erica057 (erica057) wrote in ed_ucate,
erica057
erica057
ed_ucate

Seratonin and EDs

hanacandi reminded me of a fascinating article I read about the neurobiology of eating disorders. It's dense, so I'll give you the reader's digest version first. I've done quite a bit of research in peer-reviewed scientific journals, and there is conclusive information that various neuroreceptors are damaged from eating disorders. This is probably not news to anyone in this community. However, it seems that full nutritional restoration repairs most receptors -- EXCEPT for 5-HT (seratonin) receptors. Here's an excerpt from my findings. If anyone wants the full-text PDF for a research project or something, reply with your email addy and I'll send.

Via http://dx.doi.org/10.1016/j.physbeh.2007.11.037 :

Anorexia nervosa (AN) and bulimia nervosa (BN) are related disorders of unknown etiology that most commonly begin during adolescence in women. AN and BN have unique and puzzling symptoms, such as restricted eating or binge-purge behaviors, body image distortions, denial of emaciation, and resistance to treatment. These are often chronic and relapsing disorders, and AN has the highest death rate of any psychiatric disorder. The lack of understanding of the pathogenesis of this illness has hindered the development of effective interventions, particularly for AN. Individuals with AN and BN are consistently characterized by perfectionism, obsessive–compulsiveness, and dysphoric mood. Individuals with AN tend to have high constraint, constriction of affect and emotional expressiveness, ahendonia and asceticism, whereas individuals with BN tend to be more impulsive and sensation seeking. Such symptoms often begin in childhood, before the onset of an eating disorder, and persist after recovery, suggesting they are traits that create a vulnerability for developing an ED. There is growing acknowledgement that neurobiological vulnerabilities make a substantial contribution to the pathogenesis of AN and BN. Considerable evidence suggests that altered brain serotonin (5-HT) function contributes to dysregulation of appetite, mood, and impulse control in AN and BN. Brain imaging studies, using 5-HT specific ligands, show that disturbances of 5-HT function occur when people are ill, and persist after recovery from AN and BN. It is possible that a trait-related disturbance of 5-HT neuronal modulation predates the onset of AN and contributes to premorbid symptoms of anxiety, obsessionality, and inhibition. This dysphoric temperament may involve an inherent dysregulation of emotional and reward pathways which also mediate the hedonic aspects of feeding, thus making these individuals vulnerable to disturbed appetitive behaviors. Restricting food intake may become powerfully reinforcing because it provides a temporary respite from dysphoric mood. Several factors may act on these vulnerabilities to cause AN to start in adolescence. First, puberty-related female gonadal steroids or age-related changes may exacerbate 5-HT dysregulation. Second, stress and/or cultural and societal pressures may contribute by increasing anxious and obsessional temperament. Individuals with AN may discover that reduced dietary intake, by reducing plasma tryptophan availability, is a means by which they can modulate brain 5-HT functional activity and anxious mood. People with AN enter a vicious cycle which accounts for the chronicity of this disorder because caloric restriction results in a brief respite from dysphoric mood. However, malnutrition and weight loss, in turn, produce alterations in many neuropeptides and monoamine function, perhaps in the service of conserving energy, but which also exaggerates dysphoric mood. In summary, this article reviews findings in brain chemistry and neuroimaging that shed new light on understanding the psychopathology of these difficult and frustrating disorders.

While BN individuals show a response to higher doses of fluoxetine [87] (ed: Prozac), the efficacy of such medication has been questioned since relatively few individuals abstain from binge and purge behaviors, and relapse during treatment is common[88]. Despite the abundance of data implicating 5-HT dysregulation in AN, it remains controversial whether SSRIs are effective in restricting type AN (RAN) individuals [89,90]. Our clinical experience [91] suggests that RAN respond better to fluoxetine than do binge eating-purging type AN (BAN) and that some BN individuals can be relatively insensitive to high doses of SSRIs. Few control trials of any therapy have been performed, in part, because it has been difficult to enlist cooperation of individuals with AN, and in part because psychological and pharmacological strategies that have been successful in other disorders appear to be less effective in this illness. For severely emaciated patients, hospitalization for supportive medical care and weight restoration may be useful or necessary. Still, relapse is common after discharge.
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