Suzy Lee (pepper51) wrote in ed_ucate,
Suzy Lee

serotonin + eating disorders

I'm sorry I x-posted this everywhere but I am really curious about everyone's opinions.

This is a very interesting article about the effect serotonin has on eating disordered individuals. It explains that bulimia is a possible result from abnormally low serotonin levels. My question is, if a bulimic person started taking supplements such as 5-htp, which is a precursor for serotonin production, could they possibly "cure" their bulimia? I makes sense to me, what do you think?

Biochemical Correlates of Anorexia and Bulimia
Lauren Hellew
Millions of people in the United States suffer from anorexia nervosa and bulimia nervosa. Anorexia nervosa is a dangerous eating disorder characterized by distorted body image, obsession with food and weight, drastic reduction in food intake often to the point of starvation, and extreme weight loss (1). Bulimia nervosa is a somewhat similar eating disorder more specifically characterized by recurring episodes of uncontrollable binge eating followed by self-induced vomiting or abuse of laxatives or diuretics (2).
The vast majority - more than 90 percent - of those afflicted with eating disorders are adolescent and young adult women (1). This has led to the popular belief that eating disorders can be attributed to social factors, specifically the heavy emphasis which is placed on thinness as a measure of physical attractiveness and feminine beauty in our culture. It is thought that women, especially young women, develop eating disorders in an attempt to conform to this ideal (1). While it is likely that such social factors do play an important role in the development of eating disorders, research has shown that several other psychological and biological factors are also involved. This paper will focus specifically on the biochemical factors, including abnormal activity of brain neurotransmitters, hormones and other brain chemicals, which have been implicated in these disorders.
Disturbances of the serotonergic pathways within the brain have been linked to the onset, persistence, and recurrence of eating disorders. In particular, it seems that increased serotonin activity in the brain may be responsible for anorexic behavior, while decreased serotonin activity may be responsible for bulimic behavior (4).
There is considerable evidence that increased serotonin activity in the brain is associated with appetite suppression (4). In fact, drugs which act on serotonin pathways in the brain are commonly used for the short-term management of obesity. Fenfluramine, one of the two drugs which make up the controversial diet pill "Fen-Phen," is an example of one such drug. Fenfluramine, along with dexfenfluramine (a similar, purified version of fenfluramine), acts by increasing serotonin activity in the brain, thus suppressing appetite and facilitating weight loss (5). It has been suggested that food restriction and several other behaviors which are characteristic of anorexia may be associated with increased serotonin activity (4).
Conversely, it has been shown that decreased serotonin activity in the brain is associated with enhanced appetite, and thus may be related to bulimia (4). Researchers working in conjunction with Harvard Medical School have demonstrated a link between bulimia and impaired serotonergic responsiveness in the brain. The study compared serotonergic activity and the presence of several behavioral symptoms of bulimia among bulimic and healthy women. Serotonergic responsiveness was assessed by measuring the activity of the pathway following administration of a serotonin agonist. It was found that the women with bulimia showed significantly less serotonergic activity following administration of the agonist than did the healthy women. In other words, the agonist did not have as great an effect on serotonin activity in bulimic women as it did on serotonin activity in healthy women. This suggests that individuals with bulimia demonstrate impaired serotonergic responsiveness which, in turn, results in an overall decrease in serotonin in the brain. In addition, the frequency of binge eating during the four weeks prior to the study was shown to be inversely correlated with serotonin activity (6).
Another recent study conducted by researchers at the University of Pittsburgh Medical Center assessed neurotransmitter levels and several behavioral symptoms of bulimia (including negative moods, obsessions with perfectionism and exactness) in recovered bulimic women and healthy women. It was found that the women with bulimia had abnormal levels of serotonin activity relative to healthy women. Such evidence suggests that bulimia is correlated with an alteration in brain chemistry which persists even after recovery from the disorder (7).
Many people with eating disorders also appear to suffer from depression or obsessive-compulsive disorder (OCD). This is especially interesting given that depression and OCD are also known to involve abnormal serotonergic activity (3). The link between the disorders is further supported by the fact the antidepressants which increase serotonin activity in the brain are also often effective treatments for individuals with bulimia (8).
Several other brain chemicals have also been implicated as possible correlates of eating disorders. For example, patients with anorexia and bulimia have been shown to have elevated levels of neuropeptide Y and peptide YY. This finding is particularly interesting given that these chemicals have been shown to stimulate eating behavior in laboratory animals. In addition, the hormone cholecystokinin (CCK) which seems to cause satiation in laboratory animals, is known to be low in some women with bulimia. This finding may help explain the lack of satiety which is characteristic of bulimic binges (3).
Two regions of the hypothalamus, the ventromedial hypothalamus and the lateral hypothalamus, have been shown to effect feeding behavior. In particular, the ventromedial hypothalamus is thought to contain a satiety center, while the lateral hypothalamus is thought to contain an eating center. This hypothesis comes from animal experiments in which these areas are selectively stimulated or damaged. Thus, the ventromedial hypothalamus is thought to be the satiety center because stimulation of this area suppresses eating, while damage to this area results in obesity. The opposite effects are seen following stimulation and damage to the lateral hypothalamus, thus suggesting that it may be responsible for promoting eating behavior. The mechanisms underlying these regulatory processes seem to involve the activity of the neurotransmitters norepinephrine, serotonin, and dopamine. It is suggested that further investigation into the role of these hypothalamic regions and the neurotransmitter pathways within them may provide important information about the biochemical and neurological basis of eating disorders (2).
Thus, eating disorders seem to be caused by a combination of many social, psychological, and biological factors, and it is apparent that additional research will be necessary in order to better understand the complex etiology of these disorders.
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