Carol Hayes posted a query on TIPS about the biological basis of
anorexia and bulimia which reached me with an error message, and it
won't let me quote it back to the list. So it's possible it never made
it to many on the list.
Anyway, in answer to her question, I know of a rare case (Weller &
Weller, 1982) in which an adolescent who had the classic signs of
anorexia turned out to have a hypothalmic tumor. The well-known
"lateral hypothalamic syndrome" of failure to eat or drink (with slow
recovery) results from damage to the lateral hypothalamus in animals.
However, it wasn't clear in this case whether the tumor specifically
damaged the lateral area (probably caused massive damage everywhere in
the hypothalamus).
However, this is a rare case, and as far as I know, hypothalamic
damage is otherwise never found in association with anorexia. In fact,
Mrosovsky (1984), an animal researcher, specifically rejects the
Wellers' claim that the tumor and the anorexia were "related".
As for more recent work, I'm not aware of any progress in linking
anorexia to biology. Kalat (1998) confirms this, noting "the
biological predispositions to anorexia are as yet unknown".
As for bulimia, there's interest in hormonal mediation. For example, a
study I talk about in class is Geracioti & Liddle (1988). They
reported that bulimics release less CCK, long under investigation as a
satiety hormone for food intake, after a meal than do normals. This
suggests that the cause of bulimia (the binging, anyway) is due to
lessened ability to stop eating because of deficient release of the
CCK stop hormone. However, I believe that no one has shown that
exogenous CCK is an effective treatment for bulimia (and it apparently
can cause horrible panic attacks).
Recent animal research implicating another stop hormone, leptin, may
turn out to be more promising. It's mostly in the news in relation to
attempts to use it to control obesity (it doesn't, apparently)
but it's possible that it or a similar hormone has a role in bulimia.
Turning again to handy Kalat, he says that "people with bulimia tend
to have higher-than-normal levels of peptide YY [a start eating
hormone]...lower-than-normal levels of CCK...and signs of either
decreased serotonin production or decreased receptor sensitivity for
serotonin (p. 294). Of course, whether this is cause or effect of the
bulimia isn't clear.
-Stephen
References
Weller, R., & Weller, E. Anorexia nervosa in a patient with an
infiltrating tumor of the hypothalamus. American Journal of
Psychiatry, 139, 824--
Mrosovsky, N. (1984). Animal models: anorexia yes, nervosa no.
In: The psychobiology of Anorexia Nervosa. K Pirke and D.
Ploog, Eds. Heidelberg: springer-Verlag.
Kalat, J. (1998) Biological psychology (6th ed.)
Geracioti, T., & Liddle, R. (1988). Impaired cholecystokinin secretion
in bulimia nervosa. The New England Journal of Medicine, 319, 683--
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Stephen Black, Ph.D. tel: (819) 822-9600 ext 2470
Department of Psychology fax: (819) 822-9661
Bishop's University e-mail: [EMAIL PROTECTED]
Lennoxville, QC
J1M 1Z7
Canada Department web page at http://www.ubishops.ca/ccc/div/soc/psy
Check out TIPS listserv for teachers of psychology at:
http://www.frostburg.edu/dept/psyc/southerly/tips/
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