FitSugar

Does Your Weight Fluctuate by Season?

FitSugar — Mon, 30 Mar 2009 09:00:00 -0700

Believe it or not, bikini season is right around the corner. The thought of tying up a two-piece suit may cause subtle panic in some of you, and for others, it's no biggie. The difference could have something to do with the tendency to let go a little during the Winter, indulging in warm comfort foods and saying cheers with libations more often than usual. Does your weight fluctuate by season?

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Don't Stress Over Weight Fluctuations

FitSugar — Thu, 13 Mar 2008 03:00:00 -0700

If you're someone who weighs yourself daily, then you know that our weight is hardly static. If you weighed 130 before you went to bed and then 134 in the morning (after you pee) this does not mean you gained four pounds overnight. Well, unless you consumed 14,000 calories while you were sleeping. So don't sweat it and take a look at the common reasons for day-to-day weight fluctuations:

Drinking water: Two cups of water weighs one pound, so if you've been busy hydrating yourself then you'll definitely see an immediate and temporary gain in your weight.
Not drinking water: Not drinking enough water actually causes the body to retain fluid, which can also lead to a temporary weight gain.
Eating and drinking: Food and drinks have a weight too, you know. Just as you wouldn't stand on the scale holding a box of Girl Scout Cookies, nor should you weigh yourself after eating one. Wait until your body has had time to digest before stepping on the scale.

There's more so read more.

Salt: Taking in too much sodium is a sure way to cause the body to retain water, which can cause a temporary weight gain.
Exercise: Exercise can result in an immediate weight loss from sweating and dehydration. This is why many people like to weigh themselves after working out. Remember that if you don't rehydrate your body will start to retain water.
That time of the month: Most women know that weight gain that can occur before menstruation due to water retention - it too is temporary and will pass.

I like to weigh myself at the same time each day to avoid hitting all these fluctuations at once, at least then I have a benchmarking point.

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5 Things That Can Affect The Number on The Scale

FitSugar — Tue, 24 Apr 2007 10:15:00 -0700

If you religiously live by the scale, you've probably noticed that your weight can (and will) fluctuate a few pounds. Women's Health gives us five reasons that the number on the scale may be up (or down) a few pounds:

You were thirsty! Downing 16 ounces of any fluid can cause an immediate "gain" of 1 pound.
You're backed up. Constipation can tilt the scale by as much as 2 pounds if it's been more than a couple of days since your bowels did their thing.
You're going on vacation. To Thailand. The changes in air pressure can make you retain water on flights longer than 4 hours, which can show up as an extra 1 to 3 pounds on the scale.
You ate the Chicken Kung Pao. Have a salty dinner and you could wake up 2 to 3 pounds heavier - your body retains water to dilute all that sodium.
Aunt Flo's on her way. Hormone fluctuations in the 3 days leading up to your period can make you retain up to 5 pounds of water.

How Long Does it Take To Gain Weight?

FitSugar — Tue, 17 Jul 2007 15:45:00 -0700

We all have those days where we may have had one or two (or three) extra pieces of cake at your niece's 4th birthday party. Does this mean that by morning the damage is done? After all a moment on the lips is a lifetime on the hips...

Fortunately, this is not quite how it works. In fact from what I've researched (and since I am no doctor), all I have found is that there is no real way to figure out how long it takes for excess calories to turn into fat. Of course there is a balancing act of calories in with calories out, but many other factors that impact the answer to that vary from person to person based on genetics, metabolism and hormonal factors.

Temporary weight gain could appear quickly after a large meal or two, but that does not mean that if you've overdone it, you're doomed. After all, daily weight fluctuations are normal.

Generally speaking though, if you keep your calories burned in line with your calories consumed over a week's time, you shouldn't gain -- 3,500 calories is equal to one pound. If you do have a surplus of 3,500 calories by the end of one week, most people will be up a pound from the prior week. The most worrisome is the gradual weight gain that people experience, which is more likely to represent new pounds that you truly gain over time. Keep a food diary to try and help combat this gradual weight gain and (you knew this was coming) exercise regularly!

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Why Does My Weight Fluctuate?

FitSugar — Fri, 12 Jan 2007 16:35:00 -0800

I talk a lot about maintenance when it comes to your healthy goal weight. This simply means keeping your current weight fairly constant rather than losing or gaining weight each week.

If you think that this means the number on the scale should remain static, you're wrong. For most people, maintenance means weighing within three or five pounds of their goal.

The reason for this is because everyone's body weight will fluctuate from day to day, even during the course of one day. Daily fluctuations in weight of about a pound can be normal when you are trying to maintain your weight -- and they may be due to:

Normal body fluctuations related to eating and elimination
The amount of salt or high-sodium foods you consume
Temporary water-weight gain, for women, near the time of menstruation
A decrease in physical activity

So stop stressing over every single pound fluctuation your body is just being totally normal.

The Ups & Downs of Weight Loss

FitSugar — Tue, 24 Jul 2007 11:45:00 -0700

Do you understand the ups and downs of weight loss? Here are a few questions for you to see just how much you know.

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Take the quiz

Body Acceptance: Are You More Like Kelly or Jessica?

FitSugar — Mon, 10 Aug 2009 03:30:36 -0700

Both Kelly Clarkson and Jessica Simpson have gotten flack for their fluctuating weight, but the starlets don't let it get to them. Jessica talks about embracing her curves, while Kelly complains about being Photoshopped. Now, both ladies are gracing magazine covers and discussing, among other things, their body acceptance.

In the August issue of Glamour, Jessica admits to worrying about her weight from a young age: "I was always disconnected from myself; there was this idea of perfection I couldn't ever get to. But all women struggle with insecurity, and we all have something we don't like about ourselves." Kelly is a bit more laid-back, saying: "My happy weight changes. Sometimes I eat more; sometimes I play more. I'll be different sizes all the time."

While it sounds like both women have a healthy relationship with their bodies, Kelly sounds like she gives it less thought than Jess does. Who are you more like?

Eating disorders

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

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.

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adam.com

Where's the First Place You Gain Weight?

FitSugar — Mon, 13 Jul 2009 03:30:49 -0700

It's normal to have weight fluctuations, depending on our diet, workout routine, and stress. Others may not be aware that you've put on some weight, but you're sure to notice either by the mirror, the scale, or how your clothes fit. People gain weight differently so tell me . . .

Parkinson's disease

FitSugar — Wed, 08 Oct 2008 17:35:13 -0700

In This Report

Highlights
Introduction
Symptoms
Risk Factors
Complications
Diagnosis
Treatment
Levadopa (L-dopa)
Other Medications
Surgery
Lifestyle Changes
Resources
References

HEALTH GUIDE REFERENCE FROM A.D.A.M

Highlights

Drug Approvals

In 2007, the FDA approved the first skin patch drug for treatment of Parkinson’s disease. Transdermal rotigotine (Neupro) is a dopamine agonist drug that may help improve symptoms of early-stage Parkinson’s disease. The patch is applied daily.
Rivastigimine (Exelon), an Alzheimer’s disease drug, was approved in 2006 for treatment of mild-to-moderate dementia associated with Parkinson’s disease.

Drug Withdrawal

In 2007, the FDA withdrew the dopamine agonist pergolide (Permax) from the market due to safety concerns. Several articles published in 2007 in the New England Journal of Medicine indicated that pergolide and a similar drug, cabergoline (Dostinex), are associated with heart valve problems. Cabergoline is not approved in the U.S. for treatment of Parkinson’s disease.

Dietary Supplements

In 2007, the U.S. National Institutes of Health launched a large-scale clinical trial to study whether creatine may help slow the progression of Parkinson’s disease. Creatine is a nutritional supplement that is sometimes used to enhance exercise performance.
Coenzyme Q10, an antioxidant dietary supplement, does not help improve Parkinson’s disease symptoms, according to a study published in 2007 in the Archives of Neurology.

Deep-Brain Stimulation

Deep-brain stimulation outperformed drug therapy in a randomized trial comparing these two treatment approaches. In a study published in 2006 in the New England Journal of Medicine, patients who received deep-brain stimulation had better symptom and quality of life improvement than those who were treated with only medications. However, more serious side effects were reported in the deep-brain stimulation group. Deep-brain stimulation is a surgical technique that involves implanting electrodes in a target area of the brain.

Introduction

Parkinson's disease (PD) is a slowly progressive disorder that affects movement, muscle control, and balance. Parkinson's disease is referred to as idiopathic, which means that the cause is unknown. This term distinguishes the primary disease from parkinsonism, which are the symptoms occurring from a known cause. In addition to its effects on motor control, Parkinson's disease is now recognized as a broader condition that can include cognitive and behavioral disturbances, sleep disorders, speech difficulties, and other problems.

Parkinson's disease occurs from the following process in the brain:

PD develops as cells are destroyed in certain parts of the brain stem, particularly the crescent-shaped cell mass known as the substantia nigra.

Parkinson's disease is a slowly progressive disorder that affects movement, muscle control, and balance. Part of the disease process develops as cells are destroyed in certain parts of the brain stem, particularly the crescent-shaped cell mass known as the substantia nigra. Nerve cells in the substantia nigra send out fibers to tissue located in both sides of the brain. There the cells release essential neurotransmitters that help control movement and coordination.

Nerve cells in the substantia nigra send out fibers to the corpus stratia, gray and white bands of tissue located in both sides of the brain.
There the cells release dopamine, an essential neurotransmitter (a chemical messenger in the brain). Loss of dopamine in the corpus stratia is the primary defect in Parkinson's disease.

Dopamine. Dopamine deficiency is the hallmark feature in PD. It is one of three major neurotransmitters known as catecholamines, which help the body respond to stress and prepare it for the fight-or-flight response. Loss of dopamine negatively affects the nerves and muscles controlling movement and coordination, resulting in the major symptoms characteristic of Parkinson's disease. Dopamine also appears to be important for efficient information processing, and deficiencies may also be responsible for problems in memory and concentration that occur in many patients.

Although it is clear that dopamine deficiency is the primary defect in Parkinson's disease, it is not clear what causes dopamine loss. The culprit is less likely to be a single cause than a combination of genetic and biologic factors, which are triggered by some environmental assault.

Other Changes. The PD disease process also appears to impair nerve endings in the heart to cause dysautonomia-- changes in the autonomic (also called sympathetic) nervous system. Such changes may impair the release of norepinephrine, a hormone that regulates blood pressure, pulse rate, perspiration, and other automatic responses to stress. Evidence suggests this may be responsible for the abrupt drops in blood pressure when standing that occur in PD. Further research is underway to determine if the loss of nerve terminals is confined to the heart or if it affects other organs as well.

Click the icon to see an animation about Parkinson's disease.

Apoptosis and Alpha Synuclein. Important research now suggests that three molecules are critical in the development of inherited PD: alpha synuclein, parkin, and ubiquitin, which all interact in the normal brain. Abnormally high levels of alpha synuclein, which is produced in dopamine-rich nerve cells, may play a central role. Normally, two other molecules, parkin and ubiquitin, are involved in the natural self-destruction of synuclein -- a natural process of programmed cell death called apoptosis. If this process goes awry, for instance, with a defective parkin gene, cell death fails to occur. If synuclein is not eliminated in these cells, it builds up and becomes toxic to dopamine. In such cases, synuclein accumulates in Lewy bodies, the deposits of fibrous tissue found in all patients with PD.

Another protein, beta amyloid, also increases the build-up of synuclein. Beta amyloid is a known factor in Alzheimer's disease, and may help explain the co-existence between Alzheimer's and Parkinson's disease in many patients.

Lewy Bodies. The fibrous deposits known as Lewy bodies are the hallmark signs of Parkinson's disease. They are found in the substantia nigra, the place in the brain where dopamine is first released. It is not clear whether Lewy bodies are the major killers of the nerve cells or whether they are simply a byproduct of the degenerative process. They are found not only in the brains of patients with Parkinson's disease but, in rare cases, may show up in cells in other parts of the body (the heart, intestine), causing severe disabling symptoms. These substances are also present in other diseases that cause dementia, such as Alzheimer's, and can occur in people without neurologic symptoms.

The Mitochondria and Oxygen-Free Radicals. Some research has observed that certain patients with PD have significantly low levels of complex I, an enzyme found in the mitochondria, sausage-like structures that are the primary source of energy within cells. Some theories suggest that low amounts of complex I may make nerve cells vulnerable to the assault of oxygen free radicals (also called oxidants). Oxidants are unstable molecules that bind to other molecules in the body. They are normally produced by the natural chemical processes in the body. If the body is subjected to environmental stresses, however, they can be over-produced. In excess, they can damage any cell, including nerve cells in the brain, and even interfere with their DNA.

NMDA Receptors. Also of interest in PD are processes that occur in an area of the brain called the subthalamic nucleus. Here, receptors known as glutamatergic N-methyl-D-aspartate (NMDA) become persistently overexcited and produce high levels of calcium ions within brain cells. This in turn leads to a cascade of events that trigger oxygen-free radicals and cell damage.

Immune Factors and the Inflammatory Response. An over-responsive immune system triggered by initial damage may also play a role in perpetuating Parkinson's disease. When the immune system becomes overactive, it produces excessive numbers of potent factors called cytokines, which cause inflammation and further injury in brain cells. Important cytokines under investigation are interleukin-1 and tumor necrosis factor.

Specific genetic factors appear to play a strong role in early-onset Parkinson's disease, an uncommon form of the disease. Research from the last several years suggests that multiple genetic factors may also be involved in late-onset Parkinson’s disease. Several important studies, published in 2005, lay the groundwork for potential genetic screening for this disease. Researchers identified the leukine-rich repeat kinase 2 (LRRK2) gene, located on a region of chromosome 12 known as PARK8, as a key gene involved in inherited forms of Parkinson’s. The researchers estimate that a single gene mutation in LRRK2 may be responsible for 5% of inherited Parkinson’s cases and about 2% of isolated cases.

Early Onset PD. The cases of genetic early-onset Parkinson's disease have most often been detected in specific family groups.

Defective genes that regulate the molecules alpha synuclein and parkin, which are important in the PD disease process, may be responsible for a number of early-onset cases. For example, genetic abnormalities the alpha synuclein protein have been detected in some early-onset Parkinson's patients of European descent.
The parkin gene may be the cause of many cases of early-onset Parkinson's in young adults. (Parkinson's cases associated with this mutation tend to progress slowly and respond well to treatment, even after years of symptoms. Dementia is also rare with this form.)

Late Onset PD. Two landmark studies published in the Journal of the American Medical Association provided the first evidence of a genetic link to late-onset Parkinson’s disease. In these 2001 studies, researchers found that regions on chromosomes 5, 6, 8, 9, and 17 were implicated with Parkinson’s. The parkin gene (located on chromosome 6) and the tau gene (located on chromosome 17) were both found in families that had late onset Parkinson’s. Parkin was previously thought to be responsible only for early-onset Parkinson’s, but this research identified it in families that had both early- and late-onset disease forms. These studies also bolstered the theory that Parkinson’s does have a genetic component and is not caused solely by environmental factors. A 2005 study found that a G2019S mutation in the LRRK gene, located on the PARK8 region of chromosome 12, was definitively associated with late-onset Parkinson’s disease in North American and European families.

Environmental toxins, infections, and other triggers can provoke excessive production in the body of oxygen free-radicals, damaging particles that may play a major role in the deterioration of nerve cells that lead to Parkinson's.

Infectious Organisms. Some research has identified immune factors that suggest a viral presence in the Lewy bodies and swollen nerve pathways of Parkinson's brains. Influenza and other potent viruses have long been known to be a cause of parkinsonism. In one well-known example, a major flu epidemic causing encephalitis in the early twentieth century left many of its victims with parkinsonism.

Environmental and Industrial Chemicals. Intense exposure to certain environmental and industrial chemicals is also being studied.

Pesticides and Herbicides. Some evidence implicates pesticides and herbicides as important factors in many cases of Parkinson's disease. A higher incidence of parkinsonism has long been noted in people who live in rural areas, particularly those who drink private well water or are agricultural workers. A large 2000 study found a strong link between high exposure to insecticides and herbicides at home and a 50 - 70% increase in risk of Parkinson's.
Other Chemicals. Intense exposure to other industrial chemicals and metals (manganese, copper, lead, iron, mercury, zinc, aluminum, and others) has also been linked with parkinsonism, a cause that is often reversible. The role of long-term exposure in the development of Parkinson's disease is unclear. High levels of iron content observed in critical parts of the brain in PD are under particular scrutiny.

Most, but not all, Parkinson's victims are elderly. Some studies indicate that the very elderly are not susceptible to the disease, indicating that the aging process itself is not the major player in the disease. Aging does appear to reduce the concentration of dopamine in structures called dopamine transporters, which carry the neurotransmitter back and forth between nerve cells. Some researchers posit that any excessive stress on these transporters might trigger Parkinson's disease in the aging, and more vulnerable, brain.

Symptoms

Parkinson's disease (PD) symptoms often start with tremor, which may occur in the following ways:

Tremors may first be only occasional, starting in one finger and spreading over time to involve the whole arm. The tremor is often rhythmic, 4 - 5 cycles per second, and frequently causes an action of the thumb and fingers known as pill rolling.
Tremors can occur when the limb is at rest or when it is held up in a stiff unsupported position. They usually disappear briefly during movement and do not occur during sleep.
Tremors can also eventually occur in the head, lips, tongue, and feet. Symptoms can occur on one or both sides of the body. In one study, 44% of patients reported experiencing internal tremors lasting less than half an hour, but occurring several times a week.

In younger patients tremor is usually predominant and often suggests a less aggressive form of the disease. Some evidence suggests that tremor in PD may occur from mechanisms in the brain that are different from those that cause other PD symptoms.

A number of PD symptoms involve motor impairment caused by the abnormalities in the brain that regulate movement:

Slowness of motion (bradykinesia) is one of the classic symptoms of Parkinson's disease. Patients may eventually develop a stooped posture and a slow, shuffling walk. The gait can be erratic and unsteady. After a number of years, muscles may freeze up or stall, usually when a patient is making a turn or passing through narrow spaces, such as a doorway.
Intestinal motility (the ability to swallow, digest, and eliminate) may slow down, causing eating problems and constipation.
Muscles may become rigid (akinesia). This symptom often begins in the legs and neck. Muscle rigidity in the face can produce a mask-like, staring appearance.
Motor abnormalities that limit action in the hand may develop in late stages. Handwriting, for instance, often becomes diminutive.
Normally spontaneous muscle movements, such as blinking, may need to be done consciously.

The traditional view of Parkinson's disease is shifting to reflect growing awareness that it is much more than a motor disease. Many non-motor components and their treatments are now under study. The following symptoms should be carefully monitored by doctors and caregivers:

Depression is the most common psychiatric problem associated with PD, affecting about 40% of patients. Because depression is a common problem in older people, it is likely not to be recognized as a symptom.
Anxiety affects about 30% of patients.
Dementia and paranoia are more common than previously understood.
Orthostatic hypotension -- some patients experience a sudden drop in blood pressure when they stand. This can cause dizziness and fainting.
Changes in sensations of temperature, hot flashes, and excessive sweating.
Daytime sleepiness and other sleep disorders are common.

Risk Factors

Parkinson's disease affects about 3% of Americans over 65 years old. Experts estimate that this percentage could double in the next 30 - 40 years. The symptoms of parkinsonism (tremor, gait disturbance, bradykinesia, and rigidity) occur in even more people, estimated to be 8 million over age 65. In a study that included very mild symptoms, parkinsonism occurred in about 15% of people 65 - 74 years of age, about 30% in those 75 - 84, and over half of people older than age 85.

The average age of onset of Parkinson's disease is 55. About 10% of Parkinson's cases are in people younger than 40 years old. Older adults are at higher risk for both parkinsonism and Parkinson's disease. There is some evidence, however, that the risk declines significantly after age 75 and that the very elderly are at low risk.

Some research indicates that men may face up to twice the risk as women. Estrogen may offer some protection for women up until menopause. A 2001 study, for example, reported a higher rate of Parkinson's disease in women who had undergone hysterectomy. Other studies suggest that the disease also progresses more rapidly in men than women. Older women seem to be more at risk for gait disturbance and men for rigidity and tremor.

People with siblings or parents who developed Parkinson's at a younger age are at higher risk for Parkinson's disease, but relatives of those who were elderly when they had the disease appear to have an average risk.

African- and Asian-Americans have a lower risk than Caucasians. Some evidence suggests that non-Caucasians may be more vulnerable to an atypical form of PD, which causes early impairment in thinking and has a poor response to levodopa, the primary PD treatment.

Increasing weight gain in middle age was associated with a higher risk of PD in a 2002 study.

Complications

Parkinson's disease (PD) is not fatal, but it can reduce longevity. The disease progresses more quickly in older than younger patients, and may lead to severe incapacity within 10 - 20 years. Older patients also tend to experience freezing and greater declines in mental function and daily functioning than younger people. If PD starts without signs of tremor, it is likely to be more severe than if tremor had been present. Having other family members with PD does not appear to have any effect on the severity of the disease.

Parkinson's disease can seriously impair the quality of life in any age group. The physical and emotional impact on the family should not be underestimated as the patient becomes increasingly dependent on their support.

Treatment advances are increasingly effective in alleviating symptoms and even slowing progression of the disease. Taking many of the medications over time, however, can produce significant side effects. Newer drugs may help reduce these occurrences.

The negative effect of overall motor and muscle impairment on daily life can be considerable. Some motor complications can be life-threatening.

Disturbed gait and unstable posture are common and serious problems in elderly patients, since they increase the risk for falling and injury. Some studies have suggested that the appearance of these symptoms early in the course of the disease predict a faster decline than having tremor as the predominant symptom.
Swallowing problems (dysphagia). The presence of dysphagia is associated with shorter survival time. Motor impairment of the muscles in the throat not only impairs swallowing but it also poses a risk for aspiration pneumonia.
Constipation is a major problem and occurs both as a result of the disease and a side effect of its treatment. Laxatives, stool softeners, and other medications may be prescribed.
Bladder control and urinary incontinence are also important complications of PD.
Speech problems occur in more than 70% of patients, by some estimates. Speech difficulty can be caused by rigidity of the facial muscles, loss of motor control, and impaired breath control. Tone can become monotonous, words may be repeated over and over, or the rate of speech may even be very fast.

Depression is extremely common, affecting up to 40% of patients with Parkinson's. PD poses multiple threats on the emotional health:

The disease process itself causes changes in chemicals in the brain that affect mood and well-being.
The complications of its symptoms have a profound impact on daily life that can be emotionally devastating without help and support.
Some drug treatments (levodopa combined with a dopamine agonist) can cause compulsive behavior, such as gambling, shopping, and increased sexuality. Patients who have pre-existing tendencies to novelty-seeking behavior, or a family or personal history of alcohol abuse, may be more likely to develop compulsive gambling. Deep brain stimulus (DBS) surgery may also increase the risk for compulsive gambling in patients who have a history of gambling.

Impaired Thinking (Cognitive Impairment). Defects in thinking, memory, language, and problem solving skills may occur early on in untreated patients or late in the course of the disease. Medications may play a role in thinking problems. In one study, for example, patients with PD were slower in detecting associations, although (unlike in Alzheimer's disease) once they discovered them they were able to apply this knowledge to other concepts. After they were taken off medication, however, they had no problems with the tasks.

Dementia. Dementia is three to six times more common in the elderly Parkinson patient than in the average older adult. It is most likely to occur in older patients who have had major depression. PD marked by muscle rigidity (akinesia), rather than tremor, and early hallucinations also increase the risk for dementia. (Visual hallucinations can also occur in about a third of patients from PD medication.) Unlike in Alzheimer's, language is not usually affected in Parkinson's related dementia.

A number of other problems associated with Parkinson's disease affect daily life:

Vision Problems. Vision is also affected, including impaired color perception and contrast sensitivity. These problems progress and can impair motor functioning.

Sleep Disorders. Excessive daytime sleepiness and other sleep disorders are common in PD, both from the disease itself and from the drugs that treat it. In general, patients have a 25% higher risk for daytime sleepiness, including suddenly falling asleep, than patients with other neurologic diseases.

Restless legs syndrome, an irresistible urge to move the calves, which often occurs at night, affects many patients. However, Parkinson's disease itself does not seem to increase the risk for RLS. Nor does RLS early in life predispose to Parkinson's later on. The common connection between RLS and Parkinson's disease may derive from iron deficiencies that can play a role in both conditions.

Many patients also suffer from nighttime leg cramps. And, some of the medications cause vivid dreams as well as waking hallucinations.

Impaired Sexuality. Although Parkinson's disease and its treatments can cause compulsive sexual behavior, the disease can also affect patients' self-esteem and inhibit sexuality. This is an area not often studied but which is important for many patients' well-being. A 2000 study reported that not only did sexual dysfunction occur, but also affectionate touching and expression of feelings were reduced, even though both partners maintained a desire for intimacy.

Worsened Sense of Smell. The sense of smell is impaired in about 70% of patients.

Osteoporosis. Parkinson’s disease may increase the risk for low bone density and osteoporosis. Both men and women are at risk. Experts recommend that patients with Parkinson’s disease get tested for osteoporosis, especially if they have problems with walking.

Diagnosis

It is difficult to diagnose Parkinson's in early stages. The disease is primarily diagnosed by its symptoms, and studies indicate that doctors make an incorrect initial diagnosis of Parkinson's disease in 8 - 35% of cases. Even neurologists have difficulties in correctly identifying the disease.

A medical and personal history should include any relevant symptoms as well as any medications taken, and information on exposure to environmental toxins.

Early Symptoms. Early treatment may help slow progression, so an early diagnosis of Parkinson's is highly desirable. Early symptoms are often mild, however, so Parkinson's disease can be missed, particularly in young adults. Repeated assessment of symptoms over time is important for improving the accuracy of diagnosis. Too often a younger person with Parkinson's may be diagnosed with mental illness, because the doctor associates the disease only with older people.

Parkinson's may be suspected in patients with the following symptoms:

Slowness and difficulty of movement. These are usually the first symptoms. The patient will be asked to walk and to get out of a chair, preferably a deep one. Early gait disturbance, however, often indicates a disease other than Parkinson's disease.
A tremor when their limb is relaxed. (As many as 25% of patients, however, will not have a tremor.)
Symptoms on one side of the body.

Later Symptoms. In later stages of Parkinson's disease, the symptoms are usually unmistakable, and the problem can often be diagnosed using simple physical tests and a medical and personal history.

The loss of smell is associated with loss of dopamine receptors in the brain. “Scratch and sniff” smell tests can help a doctor diagnose Parkinson’s disease. Smell tests can help differentiate Parkinson’s disease from other conditions with similar symptoms. Some patients with a very similar condition called multiple system atrophy will have a good initial response to levodopa, but it is not usually sustained.

Levodopa and apomorphine can confirm a diagnosis of Parkinson’s disease. If patients’ symptoms improve when they take these drugs, they likely have Parkinson’s, ruling out other neurological diseases.

According to 2006 guidelines from the American Academy of Neurology, there is not enough evidence to recommend for or against the use of imaging techniques such as computerized tomography (CT), magnetic resonance imaging (MRI), or positron-emission tomographic (PET) to diagnose PD.

When symptoms resemble Parkinson's disease but have an identifiable cause, the syndrome is known as parkinsonism. People who have parkinsonism, but not Parkinson's disease, often have additional neurologic symptoms. A number of conditions can also have similar or some of these symptoms.

Other Neurologic Conditions. Many medical conditions may cause symptoms of Parkinson's disease:

Hardening of the arteries (arteriosclerosis) in the brain can cause multiple small strokes, which can produce loss of motor control.

Click the icon to see an image of plaque in an artery.

Alzheimer's disease can be very similar. In one study 23% of people with Alzheimer's also met the criteria for Parkinson's disease. The two diseases often coexist, and research suggests that Alzheimer's and Parkinson's disease may sometimes share a common biologic origin, the accumulation of the protein alpha synuclein and Lewy bodies in the brain.
Lewy bodies variant (LBV), also called dementia with Lewy bodies, is a separate disease from both Alzheimer's and Parkinson's disease. It has similar symptoms to both but is marked by early dementia.
Encephalitis caused by influenza has been known to cause parkinsonism.
Primary progressive freezing gait is a progression condition, in which freezing gait occurs at the onset. Other Parkinson-like features, such as slow movement, often develop. Although very similar to PD, this condition does not respond to L-dopa or other PD medications.
Essential tremor, unlike the tremor of Parkinson's disease, often occurs in the head and voice and is usually worse during motion, as opposed to rest.
Progressive supranuclear palsy has similar symptoms, but involves less tremor and earlier rigidity, and it tends to affect both sides of the body symmetrically. Magnetic resonance imaging scans that measure parts of the midbrain may be a reliable method for distinguishing between PD and progressive supranuclear palsy.
Multiple system atrophy (previously called Shy-Drager syndrome) is a degenerative nerve disease that also affects movement and blood pressure and has many of the symptoms of Parkinson's disease. Some research suggests that a trial using the drug apomorphine may help differentiate between the two.
Other problems that may mimic Parkinson's disease include Wilson's disease, thyroid abnormalities, hydrocephalus, tumors, having the fragile X trait (but not the full disorder), and a number of degenerative neurologic diseases.

Drugs. Certain drugs or medications account for about 4% of all cases of parkinsonism. According to some studies, patients who experience drug-induced parkinsonism may actually be at an increased risk of developing Parkinson's disease later in life. A number of drugs can cause these symptoms, including antipsychotic and antiseizure drugs. Anyone with parkinsonism should discuss their medications with their doctor.

The American Academy of Neurology (AAN) recommends the Beck Depression Inventory or the Hamilton Depression Rating Scale to screen for depression in patients with Parkinson’s disease. The AAN recommends the MMSE and CAMCOG tests to screen for dementia. During these tests, the patient answers a series of questions.

Treatment

Drugs, physical therapy, and surgical interventions can manage Parkinson's disease. The goals of treatment for Parkinson's disease are to:

Relieve disabilities
Balance the problems of the disease with the side effects of the medications

Treatment is very individualized for this complicated disease. Patients must work closely with doctors and therapists throughout the course of the disease to customize a program suitable for their particular and changing needs. Patients should never change their medications without consulting their doctor, and they should never stop taking their medications abruptly.

The American Academy of Neurology recommends the following therapies for the initial treatment of Parkinson’s disease:

Levodopa (L-dopa). Levodopa, or L-dopa, has been used for years and is the gold standard for treating Parkinson's disease. The drug increases brain levels of dopamine. It is used in nearly all phases of the disease. The standard preparations (Sinemet, Atamet) combine levodopa with carbidopa, a drug that slows the breakdown of levodopa. Levodopa is better at improving motor problems than dopamine agonists but increases the risk of involuntary movements (dyskinesia).

Dopamine Agonists. Dopamine agonist drugs mimic dopamine to stimulate the dopamine system in the brain. These drugs include pramipexole (Mirapex), ropinirole (Requip), bromocriptine (Parlodel), and rotigotine (Neupro). The Food and Drug Administration (FDA) pulled the dopamine agonist pergolide (Permax) from the market in March 2007 over safety concerns that included potentially fatal heart valve damage.

Selegiline (Eldepryl) and rasagiline (Azilect). Selegiline is a monoamine oxidase B (MAO-B) inhibitor that may have some mild benefit as an initial therapy. However, unlike levodopa, it does not slow the progression of Parkinson’s disease. Another MAO-B inhibitor, rasagiline (Azilect), was approved in May 2006. Unlike selegiline, which needs to be taken by mouth twice a day, rasagiline needs to be taken only once a day.

Drug treatments for Parkinson disease do not consistently control symptoms. At certain points during the day, the beneficial effects of drugs wear off, and patients can experience a return of symptoms, such as uncontrolled muscular motor function, difficulty walking, and loss of energy. In 2006, the American Academy of Neurology (AAN) reviewed evidence for the various drugs used to treat “off time.” The AAN found that the following drugs had the strongest evidence for controlling off time symptoms:

Entacapone (Comtan) belongs to a class of drugs called catechol-o-methyl transferase (COMT) inhibitors. COMT inhibitors help prolong the effects of levodopa by blocking an enzyme that breaks down dopamine.
Rasagiline (Azilect) belongs to a class of drugs called monoamine oxidase (MAO) inhibitors. These drugs slow the breakdown of dopamine that occurs naturally in the brain and dopamine produced from levodopa.

The AAN also found good evidence for the dopamine agonists ropinirole (Requip) and pramipexole (Mirapex), and the COMT inhibitor tolcapone (Tasmar). Deep brain stimulation is a surgical treatment that may help improve motor fluctuations in some patients.

Both Levodopa and dopamine agonists can cause involuntary movements (dyskinesia). The AAN has not found any strong evidence to recommend any drug for treating dyskinesia. However, weak evidence suggests that the antiviral drug amantadine (Symmetrel) may help reduce stiffness and improve dyskinesia. There is also weak evidence that deep brain stimulation of the subthalamus area may be helpful.

Conditions associated with motor impairment and other symptoms of Parkinson's disease may require a variety of treatments.

Depression. Although depression is very common in PD, there have been surprisingly few controlled studies. Antidepressants used for PD include tricyclics, particularly amitriptyline (Elavil). Some studies have found that selective serotonin-reuptake inhibitors (SSRIs) -- which include fluoxetine (Prozac), sertraline (Zoloft), and paroxetine (Paxil) -- may worsen symptoms of Parkinson's. Doctors should monitor patients taking SSRIs.

Psychotic Side Effects. Studies indicate that clozapine (Clozaril) and quetiapine (Seroquel), antipsychotic drugs used to treat schizophrenia, may be the best drugs for treating psychosis in patients with Parkinson's disease. A similar drug, olanzapine (Zyprexa), should not be used for patients with PD because it can worsen their psychotic symptoms.

Dementia. The cholinesterase inhibitor drugs donepezil (Aricept) and rivastigmine (Exelon) are used to treat Alzheimer’s disease. Studies suggest that these drugs may also help treat dementia associated with Parkinson’s disease. In 2006, rivastigimine was approved for treatment of mild-to-moderate dementia associated with Parkinson’s disease.

Daytime Sleepiness. Modafinil (Provigil), a drug used to treat narcolepsy, is proving to be very helpful for patients with sleepiness related to their disease.

Drooling. In search of a simple solution for the problem of drooling, scientists have reported that injections of very small amounts of botulinum toxin effectively reduce saliva production and drooling. In such small amounts the toxin is safe.

Voice Loss. A relatively simple procedure using collagen injections in the neck appears to be a safe and effective method of improving the voice and speech disorders caused by PD. The procedure augments the collagen in the vocal fold and works best in patients who can still initiate speech. A 2001 study reported improvements that lasted from 2 - 7 months in 61% of patients.

Erectile Dysfunction. Sildenafil (Viagra) is proving to be very helpful for men who suffer from impotence from Parkinson's disease. However, the drug may worsen orthostatic hypotension, a side effect of some PD medications.

Eventually, symptoms such as stooped posture, freezing, and speech difficulties may not respond to drug treatment. (Total unresponsiveness is unlikely, however, even after 20 years of treatment.) The following approaches may be tried:

Simply increasing the dose of levodopa or its frequency raises an unacceptable risk of the distressing side effects. Some doctors have tried hospitalizing patients, totally withdrawing the levodopa, and then re-administering it. Benefits were seen for only a few months, however, and there were some dangerous risks to the process of withdrawal, including pneumonia and blood clots in the lungs.

An embolus is a blockage of an artery in the lungs by fat, air, tumor tissue, or blood clot.

Surgical treatments, including deep brain stimulation and pallidotomy, may help some patients.
Research is ongoing to develop drugs and procedures that will manage advanced disease and possibly even reverse the process.

Levadopa (L-dopa)

Levodopa, also called L-dopa, which is converted to dopamine in the brain, remains the gold standard for treating Parkinson's disease. The standard preparations (Sinemet, Atamet) combine levodopa with carbidopa, which improves the action of levodopa and reduces some of its side effects, particularly nausea. Levodopa can also be combined with benserazide (Madopar) with similar results, but Sinemet is almost always used in America. Dosages vary, although the preparation is usually taken in three or four divided doses per day. In 2004, the FDA approved a new oral form of carbidopa-levodopa (Parcopa) that dissolves on the tongue.

In general L-dopa has the following effects on Parkinson's disease:

It is most effective against rigidity and slowness.
It produces less benefit for tremor, balance, and gait.

In many patients, levodopa significantly improves the quality of life for many years. If symptoms do not improve after 2 - 3 months, one of the following reasons may account for the failure:

Other neurologic problems may be causing the symptoms.
Some patients have abnormalities in other brain sites that do not respond to L-dopa.
Sometimes patients are so depressed they cannot tell if the drug is beneficial or not. Only a series of physical examinations by the doctor will indicate that the drug is actually helping.

Studies suggest that levodopa may help slow disease progression and protect against brain cell degeneration.

The toxic effects of levodopa with or without carbidopa are considerable.

Physical Side Effects. The physical side effects are as follows:

Low blood pressure. Low blood pressure is a common problem during the first few weeks, particularly if the initial dose is too high. The addition of extra supplements of carbidopa reduces this effect to some degree. The patient should drink lots of fluids and possibly increase salt intake to maintain normal blood pressure.
Arrhythmia. In some cases the drug may cause abnormal heart rhythms.
Gastrointestinal effects. Stomach and intestinal side effects are common even with carbidopa. Taking the drug with food can alleviate the nausea. However, proteins interfere with intestinal absorption of levodopa, and some doctors recommend not eating any protein until nighttime in order to avoid this interference. The drug can also cause gastrointestinal bleeding.
Effects in the lung. Levodopa can cause disturbances in breathing function, although it may benefit patients who have upper airway obstruction.
Hair loss.

Psychiatric and Mental Side Effects. The major adverse effects of the drug are psychiatric. Patients taking levodopa, especially in combination with other drugs, can experience:

Confusion.
Extreme emotional states, particularly anxiety.
Vivid dreams.
Visual and possibly auditory hallucinations. The drug may even unmask dementia that had not been previously noticed.
Effects on learning. L-dopa appears to have mixed effects on learning. It may improve working memory. However, some evidence suggests that it impairs areas of the brain related to other learning functions and social behavior.
Sleepiness and sleep attacks.

Levodopa causes fewer psychiatric side effects than other drugs used for Parkinson's disease, including anticholinergics, selegiline, amantadine, and dopamine agonists. Because psychiatric side effects often occur at night, if they are severe some doctors recommend reducing or stopping the evening dose.

Within 4 - 6 years of treatment with levodopa, the effects of the drug in many patients begin to last for shorter periods of time (called the wearing-off effect) and the following pattern may occur:

Patients may first notice slowness (bradykinesia) or tremor in the morning before the next dose is due.
Less commonly, some experience painful dystonia, muscle spasms that can cause sustained contortions of various parts of the body, particularly the neck, jaw, trunk, and eyes and possibly the feet.
Patients must increase the frequency of levodopa doses. This puts them at risk for dyskinesia (the inability to control muscles), which usually occurs when the drug level peaks. Dyskinesia can take many forms, most often uncontrolled flailing of the arms and legs or chorea, rapid and repetitive motions that can affect the limbs, face, tongue, mouth, and neck. Dyskinesia is not painful, but it is very distressing.
In some people, eventually L-dopa is effective only for 1 - 2 hours and most patients start to experience motor fluctuations. In about 15 - 20% of patients such fluctuations become extreme, a phenomenon known as the on-off effect, which consists of unpredictable, alternating periods of dyskinesia and immobility. Sometimes the symptoms switch back in forth within minutes or even seconds. (The transition may follow such symptoms as intense anxiety, sweating, and rapid heartbeats.)

Reasons for the Wearing-Off Effect. Debate is ongoing about the cause of the wearing-off effect and dyskinesia. Some theories suggested for these effects are:

The disease progresses beyond the ability of levodopa to control it.
Some patients become tolerant to prolonged exposure to dopamine and, at the same time, the disease is progressing.
The brain's own dopamine neurons become incapable of storing dopamine. When the levodopa wears off, little or no natural dopamine remains.
Levodopa itself accelerates the disease by producing oxygen free radicals, unstable particles that increase injuries to the brain and dopamine degradation.

Preventing the Wearing-Off Effect. To reduce the effects of fluctuation and the wearing-off effect, it is important to maintain as consistent a level of dopamine as possible. Unfortunately, levodopa is poorly absorbed and may remain in the stomach a long time. A number of strategies are being developed to take care of these problems:

Some patients take multiple small doses on an empty stomach, crushing the pills and mixing them with a lot of liquid.
A liquid form of Sinemet may produce fewer fluctuations and a prolonged "on" time compared with the tablet.
A prolonged release version of levodopa and carbidopa (Sinemet CR) is also available to control fluctuations for some people. (Some evidence suggests that there is no actual difference in symptom control between the sustained and immediate release forms, but patients on Sinemet CR tend to experience a better quality of life.)

Other Medications

Selegiline (Eldepryl, Movergan, Zelepar), also known as deprenyl, is an antioxidant drug that blocks monoamine oxidase B (MAO-B), an enzyme that degrades dopamine. Until recently, selegiline was the drug most commonly used in early-onset disease and in combination with levodopa for maintenance. A major 2002 study reported, however, that although selegiline delays the need for L-dopa by a few months, it has no effect on long-term progression.

Rasagiline (Azilect), another MAO-B inhibitor, was approved in May 2006 for the initial treatment of Parkinson’s disease. It is used alone during early-stage PD and in combination with L-dopa for moderate-to-advanced PD. Unlike selegiline, which is taken twice a day, rasagiline is taken once a day.

Other Adverse Effects. MAO-B inhibitors may have severe side effects:

One of the most important side effects is orthostatic hypotension, particularly in people taking Sinemet plus selegiline. This condition is a sudden drop in blood pressure that causes dizziness and lightheadedness when a patient stands up. Orthostatic hypotension can also occur with other Parkinson's drugs.
Can cause high blood pressure (hypertension) if combined with drugs that increase serotonin levels -- such drugs include nearly every major antidepressant. Patients suffering from depression and taking selegiline should discuss all treatment options with their doctor.
Can also cause a dangerous increase in blood pressure if patients eat foods rich in the amino acid tyramine. Patients should avoid the following foods while taking selegiline or rasagiline and for 2 weeks after stopping medication: aged cheeses, air-dried meats, pickled herring, yeast extract, aged red wines, draft beers, sauerkraut, and soy sauce

Debate over Mortality Rates. Some major studies have reported higher mortality rates in patients with advanced PD. Such findings may be due to adverse effects on the heart and blood vessels. Although other studies have not reported lower survival rates, some experts believe that, given its modest effects, selegiline may be a poorer drug choice than others, particularly in patients with risk factors for heart disease.

Dopamine agonists stimulate dopamine receptors in the substantia nigra, the part of the brain in which Parkinson's is thought to originate. Dopamine agonists are effective in delaying motor complications during the first 1 or 2 years of treatment.

Newer Dopamine Agonists. The most commonly prescribed dopamine agonists are pramipexole (Mirapex) and ropinirole (Requip). They are used either alone or in combination with L-dopa. Pramipexole appears to work better and have fewer side effects than ropinirole.

Studies still report, however, that L-dopa is superior for improving motor function. In one study, motor function was no different in disease progression among all of the drugs by the third year of treatment. Recent research suggests that L-dopa is better at improving motor disability and dopamine agonists are better at reducing motor complications. L-dopa has a higher risk for dyskinesia side effects than dopamine agonists, but dyskinesia can also occur with dopamine agonists.

Side Effects. Side effects of pramipexole and ropinirole vary but can be severe and include:

Gastrointestinal side effects (nausea and constipation). Nausea can be controlled by drugs, such as domperidone.
Headache
Orthostatic hypotension (sudden drop in blood pressure upon standing up)
Nasal congestion
Nightmares, hallucinations, and psychosis (more severe than with L-dopa for both drugs)
Sudden sleep attacks. These can be very serious, particularly if patients are driving. (Sleep attacks may occur -- although less commonly -- with other PD drugs.)

Other Dopamine Agonists.

Specific dopamine agonists that contain ergot alkaloids include bromocriptine (Parodel), pergolide (Permax), cabergoline (Dostinex), and lisuride (Dopergin). As of 2007, bromocriptine is the only ergot dopamine agonist approved for Parkinson’s treatment in the United States. In January 2007, the New England Journal of Medicine (NEJM) published two studies indicating that pergolide and cabergoline are associated with heart valve damage. In March 2007, due to these safety concerns, the FDA withdrew pergolide from the U.S. market. Cabergoline and lisuride are not approved in the U.S. for Parkinson’s disease treatment but are used for this purpose in other countries. The NEJM studies did not find any heart valve problems associated with bromocriptine or lisuride.
Rotigotine transdermal (Neupro) is a dopamine agonist that is delivered through a skin patch that is changed daily. In 2007, the FDA approved rotigotine transdermal for treatment of symptoms of early Parkinson’s disease. It is the first skin patch approved for Parkinson’s disease. Side effects are similar to those of other dopamine agonists.
Apomorphine is a dopamine agonist used as a "rescue" drug in people experiencing on-off effects severe enough to require going off L-dopa for a few days. In 2004, the FDA approved apomorphine for treating off-time episodes of Parkinson’s disease. Apomorphine is given by injection. Because it causes severe nausea and vomiting, it must be taken with an anti-nausea drug.

Catechol-O-methyl transferase (COMT) inhibitors increase concentrations of existing dopamine in the brain. Entacapone (Comtan, Stalevo) is the current standard COMT inhibitor. (Stalevo combines entacapone and levodopa into a single pill.) It improves motor fluctuations related to the wearing-off effect and has shown good results in improving on time and reducing the requirements for L-dopa. If the patient does not respond to the drug within 3 weeks, it should be withdrawn. No one should withdraw abruptly from these drugs.

Side Effects. Side effects include:

Involuntary muscle movements
Mental confusion and hallucinations
Cramps, nausea, and vomiting
Insomnia
Headache
Urine discoloration (a harmless side effect but should be reported to the doctor)
Diarrhea
Less commonly, constipation, susceptibility to respiratory infection, sweating, dry mouth

Of major concern are reports of a few deaths from liver damage in patients taking the COMT inhibitor tolcapone (Tasmar). The drug has been taken off the market in many countries and is recommended in the U.S. only for patients who cannot tolerate another other drugs. Entacapone does not appear to have the same effects on the liver and does not require monitoring. A 2003 3-year study suggested that the drug is safe and effective over the long term. Still, patients should watch out for symptoms of liver damage, including jaundice (yellowish skin), fatigue, and loss of appetite.

Jaundice is a condition produced when excess amounts of bilirubin circulating in the bloodstream dissolve in the subcutaneous fat (the layer of fat just beneath the skin), causing a yellowish appearance of the skin and the whites of the eyes. With the exception of normal newborn jaundice in the first week of life, all other jaundice indicates overload or damage to the liver, or inability to move bilirubin from the liver through the biliary tract to the gut.

Anticholinergics were the first drugs used for PD, but have largely been replaced by dopamine drugs. They are generally used only against tremor in the early stages. They are not as effective against bradykinesia and posture problems and may increase the risk for dementia in late stages. Among the many anticholinergics are trihexyphenidyl (Artane, Trihexy), benztropine (Cogentin), biperiden (Akineton), procyclidine (Kemadrin), and ethopropazine (Parisdol). Orphenadrine (Norflex) is a drug with anticholinergic properties, but is also a muscle relaxant and does not cause urinary retention.

Side effects of Anticholinergics. Anticholinergics commonly cause dryness of the mouth (which can actually be an advantage in some people who experience drooling). Other side effects are nausea, urinary retention, blurred vision, and constipation. These drugs can also increase heart rate and worsen constipation. Anticholinergics can sometimes cause significant mental problems, including memory loss, confusion, and even hallucinations. People with glaucoma should use these drugs cautiously.

Amantadine (Symadine, Symmetrel) stimulates the release of dopamine and may be used for patients with early mild symptoms. It has some benefit against muscle rigidity and slowness and may help some patients in advanced stages who are unresponsive to other drugs. It is less powerful than levodopa and may lose its effectiveness after 6 months. It may also reduce motor fluctuations brought on by levodopa, however, and these benefits appear to persist for at least a year. Large, well-conducted studies are still needed to determine its true benefits and safety.

Side Effects. Side effects are similar to those of anticholinergic drugs and also may include swollen ankles and mottled skin. It can also cause visual hallucinations. Overdose can cause serious and even life-threatening toxicity. Patients with Parkinson's should not withdraw from this drug abruptly. In rare instances, it can cause acute delirium or a life-threatening condition called neuroleptic malignant syndrome. Pregnant or nursing women should not use this drug.

Anticonvulsants. Zonisamide (Zonegran), a drug used to treat epilepsy, is showing promise in treating tremors, motor problems, and involuntary movements in patients with Parkinson’s disease.

Budipine and Other Glutamate Blockers. A number of experimental drugs are being investigated for Parkinson's disease because they block the actions of glutamate, an amino acid that is a particularly potent nerve cell killer. Some of these drugs block a receptor group to glutamate called N-methyl-D-aspartate (NMDA). Investigational NMDA antagonists include remacemide, memantine, riluzole, and budipine.

Stem Cell Transplantation. Scientists are investigating whether transplanting embryonic stem cells into the brain may help treat Parkinson’s disease. Researchers hope that the transplanted stem cells may be able to stimulate dopamine production. However, stem cell transplantation research is still in its very early stage. It will be many years before clinical trials will be conducted in humans.

Surgery

Surgical procedures are recommended for specific patients with advanced Parkinson’s disease who no longer respond to drug treatments. Surgical treatment cannot cure Parkinson's disease, but it may help control symptoms such as motor fluctuations and dyskinesia. Pallidotomy and thalamotomy are older procedures that destroy tissue in certain parts of the brain. Deep brain stimulation, the current standard surgical practice for Parkinson’s disease, has largely replaced the older operations.

In deep brain stimulation (DBS), also called neurostimulation, an electric pulse generator controls symptoms. The generator is similar to a heart pacemaker. It sends electrical pulses to specific regions of the brain. Candidates for surgery are generally patients who have responded well to levodopa drug treatment. Patients who have had PD for fewer than 16 years may experience greater benefit from DBS than patients who have had the disease longer.

Evidence indicates that DBS improves motor function and reduces dyskinesia best when the procedure targets the subthalamic nucleus (STN) of the brain. Many studies demonstrate the effectiveness of STN stimulation. Procedures that target the globus pallidus interna or ventral intermediate nucleus of the thalamus can also sometimes treat rigidity and tremors. However, there is not yet enough evidence to support stimulation of these parts of the brain.

The procedure is performed as follows:

The surgeon implants a tiny pulse generator near the collarbone, which is connected to four electrodes that have been implanted in the target area in the brain.
The generator delivers programmed pulses to this area, which the patient can turn on and off using a magnet held over the skin.
When on, the pulses suppress symptoms. Complications occur in 2 - 4% of operations. The most serious ones are bleeding in the brain and infection. Depression is common.

In a 2006 study of patients with advanced Parkinson’s disease and severe motor symptoms, patients who received DBS had better improvement in symptoms and quality of life than those who received only drug therapy. However, patients in the neurostimulation group had more serious side effects than those who were treated only with medications. Researchers are also studying whether DBS can benefit patients with earlier-stage Parkinson’s disease.

Pallidotomy and thalamotomy are surgical procedures that destroy brain tissue in regions of the brain associated with Parkinson’s symptoms such as dyskinesia, rigidity, and tremor. In these procedures, a surgeon drills a small hole in the patient’s skull and inserts an electrode to destroy brain tissue. Pallidotomy targets the global pallidus area. Thalamotomy targets the thalamus. Because these procedures permanently eliminate brain tissue, most experts now recommend deep brain stimulation instead of pallidotomy or thalamotomy.

Surgical complications may include behavioral or personality changes, trouble speaking and swallowing, facial paralysis, and vision problems. Weight gain after surgery is also common.

Scientists are investigating whether stem cells may eventually help treat Parkinson disease. Experimental surgery has shown promise using fetal brain cells rich in dopamine implanted in the substantia nigra area of the brain. Because the use of embryonic stem cells is controversial, researchers are studying alternative types of cells, including stem cells from adult brains and cells from human placentas or umbilical cords. Studies are also using gene therapies and other advanced treatments for transplanting dopamine-producing cells or nerve-protecting cells into the brain. All of this research is still in preliminary stages.

Lifestyle Changes

No special diets or natural foods have been shown to slow down the progression of Parkinson's disease, but there are some dietary recommendations.

Protein. High levels of proteins compete with levodopa for transport to the brain and reduce its effectiveness. Avoiding protein altogether is not the solution, since malnutrition can result. Most experts now recommend trying to maintain a carbohydrate-to-protein ratio of 7:1 throughout the day. This may be difficult to calculate and some doctors recommend simply keeping proteins to 12% of total daily calories.

As an aid in calculation, food labels indicate proteins in grams. One gram of protein equals four calories. Good control of protein intake may help minimize fluctuations and wearing-off and may allow some patients to reduce their daily levodopa dosage.

Fruits and Vegetables and Increasing Fiber. Eating whole grains, fresh fruits, and vegetables is the best approach for any healthy life. A diet rich in fruits and vegetables may help protect nerve cell function. Many of these foods are also often rich in fiber, which is particularly important for helping to prevent constipation.

Dietary fiber is the part of food that is not affected by the digestive process in the body. Only a small amount of fiber is metabolized in the stomach and intestine, the rest is passed through the gastrointestinal tract and makes up a part of the stool. There are two types of dietary fiber, soluble and insoluble. Soluble fiber retains water and turns to gel during digestion. It also slows digestion and nutrient absorption from the stomach and intestine. Soluble fiber is found in foods such as oat bran, barley, nuts, seeds, beans, lentils, peas, and some fruits and vegetables. Insoluble fiber appears to speed the passage of foods through the stomach and intestines and adds bulk to the stool. It is found in foods such as wheat bran, vegetables, and whole grains. Fiber is very important to a healthy diet and can be a helpful aid in weight management. One of the best sources of fiber comes from legumes, the group of food containing dried peas and beans.

People whose diets have been low in fiber should increase it gradually. It is best to obtain dietary fiber, soluble or insoluble, in the natural form of whole grains, nuts, legumes, fruits, and vegetables. If it proves difficult to do so, psyllium, a grain naturally found in India, is an excellent soluble fiber supplement (Metamucil, Fiberall, Perdiem Fiber). Fluids are particularly important in preventing constipation.

Fish Oil. Omega-3 fatty acids, which are found in oily fish, are proving to have powerful anti-inflammatory effects and may also be nerve protective.

Click the icon to see an image of foods that contain omega-3 fatty acids.

Dairy Products. A 2002 study reported a higher risk for Parkinson's disease in men (but not in women) who consumed high amounts of dairy products. This association was not linked to fats in dairy foods and high intake of calcium or protein from other sources did not increase the risk. A 2005 prospective study of men found that milk consumption in midlife was associated with increased risk of Parkinson’s disease. As with prior research, the researchers did not find that calcium itself carried a risk. They suggested that some unidentified neurotoxic contaminant in milk may be responsible.

Vitamins.

B Vitamins. Most B vitamins play important roles in the brain and central nervous system. Vitamin B6 (pyridoxine) theoretically has benefits for PD because it is necessary in the production and metabolism of dopamine. Folate deficiency may increase toxic effects against dopamine neural pathways, perhaps by increasing levels of homocysteine, an amino acid that may play a destructive role in many diseases, including heart and neurologic disorders. Some evidence suggests that L-dopa elevates homocysteine levels, so folate supplements may be particularly important for patients. Although the major food sources of B vitamins are meats and dairy products, which are high in protein, these vitamins are also found in whole grains and are added as supplements to commercial cereals.

Click the icon to see an image of the benefits of vitamin B6.

Click the icon to see an image of foods that contain vitamin B6.

Click the icon to see an image of foods that contain folate.

Vitamin E. Researchers have investigated antioxidant vitamins, especially vitamin E, for their effect on the brain. Some, but not all, studies have reported slower mental decline and lower risk for Parkinson's and Alzheimer's disease in people who ate large amounts of foods rich in vitamin E. Such foods include vegetable oils (particularly wheat germ oil), sweet potatoes, turnip greens, mangos, avocados, nuts, sunflower seeds, and soybeans. Vitamin E supplements, however, do not appear to be helpful for slowing disease progression or improving symptoms.

Both smoking and coffee drinking have been associated with lower risk for PD. Researchers are attempting to discover if these substances protect nerve cells. One interesting study suggested that the early disease process in PD produces changes in the dopamine pathway that actually protects an individual from caffeine and nicotine addiction, so that fewer patients have a history of smoking and caffeine. Research is needed to determine why these toxic substances protect against PD.

Smoking and Nicotine Replacement. Cigarette smokers appear to have a 40% lower risk for Parkinson's disease, indicating some protection by nicotine. This finding, of course, is no excuse to smoke, but such protection may help researchers develop new therapies. Studies on nicotine replacement, such as gum or patches, have been conflicting, however, with some short-term studies reporting no benefits. A 2002 study suggested that nicotine replacement may help smokers with early PD, but not nonsmokers.

Coffee Consumption. Studies have indicated that the risk for PD in coffee drinkers is about 30% lower than for non-coffee drinkers. In a 30-year study of Japanese-American men, coffee consumption was associated with a lower risk for Parkinson's disease, and the more coffee they drank, the lower their risk became. Coffee and tea can reduce fluids by increasing urination, however, and so may increase constipation in PD.

Regular use of ibuprofen may reduce the risk of Parkinson’s disease according to research presented at the 2005 annual meeting of the American Academy of Neurology. In this prospective study, people who took at least two ibuprofen tablets per week for at least 1 year lowered their risk of developing Parkinson’s by 35% compared to nonusers or irregular users. For those who took ibuprofen daily, the comparative risk was 38% lower. Other non-steroidal anti-inflammatory drugs (NSAIDS) did not appear to affect disease risk.

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.

The following dietary supplements are being studied for treatment of Parkinson's disease:

Creatine. Creatine is a nutritional supplement that is sometimes used to improve exercise performance. In 2007, the U.S. National Institutes of Health launched a large-scale clinical trial to study whether creatine can slow the progression of Parkinson’s disease. The trial will enroll patients who have been diagnosed with PD within the last 5 years and who have received levodopa therapy for no more than 2 years.

Coenzyme Q10 (Ubiquinone). Coenzyme Q10 (also called ubiquinone) is an antioxidant being studied for the treatment of Parkinson's disease. This enzyme is important for cellular energy, which may be impaired in PD. In one study, patients who took coenzyme Q10 had slower decline in daily activities and mental and motor skills compared to patients on placebo. However, a 2007 study found that small doses of coenzyme Q10 had no effect on improving Parkinson’s symptoms. Researchers are still investigating whether larger doses given over a long period of time may benefit patients.

Exercise early in adult life may help protect against later development of Parkinson’s disease. Exercise is also an important component of rehabilitation. Physical therapy is extremely important and usually includes active and passive exercise, gait training, practice in normal activities, and if needed, hot or cold treatments, water therapy, and electrical stimulation. Exercise is also essential for well-being and helps patients maintain productive years. To date, no specific approach has been proven to be better than others.

Exercise Programs. Exercise programs are defined as passive or active.

Passive exercise, mostly stretching and manipulation of muscles by a physical therapist, is aimed at preventing muscles from shortening. A passive exercise program that begins with slow and gentle exercises and becomes progressively more intense may improve mobility in patients with early and mid-stage Parkinson's disease.
Active exercises are used to help range-of-motion, coordination, and speed. Patients should continually make efforts to practice movement, even simple ones, such as marching in place, making circular arm movements, and raising the legs up and down while sitting. Patients who enjoy sports or the use of exercise equipment should continue with these activities even if their skills diminish, assuming there are no other medical conditions that would prevent participation.

Gait Training. Practicing new methods for standing, walking, and turning may help retain balance. The following tips may be helpful:

Take large steps when walking forward, raising the toes at the forward step, and hitting the ground with the heel.
Take small steps while turning.
When walking or turning, have the legs 12 - 15 inches apart to provide a wide base.
Do not wear rubber or crepe-soled shoes because they grip the floor and may cause the patient to fall forward.
Using devices that keep a rhythmic beat, such a metronome (a simple device used by musicians to keep time), may be very effective, possibly more than music itself, in helping patients to walk faster and take longer steps. One study found that setting a metronome rhythm to about 10% faster than the patient's fastest gait offers significant improvement over walking to no rhythm at all or to a rhythm that matches the gait.

Reducing Muscle Freezing. The patient should practice regular daily activities that simplify actions and reduce the incidence of muscle freezing. Most often, freezing occurs when a patient begins to move or is presented with an obstacle. The following tips may be helpful:

Rock from side to side.
If the legs feel frozen, lift the toes. This simple action may free spasm in some cases.
Hum marching tunes. In fact, music has been shown to help people move and to get out of bed in the morning. Some studies report that wearing a Walkman and turning music on in situations associated with freezing, such as crossing a street, is helpful.
Divide actions into separate events, which may prevent freezing that occurs from trying to coordinate too many physical operations at one time. For instance, when going through a doorway, approach the door, stop at the door, open it, stop, and then walk through the doorway.
A cane equipped with a laser pointer may be helpful, at least temporarily.
Simply being touched by another person can sometimes release the patient (although a patient with PD should never be pulled or pushed).

Sleep Deprivation Therapy. Sleep deprivation therapy may have a role in treating some cases of depression and some studies are finding some benefits on the depression, tremor, and rigidity experienced by patients. Scientists believe that sleep deprivation produces certain anticholinergic effects, which may improve both depression and Parkinson's symptoms.

Mental Tasks. Mental training may increase dopamine in the brain. Some studies indicate that being mentally fit may be as important for patients as being physically fit. Helpful approaches include:

Select and learn new hobbies that require finger and hand mobility, such as sewing, carpentry, fishing, or playing cards.
Practice deep breathing and relaxation exercises. These may help maintain proper speech control, control tremor, and reduce anxiety.
Both the patient and any caregivers should consider psychological therapy and support for depression and loss of motivation. If psychological therapy is too costly, inexpensive support programs and groups are widely available and can be invaluable for the patient and the family.

Speech Therapy. Speech therapy may help those who develop a monotone voice and lose volume, particularly in combination with medications. There are no well-conducted studies comparing specific speech therapies, but the Lee Silverman Voice Treatment (LSVT) appears to be an example of an effective technique. It has five major components:

Focus on the voice ("think loud/think shout")
High effort (pushes patients to overcome limitations)
Intensive treatment (16 sessions in 1 month)
Calibration (learning to know and accept the amount of effort needed to produce normal sound so it becomes automatic)
Quantification (continuous feedback to objectively document success)

LSVT may help swallowing as well as speech.

Equipment and Devices. A number of devices can be helpful for maintaining stability and preventing falls. The following are some examples:

Rails installed where the patient needs support in getting up or down, such as along the bed and in the bathroom.
Walkers with locking wheels. (Walkers do not appear to be helpful for freezing.)
Chairs with straight backs, firm seats, and arm rests.
Firm mattresses and satin sheets or less expensive sheets with high thread counts. (These are useful for helping patients slide out of bed.)

Resources

www.ninds.nih.gov -- National Institute of Neurological Disorders and Stroke
www.aan.com -- American Academy of Neurology
www.apdaparkinson.org -- American Parkinson's Disease Association
www.pdf.org -- Parkinson's Disease Foundation
www.parkinson.org -- National Parkinson Foundation
www.michaeljfox.org -- Michael J. Fox Foundation for Parkinson's Research
www.wemove.org -- Worldwide Education and Awareness for Movement Disorders
www.parkinsonsaction.org -- Parkinson's Action Network

References

Deuschl G, Schade-Brittinger C, Krack P, Volkmann J, Schafer H, Botzel K, et al. A randomized trial of deep-brain stimulation for Parkinson's disease. N Engl J Med. 2006 Aug 31;355(9):896-908.

Murata M, Hasegawa K, Kanazawa I. Zonisamide improves motor function in Parkinson disease: a randomized, double-blind study. Neurology. 2007 Jan 2;68(1):45-50.

Schade R, Andersohn F, Suissa S, Haverkamp W, Garbe E. Dopamine agonists and the risk of cardiac-valve regurgitation. N Engl J Med. 2007 Jan 4;356(1):29-38.

Schupbach WM, Maltete D, Houeto JL, du Montcel ST, Mallet L, Welter ML, et al. Neurosurgery at an earlier stage of Parkinson disease: a randomized, controlled trial. Neurology. 2007 Jan 23;68(4):267-71. Epub 2006 Dec 6.

Storch A, Jost WH, Vieregge P, Spiegel J, Grelich W, Durner J, et al. Randomized, double-blind, placebo-controlled trial on symptomatic effects of coenzyme Q10 in Parkinson disease. Arch Neurol. 2007 July;64.

Voon V, Thomsen T, Miyasaki JM, de Souza M, Shafro A, Fox SH, et al. Factors associated with dopaminergic drug-related pathological gambling in Parkinson disease. Arch Neurol. 2007 Feb;64(2):212-6.

Watts RL, Jankovic J, Waters C, Rajput A, Boroojerdi B, Rao J. Randomized, blind, controlled trial of transdermal rotigotine in early Parkinson disease. Neurology. 2007 Jan 23;68(4):272-6. Epub 2007 Jan 3.

Zanettini R, Antonini A, Gatto G, Gentile R, Tesei S, Pezzoli G. Valvular heart disease and the use of dopamine agonists for Parkinson's disease. N Engl J Med. 2007 Jan 4;356(1):39-46.

Review Date:
6/4/2007
Reviewed By:
Harvey Simon, MD, Associate Professor of Medicine, Harvard Medical School; Physician, Massachusetts General Hospital.

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