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Speak Up: How Have Eating Disorders Affected You?

FitSugar — Tue, 24 Feb 2009 16:30:00 -0800

National Eating Disorders Awareness Week encourages eating disorder sufferers to get help and educates the public. Some of you are all too aware of them, whether you've personally suffered or watched someone close to you.

Part of raising awareness is speaking out. Whether it's recognizing their effects on the mind, body, and relationships or understanding recovery is possible, opening up about your story could help someone else. How have eating disorders affected you?

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National Eating Disorder Awareness Week

FitSugar — Mon, 26 Feb 2007 03:00:03 -0800

I want to make you all aware that it is National Eating Disorder Awareness Week. Eating disorders are serious issues and there are a lot of folks out there suffering. Most of us have heard of anorexia and bulimia, but MSNBC recently reported that binge eating is the most common eating disorder in the US. Just as it not easy to assume that all eating disorders are the same, it is not easy to determine the cause of eating disorders.

The National Eating Disorder Association sponsors the week of awareness, and events are held all over the nation. Check their website calendar to see if there is an event happening near you. The site has a wealth of information. Best of all the NEDA website has treatment referrals for folks at risk for eating disorders.

The theme this year for National Eating Disorder Awareness week is: "Be comfortable in your genes. Wear jeans that fit the REAL you." A sentiment we can all appreciate, especially since this is the year the dreaded "skinny jeans" become a fashion staple.

National Eating Disorders Awareness Week

FitSugar — Mon, 23 Feb 2009 03:00:00 -0800

This may not be a sunny, happy topic, but it needs to be discussed. In fact, it merits an entire week of discussion, if not more. It is National Eating Disorders Awareness Week. The eating disorders, anorexia, bulimia, and compulsive eating disorder, seem to work on a spectrum and have doubtlessly touched many of our lives. This awareness week is an important tool for reaching people who are at risk of developing an eating disorder or are already suffering from one.

The National Eating Disorders Association sponsors the week of awareness, and events are held all over the nation. Check their website calendar to see if there is an event happening near you. If you're in the NYC area, there will be a free discussion, open to the public on Feb. 28. In Seattle, on Feb. 26, there will be a walk and silent art auction.

The theme this year for National Eating Disorders Awareness week is: ". . .until eating disorders are history." The goal is to ultimately prevent eating disorders and body image issues while reducing the stigma surrounding eating disorders and improving access to treatment. The NEDA website has treatment referrals for people at risk for eating disorders.

Source

National Eating Disorders Awareness Week

FitSugar — Mon, 25 Feb 2008 02:00:00 -0800

This may not be a sunny, happy topic, but it needs to be discussed. In fact, it merits an entire week of discussion. It is National Eating Disorders Awareness Week. The eating disorders, anorexia, bulimia, and compulsive eating disorder, seem to work on a spectrum and doubtlessly touched many of our lives. This awareness week is an important tool for reaching people who are at risk of developing an eating disorder or are already suffering from one.

The National Eating Disorders Association sponsors the week of awareness, and events are held all over the nation. Check their website calendar to see if there is an event happening near you. The site has a wealth of information. Best of all, the NEDA website has treatment referrals for people at risk for eating disorders.

The theme this year for National Eating Disorders Awareness week is: "Be comfortable in your genes. Wear jeans that fit the REAL you." A sentiment we can all appreciate, especially since this is the year the dreaded "skinny jeans" became a fashion staple.

To read the inspirational poster text, just read more

Be comfortable in your genes.
Your genes play a role in determining your
body size and shape. Embrace your genes.
Stop trying to turn your body
into something it’s not.
Wear jeans that fit the TRUE you.

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Anxiety disorders

FitSugar — Wed, 08 Oct 2008 17:34:56 -0700

HEALTH GUIDE REFERENCE FROM A.D.A.M

Highlights

Drug Approval

In 2007, duloxetine (Cymbalta) was approved for treatment of generalized anxiety disorder. Duloxetine is a dual inhibitor antidepressant.

Anxiety Disorders Under-Recognized and Under-Treated

About 41% of patients with an anxiety disorder do not receive any treatment, indicates a 2007 study in the Annals of Internal Medicine. Anxiety disorders can interfere with daily functioning, and problems worsen when people have more than one type of anxiety disorder. The study’s researchers recommend that screening for anxiety become a regular part of office visits in the same way that primary care doctors screen patients for depression.

Antidepressants and Children

The benefits of antidepressants for treating pediatric anxiety disorders appear to outweigh the risks for suicide, according to a 2007 review in the Journal of the American Medical Association. Researchers also found that antidepressants did not work as well for treating obsessive compulsive disorder compared to other types of anxiety disorders. This review was the largest to date of antidepressant use in children and adolescents. Most doctors recommend cognitive behavioral therapy as the first treatment approach for childhood anxiety disorders.

Psychological Therapies for Post-Traumatic Stress Disorder

Specially designed psychotherapies -- such as trauma-focused cognitive behavioral therapy, eye movement desensitization and reprocessing, and stress management -- are the most effective therapies for patients with post-traumatic stress disorder, according to a 2007 review in the Cochrane Database.

Introduction

Fear and stress reactions are essential for human survival. They enable people to pursue important goals and to respond appropriately to danger. In a healthy individual, the stress response (fight, fright, or flight) is provoked by a genuine threat or challenge and is used as a spur for appropriate action.

An anxiety disorder, however, involves an excessive or inappropriate state of arousal characterized by feelings of apprehension, uncertainty, or fear. The word is derived from the Latin, angere, which means to choke or strangle. The anxiety response is often not attributable to a real threat. Nevertheless it can still paralyze the individual into inaction or withdrawal. An anxiety disorder persists, while a healthy response to a threat resolves, once the threat is removed.

Anxiety disorders have been classified according to the severity and duration of their symptoms and specific behavioral characteristics. Categories include:

Generalized anxiety disorder (GAD), which is long lasting and low-grade
Panic disorder, which has more dramatic symptoms
Phobias
Obsessive-compulsive disorder (OCD)
Post-traumatic stress disorder (PTSD)
Separation anxiety disorder (which is almost always seen in children)

GAD and panic disorder are the most common. Anxiety disorders are usually caused by a combination of psychological, physical, and genetic factors, and treatment is, in general, very effective.

Generalized anxiety disorder (GAD) is the most common anxiety disorder. It affects about 5% of Americans over the course of their lifetimes. It is characterized by the following:

A more-or-less constant state of worry and anxiety, which is out of proportion to the level of actual stress or threat in their lives.
This state occurs on most days for more than 6 months despite the lack of an obvious or specific stressor. (It worsens with stress, however.)
It is very difficult to control worry. For a clear diagnosis of GAD, the specific worries should be differentiated from those that would define other anxiety disorders, such as fear of panic attacks or appearing in public. Moreover, they are not obsessive like people with obsessive-compulsive disorder. (It should be noted, however, that over half of those with GAD also have another anxiety disorder or depression.)
Patients with anxiety may experience physical symptoms (such as gastrointestinal complaints) in addition to, or even in place of, mental worries. (This latter case may be more common in people from non-Western cultures such as those with Asian backgrounds.)
People with GAD tend to be unsure of themselves, overly perfectionist, and conforming.

Given these conditions, a diagnosis of GAD is confirmed if three or more of the following symptoms are present (only one for children) on most days for 6 months:

Being on edge or very restless
Feeling tired
Having difficulty with concentration
Being irritable
Having muscle tension
Experiencing disturbed sleep

Symptoms should cause significant distress and impair normal functioning and not be due to a medical condition, another mood disorder, or psychosis. It should be noted that pure GAD is uncommon. It typically occurs with other mood disorders (anxiety or depression) or substance use.

Panic disorder is characterized by periodic attacks of anxiety or terror (panic attacks). They usually last 15 - 30 minutes, although residual effects can persist much longer. The frequency and severity of acute states of anxiety determine the diagnosis. (It should be noted that panic attacks can occur in nearly every anxiety disorder, not just panic disorder. In other anxiety disorders, however, there is always a cue or specific trigger for the attack.) A diagnosis of panic disorder is made under the following conditions:

A person experiences at least two recurrent, unexpected panic attacks.
For at least a month following the attacks, the person fears that another will occur.

Symptoms of a Panic Attack. During a panic attack a person feels intense fear or discomfort with at least four or more of the following symptoms:

Rapid heart beat
Sweating
Shakiness
Shortness of breath
A choking feeling or a feeling of being smothered
Dizziness
Nausea
Feelings of unreality
Numbness
Either hot flashes or chills
Chest pain
A fear of dying
A fear of going insane

Women may be more likely than men to experience shortness of breath, nausea, and feelings of being smothered. More men than women have sweating and abdominal pain. Panic attacks that include only one or two symptoms, such as dizziness and heart pounding, are known as limited-symptom attacks. These may be either residual symptoms after a major panic attack or precursors to full-blown attacks. (It should be noted that panic attacks can also accompany other anxiety disorders, such as phobias and post-traumatic stress disorder. In such cases, however, additional characteristics differentiate these disorders from panic disorder.)

Frequency of Panic Attacks. Frequency of attacks can vary widely. Some people have frequent attacks (for example, every week) that occur for months; others may have clusters of daily attacks followed by weeks or months of remission.

Triggers of Panic Attacks. Panic attacks may occur spontaneously or in response to a particular situation. Recalling or re-experiencing even harmless circumstances surrounding an original attack may trigger subsequent panic attacks.

Phobias, manifested by overwhelming and irrational fears, are common. In most cases, people can avoid or at least endure phobic situations, but in some cases, as with agoraphobia, the anxiety associated with the feared object or situation can be incapacitating.

Agoraphobia. Agoraphobia has been somewhat misleadingly described as fear of open spaces, the term having been derived from the Greek word agora, meaning outdoor marketplace. In its severest form, agoraphobia is characterized by a paralyzing terror of being in places or situations from which the patient feels there is neither escape nor accessible help in case of an attack. (One patient described the terror of going outside as opening a door onto a landscape filled with snakes.) Consequently, people with agoraphobia confine themselves to places in which they feel safe, usually at home. The patient with agoraphobia often makes complicated plans in order to avoid confronting feared situations and places.

Social Phobia. Social phobia, also known as social anxiety disorder, is the fear of being publicly scrutinized and humiliated and is manifested by extreme shyness and discomfort in social settings. This phobia often leads people to avoid social situations and is not due to a physical or mental problem (such as stuttering, acne, or personality disorders). The incidence of social phobia is about 13% and has been termed "the neglected anxiety disorder" because it is often not properly diagnosed.

The associated symptoms vary in intensity, ranging from mild and tolerable anxiety to a full-blown panic attack. (Unlike a panic attack, however, social phobia is always directly related to a social situation.) Symptoms include sweating, shortness of breath, pounding heart, dry mouth, and tremor.

The disorder may be further categorized as generalized or specific social phobia:

Generalized social phobia is the fear of being humiliated in front of other people during nearly all social situations. People with this subtype are the most socially impaired and also the most likely to seek treatment.
Specific social phobia usually involves a phobic response to a specific event. Performance anxiety ("stage fright") is the most common specific social phobia and occurs when a person must perform in public. These patients usually feel comfortable in informal social situations.

Children with social anxiety develop symptoms in settings that include their peers, not just adults, and they may include tantrums, blushing, or not being able to speak to unfamiliar people. These children should be able to have normal social relationships with familiar people, however.

Specific Phobias. Specific phobias (formerly simple phobias) are an irrational fear of specific objects or situations. Specific phobias are among the most common medical disorders. Most cases are mild and not significant enough to require treatment.

The most common phobias are fear of animals (usually spiders, snakes, or mice), flying (pterygophobia), heights (acrophobia), water, injections, public transportation, confined spaces (claustrophobia), dentists (odontiatophobia), storms, tunnels, and bridges.

When confronting the object or situation, the phobic person experiences panicky feelings, sweating, avoidance behavior, difficulty breathing, and a rapid heartbeat. Most phobic adults are aware of the irrationality of their fear, and many endure intense anxiety rather than disclose their disorder.

Obsessive-compulsive disorder (OCD) has been described as hiccups of the mind. OCD is time-consuming, distressing, and can disrupt normal functioning. Much research suggests that a critical feature in this disorder is an overinflated sense of responsibility, in which the patient's thoughts center around possible dangers and an urgent need to do something about it.

Obsessions are recurrent or persistent mental images, thoughts, or ideas. The obsessive thoughts or images can range from mundane worries about whether one has locked a door to bizarre and frightening fantasies of behaving violently toward a loved one.
Compulsive behaviors are repetitive, rigid, and self-directed routines that are intended to prevent the manifestation of an associated obsession. Such compulsive acts might include repetitive checking for locked doors or unlit stove burners or calls to loved ones at frequent intervals to be sure they are safe. Some people are compelled to wash their hands every few minutes or to spend inordinate amounts of time cleaning their surroundings in order to subdue the fear of contagion.

Over half of OCD-sufferers have obsessive thoughts without the ritualistic compulsive behavior. Although individuals recognize that the obsessive thoughts and ritualized behavior patterns are senseless and excessive, they cannot stop them in spite of strenuous efforts to ignore or suppress the thoughts or actions. OCD often accompanies depression or other anxiety disorders. There is some evidence that the symptoms improve over time and that nearly half will eventually recover completely or have only minor symptoms.

Symptoms in children may be mistaken for behavioral problems (taking too long to do homework because of perfectionism, refusing to perform a chore because of fear of germs). Children do not usually recognize that their obsessions or compulsions are excessive.

Associated Obsessive Disorders. Certain other disorders that may be part of, or strongly associated with, the OCD spectrum include the following:

Body dysmorphic disorder (BDD). In BDD, people are obsessed with the belief that they are ugly, or part of their body is abnormally shaped.
Hypochondriasis. People who have hypochondiasis have an excessive fear of having a serious disease.
Anorexia nervosa. OCD frequently accompanies this eating disorder, where the compulsive behavior focuses on food restriction and thinness.
Trichotillomania. People with trichotillomania continually pull their hair, leaving bald patches.
Tourette syndrome. Symptoms of Tourette syndrome include jerky movements, tics, and uncontrollably uttering obscene words.

Obsessive-Compulsive Personality. OCD should not be confused with obsessive-compulsive personality, which defines certain character traits (being a perfectionist, excessively conscientious, morally rigid, or preoccupied with rules and order). These traits do not necessarily occur in people with obsessive-compulsive disorder.

Post-traumatic stress disorder (PTSD) is a severe, persistent emotional reaction to a traumatic event that severely impairs one’s life. It is classified as an anxiety disorder because of its symptoms. Not every traumatic event leads to PTSD, however. There are two criteria that must be present to qualify for a diagnosis of PTSD:

The patient must have directly experienced, witnessed, or learned of a life-threatening or seriously injurious event.
The patients' response is intense fear, helplessness, or horror. Children may behave with agitation or with disorganized behavior.

Triggering Events. PTSD is triggered by violent or traumatic events that are usually outside the normal range of human experience. There is some evidence that events most likely to trigger PTSD are those that involve deliberate and destructive behavior (murder, rape) and those that are prolonged or physically challenging. Such events include, but are not limited to, experiencing or witnessing sexual assaults, accidents, military combat, natural disasters (such as earthquakes), or unexpected deaths of loved ones. PTSD may also occur in people who have serious illness and receive aggressive treatments or who have close family members or friends with such conditions.

Symptoms of PTSD. There are three basic sets of symptoms associated with PTSD. They may begin immediately after the event or can develop up to a year afterward:

Re-experiencing. In such cases, patients persistently re-experience the trauma in at least one of the following ways: in recurrent images, thoughts, flashbacks, dreams, or feelings of distress at situations that remind them of the traumatic event. Children may engage in play, in which traumatic events are enacted repeatedly.
Avoidance. Patients may avoid reminders of the event, such as thoughts, people, or any other factors that trigger recollection. They tend to have an emotional numbness, a sense of being in a daze or of losing contact with their own identity or even external reality. They may be unable to remember important aspects of the event.
Increased Arousal. This includes symptoms of anxiety or heightened awareness of danger (sleeplessness, irritability, being easily startled, or becoming overly vigilant to unknown dangers).

To further qualify for a diagnosis of PTSD, patients must have at least one symptom in the re-experiencing category, three avoidance symptoms, and two arousal symptoms. Symptoms are chronic (3 months or more). Symptoms should also not be associated with alcohol, medications, or drugs and should not be intensifications of a pre-existing psychological disorder.

Acute Stress Disorder. Experts have identified a syndrome called acute stress disorder, in which symptoms of PTSD occur within 2 days to 4 weeks after the traumatic event. Acute stress disorder can accurately identify up to 94% of victims at risk for PTSD. Between 50 - 80% of these patients actually develop the more chronic and serious disorder. In other words, it is very sensitive for identification of those at highest danger for PTSD but less successful in determining specifically who will or will not recover emotionally.

Long-Term Outlook. The long-term impact of a traumatic event is uncertain. In one study of people who survived a mass killing spree in Texas, less than half of those who suffered PTSD (28% of all survivors) had recovered after a year. In another study, PTSD became chronic in 46% of the subjects. In fact, PTSD may cause physical changes in the brain, and in some cases the disorder can last a lifetime.

Separation anxiety disorder almost always occurs in children. It is suspected in children who are excessively anxious about separation from important family members or from home. For a diagnosis of separation anxiety disorder, the child should also exhibit at least three of the following symptoms for at least 4 weeks:

Extreme distress from either anticipating or actually being away from home or being separated from a parent or other loved one
Extreme worry about losing or about possible harm befalling a loved one
Intense worry about getting lost, being kidnapped, or otherwise separated from loved ones
Frequent refusal to go to school or to sleep away from home
Physical symptoms such as headache, stomach ache, or even vomiting, when faced with separation from loved ones

Separation anxiety often disappears as the child grows older, but if not addressed, it may lead to panic disorder, agoraphobia, or combinations of anxiety disorders.

Studies suggest that an imbalance of certain substances called neurotransmitters (chemical messengers in the brain) may contribute to anxiety disorders. The neurotransmitters targeted in anxiety disorders are gamma-aminobutyric acid (GABA), serotonin, dopamine, and epinephrine. Serotonin appears to be specifically important in feelings of well-being, and deficiencies are highly related to anxiety and depression.

Examples of study findings on some neurotransmitters are:

Abnormalities in the neurotransmitters gamma-aminobutyric acid (GABA) and serotonin may have a particular role in susceptibility to generalized anxiety disorder. GABA helps prevent nerve cells from over-firing and serotonin is a brain chemical important in feelings of well-being.
Serotonin is a major player in OCD.
Changes in serotonin and dopamine have been observed in social phobia.
People with post-traumatic stress disorder have abnormalities in stress hormones (cortisol) and neurotransmitters associated with stress (epinephrine and norepinephrine). Such imbalances could account for the higher anxiety levels and a tendency to startle easily after a threat in people with PTSD.
Corticotropin-releasing factor (CRF), which is believed to be a stress hormone and a neurotransmitter, is thought to be involved in depression and anxiety by causing changes in serotonin levels.

The best way to envision the brain's response to a threat is to imagine a primal situation, such as being chased by a bear.

The Brain's Response to Acute Stress. In response to seeing the bear, a part of the brain called the hypothalamic-pituitary-adrenal (HPA) system is activated.

Release of Steroid Hormones and the Stress Hormone Cortisol. The HPA systems trigger the production and release of steroid hormones (glucocorticoids), including the primary stress hormone cortisol. Cortisol is very important in marshaling systems throughout the body (including the heart, lungs, circulation, metabolism, immune systems, and skin) to deal quickly with the bear.

Release of Catecholamines and Activation of the Amygdala. The HPA system also releases certain neurotransmitters (chemical messengers) called catecholamines, particularly those known as dopamine, norepinephrine, and epinephrine (also called adrenaline).

Catecholamines activate the amygdala, a small structure deep in the brain, which regulates control of major emotional activities, including anxiety, depression, aggression, and affection. In fact, the amygdala is sometimes known as the "fear" center.

Effects on Long- and Short-Term Memory. During the stressful event, catecholamines also suppress activity in areas at the front of the brain concerned with short-term memory, concentration, inhibition, and rational thought. This sequence of mental events allows a person to react quickly to the bear, either to fight or to flee from it. (It also hinders the ability to handle complex social or intellectual tasks and behaviors during that time.)

On the other hand, neurotransmitters at the same time signal the hippocampus (a nearby area in the brain) to store the emotionally loaded experience in long-term memory. In primitive times, this brain action would have been essential for survival, since long-lasting memories of dangerous stimuli (the large bear) would be critical for avoiding such threats in the future.

Response by the Heart, Lungs, and Circulation to Acute Stress. The stress response also affects the heart, lungs, and circulation:

As the bear comes closer, the heart rate and blood pressure increase instantaneously.
Breathing becomes rapid and the lungs take in more oxygen.
The spleen discharges red and white blood cells, allowing the blood to transport more oxygen throughout the body. Blood flow may actually increase 300 - 400%, priming the muscles, lungs, and brain for added demands.

The Immune System's Response to Acute Stress. The effect on the immune system from confrontation with the bear is similar to marshaling a defensive line of soldiers to potentially critical areas. The steroid hormones dampen parts of the immune system, so that specific infection fighters (including important white blood cells) or other immune molecules can be redistributed. These immune-boosting troops are sent to the body’s front lines where injury or infection is most likely, such as the skin, the bone marrow, and the lymph nodes.

The Acute Response in the Mouth and Throat. As the bear gets closer, fluids are diverted from nonessential locations, including the mouth. This causes dryness and difficulty in talking. In addition, stress can cause spasms of the throat muscles, making it difficult to swallow.

The Skin's Response to Acute Stress. The stress effect diverts blood flow away from the skin to support the heart and muscle tissues. (This also reduces blood loss in the event that the bear catches up.) The physical effect is a cool, clammy, sweaty skin. The scalp also tightens so that the hair seems to stand up.

Metabolic Response to Acute Stress. Stress shuts down digestive activity, a nonessential body function during short-term periods of physical exertion or crisis.

The Relaxation Response: the Resolution of Acute Stress. Once the threat has passed and the effect has not been harmful (the bear has not eaten or seriously wounded the human), the stress hormones return to normal. This is known as the relaxation response. In turn, the body's systems also normalize.

Causes

A person's genetics, biochemistry, environment, history, and psychological profile all seem to contribute to the development of anxiety disorders. Most people with these disorders seem to have a biological vulnerability to stress, making them more susceptible to environmental stimuli than the rest of the population.

Abnormalities in the Brain. Scientists are using imaging techniques, particularly magnetic resonance imaging (MRI), to identify different areas of the brain associated with anxiety responses.

An MRI (magnetic resonance imaging) of the brain creates a detailed image of the complex structures in the brain. An MRI can give a three-dimensional depiction of the brain, making location of problems such as tumors or aneurysms more precise.

Important research in anxiety disorders is focusing on changes in the amygdala, which is sometimes referred to as the "fear center." This part of the brain regulates fear, memory, and emotion and coordinates these resources with heart rate, blood pressure, and other physical responses to stressful events. Some evidence suggests that the amygdala in people with anxiety disorders is highly sensitive to novel or unfamiliar situations and reacts with a high stress response.

Obsessive-compulsive disorder (OCD) is the anxiety disorder most strongly associated with specific brain dysfunction. For example, abnormalities in a specific pathway of nerves have been linked to OCD, attention deficit disorder, and Tourette syndrome. The symptoms of the three disorders are similar and they often coexist.

A number of imaging studies have reported less volume in the hippocampus in people with post-traumatic stress disorder. This important region is related to emotion and memory storage.

The influence of the family on anxiety is complicated by both genetic and psychological factors.

Panic Disorder and Family Influence. Certain psychodynamic theories suggest, and a few studies support the idea, that some people may develop panic disorder if they cannot resolve the early childhood conflict of dependence vs. independence. In one study, for example, young adults who had experienced childhood anxiety were more likely to live with their parents until their early to mid-twenties. Many people with panic disorder perceive their parents as being extremely controlling and overly protective while showing little actual affection.

Phobias and Family Influence. Several studies show a strong correlation between a parent's fears and those of the offspring. Although an inherited trait may be present, some researchers believe that many children can "learn" fears and phobias, just by observing a parent or loved one's phobic or fearful reaction to an event. People who have social phobias and severe agoraphobia generally report less parental affection and more strictness, overprotection, and encouragement of dependence than those without these disorders.

Obsessive-Compulsive Disorder and Family Influence. One study found that parental influence played no part in obsessive-compulsive disorder if the OCD patient was also not suffering from depression. However, depression coexists in two-thirds of OCD patients, and in the study patients who had both OCD and depression reported lower levels of parental care and overprotectiveness.

Traumatic events generally trigger anxiety disorders in individuals who are susceptible to them because of psychological, genetic, or biochemical factors. The clearest example is post-traumatic stress disorder. Specific traumatic events in childhood, particularly those that threaten family integrity, such as spousal or child abuse, can also lead to other anxiety and emotional disorders. Some individuals may even have a biological propensity for specific phobias, for instance of spiders or snakes, that have been triggered and perpetuated after a single exposure.

The acronym PANDAS (Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcus) is a term for an autoimmune condition associated with group A streptococcal infection in children (the cause of "strep throat" and rheumatic fever). Children with PANDAS develop tic-related disorders, including OCD and Tourette syndrome. In such cases, the OCD symptoms develop abruptly soon after the infection. It is unlikely to be an important cause of OCD.

Risk Factors

As many as 25% of all American adults experience intense anxiety sometime in their lives. The prevalence of true anxiety disorders is much lower, although they are still the most common psychiatric conditions in the United States and affect more than 20 million Americans.

Gender. With the exception of obsessive-compulsive disorder (OCD), women have twice the risk for most anxiety disorders as men. A number of factors may increase the reported risk in women, including cultural pressures to meet everyone else's needs except their own, and fewer self-restrictions on reporting anxiety to doctors.

Age. In general, phobias, OCD and separation anxiety show up early in childhood, while social phobia and panic disorder are often diagnosed during the teen years. Studies suggest that 3 - 5% of children and adolescents have some anxiety disorder. Children and adolescents who have an anxiety disorder are at risk of later developing other anxiety disorders, depression, and substance abuse.

Personality Factors. Children's personalities may indicate higher or lower risk for future anxiety disorders. For example, research suggests that extremely shy children and those likely to be the target of bullies are at higher risk for developing anxiety disorders later in life. Children who cannot tolerate uncertainty tend to be worriers, a major predictor of generalized anxiety. In fact, such traits may be biologically based and due to a hypersensitive amygdala -- the "fear center" in the brain.

Family History and Dynamics. Anxiety disorders tend to run in families. Genetic factors may play a role in some cases, but family dynamics and psychological influences are also often at work.

Social Factors. Several studies have reported a significant increase in anxiety levels in children and college students in the past two decades compared to children in the 1950s. In several studies, anxiety was associated with a lack of social connections and a sense of a more threatening environment. It also appears that more socially alienated populations have higher levels of anxiety. For example, a study of Mexican adults living in California reported that native-born Mexican Americans were three times more likely to have anxiety disorders (and even more likely to be depressed) as those who had recently immigrated to the U.S. The longer the immigrants lived in the U.S., the greater their risk for psychiatric problems. Traditional Mexican cultural and social ties seemed to protect recently arrived immigrants from mental illness.

Genetic Factors. Up to 50% of people with panic disorder and 40% of patients with generalized anxiety (GAD) have close relatives with the disorder. (About half of GAD patients also have family members with panic disorder, and about 30% have relatives with simple phobias.)

Obsessive-compulsive disorder (OCD) is also strongly related to a family history of the disorder. Close relatives of people with OCD are up to 9 times more likely to develop OCD themselves. Researchers are making progress in identifying specific genetic factors that might contribute to an inherited risk. Of particular interest are genes that regulate specific neurotransmitters (brain chemical messengers), including serotonin and glutamate. Recent research has suggested that the SLC1A1 gene, which is associated with glutamate regulation, may play an important role in early-onset OCD in boys. Research is also beginning to pinpoint regions on specific chromosomes (1, 3, 7, 6, 9, 15) that may contain genes linked to OCD.

However, there are no genetic tests to date that can identify patients at risk for anxiety disorders.

Medical Conditions. Although no causal relationships have been established, certain medical conditions have been associated with panic disorder. They include migraines, obstructive sleep apnea, mitral valve prolapse, irritable bowel syndrome, chronic fatigue syndrome, and premenstrual syndrome.

GAD affects about 1 - 5% of Americans in the course of their lives and is more common in women than in men. Some experts believe that it is underdiagnosed and more common than any other anxiety disorder. It is certainly the most common anxiety disorder among the elderly. GAD usually begins in childhood and often becomes a chronic ailment, particularly when left untreated. Depression in adolescence may be a strong predictor of GAD in adulthood. Depression commonly accompanies this anxiety disorder in any case.

Age and Panic Disorder. Studies indicate that the prevalence of panic disorder among adults is between 1.6 - 2% and is much higher in adolescence, 3.5 - 9%. Panic disorder usually first occurs either in late adolescence or in the mid-30s.

Gender and Panic Disorder. Women have about twice the risk for panic disorder as men. Panic attacks are very common after menopause. In one study, nearly 18% of older women reported panic attacks within a 6-month period, with over half of these attacks being full-blown. They tended to be associated with stressful life events and poor health. The effects of pregnancy on panic disorder appear to be mixed. It seems to improve the condition in some women and worsen it in others.

Obsessive-compulsive disorder occurs equally in men and women, and it affects about 2 - 3% of people over a lifespan. Most cases of OCD first develop in childhood or adolescence, although the disorder can occur throughout the life span.

Social anxiety disorder is currently estimated to be the third most common psychiatric disorder in the U.S. Studies have reported a prevalence of 7 - 12% in Western nations.

Age and Phobias. The onset of social anxiety disorder is usually during the early teenage years.

Gender and Phobias. Women are more likely to develop social anxiety disorder than men, although equal numbers of men and women seek treatment for it. Most people seeking treatment have had symptoms for at least 10 years.

Studies estimate a lifetime risk for PTSD in the U.S. of up to 8%. People exposed to traumatic events, of course, are at highest risk, but many people can go through such events and not experience PTSD. Studies estimate that 6 - 30% or more of trauma survivors develop PTSD, with children and young people being among those at the high end of the range. Women have the twice the risk of PTSD as men.

Furthermore, PTSD can occur in people not directly involved with a traumatic event. For example, 17% of the U.S. population outside New York City reported some symptoms of post-traumatic stress 2 months after the September 11 attack on the World Trade Towers. (In the city itself, where the attack occurred, an estimated 7.5% of New York's population reported PTSD within the month of the event, which declined to 0.6% at 6 months.)

Researchers are trying to determine factors that might increase vulnerability to catastrophic events and put people at risk for develop PTSD. Some studies report the following may be risk factors:

Pre-existing emotional disorder. People who have a history of an emotional disorder, particularly depression, before the traumatic event are at higher risk for PTSD.
Drug or alcohol abuse
A family history of anxiety
A history of abuse, particularly that which threatens family integrity, such as spousal or child abuse. Studies of individuals who had suffered physical or sexual abuse or neglect as children suggest that up to one-third develop PTSD.
An early separation from parents
Lack of social support and poverty
Sleep disorders. Insomnia and excessive daytime sleepiness even within a month after a traumatic event are important predictors for the development of PTSD. One specific sleep disorder -- sleep apnea -- may even intensify symptoms of PTSD, including sleeplessness and nightmares. Sleep apnea occurs when tissues in the upper throat (or airway) collapse at intervals during sleep, thereby blocking the passage of air. In one study, 91% of crime victims with PTSD had either sleep apnea or a lesser condition that partially blocked the airways during sleep. In fact, in one study treatment of sleep apnea eased PTSD. Sleep apnea has also been associated with a risk for panic disorder. [For more information, see In-Depth Report #65: Sleep apnea.]

Complications

Studies consistently report that all types of anxiety disorders can be very debilitating and seriously affect a person’s quality of life.

Depression. Depression is very common in people with an anxiety disorder, and it is sometimes difficult to distinguish one from the other because either or both can be accompanied by anxious feelings, agitation, insomnia, and problems with concentration.

Depression and nearly every anxiety disorder often go hand in hand, in both the young and old. In fact, the lifetime risk for depression in people with anxiety disorders may be higher than 70%. Furthermore, the combination of depression and anxiety is a major risk factor for both substance abuse and suicide. The following are examples of depression in specific anxiety disorders:

Between 50 - 65% of people with panic disorder also have major depression. Some studies have suggested that treating panic disorder early enough may help prevent major depression later on.
More than two-thirds of OCD patients suffer from depression.
Most patients with GAD will experience at least one episode of significant depression and many develop recurrent episodes. In patients with both disorders, GAD usually precedes the onset of depression.
Social anxiety during adolescence or young adulthood has been associated with a higher risk for depression, and the presence of both increases the chances for severe depression.
People with PTSD are four to seven times as likely to be depressed as are people without PTSD.

Bipolar Disorder. Symptoms of panic disorder are very common in people with bipolar disorder (manic-depression). In fact, people with bipolar have 26 times the rate of panic disorder as in the general population. Furthermore, anxiety worsens bipolar disorder. According to one study, anxiety disorders in teenagers were associated with bipolar disorder in adulthood, while manic behavior in adolescence was linked to later anxiety disorders.

Evidence now strongly supports an association between panic disorder and a risk for suicidal thoughts. Studies report that up to 18% of people with panic disorder attempt suicide and up to 38.5% regularly harbor suicidal thoughts, with the risks being higher in people with both panic disorder and depression. One study reported suicide attempts in about 12% of people with social phobias or OCD. If a person has an anxiety disorder and a mood disorders (such as depression), the risk for suicide is even higher.

Suicide is the third most common cause of death among adolescents, and is one of the most devastating events than can happen to a family. Suicide is most commonly associated with depression in young people, but it is also commonly associated with anxiety, psychosis, substance abuse, or impulsivity. More girls attempt suicide but more boys succeed, most often because they choose guns or violent methods while girls tend to overdose, which is more treatable. Nevertheless, unsuccessful attempts are major risk factors for a later suicide. Any expression of suicidal intent should be treated very seriously.

The following are danger signs in young people:

Withdrawal from friends
Sudden decrease in school performance
Loss of interest in activities that were previously pleasurable
Unusual irritability
Unusual changes in sleep or eating habits

Risk factors for suicide include a history of neglect or abuse, history of deliberate self-harm, a family member who committed suicide (nearly always one who shared a common mood disorder), access to firearms, and living in communities where there have been recent outbreaks of suicide in young people. A romantic break-up is often the trigger for a suicidal attempt in teenagers. Feeling connected with parents and family protected young people with depression in one study, regardless of gender or ethnicity.

In one study, adolescents failed to seek help for suicidal thoughts for the following reasons:

They believed nothing would help.
They were reluctant to tell anyone they had problems.
They thought it was a sign of weakness to seek help.
They did not know where to go.

Parents should not hesitate to seek professional help for their children if they suspect they are thinking about killing themselves. This is a medical emergency and requires immediate treatment.

[For more information on suicide, see In-Depth Report #8: Depression.]

Severely depressed or anxious people are at high risk for alcoholism, smoking, and other forms of addiction. Anxiety disorders are highly prevalent among people with alcoholism. Moreover, long-term alcohol use can itself cause biologic changes that may actually produce anxiety and depression.

Risk for Substance Abuse in Specific Anxiety Disorders. The following are some observations on specific anxiety disorders and substance abuse:

Some people with GAD and panic disorders may use alcohol or drugs to self-medicate.
Social phobia appears to pose a particular risk for alcohol abuse. People with this disorder are likely to drink in order to boost confidence. Alcohol itself has no direct beneficial effect on anxiety, but studies suggest that the belief in its effect appears to relieve anxious feelings. (Alcohol or substance abuse is not associated with specific phobias -- such as a fear of flying or spiders.)
Heavy smoking and substance abuse are common in people with PTSD. In adolescents, the disorder not only increases the risk for drug and alcohol use but also for eating disorders.

Studies consistently report that anxiety disorders have negative effects on work and relationships. Some examples:

In one study, more than 10% of patients with GAD missed at least 6 days of work within the previous month.
In a survey of OCD sufferers, 40% reported that they had to stop working because of the disorder. Only 40% worked full-time, while only half were married.
A 2006 study indicated that children with OCD are more likely to be bullied than other children.
Studies report that people with social phobias are less likely to get married, to leave home, and to finish school than those without this disorder. Their outlook worsens if they have other emotional disorders.

Anxiety disorders are associated with many different physical illnesses. Research suggests that people who have both an anxiety disorder and a physical illness have a worse quality of life and greater risk for disability than those who have only a physical illness. Anxiety disorders often tend to occur before the development of physical disorders.

Heart Disease. Anxiety has been associated with several heart problems, including unhealthy cholesterol levels, thicker blood vessels, and high blood pressure. Both anxiety and depression have been associated with a poorer response to treatment in heart patients, including a worse outcome after heart surgery.

Cholesterol is a soft, waxy substance that is present in all parts of the body including the nervous system, skin, muscle, liver, intestines, and heart. It is made by the body and obtained from animal products in the diet. Cholesterol is manufactured in the liver and is needed for normal body functions including the production of hormones, bile acid, and vitamin D. Excessive cholesterol in the blood contributes to atherosclerosis and subsequent heart disease. The risk of developing heart disease or atherosclerosis increases as the level of blood cholesterol increases.

Some researchers speculate that intense anxiety might trigger abnormal and dangerous heart rhythms in people with existing heart problems. In other studies, panic disorders, post-traumatic stress disorder, and phobias have been associated with a higher rate of sudden death from cardiac events, including heart attack.

Gastrointestinal Disorders. Anxiety frequently accompanies gastrointestinal conditions. Of note, half the cases of irritable bowel syndrome are associated with anxiety.

Headache. Both tension and migraine headaches are associated with anxiety disorders. One study reported that 32% of people with chronic tension headaches met criteria for anxiety. Similarly, another study reported that young girls with anxiety disorders were three times more likely to have chronic headaches than those without the disorder. (Headaches in both studies were also strongly associated with depression.)

Respiratory Problems. Studies report an association between anxiety in patients with obstructive lung conditions (asthma, emphysema, and chronic bronchitis) and more frequent relapses.

Obesity. Anxiety disorders may lead to obesity, and the reverse may also be true. A 2006 study suggested that anxiety disorders and depression in childhood may lead to higher body mass index (BMI) in adult women (but not men). Another 2006 study indicated that obesity is associated with a 25% increased risk of developing anxiety and mood disorders.

Allergic Conditions. Anxiety disorders are associated with numerous allergic conditions including hay fever, eczema, hives, food allergies, and conjunctivitis.

Other Conditions. Other physical conditions associated with anxiety disorders include thyroid problems and arthritis.

People with obsessive-compulsive disorders can experience skin problems from excessive washing, injuries from repetitive physical acts, and hair loss from repeated hair pulling (behavior known as trichotillomania).

Effect of PTSD on the Brain. Studies are reporting that PTSD is associated with shrinkage in the hippocampus, the part of the brain important for memory and learning. Some animal studies indicate that such damage may result from long-term exposure to cortisol, the major stress hormone. In one study, people who had suffered severe trauma scored 40% lower in tests of verbal memory than did the general population. There was no difference in IQ or in scores of other types of memory. Some studies suggest that exposure to chronic stress, common in PTSD patients, may even compromise the function of the brain’s receptors for anti-anxiety medication. On the other hand, a small hippocampal volume may itself increase stress hormone levels, so people with genetically smaller hippocampi may be susceptible to PTSD.

Effects of PTSD on Health. Studies of military veterans who have endured major traumatic events have found a higher risk for health problems. One study of Vietnam veterans reported that PTSD was associated with greater physical limitations, poorer physical health, and a lower quality of life than was found in the general population, regardless of other accompanying emotional or medical disorders. In another study of these veterans, PTSD sufferers had twice the risk for abnormal heart rhythms and four times the risk of a heart attack compared to men without PTSD.

Evidence suggests an association between anxiety in children and recurrent stomach aches. Anxiety has been associated with a higher risk for sleep disorders in children, such as frequent nightmares, restless legs syndrome, and bruxism (grinding and gnashing of the teeth during sleep).

Diagnosis

A physical examination and medical and personal history is essential. Because anxiety accompanies so many medical conditions, some serious, it is extremely important for the doctor to uncover any medical problems or medications that might underlie or be masked by an anxiety attack.

The patient should describe any occurrence of anxiety disorders or depression in the family and mention any other contributing factors, such as excessive caffeine use, recent life changes, or stressful events.

It is very important to be honest with your doctor about all conditions, including excessive drinking, substance abuse, or other psychological or mood states that might contribute to, or result from, the anxiety disorder.

Diagnosing children with an anxiety disorder can be very difficult, since anxiety often results in disruptive behaviors that overlap with attention-deficit hyperactivity or oppositional disorder. Other conditions with symptoms similar to anxiety disorders include pervasive developmental disorders such Asperger syndrome, learning disabilities, bipolar disorder, and depression. Many children have anxiety disorder and a co-occurring condition, which should be treated along with anxiety.

People with anxiety disorders are more likely to see a family doctor before a mental health specialist, since their symptoms are often physical. Symptoms can include muscle tension, trembling, twitching, aching, soreness, cold and clammy hands, dry mouth, sweating, nausea or diarrhea, or urinary frequency. Anxiety attacks can mimic or accompany nearly every acute disorder of the heart or lungs, including heart attacks and angina (chest pain). In fact, nearly all individuals with panic disorders are convinced that their symptoms are physical and possibly life-threatening.

Heart Problems. Studies suggest that up to a third of patients entering the emergency room with chest pain and who are low-to-moderate risk for a heart attack are actually suffering from panic attacks. It is often difficult even for specialists to distinguish between heart conditions and a panic attack:

Women who are having an actual heart attack or acute heart problem are much more likely to be misdiagnosed as having an anxiety attack than are men with similar symptoms.
Mitral valve prolapse, a common and usually mild heart problem, may have symptoms that are nearly identical to those of panic disorder. The two conditions, in fact, frequently occur together.

Mitral valve prolapse is a disorder in which the mitral valve does not close properly when the heart contracts. When the valve does not close properly it allows blood to backflow into the left atrium. Some symptoms can include palpitations, chest pain, difficulty breathing after exertion, fatigue, cough, and shortness of breath while lying down.

People with a heart-rhythm disturbance called paroxysmal supraventricular tachycardia have many of the same symptoms as those with panic attacks.

Asthma. Asthma attacks and panic attacks have similar symptoms and can also coexist.

Hyperthyroidism. Hyperthyroidism can cause many of the same symptoms of generalized anxiety disorder and must be ruled out.

Click the icon to see an image of hyperthyroidism.

Epilepsy. The symptoms of partial seizures and panic attacks often overlap.

Other Medical Conditions. In addition, anxiety-like symptoms are seen in many other medical problems, including hypoglycemia, recurrent pulmonary emboli, and adrenal-gland tumors. Women can also experience intense anxiety attacks with hot flashes during menopause.

Medication Side Effects. Many drugs, including some for high blood pressure, diabetes, and thyroid disorders, can produce symptoms of anxiety. Withdrawal from certain drugs, often those used to treat sleep disorders or anxiety, can also precipitate anxiety reactions.

Substance Abuse. People with anxiety disorders often drink alcohol or abuse drugs in order to conceal or eliminate symptoms, but substance abuse and dependency can also cause anxiety. In addition, withdrawal from alcohol can produce physiologic symptoms similar to panic attacks. Clinicians often have difficulty determining whether alcoholism or anxiety is the primary disorder. Overuse of caffeine or abuse of amphetamines can cause symptoms resembling a panic attack.

Clinicians use various screening tests to determine the causes, type, severity, and frequency of anxiety. Such tests include the Hamilton Anxiety Rating Scale, the Beck Anxiety Inventory, the Penn State Worry Questionnaire, and the Yale-Brown Obsessive Compulsive Scale.

Treatment

Anxiety disorders require treatment. Simply trying to talk oneself out of anxiety is as futile as trying to talk oneself out of a heart or stomach problem. Most anxiety disorders, especially phobias, respond well to treatment. They may, however, require long-term treatment. Many patients have a recurrence and may require additional medications. Nevertheless, most patients do not receive appropriate care for anxiety disorders. Many patients do not receive any treatment at all.

The standard current approach to most anxiety disorders is a combination of cognitive-behavioral therapy (CBT) and an antidepressant medication. A selective serotonin reuptake inhibitor (SSRI) is typically the first choice, with the serotonin-norepinephrine reuptake inhibitor (SNRI) venlafaxine (Effexor) an alternative. If patients do not respond to these drugs, tricyclic antidepressants or monoamine oxidase inhibitors (MAOIs) may be helpful. Benzodiazepines may be recommended for patients who are not helped by antidepressants. A healthy lifestyle that includes exercise, adequate rest, and good nutrition can also help to reduce the impact of anxiety.


Anxiety Disorder	Medications	Cognitive-Behavioral Therapy (CBT) and other Non-Drug Therapies
Generalized Anxiety Disorder	Antidepressants, benzodiazepines, and buspirone are helpful but have varying side effects. Investigational drugs include pregabalin and other anticonvulsants.	Cognitive-behavioral therapy or anxiety management therapy. Anxiety management therapy involves education, relaxation training, and exposure to anxiety-provoking stimuli but does not include cognitive restructuring.
Panic Attacks	SSRIs are treatment of choice. If patients do not respond to SSRIs, short-term treatment with a benzodiazepine may be used, or patients may switch to another type of antidepressant such as venlafaxine or tricyclics.	Cognitive-behavioral therapy, provided in 12 - 16 sessions over 3 - 4 months, focuses on recreating fear symptoms and helping patients change their response to them.
Social Anxiety Disorder	SSRIs or venlafaxine are first-line drug treatments. Benzodiazepines may help patients who do not respond to these antidepressants. In severe cases, an MAOI antidepressant may be prescribed. Anticonvulsants such as gabapentin (Neurontin) and pregabalin (Lyrica) are being investigated.	Cognitive-behavioral therapy can help improve symptoms after 6 - 12 weeks.
Obsessive-Compulsive Disorder	SSRIs are the first choice for adults. Clomipramine (a tricyclic antidepressant) is an alternative for adult patients who do not respond to SSRIs. For children, SSRIs do not seem to work as well for OCD as for other types of anxiety disorders.	Cognitive-behavioral therapy is the first treatment choice for children. For adults, either CBT or drug therapy may be offered as initial treatment. CBT techniques focus on exposure and response prevention (ERP).
Post-Traumatic Stress Disorder	Antidepressants, particularly SSRIs (sertraline and paroxetine approved for PTSD). The atypical antipsychotic olanzapine may be added to an antidepressant for patients who do not respond to a SSRI alone.	Trauma-focused psychological treatments include exposure therapy, trauma-focused cognitive therapy, and eye movement desensitization and reprocessing.
Note: For anxiety disorders in adults, the most effective treatments are usually combinations of drugs and CBT techniques. For children, CBT is usually the first treatment.

Medications

Selective serotonin-reuptake inhibitors (SSRIs), or the serotonin-norepinephrine reuptake inhibitor (SNRI) venlafaxine (Effexor), are the primary first-line treatment for anxiety disorders. For patients who are not helped by these drugs, benzodiazepines, either alone or in combination with an antidepressant, may be prescribed. Other types of antidepressants, including tricyclic antidepressants and monoamine oxidase inhibitors (MAOIs), may also be used to treat patients with severe or chronic forms of anxiety disorders.

Drug therapies for anxiety disorders work best in combination with cognitive behavioral therapy.

Selective Serotonin Reuptake Inhibitors (SSRIs). SSRIs include fluoxetine (Prozac), sertraline (Zoloft), paroxetine (Paxil), fluvoxamine (Luvox), citalopram (Celexa), and escitalopram (Lexapro).

SSRIs can cause agitation, nausea, and diarrhea. Sexual function side effects include low sex drive, inability to have an orgasm, and impotence. Over time, many SSRI-treated patients gain weight, although the degree of weight gain varies depending on the drug. Elderly people taking these drugs should take the lowest effective dose possible, and those with heart problems should be monitored closely.

There have been many concerns about SSRIs and increased risk for suicidal behavior. Both adults and children who are treated with SSRIs should be carefully monitored for any worsening of depressive symptoms or changes in behavior. This is especially important during the first few months of antidepressant treatment.

Paroxetine has been linked to heart-related birth defects when women took this drug during the first trimester of pregnancy. Experts are also advising caution in prescribing other types of SSRIs to pregnant women. While certain SSRIs may carry increased risks for some specific type of rare birth defects, research suggests that the overall risks are minimal. Still, women who are pregnant or who are considering becoming pregnant should discuss the potential risks of these drugs with their doctors.

Serotonin-norepinephrine reuptake inhibitors (SNRIs). SNRIs are known as dual inhibitors because they work on two neurotransmitters -- norepinephrine and serotonin. Venlafaxine (Effexor) is an SNRI that is approved for treatment of generalized anxiety disorder, social anxiety disorder, and panic disorder in adults. (It is not approved for children.) As with many SSRIs, venlafaxine impairs sexual function. Venlafaxine can increase blood pressure and heart rate and should be used with caution in patients with high blood pressure or heart disease. Some patients report severe withdrawal symptoms, including dizziness and nausea. This drug has a serious risk for overdose. Venlafaxine should not be taken during the last trimester of pregnancy because the drug can cause complications in newborn infants.

Duloxetine (Cymbalta) also acts on both serotonin and norepinephrine. In 2007, it was approved for treatment of generalized anxiety disorder. Side effects are generally mild and include dry mouth, nausea, and sleepiness. Patients with narrow-angle glaucoma or patients with liver or kidney diseases should not take duloxetine. Because duloxetine can cause liver damage, patients who drink large quantities of alcoholic beverages should not take it.

Mitrazapine (Remeron) is another type of SNRI that is sometimes used for treatment of post-traumatic stress disorder and social anxiety disorder.

Tricyclic Antidepressants. Tricyclics are an older type of antidepressant. Tricyclics used for treatment of anxiety disorder include imipramine (Tofranil, for generalized anxiety disorder, panic disorder), nortriptyline (Pamelor, for panic disorder), desipramine (Norpramin, for panic disorder), and clomipramine (Anafranil, for obsessive compulsive disorder). Clomipramine is approved specifically for OCD, but because of its severe side effects it is usually used only if SSRIs have failed to help.

Side effects of TCAs include sleep disturbance, abrupt reduction in blood pressure upon standing, weight gain, sexual dysfunction, and mental disturbance. Elderly patients and those with a history of seizures, cardiac problems, closed-angle glaucoma, and urinary retention or obstruction should be closely supervised when taking tricyclics.

Monoamine Oxidase Inhibitors. Monoamine oxidase inhibitors (MAOIs) are the oldest type of antidepressant. The MAOI phenelzine (Nardil) is sometimes used to treat social anxiety disorder or post-traumatic stress disorder that has not responded to other treatments.

MAOIs commonly cause weight gain, drowsiness, dizziness, sexual dysfunction, and insomnia. Dietary restrictions are the main problem with these drugs. Severe high blood pressure (hypertension) can be brought on by eating certain foods that have a high tyramine content, including cheese, red wine, and processed meats. High blood pressure can also occur when MAOIs are taken with certain drugs, including some common over-the-counter cough medications and decongestants. MAOIs can cause birth defects and should not be taken by pregnant women.

Most serious, fatal reactions can occur when MAOIs and SSRIs or venlafaxine are taken at the same time. There should be at least a 2- to 5-week break if a patient is changing from one type of antidepressant to the other.

Benzodiazepines are safe and effective medications for most anxiety disorders and have been the standard of treatment for years. However, their on-going use has been associated with a high risk for dependency and abuse. Therefore, they have been supplanted in most cases by SSRIs and other newer antidepressants. For anxiety disorders, benzodiazepines are most often used to treat panic disorder, and are sometimes used for social anxiety disorder and generalized anxiety disorder. These drugs include alprazolam (Xanax), clonazepam (Klonopin), and lorazepam (Ativan).

Benzodiazepines have many side effects, generally associated with chronic use. The most common are daytime drowsiness and a hung-over feeling. In rare cases, they can cause agitation. They may worsen respiratory problems. Benzodiazepines are potentially dangerous when used in combination with alcohol. Overdoses can be serious, although they are very rarely fatal.

The elderly are more susceptible to side effects and should usually start at half the dose prescribed for younger people. These drugs increase the risk of falling, which can increase the risk for hip fracture in older people. Also of concern are studies showing a high risk of automobile accidents in people who take benzodiazepines. Benzodiazepines taken during pregnancy are associated with birth defects, and they should not be used by pregnant women or by nursing mothers.

Loss of Effectiveness and Dependence. Eventually these drugs can lose their effectiveness with continued use at the same dosage. As a result, patients may want to increase their dosage to prevent anxiety. This causes dependency, which can occur after taking these drugs for several weeks.

Withdrawal and its Treatments. Withdrawal symptoms can be very severe, even in people who rapidly discontinue benzodiazepines after taking them for only 4 weeks. Symptoms include sleep disturbance and anxiety, which can develop within hours or days after stopping the medication. Some patients experience stomach distress, sweating, and insomnia, which can last 1 - 3 weeks. The longer the drugs are taken and the higher their dose, the more severe these symptoms can become. Simply tapering off gradually helps about 60% of people stop taking these drugs. Certain medications (anti-seizure drugs, antidepressants, buspirone) may also help with withdrawal.

Azapirones, such as buspirone (BuSpar), act on serotonin receptors called 5-HT(1A). Buspirone appears to work as well as a benzodiazepine for treating generalized anxiety disorder. It usually takes several days to weeks for the drug to be fully effective. It is not useful against panic attacks.

Buspirone does not produce any immediate euphoria or change in sensation, so some people believe, erroneously, that the drug doesn't work. Such qualities result in a very low potential for abuse. In fact, unlike the benzodiazepines, buspirone is not addictive, even with long-term use, so it may be particularly useful for the patient whose anxiety disorder coexists with alcoholism or drug abuse.

Buspirone also seems to have less pronounced side effects than benzodiazepines and no withdrawal effects, even when the drug is discontinued quickly. Common side effects include dizziness, drowsiness, and nausea. Buspirone should not be used with monoamine oxidase inhibitors (MAOIs).

Beta-blockers, including propranolol (Inderal) and atenolol (Tenormin), block the nerves that stimulate the heart to beat faster. They affect only the physiologic symptoms of anxiety (particularly rapid heart rate) and are most helpful for phobias, particularly performance anxiety. They may be taken before entering a situation where anxiety symptoms tend to occur. Beta-blockers are less effective for other forms of anxiety.

Atypical antipsychotics are mostly used for treating schizophrenia, bipolar disorder, and major depressive disorder. Doctors sometimes use the atypical antipsychotic olanzapine (Zyprexa) for treating severe cases of post-traumatic stress disorder. However, olanzapine has severe side effects, including weight gain and increased high blood sugar levels, which can increase the risk for diabetes. [For more information, see In-Depth Report #47: Schizophrenia.]

Pregabalin (Lyrica) and gabapentin (Neurontin) are drugs used to treat seizures and other conditions. Researchers are investigating whether these drugs may be useful for certain anxiety disorders, such as social anxiety disorder and general anxiety disorder. Their exact role in the treatment of anxiety disorders is not clear, however.

Generally, manufacturers of herbal remedies and dietary supplements do not need FDA approval to sell their products. Just like a drug, herbs and supplements can affect the body's chemistry, and therefore have the potential to produce side effects that may be harmful. There have been a number of reported cases of serious and even lethal side effects from herbal products. Always check with your doctor before using any herbal remedies or dietary supplements.

Studies indicate that the dietary supplement inositol may have benefits for panic disorder and, possibly, obsessive compulsive disorder. Inositol is part of the vitamin B complex.

Some patients use aromatherapy as a relaxation aid. Aromatherapy is in general safe, but some plant extracts in these formulas have been linked to skin allergies.

There is no evidence supporting the efficacy of valerian, St. John’s wort, or passionflower for treatment of anxiety. The herbal remedy kava has been associated with liver problems and should not be avoided, especially by patients with liver disease or those who use alcohol. Kava can also interact dangerously with medications that are metabolized by the liver.

Other Treatments

The goal of cognitive-behavioral therapy (CBT) is to regain control of reactions to stress and stimuli, thus reducing the feeling of helplessness that often accompanies anxiety disorders. CBT works on the principle that the thoughts that produce and maintain anxiety can be recognized and altered using various techniques that change behavioral responses and eliminate the anxiety reaction. Many studies have shown that a combination of CBT and medication works best for treating anxiety disorders.

A number of CBT approaches work well for treating many types of anxiety disorders. Studies suggest that CBT is also helpful for patients who have additional conditions, such as depression, a second anxiety disorder, or alcohol dependency. (It may take longer to achieve a successful outcome in such cases, however.) CBT is often given along with drug treatment. A study in the Journal of the American Medical Association found that children and adolescents with OCD responded better to CBT alone than the antidepressant setraline (Zoloft) alone, but most patients did best when they were treated with a combination of CBT and sertraline.

Both individual and group treatments work well. (However, people with social phobia may do better in individual sessions.) Several recent studies also indicate that telephone-based behavioral therapy works well for people with OCD, generalized anxiety disorder, and panic disorders.

Anxiety disorders are chronic, however, and recurrence is common. Some studies indicate that 30 - 82% of people with panic disorder and phobias have a recurrence of attacks at an average of 9 months, even after successful short-term therapy. Medications, then, are also generally recommended for most patients.

Basic Cognitive Therapy Techniques. Treatment usually takes about 12 - 20 weeks. The essential goal of cognitive therapy is to understand the realities of an anxiety-provoking situation and to respond to reality with new actions based on reasonable expectations.

First, the patient must learn how to recognize anxious reactions and thoughts as they occur. One way of accomplishing this is by keeping a daily diary that reports the occurrences of anxiety attacks and any thoughts and events associated with them. A patient with OCD, for instance, may record repetitive thoughts.
These entrenched and automatic reactions and thoughts must be challenged and understood. Again, using the OCD example, one approach is to record and play back the words of the repetitive thoughts, over exposing the patient to the thoughts and reducing their effect. One effective approach for patients with generalized anxiety disorder targets their intolerance of uncertainty and helps them develop methods to cope with it.
Patients are usually given behavioral homework assignments to help them change their behavior. For example, a person with generalized social phobia may be asked to buy an item and then return it the next day. As the patient performs this action, they observe any unrealistic fears and thoughts triggered by such an event.
As the patient continues with self-observation, they begin to perceive the false assumptions that underlie the anxiety. For example, OCD patients may learn to recognize that their heightened sense of responsibility for preventing harm in non-threatening situations is not necessary or even useful.
At that point, the patient can begin substituting new ways of coping with the feared objects and situations.

Systematic Desensitization. Systematic desensitization is a specific technique that breaks the link between the anxiety-provoking stimulus and the anxiety response. This treatment requires the patient to gradually confront the object of fear. There are three main elements to the process:

Relaxation training
A list composed by the patient that prioritizes anxiety-inducing situations by degree of fear
The desensitization procedure itself, confronting each item on the list, starting with the least stressful

This treatment is especially effective for simple phobias, social phobias, agoraphobia, and post-traumatic stress syndrome.

Exposure and Response Treatment. Exposure treatment purposefully generates anxiety by exposing the patient repeatedly to the feared object or situation, either literally or using imagination and visualization. It uses the most fearful stimulus first. (This differs from the desensitization process because it does not involve relaxation or a gradual approach to the source of anxiety.)

Exposure treatments are usually known as either flooding or graduated exposure:

Flooding exposes the person to the anxiety-producing stimulus for as long as 1 - 2 hours.
Graduated exposure gives the patient a greater degree of control over the length and frequency of exposures.

In both cases, the patient experiences the anxiety over and over until the stimulating event eventually loses its effect. Combining exposure with standard cognitive therapy may be particularly beneficial. This approach has helped certain patients in most anxiety disorder categories, including post-traumatic stress disorder.

Modeling Treatment. Phobias can often be treated successfully with modeling treatment:

The therapy typically uses an actor who approaches an anxiety-producing object or engages in a fear-provoking activity that is similar to the patient's specific problem. Either a live or videotaped situation may be used, although the live model is considered to be more effective.
The patient observes this event and tries to learn how to behave in a comparable manner.

Other forms of psychotherapy, commonly called emotion-based psychotherapy (EBT), psychodynamic therapy, or "talk" therapy, deal more with childhood roots of anxiety and usually, although not always, require longer treatments. They include interpersonal therapy, supportive psychotherapy, attention intervention, and psychoanalysis. All work is done during the sessions. Some research indicates that such therapies might be more useful for generalized anxiety, which may require more sustained work to process and recover from early traumas and fears. Studies suggest that although emotion-based psychotherapies are not as effective as cognitive-behavioral therapy (CBT) in treating panic disorders, patients tend to stay longer in EBT than in CBT. Some doctors suggest adding elements of EBT to the usual CBT and medication treatments.

Anxiety Management Therapy. Anxiety management therapy is sometimes used as an alternative to CBT for generalized anxiety disorder. It involves patient education, relaxation training, and exposure to anxiety-provoking stimuli but does not include exercises in cognitive retraining.

Relaxation Training. Relaxation techniques use muscle relaxation and mental visualization to help focus attention towards a calming feeling. Some people find meditation helpful.

Breathing Retraining. Breathing retraining techniques may help reduce the physical effects of anxiety. For example, hyperventilation is one of the primary physical manifestations of panic disorders. This involves rapid, tense breathing, resulting in chest pain, dizziness, tingling of the mouth and fingers, muscle cramps, and even fainting. By practicing measured, controlled breathing at the onset of a panic attack, patients may be able to prevent full attacks.

Biofeedback. Biofeedback uses special sensors that allow patients to recognize anxiety states by changes in specific physical functions, such as changes in pulse rate, skin temperatures, and muscle tone. Eventually they learn to modify these changes, which in turn helps relieve anxiety. While commonly used, there are not many rigorous studies showing that biofeedback helps patients reduce or eliminate their symptoms over the long term.

Several types of psychological treatments have been designed specifically for treating patients with PTSD. These approaches include a special type of CBT known as trauma-focused cognitive behavioral therapy (TFCBT), and a psychotherapy treatment called eye movement desensitization and reprocessing (EMDR).

With TFCBT, patients are taught stress management skills. The therapist helps the patient develop a narrative (verbal, written, or artistic) about the traumatic event. Patients may be exposed to reminders about the trauma and are taught how to cope with future reminders. Through the process, the patient learns how to reprocess their thoughts, feelings, and behaviors.

With EMDR, the patient focuses on remembering the traumatic experience while visually following the rhythmic movement of the therapist’s fingers. The patient recounts to the therapist what memories have been provoked during the exercise. EMDR may help patients recall details and sensations that they had blocked out. Through this breakthrough, patients learn how to regain emotional control.

Transcranial magnetic stimulation (TMS) uses high frequency magnetic pulses to target and stimulate specific areas of the brain. Research has particularly focused on possible benefits for obsessive-compulsive behavior. Some studies have found some improvement in mood, but more research is needed to determine its value for reducing anxiety and obsessions.

In 2006, the U.S. National Institutes of Health funded a large study to examine whether deep brain stimulation (DBS) can help patients with OCD. DBS involves implanting tiny stimulators into the brain to block abnormal nerve signals that cause obsessive symptoms. These “brain pacemakers” are approved to treat epilepsy and Parkinson’s disease. Researchers hope that DBS may eventually provide a new treatment option for patients with severe OCD.

A surgical technique called cingulotomy involves interrupting the cingulate gyrus, a bundle of nerve fibers in the front of the brain. It is sometimes used as a last resort for patients with severe OCD. A variation of this procedure using magnetic resonance imaging (MRI) to guide the surgeon has resulted in long-term improvement in about 25 - 33% of OCD patients in whom it is performed. The procedure is generally safe with few serious complications and does not affect intellect or memory.

Resources

www.nimh.nih.gov -- National Institute of Mental Health
www.adaa.org -- Anxiety Disorders Association of America
www.nami.org -- National Alliance on Mental Illness
www.psych.org -- The American Psychiatric Association
www.apa.org -- The American Psychological Association
www.istss.org -- International Society for Traumatic Stress Studies
www.ncvc.org -- National Center for Victims of Crime
www.ncptsd.va.gov -- National Center for Post-Traumatic Stress Disorders
www.rainn.org -- Rape, Abuse, and Incest National Network
www.aacap.org -- American Academy of Child and Adolescent Psychiatry
www.aabt.org -- Association for Behavioral and Cognitive Therapies
www.ocfoundation.org -- Obsessive Compulsive Foundation

References

Bisson J, Andrew M. Psychological treatment of post-traumatic stress disorder (PTSD). Cochrane Database Syst Rev. 2007 Jul 18;(3):CD003388.

Bisson JI. Post-traumatic stress disorder. BMJ. 2007 Apr 14;334(7597):789-93.

Bridge JA, Iyengar S, Salary CB, et al. Clinical response and risk for reported suicidal ideation and suicide attempts in pediatric antidepressant treatment: a meta-analysis of randomized controlled trials. JAMA. 2007 Apr 18;297(15):1683-96.

Connolly SD, Bernstein GA; Work Group on Quality Issues. Practice parameter for the assessment and treatment of children and adolescents with anxiety disorders. J Am Acad Child Adolesc Psychiatry. 2007 Feb;46(2):267-83.

Gale C, Davidson O. Generalised anxiety disorder. BMJ. 2007 Mar 17;334(7593):579-81.

Heyman I, Mataix-Cols D, Fineberg NA. Obsessive-compulsive disorder. BMJ. 2006 Aug 26;333(7565):424-9.

Hunot V, Churchill R, Silva de Lima M, Teixeira V. Psychological therapies for generalised anxiety disorder. Cochrane Database Syst Rev. 2007 Jan 24;(1):CD001848.

Ipser JC, Carey P, Dhansay Y, Fakier N, Seedat S, Stein DJ. Pharmacotherapy augmentation strategies in treatment-resistant anxiety disorders. Cochrane Database Syst Rev. 2006 Oct 18;(4):CD005473.

Katon WJ. Clinical practice. Panic disorder. N Engl J Med. 2006 Jun 1;354(22):2360-7.

Koran LM, Hanna GL, Hollander E, Nestadt G, Simpson HB; American Psychiatric Association. Practice guideline for the treatment of patients with obsessive-compulsive disorder. Am J Psychiatry. 2007 Jul;164(7 Suppl):5-53.

Kroenke K, Spitzer RL, Williams JB, Monahan PO, Löwe B. Anxiety disorders in primary care: prevalence, impairment, comorbidity, and detection. Ann Intern Med. 2007 Mar 6;146(5):317-25.

Saeed SA, Bloch RM, Antonacci DJ. Herbal and dietary supplements for treatment of anxiety disorders. Am Fam Physician. 2007 Aug 15;76(4):549-56.

Schneier FR. Clinical practice. Social anxiety disorder. N Engl J Med. 2006 Sep 7;355(10):1029-36.

Smoller JW, Pollack MH, Wassertheil-Smoller S, et al. Panic attacks and risk of incident cardiovascular events among postmenopausal women in the Women's Health Initiative Observational Study. Arch Gen Psychiatry. 2007 Oct;64(10):1153-60.

Review Date:
12/25/2007
Reviewed By:
Harvey Simon, MD, Editor-in-Chief, Associate Professor of Medicine, Harvard Medical School; Physician, Massachusetts General Hospital. Also reviewed by David Zieve, MD, MHA, Medical Director, A.D.A.M., Inc.

A.D.A.M., Inc. is accredited by URAC, also known as the American Accreditation HealthCare Commission (www.urac.org). URAC's accreditation program is an independent audit to verify that A.D.A.M. follows rigorous standards of quality and accountability. A.D.A.M. is among the first to achieve this important distinction for online health information and services. Learn more about A.D.A.M.'s editorial policy, editorial process and privacy policy. A.D.A.M. is also a founding member of Hi-Ethics and subscribes to the principles of the Health on the Net Foundation (www.hon.ch).

A.D.A.M. Copyright

The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition. A licensed medical professional should be consulted for diagnosis and treatment of any and all medical conditions. Call 911 for all medical emergencies. Links to other sites are provided for information only -- they do not constitute endorsements of those other sites. © 1997-2009 A.D.A.M., Inc. Any duplication or distribution of the information contained herein is strictly prohibited.

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Eating disorders

FitSugar — Wed, 08 Oct 2008 17:35:00 -0700

In This Report

Highlights
Introduction
Risk Factors
Causes
Complications of Bulimia...
Complications of Anorexia...
Symptoms
Diagnosis
Treatment
Treatment for Bulimia
Treatment for Anorexia
Therapy
Resources
References

HEALTH GUIDE REFERENCE FROM A.D.A.M

Highlights

Eating Disorders Overview

Eating disorders typically occur among young women.
Bulimia nervosa involves a pattern of bingeing and purging. Many people with bulimia nervosa also suffer from depression.
Anorexia nervosa involves a pattern of self-starvation. Patients often have an accompanying anxiety disorder (such as obsessive compulsive disorder) or depression. Patients who have anorexia and depression have a high risk for suicide. Some studies estimate that anorexia nervosa has the highest death rate of any psychiatric disorder.

Treatment of Bulimia Nervosa

Bulimia nervosa is treated with a combination of psychotherapy and medication. Cognitive behavioral therapy, which is given along with nutritional counseling, is the preferred psychotherapeutic approach. Selective serotonin reuptake inhibitors (SSRIs), such as fluoxetine (Prozac), are the first choice for drug therapy.

Treatment of Anorexia Nervosa

Unlike bulimia nervosa, anorexia nervosa does not respond as well to drug treatment, although SSRIs are sometimes used as an adjunct to psychotherapy. Therapy that includes the entire family -- not just the patient -- is an important part of the treatment process, as is nutritional education. Patients who are severely underweight and who have other physical risks may need to be hospitalized while weight is restored. Recovery is a long process that can take 5 - 6 years to achieve.

Introduction

Eating disorders are behavioral issues brought on by a complex interplay of factors, which may include emotional and personality disorders, family pressures, a possible genetic or biologic susceptibility, and a culture in which there is an overabundance of food and an obsession with thinness. There are four general categories of eating disorders:

Bulimia nervosa
Anorexia nervosa
Binge eating
Eating disorders not otherwise specified

These are not new disorders. Although anorexia nervosa was first defined as a medical problem in the late 1800s, descriptions of self-starvation have been found even in medieval writings.

Bulimia nervosa is more common than anorexia, and it usually begins early in adolescence. It is characterized by cycles of bingeing and purging, and typically takes the following pattern:

Bulimia is often triggered when young women attempt restrictive diets, fail, and react by binge eating. (Binge eating involves consuming larger than normal amounts of food within a 2-hour period.)
In response to the binges, patients compensate, usually by purging, vomiting, using enemas, or taking laxatives, diet pills, or drugs to reduce fluids.
Patients then revert to severe dieting, excessive exercise, or both. (Some patients with bulimia follow bingeing only with fasting and exercise. They are then considered to have non-purging bulimia.)
The cycle then swings back to bingeing and then to purging again.
Some studies have reported that patients with bulimia average about 14 episodes of binge-purging per week. To be diagnosed with bulimia, however, a patient must binge and purge at least twice a week for 3 months. (Some experts believe that going through the cycle only once a week is sufficient for a diagnosis.)
In some cases, the condition progresses to anorexia. Most people with bulimia, however, have a normal to high-normal body weight, although it may fluctuate by more than 10 pounds because of the binge-purge cycle.

Young people who occasionally force vomiting after eating too much are not considered bulimic, and most of the time this occasional unhealthy behavior does not continue beyond youth.

The term "anorexia" literally means absence of appetite. Anorexia nervosa involves an aversion to food that leads to a state of starvation and emaciation. It is a very serious illness that some experts believe is an entirely different condition from bulimia and should be not be diagnosed as a simple eating disorder.

Facts associated with anorexia nervosa:

At least 15% to as much as 60% of normal body weight is lost.
The patient with anorexia nervosa has an intense fear of gaining weight, even when severely underweight.
Individuals with anorexia nervosa have a distorted image of their own weight or shape and deny the serious health consequences of their low weight.
Women with anorexia nervosa miss at least three consecutive menstrual periods. (Some experts believe women can be anorexic without this occurrence.)

Patients with this condition are often characterized as anorexia restrictors or anorexic bulimic patients. Each type is equally prevalent.

Anorexia restrictors reduce their weight by severe dieting.
Anorexic bulimic patients maintain emaciation by purging. Although both types are serious, the bulimic type, which imposes additional stress on an undernourished body, is the more damaging.

Severe anorexia is common in the elderly, who may experience weight loss because of social isolation, impaired gastrointestinal function, or loss of certain chemicals related to the feeding drive. Such age-related anorexia, however, is not synonymous with anorexia nervosa, a psychologic disorder.

Bingeing without purging is characterized as compulsive overeating (binge eating) with the absence of bulimic behaviors, such as vomiting or laxative abuse (used to eliminate calories). Binge eating usually leads to becoming overweight.

To be diagnosed as a binge eater, a person typically has the following characteristics:

Bingeing at least twice a week for 6 months
Consuming 5,000 - 15,000 calories in one sitting
Eating three meals a day plus frequent snacks
Overeating continually throughout the day, rather than consuming large amounts of food during binges

Since binge eating disorder is generally associated with weight gain, it will not be further discussed in this report. [For more information, see In-Depth Report #53: Weight control and diet.]

A fourth category called eating disorders not otherwise specified (NOS) has been established to define eating disorders not specifically defined as anorexia or bulimia. This category includes:

Infrequent binge-purge episodes (occurring less than twice a week or having such behavior for less than months)
Repeated chewing and spitting without swallowing large amounts of food
Normal weight and anorexic behavior

Such patients tend to be older at diagnosis. Although less serious than other eating disorders, these patients still face similar health problems, including a higher risk for fractures and other conditions.

Risk Factors

Many factors contribute to the risk of developing an eating disorder. In the United States, about 7 million women and 1 million men suffer from eating disorders.

Eating disorders occur most often in adolescents and young adults. However, new research finds that they are increasingly prevalent among young children. Eating disorders are more difficult to identify in young children because they are rarely suspected.

Studies indicate that eating disorders occur predominantly among girls and women. About 90 - 95% of patients with anorexia nervosa, and about 80% of patients with bulimia nervosa, are female.

Most studies of individuals with eating disorders have been conducted using Caucasian middle-class females. Studies now indicate, however, that minority populations (including Hispanic Americans and African-Americans) are increasingly affected.

Living in any economically developed nation on any continent appears to pose a risk for eating disorders. Within nations, eating disorders can affect people of all socioeconomic levels.

People with eating disorders tend to share similar personality and behavioral traits, including low self-esteem, dependency, and problems with self-direction. Specific psychiatric personality disorders may put people at higher risk for eating disorders.

Avoidant Personalities. Some studies indicate that many patients with anorexia nervosa have avoidant personalities. This personality disorder is characterized by:

Being a perfectionist
Being emotionally and sexually inhibited
Having less of a fantasy life than people with bulimia or those without an eating disorder
Being perceived as always being "good," not being rebellious
Being terrified of being ridiculed or criticized or of feeling humiliated

People with anorexia are extremely sensitive to failure, and any criticism, no matter how slight, reinforces their own belief that they are "no good".

Obsessive-Compulsive Personality. Obsessive-compulsive personality defines certain character traits (being a perfectionist, morally rigid, or preoccupied with rules and order). This personality disorder has been strongly associated with a higher risk for anorexia. These traits should not be confused with the anxiety disorder called obsessive-compulsive disorder (OCD), although they may increase the risk for this disorder.

Borderline Personalities. Borderline Personality Disorder (BPD) is associated with self-destructive and impulsive behaviors. People with BPD tend to have other co-existing mental health problems, including eating disorders.

Narcissistic Personalities. Studies have also found that people with bulimia or anorexia are often highly narcissistic and tend to:

Have an inability to soothe oneself
Have an inability to empathize with others
Have a need for admiration
Be hypersensitive to criticism or defeat

Many patients with eating disorders experience depression and anxiety disorders. Depression, anxiety, or both is also common in families of patients with eating disorders. It is not clear if emotional disorders, particularly obsessive-compulsive disorder (OCD), cause the eating disorders, increase susceptibility to them, or share common biologic cause.

Obsessive-Compulsive Disorder (OCD). Obsessive-compulsive disorder is an anxiety disorder that occurs in up to two thirds of patients with anorexia and up to one third of patients with bulimia. In fact, some experts believe that eating disorders are variants of OCD. Obsessions are recurrent or persistent mental images, thoughts, or ideas, which may result in compulsive behaviors (repetitive, rigid, and self-prescribed routines) that are intended to prevent the manifestation of the obsession. Women with anorexia and OCD may become obsessed with exercise, dieting, and food. They often develop compulsive rituals (weighing every bit of food, cutting it into tiny pieces, or putting it into tiny containers). The presence of OCD with either anorexia or bulimia does not, however, appear to have any influence on whether a patient improves or not.

Obsessive-compulsive disorder is an anxiety disorder characterized by an inability to resist or stop continuous, abnormal thoughts or fears combined with ritualistic, repetitive, and involuntary defense behavior.

Other Anxiety Disorders. A number of other anxiety disorders have been associated with both bulimia and anorexia, including:

Phobias. Phobias often precede the onset of the eating disorder. Social phobias, in which a person is fearful about being humiliated in public, are common in both types of eating disorders.
Panic Disorder. Panic disorder often follows the onset of an eating disorder. It is characterized by periodic attacks of anxiety or terror (panic attacks).
Post-Traumatic Stress Disorder. Many women with serious eating disorders report a past traumatic event, and many exhibit symptoms of post-traumatic stress disorder (PTSD) -- an anxiety disorder that occurs in response to life-threatening circumstances.

Depression. Depression is common in people with eating disorders, for both anorexia and bulimia. Major depression is unlikely to be a cause of eating disorders, however, because treating and relieving depression rarely cures an eating disorder. In addition, depression often improves after anorexic patients begin to gain weight.

Extreme eating disorder behaviors, including use of diet pills, laxatives, diuretics, and vomiting, are reported more often in overweight teenagers. Researchers are working on strategies for preventing the development of eating disorders among overweight adolescents. A 2006 study that targeted overweight college-age women reported success with an Internet-based cognitive behavioral therapy program that helped these women become more comfortable with their body weight and shape. The program also included information on the risks of eating disorders, and education on healthy eating and weight maintenance.

Body Dysmorphic Disorder. Body dysmorphic disorder (BDD) involves a distorted view of one's body that is caused by social, psychologic, or possibly biologic factors. It is often associated with anorexia or bulimia, but it can also occur without any eating disorder. People with this disorder commonly suffer from emotional disorders, including obsessive-compulsive disorder and depression. As part of obsessive thinking, some people with BDD may obsess about a perceived deformity in one area of their body, and may repeatedly seek cosmetic surgery to "correct" it. People with BDD are also at higher risk for suicidal thinking and attempts. Some evidence suggests that treatment with fluoxetine (Prozac), a common antidepressant known as an SSRI helps reduce this problem, even in people without an eating disorder.

Muscle Dysmorphia. Experts are also increasingly reporting a disorder in which people have distorted body images involving their muscles. It tends to occur in men who perceive themselves as being "puny," which results in excessive body building, preoccupation with diet, and social problems. Such individuals are prone to eating disorders and other unhealthy behaviors, including the use of anabolic steroids.

Highly competitive athletes are often perfectionists, a trait common among people with eating disorders.

Female Athletes. Excessive exercise is associated with many cases of anorexia (and, to a lesser degree, bulimia). In young female athletes, anorexia postpones puberty, allowing them to retain a muscular boyish shape without the normal accumulation of fatty tissues in breasts and hips that may blunt their competitive edge. Many coaches and teachers compound the problem by overstressing calorie counting and loss of body fat.

In response, people who are vulnerable to such criticism may lose excessive weight, which has been known to be deadly even for famous athletes. The term "female athlete triad" in fact, is now a common and serious disorder facing young female athletes and dancers and describes the combined presence of the following problems:

Eating disorders, including anorexia
Amenorrhea (absence or irregular menstruation)
Osteoporosis (bone loss, which appears to be related to low weight)

Male Athletes. Male wrestlers and lightweight rowers are also at risk for excessive dieting. One-third of high school wrestlers use a method called weight-cutting for rapid weight loss. This process involves food restriction and fluid depletion by using steam rooms, saunas, laxatives, and diuretics. Although male athletes are more apt to resume normal eating patterns once competition ends, studies show that the body fat levels of many wrestlers are still well below their peers during off-season and are often as low as 3% during wrestling season.

Men and Women in the Military. Studies also show a higher-than-average risk for eating disorders in men and women in the military. A study of eating behavior on one Army base reported that 8% of the women had an eating disorder, compared to 1 - 3% in the civilian female population.

In general, vegetarianism, with careful planning, is a healthy practice for both adults and adolescents. Studies report, however, that vegetarianism in adolescence may be a risk factor for eating disorders in both males and females. Vegetarian teens have been found to be twice as likely to diet frequently, four times as likely to intensively diet, and eight times as likely to use laxatives as their non-vegetarian peers.

These studies do not mean that being a vegetarian equates with having an eating disorder. They do suggest, however, that parents with children who suddenly become vegetarians should be sure that their children are eating a balanced meal with sufficient protein, calories, and important minerals, such as calcium. Parents also might suspect anorexic behavior in their child under certain conditions:

If the child has stopped eating meat only to avoid fat rather than from other motives, such as love of animals or to improve health.
If the vegetarian diet coincides with rapid weight loss.
If the child avoids important vegetable products because of calories (such as whole grains) or because of fats and oils (such as tofu, nuts, and dairy products).

Eating disorders may be more common in teenagers with chronic illness, such as diabetes or asthma. Some recent research suggests an endocrinological link between obesity, diabetes, and eating disorders.

Diabetes. Eating disorders are particularly serious problems for people with either type 1 or type 2 diabetes.

Binge eating (without purging) is most common in type 2 diabetes and, in fact, the obesity it causes may even trigger this diabetes in some people.
Both bulimia and anorexia are common in type 1 diabetes. A 2005 study indicated that as many as 25% of young women with type 1 diabetes may develop abnormal eating habits, and that the combination of diabetes and an eating disorder can have serious health consequences in the women's future. Diabetic women often omit or underuse insulin in order to control weight. If such patients develop anorexia, their extremely low weight may appear to control the diabetes for a while. Eventually, however, if they fail to take insulin and continue to lose weight, these patients develop life-threatening complications.

Click the icon to see an image of type 1 diabetes.

There is a greater risk for eating disorders and other emotional problems for girls who undergo early puberty, when the pressures experienced by all adolescents are intensified by experiencing, possibly alone, these early physical changes, including normal increased body fat. One interesting study reported that:

Before puberty, girls ate quantities of food appropriate to their body weight, were satisfied with their bodies, and noted their depression increased with lower food intake.
After puberty, girls ate about three-quarters of the recommended calorie intake, had a worse body self-image, and noted their depression increased with higher food intake.

This study reported on girls without eating disorders, but it certainly suggests patterns that can lead to eating problems, particularly in girls who go through puberty early. Other studies also indicate that girls who start menstruating at a younger age are more likely to develop eating disorders.

Causes

There is no single cause for eating disorders. Although concerns about weight and body shape play a role in all eating disorders, the actual cause of these disorders appear to result from many factors, including cultural and family pressures and emotional and personality disorders. Genetics and biologic factors may also play a role.

Negative influences within the family may play a major role in triggering and perpetuating eating disorders. Some studies have produced the following observations and theories regarding family influence.

Insecure Infancy. Some experts theorize that parents who fail to provide a safe and secure foundation in infancy may foster eating disorders. In such cases, children experience so-called insecure attachments. They are more likely to have greater weight concerns and lower self-esteem than are those with secure attachments.
Parental Behaviors. Poor parenting by both mothers and fathers has been implicated in eating disorders. One study found that 40% of 9- and 10-year-old girls trying to lose weight generally with the urging of their mothers. Some studies have found that mothers of anorexics tend to be over-involved in their child's life, while mothers of people with bulimia are critical and detached. Overly critical fathers, brothers, or both may play a factor in the development of anorexia in both girls and boys.
Family Meals. How often a family eats together may influence whether a child develops an eating disorder. A study published in the Journal of Adolescent Health found that young girls who ate 3 - 4 meals per week with their families were about half as likely to engage in extreme weight control behaviors as girls who ate family meals less often.
Family History of Addictions or Emotional Disorders. Studies report that people with either anorexia or bulimia are more likely to have parents with alcoholism or substance abuse than are those in the general population. Parents of people with bulimia appear to be more likely to have psychiatric disorders than parents of patients with anorexia.
History of Abuse. Women with eating disorders, particularly bulimia, appear to have a higher incidence of sexual abuse. Studies have reported sexual abuse rates as high as 35% in women with bulimia.
Family History of Obesity. People with bulimia are more likely than average to have an obese parent or to have been overweight themselves during childhood.

At least one study has reported that the most positive way for parents to influence their children's eating habits and to prevent weight problems and eating disorders is to have healthy eating habits themselves.

Anorexia is eight times more common in people who have relatives with the disorder, and some experts estimate that genetic factors are the root cause of many cases of eating disorders. Twins had a tendency to share specific eating disorders (anorexia nervosa, bulimia nervosa, and obesity). Researchers have identified specific chromosomes that may be associated with bulimia and anorexia. In particular, regions on chromosome 10 have been linked to bulimia as well as obesity. Some evidence has also reported an association with genetic factors responsible for serotonin, the brain chemical involved with both well-being and appetite. Researchers have also pinpointed certain proteins such as brain-derived neurotrophic factor (BDNF). This protein may influence an individual's susceptibility to developing an eating disorder.

The approach to food in Western countries is extremely problematic. Enough food is produced in the U.S. to supply 3,800 calories every day to each man, woman, and child, far more than any single person needs to sustain life. Obesity is a global epidemic, and few people living in this over-fed and sedentary culture eat a meal guiltlessly.

One interesting anthropologic study reported the following observations:

During historical periods or in cultures where women are financially dependent and marital ties are stronger, the standard is toward being curvaceous, possibly reflecting a cultural or economic need for greater reproduction.
During periods or in cultures where female independence has been possible, the standard of female attractiveness tends toward thinness.

The response of the media to the cultural drive for thinness and the overproduction of food both likely play major roles in triggering obesity and eating disorders.

On the one hand, advertisers heavily market weight-reduction programs and present anorexic young models as the paradigm of sexual desirability.
Clothes are designed and displayed for thin bodies in spite of the fact that few women could wear them successfully.
On the other hand, the media floods the public with attractive ads for consuming foods, especially "junk" foods.

Hormonal abnormalities are common in eating disorders and include chemical abnormalities in the thyroid, the reproductive regions, and areas related to stress, well-being, and appetite. Many of these chemical changes are certainly a result of malnutrition or other aspects of eating disorders, but they also may play a role in perpetuating or even creating susceptibility to the disorders.

The primary setting of many of these abnormalities originate in a small area of the brain called the limbic system. A specific system called hypothalamic-pituitary-adrenal axis (HPA) may be particularly important in eating disorders. It originates in the following regions in the brain:

Hypothalamus. The hypothalamus is a small structure that plays a role in controlling our behavior, such as eating, sexual behavior and sleeping, and regulates body temperature, emotions, secretion of hormones, and movement.

Click the icon to see an image of the hypothalamus.

The pituitary gland. The pituitary gland is involved in controlling thyroid functions, the adrenal glands, growth, and sexual maturation.
Amygdala. This small almond-like structure lies deep in the brain and is associated with regulation and control of major emotional activities, including anxiety, depression, aggression, and affection.

Click the icon to see an image of the brain-thyroid link.

Stress Hormones. The HPA systems trigger the production and release of stress hormones called glucocorticoids, including the primary stress hormone cortisol. Chronically elevated levels of stress chemicals have been observed in patients with anorexia and bulimia. Cortisol is very important in marshaling systems throughout the body (including the heart, lungs, circulation, metabolism, immune systems, and skin) to deal quickly with any threat.

Release of Neurotransmitters. The HPA system also releases certain neurotransmitters (chemical messengers) that regulate stress, mood, and appetite and are being heavily investigated for a possible role in eating disorders. Abnormalities in the activities of three of them, serotonin, norepinephrine, and dopamine, are of particular interest. Serotonin is involved with well-being, anxiety, and appetite (among other traits), and norepinephrine is a stress hormone. Dopamine is involved in reward-seeking behavior. Recent research suggests that people with anorexia have increased activity in the brain's dopamine receptors. This overactivity may explain why people with anorexia do not experience a sense of pleasure from food and other typical comforts.

Ghrelin. High levels of ghrelin, a hormone that increases the feeling of hunger and slows metabolism, have been noted in patients with anorexia and bulimia.

Low-Leptin Levels. Leptin is a hormone that appears to trigger the hypothalamus to stimulate appetite, and low levels have been observed in people with anorexia and bulimia.

Low Reproductive Hormones. The hypothalamic-pituitary system is also responsible for the production of important reproductive hormones that are severely depleted in anorexics. Although most experts believe that these reproductive abnormalities are a result of anorexia, others have reported that in 30 - 50% of people with anorexia, menstrual disturbances occurred before severe malnutrition set in and remained a problem long after weight gain, indicating that hypothalamic-pituitary abnormalities precede the eating disorder itself.

In some cases, infection has been associated with anorexia. In such cases, immune factors released to fight these infections may cause inflammation and injury in the areas of the brain that affect appetite and behavior.

Streptococcal Infection. The bacteria responsible for strep throat and rheumatic fever -- called group A beta-hemolytic streptococcal (GABHS) -- is now a suspect in some cases of anorexia. Some children who have been infected with these bacteria develop a syndrome that includes obsessive-compulsive disorder (OCD), tics, and anorexia nervosa. The syndrome is called PANDAS (Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcus). More research is needed to confirm this as an actual cause of anorexia and to determine if it may be treatable with antibiotics.

Epstein Barr Virus. Epstein Barr, the virus that causes mononucleosis, has also been associated with the development of anorexia.

Click the icon to see an image of infectious mononucleosis.

Complications of Bulimia

Most studies report that patients who have bulimia without severe weight loss have a much better outlook than patients with anorexia. Some studies have suggested that 60 - 80% of bulimic patients are in remission within 3 months of treatment. However, relapse is common, and over half of women with bulimia continue to battle disordered eating habits for years. In one study, bulimia itself persisted in 10 - 25% of patients after treatment.

Many medical problems are directly associated with bulimic behavior, including:

Tooth erosion, cavities, and gum problems
Water retention, swelling, and abdominal bloating
Acute stomach distress
Fluid loss with low potassium levels (due to excessive vomiting or laxative use; can lead to extreme weakness, near paralysis, or lethal heart rhythms)
Irregular periods
Swallowing problems and esophagus damage

Forced vomiting causes repetitive assaults on the esophagus (the food pipe) from forced vomiting. It is not clear, however, if swallowing problems are common.

The esophagus connects the nose and mouth with the stomach. The epiglottis folds over the trachea when a swallow occurs, to prevent the swallowed substance from being inhaled into the lungs. When a person is unable to swallow because of illness or coma, a tube may be inserted either through the mouth or nose, past the epiglottis, through the esophagus and into the stomach. Nutrients pass directly through the tube into the stomach.

Rupture of the esophagus, or food pipe
Weakened rectal walls (rare, but serious condition that requires surgery)

Click the icon to see an image of the rectum.

A number of self-destructive behaviors occur with bulimia:

Smoking. Many teenage girls with eating disorders smoke because it is thought to help prevent weight gain.
Impulsive Behaviors. Women with bulimia are at higher-than-average risk for dangerous impulsive behaviors, such as sexual promiscuity, self-cutting, and kleptomania. Some studies have reported such behaviors in half of those with bulimia.
Alcohol and Substance Abuse. An estimated 30 - 70% of patients with bulimia abuse alcohol, drugs, or both. This rate is higher than that of the general population and for people with anorexia. However, this higher rate of substance abuse may be a distortion because studies are conducted only on diagnosed patients. Bulimia tends not to get diagnosed. And reports of bulimia in the community (where the incidence of the eating disorder is higher than statistics suggest) indicate that substance abuse is actually lower than in people with anorexia.

Women with bulimia frequently abuse over-the-counter medications, such as laxatives, appetite suppressants, diuretics, and drugs that induce vomiting (ipecac). None of these drugs is without risk. For example, ipecac poisonings have been reported, and some people become dependent on laxatives for normal bowel functioning. Diet pills, even herbal and over-the-counter medications, can be hazardous, particularly if they are abused.

Complications of Anorexia

Anorexia nervosa is a very serious illness that has a wide range of effects on the body and mind. It is also associated with other problems, ranging from frequent flus and general poor health to life-threatening conditions. Some experts believe that it should not be approached as a simple eating disorder but as a serious condition requiring staging according to severity.

At this time, no treatment program for anorexia nervosa is completely effective. Recovery rates vary between 23 - 50%, and relapses range from 4 - 27%. Recovery takes an average of 5 - 6 years from the time of diagnosis. Up to 30% of patients do not recover.

Even after treatment and weight gain, many patients continue to display characteristics of the disorder, including perfectionism and a drive for thinness, which could keep them at risk for recurrence.

Some research suggests that anorexia nervosa has the highest death rate of any psychiatric disorder. According to different studies, the risk for early death is higher for people with the following conditions or characteristics:

Being younger
Having bulimia anorexia (twice as high in this group than in the anorexic-restrictor types)
Being severely low in weight at the time of treatment
Being sick for more than 6 years
Having been previously obese
Having an accompanying severe psychological disorder including personality disorders

One of the most serious effects of anorexia is hormonal changes, which can have severe health consequences.

Reproductive hormones, including estrogen and dehydroepiandrosterone (DHEA), are lower. Estrogen is important for healthy hearts and bones. DHEA, a weak male hormone, may also be important for bone health and for other functions.
Thyroid hormones are lower.
Stress hormones are higher.
Growth hormones are lower. Children and adolescents with anorexia may experience retarded growth.

The result of many of these hormonal abnormalities in women is long-term, irregular or absent menstruation (amenorrhea). This can occur early on in anorexia, even before severe weight loss. Over time this causes infertility, bone loss, and other problems. Low weight alone may not be sufficient to cause amenorrhea. Extreme fasting and purging behaviors may play an even stronger role in hormonal disturbance.

Adolescents with eating behaviors associated with anorexia (fasting, frequent exercise to lose weight, and self-induced vomiting) are at high risk for anxiety and depression in young adulthood. Alcohol and drug abuse are more common in patients with anorexia. Suicide has been estimated to account for as many as half the deaths in anorexia with studies showing up to a fifth of anorexic patients attempting suicide.

Heart disease is the most common medical cause of death in people with severe anorexia. The effects of anorexia on the heart are:

Dangerous heart rhythms, including slow rhythms known as bradycardia, may develop. Such abnormalities can show up even in teenagers with anorexia.

Bradycardia is a slowness of the heartbeat, usually at a rate under 60 beats per minute (normal resting rate is 60 - 100 beats per minute).

Blood flow is reduced
Blood pressure may drop
The heart muscles starve, losing size
Cholesterol levels tend to rise

Click the icon to see an image of cholesterol.

A primary danger to the heart is from abnormalities in the balance of minerals, such as potassium, calcium, magnesium, and phosphate, which are normally dissolved in the body's fluid. The dehydration and starvation that occurs with anorexia can reduce fluid and mineral levels and produce a condition known as electrolyte imbalance. Electrolytes (calcium and potassium) are critical for maintaining the electric currents necessary for a normal heartbeat. An imbalance in these electrolytes can be very serious and even life threatening unless fluids and minerals are replaced. Heart problems are a particular risk when anorexia is compounded by bulimia and the use of ipecac, a drug that causes vomiting.

After treatment and an increase in weight, estrogen levels are usually restored and periods resume. In severe anorexia, however, even after treatment, normal menstruation never returns in 25% of such patients.

If a woman with anorexia becomes pregnant before regaining normal weight, she faces a higher risk for miscarriage, cesarean section, and for having an infant with low birth weight or birth defects. She is also at higher risk for postpartum depression.
Women with anorexia who seek fertility treatments have lower chances for success.

Most pregnant women with a history of eating disorders have healthy pregnancies. However, some studies suggest that they may face higher risks for a number of complications, including cesarean sections, postpartum depression, miscarriages, complicated deliveries, and premature birth. Many studies indicate that babies born to mothers with eating disorders have a higher risk for low birth weight. However, an encouraging 2006 study reported that mothers with a history of anorexia nervosa do not have a higher risk for pregnancy complications or poor birth outcomes.

Almost 90% of women with anorexia experience osteopenia (loss of bone minerals), and 40% have osteoporosis (more advanced loss of bone density). Up to two-thirds of children and adolescent girls with anorexia fail to develop strong bones during their critical growing period. Boys with anorexia also suffer from stunted growth. The less the patient weighs, the more severe the bone loss. Women with anorexia who also binge-purge face an even higher risk for bone loss.

Bone loss in women is mainly due to low estrogen levels that occur with anorexia. Other biologic factors in anorexia also may contribute to bone loss, including high levels of stress hormones (which impair bone growth) and low levels of calcium, certain growth factors, and DHEA (a weak male hormone). Weight gain, unfortunately, does not completely restore bone. Only achieving regular menstruation as soon as possible can protect against permanent bone loss. The longer the eating disorder persists the more likely the bone loss will be permanent.

Testosterone levels decline in boys as they lose weight, which also can affect their bone density. In young boys with anorexia, weight restoration produces some catch-up growth, but it may not produce full growth.

People with severe anorexia may suffer nerve damage that affects the brain and other parts of the body. The following nerve-related conditions have been reported:

Seizures
Disordered thinking
Numbness or odd nerve sensations in the hands or feet (peripheral neuropathy)

Brain scans indicate that parts of the brain undergo structural changes and abnormal activity during anorexic states. Some of these changes return to normal after weight gain, but there is evidence that some damage may be permanent. Still, the extent of the neurologic problems is unclear.

Anemia is a common result of anorexia and starvation. In one study, 38% of anorexic participants had anemia. A particularly serious blood problem is pernicious anemia, which can be caused by severely low levels of vitamin B12. If anorexia becomes extreme, the bone marrow dramatically reduces its production of blood cells, a life-threatening condition called pancytopenia.

Bloating and constipation are both very common problems in people with anorexia.

In very late anorexia, the organs simply fail. The main warning sign is high blood levels of liver enzymes, which require immediate administration of calories.

Eating disorders are very serious for young people with type 1 diabetes. A study of over 2,000 women found that bulimia, or a combination of bulimia and anorexia, was more common among women with type 1 diabetes.

The complications of eating disorders that affect all patients are even more dangerous in this group of patients. Low blood sugar, for example, is a danger for anyone with anorexia, but it is a particularly dangerous risk for those with diabetes. If patients do not take their insulin, high blood sugar, which is also very dangerous, can occur. Unfortunately, patients with eating disorders may skip or reduce their daily insulin in order to decrease their intake of calories. Extremely high blood sugar levels can cause diabetic ketoacidosis, a condition in which acidic chemicals (ketones) accumulate in the body. This condition can lead to coma and death.

Symptoms

Possibly the most bewildering symptom of eating disorders is the distorted body image (body dysmorphia ). Although people typically associate distorted body image with severe anorexia, one study indicated that distortion may be more prevalent in people with bulimia. People with bulimia were more likely than those with anorexia to overestimate their size. There was also a greater disparity between what they wanted to look like and what they believed they looked like.

People with bulimia nearly always practice it in secret, and, although they may be underweight, they are not always anorexic. Symptoms or signs of bulimia may, therefore, be very subtle and go unnoticed. They may include:

Evidence of discarded packaging for laxatives, diet pills, emetics (drugs that induce vomiting), or diuretics (medications that reduce fluids)
Regularly going to the bathroom right after meals
Suddenly eating large amounts of food or buying large quantities that disappear right away
Compulsive exercising
Broken blood vessels in the eyes (from the strain of vomiting)
Pouch-like appearance to the corners of the mouth due to swollen salivary glands (occurs within days of vomiting in about 8% of people with bulimia)
Dry mouth
Tooth cavities, diseased gums, and irreversible enamel erosion from excessive acid
Rashes and pimples
Small cuts and calluses across the tops of finger joints due to self-induced vomiting

Weight Loss. The primary symptom of anorexia is major weight loss from excessive and continuous dieting, which may either be restrictive dieting or binge-eating and purging.

Other symptoms of anorexia may include:

Infrequent or absent menstrual periods
Compulsive exercising coupled with excessive thinness
Refusal to eat in front of others
Ritualistic eating, including cutting food into small pieces
Hypersensitivity to cold -- some women wear several layers of clothing to both keep warm and hide their thinness
Yellowish skin, especially on the palms of the hands and soles of the feet -- from eating too many vitamin A-rich vegetables such as carrots
Dry skin covered with fine hair
Thin scalp hair
Cold or swollen feet and hands
Stomach problems, including bloating after eating
Confused or slowed thinking
Poor memory or judgment

Diagnosis

The first step towards a diagnosis is to admit the existence of an eating disorder. Often, the patient needs to be compelled by a parent or others to see a doctor because the patient may deny and resist the problem. Some patients may even self-diagnose their condition as an allergy to carbohydrates, because after being on a restricted diet, eating carbohydrates can produce gastrointestinal problems, dizziness, weakness, and palpitations. This may lead such people to restrict carbohydrates even more severely.

It is often extremely difficult for parents as well as the patient to admit that a problem is present. For example, because food is such an intrinsic part of the mother-child relationship, a child's eating disorder might seem like a terrible parental failure. Parents may have their own emotional issues with weight gain and loss and perceive no problem with having a "thin" child.

It is recommended that a supportive companion be present during part of the initial medical interview to offer additional information on the patient's eating history and to help offset any resistance or denial the patient may express.

Various questionnaires are available for assessing patients. The Eating Disorders Examination (EDE), which is an interview of the patient by the doctor, and the self-reported Eating Disorders Examination-Questionnaire (EDE-Q) are both considered valid tests for assessing eating disorder diagnosis and determining specific features of the individual’s condition (such as vomiting or laxative use).

Another test is called the SCOFF questionnaire. It is proving to be very reliable in accurately identifying both very young and adult patients who meet the full criteria for anorexia or bulimia nervosa. (It may not be as accurate in people who do not meet the full criteria.)

SCOFF Questionnaire

Do you make yourself Sick because you feel uncomfortably full?

Do you worry you have lost Control over how much you eat?

Have you recently lost more than One stone 's worth of weight (14 pounds) in a 3-month period?

Do you believe yourself to be Fat when others say you are too thin?

Would you say that Food dominates your life?

Answering yes to two of these questions is a strong indicator of an eating disorder.

In spite of the prevalence of bulimia, a majority of doctors have never diagnosed bulimia in a patient. Younger and female doctors are more likely to detect bulimia. A doctor should make a diagnosis of bulimia if there are at least two bulimic episodes per week for 3 months. Because people with bulimia tend to have complications with their teeth and gums, dentists could play a crucial role in identifying and diagnosing bulimia.

Generally, an observation of physical symptoms and a personal history will quickly confirm the diagnosis of anorexia. The standard criteria for diagnosing anorexia nervosa are:

The patient's refusal to maintain a body weight normal for age and height
Intense fear of becoming fat even though underweight
A distorted self-image that results in diminished self-confidence
Denial of the seriousness of emaciation and starvation
The loss of menstrual function for at least 3 months

The doctor then categorizes the anorexia further:

Restricting (severe dieting only)
Anorexia bulimia (binge-purge behavior)

Because the disorder rarely shows up in men, doctors may not be on the lookout for it in male patients, even if they show classic symptoms of anorexia. Doctors should be very aware of these symptoms in anyone, particularly in athletes and dancers.

Once a diagnosis is made, doctors should immediately check for any serious complications of starvation. They should also rule out other medical disorders that might be causing the anorexia. Tests should include:

A complete blood count
Tests for electrolyte imbalances (low potassium levels mean the disorder is more likely to be accompanied by the binge-purge syndrome)
Test for protein levels
An electrocardiogram and a chest x-ray
Tests for liver, kidney, and thyroid problems
A bone density test

Treatment

Treatment goals for eating disorders include:

Restore normal weight for anorexia nervosa
Reduce, and hopefully stop, binge eating and purging for bulimia nervosa
Treat physical complications and any associated psychiatric disorders
Teach patients proper nutritional habits and how to develop healthy eating patterns and meal plans
Change patients’ dysfunctional thoughts about the eating disorder
Improve self-control, self-esteem, and behavior
Provide family counseling
Prevent relapse

The first major difficulty in treating eating disorders is resistance by everyone involved:

The anorexic patient often believes that the emaciation is normal and even attractive.
The bulimic patient may feel that purging is the only way to prevent obesity.
Even worse, the anorexic condition may be encouraged by friends who envy thinness or by dance or athletic coaches who encourage low body fat.
The family itself may deny the problem and be obstructive or manipulative, adding to the difficulties of treatment.

It is very important that the patient and any close friends and relatives be informed about the serious potential of these conditions and the importance of receiving immediate help.

A multidisciplinary team approach with consistent support and counseling is essential for long-term recovery from all severe eating disorders. Depending on the severity and type of disorder, team members may include:

Doctors specializing in relevant medical complications
Dietitians
Cognitive-behavioral therapists
Psychotherapists
Nurses

All should be skilled in treating eating disorders. Studies have found that people treated by such specialists have a lower mortality rate than those treated only as psychiatric patients.

Patients may drop out of programs if they have unrealistic expectations of being "cured" simply through the therapists' insights. Before a program begins, the following possibilities should be made clear:

The process is painful and requires hard work on the part of the patient and family.
A number of therapeutic methods are likely to be tried until the patient succeeds in overcoming these difficult disorders.
Relapse is common but should not be greeted with despair. (In one study, about 90% of bulimic patients responded to treatments after 6 years.)

Although the outcome for bulimics is generally more favorable than for anorexics, long-term studies are showing recovery in most people treated for anorexia.

Psychotherapies. Eating disorders are nearly always treated with some form of psychiatric or psychologic treatment. Depending on the problem, certain psychologic approaches may work better than others.

Medications. Various medications may be helpful for patients depending on the type of eating disorder, psychiatric state, and severity of the condition.

Nutritional Rehabilitation. Nutritional counseling can help patients regain weight and learn normal expectations concerning hunger and eating patterns.

The patient’s condition, social circumstances, and health insurance coverage determine the type of treatment facility -- inpatient hospitalization, residential hospitalization, partial hospitalization, or outpatient care. Weight is not the sole determining factor. The patient’s overall physical condition, psychological state, behavior patterns, and family support are all factors. Patients and their families should discuss with their doctors the various options available and how structured and intense the treatment should be.

Treatment for Bulimia

Some experts recommend a stepped approach for patients with bulimia, which follow specific stages depending on the severity and response to initial treatments:

Support groups. This is the least expensive approach and may be helpful for patients who have mild conditions with no health consequences.
Cognitive-behavioral therapy (CBT) along with nutritional therapy is the preferred first treatment for bulimia that does not respond to support groups.
Drugs. The drugs used for bulimia are typically antidepressants known as selective serotonin-reuptake inhibitors (SSRIs). A combination of CBT and SSRIs is very effective if CBT alone is not helpful.

Patients with bulimia rarely need hospitalization except under the following circumstances:

Binge-purge cycles have led to anorexia
Drugs are needed for withdrawal from purging
Major depression is present

Psychologic Therapy. Cognitive-behavioral therapy (CBT) is the first-line of therapy for most patients with bulimia and is successful in about 60% of cases. Patients who do not respond to CBT tend to be less committed to the treatment, are more preoccupied with their symptoms, and have ritualized eating behaviors. Interpersonal therapy may be tried if CBT fails. Some studies have found that bulimic patients respond well to self-help CBT with a CD-ROM or manual. These methods, the research found, reduced the incidence of both binging and vomiting. Patients who do not respond to CBT may wish to try interpersonal therapy (also known as “talk therapy’), where therapists help patients explore how social and family relationships may affect their eating disorder.

Antidepressants. The most common antidepressants prescribed for bulimia are selective serotonin reuptake inhibitors (SSRIs) such as:

Fluoxetine (Prozac)
Sertraline (Zoloft)
Paroxetine (Paxil)
Fluvoxamine (Luvox)

Studies are mixed, however, on whether SSRIs offer an additional advantage in reducing binge-eating compared to CBT. Fluoxetine has been approved for bulimia and is considered the drug of choice, although some studies suggest that other SSRIs work just as well.

Antidepressants may increase the risks for suicidal thoughts and actions during the first few months of treatment. In particular, adolescents and young adults should be carefully monitored during this time period for any changes in behavior.

Topiramate. The antiepileptic drug topiramate (Topamax) has been shown in studies to reduce bingeing and purging episodes in patients with bulimia. However, due to this drug’s risk for serious side effects, topiramate should be used only if other medication has failed. In addition, because people tend to lose weight while taking topiramate, it should not be used by patients who have low or even normal body weight.

Treatment for Anorexia

Treatment goals for patients with anorexia require a team approach. Doctors should immediately check and treat any medical problems related to the condition, such as bone loss, imbalances in important electrolytes, and any hormonal deficiencies, including thyroid and reproductive hormones. Nutrition rehabilitation and psychotherapy also plays an important part in anorexia therapy.

Many moderately to severely ill anorexic patients require hospitalization when:

Weight loss continues even with outpatient treatment
Weight is 30% below ideal body weight
Depression is severe or the patient is suicidal
There are symptoms of medical complications (disturbed heart rate, low potassium levels, altered mental status, low blood pressure, severe sensations of cold)

When severe metabolic or medical problems occur, patients with anorexia may need to be hospitalized either voluntarily or involuntarily. A variety of partial hospitalization or day care programs are also available.

Duration of Inpatient Treatment. For people with severe anorexia, many experts believe that 10 - 12 weeks of hospitalization with full nutritional support are required to reach ideal body weight. Check to see how many days your insurance company allows for inpatient treatment. Many rarely cover more than 15 days in the hospital. It is particularly important for women with both diabetes and anorexia to achieve 100% of ideal weight before being released.

The body mass index (BMI) is the measurement of body fat. It is derived by multiplying a person's weight in pounds by 703 and then dividing it twice by the height in inches.

A healthy BMI for women over age 20 is 19 - 24.
Those over 24 are considered to be at risk for health problems related to obesity.
Those under 17.5 are considered to be at risk for health problems related to anorexia. (However, young teenagers can have lower BMIs without necessarily being anorexic.)

For example, a woman who is 5'5" and weighs 125 pounds has a healthy BMI of 21. A woman at the same height who weighs 90 pounds would have a dangerously low BMI of 15.

Nutritional intervention is essential. Weight gain is associated with fewer symptoms of anorexia and with improvements in both physical and mental function. Restoring good nutrition can help reduce bone loss, and raising the level of energy available to the body by balancing food intake and exercise can normalize hormonal function. Restoring weight is also essential before the patient can fully benefit from additional psychotherapeutic treatments.

Goals for Weight Gain and Good Nutrition. A weight-gain goal of 2 - 3 pounds a week for hospitalized patients, and 0.5 - 1 pound a week for outpatients, is strongly encouraged. Patients typically begin with a calorie count as low as 1,000 - 1,600 calories a day, which is then gradually increased to 2,000 - 3,500 calories a day. Patients may initially experience intensified anxiety and depressive symptoms, as well as fluid retention, in response to weight gain. These symptoms decrease as the weight is maintained.

Tubal Feedings. Feeding tubes that pass through the nose to the stomach are not commonly used, since many experts believe they discourage a return to normal eating habits and because many patients interpret their use as punishing forced feeding. However, for patients who are at significant risk or for those who refuse to eat, tube feeding through the nose or through a tube inserted through the abdomen into the stomach can help with weight gain and improve the nutritional status of the patient. One method is to administer such feedings only at nighttime, with the patient eating normally during the day.

Intravenous Feedings. Intravenous feedings may be needed in life-threatening situations. This involves inserting a needle into the vein and infusing fluids containing nutrients directly into the bloodstream. Intravenous feedings must be administered carefully. When given at home, no more than the prescribed amount should be used. Overzealous administration of glucose solutions can trigger the so-called refeeding syndrome, in which phosphate levels drop severely and cause a condition called hypophosphatemia. Emergency symptoms include irritability, muscle weakness, bleeding from the mouth, disturbed heart rhythms, seizures, and coma.

The role of exercise in recovery is complex, since, for those with anorexia, excessive exercise is often a component of the original disorder. However, very controlled exercise regimens may be used as both a reward for developing good eating habits and as a way to reduce the stomach and intestinal distress that accompanies recovery. Exercise should not be performed if severe medical problems still exist and if the patient has not gained significant weight. The goal of exercise should be on improving physical fitness and health, not on burning off calories.

Psychologic Therapies Used in Anorexia. Family therapy is an important component of anorexia treatment, especially for children and adolescents. Adults usually begin with motivational psychotherapy that provides an empathetic setting and rewards positive efforts towards weight gain. After weight is restored, cognitive behavioral therapy techniques are helpful.

Antidepressants. Studies have not reported many benefits for treating anorexia nervosa with selective serotonin reuptake inhibitors (SSRIs), the antidepressants that are often useful for patients with bulimia. A few studies suggest that these drugs could be useful for people with anorexia nervosa who also have obsessive-compulsive disorder (OCD).

Doctors hoped that SSRIs could help prevent relapse in patients who have successfully restored their body weight. However, in a well-designed study in the Journal of the American Medical Association there was no difference in the time to relapse between patients who received fluoxetine (Prozac) and those who received placebo.

Nutritional Supplements. Calcium and vitamin D supplements are often recommended. Some studies have reported that zinc supplements may help patients gain weight.

Therapy

Eating disorders are nearly always treated with some form of psychiatric or psychologic treatment. Depending on the problem, different psychologic approaches may work better than others.

Cognitive-behavioral therapy (CBT) works on the principle that a pattern of false thinking and belief about one's body can be recognized objectively and altered, thereby changing the response and eliminating the unhealthy reaction to food. One approach for bulimia is the following:

Over a period of 4 - 6 months the patient builds up to eating 3 meals a day, including foods that the patient has previously avoided.
During this period, the patient monitors and records the daily dietary intake along with any habitual unhealthy reactions and negative thoughts toward eating while they are occurring.
The patient also records any relapses (binges or purging). Such lapses are reported objectively and without self-criticism and judgment.
The patient discusses the responses with a cognitive therapist at regular sessions. Eventually the patient is able to discover the false attitudes about body image and the unattainable perfectionism that underlies the opposition to food and health.
Once these habits are recognized, food choices are broadened, and the patient begins to challenge any entrenched and automatic ideas and responses. The patient then replaces them with a set of realistic beliefs along with actions based on reasonable self-expectations.

Interpersonal therapy deals with depression or anxiety that might underlie the eating disorders along with social factors that influence eating behavior. This therapy does not deal with weight, food, or body image at all.

The goals are the following:

To express feelings
To discover how to tolerate uncertainty and change
To develop a strong sense of individuality and independence
To address any relevant sexual issues or traumatic or abusive event in the past that might be a contributor of the eating disorder

Studies generally report that interpersonal therapy is not as effective as cognitive therapy for bulimia and binge eating, but may be useful for some patients with anorexia. The skill of the therapist plays a strong role in its success.

Because of the major role family attitudes play in eating disorders, one of the first steps in treating the patient with early-onset anorexia is to also treat the family. Family therapy can be useful for both younger and older patients.

If the patient is hospitalized, experts recommend that family therapy start after the patient has gained weight, but before discharge. It should usually continue after the patient has left the hospital.

The feelings of intense guilt and anxiety that caregivers experience are probably similar to those produced by living with a person who is suicidal. An over-involved parent may even support the patient's eating disorder for various reasons:

Some parents may be afraid of releasing some underlying anger or grief directed at the patient.
Other parents may identify with the goal of thinness and not even perceive that their child is unhealthily underweight.

In such cases, it is extremely important that the family members fully understand the danger of this disorder and that they are collaborating in their child's illness, or even death, by encouraging this state.

Resources

www.nimh.nih.gov -- National Institute of Mental Health
www.anad.org -- National Association of Anorexia Nervosa and Associated Disorders
www.aedweb.org -- Academy for Eating Disorders
www.nationaleatingdisorders.org -- Eating Disorders Awareness and Prevention
www.eatright.org -- American Dietetic Association
www.aabt.org -- Association for Behaviorial and Cognitive Therapies
www.psych.org -- The American Psychiatric Association
www.aacap.org -- American Academy of Child and Adolescent Psychiatry

References

American Psychiatric Association. Treatment of patients with eating disorders, third edition. American Psychiatric Association. Am J Psychiatry. 2006 Jul;163(7 Suppl):4-54.

Berkman ND, Lohr KN, Bulik CM. Outcomes of eating disorders: a systematic review of the literature. Int J Eat Disord. 2007 May;40(4):293-309.

Bulik CM, Berkman ND, Brownley KA, Sedway JA, Lohr KN. Anorexia nervosa treatment: a systematic review of randomized controlled trials. Int J Eat Disord. 2007 May;40(4):310-20.

Morris J, Twaddle S. Anorexia nervosa. BMJ. 2007 Apr 28;334(7599):894-8.

Signorini A, De Filippo E, Panico S, De Caprio C, Pasanisi F, Contaldo F. Long-term mortality in anorexia nervosa: a report after an 8-year follow-up and a review of the most recent literature. Eur J Clin Nutr. 2007 Jan;61(1):119-22. Epub 2006 Aug 2.

Schmidt U, Lee S, Beecham J, et al. A randomized controlled trial of family therapy and cognitive behavior therapy guided self-care for adolescents with bulimia nervosa and related disorders. Am J Psychiatry. 2007 Apr;164(4):591-8.

Review Date:
12/31/2007
Reviewed By:
Harvey Simon, MD, Editor-in-Chief, Associate Professor of Medicine, Harvard Medical School; Physician, Massachusetts General Hospital. Also reviewed by David Zieve, MD, MHA, Medical Director, A.D.A.M., Inc.

A.D.A.M. Copyright

adam.com

Attention deficit hyperactivity disorder

FitSugar — Wed, 08 Oct 2008 17:35:28 -0700

In This Report

Highlights
Introduction
Risk Factors
Causes
Diagnosis
Other Disorders Associated ...
Complications
Treatment
Medications
Behavioral Management
Other Treatments
Resources
References

HEALTH GUIDE REFERENCE FROM A.D.A.M

Highlights

Drug Approval

In 2007, the Food and Drug Administration (FDA) approved lisdexamfetamine (Vysvanse), a new stimulant drug for the treatment of attention-deficit/hyperactivity disorder (ADHD). The active ingredient in lisdexamfetamine is similar to dextroamphetamine, the drug used in Dexedrine and Adderall.

Drug Warning

In 2007, the FDA instructed the manufacturers of all ADHD drugs to include drug warning labels describing the risks for heart and psychiatric side effects. Doctors should carefully evaluate patients for any risk factors. Reports have linked ADHD drugs to sudden death in patients with serious heart problems. There is also a slightly increased risk for auditory hallucinations, paranoia, and manic behavior even in patients with no history of psychiatric problems. The FDA warning applies to all stimulant ADHD drugs and to the non-stimulant drug atomoxetine (Strattera).

Ritalin Can Stunt Growth

After 3 years of methylphenidate (Ritalin) treatment, children are about an inch shorter and 6 pounds lighter than their peers who do not take this drug, according to a 2007 study in the Journal of the American Academy of Child and Adolescent Psychiatry.

ADHD Improves Over Time

ADHD symptoms may improve over time regardless of the treatment approach, indicates a 2007 study in the Journal of the American Academy of Child and Adolescent Psychiatry. Researchers found that medication, behavioral therapy, or a combination of the two all helped produce improvement after 3 years. There appeared to be no significant difference between children who took medication and those who did not.

Neurofeedback May Help ADHD

Neurofeedback (also known as biofeedback) is a non-drug treatment that may help improve attention and behavior problems associated with ADHD. This treatment approach involves teaching children to control their brain wave activity.

Introduction

According to the U.S. National Institute of Mental Health, attention deficit hyperactivity disorder (ADHD) is a legitimate psychologic condition.

ADHD is a syndrome generally characterized by the following symptoms:

Inattention
Distractibility
Impulsivity
Hyperactivity

Some experts categorize ADHD into three subtypes:

Behavior marked by hyperactivity and impulsivity, but not inattentiveness
Behavior marked by inattentiveness, but not hyperactivity and impulsivity
A combination of the above two

There is some debate over these criteria. Some argue the condition is over-diagnosed. Others say it's underdiagnosed. (See Difficulties in Identifying Children with ADHD later in this article.) One-third of cases are accompanied by learning disabilities and other neurologic or emotional problems, making an ADHD diagnosis particularly difficult. It is likely that the term attention-deficit hyperactivity disorder will eventually give way to subgroups of problems that include some of these general symptoms.

In the United States, about 4.7 million children ages 3 - 17 have been diagnosed at some point with ADHD. This accounts for 7.4% of all American children in this age range.

ADHD is a genuine disorder, but it is telling that the U.S. accounts for 90% of worldwide prescriptions for stimulants for ADHD. It is not known whether this reflects a real increase in ADHD, or a better ability to recognize it. Some say it may be an indication of a culture that places excessive value on normalcy and academic achievement at the expense of more frequent diagnoses.

Symptoms of ADHD usually occur before the age of 7. Studies indicate that ADHD symptoms in preschool children with ADHD do not differ significantly from older children.

The classic ADHD symptoms do not always adequately describe the child's behavior, nor do they describe what is actually happening in the child's mind. Some experts are focusing on deficits in "executive functions" of the brain to understand and describe all ADHD behaviors. Such impaired executive functions in ADHD children can cause the following problems:

Inability to hold information in short-term memory
Impaired organization and planning skills
Difficulty in establishing and using goals to guide behavior, such as selecting strategies and monitoring tasks
Inability to keep emotions from becoming overpowering
Inability to shift efficiently from one mental activity to another

Hyperactivity. The term hyperactive is often confusing since, for some, it suggests a child racing around non-stop. A boy with ADHD playing a game, for instance, may have the same level of activity as another child without the syndrome. But when a high demand is placed on the ADHD child's attention, his brain motor activity intensifies beyond the levels of the other children. In a busy environment, such as a classroom or a crowded store, ADHD children often become distracted and react by pulling items off the shelves, hitting people, or spinning out of control into erratic, silly, or strange behavior.

Impulsivity and Temper Explosions. Even before the "terrible twos," impulsive behavior is often apparent. The toddler may gleefully make erratic and aggressive gestures, such as hair pulling, pinching, and hitting. Temper tantrums, normal in children after age 2, are usually exaggerated and not necessarily linked to a specific negative event in the life of an ADHD child. One of the most painful events a parent may experience is an abrupt and aggressive attack that may occur after cuddling a young ADHD child. Often this reaction seems to be caused not by anger, but by the child's apparent inability to endure overstimulation or displays of physical affection.

Attention and Concentration. ADHD children are usually distracted and made inattentive by an overstimulating environment (such as a large classroom). They are also inattentive when a situation is low-key or dull. Some experts believe that certain parts of the brain in ADHD children may be underactive, so the children fail to be aroused by nonstimulating activities. In contrast, they may exhibit a kind of "super concentration" to a highly stimulating activity (such as a video game or a highly specific interest). Such children may even become over-attentive -- so absorbed in a project that they cannot modify or change the direction of their attention.

Impaired Short-Term Memory. Many experts now believe that an essential feature in ADHD, as well as in learning disabilities, is an impaired working (also called short-term) memory. People with ADHD can't hold groups of sentences and images in their mind long enough to extract organized thoughts. They are not necessarily inattentive. Instead, a patient with ADHD may be unable to remember a full explanation (such as a homework assignment), or unable to complete processes that require remembering sequences, such as model building. In general, children with ADHD are often attracted to activities (television, computer games, or active individual sports) that do not tax the working memory, or produce distractions. Children with ADHD have no differences in long-term memory compared with other children.

Inability to Manage Time. Studies suggest that children with ADHD have difficulties being on time and planning the correct amount of time to complete tasks. (This may coincide with short-term memory problems.) In one study, although children with probable ADHD were able to self-report many ADHD symptoms, they tended to believe they used their time wisely, in contrast to reports by their teacher.

Lack of Adaptability. ADHD children have a very difficult time adapting to even minor changes in routines, such as getting up in the morning, putting on shoes, eating new foods, or going to bed. Any shift in a situation can precipitate a strong and noisy negative response. Even when they are in a good mood, they may suddenly shift into a tantrum if met with an unexpected change or frustration. In one experiment, ADHD children could closely focus their attention when directly cued to a specific location, but they had difficulty shifting their attention to an alternative location.

Hypersensitivity and Sleep Problems. ADHD children are often hypersensitive to sights, sounds, and touch. They usually complain excessively about stimuli that seem low key or bland to others. Sleeping problems usually occur well after the point when most small children sleep through the night. In one study, 63% of children with ADHD had trouble sleeping.

A. Either 1 or 2 should be present:

1. Should have 6 or more of the following symptoms of inattention, persisting for at least 6 months to a degree that is maladaptive and inconsistent with developmental level:

Often fails to give close attention to detail, makes careless mistakes

Often has difficulty sustaining attention in tasks or play

Often does not seem to listen when spoken to directly

Often does not follow through and fails to finish tasks

Has difficulty organizing tasks and activities

Avoids or dislikes tasks requiring sustained mental effort

Often loses things necessary for tasks or activities

Is often easily distracted by extraneous stimuli

Is often forgetful in daily activities

2. Should have 6 or more of the following symptoms of hyperactivity-impulsivity that lasts for at least 6 months to a degree that is maladaptive and inconsistent with developmental level:

Often fidgets or squirms when sitting

Has difficulty remaining seated when required to do so

Often runs about or climbs excessively in inappropriate situations

Has difficulty playing quietly

Is often "on the go"

Often talks excessively

Often blurts out answers to questions before they have been completed

Has difficulty waiting for his or her turn

Often interrupts or intrudes on others

Note: Patients with A1 symptoms are diagnosed with ADHD, predominantly inattentive type. Those with A2 are diagnosed with ADHD, predominantly hyperactive-impulsive type. Those with both A1 and A2 are diagnosed as ADHD, combined-type.

B. Onset of some symptoms before the age of 7. However, children with the inattentive subtype are not often diagnosed until they are above 7 years of age.

C. Symptoms occur in two or more settings. For example, at home and at school.

D. Clear evidence of significant impairment in social or academic functioning.

E. Not caused by a pervasive developmental disorder, schizophrenia, or any other psychotic disorder, and is not better accounted for by another mental disorder, including anxiety or depression.

Source: American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 4th Ed. (Text Revision). Washington, DC: 2000.

Risk Factors

ADHD is most often diagnosed in boys. However, there is some evidence that it is underdiagnosed in girls. Until recently, all major studies were conducted using boys as subjects. Important studies on girls with ADHD are now underway. A major study reported that girls with the condition experience the same multiple impairments as boys do.

Although ADHD is primarily thought of as a childhood disorder, diagnoses of attention-deficit disorder in adults are on the rise. Methylphenidate (Ritalin) was prescribed for nearly 800,000 adults in the U.S. in 1997, nearly three times the number in 1992. As of 2005, experts estimated that ADHD affects about 4.1% of adults ages 18 - 44 years in a given year.

How Is ADHD Identified in Adults?

Research suggests that ADHD affects 2 - 6% of the adult population, assuming that one- to two-thirds of cases persist into adulthood. ADHD in adults always occurs as a continuum of the childhood condition. Adult-onset symptoms are likely due to other factors. Diagnosing adult ADHD can be a difficult problem since hyperactivity typically wanes as children get older, while attention and organizational problems may develop in older people. Some experts believe, then, that the number of adults with ADHD is underestimated.

A rating scale using four factors may be useful in identifying adults with ADHD:

Inattention and memory problems. (Examples: losing or forgetting things, being absent-minded, not finishing things, misjudging time, depending on others for order, having trouble getting started, changing jobs or projects in the middle.)
Hyperactivity and restlessness. (Examples: always being on the go, fidgety, easily bored, taking risks, liking active and fast paced jobs and activities, such as being a sales representative or stockbroker.)
Impulsivity and emotional instability. (Examples: saying things without thinking first, interrupting others, being annoying to others, easily frustrated, easily angered, having unpredictable moods, driving recklessly, having high relationship and job turnover.)
Problems with self worth. (Examples: Avoids new challenges, appears confident to others but not to oneself.)

Doctors use adult reports of their childhood behaviors and experiences when searching for clues for a diagnosis. Interestingly, the disorder seems to be distributed equally between adult women and men.

How Serious Is Attention Deficit Disorder in Adults?

Accompanying Emotional, Personality, and Learning Disorders. Between 19 - 37% of adults with ADHD have depression or bipolar disorder. Between 25 - 50% have an anxiety disorder. Bipolar disorder plus ADHD, in fact, may be very difficult to differentiate from ADHD alone in adults.

Accompanying Learning Disorders. About 20% of adults with ADHD have learning disorders, usually dyslexia and auditory processing problems. These problems should be considered in any treatment plan.

Effect on Work. Compared to adults without ADHD, those with the condition tend to reach lower educational levels, earn less money, and be fired more often. In fact, one article reported that by the time they are in their 30s, about 35% of ADHD adults are self-employed.

Substance Abuse. About 1 in 5 adults with ADHD also contend with substance abuse. Studies indicate that adolescents with ADHD are twice as likely to smoke cigarettes as their peers who do not have ADHD. Cigarette smoking during adolescence is a risk factor for the development of substance abuse in adulthood.

Sleep Disorders. Sleep disorders, especially restless legs syndrome and sleep apnea, are common in adults and children with ADHD. Sleep apnea is a disorder in which a person temporarily stops breathing during sleep, perhaps hundreds of times. In most cases the person is unaware of it, although sometimes they awaken and gasp for breath. It is usually accompanied by snoring. One report suggested that treating sleep apnea in adults with both conditions may help reduce ADHD symptoms. [For more information, see In-Depth Report #65: Sleep apnea.]

Causes

Brain Structures. Research using advanced imaging techniques shows there is a difference in the size of certain parts of the brain in children with ADHD compared to children who do not have ADHD. The areas showing change include the prefrontal cortex, the caudate nucleus and globus pallidus, and the cerebellum:

The prefrontal cortex is located in the front of the brain. It is thought to be the brain's command center. It regulates the brain’s ability to block certain responses. Numerous imaging studies have indicated that the prefrontal cortex of the brain in people with ADHD may be less active than in those without the disorder.
The caudate nucleus and globus pallidus, located near the center of the brain, speed up or stop orders coming from the prefrontal cortex. In some reports, these areas have been smaller than average in young children with ADHD, but tended to become normal as the children got older. Abnormalities in these areas may impair a person's ability to stop certain actions, resulting in the impulsivity typical of people with ADHD.
The cerebellum is the area above the brain stem. This area helps control muscle tone and balance, and synchronizes muscle activity. This has been found to be smaller in children with ADHD compared to those without the condition.

Brain Chemicals. Abnormal activity of certain brain chemicals in the prefrontal cortex may contribute to ADHD. The chemicals dopamine and norepinephrine are of special interest. Dopamine and norepinephrine are neurotransmitters, or chemical messengers, that affect both mental and emotional functioning. They also play a role in the "reward response." This response occurs when a person experiences pleasure in response to certain stimuli (such as food or love). Studies suggest that increased levels of the brain chemicals glutamate, glutamine, and GABA -- collectively called Glx -- interact with the pathways that transport dopamine and norepinephrine.

Nerve Pathways. Another area of interest is a network of nerves called the basal-ganglia thalamocortical pathways. Abnormalities along this neural route have been associated with ADHD, Tourette syndrome, and obsessive-compulsive disorders, all of which share certain symptoms.

Genetic factors may play the most important role in ADHD. The relatives of ADHD children (both boys and girls) have much higher rates of ADHD, antisocial, mood, anxiety, and substance abuse disorders than the families of non-ADHD children. A study reported that 90% of children with a diagnosis of ADHD shared it with their twin.

Genetic Factors Regulating Dopamine and Advantages in Early Man. Most of the research on the underlying genetic mechanisms targets the neurotransmitter dopamine. Variations in genes that regulate specific dopamine receptors have been identified in a high proportion of people with addictions and ADHD. Such genes have been associated with novelty seeking and extroversion. Some experts theorize that the genetic variants may have first appeared thousands of years ago, and affect as many as half of ADHD children. Furthermore, the genetic variations may have offered some benefits to their early carriers. In such people, a genetic predilection for novelty-seeking and risk-taking may have supplied an advantage in reproduction, mating, hunting, and achieving dominance.

Genetic Resistance to Thyroid Hormone. About 50% of adults and 70% of children with a genetic resistance to thyroid hormone, essential for normal brain development, have ADHD. People who have this condition appear to have a more severe form of ADHD. The thyroid disorder is not a common cause of ADHD. Only those with a family history of thyroid disease are at risk.

Infant malnutrition is a strong risk indicator of ADHD. Even if children receive enough food later on, infants who suffer from malnutrition may develop behavior problems, the most prevalent being attention-deficit disorder.

Deficiencies in Zinc and Essential Fatty Acids. Several dietary factors have been researched in association with ADHD, including sensitivities to certain food chemicals, deficiencies in fatty acids (compounds that make up fats and oils) and zinc, and sensitivity to sugar.

Some studies have found an association between deficiencies in certain fatty acids and ADHD. Other research reports an association between zinc deficiencies and ADHD. Zinc aids in the breakdown of fatty acids, which affects dopamine, the neurotransmitter likely to be involved with ADHD.

No clear evidence has emerged, however, that implicates any of these nutritional factors in ADHD.

Research suggests that prenatal exposure to tobacco, alcohol, environmental lead, and other toxins may increase the risk for ADHD and conduct disorders.

Diagnosis

Important factors for making a diagnosis of attention-deficit hyperactivity disorder (ADHD) include:

Children between ages 6 - 12 should first be evaluated for ADHD if they show symptoms of inattention, hyperactivity, impulsivity, academic underachievement, or behavior problems in at least two settings. Such behaviors should have been harmful for the child academically or socially for at least 6 months.
The child should meet the official symptom guidelines.
A diagnosis requires detailed reports by parents or caregivers. It should be noted that a mother's description of her child's behavior is a very accurate and reliable guide for diagnosing ADHD. Parents should not be shy about insisting on further evaluation if their experience does not match a doctor's single observation of their child.
Guidelines for primary care doctors emphasize the importance of obtaining direct evidence from the classroom teacher or other school-based professionals about the child's symptoms and their duration, and evidence of functional impairment in the school setting.
The child should be assessed for accompanying conditions (such as learning difficulties).

No laboratory or imaging tests exist to reliably diagnose ADHD. A diagnosis relies only on behavioral symptoms and ruling out other disorders. Many experts believe that the disorder is both over- and underdiagnosed. Diagnosis of attention-deficit hyperactivity disorder is difficult for some of the following reasons:

Factors Leading to the Over-Diagnosis of ADHD:

The popularity methylphenidate (Ritalin) has encouraged some parents and teachers to pressure doctors into prescribing this standard ADHD drug for children who are aggressive or who have poor grades. Often with careful testing many of these children do not meet the criteria for the illness. Children may have other diagnoses, other behavioral or emotional problems, or no problems at all.
Other factors that may contribute to misdiagnosis include children who are young for their grade and therefore socially and intellectually immature, and social and economic problems such as single parent households.

Factors Leading to the Under-Diagnosis of ADHD:

Some evidence suggests that many girls with ADHD may go underdiagnosed. Research indicates that girls with ADHD are often inattentive but not hyperactive or impulsive. In fact, older girls with ADHD tend to have social problems due to withdrawal and internalized emotions, showing symptoms of anxiety and depression. The inattentive subtype, in any case, may first show up in older children and adolescents.
Doctors may fail to diagnose children with ADHD because they often behave normally in the quiet doctor's office where there are no distractions to trigger symptoms. In addition, doctors may be unfamiliar with how to diagnose the condition.
In spite of the fact that there seems to be no differences in response to treatment among population groups, African-American, Hispanic, and Asian children with ADHD are half as likely to be diagnosed and treated as Caucasian children. By high school, the racial disparity increases to the level that the medication rate for blacks is one-fifth of that for whites.

The doctor will first require a detailed history of the child's behavior. Doctors will match this against a standardized checklist to define the disorder.

The parents should describe the following:

Specific problems, beginning as early as possible, they have encountered during the child's development -- school reports are very helpful
Sibling relationships
Recent life changes
A family history of ADHD
Eating habits
Sleep patterns
Speech and language development
Any problems during the mother's pregnancy or during delivery
Any history of medical or physical problems, particularly allergies, chronic ear infections, and hearing difficulties

The health professional will want to know how the parents handle different situations, and may want to observe them interacting with the child.

The child should also be given a general physical examination to determine if any medical conditions are present. The child should be given a hearing test to rule out hearing abnormalities as a source of behavioral problems.

Various tests are available to test neurologic, intellectual, and emotional development problems. Most involve learning and problem solving tasks that help define the particular areas that are most disabling. Blood or other laboratory tests are currently recommended only if the doctor suspects lead toxicity or other medical problems.

Although some doctors use a trial of a psychostimulant (usually Ritalin) to facilitate diagnosis, most experts strongly recommend against this method of diagnosis, because it is not always accurate. An improvement in symptoms is considered suggestive of ADHD, while in non-ADHD children the stimulant often increases agitation and hyperactivity. Many children and adults without the disorder have a similar response, and such a diagnostic trial may lead to unnecessary prescriptions of this drug.

Other Disorders Associated with ADHD

Several disorders may mimic or accompany attention-deficit disorder. ADHD exists alone in only about one-third of children. Many professionals object to the use of the single term "attention-deficit hyperactivity disorder" to encompass such a wide spectrum of behaviors, which they believe should be categorized into subgroups. Many of these problems require other modes of treatment and should be diagnosed separately, even if they accompany ADHD.

Attention-deficit disorder can appear without hyperactivity, in which case the child's primary symptoms are distractibility and an inability to persist in tasks.

About 14% of children diagnosed with ADHD also have oppositional-defiant disorder (ODD). The most common symptom for this disorder is a pattern of negative, defiant, and hostile behavior toward authority figures that lasts more than 6 months. In addition to displaying inattentive and impulsive behavior, these children demonstrate aggression, have frequent temper tantrums, and display antisocial behavior. A significant number of children with ODD also have anxiety disorders and depression, which should be treated separately. Many children who develop ODD at an early age go on to develop conduct disorder.

Some children with ADHD also have conduct disorder, which describes a complex group of behavioral and emotional disturbances seen in children. It includes aggression towards people and animals, destruction of property, deceitfulness, lying, or stealing, and general violation of rules.

Pervasive developmental disorder (PDD) is rare and usually marked by autistic-type behavior, hand-flapping, repetitive statements, slow social development, and speech and motor problems. If a child who has been diagnosed with ADHD does not respond to treatment, the parents might inquire about PDD, which often responds to antidepressants. Some children with PDD may also benefit from stimulants.

Children with ADHD often have difficulties with tasks that involve listening or hearing. Research is indicating that symptoms of the two disorders often overlap but may actually be two distinct disorders. Hearing problems themselves may cause ADHD symptoms.

Children diagnosed with attention-deficit disorder may also have bipolar disorder, commonly called manic depression. Indications of this problem include episodes of depression and mania (with symptoms of irritability, rapid speech, and disconnected thoughts), sometimes occurring at the same time. [For more information, see In-Depth Report #66: Bipolar disorder.] Both disorders often cause inattention and distractibility and may be difficult to distinguish, particularly in children. Children with mania and ADHD may have more aggression, behavioral problems, and emotional disorders than those with ADHD alone. In some cases, ADHD in children or adolescents can even be a marker for an emerging bipolar disorder. The primary way to differentiate bipolar disorder from ADHD is by the presence of a manic or hypomanic episode, which occurs in patients with bipolar disorder but not with ADHD. Most children with bipolar will also respond to the drug valproate, which does not typically work for ADHD in children.

Anxiety disorders commonly accompany ADHD. Obsessive-compulsive disorder is a specific anxiety disorder that shares many characteristics with ADHD and may share a genetic component. Young children who have experienced traumatic events, including sexual or physical abuse or neglect, exhibit characteristics of ADHD, including impulsivity, emotional outbursts, and oppositional behavior.

Sleep disorders or disturbances are very common with ADHD patients. Insomnia is common. In addition, specific sleep disorders -- restless legs syndrome and sleep-disordered breathing -- have been identified with hyperactivity and conduct disorder.

Restless Legs Syndrome (RLS). Some experts believe RLS and periodic limb movement disorder are strongly associated with ADHD in some children. One theory is that the two are linked by a common mechanism. The disorders have much in common, including poor sleep habits, twitching, and the need to get up suddenly and walk about frequently. They may even be genetically linked. For example, both have been associated with lower levels of dopamine in the brain, which is associated with faulty motor control, a common problem in both disorders.

Sleep-Disorder Breathing and Sleep Apnea. Some research has shown an association between mild symptoms of ADHD and sleep-disordered breathing, including snoring and obstructive sleep apnea in children and adults. Treating the sleep-related breathing disorders may improve the attention disorder in some children. (One study indicated that such problems are unlikely to be associated with children with moderate to severe ADHD.) [For more information, see In-Depth Report #65: Sleep apnea.]

Tourette Syndrome and Other Genetic Disorders. Several genetic disorders cause symptoms resembling ADHD, including fragile X and Tourette syndrome. About 50% of those with Tourette syndrome also have ADHD, and some of the treatments are similar.

Other Medical Conditions. A number of medical conditions, including hyperthyroidism and vision problems, can produce ADHD-like symptoms.

Lead. Children who ingest even low amounts of lead may manifest symptoms similar to those of ADHD. A child may be easily distractible, disorganized, and have trouble thinking logically. The major cause of lead toxicity is exposure to leaded paint, particularly in homes that are old and in poor repair.

Complications

More than half of children with attention-deficit disorder have accompanying disorders, including anxiety, depression, and conduct disorders. Children with ADHD who experience anxiety or depression are also more likely to suffer from low self-esteem.

Anti-Social Behavior. Even if these emotional disorders are absent in childhood, the ADHD child's relationship with others is volatile, and they are often unhappy from a very young age. Research indicates that any boy or girl with ADHD, particularly an aggressive child, has trouble getting along with others, and is less liked by his or her peers.

Children with the inattentive subtype of ADHD are more likely to be picked on and to spend time alone.
Children with the combined subtypes tend to have different problems. Boys with ADHD are less likely than others to empathize with people in difficult circumstances. A best friend can turn into an enemy overnight when, for example, a boy with ADHD does not perceive his friend's fearful response to over-aggressive roughhousing and fails to let up. The next day the child with ADHD has forgotten the event; the ex-friend hasn't. When a child with ADHD hurts someone, the child either may go into a state of denial or blame himself excessively. As ostracism, fear, and ridicule from peers persist from year to year, the unstable behavior, originally neurologic, becomes emotionally based. Unless this cycle is broken, serious adult problems can evolve.

Substance Abuse in Young People. Studies consistently report that young people with ADHD -- in particular those with conduct or mood disorders -- have a higher than average risk for substance abuse and that it starts in younger ages. In one study, for example, by age 11 nearly 20% of children with ADHD had tried smoking cigarettes, drinking alcohol, or both. Biologic factors associated with ADHD may make these individuals susceptible to substance abuse. Many of these young people are self-medicating their condition. In fact, according to a major analysis, Ritalin or other stimulants used to treat ADHD may help protect such patients against substance abuse. (Boys with ADHD and conduct disorder, however, still face a high risk for substance abuse. Girls with ADHD and emotional disorders may also still have a higher risk.)

High-Risk Behavior. Impulsivity in young people with ADHD can certainly cause them to take chances before thinking them through, putting them in situations where the consequences become clear only after the action has been taken. Children with ADHD and high levels of aggression are at higher risk for delinquent behavior in adolescents and criminal activity in adulthood. However, children with ADHD who are not aggressive have a lower and even normal risk for dangerous activities. Even in aggressive children with ADHD, close parental attention and early treatment can limit the risk considerably.

Although speech and learning disorders are common in children with ADHD, the disorder does not affect intelligence. People with ADHD span the same IQ range as the general population.

Many children with ADHD are underachievers, and half are held back in school at least once. Some evidence suggests that inattention may be a major factor in low academic performance in these children. About 20% also have reading difficulties, and 60% have serious handwriting problems. Adults with ADHD are also at very high risk for these conditions.

Some research suggests that ADHD persists in one- to two-thirds of those diagnosed with the condition in childhood. Many researchers describe the pattern of ADHD as they would a chronic illness, with remission and periods of worsening.

The time and attention needed to deal with a child with ADHD can change internal family relationships and have devastating effects on parents and siblings.

Effect on Parents. Studies indicate that any intervention for the child must include the parents. Parents who are responsive to their child in a positive way can help reduce the chances for oppositional behaviors. But it can be very difficult. A child with ADHD is wonderful one day and terrible the next, for no apparent reason. The parent can feel betrayed and hurt, and believe they have no control over their child. Parents must protect themselves and their child by establishing tough but kind rules about where their space ends and the child's begins. The are many effects on parents:

Mothers generally get the brunt of the emotional and physical abuse that a child with ADHD can produce.
Parents may have to give up on the idea of an immaculate house and a hot meal every night. Parents must learn that striving for perfection is among the most counterproductive goals to pursue in raising a child with ADHD, or any child.
Parents must face the hostility and anger of other parents and see their own child rejected. It is very easy to fall into an emotional black hole, and feel alone, inadequate, and helpless.
Marriages are often stressed to the breaking point because of exhaustion and disagreements between the husband and wife on how to respond to the child.

Effect on Siblings. Siblings of children with ADHD have particular difficulties, and are also at risk for psychologic impairment, depression, drug abuse, and language disorders. The non-ADHD sibling does not have the control a parent does in the management of the ADHD child's behavior and is very likely to feel alienated and alone. Children without ADHD are often victimized by siblings with ADHD who may be demanding or bullying.

A sibling who does not receive attention in their own right may begin to imitate undesirable behaviors or to act out negatively in other ways. It is very important to make the brothers and sisters equally vital to the family's functioning. However, they should never be made to feel that their value in the family is as caregivers of the ADHD sibling.

Treatment

A combination of a psychostimulant, most commonly methylphenidate (Ritalin), and cognitive-behavioral therapy is proving to be the best option for treatment of children with ADHD. Although medication can be helpful during the initial years of treatment, some research indicates that the benefits of medication eventually wear off. It appears that for ADHD symptoms may improve naturally over time, regardless of the treatment approach.

Signs that ADHD may be easing include not having to adjust medication dosages during growth spurts, no deterioration when a drug dose is missed, or new abilities to concentrate during “drug holidays.” (School vacation times are a good period to test the effectiveness of temporarily stopping medication.) The American Academy of Child and Adolescent Psychiatry suggests that parents evaluate whether medication can safely be withdrawn when children with ADHD have been free of symptoms for at least 1 year. If a child’s condition worsens after medication withdrawal, the drug should be resumed.

Developing a Treatment Approach. The following guidelines may be useful in determining a treatment approach for children with ADHD:

Behavioral techniques, possibly including dietary changes, should be tried first, if possible.
If the symptoms are severe or do not respond, a trial using medication (usually psychostimulants), in conjunction with behavior modification therapy, is advisable.

Cognitive behavioral therapy (CBT) is often administered by mental health providers, with both primary care physicians and psychiatrists prescribing medications. Unfortunately, many children do not have access to behavioral therapies, either because of lack of time or available resources.

Specific Patient Populations. Unfortunately, such guidelines do not address the following specific patient groups:

There are no definite guidelines for treating preschool children with severe ADHD. Some parents have reported very good long-term results with behavioral interventions at this age.
There are no reliable guidelines on how to treat the inattentive subtype of ADHD, which might be more common in girls.
There are no defined treatments for ADHD patients with accompanying conditions, including impaired working memory and deficits in language processing.
There are no defined treatments for children with ADHD and accompanying emotional problems, such as bipolar or anxiety disorders. (There is some evidence, for example, that children with ADHD plus anxiety disorders do worse on psychostimulants.)

Determining a Medication Regimen. Doctors still have a difficult time predicting which medications will produce beneficial results, so treatment is individualized and performed on a trial and error basis, which requires close observation and cooperation between all participants. In developing an effective medication plan, the following steps may be helpful:

Before any drug is administered, a child should be given a thorough examination for any medical problems to be sure there are no medical conditions that interfere with the medication.
Both the doctor and the parents should be very clear about the specific behaviors they hope the medication will target.
The goal is to use the lowest possible dosage that produces improved behavior.
If an initial regimen doesn't work, changing the dosage, or changing to a different medication often brings improvement.
Frequent follow-up visits should be scheduled to assess the response and to detect possible side effects.

Arguments For and Against Psychostimulants. Many parents are very disturbed by the idea of putting their children on intensive stimulant drug regimens, possibly for years, particularly given the uncertainties in diagnosis and the negative publicity surrounding the use of these drugs. Although the decision to use these drugs should not be made lightly, the negative social and emotional effects of the disorder itself for many children with ADHD are far more severe and long-lasting than the use of these drugs. For some parents and children, medication seems like a miracle and can provide desperate families with a quality of life for which they had almost given up hope. Whether or not psychostimulants are used, children and families should understand that ongoing efforts around behavior control will be necessary.

Of great concern is the dramatic increase in prescriptions for psychostimulants among preschool children. Although low doses of methylphenidate (Ritalin) may help preschoolers (ages 3 - 5 years) with ADHD, the drug can cause considerable side effects in many children. These side effects include insomnia, nervousness, anxiety, loss of appetite and weight, and slowed growth. Children in one large study grew about an inch less and weighed about 6 pounds less than normal after 3 years of methylphenidate treatment. Doctors must carefully consider the risks versus benefits when prescribing ADHD drugs to preschoolers. Children who do receive these drugs need to be carefully monitored by their doctors.

Treatment for Adult ADHD. As with children, adults with ADHD are treated with a combination of medication and psychotherapy. For medication, stimulant drugs or the non-stimulant drug atomoxetine (Strattera) are usually first-line treatments, with antidepressants a secondary option. Atomoxetine is approved specifically for adults with ADHD. Adults who have heart problems or heart condition risk factors should be aware of the cardiovascular risks associated with ADHD medication. There have been ADHD medication-associated incidents of sudden death in patients with underlying serious heart problems, and reports of stroke and heart attack in adults with cardiac risk factors.

Research increasingly supports the view that interventions for the ADHD child must also include the parents if they are to be successful. Teachers and school officials should also be educated and involved in the process.

Parents who feel they have the most control over their child's situation experience the least psychological stress and depression. Parents who are responsive in a positive way also help reduce the chances for their child developing oppositional behaviors. But it can be very difficult, particularly for parents who have ADHD themselves. In fact, parents who have severe ADHD symptoms are less likely to respond to parent training programs unless they get help for themselves.

In addition to behavioral therapy for the child, family therapy may help ADHD children and their parents and siblings cope with the emotional conflicts that nearly always arise in the lifelong process of managing the condition. Separate psychological therapies for specific family members might be needed, particularly in light of the high incidence of psychiatric and other emotional problems in families with ADHD children.

Medications

Several types of medication are available to treat ADHD.

Psychostimulants are the primary drugs used to treat ADHD. Although these drugs stimulate the central nervous system, they have a calming effect on people with ADHD.

These drugs include:

Methylphenidate (Ritalin, Concerta, Metadate, Daytrana)
Dexmethylphenidate (Focalin)
Amphetamine-Dextroamphetamine (Adderall)
Dextroamphetamine (Dexedrine, Dextrostat)
Lisdexamfetamine (Vyvanse)

Pemoline (Cylert), another stimulant drug, was withdrawn from the U.S. market in 2005 after several reports of liver failure.

Methylphenidate and Dexmethylphenidate. Methylphenidate drugs (Ritalin, Metadate, Concerta, Daytrana) are the most commonly used psychostimulants for treating ADHD in both children and adults. Dexmethylphenidate (Focalin) is a similar drug. These drugs increase dopamine, a neurotransmitter important for cognitive functions such as attention and focus.

With the exception of Daytrana, all of these drugs are pills taken by mouth. Daytrana, approved in 2006, is the first skin patch drug for ADHD. A patch is applied to the hip each day and delivers a 9-hour dose of methylphenidate.

These drugs are available in short-acting and long-acting dosage forms. The short-acting forms need to be taken several times a day, including during school hours. As the drug wears off, a rebound effect can occur, and ADHD symptoms can intensify. For this reason, the long-acting dosage forms have become popular.

Amphetamine, Dextroamphetamine, and Lisdexamfetamine. Amphetamine-dextroamphetamine (Adderall), dextroamphetamine (Dexedrine, Dextrostat), and lisdexamfetamine (Vyvanse) work by blocking the reabsorption of the brain chemicals dopamine and norepinephrine. Side effects can include stomach problems and mood changes, including sadness, anxiety, and irritability.

Psychostimulant medications are associated with some significant risks. All ADHD stimulant drugs carry warnings that they should not be used by patients with structural heart problems or pre-existing heart conditions (high blood pressure, heart failure, or heart rhythm disturbances). These drugs have been associated with sudden death in children with heart problems. They have also been associated with sudden death, stroke, and heart attack in adults with a history of heart disease. In addition, these drugs may slightly increase the risk for auditory hallucinations, paranoia, and manic behavior even in patients who do not have a history of psychiatric problems. The FDA has directed manufacturers of ADHD medications to warn all patients taking these medicines of their potential cardiovascular and psychiatric risks.

Stimulant drugs may also:

Worsen behavior and thought disturbance in patients with a pre-existing psychotic disorder.
Cause a mixed or manic episode in patients who have both ADHD and bipolar disorder.
Increase aggressive behavior or hostility. Patients beginning stimulant drug treatment should be monitored for worsening of these behaviors.
Slow growth and weight gain in children. Children who take stimulant drugs should have their growth monitored. If they do not gain height or weight at a normal rate, they may need to stop taking the drug.

Side Effects. All stimulants have a number of side effects:

The most common side effects of any stimulant are nervousness and sleeplessness, although some parents have reported improved sleep patterns in their children after taking stimulants.
Tics or jerky, disordered movements occur in about 9% of children.
Other side effects include irritability, stomach pain, headache, depression, hair loss, and lack of spontaneity.

Symptoms of Overdose. Symptoms of overdose include changes in heart rhythm and rate, hypertension, confusion, breathing difficulties, sweating, vomiting, and muscle twitches. If they occur, parents should call the doctor immediately. Even among young people who abuse Ritalin, however, less than 1% experience severe side effects (rapid heart rate, hypertension), and outcomes are generally good. Side effects may be very severe, however, if Ritalin is overused and taken with other drugs. A 2006 study reported that over 3,000 people are treated in hospital emergency rooms due to side effects from ADHD drugs. Sixty-one percent of these visits involved accidental ingestion or overdose.

Concerns for Abuse. Studies on both animals and humans suggest that Ritalin lacks the properties that create addiction, particularly in doses used for treating ADHD. Although methylphenidates have properties similar to amphetamines, their drug levels rise very slowly in the brain at the oral doses given for ADHD. This slow rise prevents a so-called "high" and subsequent addiction to the drug. Some stimulant drugs, such as lisdexamfetamine, may pose a lower risk for abuse than others.

The primary danger for drug abuse from stimulants appears to occur in non-ADHD young people who purchase these drugs illegally. In one study, for instance, 16% of children with ADHD reported pressure from their fellow students to sell or give them their medication. While people ages 18 - 25 are more likely to use ADHD drugs for non-medical uses, children ages 12 - 17 are more likely to suffer adverse effects from medication misuse and to require treatment at an emergency room. If a child abuses another drug (alcohol, prescription medication) along with the ADHD medication, the chance for serious side effects is even greater.

Atomoxetine (Strattera) was the first non-stimulant approved for ADHD in children and the first treatment approved for adult ADHD. The drug works by increasing levels of both norepinephrine and dopamine, which are generally lower than normal in ADHD. The most common side effect is decreased appetite. A few cases of atomoxetine-associated liver injury have been reported, and the FDA has warned doctors that the drug should be discontinued at the first signs of jaundice or liver problems. Long-term effects, such as any impact on growth, are still unknown. Atomoxetine may cause suicidal thinking in children and adolescents, especially during the first few months of treatment. Parents should monitor children taking atomoxetine for any changes in mood or behavior, and immediately contact their doctor if changes occur.

Antidepressants are not FDA-approved for ADHD treatment, but may be helpful in certain circumstances. Because antidepressants appear to work about as well as behavioral therapy, doctors recommend that patients first try psychotherapy before using antidepressants.

Bupropion (Wellbutrin) and tricyclics are the types of antidepressants used for ADHD. Bupropion affects the reuptake of the serotonin, norepinephrine, and dopamine neurotransmitters. Side effects include restlessness, agitation, sleeplessness, headache, and stomach problems. Bupropion should not be used by patients who have a seizure disorder.

Tricyclics are an older type of antidepressant that are effective but have many side effects. Imipramine (Tofranil) and nortriptyline (Pamelor, Aventil) are the tricyclics most commonly prescribed for ADHD. A third tricyclic, desipramine (Norpramin) should only be used if patients are not helped by other tricyclics. (Desipramine has caused sudden death in some children and adolescents.)

Tricyclic antidepressants can cause disturbances in heart rhythm. Children should have an electrocardiogram when they first begin to take this drug, and after any dose increase.

[For more information, see In-Depth Report #8: Depression ].

Alpha-2 agonists stimulate the neurotransmitter norepinephrine, which appears to be important for concentration. They include clonidine (Catapres) and guanfacine (Tenex). They are used for Tourette syndrome and may be beneficial when other drugs have failed for ADHD children with tics or those whose primary symptoms are severe impulsivity and aggression. These drugs are mainly prescribed in combination with a stimulant.

These drugs have a number of side effects. Sedation is the most common. A clonidine skin patch, which gradually releases the medication, helps reduce the sedative effect. Because clonidine slows the heart down, it can have adverse effects in some children. Going off too quickly or missing doses can cause rapid heartbeats and other symptoms that may lead to severe problems. Doctors strongly recommend that no child be given this medication without a preliminary examination for heart problems, and no child with existing heart, kidney, or circulatory problems should take it.

Behavioral Management

Behavioral techniques for managing the child with ADHD are not intuitive for most parents and teachers. To learn them, caregivers may need help from qualified health care professionals or from ADHD support groups. At first, the idea of changing the behavior of a highly energetic, obstinate child is daunting. It is futile and damaging to try to force a child with ADHD to be like most children. It is possible, however, to limit destructive behavior and to instill a sense of self-worth that will help overcome negativity toward life, which is one of the great dangers of the disorder.

Bringing up a child with ADHD, like bringing up any child, is a process. No single point is ever reached where the parent can sit back and say, "That's it. My child is now OK, and I don't have to do anything more." The child's self worth will evolve with an increasing ability to step back and consider the consequences of an action and then to control that action before taking it. But this does not happen overnight. A growing child with ADHD is different from other children in very specific ways, presenting challenges at every age.

Setting Priorities for the Parent. Parents must first establish their own levels of tolerance. Some parents are easygoing and can accept a wide range of behaviors, while others cannot. To help a child achieve self-discipline requires empathy, patience, affection, energy, and toughness. Some tips to help the parents include:

Parents should prepare a list giving priority to those behaviors they think are the most negative, such as fighting with other children or refusing to get up in the morning. The least negative behaviors on the bottom of the list should be ignored temporarily or even permanently (refusing to wear anything but red T-shirts).
Certain odd behaviors that are not hurtful to the child or to others may be an indication of creative or humorous attempts to adapt (making up silly songs or drawing violent pictures). These should be accepted as part of the child's unique and positive development, even if they seem peculiar to the parent.
It is important to keep in mind that no one is a saint. Loving parents who occasionally lose their tempers will not damage their children forever. In fact, non-abusive open disapproval or dismay is far less destructive to both parent and child than harboring resentment beneath a false calm.

Establishing Consistent Rules for the Child. Parents must be as consistent as possible in their approach to the child, which should reward good behavior and discourage destructive behavior. Rules should be well-defined but flexible enough to incorporate harmless idiosyncrasies. It is very important to understand that children with ADHD have much more difficulty adapting to change than do children without the condition. (For example, the child should do homework every day but might choose to start it after a TV show or computer game.)

Managing Aggression. Some useful tips for managing aggression include:

Parents should try to give little attention to mildly disruptive behaviors that allow this energetic child to let off some harmless steam. The parent will also be wasting energy that will be needed when the negative behavior becomes destructive, abusive, or intentional.
The use of "time-out," isolating the child immediately for a short period of time, is an effective measure for allowing both the caregiver and the child to cool down. The child should immediately (and without emotion) be removed from a situation in which they are endangered or endangering others. The child should view time out as a way of cooling off and getting a distance on their behavior, not as isolation from others.
To channel physical aggression and impulsivity in the ADHD toddler, the parents must teach them to use verbal responses. (A parent may need to allow verbal responses that would be unacceptable in another child.)
When the ADHD child becomes older and if the verbal responses become intentionally abusive and socially undesirable, the parent must redirect this form of aggression into more acceptable activities, such as competitive one-on-one sports, energetic music, video games, or big colorful paintings. Competitive video games, such as sports games, may also be an option.
Sometimes a parent can anticipate situations when an ADHD child is likely to misbehave, but all too often the child explodes for no apparent reason. If the blow-up occurs in public, the parents should complete their activities and leave as quickly as possible.

Establishing a Reward System. Children with ADHD respond particularly well to reward systems. One study reported that they performed equally well when encouraged either by a direct reward for a correct response or with the use of a system called response-cost. With this system, the child is given the reward first and allowed to keep it if their behavior remains appropriate.

Some suggested tips for rewarding the ADHD child are:

Create charts with points or stars for good behavior or for completed tasks. It is important to give points for even simple positive behaviors, which may be taken for granted in other children (responding happily to a change in plans, changing an obscenity to a more acceptable expletive).
Rewards for any child can include playing a favorite game with the child, extending bedtime by an hour, or allowing an extra half-hour of TV.
Rewards of food or gifts should be used infrequently, if at all. They can create other problems, such as being overweight, having a bad diet, or making continuous demands for objects.
A reward system should rotate different types of rewards, because such children are easily bored.
Children with ADHD respond better with small rewards promised in the short-term than large rewards offered in the future. One approach that employs both short- and long-term rewards uses a system that gives the child points for specific positive behaviors. As the children accumulate points, they can use them for larger tangible rewards, such as a favorite video game or CD.
Rewards should be promised only when caregivers are fairly certain they can follow through. ADHD children respond with much greater frustration than non-ADHD children to disappointment, and are likely to have a strong (and noisy) negative reaction. A parent must remember that this response is part of the ADHD child's make-up and not necessarily in their control.

Improving Concentration and Attention. Research indicates that ADHD children perform significantly better when their interest is engaged. Parents should be on the lookout for activities that hold the child's concentration. Some options that may help an ADHD child to focus include:

Many ADHD children are particularly lured by the computer, which is a very promising tool. A number of non-violent computer games are available that offer problem-solving techniques using characters, narrative, and humor.
Swimming, tennis, and other sports that focus attention and limit peripheral stimuli are often appealing. ADHD children often do not do well with team sports, although they are interested. Children with ADHD are less likely to become distracted in sports that require constant alertness, such as football or basketball. In baseball, positions such as pitching or catching are preferable to the outfield, where attention easily wanders. Finding a coach that understands the child’s difficulties is very helpful.
Some experts are enthusiastic about martial arts, such as Tae Kwon Do, which can offer an appropriate and controlled emotional outlet, help to focus attention, and teach self-restraint, self-discipline, and tolerance. Care should be taken to select an instructor who makes such goals a priority.
Learning an instrument may be one of the best ways for an ADHD child to develop a more rhythmic and balanced sense of self. Music, even simply listening to it, is often very important for these children. (Parents may have to tolerate music that does not please them.)

Even if a parent is successful in managing the child at home, difficulties often arise at school. The ultimate goal for any educational process should be the happy and healthy social integration of the ADHD child with their peers.

Preparing the Teacher. Although teachers can expect at least one student in every classroom to have ADHD, there is currently little training that prepares them for managing these children. The teacher should be prepared for the certain behaviors in the child with ADHD:

Students with ADHD are often demanding, talkative, and highly visible.
Inattention is a major factor in low academic performance. It causes them to frequently forget homework or miss assignments. Children with ADHD often require frequent reminders or visual cues (such as posters) for rules and regulations. Having the child sit in the front of the classroom may be helpful for both increasing attention and reducing noisy activity.
Lack of fine motor control makes taking notes very difficult, and handwriting is often poor. Using a typewriter or computer can compensate for this. One useful skill that has helped some children is learning to type at an early age, around the third or fourth grade.
Rote memorization and math computation, which require following a set of ordered steps, are often difficult. (Children with ADHD may do better with math concepts.)
Many children with ADHD respond well to school tasks that are rapid, intense, novel, or of short duration (such as spelling bees or competitive educational games), but they almost always have problems with long-term projects where there is no direct supervision.

The Role of the Parent in the School Setting. The parent can help the child by talking to the teacher before the school year starts about their child's situation:

The first priority for the parent is to develop a positive, not adversarial, relationship with the child's teacher.
The parent must acknowledge the teacher's situation, for the teacher must deal not only with the ADHD child's behavior but also with the needs of all the other children.
Frequent brief and sympathetic conversations with the teacher can be helpful and can lead to coordination of efforts, particularly if they provide reciprocal information about progress or setbacks.
Finding a tutor to help after school may be helpful. It is not clear, however, if tutoring offers significant benefits for children whose academic problems stem from inattention unless it is structured specifically to address this problem.

Special Education Programs. The Individuals with Disabilities Education Act (IDEA) requires the school to identify and evaluate children who may need help and to provide special services. However, parents sometimes report pressure by the school to put their children on medication or force them into special classrooms without clear educational justification. The schools, in these cases, may be acting illegally.

High-quality special education can be extremely helpful in improving learning and developing a child's sense of self worth. Many families, however, may not have appropriate programs available for them. Programs vary widely in their ability to provide quality education. Parents must be aware of certain limitations and problems with special education:

Special education programs within the normal school setting often increase the child's feelings of social alienation.
If the educational strategy focuses only on abnormal behavior, it will fail to take advantage of the creative, competitive, and dynamic energy that often accompanies ADHD behavior.
There is no federally funded special education category specifically targeted to ADHD.

If, in fact, ADHD is as common as studies are indicating, the best approach may be to treat the syndrome as a variant of the norm and train teachers to manage these children within the context of a normal classroom.

Special programs are also required under the Rehabilitation Act and by the Americans with Disabilities Act (ADA) for students at institutions of higher learning. It is the student's responsibility, however, to inform the administration at their college or university that they need such services. Unfortunately, many college students are reluctant to do this, although such programs can provide important and beneficial assistance in improving their academic performance.

Other Treatments

A number of diets have been suggested for people with ADHD. Several well-conducted studies have failed to support dietary effects of sugar and food additives on behavior, except possibly in a very small percentage of children. Still various studies have reported behavioral improvement with diets that restrict possible allergens in the diet. Parents may want to discuss with their doctor implementing an elimination diet of certain foods that would not be harmful and that might help.

Food Allergies. Evidence suggests that children with behavioral difficulties may be sensitive to certain chemicals in foods. Studies vary widely, however, on how many cases of ADHD may be associated with sensitivities or allergies to food chemicals or additives, with results ranging widely from 5 - 62%. Among the suspected additives and foods that parents and studies report as inciting behavioral changes are the following:

Any artificial colorings (particularly yellow, red, or green)
Other chemical additives -- for example, BHT or BHA
Milk
Chocolate
Eggs
Wheat
Foods containing salicylates, including all berries, chili powder, apples and cider, cloves, grapes, oranges, peaches, peppers (bell & chili), plums, prunes, tomatoes

In one small study, 62% of children who were given only rice, turkey, pears, and lettuce to eat for 2 weeks experienced at least a 50% improvement in symptoms. Nevertheless, about a quarter of the children pulled out because they could not stick with the diet or they became ill.

Feingold Diet. The most well-known diet for ADHD is the Feingold diet, a salicylate- and additive-free diet, which requires rigorous vigilance over a child's eating habits. This diet also prohibits aspirin, which contains salicylates. Some parents report great success with this diet, although it may be difficult to impose. One study that reported the diets efficacy suggested that it might not provide enough nutritive value, although the diet provides a wide range of healthy foods to select from. It is certainly wise, in any case, to avoid food with artificial colors and flavors and to provide a healthy balance of fresh, natural foods.

Essential Fatty Acids. Omega-3 fatty acids, found in fatty fish and certain vegetable oils, are important for normal brain function and may have some benefits for people with ADHD. It is not clear if supplements of fatty acid compounds, such as docosahexaenoic acid (DHA) and eicosapentaneoic acid (EPA), provide any advantages.

Zinc. Zinc is important for the metabolism of certain neurotransmitters that play a role in ADHD, and deficiencies have been associated with some cases of ADHD. Long-term use of zinc, however, can cause anemia and other side effects in people without deficiencies and it has no effect on ADHD in these patients. In any case, testing for trace minerals, such as zinc, is not standard procedure when evaluating children suspected to have ADHD.

Sugar. Although parents often blame sugar for causing children to become impulsive or hyperactive, a number of studies strongly indicate that sugar plays no role in hyperactivity. One study reported, in fact, that ADHD children had fewer problems after a high-carbohydrate breakfast than after a high-protein one. Another reported that children actually moved more slowly after a high-sugar meal, suggesting the carbohydrates may have a sedative effect. (Still, it's probably always wise for any child to cut down on sugar.)

Techniques that use biologic or auditory feedback are proving to be effective tools for increasing children's attention -- a primary factor in low academic performance.

Neurofeedback. Neurofeedback is an approach that uses electronic devices to help the child control their own brain wave activity. Electrodes are pasted to the child's head and pick up signals from the brain. The child watches images, such as moving graphs, on a computer monitor that reflect the child's brain wave activity. Children are then taught certain high-level mental activities at the point when feedback information on the screen indicates that they are fully concentrating. Children usually attend forty 50-minute sessions, usually twice a week. Small studies have reported significant improvement in inattention, impulsivity, and response time.

Interactive Metronome and Musical Therapy. Interactive metronome uses feedback from sound to improve attention, motor control, and certain academic skills. In this technique study, children wear headphones and sensors on their hands and feet. They perform a number of exercises to a rhythmic computer-beat. Training sessions are completed in 3 - 5 weeks. Some small studies have reported improvement in attention, motor control, language processing, and behavior. (In support of this, some parents report that learning a musical instrument helped their children significantly.)

Procedures and Non-Drug Therapies. A number of alternative approaches are used for children and adults with mild ADHD symptoms. For example, daily massage therapy may help people with ADHD feel happier, fidget less, be less hyperactive, and focus on tasks. Other alternative approaches that may be helpful include relaxation training, meditation, and music therapy. Based on existing evidence, these treatments may be helpful for symptom management but are not proven to benefit the underlying disorder.

Natural Remedies. A number of parents resort to alternative remedies as an alternative to psychostimulants and other drugs. Small trials have found some herbs and supplements -- such as oral flower essence, ginkgo biloba, panax ginseng, melatonin, and pine bark extract (Pycnogenol) --may possibly have benefits for ADHD. Based on existing evidence, however, none can be recommended, particularly for children.

The following are special concerns for people taking natural remedies for attention-deficit disorders:

Melatonin. High doses of melatonin have been associated with an increased risk for seizures in children with existing neurologic disorders.
Gingko. The risk for side effects from gingko appear to be low, but there is an increased risk for bleeding and interaction with anti-clotting medications at high doses.
Ginseng. There have been contaminated forms of imported ginseng. Ginseng also has been associated with low blood sugar and a higher risk for bleeding. In addition, a great number of ginseng products have been found to contain little or no ginseng.

Resources

www.aap.org -- American Academy of Pediatrics
www.nimh.nih.gov -- National Institute of Mental Health
www.chadd.org -- Children and Adults with Attention-Deficit Disorder
www.add.org -- Attention Deficit Disorder Association
www.aabt.org -- Association for Behavioral and Cognitive Therapies
www.psych.org -- American Psychiatric Association
www.parentsmedguide.org -- Medication Guide for Treating ADHD
www.aacap.org -- American Academy of Child and Adolescent Psychiatry
www.nichcy.org -- National Dissemination Center for Children with Disabilities
www.ncld.org -- National Center for Learning Disabilities
www.ldaamerica.org -- Learning Disabilities Association of America

References

Braun JM, Kahn RS, Froehlich T, Auinger P, Lanphear BP. Exposures to environmental toxicants and attention deficit hyperactivity disorder in U.S. children. Environ Health Perspect. 2006 Dec;114(12):1904-9.

Heinrich H, Gevensleben H, Strehl U. Annotation: neurofeedback - train your brain to train behaviour. J Child Psychol Psychiatry. 2007 Jan;48(1):3-16.

Jensen PS, Arnold LE, Swanson JM, et al. 3-year follow-up of the NIMH MTA study. J Am Acad Child Adolesc Psychiatry. 2007 Aug;46(:989-1002.

Nigg JT, Breslau N. Prenatal smoking exposure, low birth weight, and disruptive behavior disorders. J Am Acad Child Adolesc Psychiatry. 2007 Mar;46(3):362-9.

Pliszka S; AACAP Work Group on Quality Issues. Practice parameter for the assessment and treatment of children and adolescents with attention-deficit/hyperactivity disorder. J Am Acad Child Adolesc Psychiatry. 2007 Jul;46(7):894-921.

Steiner H, Remsing L; Work Group on Quality Issues. Practice parameter for the assessment and treatment of children and adolescents with oppositional defiant disorder. J Am Acad Child Adolesc Psychiatry. 2007 Jan;46(1):126-41.

Swanson JM, Elliott GR, Greenhill LL, et al. Effects of stimulant medication on growth rates across 3 years in the MTA follow-up. J Am Acad Child Adolesc Psychiatry. 2007 Aug;46(:1015-27.

Valera EM, Faraone SV, Murray KE, Seidman LJ. Meta-analysis of structural imaging findings in attention-deficit/hyperactivity disorder. Psychiatry. 2007 Jun 15;61(12):1361-9. Epub 2006 Sep 1.

Wilens TE, Upadhyaya HP. Impact of substance use disorder on ADHD and its treatment. J Clin Psychiatry. 2007 Aug;68(:e20.

Williams JH, Ross L. Consequences of prenatal toxin exposure for mental health in children and adolescents: a systematic review. Eur Child Adolesc Psychiatry. 2007 Jun;16(4):243-53. Epub 2007 Jan 2.

Review Date:
12/27/2007
Reviewed By:
Harvey Simon, MD, Editor-in-Chief, Associate Professor of Medicine, Harvard Medical School; Physician, Massachusetts General Hospital. Also reviewed by David Zieve, MD, MHA, Medical Director, A.D.A.M., Inc.

A.D.A.M. Copyright

adam.com

Depression

FitSugar — Wed, 08 Oct 2008 17:34:57 -0700

In This Report

Highlights
Introduction
Causes
Risk Factors
Complications of Depression...
Diagnosis
Treatment
Antidepressants and Drug Tr...
Psychotherapy
Other Treatments
Lifestyle Changes
Resources
References

HEALTH GUIDE REFERENCE FROM A.D.A.M

Highlights

Drug Approval

In 2007, the Food and Drug Administration (FDA) approved the atypical antipsychotic drug aripiprazole (Abilify) for treatment of major depression in adults. Aripiprazole is used for treatment of schizophrenia and bipolar disorder. For depression, it is used in combination with antidepressant drug therapy. Researchers are also investigating other atypical antipsychotics for major depression treatment.

Antidepressants and Suicide Risk

In 2007, the FDA proposed adding new information to antidepressant warning labels concerning the increased risk for suicidal thinking and behavior among young adults ages 18 - 24 during the initial months of drug therapy.
The benefits of antidepressants for children and adolescents outweigh their potential risks, suggests a 2007 study in the Journal of the American Medical Association.

Antidepressants During Pregnancy

Most selective serotonin reuptake inhibitors (SSRIs) do not significantly increase the risk for birth defects when taken during early pregnancy, indicate several 2007 studies in the New England Journal of Medicine. However, some SSRIs -- such as paroxetine (Paxil) -- carry a higher risk than others. Researchers are still studying the overall safety of SSRIs during pregnancy. Women with depression should discuss with their doctors all potential risks and benefits.

Introduction

Everyone experiences some unhappiness, often as a result of a change, either in the form of a setback or a loss, or simply, as Freud said, "everyday misery." The painful feelings that accompany these events are usually appropriate, necessary, and transitory, and can even present an opportunity for personal growth. However, when depression persists and impairs daily life, it may be an indication of a depressive disorder. Severity, duration, and the presence of other symptoms are the factors that distinguish normal sadness from a depressive disorder.

Depression has been alluded to by a variety of names in both medical and popular literature for thousands of years. Early English texts refer to "melancholia," which was for centuries the generic term for all emotional disorders.

Depression is now referred to as a mood disorder, and the primary subtypes are major depression, dysthymia (chronic and usually milder depression), and atypical depression. Other important forms of depression are premenstrual dysphoric disorder (PDD or PMDD) and seasonal affective disorder (SAD).

Depression is defined as a mood disorder, and there are several subtypes. Bipolar disorder, also known as manic-depressive illness, is considered in a separate category.

The other major mood disorder is bipolar disorder, or manic-depressive illness, which is characterized by periods of depression alternating with episodes of excessive energy and activity. Bipolar disorder is not discussed in this report. [For more information, see In-Depth Report #66: Bipolar disorder.]

In major, or acute, depression, at least five of the symptoms listed below must occur for a period of at least 2 weeks, and they must represent a change from previous behavior or mood. Depressed mood or loss of interest must be present. Symptoms include:

1. Depressed mood on most days for most of each day -- irritability may be prominent in children and adolescents

2. Total or very noticeable loss of pleasure most of the time

3. Significant increases or decreases in appetite, weight, or both

4. Sleep disorders, either insomnia or excessive sleepiness, nearly every day

5. Feelings of agitation or a sense of intense slowness

6. Loss of energy and a daily sense of tiredness

7. Sense of guilt or worthlessness nearly all the time

8. Inability to concentrate occurring nearly every day

9. Recurrent thoughts of death or suicide

In addition, other criteria must be met:

The symptoms listed above do not follow or accompany manic episodes (such as in bipolar disorder or other disorders).
They impair important normal functions (such as work or personal relationships).
They are not caused by drugs, alcohol, or other substances.
They are not caused by normal grief.

A long-term study found that episodes of major depression usually last about 20 weeks. Between 30 - 40% of depressed patients experience sudden attacks of anger that they describe as uncharacteristic and inappropriate.

Click the icon to see an image of childhood depression.

Dysthymia, or chronic depression, afflicts 3 - 6% of the general population and is characterized by many of the same symptoms that occur in major depression. Symptoms of dysthymia are less intense and last much longer, at least 2 years. The symptoms of dysthymia have been described as a "veil of sadness" that covers most activities. Possibly because of the duration of the symptoms, patients who suffer from chronic minor depression do not exhibit marked changes in mood or in daily functioning, although they have low energy, a general negativity, and a sense of dissatisfaction and hopelessness.

Double Depression. Often, symptoms become more severe over time. In one long-term study, nearly all patients with dysthymia suffered at least one episode of major depression superimposed over chronic depression (sometimes called double depression) at some time in their life. Some experts believe that such double depression should be considered as part of the natural course of dysthymic disorder. Women may be more susceptible to double depression. In one study, more than one-third of those who recovered from dysthymia relapsed within 5 years.

About a third of patients with depression have atypical depression. Symptoms include overeating and oversleeping. Such patients tend to have a feeling of being weighed down and react strongly to rejection. It tends to occur more in women, unmarried people, and those with other emotional disorders, such as anxiety or substance abuse. It also may impair functioning more severely than ordinary depression does.

Seasonal affective disorder (SAD) is characterized by annual episodes of depression during fall or winter that remit in the spring or summer. Other SAD symptoms include fatigue and a tendency to overeat (particularly carbohydrates) and oversleep in winter. A minority of individuals with SAD has the more common depressive symptoms of undereating and being sleepless. SAD tends to last about 5 months in those who live in the northern part of the U.S.

Seasonal changes affect many people's moods, regardless of gender and whether or not they have SAD. Simply being mildly depressed during the winter does not mean that one has SAD. Living in a northern country with long winter nights does not guarantee a higher risk for depression. Changes in light may not be the only contributor to SAD.

Causes

The causes of depression are not fully known. Most likely a combination of genetic, biologic, and environmental factors are at work.

Because depression runs in families, and has a strong genetic component, compelling evidence suggests that depression is a biologic phenomenon. Data from family, twin, adoption, and genetic studies have confirmed this. Studies have found that first-degree relatives of patients with depression are two to six times more likely to develop the problem than individuals without a family history.

Evidence supports the theory that depression has a biologic basis. The basic biologic causes of depression are strongly linked to abnormalities in the delivery of certain key neurotransmitters (chemical messengers in the brain). These neurotransmitters regulate mood and associated behaviors. Scientists hope that by identifying the gene mutations that code the regulation of these neurotransmitters, they may eventually be able to predict which patients are most likely to respond to specific antidepressant drugs.

Serotonin. Perhaps the most important neurotransmitter in depression is serotonin. Among other functions, it is important for feelings of well-being. Imbalances in the brain’s serotonin levels can trigger depression and other mood disorders.
Other Neurotransmitters. Other neurotransmitters possibly involved in depression include acetylcholine and catecholamines, a group of neurotransmitters that consists of dopamine, norepinephrine, and epinephrine (also called adrenaline). Corticotropin-releasing factor (CRF), which is believed to be a stress hormone and a neurotransmitter, is thought to be involved in depression and anxiety. Increased CRF concentrations appear to interact with serotonin and have been detected in patients with either depression or anxiety.

Endocrine glands release hormones into the bloodstream that are transported to various organs and tissues throughout the body. For instance, the pancreas secretes insulin, which allows the body to regulate levels of sugar in the blood. The thyroid gets instructions from the pituitary gland to secrete hormones that determine the pace of chemical activity in the body. The more hormone in the bloodstream, the faster the chemical activity; the less hormone, the slower the activity.

The degree to which these chemical messengers are disturbed is determined by other factors, such as light, structural abnormalities in the brain, sleep disorders, or genetic susceptibility. For example, researchers have identified a defect in the gene known as SERT, which regulates serotonin and has been linked to depression.

Reproductive Hormones. In women, the female hormones estrogen and progesterone most likely play a role in depression.

Women, regardless of nationality or socioeconomic level, have significantly higher rates of depression than men. The causes of such higher rates appear to be a mix of biologic and cultural factors.

Social and Economic Factors. The role that work, marriage, and children play in a woman's depression is complex. Many women feel that they must be everything to everyone and at the same time feel as if they are no one at all. Such a self-image is common and should be strongly considered as a major contributor to depression in many women, particularly those who work and have small children.

Hormonal Fluctuations and Life Stages. Extreme hormonal shifts can trigger emotional swings in all women. The role of hormones in depression is not clear, however, and is mostly based on observations of depression during specific stages in female development. Female hormones undoubtedly play some role in premenstrual dysphoria, postpartum depression, and SAD. These forms of depression recede or stop after menopause.

Early Puberty. Girls who go through puberty early (reaching the midpoint at 11 years or younger) are more likely to experience depression during adolescence than girls who mature later.

Premenopause. Premenopausal women ages 20 - 45 are most susceptible to depression, with 22% of this age group reporting symptoms of major depression. Specifically, premenstrual dysphoric disorder (severe depression before a period) affects an estimated 3 - 8% of women during their reproductive years. [For more information, see In-Depth Report # 79: Premenstrual syndrome.]

Perimenopause. Depression often occurs around menopause (the perimenopausal period), when, in addition to hormonal changes, other factors such as cultural pressures favoring young women, sudden recognition of aging, and sleeplessness are involved.

Postmenopause. Once women pass into the postmenopausal period, studies suggest that average depression scores are nearly as low as those in premenopausal women. In fact, many women report that after menopause, previous bouts of depression, particularly when caused by seasonal changes or premenopausal syndrome, recede or stop completely.

Premenstrual Dysphoric Disorder. The syndrome of severe depression, irritability, and tension before menstruation is known as premenstrual dysphoric disorder (PDD or PMDD), also called late-luteal dysphoric disorder. It affects an estimated 3 - 8% of women in their reproductive years. A diagnosis of PDD depends on having five or more standard symptoms of major depression that occur during most menstrual cycles, with symptoms worsening a week or so before the menstrual period and resolving afterward. PMDD has features of both anxiety and depression disorders, although experts increasingly believe it is a distinct disorder with specific biochemical abnormalities. [For more information, see In-Depth Report #79: Premenstrual disorder.]

Depression During Pregnancy. Pregnancy is certainly an occasion of great celebration for most women most of the time. However, emotions during that time are not always straightforward, and depression is a common (although most often a temporary) companion. Prenatal depression can affect a mother's sleep, physical activity, adherence to care, and appetite.

Miscarriage. Miscarriage poses a very high risk for depression, particularly in the first month after the loss. Older women with no previous successful pregnancies and those with a history of depression are at particular risk during this time. (Despite some concern that depression increases the risk for miscarriage in the first place, there is no evidence to support this.)

Postpartum Depression. Most new mothers experience weeping, irritability, and confusion for a few days following childbirth. Such symptoms, known as the "baby blues," are not considered signs of postpartum depression unless they persist in severe form nearly every day for more than 1 - 2 weeks.

Women are most likely to develop postpartum depression and other mental disorders in the first 3 months following delivery. (The risk is highest for first-time mothers, especially in the 10 - 19 days after delivery.) Other studies have reported that 8 - 20% of women have diagnosable postpartum depression within that 3-month period. In one study, 5% of these women had suicidal thoughts.

Studies have not found any association between a higher risk for postpartum depression in women and the following:

Educational level
Gender of the child
Whether or not the woman breast-feeds
Whether or not the pregnancy was planned
Whether the delivery was vaginal or cesarean

The rapid decline of reproductive hormones that accompany childbirth is likely to play the major role in postpartum depression in susceptible women. Fluctuating thyroid hormones can also contribute to depression. Studies suggest that women who are more sensitive to hormone fluctuations are at greater risk for postpartum depression if they have one or more of the following conditions:

A history of prior depressive episodes
A family history of mood disorders
Stressful life events (such as being a new mother and having an infant with medical problems)
Lack of social support or feeling as if it is lacking

Depressed children often suffer in silence, and depression may be evident only from reports of problems in school. It is also often difficult for adults to believe that children can be chronically depressed. Symptoms for depression in children often differ from those in adults and may include the following:

An inability to enjoy favorite activities
Persistent sadness
Increased irritability
Complaints of physical problems, such as headaches and stomachaches
Poor performance in school
Persistent boredom
Low energy
Poor concentration
Changes in eating and/or sleeping patterns
A greater tendency to bully others -- anxious children are more often bullied.

Risk Factors for Depression in Children and Adolescents. Depression can occur in children of all ages, including preschoolers, although adolescents have the highest risk (about 20%). Risk factors for depression in young people include having parents, particularly mothers with depression. Early negative experiences and exposure to stress, neglect, or abuse also pose a risk for depression. Sometimes depression develops after a physical illness. In adolescents, feeling alienated from parents is a strong predictor for depression.

Outlook for Future Emotional Problems. Adolescents who have depression are at significantly higher risk for substance abuse, recurring depression, and other emotional problems (such as bipolar disorder) in adulthood.

Risk for Suicide in Adolescents. Suicide is the third most common cause of death among adolescents, and is one of the most devastating events than can happen to a family. Suicide is most commonly associated with depression in young people but it is also linked with anxiety, psychosis, substance abuse, or impulsivity. More girls attempt suicide but more boys succeed, most often because they choose guns or violent methods while girls tend to overdose, which is more treatable. Nevertheless, attempts are major risk factors for a later suicide. Any expression of suicidal intent should be treated very seriously.

The following are danger signs in young people:

Withdrawal from friends
Sudden decrease in school performance
Loss of interest in activities that were previously pleasurable
Unusual irritability
Unusual changes in sleep or eating habits

Adolescents may fail to seek help for suicidal thoughts for the following reasons:

They believe nothing would help
They are reluctant to tell anyone they had problems
They think it is a sign of weakness to seek help
They do not know where to go

Parents should not hesitate to seek professional help for their children if they suspect they are thinking about killing themselves. This is a medical emergency and requires immediate treatment.

Behavioral therapies and antidepressants are promising treatments for preventing suicide but need study. There has been a decline in adolescent suicides over the past decade, which some experts attribute to the increased use of antidepressants in this population. However, recent evidence has indicated that antidepressants can also raise the risk for suicidality (suicidal thoughts and behavior) in some people. Children, adolescents, and young adults who are prescribed antidepressant medication should be carefully monitored by both their parents and doctor, especially during the first few months of treatment, for any worsening of depression symptoms or changes in behavior. [See Suicide Risk and Antidepressant Medications in Medication section.]

Although depression in the elderly is very common, the aging process itself is unlikely to be the cause in most cases. An Italian study, for example, indicated that the very old (people who lived beyond 90 years of age) were no more likely to be depressed than younger adults. (The rate was 10% in both groups.) Studies on the cause or extent of depression in the elderly are not clear.

The severity of depression in elderly patients is strongly associated with poor health and less ability to function. In one study of older adults undergoing rehabilitation, half of whom were depressed, as their function improved so did their mood.

Anyone who experiences cumulative negative life events, physical illness, the death of a loved one, impaired functioning, or loss of independence can become deeply depressed. The elderly are at highest risk for such events.

Diagnosing Depression in the Elderly. Because of the complex relationship between depression, drug interactions, and serious physical illness in the elderly, an accurate diagnosis in this group is important but not always straightforward. The characteristic symptoms of depression are not always present or readily apparent in older people:

Some older people may be aware of their depression but believe that nothing can be done about it.
Many elderly people who are depressed may report only physical symptoms (aches and pains) or other mood states (confusion, agitation, anxiety, and irritability) related to depression rather than depression itself.
Often they are unable or unwilling to express their feelings or are even unaware that they are depressed.
Their symptoms are often ignored or confused with other ailments common in the elderly, including Parkinson's or Alzheimer's disease, dementia, thyroid disorders, arthritis, stroke, cancer, heart disease, and other chronic conditions.
Depression is also a side effect of many drugs that are commonly prescribed for the elderly. It is often very difficult, then, to determine if the patient's depression is a psychologic reaction to the illness, caused by the disease itself, or completely independent from the medical condition. Both physical and emotional conditions should be considered in making a diagnosis in older people.

Many studies suggest strong associations between even mild depression and poorer quality of life as well as a shorter lifespan.

Risk for Suicide in the Elderly. Suicide in the elderly is the third-leading cause of death related to injury. Men account for 81% of these suicides, with divorced or widowed men at highest risk.

Effects of Depression on the Ability to Function. Even mild depressive symptoms in people aged 65 and above are associated with a higher risk of becoming disabled and having a lower chance of recovery.

Heart Disease and Heart Attacks. Depression increases the severity of a heart attack and may even impair a patient's response to medication for heart disease. Although people with heart disease may certainly become depressed, this does not explain entirely the link between the two problems. Data suggest that depression itself may be a true risk factor for heart disease as well as its increased severity. A number of studies indicate that depression has biologic effects on the heart, including a higher risk for blood clotting, changes in heart rate, and impaired blood flow to the heart (particularly in response to mental stress). The more severe the depression, the more dangerous to the health, although even mild depression, including feelings of hopelessness, experienced over many years, may harm the heart, even in people with no early signs of heart disease.

Mental Decline. Depression in the elderly is associated with a decline in mental functioning, regardless of the presence of dementia. Depression may be a predictor or even a cause of Alzheimer's disease. Brain scans in the elderly, for example, have reported greater atrophy in the brains of depressed individuals than in those of nondepressed ones.

Risk Factors

According to a major surveys, more than 13% of Americans have major depression disorder over the course of their lifetimes. Furthermore, an estimated 18 million Americans experience major depression each year. Depression is second only to high blood pressure as a chronic condition encountered by primary care doctors. Depression is an illness that can afflict anyone, regardless of age, race, class, or gender. A third of all depressed people consider suicide, and 9% attempt it.

Depression in Women. At any given time, 5 - 9% of women are depressed, compared to 1 - 3% of men. In one study, nearly half of all women surveyed had experienced depression at some point in their lives and over half of those who suffered from it had sought treatment. Women are also more apt to have multiple types of depression (dysthymia and major depression). [For more information, see Depression in Women.]

Depression in Men. Depression is not rare in men. In fact, prepubescent boys are more likely than girls of the same age to be depressed. Older men are also at much higher risk for suicide and, as with women, they are at risk for health complications of depression. Some evidence suggests that men are more apt than women to mask their depression by using alcohol, which may result in a lower reported (but not actual) incidence of depression in men. Some experts suggest that men with depression might be identified with the following indicators:

Low tolerance to stress
Behaviors such as "acting out" and being impulsive
A history of alcohol or substance abuse
A family history of depression, alcohol abuse, or suicide

Depression is less reported in the male population, but this may be caused by male tendency to mask emotional disorders with behavior such as alcohol abuse.

Depression in Children and Adolescents. Children ages 12 - 16 are at high risk for depression. Studies suggest that 3 – 5% of children and adolescents suffer from depression, and 10 – 15% have some depressive symptoms. Depression before puberty is more likely to occur in boys and after puberty in girls.

Depression in Adults. Surveys indicate that depression usually begins around the age of 30, although people do not generally seek treatment until they are about 33 years old. Statistics also suggest that depression is becoming more common among middle-aged people ages 45 - 64. According to a 2005 survey, middle-aged adults have the highest lifetime risk for depression.

Depression in the Elderly. Studies suggest that 5 – 14% of the elderly population suffer from some form of depression. In addition, the elderly are highly vulnerable to suicide. Elderly people comprise 13% of the U.S. population but account for 18% of all suicide deaths.

The role of society and economics has specific implications for women. [See Depression in Women.] Being in a low socioeconomic group is a major risk factor for depression in anyone. Money, of course, allows greater access to good medical care, but this factor does not fully explain the higher rates of depression in impoverished people. People at any income level are likely to be depressed if they have poor health and are socially isolated. Some studies suggest that Western cultural attitudes that link income to social status may play a significant role in the connection between poverty and depression:

In one British study, actual poverty or unemployment increased the duration of any existing depression, but it did not appear to play any important causal role. Feelings of financial insecurity, however, both caused and prolonged depression.
Another study reported that Mexican adults who immigrated to America had half the psychiatric illnesses as did Mexican-Americans born in the U.S., regardless of their income. But the longer the immigrants lived in the U.S., the greater their risk for psychiatric problems. Traditional influences of Mexican culture and social ties appeared to protect newly arrived immigrants from mental illness, even when they were poor. Eventually, however, the consequences of Americanization added to poverty and led to feelings of alienation and inferiority.

Depression in family members increases the risk for depression in other family members. Studies report that depression for even 1 - 2 months in a mother increases the risk for depression in her children. The more severe the maternal depression, the higher the risk for depression in the children. In a perpetuating cycle, being depressed as a child increases the risk for depression during adulthood. In such cases, genetic or environmental factors or both may be responsible. Spouses of partners with depression are themselves at higher risk for depression.

Patients who have had serious bouts of depression usually cite a stressful life event as the precipitating factor for their illness. Adverse events during childhood pose a higher risk for depression in adulthood. In one study, parental divorce, physical abuse, and frightening experiences were particularly associated with onset of depression in adulthood. Only divorce was associated with recurrence, however.

Adverse events in adulthood also trigger depression. Losing a spouse through divorce or death is a major risk factor for depression in anyone. In fact, recent loss of a loved one is the most frequently reported precipitant of acute depression. All major (and even minor) losses, however, cause grief reactions. People who develop acute or chronic depression after a loss may have predisposing factors, including genetic or biologic ones, which make them more vulnerable. The existence or absence of a strong social network of family, friends, or both also has a major positive or negative effect, respectively, on recovery. Most people are able to cope with the emotional pain and eventually move beyond it without becoming chronically depressed. [See Ruling out Grief and Loneliness in the diagnosis section of this report.]

Traumatic events such as abuse or even natural disasters can cause severe immediate or delayed depression from which recovery takes a long time.

Severe or Chronic Medical Conditions. Any chronic or serious illness that is life-threatening or out of a person's control can lead to depression.

Thyroid Disease. Hypothyroidism (a condition caused when the thyroid gland does not produce enough hormone) can cause depression. However, hypothyroidism may also be misdiagnosed as depression and go undetected.

Chronic Pain Conditions. Studies have reported a strong association between depression and headaches, including chronic tension-type and migraine. Some experts believe that a syndrome of migraine headaches (and also possibly tension-type), anxiety, and depression is caused by common factors, such as abnormalities in chemical messengers, particularly dopamine or serotonin. Fibromyalgia and other chronic pain syndromes are also associated with depression.

Stroke and Other Neurological Conditions. Having a stroke increases the risk of developing depression. Also, patients with Parkinson's disease, spinal cord injuries, and other similar problems that impair movement or thinking are associated with depression.

Heart Failure. Patients with heart failure or patients who have suffered a heart attack may also suffer from depression.

A number of drugs taken for chronic problems cause depression. Among them are pain relievers for arthritis, cholesterol-lowering drugs, medications for high blood pressure and heart problems, and bronchodilators used for asthma and other lung disorders.

There is a significant association between cigarette smoking and a susceptibility to depression. People who are prone to depression face a 25% chance of becoming depressed when they quit smoking, and this increased risk persists for at least 6 months. What's more, depressed smokers are unlikely to stop smoking. Only about 6% remain smoke-free after a year. Smokers with a history of depression are not encouraged to continue smoking, but rather to keep a close watch on recurrence of depressive symptoms if they do stop smoking. The antidepressant bupropion (Wellbutrin), which is approved for helping people quit smoking (marketed under the name Zyban), is proving to be very useful in helping smokers to quit.

Chronic depression is a frequent companion to anxiety disorders. In one study, up to 96% of patients with depressive disorders experienced concurrent anxiety. More than two-thirds of people with obsessive-compulsive disorder, a common anxiety disorder, also suffer from depression.

Some evidence suggests that certain personality styles, which include an intense need for close relationships and concern for disapproval or need for control, pose a high risk for depression, particularly after an adverse life event. In line with these findings, the following specific personality disorders have been associated not only to a first episode of depression, but also to relapses:

A person with borderline personality disorder acts impulsively and has a poor self-image and unstable relationships. In one study, patients with borderline personality disorder and major depression were more likely than those with either condition alone to plan and attempt suicide.
An individual with an avoidant personality avoids strangers and unfamiliar situations.

(Personality disorders, as opposed to emotional disorders, are those with abnormal behavioral patterns rather than abnormal emotions.)

Sleep abnormalities are an integral part of depressive disorders, with more than 90% of depressed patients experiencing insomnia. Although stress and depression are major causes of insomnia, insomnia may also increase the activity of the hormones and pathways in the brain that can produce emotional problems. Even modest alterations in waking and sleeping patterns can have significant effects on a person's mood. Persistent insomnia may even predict the future development of emotional disorders. Some experts think that some psychiatric disorders can be prevented by early recognition and treatment of insomnia.

Seasonal affective disorder (SAD) affects about one in 20 adults. About 80% of people who suffer from SAD are women. People who live in the north are more apt to experience SAD than people who live in southern latitudes.

Complications of Depression

Depression is often chronic, with episodes of recurrence and improvement. About one-third of patients with a single episode of major depression will have another episode within 1 year after discontinuing treatment, and more than 50% will have a recurrence at some point in their lives. Depression is more likely to recur if the first episode was severe or prolonged, or if there have been recurrences. To date, even newer antidepressants have failed to achieve permanent remission in most patients with major depression, although the standard medications are very effective in treating and preventing acute episodes.

About 90% of suicides are due to treatable disorders, most commonly depression or substance abuse. People with depression have up to a 15% risk for suicide, with the highest risk in patients who are hospitalized for depression. Some studies indicate that atypical depression poses a higher risk for suicide than typical depression and that dysthymia may pose a higher risk than episodic major depressive disorder. Depressed men are more likely to commit suicide than depressed women. Around the world, suicide is most common in men older than 60. Suicidal preoccupation or threats of suicide should always be treated seriously in anyone, however. [See Depression in the Elderly or Depression in Children in this report.]

Major depression in the elderly or in people with serious illness seems to reduce their survival rates, even independently of any accompanying illness. Decreased physical activity and social involvement certainly play a role in the association between depression and illness severity.

Effect on Heart Disease and Other Age-Related Problems. Many studies report strong associations between depression and a worse and even shorter old age. Depression is also associated with mental decline in older people.

Studies are now showing that depression may contribute to poor outcomes for patients with heart disease.

Obesity. Both obesity and depression are increasing in Americans. Adolescents who are depressed have a high risk for obesity. Conversely, obese people are about 25% more likely than non-obese people to develop depression or other mood disorders. The conditions may have common risk factors. For example, being in a lower social and economic group increases the risk for both obesity and depression. Low physical activity may also be a common factor.

Increasing Sensations of Pain. Depression coincides with increased pain in people with conditions such as those arthritis or fibromyalgia.

Cancer. The relationship between depression and cancer has been explored for years with only a few clear-cut associations. Certainly depression and anxiety can have a profound impact on quality of life in cancer patients.

Effects of Parental Depression on Children. Depression in parents can have profound effects on their children and may increase the risk for childhood depression.

Effects on Marriage. In one survey, nearly half of people who suffered from psychiatric disorders before or during their first marriage were divorced, compared to a divorce rate of 36% in those who never suffered from emotional disorders. Spouses of partners with depression are themselves at higher risk for depression.

Effect on Work. Depression is well-known to adversely affect a person's work life. It significantly increases the risk for unemployment and lower income. Nearly half of the nation's excess lost productive time (in most cases because of reduced performance at work) may be a result of depression. Workers with depression also lose significantly more time due to ill health than non-depressed workers. Such lost time is estimated to cost the country billions of dollars each year.

Alcohol and Drug Abuse. About 14% of people with major depression also have an alcohol use disorder and 5% have drug abuse problems. Studies on the connections between alcohol dependence and depression have still not resolved whether one causes the other or if they both share some common biologic cause.

Smoking. Depression is a well-known risk factor for smoking, and 26% of people with major depression are nicotine dependent. Nicotine may stimulate receptors in the brain that improve mood in certain people with genetically induced depression.

Diagnosis

Most people who are depressed do not seek psychiatric help and must rely on their family doctor. Unfortunately, it is often difficult for a primary care doctor to recognize the problem if the patient does not bring it up directly.

Patients themselves may be unable to sense or admit their own depression. In one study, although 21% of patients who visited their family doctors were depressed, only 1% described their problem as depression.

Depression can also be confused with other medical illnesses. Weight loss and fatigue, for example, accompany many conditions, some serious, but they can also occur with depression.

Although not all patients who visit their doctor should be screened for depression, individuals who have certain factors might ask their doctor if they should be screened for depression. For example, the following people may be at higher risk and therefore warrant a screening test:

People with a family or personal history of depression
Patients with multiple medical problems
Patients with physical symptoms that have no clear medical cause
Patients with chronic pain
Individuals who visit their doctor more frequently than expected

A mental health specialist, such as a psychiatrist, social worker, or psychologist, is the best source for a diagnosis of depression. Such health professionals may administer a screening test such as the Beck Depression Inventory or the Hamilton Rating Scale, both of which consist of about 20 questions that assess the individual for depression. Studies are finding that even computerized phone interviews are valuable as screening tools for depression. However, most mental health professionals generally diagnose depression based on symptoms and other criteria.

Specific ethnic groups may present different symptoms of depression. People from non-Western countries are more apt to report physical symptoms (such as headache, constipation, weakness, or back pain) related to the depression, rather than mood-related symptoms.

Grief. The symptoms of grief (bereavement) and depression have much in common; indeed, it may be difficult to separate the two. Grief, however, is considered to be a healthy and important emotional response for dealing with loss, and it generally follows a characteristic path:

Grief normally has a limited duration. In people without any co-existing emotional disorder, bereavement usually lasts between 3 - 6 months.
The grieving person typically endures a succession of emotions that include shock and denial, loneliness, despair, social alienation, and anger.
The recovery period following this process, during which the individual becomes re-involved with life, takes about the same amount of time as the bereavement cycle.

If the grief is still severe after this period, however, it may affect a person's health or increase the risk for on-going depression. Some experts suggest that such a severe persistent grieving state be categorized as a separate psychologic diagnosis, termed complicated grief disorder, which would be related to post-traumatic stress syndrome and require special treatment.

Loneliness. Like grief, loneliness is a condition that may often be mistaken for depression. In fact, while loneliness and depression often go hand in hand, some researchers believe that some people with loneliness may be effectively treated for depression. Of course, every person feels loneliness now and then. Debilitating loneliness, however, is often characterized by misery, a feeling of hollowness, unrealistic expectations for one's life, and feeling removed from others. Shy people may be more prone to loneliness. Psychotherapy of various kinds may help people address and allay loneliness.

Treatment

Depression is a treatable illness, with many therapeutic options available. Increasingly, professionals are viewing major depression as a chronic illness (the condition nearly always returns when treatment is stopped). Therefore, medical intervention and help must be ongoing.

Patients with chronic depression have a number of options, including psychotherapy, antidepressants, or both. In general, the treatment choice depends on the degree and type of depression and other accompanying conditions. It also may depend on age, pregnancy status, or other individual factors.

Unfortunately, many Americans with major depression receive either inadequate treatment or no treatment at all. Reasons may include treatment by providers who may not have sufficient information or training on dosages or specific drugs that would be best suited for individual cases, lack of recognition of depression symptoms by providers, poor access to health care services, lack of health insurance, and poor compliance with medications.

Patients with Major Depression. Numerous studies support a combination of cognitive behavioral therapy (CBT) plus antidepressants, typically a selective serotonin reuptake inhibitor (SSRI) or serotonin norepinephrine reuptake inhibitor (SNRI). Although some people may feel better after taking antidepressants for a few weeks, most people need to take medication for at least 6 - 12 months to ensure a full response. Research indicates that patients respond better to medications when drug therapy is combined with CBT. Exercise is also important in helping relieve depressive symptoms.

For patients who are not helped by SSRIs or SNRIs, other types of antidepressants are available. Sometimes an atypical antipsychotic drug may be given in combination with an antidepressant for patients with severe major depressive disorder.

Brain stimulation techniques, such as electroconvulsive therapy (ECT) and vagus nerve stimulation, are also options. In recent years, experimental procedures, such as repetitive transcranial magnetic stimulation, have also been found to help in some cases of treatment-resistant depression. Researchers are also investigating new types of drugs (such as ketamine), which may provide a rapid, if temporary, improvement for these patients. In general, the more treatment strategies that patients need, the less likely they are to recover completely from depression.

Patients with Minor Depression. Patients with minor depression (fewer than five symptoms that persist for fewer than 2 years) may respond well to watchful waiting to see if antidepressants are necessary. Some studies indicate that antidepressants do not work that well for mild depression. Counseling or cognitive behavioral therapy may be helpful, as is regular exercise.

Patients with Depression and Other Psychiatric Problems. Other psychiatric problems often coexist with depression. If patients also suffer from anxiety, treating the depression first often relieves both problems. More severe psychiatric problems, such as bipolar disorder or schizophrenia, require specialized treatments.

Patients with Depression and Medical Conditions. Depression can worsen many medical conditions and may even increase mortality rates from some disorders, such as heart attack and stroke. Depression, then, should be aggressively treated in anyone with a serious medical problem.

Patients with Depression and Substance Abuse Problems. Treating depression in patients who abuse alcohol or drugs is important and can sometimes help patients quit. However, absence from substance abuse is considered essential for adequate treatment of depression.

Most people with depression can be treated in an office setting by a psychiatrist or other therapist. Infrequently, the level of dysfunction may be serious enough to warrant hospitalization to provide protection from further deterioration or self-harm.

Health professionals who can prescribe antidepressants include:

Doctors, including psychiatrists
Some nurse clinicians

Although other mental health professionals cannot prescribe drugs, most therapists have arrangements with a psychiatrist for providing medications to their patients. In general, mental health professionals are categorized by their training:

Psychoanalysts tend to have a degree in psychiatry, psychology, or social work as well as several years of training at a psychoanalytic institute.
Psychologists have received a Ph.D, including an internship in a mental healthcare facility.
A clinical social worker has a master's degree and 2 years of supervised experience in mental health and human services.
Advanced-practice psychiatric nurses have a master's degree and can provide therapeutic services.

Tips for Selecting a Therapist:

Patients can locate a mental health professional in their area by asking their doctor for a referral or by contacting a mental health organization. [See Resources.]
The patient should describe problems briefly but specifically over the phone to any prospective therapist to get a sense of whether he or she will suit the patient's needs.
An advanced degree does not necessarily guarantee quality therapy. The patient's belief in their health care provider may be the most important component in recovery.
Patients should not be shy about considering a change in their therapist if they lack confidence in their current one.

Although a mother's depression during and after pregnancy can have serious effects on her child, researchers are still trying to determine the best methods for preventing and treating pregnancy-related depression.

The use of antidepressants during pregnancy is controversial, especially for women with major depression who regularly take antidepressant medication. Most doctors advise women to avoid, if possible, any medications during pregnancy and nursing. But, women with depression who stop taking antidepressants during pregnancy may be likely to have a relapse of depression. Women who are pregnant or thinking about becoming pregnant should not stop taking antidepressants without first talking to their doctors.

Some research suggests that certain serotonin reuptake inhibitors (SSRIs) may increase risks for the fetus. The strongest evidence concerns the SSRI paroxetine (Paxil), which can cause major birth defects -- including heart abnormalities -- if taken during the first trimester of pregnancy. In 2006, the American College of Obstetricians and Gynecologists recommended that doctors should not prescribe paroxetine to women who are pregnant or planning on becoming pregnant.

Other research indicates that first-trimester use of SSRIs may increase the risk for rare skull and neural tube defects. Venlafaxine (Effexor), a dual inhibitor antidepressant, has been associated with birth complications when taken during the last trimester. In addition, some studies have shown that babies may experience withdrawal symptoms if their mothers take SSRIs late in pregnancy. However, the overall evidence indicates that there is a very low overall risk for antidepressant-associated birth defects and problems. Still, women should discuss all potential risks with their doctors.

In terms of non-drug treatment of postpartum depression, a review of 15 clinical trials suggested that postpartum depression is best treated by intensive and individualized psychotherapy within a month after a woman gives birth. The researchers found that women are too busy in the weeks before birth to attend prenatal classes that focus on preventing postpartum depression.

Some experts recommend only psychotherapy or attention intervention for elderly patients with mild depression. In many older patients, a regular exercise program may be sufficient to improve mood. Ideally, elderly people with more serious depression should be treated with a combination of psychotherapy and antidepressants on an ongoing basis, even after their depressive symptoms are relieved.

The use of antidepressants in the elderly is problematic:

Tricyclics are as effective as, and less expensive than, SSRIs, but they have more side effects. Specifically, they pose a higher risk for adverse effects on the heart and possibly the lungs. (The older tricyclics, such as amitriptyline and imipramine, have other severe side effects in older adults.)
SSRIs have fewer side effects than tricyclics. However, SSRIs may not pose any lower risk for falls than the older tricyclic antidepressants. In addition, researchers are investigating whether SSRIs are associated with an increased rate of osteoporosis (“thin bones”) and fractures in older adults.

About 2% of American primary school-age children and 4 - 8% of adolescents suffer from depression. Studies suggest that when children or adolescents are treated, up to 80% recover. Still, 25 - 50% of these young people have a recurrence of depression within 2 years of their first episode of depression.

It is important to recognize that childhood depression differs from adult depression and that children may respond differently than adults to antidepressant medication. These variances are due to childhood brain development processes as well as age-related differences in drug metabolism. Children may experience medication side effects not seen in adults, and some antidepressants that are effective for adults may not work for children.

Mild-to-Moderate Depression. The pediatrician may want to monitor a child with mild depression for 6 - 8 weeks before deciding whether to prescribe psychotherapy, antidepressant medication, or a referral to a mental health professional. Once medication has been started, the doctor will decide if the dosage needs to be increased after another 6 - 8 weeks. Medication may need to be continued for 1 year after the symptoms have resolved, and the doctor should continue to monitor the child on a monthly basis for 6 months after full remission of depression. For psychotherapy, cognitive therapy may be the best approach for children and adolescents with depression. Some studies suggest that other types of psychotherapy, such as family therapy and supportive therapy, can also be very effective.

Severe Depression. The American Academy of Child and Adolescent Psychiatry recommends an SSRI antidepressant for children and adolescents with very severe depression that does not respond to psychotherapy. Tricyclic antidepressants do not tend to help adolescents and children and these drugs have many side effects. MAOIs are also not commonly prescribed.

Many SSRIs appear to be safe and effective, but at this time fluoxetine (Prozac) is the only one approved for children over age 7 and for adolescents. The FDA strongly advises against the use of specific SSRIs, such as paroxetine (Paxil), due to concerns about an increased risk for suicidal behavior as well as the lack of any evidence supporting the drug's efficacy in pediatric patients. On an encouraging note, a 2007 review in the Journal of the American Medical Association indicated that the overall benefits of antidepressants for children and adolescents appear to be much greater than the risks for suicidal behavior. Still, the study found that antidepressants have only modest benefits for major depressive disorder, which underlines the importance of adjunctive psychotherapy.

For optimal results, SSRIs should be combined with either cognitive-behavioral or interpersonal psychotherapies. A study of adolescents with depression reported that combination treatment with fluoxetine and cognitive behavioral therapy was more effective than either treatment alone.

Due to potential suicide risks, children and adolescents should be monitored regularly during the initial months of antidepressant treatment. [For more detailed information, see Suicide Risk and Antidepressant Medications.]

Antidepressants and Drug Treatment Guidelines

Major classes of antidepressants include:

Selective serotonin-reuptake inhibitors (SSRIs). These have become the standard antidepressants. They target the brain chemical (neurotransmitter) serotonin. They are effective and have very moderate side effects. Some may be beneficial in treating anxiety and certain subtypes of depressive disorders unresponsive to previous drugs, including premenstrual dysphoric disorder and seasonal affective disorder, atypical depression, and recurrent brief depression.
Other neurotransmitter inhibitors. These drugs target neurotransmitters other than or in addition to serotonin, such as norepinephrine. Many are proving to be effective in patients who do not respond to standard antidepressants or in specific patients, such as smokers who want to quit or patients with chronic pain.
Tricyclic antidepressants (TCAs). These drugs are effective but can have severe adverse effects, particularly in older people.
Monoamine oxidase inhibitors (MAOIs). These drugs include newer selective MAOIs. MAOIs are the most effective antidepressants for atypical depression, but have some severe side effects and require restrictive dietary rules.
St. John's wort and other herbal remedies are included in the Lifestyle section of this report.

Approach and Duration of Initial Treatment. The guidelines for the duration of an initial antidepressant regimen is as follows:

Patients should start at a low dose, which is increased over a period of 5 - 10 days.
Patients should see their doctor every 1- 2 weeks until substantial improvement occurs. It may take 4 - 8 weeks before a patient experiences the effects of any antidepressant.
Side effects usually diminish within 1 - 4 weeks. (Exceptions may be weight gain and sexual dysfunction.)
If no improvement occurs, an alternative drug may be tried. More than 80% of patients respond to some antidepressant, although specific drugs are helpful for only about half of patients. This suggests that if one medication fails, another has a good chance of being helpful. In general, the fewer drug treatment strategies required, the better a patient’s chances of recovering completely from depression. Patients who become symptom-free have the best chance for complete recovery compared to patients whose symptoms merely improve.
In general, patients should continue taking antidepressants for at least 6 months after symptom relief to help prevent relapse. (Patients who improve within 2 weeks of taking medications may not require lengthy treatment.)

Treating Recurrence. Recurrence of depression is very common. About a third of patients will relapse after a first episode within a year of ending treatment, and more than half will experience a recurring bout of depression at some point during their lives. Among those at highest risk for early relapse and who may require ongoing antidepressants are:

Patients with at least two episodes of major depression or major depression that lasts for 2 years or longer before initial treatment.
Patients who continue to have low-level depression for 7 months after starting antidepressant treatments.

Patients may need maintenance therapy. Experts disagree, however, on the optimal length or the appropriate dosage of maintenance therapy. Some patients may need to stay on antidepressants for 1 - 2 years -- or even indefinitely. Some experts recommend withdrawing from medication after a year. (This should be done gradually, over 2 - 3 months.) If depression recurs, the patient should go back on the antidepressants.

There is no risk for addiction with current antidepressants, and many of the common antidepressants, including most standard SSRIs, have been proven safe when taken for a number of years.

Common Side Effects of Most Antidepressants. No matter how well a drug treats depression, the ability of the patient to tolerate its side effects strongly influences their compliance with therapy. Lack of compliance is probably the major barrier to success. Side effects can be avoided or moderated if any regimen is started at low doses and built up over time. Although specific side effects are discussed under individual drugs, there are a few that are common to many of them:

Sexual dysfunction is a common side effect of many of the standard antidepressants and some of the newer drugs. These side effects can be particularly distressing for patients on maintenance treatment who otherwise feel well. Some of the newer antidepressants, such as bupropion, may be effective alternatives without as high a risk for this problem. Sildenafil (Viagra), used for erectile dysfunction in men, may help reverse sexual dysfunction from antidepressants. It does not heighten sexual interest, however.
An increased risk of oral health problems caused by dry mouth is associated with long-term use of most antidepressants. Patients can increase salivation by chewing gum, taking vitamin C tablets, using saliva substitutes, and rinsing the mouth frequently.
Virtually all antidepressants have complicated interactions with other drugs; some are very important. Patients should inform the doctor of any drugs they are taking, including over-the-counter medications and herbal remedies.
Nearly all antidepressants are metabolized in the liver, so anyone with liver abnormalities should use them with caution.
Abrupt withdrawal from many antidepressants can produce severe side effects; no antidepressant should be stopped abruptly without consultation with a doctor.

In recent years, there has been concern that SSRI antidepressants may increase the risk for suicidal behavior. Of particular concern is a greater risk for suicide in young people taking these medications. While depression is itself the major risk factor for suicide, and antidepressant medication may revitalize suicidal attempts in patients who were too despondent before treatment to make the effort, evidence suggests that in some cases the medication itself can cause suicidal behavior. One specific SSRI, paroxetine (Paxil), has been definitely linked with suicidal behavioral risk in adults ages 18 - 30. In May 2006, the drug’s manufacturer warned doctors that all patients, and particularly young adults, should be carefully monitored during paroxetine therapy.

The U.S. Food and Drug Administration (FDA) has been conducting in-depth research on suicide risk and antidepressant medications. In October 2004, after careful review of scientific evidence, the FDA issued a public health advisory instructing drug manufacturers to include a "black box" warning explaining the association between antidepressant use and increased risk for suicidality (suicidal thoughts and behavior) in children and adolescents. In May 2007, the FDA proposed that the labels of antidepressant medications should include additional warnings about the risk of suicidal thoughts and behavior in young adults (ages 18 - 24) during the first 1 - 2 months of treatment. The FDA also notes there is a decreased risk of suicidality for adults age 65 years and older taking antidepressants.

The FDA based its recommendations for children and adolescents on a review of 24 clinical trials of nine antidepressant drugs. These trials enrolled over 4,400 pediatric patients and tested the safety and efficacy of SSRIs as well as other classes of antidepressants. The data suggested a greater risk for suicidality within the first few months of treatment. The average risk was minimal. Children and adolescents treated with these drugs had a 4% risk for suicidality compared with 2% for patients who received placebo. No patients in these studies actually committed suicide.

Based on these findings, the FDA recommends that caregivers monitor children being treated with antidepressants for sudden behavioral changes, and immediately notify their doctor if such changes occur. These behavioral signs include:

Agitation
Irritability
Anxiety
Panic attacks
Insomnia
Aggressiveness
Impulsivity
Hyperactivity in actions and speech
Worsening of depression
Increased thoughts of suicide

The FDA’s guidelines for medication usage recommend that patients see their doctor regularly after initiating drug treatment. The recommended schedule is:

Once per week for 4 weeks (1st month)
Every 2 weeks for the next month (2nd month)
At the end of week 12 following the start of drug treatment (3rd month)
More frequently if changes in mood or behavior occur
Patients should also be closely monitored if their drug dosage is changed.

Patients should immediately contact their doctor if depression symptoms worsen or if suicidal thoughts or behavior increase.

Selective serotonin-reuptake inhibitors (SSRIs) are now the first-line treatment of major depression. They work by increasing levels of serotonin in the brain. SSRIs include fluoxetine (Prozac), sertraline (Zoloft), paroxetine (Paxil), fluvoxamine (Luvox), citalopram (Celexa), and escitalopram (Lexapro). There are no significant differences among SSRI brands in effectiveness for treating major depressive disorder, although individual drugs may have different side effects or benefits for specific patients. At this time, fluoxetine is the only one of these drugs to be approved for children over age 7 and adolescents.

Because they act specifically on serotonin, SSRIs have fewer side effects than older antidepressants, which have more widespread effects in the body.

Candidates for SSRIs. SSRIs appear to help people with the following conditions:

Mild to moderately severe major depression
Seasonal affective disorder
Dysthymia
Severe premenstrual syndrome and premenstrual dysphoric disorder (PMDD) -- a repackaged form of fluoxetine (Sarafem) is the first SSRI specifically FDA-approved for PMDD. Other SSRIs and newer antidepressants are also proving to be effective
Anxiety disorders
Bulimia
Impulsive and aggressive behaviors in psychiatric patients and in people with no mental health problems

Duration of Effectiveness and Use. SSRIs take, on average, 2 - 4 weeks to be effective in most adults. They may take even longer, up to 12 weeks, in the elderly and in those with dysthymia. By 14 weeks, depression should be in remission in everyone who responds to the drugs. Unfortunately, recurrence is common once the drugs are stopped. Studies indicate that the standard SSRIs are generally safe, although it is still unclear which patients would most benefit from on-going medication. Some doctors recommend withdrawing from medication after a year. If depression recurs, then the patient should go back on the antidepressant.

Side Effects of SSRIs. Side effects may include:

Nausea and gastrointestinal (GI) symptoms usually wear off over time.
Agitation, insomnia, mild tremor, and impulsivity occur in 10 - 20% of people who take SSRIs. These symptoms may be particularly problematic in patients who also suffer from anxiety, sleeplessness, or both.
Drowsiness affects about 20% of SSRI-treated patients. Newer SSRIs, such as escitalopram (Lexapro), may have fewer of these adverse effects.
Dry mouth is a common side effect.
Patients may lack motivation, feel tired, be confused, and experience mental dullness, but this side effect is fairly rare.
Headache and flu-like symptoms may occur.
Heart palpitations and chest pain may occur.
Weight gain varies depending on the SSRI. For example, in one study patients who took paroxetine (Paxil) experienced five times the weight gain as those who took citalopram (Celexa). Patients should be encouraged to maintain a low-calorie diet and to exercise. They should be aware that some of the weight-loss medications, notably sibutramine (Meridia), can have serious interactions with SSRIs.
Sexual side effects include delayed or loss of orgasm and low sexual drive. They are a well-known side effect of SSRIs. Taking a supervised drug "holiday" on the weekend may improve sexual function during that time. Some of the newer SSRIs or other antidepressants may cause less severe impairment of sexual function.
Paroxetine (Paxil) may cause birth defects if taken during the first 3 months of pregnancy. Most reported defects have been heart-related. The most common heart abnormalities are ventricular septal defects, which are holes in the muscular wall that separate the main pumping chambers of the heart. Venlafaxine (Effexor) has also been associated with birth defects. Still, recent research suggests that most types of SSRI-associated birth defects are rare and the overall risks are low. Pregnant women who are being treated for major depression should not stop taking antidepressants without first talking to their doctors. [For more information on antidepressant treatment guidelines during pregnancy, see Treating Depression During and After Pregnancy in Treatment section.]

Drug Interactions. SSRIs can interact with other antidepressants such as tricyclics and, in particular, monoamine oxidase inhibitors (MAOIs). SSRIs should never be taken in combination with an MAOI or within 2 weeks after discontinuing MAOI treatment. Other serious interactions have occurred with meperidine (Demerol) and illegal substances (such as LSD, cocaine, or ecstasy). People who take SSRIs may drink alcohol in moderation, although the combination may compound any drowsiness experienced with SSRIs, and some SSRIs increase the effects of alcohol.

Withdrawal Symptoms. Cognitive problems, sleep disturbances, increase in depressive symptoms, and electric shock-like symptoms have been known to occur with sudden discontinuation of SSRIs. The symptoms are more likely to occur with antidepressants with shorter half-lives as compared with fluoxetine, which has a long half-life. The dose of the antidepressant should be slowly reduced before stopping.

These newer antidepressants target other neurotransmitters, such as norepinephrine or dopamine, alone or in addition to serotonin. In general, the advantages of the new designer antidepressants are:

They may be better tolerated than the older tricyclic compounds and even some SSRIs, although long-term side effects are not fully known in this group.
Most of these drugs have fewer adverse effects than SSRIs on sexual function.
They may be more effective than SSRIs for severely depressed patients.
Some of these drugs are helpful for additional problems -- such as insomnia, fibromyalgia and similar chronic pain syndromes, or smoking -- that may affect people with depression.

They do share some side effects with other antidepressants, including dizziness and dry mouth.

Dual Inhibitors. Dual inhibitors act directly on two neurotransmitters -- norepinephrine and serotonin. These drugs are also known as serotonin norepinephrine reuptake inhibitors (SNRIs). The following SNRIs are approved for treatment of major depression in adults:

Venlafaxine (Effexor) is similar to Prozac in effectiveness and tolerability for most patients. As with SSRIs, venlafaxine may impair sexual function. The drug can increase blood pressure and heart rate and should be used with caution in patients with high blood pressure or heart disease. It can also cause uterine and vaginal bleeding unrelated to menstruation. Venlafaxine should not be taken during the last trimester of pregnancy as it can cause complications in newborn infants. Some patients report severe withdrawal symptoms, including dizziness and nausea. In 2006, the drug’s manufacturer warned of an increased overdose risk and advised doctors to prescribe their patients only small amounts of venlafaxine pills.
Duloxetine (Cymbalta) also acts on both serotonin and norepinephrine. Side effects are generally mild and include dry mouth, nausea, and sleepiness. Patients with narrow-angle glaucoma or patients with liver or kidney diseases should not take duloxetine. Because duloxetine can cause liver damage, patients who drink large quantities of alcoholic beverages should not take it. Signs of liver damage include itching, dark urine, yellowing of skin and eyes (jaundice), and fatigue. Patients should immediately contact their doctor if they experience these symptoms.
Mirtazapine (Remeron) can cause sleepiness, increased appetite, weight gain, and dizziness.

Other Antidepressants with Effects on Multiple Neurotransmitters. Bupropion (Wellbutrin, Zyban) affects the reuptake of serotonin, norepinephrine, and dopamine -- a third important neurotransmitter. In addition to depression, bupropion is also approved for smoking cessation and for treating seasonal affective disorder (SAD). Bupropion causes less sexual dysfunction than SSRIs. About 25% of patients experience initial weight loss. Side effects include restlessness, agitation, sleeplessness, headache, and stomach problems. Bupropion has a risk for seizures, which increases with higher doses. High doses may also cause dangerous heart arrhythmias.

Before the introduction of SSRIs, tricyclics were the standard treatment for depression.

Tricyclics are sometimes grouped into two categories:

Tertiary amines include amitriptyline (Elavil, Endep) and imipramine (Tofranil).
Secondary amines include desipramine (Norpramin) and nortriptyline (Pamelor, Aventyl). Secondary amines may have fewer side effects, including drowsiness, than tertiary amines, but they are as toxic in high amounts.

Less commonly used tricyclics include doxepin (Sinequan), amoxapine (Asendin), maprotiline (Ludiomill), protriptyline (Vivactil), trimipramine (Surmontil), mianserin (Bolvidon), and dothiepin (Prothiaden).

Tricyclics are as effective for treating depression but they have many side effects. They may offer benefits for many people with dysthymia, who generally do not respond to SSRIs. They may also be prescribed in lower dosages to be taken at night to help with insomnia.

Side Effects of Tricyclics. Side effects are common with these medications. In fact, in an analysis of studies, more tricyclic users discontinued their drugs due to side effects than did SSRI or MAOI users. Those most often reported include:

Dry mouth
Constipation
Blurred vision
Sexual dysfunction
Weight gain
Difficulty urinating
Drowsiness
Dizziness -- blood pressure may drop suddenly when sitting up or standing.

Tricyclics can have serious, although rare, side effects:

They tend to cause disturbances in heart rhythm, which can pose a danger for some patients with certain heart diseases. Care should be taken when these medications are prescribed to the elderly and to those at risk of overdose.
Also of concern are reports that tricyclics, particularly imipramine as well as mianserin and dothiepin, may increase the risk for a lung disease called idiopathic pulmonary fibrosis (IPF), which can cause lung inflammation and scarring. Initial symptoms are breathlessness and dry cough.
Tricyclics can be fatal with an overdose.
Protriptyline can cause sun sensitivity. People who take this drug should take precautions against sunlight when they go outdoors.

Monoamine oxidase inhibitors (MAOIs) block monoamine oxidase, an enzyme which has negative effects on many of the neurotransmitters that are important for well-being. MAOIs include phenelzine (Nardil), isocarboxazid (Marplan), and tranylcypromine (Parnate). Because these drugs can have very severe side effects, they are usually prescribed only when other types of antidepressants do not help. Research indicates that MAOIs are an effective option for atypical and treatment-resistant depression.

Newer MAOIs, such as selegiline (Eldepryl, Movergan), target only one form of the MAOI enzyme. They may cause fewer side effects than older MAOIs. In 2006, a skin patch form of selegiline (Emsam) was approved for treatment of major depressive disorder in adults.

Candidates for MAOIs. MAOIs may be effective for the following conditions:

Atypical depression
Eating disorders
Post-traumatic stress disorder
Borderline personality

Side Effects. MAOIs commonly cause the following side effects:

Orthostatic hypotension (a sudden drop in blood pressure upon standing)
Drowsiness or insomnia
Dizziness
Sexual dysfunction
The most serious side effect is severe hypertension (high blood pressure), which can be brought on by eating certain foods having high tyramine content. Such foods include aged cheeses, most red wines, sauerkraut, vermouth, chicken livers, dried meats and fish, canned figs, fava beans, and concentrated yeast products.
MAOIs can cause birth defects and should not be taken by pregnant women.

Very dangerous side effects, such as serotonin syndrome, can occur from interactions with other antidepressants, including SSRIs. Serotonin syndrome is a potentially fatal condition that is caused by the interaction of serotonergic drugs. Symptoms include confusion, agitation, sweating and shivering, and muscle spasms. There should be at least a 2-week break between taking MAOIs and other antidepressants. MAOIs can have serious interactions with other drugs as well, including some common over-the-counter cough medications. In such cases, severe high blood pressure or dangerous reactions can occur. It is important that patients discuss with their doctors any other medications they are taking.

If patients fail to respond to antidepressants, doctors may try adding on a different type of drug. (This combination strategy is called “augmentation” or “adjunctive treatment”.) Atypical antipsychotics are drugs that are usually prescribed for schizophrenia or bipolar disorder, but they can also play a role in the treatment of severe depression. In 2007, aripiprazole (Abilify) was approved in combination with antidepressant therapy for treatment of adults with major depressive disorder. Investigators are also studying whether combination treatment with the atypical antipsychotic risperidone (Risperdal) can help patients with major depression achieve remission.

Ketamine. Ketamine, an anesthetic drug, may be helpful for patients with severe treatment-resistant depression. In a small preliminary study, a single intravenous dose of ketamine helped patients quickly recover from depression within 2 hours, and some patients sustained benefits for up to a week. (Standard antidepressant drugs usually take about 8 weeks to have an effect.) Ketamine blocks the NMDA brain protein receptor, which is involved in glutamate regulation. Glutamate is a brain chemical that is thought to be involved in depression.

Psychotherapy

Among the various psychotherapies, cognitive-behavioral therapy appears to be the most effective approach. If psychotherapy is used alone without medications, benefits should be evident within 8 weeks and symptoms should be fully resolved by 12 weeks. If these conditions are not met, then the patient should strongly consider antidepressant drugs.

In a major analysis of four randomized comparative studies, cognitive behavior therapy worked as well as antidepressants in treating severe depression for many patients. Much of the success of psychologic therapy depends on the skill of the therapist. Many studies suggest that combining cognitive therapy with antidepressants offer the greatest benefits for many patients, particularly for dysthymia (chronic depression).

Medical evidence also has found that the benefits of cognitive therapy persist after treatment has ended. Cognitive behavioral therapy has been shown to help prevent future suicide attempts in patients with a history of suicidal behavior.

Best Candidates. Cognitive therapy may be particularly helpful for the following patients:

Patients with atypical depression
Adolescents with mild symptoms of major depression
Women with non-psychotic postpartum depression
Children of parents with the disorder -- in this case, therapy should involve the whole family.
Cognitive therapy does not appear to be as beneficial as antidepressants for most patients with dysthymia.

Approach. This approach focuses on identification of distorted perceptions that patients may have of the world and themselves, on changing these perceptions, and on discovering new patterns of actions and behavior. These perceptions, known as schemas, are negative assumptions developed in childhood that can precipitate and prolong depression. Cognitive therapy works on the principle that these schemas can be recognized and altered, thereby changing the response and eliminating the depression.

First, the patient must learn to recognize depressive reactions and thoughts as they occur, usually by keeping a journal of feelings about, and reactions to, daily events.
The patient is often given "homework" that tests old negative assumptions against reality and demands different responses.
Then, the patient and therapist examine and challenge these entrenched and automatic reactions and thoughts.
As the patient begins to understand the underlying falseness of the assumptions that cause depression, they can begin substituting new ways of coping.

Over time, such exercises help build confidence and eventually alter behavior. Patients may take group or individual cognitive therapy. Cognitive therapy is a time-limited treatment, typically lasting 12 - 14 weeks. Extending this period, however, may help prevent relapse. In one study, therapy was continued for 10 sessions over an additional 8 months. This extended treatment significantly reduced the risk of recurrence. In fact, some experts believe that short-term therapy is not effective for patients with chronic or relapsing psychiatric disorders.

Based in part on psychodynamic theory, interpersonal therapy acknowledges the childhood roots of depression, but focuses on symptoms and current issues that may be causing problems. IPT is not as specific as cognitive or behavioral therapy, and all work is done during the sessions. The therapist seeks to redirect the patient's attention, which has been distorted by depression, toward the daily details of social and family interaction. The goals of this treatment method are improved communication skills and increased self-esteem within a short period (3 - 4 months of weekly appointments) of time. Among the forms of depression best served by IPT are those caused by distorted or delayed mourning, unexpressed conflicts with people in close relationships, major life changes, and isolation.

The intent of supportive psychotherapy or attention intervention is to provide the patient with a nonjudgmental environment by offering advice, attention, and sympathy. Supportive therapy appears to be particularly helpful for improving compliance with medications by giving reassurance, especially when setbacks and frustration occur.

Other Treatments

Electroconvulsive therapy (ECT) is commonly called shock treatment. It has received bad press, in part for its potential memory-depleting effect. Since its introduction in the 1930s, ECT has been significantly refined, and is now considered an effective and safe treatment for severe depression in the appropriate situation. It is especially effective for patients with severe depression who experience delusions and hallucinations. Maintenance ECT may also help prevent relapse.

Candidates for ECT. ECT may be helpful for the following patients with severe depression:

Patients who cannot, for any reason, take antidepressant drugs
Suicidal patients
Elderly patients who are psychotic and depressed
Pregnant women with severe depression
Patients with certain heart problems
Young patients who fit the adult criteria for ECT

The Procedure. In general, hospitalization is not necessary. ECT involves the following steps:

The patient receives a muscle relaxant and short-acting anesthetic.
A small amount of electric current is sent to the brain, causing a generalized seizure that lasts for about 40 seconds.
Most patients receive 6 treatments, spaced every 2 - 5 days. Others receive up to 15 treatments, followed by 6 - 12 additional treatments spaced every other week or longer for another 2 - 4 months.

Side Effects. Side effects of ECT may include temporary confusion, memory lapses, headache, nausea, muscle soreness, and heart disturbances. Concerns about permanent memory loss appear to be unfounded.

Transcranial magnetic stimulation (TMS) uses high frequency magnetic pulses that target affected areas of the brain. This investigational treatment is similar to electroconvulsive therapy (ECT) but, unlike ECT, it is more precise. However, it is not yet clear whether it as effective as ECT. Researchers are continuing to refine rTMS techniques to improve treatment outcomes.

Vagus nerve stimulation (VNS) is a procedure that is effective for certain patients with epilepsy, and is now showing some success in patients with treatment-resistant depression

VNS involves implanting a battery-powered device under the skin in the upper left of the chest. The neurologist programs the device to deliver mild electrical stimulation to the vagus nerve. The two vagus nerves are the longest nerves in the body. They run along each side of the neck, then down the esophagus to the gastrointestinal tract. The vagus nerve travels to areas of the brain that control functions such as sleep and mood.

Studies report response rates of 35 - 46% in appropriate candidates with treatment-resistant depression. VNS is approved by the FDA for long-term treatment of chronic depression in adults who have not responded to typical treatments for their major depressive episode. Patients who use VNS may continue to show improvement in both their depression symptoms and quality of life.

Vagal stimulation can cause shortness of breath, hoarseness, sore throat, coughing, ear and throat pain, or nausea and vomiting. These side effects can be reduced or eliminated by reducing the intensity of stimulation. Long-term studies on patients with epilepsy have reported no serious adverse side effects, although the treatment may cause lung function deterioration in some people with existing lung disease.

The vagus nerves branch off the brain on either side of the head and travel down the neck, along the esophagus to the intestinal tract. They are the longest nerves in the body, and affect swallowing and speech. The vagus nerves also connect to parts of the brain involved in seizures. In many seizures disorders, electrical stimulation of the vagus nerves may help relieve symptoms.

Phototherapy is recommended as treatment for seasonal affective disorder (SAD), particularly for patients who do not wish to try antidepressants.

The Procedure. The procedure is noninvasive and simple. It is best performed immediately after waking in the morning. The patient sits a few feet away from a box-like device that emits very bright fluorescent light (10,000 lux) for about 30 minutes every day.

Some people report mood improvement as early as 2 days after treatment. In others, depression may not lift for 3 - 4 weeks. If no improvement is experienced after that, depressive symptoms will be unlikely to respond to phototherapy. Phototherapy may work best when combined with cognitive behavioral therapy.

Side Effects. Side effects include headache, eye strain, and irritability, although these symptoms tend to disappear within a week. Patients taking light-sensitive drugs (such as those used for psoriasis), certain antibiotics, or antipsychotic drugs should not use light therapy. Patients should be examined by an ophthalmologist before undergoing this treatment.

A surgical technique called cingulotomy interrupts the cingulate gyrus, a bundle of nerve fibers in the front of the brain, by applying heat or cold. A variation of this procedure using MRI scans to guide the surgeon produced long-term improvement in 53 - 78% of patients with severe intractable depression. The procedure is generally safe with few serious complications. It does not affect intellect or memory.

Some small studies have suggested that acupuncture may help in relieving depression. Larger studies are required to confirm its benefits.

Lifestyle Changes

St. John's wort (Hypericum perforatum) is an herbal remedy that may help some patients with mild-to-moderate depression. It does not appear to help patients with moderate or severe depression.

The herb St. John's wort is believed to be helpful in relieving mild-to-moderate depression, but should only be taken under a doctor's supervision. Manufacturers of herbal supplements do not need FDA approval to sell the products.

This herbal substance is not regulated, and there is no guarantee of quality in any brands currently available. In fact, in a 2003 study, only 2 of 54 St. John's products bought in Canada and the U.S. contained concentrations of the active ingredients that fell within 10% of the claims on the labels.

The following guidelines are recommended:

People with depression should not use St. John's wort without consulting a doctor. Children and pregnant or nursing women should not take this substance.
People should purchase brands only from well-established manufacturers.
Although no specific dose levels have been established, evidence suggests taking 900 mg daily (300 mg taken 3 times a day or 450 mg taken twice a day).
It takes between 2 - 3 weeks for the herb to have an effect.
St. John's wort should not be combined with other antidepressants. This herb may also interact with other types of medications and increase or decrease their potency. St. John's wort can increase the risk for bleeding when used with blood-thinning drugs. It can also reduce the strength of certain drugs including cancer and HIV treatments.

Side Effects. Side effects are uncommon but may include nausea, dry mouth, allergic reactions, and fatigue. This herb may increase sensitivity to light (photosensitivity). Some people have reported temporary nerve damage after sun exposure, specifically pain and tingling on sun-exposed areas.

Carbohydrates and Tryptophan. Some people report relief from depression by eating foods or diet supplements that boost levels of tryptophan, an amino acid involved in the production of serotonin. There are high-carbohydrate drinks available over the counter that increase tryptophan levels and may alleviate depression associated with premenstrual syndrome for about 3 hours. Simply eating a high amount of carbohydrates, however, is not a solution for depression.

Impurities found in diet supplements containing L-tryptophan itself have caused cases of eosinophilia-myalgia syndrome, a condition that elevates certain white blood cells and can be fatal. Supplements containing L-tryptophan are currently banned in the U.S. by the FDA.

Fish Oil. Some evidence suggests that an imbalance in the ratio of specific fatty acids (omega-6 to omega-3) may increase the risk for depression. Both are polyunsaturated fats, but omega-6 fatty acids are mostly found in corn, safflower, soybean, and sunflower oil whereas omega-3 fatty acids are found in fish oil, canola oil, soybeans, flaxseed, and certain nuts and seeds.

The bottom line may be to increase intake of omega-3 rich foods, such as fish, nuts, and canola oil, and reduce consumption of foods containing omega-6 fatty acids, such as corn and sunflower oils. Such a dietary approach is healthy in any case. Researchers are studying whether eating fish or taking fish oil supplements can reduce depression. Small preliminary studies suggest that these dietary approaches may be helpful for some patients. Scientists are also investigating which type of fish oil compound -- eicosapentaenoic acid (EPA) or docosahexaenoic acid (DHA) -- provides the greatest benefit.

Omega-3 fatty acids, found in oily fish and flaxseed and canola oils, may be beneficial to people with depression.

Vitamins and Other Supplements. Certain B vitamins have been associated with some protection against depression.

Vitamin B-3 (niacin) is important in the production of tryptophan and is produced from processing vitamin B3 (niacin). Dietary sources of niacin include oily fish (such as salmon or mackerel), pork, chicken, dried peas and beans, whole grains, seeds, and dried fortified cereals.
Vitamin B-12 and calcium supplements may help reduce depression that occurs before menstruation. One study also suggested that calcium might help prevent postpartum depression.
Low levels of folate, a B vitamin, may be associated with depression. Researchers are studying whether folate supplements may help enhance the effectiveness of SSRIs and other antidepressants.

Increasingly studies are reporting major benefits from exercise for people with depression.

Aerobics. Either brief periods of intense training or prolonged aerobic workouts can raise chemicals in the brain, such as endorphins, adrenaline, serotonin, and dopamine that produce the so-called runner's high. And, of course, weight loss and increased muscle tone can boost self-esteem.

Yoga. Yoga practice, which involves rhythmic stretching movements and breathing, may help improve and stabilize mood.

Click the icon to see an image depicting the practice of yoga.

A strong network of social support is important for both prevention and recovery from depression. Support from family and friends must be healthy and positive. One study of depressed women showed, however, that overprotective as well as very distant parenting was associated with a slow recovery from depression. Studies indicate that people with strong spiritual faiths have a lower risk for depression. Such faith does not require an organized religion. People with depression might find solace from less structured sources, such as those that teach meditation or other methods for obtaining spiritual self-fulfillment.

Resources

www.nimh.nih.gov -- National Institute of Mental Health
www.dbsalliance.org -- Depression and Bipolar Support Association
www.fda.gov/cder/drug/antidepressants -- FDA Antidepressant Use in Children, Adolescents, and Adults
www.parentsmedguide.org -- American Psychiatric Association-sponsored information on pediatric antidepressants
www.nami.org -- National Alliance on Mental Illness
www.nmha.org -- Mental Health America
www.aabt.org -- Association for Behavioral and Cognitive Therapies
www.psych.org -- American Psychiatric Association
www.apa.org -- American Psychological Association
www.aacap.org -- American Academy of Child and Adolescent Psychiatry
www.postpartum.net -- Postpartum Support International
www.mentalhealth.samhsa.gov -- National Mental Health Information Center
www.mentalhealth.samhsa.gov/suicideprevention/concerned.asp -- National Strategy for Suicide Prevention (if contemplating suicide, call 1-800-273-TALK)
www.suicidology.org -- American Association of Suicidology

References

Allen JJ, Schnyer RN, Chambers AS, Hitt SK, Moreno FA, Manber R. Acupuncture for depression: a randomized controlled trial. J Clin Psychiatry. 2006 Nov;67(11):1665-73.

Alwan S, Reefhuis J, Rasmussen SA, Olney RS, Friedman JM; National Birth Defects Prevention Study. Use of selective serotonin-reuptake inhibitors in pregnancy and the risk of birth defects. N Engl J Med. 2007 Jun 28;356(26):2684-92.

Cheung AH, Zuckerbrot RA, Jensen PS, Ghalib K, Laraque D, Stein RE; GLAD-PC Steering Group. Guidelines for Adolescent Depression in Primary Care (GLAD-PC): II. Treatment and ongoing management. Pediatrics. 2007 Nov;120(5):e1313-26.

Diem SJ, Blackwell TL, Stone KL, et al. Use of antidepressants and rates of hip bone loss in older women: the study of osteoporotic fractures. Arch Intern Med. 2007 Jun 25;167(12):1240-5.

Eranti S, Mogg A, Pluck G, et al. A randomized, controlled trial with 6-month follow-up of repetitive transcranial magnetic stimulation and electroconvulsive therapy for severe depression. Am J Psychiatry. 2007 Jan;164(1):73-81.

Frederikse M, Petrides G, Kellner C. Continuation and maintenance electroconvulsive therapy for the treatment of depressive illness: a response to the National Institute for Clinical Excellence report. J ECT. 2006 Mar;22(1):13-7.

George MS, Nahas Z, Borckardt JJ, et al. Brain stimulation for the treatment of psychiatric disorders. Curr Opin Psychiatry. 2007 May;20(3):250-4; discussion 247-9.

Gross M, Nakamura L, Pascual-Leone A, Fregni F. Has repetitive transcranial magnetic stimulation (rTMS) treatment for depression improved? A systematic review and meta-analysis comparing the recent vs. the earlier rTMS studies. Acta Psychiatr Scand. 2007 Sep;116(3):165-73.

Hetrick S, Merry S, McKenzie J, Sindahl P, Proctor M. Selective serotonin reuptake inhibitors (SSRIs) for depressive disorders in children and adolescents. Cochrane Database Syst Rev. 2007 Jul 18;(3):CD004851.

Institute for Clinical Systems Improvement. Health Care Guideline: Major Depression in Adults in Primary Care. Tenth addition. May 2007.

Jarema M. Atypical antipsychotics in the treatment of mood disorders. Curr Opin Psychiatry. 2007 Jan;20(1):23-9.

Kasper S, Anghelescu IG, Szegedi A, Dienel A, Kieser M. Superior efficacy of St John's wort extract WS 5570 compared to placebo in patients with major depression: a randomized, double-blind, placebo-controlled, multi-center trial. BMC Med. 2006 Jun 23;4:14.

Kellner CH, Knapp RG, Petrides G, et al. Continuation electroconvulsive therapy vs pharmacotherapy for relapse prevention in major depression: a multisite study from the Consortium for Research in Electroconvulsive Therapy (CORE). Arch Gen Psychiatry. 2006 Dec;63(12):1337-44.

Krishnan KR. Revisiting monoamine oxidase inhibitors. J Clin Psychiatry. 2007;68 Suppl 8:35-41.

Lin PY, Su KP. A meta-analytic review of double-blind, placebo-controlled trials of antidepressant efficacy of omega-3 fatty acids. J Clin Psychiatry. 2007 Jul;68(7):1056-61.

Louik C, Lin AE, Werler MM, Hernández-Díaz S, Mitchell AA. First-trimester use of selective serotonin-reuptake inhibitors and the risk of birth defects. N Engl J Med. 2007 Jun 28;356(26):2675-83.

Mahmoud RA, Pandina GJ, Turkoz I, et al. Risperidone for treatment-refractory major depressive disorder: a randomized trial. Ann Intern Med. 2007 Nov 6;147(9):593-602.

Papakostas GI, Shelton RC, Smith J, Fava M. Augmentation of antidepressants with atypical antipsychotic medications for treatment-resistant major depressive disorder: a meta-analysis. J Clin Psychiatry. 2007 Jun;68(6):826-31.

Rapaport MH. Dietary restrictions and drug interactions with monoamine oxidase inhibitors: the state of the art. J Clin Psychiatry. 2007;68 Suppl 8:42-6.

Rohan KJ, Roecklein KA, Tierney Lindsey K, et al. A randomized controlled trial of cognitive-behavioral therapy, light therapy, and their combination for seasonal affective disorder. J Consult Clin Psychol. 2007 Jun;75(3):489-500.

Ruhé HG, Huyser J, Swinkels JA, Schene AH. Switching antidepressants after a first selective serotonin reuptake inhibitor in major depressive disorder: a systematic review. J Clin Psychiatry. 2006 Dec;67(12):1836-55.

Stewart JW. Treating depression with atypical features. J Clin Psychiatry. 2007;68 Suppl 3:25-9.

Thachil AF, Mohan R, Bhugra D. The evidence base of complementary and alternative therapies in depression. J Affect Disord. 2007 Jan;97(1-3):23-35. Epub 2006 Aug 22.

Zuckerbrot RA, Cheung AH, Jensen PS, Stein RE, Laraque D; GLAD-PC Steering Group. Guidelines for Adolescent Depression in Primary Care (GLAD-PC): I. Identification, assessment, and initial management. Pediatrics. 2007 Nov;120(5):e1299-312.

A.D.A.M. Copyright

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Insomnia

FitSugar — Wed, 08 Oct 2008 17:35:00 -0700

In This Report

Highlights
Introduction
Causes of Short-Term or Tra...
Causes of Chronic Insomnia...
Risk Factors
Prognosis
Diagnosis
Treatment
Medications
Resources
References

HEALTH GUIDE REFERENCE FROM A.D.A.M

Highlights

Sedative Hypnotic Drug Warnings

In March 2007, the FDA ordered stronger warning labels on sedative hypnotic drugs. These medications include benzodiazepine and non-benzodiazepine drugs, such as zolpidem (Ambien), eszopiclone (Lunesta), ramelteon (Rozerem), and triazolam (Halcion). The FDA warned that these drugs may be associated with:

Severe allergic reactions (anaphylaxis) and severe facial swelling (angioedema), which can occur even the first time a drug is taken
Complex sleep-related behaviors, such as sleep driving, making phone calls, and preparing and eating food while asleep

Patients who take sleeping pills should be sure to follow the directions. These include not combining sleeping pills with alcohol or other drugs and not taking more than the prescribed dose. All patients prescribed sedative hypnotic drugs should receive a patient medication guide that describes the potential risks, and precautions to reduce these risks.

Behavioral and Psychological Therapies

Behavioral and psychological treatments, such as cognitive behavioral therapy and relaxation techniques, are effective approaches for insomnia and can produce long-lasting benefits, according to a 2006 study in Sleep.
Behavioral interventions help over 80% of children who try them, indicates another 2006 Sleep study.

Complementary and Alternative Medicine

More than 1.6 million adults use complementary and alternative medicine to treat their insomnia, according to results of a national survey published in the Archives of Internal Medicine. About half of patients who tried herbal medicine or relaxation techniques found that these approaches helped improve their sleep.
In 2006, the American Academy of Sleep Medicine issued a position statement advising that there is only limited scientific evidence that herbal remedies are effective sleep aids.

Insomnia and Mood Disorders

Chronic insomnia can increase the risk of developing depression and anxiety, according to a 2007 study in Sleep. Research also indicates that insomnia and daytime sleepiness can cause and worsen depression and anxiety in children as well as adults.

Introduction

Insomnia comes from the Latin words for “no sleep.” Insomnia is characterized by:

Difficulty falling asleep
Difficulty staying asleep
Waking up too early in the morning

Some experts believe that poor quality (“non-restorative”) sleep is also related to insomnia. Insomnia can cause daytime fatigue, irritability, and impaired performance. About 60 million Americans each year suffer from insomnia.

Insomnia may be primary or secondary:

Primary insomnia means that the inability to sleep is not caused by other health problems.
Secondary insomnia is due to other health conditions that interfere with sleep. Some experts prefer the term “co-morbid insomnia.”

Insomnia, usually temporary, is often categorized by how long it lasts:

Transient insomnia lasts for a few days.
Short-term insomnia lasts for no more than 3 weeks.
Chronic insomnia occurs at least 3 nights per week for 1 month or longer.

Insomnia may also be defined in terms of inability to sleep at conventional times. The following examples are referred to as circadian rhythm disorders:

Delayed Sleep-Phase Syndrome. Delayed sleep-phase syndrome is the term for a circadian clock that runs late but reliably. People who have this condition (usually adolescents) fall asleep very late at night or in early morning hours, but then sleep normally.
Advanced Sleep-Phase Syndrome. This syndrome tends to develop in older people. It produces excessive sleepiness in the morning and undesired awakening early (3 - 5 a.m.) in the morning.

In sleep studies, subjects spend about one-third of their time asleep, suggesting that most people need about 8 hours of sleep each day. Individual adults differ in the amount of sleep they need to feel well rested, however. (Infants may sleep as many as 16 hours a day.)

The daily cycle of life, which includes sleeping and waking, is called a circadian (meaning "about a day") rhythm, commonly referred to as the biologic clock. Hundreds of bodily functions follow biologic clocks, but sleeping and waking comprise the most prominent circadian rhythm. The sleeping and waking cycle is approximately 24 hours. (If confined to windowless apartments, with no clocks or other time cues, sleeping and waking as their bodies dictate, humans typically live on slightly longer than 24-hour cycles.) It usually takes the following daily patterns:

Humans are designed for daytime activity and nighttime rest.
Additionally, there is a natural peak in sleepiness at mid-day, the traditional siesta time.

In addition, daily rhythms intermesh with other factors that may interfere or change individual patterns:

The fraction-of-a-second-firing of nerve cells in the brain may be faster or slower in different individuals.
The monthly menstrual cycle in women can shift the pattern.
Light signals coming through the eyes reset the circadian cycles each day, so changes in season or various exposures to light and dark can unsettle the pattern. The importance of sunlight as a cue for circadian rhythms is dramatized by the problems experienced by people who are totally blind. They commonly suffer trouble sleeping and other rhythm disruptions.

The response to light signals in the brain is an important key factor in sleep:

Light signals travel to a tiny cluster of nerves in the hypothalamus in the center of the brain, the body's master clock, which is called the supra chiasmatic nucleus (SCN).
This nerve cluster takes its name from its location, which is just above (supra) the optic chiasm, which is a major junction for nerves transmitting information about light from the eyes.
The approach of dusk each day prompts the SCN to signal the nearby pineal gland (named so because it resembles a pine-cone) to produce the hormone melatonin.
Melatonin is thought to act as the body's time-setting hormone. The longer a person is in darkness the longer the duration of melatonin secretion. Secretion can be diminished by staying in bright light. Melatonin also appears to trigger the need to sleep.

Sleep consists of two distinct states that alternate in cycles and reflect differing levels of brain nerve cell activity:

Non-Rapid Eye Movement Sleep (NonREM). NonREM sleep is also termed quiet sleep. NonREM is further subdivided into three stages of progression:

Stage 1 (light sleep)
Stage 2 (so-called true sleep)
Stage 3 to 4 (deep "slow-wave" or delta sleep)

With each descending stage, awakening becomes more difficult. It is not known what governs NonREM sleep in the brain. A balance between certain hormones, particularly growth and stress hormones, may be important for deep sleep.

Rapid Eye-Movement Sleep (REM). REM sleep is termed active sleep. Most vivid dreams occur in REM sleep. REM-sleep brain activity is comparable to that in waking, but the muscles are virtually paralyzed, possibly preventing people from acting out their dreams. In fact, except for vital organs like lungs and heart, the only muscles not paralyzed during REM are the eye muscles. REM sleep may be critical for learning and for day-to-day mood regulation. When people are sleep-deprived, their brains must work harder than when they are well rested.

The REM/NREM Cycle. The cycle between quiet (nonREM) and active (REM) sleep generally follows this pattern:

After about 90 minutes of nonREM sleep, eyes move rapidly behind closed lids, giving rise to REM sleep.
As sleep progresses the nonREM/REM cycle repeats.
With each cycle, nonREM sleep becomes progressively lighter, and REM sleep becomes progressively longer, lasting from a few minutes early in sleep to perhaps an hour at the end of the sleep episode.

Causes of Short-Term or Transient Insomnia

A reaction to change or stress is one of the most common causes of short-term and transient insomnia. This condition is sometimes referred to as adjustment sleep disorder.

The trigger could be a major or traumatic event such as:

An acute illness
Injury or surgery
The loss of a loved one
Job loss

Temporary insomnia could also develop after a relatively minor event, including:

Extremes in weather
An exam
Traveling
Trouble at work

In most cases, normal sleep almost always returns when the condition resolves, the individual recovers from the event, or the person becomes used to the new situation. Treatment is needed if sleepiness interferes with functioning or if it continues for more than a few weeks. Individual responses to stress vary and some people may not experience insomnia at all, even during very stressful situations while others may suffer from insomnia in response to very mild stressors.

Fluctuations in female hormones play a major role in insomnia in women over their lifetimes. This insomnia is usually temporary.

During Menstruation. Progesterone promotes sleep, and levels of this hormone plunge during menstruation, causing insomnia. (When they rise during ovulation, women may become sleepier than usual.)
During Pregnancy. The effects of changes in progesterone levels in the first and last trimester can disrupt normal sleep patterns.
Menopause. Insomnia can be a major problem in the first phases of menopause, when hormones are fluctuating intensely. Insomnia during this period may be due to different factors that occur. In some women, hot flashes, sweating, and a sense of anxiety can awaken women suddenly and frequently at night. Insomnia may also be caused by psychologic distress provoked by this life passage. In many cases, insomnia is temporary. However, a 2006 study found that hot flashes in perimenopausal and postmenopausal women are strongly associated with chronic insomnia (sleep problems lasting more than 1 month). Treating hot flashes may help resolve chronic insomnia.

Air travel across time zones often causes insomnia. After long plane trips, 1 day of adjustment is usually needed for each time zone crossed. Traveling west to earlier times seems to be less traumatic than going east to a later time because it is easier to lengthen a circadian phase than to shorten it.

In one study, 20% of adults reported that light, noise, and uncomfortable temperatures caused their sleeplessness. Depending on the time of day, too much or too little light can disrupt sleep.

Excessive Light at Night. A person's biologic circadian clock is triggered by sunlight, and very bright artificial light maintains wakefulness. One study indicated that even dim artificial light might disrupt sleep.
Insufficient Light During the Day. Insufficient exposure to light during the day, as occurs in some disabled elderly patients who rarely venture outside, may also be linked with sleep disturbances. One study suggested that when a person is exposed to bright daylight, melatonin levels increase in response to darkness at night, which aids sleep.

Caffeine. Caffeine is a stimulant, which can interfere with falling asleep.

Nicotine. Nicotine is also a stimulant, but quitting smoking itself can lead to transient insomnia. In fact, it has been suggested that if sleeping could be improved during withdrawal from smoking, perhaps it would be easier to quit smoking.

Partner's Sleep Habits. In one survey, 17% of women and 5% of men reported that their partner's sleep habits impaired their own sleep. Snoring can certainly be a factor in a partner's insomnia.

Medications. Insomnia is a side effect of many common medications, including over-the-counter preparations that contain caffeine. People who suspect their medications are causing them to lose sleep should check with their doctors or pharmacists.

Causes of Chronic Insomnia

Sleep problems seem to run in families. About 35% of people with insomnia have a family history of insomnia, with the mother being the most commonly affected family member. Still, because so many factors are involved in insomnia, a genetic component is difficult to define.

Abnormal levels of certain brain chemicals have been observed in some people with chronic insomnia.

Melatonin. Low levels of melatonin, the hormone secreted by the pineal gland, have sometimes been observed in chronic insomnia.
Stress Hormones. Some studies have reported persistently high levels of stress hormones, particularly cortisol, in people with chronic insomnia, particularly insomnia related to aging and psychiatric disorders. High levels of cortisol reduce REM sleep. However, a 2003 study of people with chronic insomnia reported that cortisol levels were high only when their sleep was of poor quality. When they slept well, levels were lower. This study and other research suggests that high levels of stress hormones are caused by poor sleep, rather than being the cause.
Growth Hormone. Normal aging is associated with a blunting of regular, cyclical surges of growth hormone, which may affect sleep as one gets older. This hormone, which is normally secreted in the late night, is associated not only with growth but with deep, slow-wave sleep. (Older people generally have less slow-wave sleep.)

Chronic insomnia occurs in people who have persistently high levels of stress hormones and a shift in the levels of certain immune factors. Studies indicate that people with chronic insomnia have higher levels of interleukin-6 and tumor necrosis factor during the day, but lower levels at night. These immune factors, called cytokines, cause symptoms of fatigue. Levels are usually higher at night in people with healthy sleep. The implications of these immune changes in people with insomnia are not known.

Many cases of chronic insomnia cases have a psychologic or psychiatric basis. The disorders that most often cause insomnia are:

Anxiety.
Depression. Sleep abnormalities are an integral part of depressive disorders, with more than 90% of depressed patients experiencing insomnia.
Bipolar disorder.

Insomnia may also cause emotional problems. It is often unclear which condition has triggered the other, or if the two conditions, in fact, have a common source.

In many cases, it is unclear if chronic insomnia is a symptom of some physical or psychological condition or if it is a primary disorder of its own. In most instances, a mix of psychological and physical conditions causes the insomnia.

Psychophysiologic insomnia occurs when:

An episode of transient insomnia disrupts the person's circadian rhythm.
The patient begins to associate the bed not with rest and relaxation but with a struggle to sleep. A pattern of sleep failure emerges.
Over time, this event repeats, and bedtime becomes a source of anxiety. Once in bed, the patient broods over the inability to sleep, the consequences of sleep loss, and the lack of mental control. All attempts to sleep fail.
Eventually excessive worry about sleep loss becomes persistent and provides an automatic nightly trigger for anxiety and arousal. Unsuccessful attempts to control thoughts, images, and emotions only worsen the situation. After such a cycle is established, insomnia becomes a self-fulfilling prophecy that can persist indefinitely.

Sometimes anxiety and the inability to sleep dates back to childhood when parents used various threats to force their children into sleep for which they may not have been ready.

In one survey, 22% of adults reported that health conditions, pain, or discomfort impaired their sleep. These conditions can include:

Nightly Leg Problems. Leg disorders that occur at night, such as restless legs syndrome or leg cramps, are of special note. They are very common and an important cause of insomnia, particularly in older people.

Medical Problems. Among the many medical problems that can cause chronic insomnia are allergies, arthritis, cancer, fibromyalgia, heart disease, gastroesophageal reflux disease (GERD), hypertension, asthma, emphysema, rheumatologic conditions, Alzheimer's disease, Parkinson's disease, hyperthyroidism, and attention deficit hyperactivity disorder.

Medications. Among the many medications that can cause insomnia are antidepressants (fluoxetine, bupropion), theophylline, lamotrigine, felbamate, beta-blockers, and beta-agonists.

An estimated 10 -15% of chronic insomnia cases result from substance abuse, especially alcohol, cocaine, and sedatives. One or two alcoholic drinks at dinner, for most people, pose little danger of alcoholism and may help reduce stress and initiate sleep. Excess alcohol or alcohol used to promote sleep, however, tends to fragment sleep and cause wakefulness a few hours later. It also increases the risk for other sleep disorders, including sleep apnea and restless legs. Alcoholics often suffer insomnia during withdrawal and, in some cases, for several years during recovery.

Shift work throws off the body's circadian rhythm and may lead to chronic insomnia.

Risk Factors

Studies estimate that between 25 - 33% of adults experience some insomnia each year. In spite of this widespread problem, however, studies suggest that only about 30% of American adults who visit their doctor ever discuss sleep problems. And, doctors seem rarely to ask patients about their sleep habits or problems.

A 2003 study suggested that there were seven significant factors that predicted high risk for insomnia:

Being older
Having conflicts with relatives
Being overworked on the job
Being overworked at home
Having a sick relative
Having low social status
Having a psychiatric or psychologic problem

Stressful events do not cause insomnia in everyone. However, negative thoughts and attitudes toward events can be significant factors in insomnia. In one study, for example, the number of stressful events did not differ between good and poor sleepers. Those with insomnia, however, tended to experience these stressful events more intensively than the healthy sleepers.

In another study, patients with insomnia and good sleepers were asked to record their pre-sleep images using a handheld counter. People with insomnia not only reported fewer images, but their images also tended to be more unpleasant than those of good sleepers. More of the images in people with insomnia were related to intimate relationships and to sleep itself. The images of sleepers were more likely to be random and disconnected.

Studies report that the strongest risk factors for insomnia are psychiatric problems (particularly depression) and physical complaints (such as headaches and chronic pain) that have no identifiable cause (called somatic symptoms). About 90% of people with depression have insomnia. A study presented at the 2005 Associated Professional Sleep Societies meeting indicated that insomnia may contribute to, and prolong, depression. Researchers analyzed data from over 1,800 adults age 65 years and older. Compared with depressed patients who did not have sleep problems, depressed patients with insomnia were 11 times more likely to remain depressed after 6 months and 17 times more likely to still be depressed after a year. The researchers suggested that treating insomnia may help patients recover from depression more quickly.

Overall, insomnia is more common in women than men, although men are not immune from insomnia. Sleep efficiency deteriorates equally in men and women as they get older.

Men. One major study suggested that as men age from 16 - 50, they lose about 80% of their deep sleep. During that period, light sleep increases and REM sleep remains unchanged. (The study did not use women as subjects, and there is some evidence to suggest they are not as affected.) After age 44, REM and total sleep diminish and awakenings increase.

Women. It is not clear why women suffer more from insomnia than men. Some theories include:

In women, a number of hormonal events can disturb sleep, including premenstrual syndrome, menstruation, pregnancy, and menopause. All these conditions are short-term, however, and in most cases the wakefulness associated with them is temporary and can be eliminated with sleep hygiene and time.
After childbirth, most women develop a high sensitivity to the sounds of their children, which causes them to wake easily. Women who have had children sleep less efficiently than women who have not had children. It is possible that many women never unlearn this sensitivity and continue to wake easily long after the children have grown.
Women are at higher risk than men are for depression and anxiety, which are known risk factors for insomnia. In fact, some researchers believe that this is a main reason for the gender differences in insomnia.

After menopause, women are susceptible to the same environmental and biologic causes of insomnia as men. In fact, older women who are not bothered by sleeplessness tend to have longer and better sleep than noninsomniac men their own age.

As people grow older, sleep patterns change. In a major 2003 survey, a third of older adults reported that they woke up frequently during the night. About a quarter of participants reported waking up too early and being unable to go back to sleep. In the same study, 33% of adults age 55 - 64 reported waking up feeling unrefreshed.

Although age itself does not appear to be a risk factor for insomnia, a number of factors may interfere with sleep as one gets older:

Elderly people are more likely to be sedentary than younger adults.
Medical conditions that cause pain or nighttime distress are common in the elderly and pose a high risk for insomnia. They include arthritis, gastrointestinal distress, frequent urination, lung disease, and heart conditions.
Neurologic diseases in the elderly, such as restless legs syndrome, Parkinson's, Alzheimer's, and other forms of dementia can cause nighttime disorientation, confused wandering, and delirium.
Older people often take a number of prescription drugs whose side effects include insomnia.
The elderly are prone to grief, depression, and anxiety, emotional factors that can cause sleeplessness. One study of healthy older adults found that psychologic factors, such as anxiety and depression, were more likely to cause insomnia than illness, medications, or living conditions.
Melatonin levels are generally lower in older people. Some research suggests, however, that elderly people have lower levels simply because they stay mostly indoors and do not receive adequate sunlight.

Lack of sleep at night can lead to excessive sleepiness during the day. A 2006 study reported the following risk factors for excessive daytime sleepiness among the elderly:

Male gender
Sleep apnea or other sleep breathing disorders
Nighttime chest wheezing
Poor sleep quality
Longer time spent in REM sleep
More than 3 episodes of nighttime pain within a week
Medications that cause sleepiness

Sleep loss among the elderly is not inevitable. While older people are more susceptible to many conditions that can cause insomnia, treatments and a healthy lifestyle, particularly regular exercises, are as useful in providing relief to the elderly as to the young. And, a number of studies have found no significant increase in insomnia in older healthy adults.

Shift workers are at considerable risk for insomnia. In a major survey, 65% of shift workers reported one or more symptoms of insomnia at least a few nights a week. Workers over age 50 and those whose shifts are always changing are particularly susceptible to insomnia, although night-shift workers also have a high rate of sleeplessness. One study found that 53% of night-shift workers fall asleep on the job at least once a week, implying that their internal clocks do not adjust to unusual work times. (They are also at much higher risk than other workers for automobile accidents due to their drowsiness and may also have a higher risk for health problems in general.) A Japanese study reporting on different aspects of insomnia found that excessive computer work was associated with all forms of insomnia. People who were over-involved with their work tended to have trouble falling asleep, and they tended to awaken earlier than average.

Among the many conditions that pose a high risk for insomnia are:

Frequent travel, particularly crossing time lines
Post-traumatic stress syndrome
Brain injuries
Many chronic medical conditions ranging from seemingly minor ones, such as tinnitus (ringing in the ears) to major conditions, such as respiratory problems, heart disease, or being on dialysis

Prognosis

A 2002 study of sleeping habits in over 1 million people reported that people who slept 7 hours a night lived the longest. People who slept more than 8 hours or less than 6 hours, or who took sleeping pills, had lower survival rates.

Insomnia is not life-threatening, except in very rare cases, such as in those who have the genetic disorder called fatal familial insomnia. This rare degenerative brain disease develops in late adulthood.

Sleepiness causes as many as 200,000 automobile accidents in the U.S. and 1,500 deaths from such accidents. Studies indicate that drowsy driving is as risky as drunk driving. In a major 2003 survey, 60% of young adults reported driving while drowsy, and 20% dosed off while driving. In the study, 1% of adults who dozed off reported having an accident because of it. (One study strongly suggested that it is habitual sleepiness, however, and not just being sleepy at the time of an accident that places people at higher risk.)

Surveys show that people with severe insomnia have a quality of life that is almost as poor as those who have chronic conditions, such as heart failure. In addition to more daytime sleepiness, people with insomnia complain of more attention and memory problems compared to good sleepers.

Insomnia can also lead to irritability, mistakes at work, and poorer relationships.

Effect on Thinking and Performance. Studies suggest that insomnia makes it harder to concentrate and perform tasks.

Reduced concentration. Deep sleep deprivation impairs the brain's ability to process information.
Impaired task performance. One study reported that missing only 2 - 3 hours of sleep every night for a week significantly impaired performance and mood. An Australian study reported that 17 hours of sleep deprivation causes impaired performance levels comparable to those found in people who have blood alcohol levels indicating intoxication.
Memory problems. Whether insomnia significantly impairs learning is unclear. Some studies have reported problems in memorization, although others have found no differences in test scores between people with temporary sleep loss and those with full sleep.

Insomnia and Depression. Although stress and depression are major causes of insomnia, insomnia may also increase the activity of the hormones and pathways in the brain that can produce emotional problems. Research indicates that chronic insomnia can increase the risk of developing depression and anxiety. Some investigators are exploring the possibility of preventing psychiatric disorders by early recognition and treatment of insomnia.

Even modest alterations in waking and sleeping patterns can have significant effects on a person's mood. In both children and adults, the combination of insomnia and daytime sleepiness can produce more severe depression than either condition alone.

Effects on the Heart. Although there has been some concern that insomnia may increase the risk for heart problems, little evidence has supported any significant dangers. One study reported signs of heart and nervous system activity in people with chronic insomnia that might place such individuals at risk for coronary heart disease. If it exists, however, this increased danger is very modest compared with other risk factors for heart disease. Yet another report suggested that sleep complaints in elderly people without coronary artery disease predicted a first heart attack. Sleep disorders in such cases may have been a marker for depression, however, which is a risk factor for heart attacks in elderly people.

Effects on Weight. Lack of sleep can cause weight gain and obesity. In a 16-year study of over 68,000 women, those who slept no more than 5 hours a night were 32% more likely to gain at least 33 pounds, and those who slept 6 hours had a 12% increased risk of weight gain compared to women who slept at least 7 hours a night.

Effects on the Immune System. A 2003 study reported significant differences in immune factors among sleepers, with higher levels of certain infection-fighters observed in good sleepers than in people with chronic insomnia. The significance of these findings is still unknown, however.

Diagnosis

Diagnosing sleep disturbance and its cause is the most important step in restoring healthy sleep. However, there is little agreement, even among experts, on the best methods for effectively assessing a patient's insomnia.

A major difficulty in diagnosing this problem is its subjective nature. One study showed that there was no difference in sleep behaviors between people who said they were insomniacs and people who said they weren't. People who believe they have insomnia may have actually had frequent brief awakenings during sleep that they perceive as being continuously awake.

A number of questionnaires are available for determining whether a patient has insomnia or other sleep disorders. For example, the doctor may ask:

How would you describe your sleep problem?
How long have you had the sleep problem?
How long does it take to fall asleep?
How many times a week does it occur?
How restful is sleep?
Do you have trouble falling asleep or do you wake up too early?
What is the sleep environment like (Noisy? Not dark enough?)?
How does insomnia affect daytime functioning?
What medications do you take? (Include herbs, alcohol, and over-the-counter or prescription drugs.)
Are you taking or withdrawing from stimulants, such as coffee or tobacco?
How much alcohol is consumed per day?
What stresses or emotional factors may be present?
Have you experienced any significant life changes?
Do you snore or gasp during sleep (an indication of sleep apnea)?
Do you have leg problems (cramps, twitching, crawling feelings)?
If there is a bed partner? Is this person's behavior distressing or disturbing?
Are you a shift worker?

Sleep Diary. If the patient cannot answer these questions, keeping a sleep diary is a helpful diagnostic tool. Every day for 2 weeks, the patient should record all sleep-related information, including responses to questions listed above described on a daily basis. A bed partner can help by adding their observations of the patient's sleep behavior.

The Epworth Sleepiness Scale. The Epworth Sleepiness Scale (ESS) uses a simple questionnaire to measure excessive sleepiness during eight situations.


Situation	Chance of Dozing 0 = no chance of dozing 1 = slight chance of dozing 2 = moderate chance of dozing 3 = high chance of dozing
Sitting and reading.	(Indicate a score of 0 to 3)
Watching TV.	(Indicate a score of 0 to 3)
Sitting inactive in a public place (e.g., a theater or a meeting).	(Indicate a score of 0 to 3)
As a passenger in a car for an hour without a break.	(Indicate a score of 0 to 3)
Lying down to rest in the afternoon when circumstances permit.	(Indicate a score of 0 to 3)
Sitting and talking to someone.	(Indicate a score of 0 to 3)
Sitting quietly after a lunch without alcohol.	(Indicate a score of 0 to 3)
In a car, while stopped for a few minutes in traffic.	(Indicate a score of 0 to 3)
Score Results	1-6: Getting enough sleep 4-8: Tends to be sleepy but is average. 9-15: Very sleepy and should seek medical advice. Over 16: Dangerously sleepy

Multiple Sleep Latency Test. The multiple sleep latency test (MSLT) uses a machine to measure the time it takes to fall asleep while lying in a quiet room during the day:

The patient takes four or five scheduled naps 2 hours apart.
People with healthy sleep habits fall asleep in about 10 - 20 minutes.
The test can detect changes in sleepiness associated with sleep deprivation in patients with insomnia.

It has limitations, however, and does not take into consideration any situations that may affect the patients' mental state and the actual home situation. The test is used mainly after other sleep disorders have been ruled out and the doctor is uncertain whether or not insomnia is a correct diagnosis.

If unexplained insomnia persists after treatment or there is evidence of a primary sleep disorder, such as sleep apnea or narcolepsy, the doctor may recommend a sleep specialist or a sleep disorders center. Centers are accredited by the American Academy of Sleep Medicine. Patients should investigate centers carefully, to be sure that they offer full sleep studies.

Among the signs that may indicate a need for a sleep disorders center are:

Insomnia due to psychologic disorders
Sleeping problems due to substance abuse
Snoring and sudden awakening with gasping for breath (possible sleep apnea)
Severe restless legs syndrome
Persistent daytime sleepiness
Sudden episodes of falling asleep during the day (possible narcolepsy)

At most sleep disorders centers, patients undergo an in-depth analysis, usually supervised by a multidisciplinary team of consultants who can provide both physical and psychiatric evaluations.

Treatment

The American Academy of Sleep Medicine (AASM) recommends cognitive behavioral therapy (CBT) and prescription medications as the main treatments for insomnia. According to the AASM, these treatment options can improve both quality and quantity of sleep for people with insomnia.

Experts agree that behavioral therapies should be the first-line treatment for insomnia. For children in particular, medications should rarely be used as initial treatment. A 2006 study reported that behavioral interventions can provide sustained improvement in over 80% of children with insomnia.

Prevention of sleeplessness depends upon the patient's ability to learn how to relax and sleep well. A number of behavioral methods are aimed at achieving these goals. Behavioral techniques can actually cure chronic insomnia in many cases and studies report that they help nearly all patients with primary chronic insomnia. The benefits of psychological and behavioral therapy in managing insomnia are long-lasting.

Although medications are equally effective for helping people with insomnia to sleep, they cannot cure the condition. In addition, behavioral methods act faster. Behavioral methods work in all age groups, including children and elderly patients.

Behavioral methods include:

Stimulus control
Cognitive behavioral therapy
Progressive muscle relaxation
Paradoxical intention
Biofeedback
Sleep restriction
Imagery tasks

Studies have reported that between 70 - 80% of patients who are treated with non-drug methods experience improved sleep with an average treatment duration of only 5 hours over a 4-week period. Furthermore, studies report that 75% of those who have been taking drugs are able to stop or reduce their use.

Proper sleep hygiene is the first step and should accompany any behavioral method. A number of behavioral approaches are available, but all have the same basic goals:

To reduce the time it takes to go to sleep to below 30 minutes
Reduce wake-up periods during the night

Stimulus Control. Stimulus control is now considered the standard treatment for primary chronic insomnia and may be helpful for some patients with secondary insomnia as well. The primary goal of stimulus control is to regain the idea that the bed is for sleeping. It involves the following:

Go to bed only when ready to sleep or for sex.
If unable to sleep within 15 - 20 minutes, get up and go into another room. (People who find it physically difficult to get out of bed should sit up and do something relatively arousing, like reading a book.)
Maintain a regular wake-up time no matter how few hours you actually sleep.
Avoid naps.

Cognitive-Behavioral Therapy. Cognitive behavioral therapy (CBT) is a form of therapy that emphasizes observing and changing negative thoughts about sleep such as, "I'll never fall asleep." It uses actions intended to change behavior. A 2004 study of young and middle-aged adults suggested that CBT is more effective than medication in treating chronic insomnia, and should be considered as a first-line intervention. Adding medication to CBT did not provide additional benefit. In a 2006 study of older adults, CBT worked better than zopiclone (Imovane) in managing chronic insomnia. [Zopiclone is a European sleep medication that is similar to the American drug eszopiclone (Lunesta).] Compared to zopiclone or placebo, CBT helped patients spend less time awake at night. The benefits of 6 weeks of weekly CBT sessions lasted for 6 months.

Progressive Muscle Relaxation. Progressive muscle relaxation is another technique for inducing sleep that works well for many people. It takes about 10 minutes to perform:

Focus on one specific muscle group at a time. Most people start with the muscles in one foot. Inhale and tense the foot muscles for about 8 seconds. (Do this gently. It is not intended to cause severe pain or muscle contractions.)
Relax the foot, and let it become loose and limp. Stay relaxed for 15 seconds, then repeat with the other foot.
Move up to the next muscle group and repeat the sequence, doing one side of the body at a time. Move progressively from each foot and leg up through the abdomen and chest, to each hand and arm, then to the neck, shoulders, and face.

Paradoxical Intention. Paradoxical intention is a psychological approach that is based on doing the opposite of what one wants or fears and takes it to the extreme. The first step is to make a plan to take such a paradoxical approach to insomnia.

Instead of going through activities leading to sleep, the patient prepares for staying awake and doing something energetic.
In some cases, people may take specific psychological barriers to sleep to an extreme limit. For example, if worry is a factor in insomnia, the patient intensifies the worries.

Biofeedback. Biofeedback is also effective, but requires being monitored with an electroencephalogram (EEG), a device that measures brain waves. Patients are given feedback to recognize certain states of tension or sleep stages so that they can either avoid or repeat them voluntarily.

Sleep Restriction Therapy. Sleep restriction therapy may be effective, although evidence is inconclusive. In a 2001 study, patients practiced sleep hygiene and sleep restriction. Sleep hygiene was very helpful during the first 2 months while sleep restriction led to sustained benefits and deeper sleep. The approach is a systematic method for achieving sleep and restricting the time spent in bed.

The first step is to calculate a person's sleep efficiency number:

Keep a sleep diary for 14 days. Calculate the average hours of actual sleep and hours in bed. Then divide the average hours slept by the hours spent in bed. The result, given as a percentage, is the sleep efficiency number. (For example, if a patient sleeps an average of 5 hours out of 7 hours spent in bed then the result is .714, and the sleep efficiency percentage is 71%.)
The patient's goal is to achieve sleep efficiencies of between 85 - 90%, which means only 10 - 15% of the time is spent staying awake in bed. (Sleep efficiency in older people normally falls between 75 - 85%.)

To achieve this goal, the patient takes the following actions:

Begin by going to bed 15 minutes later than usual the first week.
If 85% sleep efficiency isn't reached by the end of the week, add another 15 minutes before going to bed. Refrain from going to bed even if tired, although bedtime should not be reduced below 5 hours.
Once efficiency reaches 90% or more, begin to go to bed 15 minutes earlier each week.

Other parts of the program include stopping any sleep medications and following good sleep hygiene. People using this treatment have reported lasting improvements after just 8 weeks, and studies suggest that it is significantly more successful than relaxation techniques.

Imagery Tasks. A 2002 study enrolled people whose chronic insomnia was associated with unwanted thoughts and worries. They were given specific positive mental tasks that gave them a sense of positive control (as opposed to their real life concerns, which felt out of their control). These images distracted them and allowed them to fall asleep faster. In support of this approach, another study evaluated patients with insomnia who were given a problem before sleep. One group was asked to think of the problem in images and the other in words. The group who used imagery fell asleep more quickly and woke up with less anxiety.

Sleep Hygiene. The term sleep hygiene is used to describe simple behaviors that may help everyone improve their sleep.

Establish a regular time for going to bed and getting up in the morning. Stick to this schedule even on weekends and during vacations.
Use the bed for sleep and sexual relations only, not for reading, watching television, or working. Excessive time in bed disrupts sleep.
Avoid naps, especially in the evening.
Exercise before dinner. A low point in energy occurs a few hours after exercise; sleep will then come more easily. Exercising close to bedtime, however, may increase alertness.
Take a hot bath about 1.5 - 2 hours before bedtime. This alters the body's core temperature rhythm and helps people fall asleep more easily and more continuously. (Taking a bath shortly before bed increases alertness.)
Do something relaxing in the 30 minutes before bedtime. Reading, meditation, and a leisurely walk are all appropriate activities.
Keep the bedroom relatively cool and well ventilated.
Do not look at the clock. Obsessing over time will just make it more difficult to sleep.
Eat light meals, and schedule dinner 4 - 5 hours before bedtime. A light snack before bedtime can help sleep, but a large meal may have the opposite effect.
Spend a half hour in the sun each day. The best time is early in the day. (Take precautions against overexposure to sunlight by wearing protective clothing and sunscreen.)
Avoid fluids just before bedtime so that sleep is not disturbed by the need to urinate.
Avoid caffeine in the hours before sleep.
If one is still awake after 15 - 20 minutes, go into another room, read or do a quiet activity using dim lighting until feeling very sleepy. (Don't watch television or use bright lights.)
If distracted by a sleeping bed partner, moving to the couch or a spare bed for a couple of nights might be helpful.
If a specific worry is keeping one awake, thinking of the problem in terms of images rather than in words may allow a person to fall asleep more quickly and to wake up with less anxiety.

Exercise may be one of the best ways to promote healthy sleep. One study found that exercise is as good for inducing sleep as the use of benzodiazepines, a prescription sleep aid. Some research has found that yoga practice may have specific benefits on sleep health. Yoga uses meditation, deep breathing techniques, and movements that emphasize stretching and balance.

The circadian rhythm is more a function of darkness and light rather than actual time of day. Bright light can discourage drowsiness, and darkness can cause sleepiness, day or night. The use of a special box that gives off very bright fluorescent light (over 4,000 lux) for about 30 minutes each day may be helpful.

The following people might benefit from light therapy:

Shift workers. Light therapy should be maximized during hours they are at work and minimized when they need to sleep.
Frequent travelers. Light therapy may be useful for adjusting to new time zones and reducing jet lag.
Nursing home patients.
People with delayed sleep-phase syndrome. These people have a natural tendency to fall asleep very late at night or in early morning hours, but then sleep normally.

Patients should check with their doctors before using light therapy. The following people should avoid light therapy or use it only under a doctor's direction:

Anyone with eyes or skin that are highly sensitive to light
Anyone taking medications that increase the risk for photosensitivity
People with bipolar disorder

Timing of the therapy depends on the type of insomnia or sleep schedule of the individual. For example, in people who cannot get to sleep at night, light therapy in the morning and restricting bright light at night may be helpful. People who wake up early in the morning may benefit from light therapy performed in the evening, although a 2002 study reported that it had no effect in this group. Some light boxes have dawn/dusk simulators that help determine the correct brightness.

Medications

According to a major 2003 survey, about 20% of American older adults use some form of sleep aid, including prescription or over-the-counter drugs or alcohol. Furthermore, 15% use such aids every night.

However, while behavioral or psychologic techniques can actually cure insomnia, prolonged use of sleeping pills can only result in dependency.

In general, the following precautions are important:

Start with non-prescription medication.
Drugs used specifically for improving sleeping are called sedative hypnotics. These drugs include benzodiazepines and non-benzodiazepines. Until recently benzodiazepines were most commonly prescribed, but newer non-benzodiazepines may be better tolerated and have less risk of dependency. These medicines, however, may be associated with potentially severe allergic reactions, such as anaphylaxis and facial swelling (angioedema). These medicines may also cause hazardous behaviors, such as driving, making phone calls, or eating while asleep. If you need to take one of these prescription drugs, start with as low a dose as possible.
For adults over age 60 years, studies suggest that the risks of sedative hypnotics may far outweigh their benefits.
As a general rule, do not take either prescription nor non-prescription sleeping pills on consecutive days or for more than 2 - 4 days a week.
If insomnia is still a problem after stopping the drug and continuing with good sleep hygiene, this pattern can be repeated again, but for only up to 4 weeks.
Medication should be withdrawn gradually, and the patient should be aware of the possibility of rebound insomnia after stopping medication.
Alcohol intensifies the side effects of all sleeping medication and should be avoided.
If chronic insomnia is a companion to depression or anxiety, treating these problems first may be the best approach.

Brands with Antihistamines. Many over-the-counter sleeping medications use antihistamines, which cause drowsiness. Diphenhydramine is the most common antihistamine used non-prescription sleep aids. Some drugs contain diphenhydramine alone (Nytol, Sleep-Eez, Sominex), while others contain combinations of diphenhydramine with pain relievers (Anacin P.M., Excedrin P.M., Tylenol P.M.). Doxylamine (Unison) is another antihistamine used in sleep medications. Certain antihistamines indicated only for allergies, such as chlorpheniramine (Chlor-Trimeton), diphenhydramine (Benadryl), or hydroxyzine (Atarax or Vistaril) may also be used as mild sleep-inducers.

Unfortunately, most of these drugs leave patients feeling drowsy the next day and may not be very effective in providing restful sleep. Side effects include:

Daytime sleepiness
Dizziness
Drunken movements
Blurred vision
Dry mouth and throat

In general, these drugs should be avoided by people with angina, heart arrhythmias, glaucoma, or problems urinating. They should not be used at the same time as medications that prevent nausea or motion sickness. Some non-prescription sleeping aids, such as those containing doxylamine, should also be avoided by patients with chronic lung disease.

Common Pain Relievers. When sleeplessness is caused by minor pain, simply taking acetaminophen (Tylenol) or a non-steroidal anti-inflammatory drug (NSAID) such as ibuprofen (Advil, Motrin), can be very helpful without causing any daytime sleepiness. The extra "P.M." antihistamine found in combination products is simply an extra, needless chemical in these situations.

Benzodiazepines, also referred to as benzodiazepine receptor agonists (BzRAs), were once the most commonly prescribed sedative hypnotics. Originally developed in the 1960s to treat anxiety, these drugs nonselectively target receptor sites in the brain that modulate the effects of the neurotransmitter gamma-aminobutyric acid (GABA).

Brands. Commonly prescribed benzodiazepines:

Long-acting benzodiazepines include flurazepam (Dalmane) and clonazepam (Klonopin), quazepam (Doral).
Medium- to short-acting benzodiazepines include triazolam (Halcion), lorazepam (Ativan), alprazolam (Xanax), temazepam (Restoril), oxazepam (Serax), prazepam (Centrax), estazolam (ProSom), and flunitrazepam (Rohypnol). Short-acting benzodiazepines may be useful for air travelers who want to reduce the effects of jet lag.

Side Effects. Elderly people are more susceptible to side effects and should usually start at half the dose prescribed for younger people. They should not take long-acting forms.

Side effects may differ depending on whether the benzodiazepine is long- or shorting acting. They include:

Severe allergic reactions, including facial swelling, can occur even with the first use of a benzodiazepine drug.
Respiratory problems may occur with overuse or in people with pre-existing respiratory illness
The drugs may increase depression, a common co-condition in many people with insomnia.
Respiratory depression may occur with overuse or with people with pre-existing respiratory illness.
Long-acting drugs have a very high rate of residual daytime drowsiness compared to other types of sleeping pills. They have been associated with a significantly increased risk for automobile accidents and falls in the elderly, particularly in the first week after taking them. Shorter-acting benzodiazepines do not appear to pose as high a risk.
Memory loss (so-called traveler's amnesia), sleepwalking, sleep driving, eating while asleep and other odd mood states may occur. These effects are enhanced by alcohol.
Incontinence. In one study, 33% of patients experienced incontinence at least twice a week. The risk is highest in the elderly and with older, long-acting drugs.
Because these drugs cross the placenta and enter breast milk, pregnant women or nursing mothers should not use them. Benzodiazepine use in the first trimester of pregnancy may be associated with the development of cleft lip in newborns.
In rare cases, overdoses have been fatal.

Interactions. Benzodiazepines are potentially dangerous when combined with alcohol. Some medications, like the ulcer medication cimetidine, can slow the metabolism of the benzodiazepine.

Withdrawal Symptoms. Withdrawal symptoms usually occur after prolonged use and indicate dependence. They can last 1 - 3 weeks after stopping the drug and may include:

Gastrointestinal distress
Sweating
Disturbed heart rhythm
In severe cases, patients might hallucinate or experience seizures, even a week or more after the drug has been stopped.

Rebound Insomnia. Rebound insomnia, which often occurs after withdrawal, typically includes 1 - 2 nights of sleep disturbance, daytime sleepiness, and anxiety. In some cases, patients may experience the return of the original severe insomnia. The chances for rebound are higher with the short-acting benzodiazepines than with the longer-acting ones.

Newer short-acting non-benzodiazepines can induce sleep with fewer side effects than the benzodiazepines. Both benzodiazepine and non-benzodiazepine sedative hypnotics act on GABA-A receptor sites in the brain, but non-benzodiazepines are more specific in the subunits they target. Developed in the late 1980s, these drugs are increasingly prescribed and are becoming the hypnotics of choice for many doctors.

Brands and Benefits. Non-benzodiazepine hypnotics currently approved in the United States are zolpidem (Ambien, Ambien CR), zaleplon (Sonata), eszopiclone (Lunesta), and ramelteon (Rozerem).

Zolpidem (Ambien, generic) is one of the most commonly prescribed drugs for insomnia. It lasts longer than zaleplon. Patients should not take it unless they plan on getting at least 7 - 8 hours of sleep. The recommended dose is 10 mg/day for adults, although elderly patients may be prescribed half that dose. A 2002 study suggested that the drug might be used on an as-needed basis, with up to 5 tablets taken a week. After 3 weeks, two-thirds of the patients taking zolpidem this way were able to reduce their tablet intake by more than 25% without losing improvements in sleep. Ambien CR, an extended-release form, received approval from the Food and Drug Administration (FDA) in late 2005. It is the first extended-release prescription medicine for insomnia. The medicine is delivered in two steps. The first layer dissolves quickly, allowing the patient to fall asleep. The second layer helps the patient stay asleep.
Zaleplon (Sonata) is the shortest-acting hypnotic available. Because it is rapidly eliminated from the body it may be best for people who have difficulty falling asleep, not those who wake up often throughout the night. The drug takes effect within 30 minutes and may be taken at bedtime or later as long as the patient can sleep for at least 4 hours. The recommended dose is 5 - 10 mg/day. The drug is usually taken for 7 - 10 days.
Eszopiclone (Lunesta) is a newer, non-benzodiazepine hypnotic approved by the FDA in 2004. It may help improve both sleep maintenance and daytime alertness. Eszopiclone is related to zopiclone (Imovane), which has been used for many years in Europe. Unlike other sleep medications, eszopiclone can be taken on a long-term basis. In clinical trials, patients used eszopiclone for up to 6 months. Recommended doses are 2 - 3 mg/day for adults and 2 mg/day for elderly patients. Patients whose main problem is falling asleep may need only 1 mg/day.
Ramelteon (Rozerem) was approved by the FDA in 2005. Ramelteon is a novel non-benzodiazepine hypnotic. Unlike most sleep drugs, which target the gamma-aminobutyric acid (GABA) receptors, ramelteon targets the MT1 and MT2 receptors. Ramelteon does not cause dependence and is the first sleep drug not designated as a controlled substance.

These drugs can be particularly helpful for preventing jet lag (but zolpidem should not be used on flights less than 7 - 8 hours). They also may be helpful for people who also have accompanying mood disorders, such as depression or post-traumatic stress disorder. Because they are short-acting, zaleplon and zolpidem may pose fewer risks for falls and memory loss in elderly patients. In general, these drugs are recommended for short-term use (7 - 10 days) and treatment should not exceed 4 weeks. No studies have yet confirmed safety for longer-term use.

Side Effects. All of these drugs have fewer morning side effects than the benzodiazepines, including morning sedation and memory loss (although they can occur to some degree). Zolpidem’s (Ambien) record of adverse effects is similar to that of triazolam (Halcion), the short-acting benzodiazepine. Zaleplon (Sonata) and Ramelteon (Rozerem) appear to have less severe morning side effects. When patients first start taking any of these drugs, they should use caution during morning activities until they are sure how the drug affects them.

General side effects are mild but may include:

Drowsiness
Dizziness
Fatigue
Headache
Unpleasant taste
Diarrhea

Rarer side effects may include sleepwalking and hallucinations. In 2006, reports emerged of zolpidem (Ambien) causing sleepwalking and, even more bizarrely, sleep-driving. Most of these cases likely were due to patients using zolpidem along with alcohol or other drugs or taking more than the recommended dose. However, in March 2007, the FDA ordered stronger warning labels for zolpidem and all other non-benzodiazepine drugs. The new labels warn that that these drugs can cause sleep-related behavior, including sleep-driving, making phone calls, and preparing and eating food while asleep. In addition, severe allergic reactions (anaphylaxis) and facial swelling (angioedema) can occur even the first time one of these drugs is taken.

Anyone who receives a prescription for these medicines will also get a patient medication guide explaining the risks of the drugs and the precautions to take. Talk to your doctor if you have any questions concerning these drugs or their potential side effects.

Patients should carefully read the information labels for all drugs and follow the directions. Some sleeping pills take 30 - 60 minutes to take effect, while others (such as zolpidem) are fast-acting. For zolpidem, patients should:

Take zolpidem immediately before going to sleep
Take zolpidem only when able to get a full night’s sleep (7 – 8 hours)
Not drink alcohol the same evening
Not take more than the prescribed dose
Use caution in the morning when getting out of bed, driving, or operating heavy machinery

Interactions. As with any hypnotics, alcohol increases the sedative effects of these drugs. These hypnotics also interact with other drugs, including rifampin, ketoconazole, erythromycin, and cimetidine. They may also interfere or be interfered by other drugs. Patients should report all medications to their doctors.

Dependency, Withdrawal Symptoms, and Rebound Insomnia. The risk for rebound insomnia, dependence, and tolerance is lower with non-benzodiazepine hypnotics than with benzodiazepine drugs. These drugs are still subject to abuse. In any case, no hypnotic should be taken for more than 7 - 10 days or at higher than the recommended dose without a doctor's approval.

Antidepressants are sometimes used to treat insomnia that may be caused by depression (secondary insomnia). In addition, some antidepressants with sedating properties are prescribed for the treatment of primary insomnia. For example, trazodone has been frequently prescribed in low doses as a hypnotic to help induce sleep. However, there are few studies that address its safety and efficacy as a drug for treating insomnia in non-depressed patients. Several studies have warned against trazodone's use in elderly patients, due to its risk for side effects (daytime sleepiness, dizziness, priapism) and drug interactions. In fact, all hypnotics can have serious side effects in the elderly, and all must be used with caution.

Chloral Hydrate. Chloral hydrate has been in use since 1832. It has significant adverse effects, however, and most experts believe it no longer has a role in the treatment of insomnia. In any case, it does not appear to be effective in the elderly. Chloral hydrate poses a risk for addiction, and it can be fatal in overdose. It also has cancer-causing properties. Side effects include irritation of the skin, mucous membranes, and stomach. People with stomach, heart, kidney, or liver disorders should not take this drug at all. If a child is given it (usually for minor surgery), that child should never be given chloral hydrate again in their lifetime.

Barbiturates. Barbiturates (Seconal, Nembutal) were the standard sleeping medications before the introduction of benzodiazepines. Overdose is dangerous and frequent; addiction and abuse are common. These drugs should rarely or never be prescribed for insomnia.

Indiplon. The FDA is reviewing indiplon, a new non-benzodiazepine hypnotic.

According to results from a national survey published in 2006 in the Archives of Internal Medicine, more than 1.6 million Americans use complementary and alternative therapies to treat insomnia. Many people choose herbal and dietary supplement remedies. Some, such as chamomile tea or lemon balm, are generally harmless for most people. Others have more serious side effects and interactions. [See Box.] According to a 2007 study, valerian and melatonin are among the most popular alternative remedies for insomnia.

Although about half of people who use herbal medicine report that these products help their sleep, experts are not sure whether these remedies really work or whether a placebo effect is the main reason for the improvement. The American Academy of Sleep Medicine (AASM) states that there is only limited scientific evidence to show that herbal and dietary supplements are effective sleep aids. The AASM recommends that these products should be taken only if approved by a doctor. Be sure to talk to your doctor if you are considering taking any herbal or dietary supplement. Some of these products can interact with prescription medications.

Melatonin is the most studied natural remedy for insomnia. A 2005 analysis of 17 melatonin studies found that melatonin significantly reduced the time to fall asleep (sleep onset) and the time spent asleep (sleep duration). However, there are no consistent standards on melatonin doses. Some research suggests that 0.3 mg may be the most effective dosage in many people with insomnia. However, higher doses may keep some people awake.

Although melatonin may not have many benefits for most people with chronic insomnia, studies suggest that it may help the following individuals:

Elderly people. It may help certain older people with insomnia, such as those with evidence of low melatonin levels and those dependent on prescription sleeping medications. It is not clear, however, how significant the benefits are.
People without sight. A 2000 study reported that melatonin can help people without sight retrain their circadian cycle so that they can sleep at regular hours. The best dosages and timing, however, need to be clarified.
Travelers suffering jet lag. Some studies have reported that melatonin may help prevent jet lag in some travelers.
Those in withdrawal from prescription sleep medication. Melatonin may help people who are dependent on sleeping medications withdraw from these drugs and maintain good quality sleep.
People with delayed sleep syndrome. It might be somewhat helpful for people who fall asleep very late at night or in early morning hours but then sleep normally.
Children. Melatonin may help some children with chronic insomnia. In one small study, or example, melatonin was specifically helpful for children with Asperger syndrome, who are at risk for sleep disturbances. More research is warranted, however. At this time, no one should give their child melatonin without a doctor's recommendation.

Melatonin is a powerful hormone that can have major effects on all parts of the body. Doses of melatonin over 0.3 mg can disrupt the circadian system in the brain. Long-term consequences are unknown. High doses have been associated with the following adverse events:

Mental impairment
Severe headaches
Nightmares

Interactions with other drugs are not completely known. Melatonin is classified as a dietary supplement and not as a drug, so its quality is not regulated in the U.S.

Generally, manufacturers of herbal remedies and dietary supplements do not need FDA approval to sell their products. Just like a drug, herbs and supplements can affect the body's chemistry, and therefore have the potential to produce side effects that may be harmful. There have been a number of reported cases of serious and even lethal side effects from herbal products. Patients should always check with their doctors before using any herbal remedies or dietary supplements.

The following are special concerns for people taking natural remedies for insomnia:

Chamomile. Many people drink chamomile tea for its sedative properties. Although it is generally safe, it may cause allergic reactions in people who have plant or pollen allergies.

Valerian root. Valerian is an herb that has sedative qualities and has been helpful in people with insomnia. One study reported that it was also useful for helping patients withdraw from benzodiazepines -- the standard prescription sleeping pills. In another study, 83% of patients rated the effects of valerian on sleep as being very good. In the same study, valerian was as effective as oxazepam, a standard prescription sleeping medication. Valerian's side effects may include vivid dreams. High doses of valerian can cause blurred vision, excitability, and changes in heart rhythm. Valerian's effects can be dangerously increased if it is used with standard sedatives.

Chinese Herbal Remedies. Studies suggest that up to 30% of herbal patent remedies imported from China are laced with potent pharmaceuticals such as phenacetin and steroids. They may also contain toxic metals. The herbal remedy Sleeping Buddha was recalled in 1998 because it contained a benzodiazepine, the major ingredient in many prescription sleeping pills, and also appeared to increase the risk for birth defects in pregnant women. Reports of a few cases of acute hepatitis have occurred from Jin Bu Huan, a Chinese herbal remedy sold as treatment for pain and insomnia.

Kava. Kava has been used to relieve anxiety and improve sleep. It is not considered safe. There have been reports of liver failure and death from this herb, with highest risk in those with liver disease. Other side effects include itchy, scaly skin, muscle weakness, and problems with coordination. It also interacts dangerously with certain medications, including alprazolam, an anti-anxiety drug. Kava also increases the strength of certain other drugs, including other sleep medications, alcohol, and antidepressants.

Tryptophan and 5-L-5-hydroxytryptophan (HTP). Tryptophan is an amino acid used in the formation of the neurotransmitter serotonin, which is known to promote well-being and has been associated with healthy sleep. L-tryptophan was marked for insomnia and other disorders but was withdrawn from the market after contaminated batches caused a rare and even fatal disorder called eosinophilia myalgia syndrome. 5-HTP, a byproduct of tryptophan, is still available as a supplement. There have been reports that some brands contain a substance called Peak X, which may be harmful. There is little evidence that 5-HTP relieves insomnia.

Resources

www.aasmnet.org -- American Academy of Sleep Medicine
www.nhlbi.nih.gov/about/ncsdr -- National Center for Sleep Disorders Research
www.sleepfoundation.org -- National Sleep Foundation
www.sleepeducation.com -- Sleep Education from the American Academy of Sleep Medicine
www.wfsrs.org -- World Federation of Sleep Research Societies
www.clinicaltrials.gov -- Find clinical trials

References

Bliwise DL, Ansari FP. Insomnia associated with valerian and melatonin usage in the 2002 National Health Interview Survey. Sleep. 2007 July 1;30(7):881-884.

Liu X, Buysse DJ, Gentzler AL, Kiss E, Mayer L, Kapornai K, et al. Insomnia and hypersomnia associated with depressive phenomenology and comorbidity in childhood depression. Sleep. 2007 Jan 1;30(1):83-90.

Mindell JA, Emslie G, Blumer J, Genel M, Glaze D, Ivanenko A, et al. Pharmacologic management of insomnia in children and adolescents: consensus statement. Pediatrics. 2006 Jun;117(6):e1223-32.

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Review Date:
7/18/2007
Reviewed By:
Harvey Simon, MD, Associate Professor of Medicine, Harvard Medical School; Physician, Massachusetts General Hospital.

A.D.A.M. Copyright

adam.com

Chronic fatigue syndrome

FitSugar — Wed, 08 Oct 2008 17:35:00 -0700

In This Report

Highlights
Introduction
Risk Factors
Causes
Diagnosis
Prognosis
Treatment
Medications
Resources
References

HEALTH GUIDE REFERENCE FROM A.D.A.M

Highlights

Causes

Four out of five people with chronic fatigue syndrome (CFS) are infected with an enterovirus -- one of the viruses that cause respiratory and gastrointestinal infections -- compared with only one out of five healthy people. The virus might be a trigger for CFS, although research has not yet confirmed a cause-and-effect relationship.

Diagnosis

According to new guidelines, symptoms that suggest a diagnosis of CFS include disabling fatigue that starts suddenly, lasts a long time, keeps coming back, and can't be explained by another condition. Other symptoms may include difficulty concentrating or sleeping, dizziness, headaches, muscle or joint pain, sore throat, and palpitations. Doctors should consider a diagnosis of CFS if symptoms have lasted for 4 months in adults or 3 months in children.
Researchers have found that people with CFS have altered amounts of slow wave sleep, which could indicate a problem with sleep regulation.

Treatment

According to one study, people with CFS who used cognitive behavioral therapy (CBT) had higher mental health scores, and were able to walk faster and with less fatigue than those who didn't use the therapy.
A 2007 study found that taking two 10 milligram doses of methylphenidate (Ritalin) each day works much better than placebo at relieving fatigue and concentration problems in people with CFS.

Introduction

Chronic fatigue syndrome (CFS), sometimes called immune dysfunction syndrome or myalgic encephalomyelitis (in Europe), is not a new disorder. In the 19th century the term neurasthenia, or nervous exhaustion, was applied to symptoms resembling CFS. In the 1930s through the 1950s, outbreaks of disease marked by prolonged fatigue were reported in the United States and many other countries. Beginning in the early- to mid-1980s, interest in chronic fatigue syndrome was revived by reports in America and other countries of various outbreaks of long-term debilitating fatigue.

Unexplained chronic fatigue describes fatigue that lasts for more than 6 months, impairs normal activities, and has no identifiable medical or psychological problems to account for it. In addition to fatigue, people may complain of other problems, such as difficulty with memory or concentration, headaches, or sore muscles or joints.

The symptoms of CFS may be categorized as follows:

Chronic fatigue syndrome (CFS). A number of criteria must be met in order for a patient's symptoms to be described as CFS. Six million patient visits are made each year because of fatigue, although only a very small percentage of these visits can be attributed to actual chronic fatigue syndrome.
Idiopathic chronic fatigue. If the symptoms do not meet the criteria for CFS, the condition is referred to as idiopathic chronic fatigue, meaning the cause is unknown.

Although the exact causes of CFS are not known, researchers think infection, genetics, hormonal imbalances, and chemical toxins play roles in different patients.

Risk Factors

In studies of large patient groups, 15 - 27% of people complain of long-term fatigue, but the majority of this fatigue can be explained by other medical or psychological problems. According to surveys, chronic fatigue syndrome (CFS) itself affects more than four out of every 1,000 Americans.

CFS occurs in both sexes, at all ages, and in all racial and ethnic groups. The Centers for Disease Control and Prevention estimates 1 million people in the U.S. have the disease, but only 20% of people with CFS may be properly diagnosed. Nevertheless, the true prevalence of CFS is very difficult to determine, since an accurate diagnosis is hard to obtain.

People ages 40 - 50 most often experience chronic fatigue. Studies have found that four out of five people with CFS are women, although a woman's symptoms do not appear to be more severe symptoms than those of men with the disorder.

Children and adolescents are not immune to CFS. Most studies indicate that girls are more likely than boys to develop CFS, although one study found the incidence of the syndrome to be equal in children among the genders.

The link between psychological disorders and chronic fatigue syndrome is problematic because so many of the symptoms overlap. The rates of depression are very high in CFS patients, possibly higher than in patients with other conditions (notably fibromyalgia and multiple chemical sensitivity).

Studies report that most children and adolescents with CFS have psychiatric disorders. Psychological factors during childhood may increase susceptibility for later CFS, although these factors are not consistent. Studies have not found any consistent association between emotional or personality disorders and CFS to explain any causal role. Some psychological factors may, however, serve as a risk factor for CFS.

Depression, in any case, is very common in the general population. It affects up to one-fifth of all Americans at some point in their lives, and most depressed people feel fatigued.

There is some evidence that stress may be a trigger for CFS in people genetically at risk for the disease.

A number of conditions overlap or coexist with chronic fatigue syndrome and have similar symptoms. Patients with CFS may also have a diagnosis of fibromyalgia, multiple chemical sensitivity, or both. It is not clear whether these conditions or others are risk factors for CFS, are direct causes, have common causes, or have no relationship at all with CFS.

Fibromyalgia. Fibromyalgia causes prolonged fatigue and widespread muscle aches. It is the disease most often confused with CFS. The two conditions also commonly appear together. In fact, many experts believe fibromyalgia is simply another variant of chronic fatigue syndrome or different manifestations of the same disease. CFS patients experience severe fatigue, whereas fibromyalgia patients experience more pain. One hypothesis proposes that the connection between the two conditions may be found in central sensitization, which is thought to cause fibromyalgia and may also cause CFS.

A characteristic feature of fibromyalgia is the existence of at least 11 distinct sites of deep muscle tenderness that hurt when touched firmly. The sites often include the following:

The side of the neck
The top of the shoulder blade
The outside of the upper buttock and hip joint
The inside of the knee

Some patients with CFS exhibit similar tender pressure points. Recurrent sore throat, headache, low fever, and depression are also common symptoms of fibromyalgia. Like CFS, fibromyalgia is chronic and not curable.

Multiple Chemical Sensitivity. Multiple chemical sensitivity (MCS) is a term now used to describe a condition in which certain chemicals are believed to cause symptoms similar to CFS in some people. It has also been observed in people with CFS. The following proposed criteria can help recognize people with MCS:

The symptoms are reproducible with repeated exposure to a chemical. (These are often common chemicals found in popular products, such as perfumes, fabric softeners, and air fresheners.)
The condition is chronic.
Symptoms can be produced by exposure to the chemical at levels lower than previously or commonly tolerated.
The symptoms improve when the chemical is removed.
Symptoms can be triggered by multiple substances that are chemically unrelated.
Symptoms involve multiple organ systems.

Still, as with CFS and fibromyalgia, there is uncertainty as to whether MCS is an actual medical condition or is psychologically based. In one study, for example, CFS patients who believed their problem was chemically triggered were exposed to either an active chemical or a placebo (an inactive substance). Both groups reported symptoms, including those exposed only to the placebo. It should be noted that everyone is exposed to many chemicals on a daily basis, and it is very difficult to determine whether chemicals are responsible for specific symptoms.

Post-ADD. Young adults who had attention deficit disorder as children can flip from hyperactivity to fatigue. Such patients have severe hypersomnolence (sleeping too much, sleeping at any time or anywhere). These patients respond well to psychostimulant medications.

Eating Disorders. Eating disorders, notably bulimia and anorexia, have been observed in patients with CFS. The conditions often have overlapping risk factors, although it is unclear whether there is a causal relationship.

Other Conditions that Commonly Coexist With CFS. A number of other conditions also often coexist with CFS and, in fact, occur at higher-than-average rates among CFS patients:

Chronic headaches
Cognitive problems such as difficulty concentrating, impaired memory, and symptoms of attention deficit disorder
Interstitial cystitis
Irritable bowel syndrome
Sleep problems
Temporomandibular disorder (TMD)

Causes

Theories abound about the causes of chronic fatigue syndrome. Indeed, no primary cause has been found that explains all cases of CFS, and no blood tests or brain scans can definitively diagnose the condition.

Convergence of Factors. A number of experts believe that CFS develops from a convergence of conditions that may include the following:

Genetic factors
Brain abnormalities
A hyper-reactive immune system
Viral or other infectious agents
Psychiatric or emotional conditions

For example, the majority of patients report some preceding moderate-to-serious physical illness (such as a chronic viral infection) or emotional event (like an episode of depression). Some experts theorize that such events, alone or in combination, may interact with certain neurologic and genetic abnormalities to trigger the event.

Still, it is not clear what sequence of events actually leads to the fatigue and other prominent symptoms of this disorder. Nor is there any specific brain or nervous system problem that experts can point to with assurance. Research indicates that CFS is more common among identical twins (who share the same genes) than fraternal twins (who share only some genes). Inheritance, then, may play a role in roughly 30 - 50% of cases, similar to the influence thought to occur in depression or alcoholism, although specific genes have not yet been identified.

New evidence suggests genes involved in the body's response to stress may play key roles in CFS. A series of 14 articles published in 2006 linked CFS with genes involved in the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system. The researchers were able to locate a common variation of DNA sequences that predicted CFS with 76% accuracy. The genes control response to trauma, injury, and other stressful events. Nevertheless, the researchers were unable to find genetic markers of CFS or to determine how the genetic variations influenced symptoms.

In 2005, English researchers found that people with CFS are more likely than people without CFS to have human leukocyte antigen (HLA) class II alleles, variations that produce antibodies to certain immune factors. Another British study of people with CFS found alterations in 16 specific genes involved with immune function, communication between cells, and transfer of energy to cells.

Abnormal levels of certain chemicals regulated in the brain system known as the hypothalamus-pituitary-adrenal (HPA) axis have been proposed as a cause of CFS. This system controls important functions, including sleep, response to stress, and depression. Of particular interest to researchers are the following chemicals and other factors controlled by the HPA axis:

Changes in Important Neurotransmitters. Research has reported that some patients with CFS have abnormally high levels of serotonin, a neurotransmitter (chemical messenger in the brain). Such elevated levels in the brain are associated with fatigue. Studies also suggest that deficiencies of dopamine, an important neurotransmitter associated with feelings of reward, may play a role in CFS. Imbalances between norepinephrine and dopamine have been identified in certain CFS patients in several studies. Unfortunately, routine clinical testing for such chemical imbalances is cost-prohibitive.
Stress Hormone Deficiencies. A number of studies on CFS patients have observed lower levels of cortisol, a stress hormone produced in the adrenal glands. Cortisol is a precursor of dehydroepiandrosterone (DHEA), a weak male hormone that may also be important in CFS. Deficiencies may be the reason why CFS patients have an impaired and weaker response to psychological or physical stresses, such as infection or exercise. (Administering replacement cortisol improves symptoms only in some patients, indicating other factors are involved.)
Disturbed Circadian Rhythms. Evidence suggests that, in certain patients, CFS is a disorder of the sleep-wake cycle, which is regulated by the so-called circadian clock, a nerve cluster in the hypothalamus-pituitary-adrenal (HPA) axis. Some mentally or physically stressful event, such as a viral infection, may disrupt natural circadian rhythms, and an inability to reset these rhythms results in a perpetual cycle of sleep disturbances. Medications that improve sleep can be very helpful for certain patients with CFS.

However, it is still not clear whether any of these changes are causes of chronic fatigue syndrome, or merely findings in some patients.

Because most of the features of CFS resemble those of a lingering viral illness, many researchers have focused on the possibility that a virus or some other infectious agent causes the syndrome in some cases.

Still, not all CFS patients show signs of infection. Although experts have long been divided on whether infections play any role in this disorder, subtypes of viral-related and non-viral CFS may both exist.

Viruses. The theory that CFS has a viral cause is not based on hard evidence, but on various observations that suggest an association, such as the following:

CFS patients typically have elevated levels of antibodies to many organisms that cause fatigue and other CFS symptoms. Such organisms include those that cause Lyme disease, candida ("yeast infection"), herpesvirus type 6 (HHV-6), human T cell lymphotropic virus (HTLV), Epstein-Barr, measles, coxsackie B, cytomegalovirus, or parvovirus. Many of these infectious agents are very common, however, and none has emerged as a significant cause of CFS.
In up to 80% of cases, chronic fatigue syndrome starts suddenly with a flu-like condition.
In the U.S., there have been reports of cluster outbreaks of CFS occurring within the same household, workplace, and community (but most have not been confirmed by the Centers for Disease Control and Prevention).
One study found that four out of five people with CFS are infected with an enterovirus -- one of the viruses that causes respiratory and gastrointestinal infections -- compared to only one out of five healthy people. The virus could be a trigger for CFS, although research has not confirmed a cause-and-effect relationship.

Some researchers are suggesting that changes in normally harmless bacteria found in the intestine may play a role in the development of CFS.

Evidence suggesting that some CFS cases may not be due to a virus includes the following:

Most cases of CFS occur sporadically. They occur in individuals and do not appear to be contagious.
There is no evidence that CFS is spread through casual contact, such as shaking hands or coughing, or by intimate sexual contact.
No single virus has been implicated in chronic fatigue syndrome. Well-designed studies of patients who met strict criteria for chronic fatigue syndrome and of patients with chronic fatigue without any known cause have not found an increased incidence of any specific infections.

CFS has sometimes been referred to as the "chronic fatigue immune dysfunction syndrome." A number of studies have found many irregularities of the immune system. Some components appear to be over-reactive, while others appear to be under-reactive, but no consistent picture has emerged to explain CFS as a disease of the immune system.

Allergies. Some studies have reported that a majority of CFS patients have allergies to foods, pollen, metals (such as nickel or mercury), or other substances. One theory is that allergens, like viral infections, may trigger a cascade of immune abnormalities leading to CFS. (Most allergic people do not have CFS.)

Autoimmune Abnormalities. The risk profile for chronic fatigue syndrome is similar to the risk profiles for a number of autoimmune diseases. Studies are inconsistent, however, in reporting the presence of autoantibodies (antibodies that attack the body's own tissues) in CFS, and the disease is unlikely to be due to autoimmunity.

Studies have observed that some patients who fit the strict criteria for chronic fatigue syndrome also have symptoms of a condition known as neurally mediated hypotension (NMH). NMH causes a dramatic drop in blood pressure when a person stands up, even for as short a time as 10 minutes. Its immediate effects can be lightheadedness, nausea, and fainting.

However, not all CFS patients experience NMH, and studies have reported no higher incidence of NMH in chronic fatigue patients.

Psychological, personality, and social factors are strongly associated with chronic fatigue in most patients. The complex relationship between physical and emotional factors has yet to be fully understood, however. Studies have not found any consistent association between emotional or personality disorders and CFS to explain a causal role. Psychological factors, then, are unlikely to be a primary cause of CFS. They may play a role in increasing susceptibility to the disorder. Certainly, in many cases, CFS promotes psychological and social dysfunction.

Overall, doctors are increasingly adopting the view that CFS is probably a disease category that includes a range of subtypes, in the same way that cancer is a broad term within which numerous specific forms occur. Mounting evidence suggests that different subtypes of CFS have different causes and manifestations, and that these various types require different treatment approaches.

Research on subgroups of CFS is underway, but it is still in the very early stages. To date, however, clinical experience and limited data suggest that subgroups of CFS may include the following:

Post-ADD CFS: Young adults who had attention deficit disorder as children, who have flipped from hyperactivity to fatigue. Such patients have severe hypersomnolence (sleeping too much, sleeping any time or anywhere). Such patients respond well to psychostimulant medications.
Neurological CFS: These patients have more severe cognitive symptoms than do patients in the other groups. They may have trouble thinking, remembering, and paying attention. Although cognitive difficulties affect the vast majority of patients with CFS, this group experiences significantly more severe symptoms. Visual-spatial problems are common, as are sensitivities to light and noise. Other symptoms in this group include seizure-like episodes and other abnormalities that suggest temporal lobe seizures. Patients in this group tend to have severe sleep problems in which they never achieve stages 3 or 4 of the sleep cycle, awaken unrefreshed, and respond well to sleep-improving drugs.
Post-viral CFS versus gradual-onset CFS: According to some experts, an estimated 70% of patients are healthy until a particular illness strikes. In gradual-onset patients, however, symptoms develop gradually, and patients are unable to recall any specific viral or infectious illness that initiated the process.
Patients with immune abnormalities versus those without such abnormalities: Immune dysfunction (such as CD4, CD8, RNase, and TH1-TH2 imbalances) can leave some CFS patients unable to fight viruses effectively and cause their bodies to launch wrongful attacks against healthy tissues. Other CFS patients, however, do not have these immune abnormalities, or have only borderline shifts in immune factors.
CFS with Orthostatic Intolerance or Neurally Mediated Hypotension (NMH). These conditions cause dizziness (or unconsciousness) when a person stands up, due to a drop in blood pressure.
CFS with neuroendocrine abnormalities: Such problems may include dysregulation of cortisol or ACTH levels.
Activity level: There may be a difference between low-active versus high-active patients.
Patients with CFS alone: This subgroup may be different than CFS in patients with other conditions, such as fibromyalgia or multiple chemical sensitivity.

Observations that different treatments work for select patients appear to support the idea that subtypes of CFS require distinct approaches. The existence of subgroups may also explain why CFS researchers are frequently unable to replicate their results in subsequent studies; patient selection in studies to date has not reflected such careful discrimination. Researchers are now, however, working to define the subgroups of CFS and identify which treatments are most effective for each.

It should be noted that while the subgroup theory is interesting, in some cases the differences among patient populations may also reflect stages of disease. For instance, in the initial stages of the disease, many patients are symptomatic and have particular psychological symptoms, including alarm, denial, and anger. In contrast, patients in later phases of the disease typically have learned to cope better with their symptoms and have a degree of acceptance. Patients' mental and emotional status may have biological consequences that bear on their physical symptoms. Such a relationship is not yet documented in CFS patients, however, and remains subject to research.

Sudden- and Gradual-Onset CFS. One interesting theory is that CFS can be categorized as either sudden- or gradual onset, with each subgroup having different causes. In over half of patients, the onset is sudden, while the remaining patients have a slow onset. Some experts believe that sudden-onset CFS may be triggered by a virus or neurologic abnormality, while gradual-onset CFS might have a psychological or other cause. Supporting this theory was a study that looked at MRI scans of the brains of CFS patients who didn't have an accompanying psychiatric problem, and showed small injuries suggesting either a viral infection or neurologic problem. Still other experts believe that in some cases, gradual-onset CFS may be traced to cognitive disorders that were present during childhood, but went unrecognized until symptoms advanced into adulthood.

Diagnosis

It is very difficult to diagnose chronic fatigue syndrome. Even experts do not have a clear definition of what chronic fatigue actually is or what mechanisms in the brain or nervous system are responsible for it. The best diagnostic approach is to determine if the patient matches the criteria for CFS and to rule out other possible causes of symptoms.

In May 2006, the Centers for Disease Control and Prevention (CDC) released a revised definition for Chronic Fatigue Syndrome based on a consensus of many of the leading CFS researchers and doctors (including input from patient group representatives). In the revised definition, chronic fatigue syndrome is considered a subset of chronic fatigue, a broader category defined as unexplained fatigue that lasts for 6 months or longer. Chronic fatigue is considered a subset of prolonged fatigue, which is defined as fatigue that lasts for 1 month or more.

Unexplained chronic fatigue can be classified as CFS if the patient meets the following criteria:

Unexplained persistent or relapsing chronic fatigue that is either new or that started at a definite period of time; is not the result of ongoing exertion; is not substantially relieved by rest; and significantly reduces activities such as work, education, and social life.
Also, four or more of the following symptoms, which must have continued or recurred during 6 or more consecutive months of illness and must not have started before the fatigue:
- Significant impairment in short-term memory or concentration
- Sore throat
- Tender lymph nodes
- Muscle pain
- Joint pain without swelling or redness
- Headaches of a new type, pattern, or severity
- Unrefreshing sleep
- Malaise that lasts more than 24 hours after exertion

Any active medical condition that may explain the presence of chronic fatigue, such as:
- Untreated hypothyroidism
- Sleep apnea and narcolepsy
- Side effects of medication
An illness (such as cancer or hepatitis B or C virus infection) that relapsed or did not completely get better during treatment, that could explain the presence of chronic fatigue.
A past or current major depressive disorder, such as:
- Bipolar affective disorder
- Schizophrenia
- Delusional disorder
- Dementia
- Anorexia nervosa or bulimia nervosa
Alcohol or other substance abuse that occurs within 2 years of the onset of chronic fatigue and any time afterward.
Severe obesity as defined by a body mass index (BMI) equal to or greater than 45. (Note: Body mass index values vary considerably among different age groups and populations. No "normal" or "average" range of values can be suggested. The range of 45 BMI or higher was selected because it falls within the range of severe obesity.)

Any other abnormality found during an exam or other tests that could explain CFS symptoms must be resolved before further attempting to classify the condition.

In 2007, the National Institute for Health and Clinical Excellence (NICE) released new guidelines for the diagnosis and management of CFS in adults and children. According to these guidelines, CFS may be diagnosed if the person has disabling fatigue that starts suddenly, lasts a long time, keeps coming back, and can't be explained by another condition.

People with CFS also can have the following symptoms:

Difficulty thinking, concentrating, remembering, finding the right words, planning, and organizing
Difficulty sleeping
Dizziness or nausea
General malaise or flu-like symptoms
Headaches
Muscle or joint pain in many areas of the body without inflammation
Painful lymph nodes without disease
Fast heartbeat (palpitations) without heart problems
Sore throat
Worsening of symptoms with physical exertion

After ruling out other possible causes, the doctor should consider a diagnosis of CFS if symptoms have lasted for 4 months in adults or 3 months in children. Children should be diagnosed by a pediatrician.

A doctor should first take a careful personal and family medical history, which may include a psychological profile, as well as perform a thorough physical examination. Patients should be prepared to answer questions such as:

When did the fatigue first begin?
Does anything make it worse or better?
Is it better at certain times of the day?
Does physical activity make it worse?
Are there any other symptoms?
Has anyone else in the family ever complained of fatigue?
Is your personal and professional life stressful?

The doctor may also ask about any changes in weight or request a patient to monitor morning and afternoon body temperatures. Patients should report any drugs they are taking, including vitamins and over-the-counter or herbal medications.

Standard tests are typically recommended to rule out specific conditions that can cause persistent fatigue. These tests include:

Blood count
Blood tests for gluten sensitivity
C-reactive protein
Creatine kinase
Erythrocyte sedimentation rate or plasma viscosity
Liver function
Random blood sugar (glucose)
Serum calcium
Serum creatinine
Serum ferritin levels (only in children)
Thyroid function
Urea and electrolytes
Urine test for protein, blood, and glucose

No blood, urine, or other laboratory test can specifically diagnose CFS. If any test is abnormal, it is not useful for diagnosing CFS specifically, and the doctor should look for other causes of these abnormalities.

That being said, research published in 2005 found that certain components in urine were unique in people with CFS, and may someday be considered biomarkers of the disease. Additionally, antibodies to Epstein-Barr virus and increased levels of isoprostanes -- markers of oxidative stress -- have been found in the blood of people with CFS.

Among the many other common conditions that can lead to feelings of temporary exhaustion are the following:

Depression
Infections
Pregnancy
Extreme exercise
Excessive stress

In most of these cases, fatigue can be relieved with adequate rest. It is important to note that longstanding fatigue can be the harbinger of a serious medical or psychological problem. A number of more serious conditions may cause persistent fatigue and other symptoms of CFS and should be ruled out. Patients and doctors should not overlook these diseases, even if the conditions have been previously treated, because they may not have completely resolved or they may cause residual fatigue. Doctors can usually distinguish these diseases from CFS after a clinical evaluation and laboratory testing.

Infectious Mononucleosis and Epstein-Barr Virus. Infectious mononucleosis is marked by fatigue and swollen glands. It primarily affects adolescents and young adults. Some patients may have lingering fatigue that lasts for many months and blood tests that indicate a persistence of the Epstein-Barr virus (EBV), which causes mononucleosis.

Autoimmune Diseases. Some diseases, including systemic lupus erythematosus, multiple sclerosis, and rheumatoid arthritis, are caused by autoimmunity, a condition in which the person's immune system attacks the body's own tissues. The early symptoms of these conditions may mimic some of those that appear in CFS, such as muscle and joint pain and fatigue. These diseases, like CFS, also occur more often in women than in men. Most of these conditions can be confirmed with laboratory or x-ray/radiologic findings. However, some autoimmune diseases may evolve slowly, and even if a diagnosis of chronic fatigue syndrome is considered, doctors should keep track of any changes in symptoms over time in order to rule out these serious illnesses.

Post-Lyme Disease Syndrome. Rarely, patients treated for a diagnosis of Lyme disease continue to have nonspecific symptoms, which can last for years after antibiotic treatment and that resemble symptoms of chronic fatigue syndrome.

Psychosis and Severe Mental Disorders. The Centers for Disease Control (CDC), which set up the definitions in the U.S. for research in chronic fatigue syndrome, recognizes depression as one of the symptoms of CFS. However, according to the CDC, anyone with a history of major depression or other severe psychiatric disorders, including bipolar disorder and schizophrenia, does not meet the criteria for chronic fatigue syndrome.

Symptoms of major depression include the following:

A depressed mood every day
Significant weight gain or loss (10% or more of an individual's typical body weight)
Insomnia or excessive sleeping
Restlessness or a sense of being slowed down
Low energy every day
Worthless or inappropriately guilty feelings
An inability to concentrate or to make decisions
Suicidal thoughts

Major depression is likely to be responsible if a person has several of these symptoms and no physical symptoms (such as sore throat, aches and pains, or fever). The longer fatigue has continued without such physical symptoms, the more likely that the diagnosis is depression.

Of note, a persistent form of minor depression called dysthymia may be more difficult to differentiate from CFS and may actually account for a subset of CFS cases. Dysthymia is characterized by many of the same symptoms that occur in major depression, but they are less intense and last much longer, at least two years. The symptoms of dysthymia have been described as a "veil of sadness" that covers most activities.

Patients with depression and those with CFS generally perceive their illnesses differently:

Patients with depression have significantly lower self-esteem, more thought distortions (for instance, focusing on the negative or personalizing their situations), and believe their conditions stemmed from psychological factors.
CFS patients, even those with concurrent depression or dysthymia, tend to identify medical causes as the source of their problems and to focus on physical symptoms.

Many previously healthy patients with CFS become depressed and anxious because they feel so exhausted all the time. CFS may also lead to highly stressful socioeconomic situations, such as social isolation and poverty, that can contribute to and even cause emotional disorders in susceptible individuals, which in turn can worsen CFS.

Sleep Disturbances. Certain sleep disorders may cause persistent fatigue and can be confused with CFS:

Sleep apnea is a common disorder that can cause daytime fatigue without the patient being aware of the problem. Apnea is actually a breathing disorder often marked by loud snoring and thrashing in bed. A person may not realize the problem exists unless it is brought to his or her attention by a sleeping partner or observer.
Narcolepsy is a peculiar and rare disorder in which a person suddenly falls asleep without any previous signs of fatigue.
Other sleep disorders that cause daytime fatigue include insomnia and restless legs syndrome.

Researchers have found that people with CFS have altered amounts of slow wave sleep, which could indicate a problem with sleep regulation. Non-restorative sleep and nighttime restlessness are the most common complaints of people with CFS.

Conditions that Cause Joint Pain, Muscle Aches, or Both. A number of illnesses cause one or more of CFS symptoms, including arthritic symptoms, fever, and fatigue.

Severe Obesity. People who are severely obese often have symptoms of chronic fatigue because of the stress imposed by the weight. People who are obese are also at particular risk for sleep apnea, which can confuse the diagnosis.

Other Medical Conditions that Usually Rule Out CFS. Many diseases, both benign and serious, can fully explain prolonged or chronic fatigue, including:

Hepatitis
Anemia
Hemochromatosis (a hereditary disease caused by iron overload) infections
Various forms of cancer
Neuromuscular diseases (such as myasthenia gravis)
Hypothyroidism
Diabetes

Drugs and Alcohol. Fatigue is a side effect of many prescription and over-the-counter medications, such as antihistamines. In addition, dependency on or abuse of alcohol or illicit drugs may manifest as chronic fatigue. Medications should be considered as a possible cause of fatigue if an individual has recently started, stopped, or changed medicines. Withdrawal from caffeine can produce depression, fatigue, and headache.

Prognosis

The physical severity of chronic fatigue syndrome varies. Most commonly, patients with CFS report that they have trouble fulfilling both home and work responsibilities.

CFS sufferers typically work part-time. In extreme cases, patients are severely disabled and even bedridden. Such patients can do virtually nothing, including even light housework.

Patients with CFS are more likely to lose their jobs, possessions, and support from friends and family than are people who have other conditions that cause fatigue.

Most patients say that while fatigue is the most incapacitating symptom, mental impairment, such as an inability to concentrate or remember, is the most distressing symptom. The effects of CFS on mental functioning are complex, however. Some experts believe that the impaired mental functioning is due to depression, which is common in CFS patients.

Some studies indicate that, although general intelligence is not impaired, CFS patients test lower in certain mental functions, particularly speed and efficiency in processing complex information, and that 40 - 60% have memory impairments. In such studies, this impaired mental function occurs regardless of the presence or absence of depression or other psychiatric disorders.

Because the illness remains elusive and poorly defined, and there are few objective measures for recovery, experts have found it difficult to determine the long-term course of the disease. Many patients are not covered by insurance or have difficulty finding good care, so available statistics may be incorrect. Bearing these factors in mind, some studies have reported that more than half of patients who complain of chronic fatigue are still fatigued at 2 years. Although a variety of studies have attempted to identify factors that predict a more chronic or severe course, no clear conclusions can be made. Even if patients get progressively worse, however, the disorder is not fatal.

Although children with symptoms of chronic fatigue have not been as rigorously studied as adults, limited evidence suggests that CFS can be significantly disabling in young people. Studies report that adolescents who meet the criteria for CFS also have greater anxiety, depression, and school absenteeism than their peers. Still, some studies indicate that children have a better prognosis than adults and that most will recover after 1 - 4 years. Several studies have indicated that cognitive-behavioral therapy is an effective treatment for adolescents with CFS.

Treatment

There is no proven or reliable cure for CFS, and no drug has been developed specifically for this disorder. Because CFS remains poorly understood, many patients have problems finding good care. Overall, the recommended strategy for treatment includes a combination of the following:

A healthy diet
Antidepressant drugs in some cases, usually low-dose tricyclics
Cognitive-behavioral therapy (CBT) and graded exercise for certain patients
Medication
Sleep management techniques

Patients with the best chance for improvement are those who remain as active as possible and who seek to have some control over the course of the disorder. Patients should choose physicians who are willing to consider the problem as a medical condition with psychiatric components. They should be very wary, however, if the physician recommends excessive and expensive treatments that may have serious adverse effects and that have no proven benefits. For patients with severe CFS that cannot be managed with lifestyle changes and standard medications, asking the physician about enrolling in any available clinical trials may be helpful.

Cognitive-Behavioral Therapy

CBT is designed to help CFS patients regain a sense of control, and is proving to have substantial benefits for some patients. Some experts believe that patients who are diagnosed with CFS should be referred to therapists trained in cognitive-behavioral therapy. (Psychoanalysis and other interpersonal psychological therapies, which are concerned with subconscious thoughts and early childhood memories, are not generally helpful for the CFS patient.)

The Goals of Cognitive-Behavioral Therapy. The primary goals of cognitive-behavioral therapy (referred to below as just cognitive therapy) are to change any distorted perceptions that individuals have of the world and of themselves, and to change their behavior accordingly. For CFS patients, this means learning to think differently about their fatigue and to improve their ability to deal with stressful situations and manage their disorder. It can also help manage their sleep problems and find the appropriate activity levels for them. Cognitive therapy is particularly helpful in defining and setting limits, behaviors that are extremely important for these patients.

The Procedure. CBT is usually performed over 6 - 20 sessions, each lasting about an hour. Patients are also given homework, which usually includes keeping a diary and attempting tasks that they have avoided because of negative attitudes.

A typical cognitive therapy program may involve the following measures:

Keep a Diary. The patient is almost always asked to keep an energy diary, which can be a key component of CFS cognitive therapy. The diary serves as a general guide for setting limits and planning activities. The patient uses the diary to track any factors, such as a job or a relationship that may be making the fatigue worse or better. It is also used to track the times of day when energy levels are at their highest and lowest peaks.
Adjust Schedule. The patient adjusts schedules to conform to energy peaks and valleys recorded in the diary. For instance, the patient may plan to take a nap during low-energy times and plan important activities during high-energy times. Developing fairly rigid daily routines around probable energy spurts or drops may help establish a more predictable pattern.
Confront Negative or Discouraging Thoughts. Patients are taught to challenge and reverse negative beliefs (such as "I'm not good enough to control this disease, so I'm a total failure."), and to use coping statements ("Where is the evidence that I can control this disease?")
Be Flexible. Energy levels will most likely never be entirely predictable. Patients must be prepared to adapt to energy variations. Instead of taking a long nap, for instance, patients may need 5- to 10-minute rest periods every hour or more, possibly involving relaxation or meditation.
Set Limits. Limits are designed to keep both mental and physical stress within a manageable framework so that patients do not get discouraged by forcing themselves into situations in which they are likely to fail. For example, tasks are broken down into incremental steps and patients focus on one step at a time.
Prioritize. Patients learn to drop some of the less critical tasks or delegate them to others.
Manage Impaired Concentration. Patients seek out activities that are appealing, focus attention, and help increase alertness. They learn to request instructions given as concise, simple statements. External distractions, such as music or talking, are kept to a minimum.
Accept Relapses. Over-coping and accomplishing too much too soon can often cause a relapse of symptoms. Patients should respect these relapses and back off. They should not consider them a sign of treatment- or self-failure.

Using both self-observation and specific tasks, patients gradually shift their fixed ideas that they are helpless against the fatigue that dominates their lives. They move to the perception that fatigue is only one negative and, to a degree, a manageable experience among many positive ones.

Success Rates. One review of CFS trials reported that, of all therapies available to CFS patients, only cognitive behavioral therapy (CBT) and graded exercise showed conclusive benefits. Although CBT doesn't appear to bring patients completely back to normal, research has found that people who used the therapy had higher mental health scores, and were able to walk faster and with less fatigue than those who didn't use CBT. A 2005 study found that cognitive therapy is an effective treatment for adolescents with CFS. Patients who received CBT reported improvements in fatigue, functional status, and school attendance.

Not all studies support the benefits of cognitive therapy for CFS. It is important to note that different therapists may have different fundamental assumptions about CBT and may use different techniques. For instance, some therapists believe that CFS is purely a psychological problem and that patients must reject the notion of physical causes, abandon all reliance on assistive devices, and participate in challenging exercise programs. In contrast, other therapists do not attempt to change patients' underlying beliefs at all, but instead focus on helping patients conserve energy and better cope with the limitations of their illness. When considering CBT, patients and their families must be aware of such important differences.

Regardless of whether specific organic causes of CFS are identified, the power of the mind to improve or oppose health problems is significant, and treatments that promote a positive outlook are beneficial for any disease.

A number of studies have suggested that a graded exercise program, in which patients perform increasingly more intense levels of exercise tailored to their individual abilities, has benefits for many patients with CFS. Exercise is best performed in combination with cognitive behavioral therapy.

Reports have found that 75% of CFS patients who were able to engage in exercise, particularly aerobic exercise, reported less fatigue and better daily functioning and fitness after a year. A 2004 review of clinical trials found that exercise therapy is beneficial for CFS, particularly when combined with patient education.

Some patient groups and experts contend that such studies use only patients with less severe conditions and do not apply to many CFS patients. Many patients have severe conditions, and some are very incapacitated (such as being wheelchair bound). These patients are unlikely to undergo even graded exercise. All CFS patients, in fact, have a lower exercise capacity than healthy individuals, and over-exercising can intensify symptoms. Some patients experience profound fatigue following even modest exercise. It is the primary factor in perpetuating the low-activity levels observed in these patients.

The following tips may be helpful for CFS patients when embarking on an exercise program:

Work with your health care provider to determine a good starting level of activity for you. Start slowly and incrementally, beginning with as few as 3 - 5 minutes of moderate exercise a day. The goal is to increase activity by about 20% every 2 - 3 weeks, until you can handle about 30 minutes a day. Once you reach 30 minutes a day, start to increase the aerobic intensity of your workouts. (Capacity varies greatly among CFS sufferers, however, and some may not be able to achieve this.)
Establish limits and keep within them in order to avoid overexertion and relapse.
Experiment with different forms of physical activity that suit your available energy levels. Some patients report great benefits from yoga or Tai Chi, which combine exercise with meditation.
Setbacks will occur, but do not become discouraged.

Work with your health care provider to find a level of activity you can handle. Then gradually increase your activity level. Activity management should involve:

Balancing your time between activity, rest, and sleep
Spreading out more challenging tasks throughout the week
Breaking big tasks into smaller, more manageable ones
Avoiding doing too much on days when you feel tired

Although there is no evidence to support any specific dietary factors in CFS, patients should be sure to maintain a healthy diet that includes:

Plenty of fresh dark-colored fruits and vegetables, which are rich in antioxidants
Fiber-rich foods
Limited saturated fats (found in animal products)
Omega-3 essential fatty acids, found in certain fish and oils
Increased salt (only for those with demonstrated low blood pressure)
Starchy foods, particularly for nausea

Stress Reduction Techniques. One panel of experts concluded that relaxation and stress-reduction techniques were helpful in managing chronic pain. These techniques also can help relieve the stress associated with the disease. They are not useful, however, as the primary treatment for CFS. A number of relaxation techniques are available:

Biofeedback
Deep breathing exercises
Hypnosis
Massage therapy
Meditation
Muscle relaxation techniques
Yoga

Light Therapy. Patients with seasonal affective disorder (SAD) experience more depression during the winter, when the hours of sunlight decrease. With light therapy (phototherapy), the patient sits for about 30 minutes each day a few feet away from a box-like device that emits very bright fluorescent light (4,000 lux). Light therapy is best performed immediately after awakening in the morning.

Some CFS patients don't have much improvement from light therapy. However, the treatment may still help some patients with CFS whose symptoms are similar to those of patients with seasonal affective disorder (SAD).

Supportive Family and Groups. Having strong, supportive relationships with family and friends can help CFS patients get better. However, CFS patients should try not to impose unreasonable expectations on loved ones that cannot be met. Ongoing support groups with fellow patients may be very helpful. In one study, sharing experiences in a group therapy setting proved to be the most valuable component in treatment, and one that improved patients' coping abilities.

Medications

No medications are specifically approved for the treatment of CFS. However, some may be useful for pain or other specific symptoms, or in cases where CFS may have a specific cause. Doctors generally use combinations of drugs to accomplish specific goals, such as medication at night to improve sleep and medication in the morning to improve cognition and energy. Treatment is very individualized.

Nonsteroidal Anti-Inflammatory Drugs (NSAIDs). Patients with CFS may find relief using NSAIDs -- common pain relievers that reduce pain and swelling. Types of NSAIDs include aspirin, ibuprofen (Motrin, Advil, Nuprin), and naproxen (Aleve, Naprosyn, Naprelan, Anaprox).

Although NSAIDs work well, long-term use can cause stomach problems, such as ulcers and bleeding. In April 2005, the FDA asked drug manufacturers of NSAIDs to include a warning label on their product that alerts users of an increased risk for cardiovascular events and gastrointestinal bleeding. Due to its proven cardiovascular benefits, aspirin was excluded from these labeling revisions.

NSAIDs can also increase blood pressure, particularly among people already being treated for hypertension. (About 12 - 15% of elderly people take both an NSAID and an antihypertensive drug.) Piroxicam, naproxen, and indomethacin appear to pose the greatest risk of high blood pressure. Sulindac has the smallest effect.

Other side effects of NSAIDs include:

Dizziness
Ringing in the ears
Headaches
Skin rashes
Possibly depression

NSAIDs can cause kidney damage. (The damage gets better once the patient stops using the drug.) People with high blood pressure, severe circulation disorders, or kidney or liver problems, as well as people taking diuretics or oral hypoglycemics, must be closely monitored if they need to use NSAIDs on a long-term basis. Because NSAIDs reduce blood clotting, NSAID users scheduled for surgery should stop taking those drugs a week before the operation.

COX-2 Inhibitors (Coxibs). Coxibs block an inflammation-promoting enzyme called COX-2. This class of drugs was initially believed to work as well as traditional NSAIDs, but with fewer stomach problems. However, numerous reports of cardiovascular events, skin rashes, and other adverse effects prompted the FDA to re-evaluate the risks and benefits of the COX-2 drugs. Rofecoxib (Vioxx) and valdecoxib (Bextra) were withdrawn from the U.S. market following reports of heart attacks in patients taking the drugs. Celecoxib (Celebrex) was still available at the time of this report, but labeled with strong warnings and a recommendation that it be prescribed at the lowest possible dose for the shortest duration possible. Patients should ask their doctor whether the drug is appropriate and safe for them.

Because of the association between depression and CFS, antidepressants are often tried, with varying degrees of success. Common side effects of many antidepressants include:

Dry mouth
Restlessness
Reduced sexual drive
Slightly increased heart rate
Constipation

Virtually all antidepressants have complicated interactions with other drugs, and some are very serious.

Tricyclic Antidepressants. Antidepressants known as tricyclics may be particularly helpful for CFS patients. For example, the tricyclic amitriptyline (Elavil) is known to relieve many of the symptoms of CFS, including sleeplessness and low energy levels. These drugs may provide benefits by promoting deep sleep and inhibiting pain pathways in the nervous system. Improvement in symptoms can take 3 - 4 weeks. Other tricyclics include doxepin (Sinequan), desipramine (Norpramin), nortriptyline (Pamelor), clomipramine (Anafranil), and imipramine (Tofranil, Janimine). Patients with CFS normally respond to much lower doses than those used to treat people with depression. In fact, many CFS patients cannot tolerate the higher doses commonly used to treat the psychiatric disorder. Like all medications, tricyclics must be taken as directed. Overdose can be life-threatening. Tricyclics should not be taken together with SSRIs, because of the possibility of dangerous side effects.

Other Antidepressants. Newer, so-called designer SSRIs, including bupropion (Wellbutrin), nefazodone (Serzone), or mirtazapine (Remeron), affect combinations of different neurotransmitters, and some may have moderate benefits for CFS patients. For example, in one study, nefazodone improved mood, fatigue, and sleep disturbances.

SSRIs. The popular antidepressants known as selective serotonin-reuptake inhibitors (SSRIs) may be helpful for the subgroup of CFS patients who experience significant depression. They include fluoxetine (Prozac), sertraline (Zoloft), and paroxetine (Paxil). Cymbalta (duloxetine) is a new antidepressant that is classified as a selective serotonin and norepinephrine reuptake inhibitor (SSNRI).

In a 2006 UK study of 275 CFS patients, those treated with antidepressants recovered faster than those who did not receive the medication. SSRIs were found to be more effective than tricyclic antidepressants, producing improvements, including a reduction in fatigue, that were maintained at the 3-year follow-up.

Psychostimulants. Psychostimulants may be helpful for a subgroup of patients with CFS who have cognitive problems, such as difficulty concentrating, memory problems, and other attention deficit disorder (ADD)-like characteristics. Psychostimulants include Dexamphetamine, Adderal, methylphenidate (Ritalin) and Ritalin-like drugs such as Focalin, Concerta, Ritalin LA, and Metadate, as well as Strattera and Provigil. The NICE guidelines for CFS do not advise taking Dexamphetamine or Ritalin. However, a 2007 study found that taking two 10 mg doses of Ritalin each day works much better than placebo at relieving fatigue and concentration problems. More research is needed to study the long-term effects of Ritalin on CFS patients.

Because of the difficulties in treating chronic fatigue syndrome, many patients seek alternative therapies. Some, such as acupuncture, yoga, and relaxation techniques, may be helpful and are not dangerous. No scientific evidence exists that vitamin and mineral supplements will relieve CFS, but some people do report that they find supplements helpful.

Herbal and Supplements. Popular herbal and dietary supplement remedies for CFS include coenzyme Q10, vitamin B12, vitamin C, magnesium, multivitamins, DHEA, ginseng, and acetylcarnitine. None have been rigorously tested. Some herbs, such as St. John’s wort, ginkgo, and comfrey, may cause serious side effects and drug interactions.

Herbal remedies and dietary supplements are not regulated by the FDA. This means that manufacturers and distributors do not need FDA approval to sell their products. In addition, any substance that can affect the body's chemistry can, like any drug, produce side effects that may be harmful. There have been a number of reported cases of serious and even lethal side effects from herbal products.

Some so-called natural remedies have been found to contain standard prescription medication. Of specific concern are studies suggesting that up to 30% of herbal patent remedies imported from China have been laced with potent pharmaceuticals, such as phenacetin and steroids. Most reported problems occur in herbal remedies imported from Asia. One study reported that a significant percentage of such remedies contain toxic metals.

CFS patients should be wary of any company that promises a cure or urges the purchase of expensive but useless and sometimes potentially dangerous treatments, such as the following:

St. John's wort. This herbal remedy is being investigated for mild depression. In one study, St. John's wort lessened fatigue in CFS patients, even in those who did not consider themselves to be depressed. However, the substance may have some serious side effects; for example, it can interact with blood thinning medication. In a brand comparison, only three St. John's wort products out of eight contained within 10% of the active ingredient amounts claimed on the labels.
Melatonin. Some patients use melatonin, based on the association between CFS and possible sleep abnormalities. However, the small amount of research available has not shown melatonin to be helpful.
Gingko. Although the risks for gingko appear to be low, there is an increased risk of bleeding at high doses. In addition, gingko can interact with high doses of vitamin E and anti-clotting medications. Commercial gingko preparations have also been reported to contain colchicine, an agent that can be harmful in pregnant women and people with kidney or liver problems. Some brands of gingko have no effect at all.
Comfrey. Comfrey is an herbal remedy used for a number of inflammatory problems. Recently, evidence has emerged that comfrey can be toxic to the liver, and animal studies have reported a possible cancer risk. Comfrey is banned in Canada and other countries, but is widely available in the U.S.

Of particular note for CFS patients are products containing the ingredient Ma Huang, which contains the stimulants ephedrine and kola nut, a caffeine source. Serious adverse reactions, including seizures, psychosis, and several deaths, have been reported in people taking this supplement for increased energy or weight loss. Products that have only one of these ingredients do not appear to have the same effect, but people should take so-called energy boosting supplements only with the knowledge and recommendation of their doctor.

Other alternative remedies with no proven benefit and possible toxic and dangerous side effects include the following:

Hydrogen peroxide injection (can cause blood clots or strokes)
Megadoses of vitamins (can be toxic and have shown no benefits)
High colonic enemas
Bee pollen (can cause an allergic reaction)
Injections of liver extract
Superoxide dismutase (SOD)

Resources

www3.niaid.nih.gov -- National Institute of Allergy and Infectious Diseases
www.cdc.gov/cfs - Centers for Disease Control and Prevention, Chronic Fatigue Syndrome information
www.cfids.org -- The Chronic Fatigue and Immune Dysfunction Syndrome Association of America
www.ncfsfa.org -- National Chronic Fatigue Syndrome and Fibromyalgia Association
www.aacfs.org -- American Association for Chronic Fatigue Syndrome
www.theacpa.org -- American Chronic Pain Association
www.ampainsoc.org -- American Pain Society
www.iasp-pain.org -- International Association for the Study of Pain
www.medicalacupuncture.org -- American Association of Medical Acupuncture
www.aabt.org -- Association for Advancement of Behavior Therapy

References

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Review Date:
1/4/2008
Reviewed By:
Harvey Simon, MD, Editor-in-Chief, Associate Professor of Medicine, Harvard Medical School; Physician, Massachusetts General Hospital. Also reviewed by David Zieve, MD, MHA, Medical Director, A.D.A.M., Inc.

A.D.A.M. Copyright

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