Central Nervous System
Neurotransmitter Activity in Anorexia
Nervosa and Bulimia Nervosa
WALTER H. KAYE
It is common to consider eating disorders as being caused by cultural pressures for thinness, since dieting and the pursuit of thinness are common in industrialized countries. (See Chapters 19, 45, and 47 for discussions of sociocultural influences.) However, the disparity between the high prevalence of pressures for thinness and the low prevalence of eating disorders (see Chapter 41), combined with clear evidence of anorexia nervosa occurring at least several centuries ago (see Chapter 27), as well as the stereotypical presentation, predominance in females, premorbid anxiety, and developmentally specific age-ofonset distribution, underscore the possibility of contributing biological vulnerabilities. Other evidence of biologic risk factors includes indications that both anorexia nervosa and bulimia nervosa are familial and heritable disorders (see Chapter 42).
In the past few decades, a substantial number of neurotransmitters that contribure to the regulation of feeding behaviors have been identified. This in turn has raised the question of whether some disturbance of neurotransmitter function may contribute to the pathophysiology of anorexia nervosa and bulimia nervosa. However, it is difficult to answer this question with in vivo studies in humans because the central nervous system has been relatively inaccessible. In the living human brain, methods of characterizing neurotransmitter function have relied upon relatively indirect measures, such as levels of neurotransmitters in cerebrospinal fluid or endocrine responses to challenges of neurotransmitter function.
Another difficulty in the study of neurotransmitter activity in people with eating disorders is that disturbances of neuropeptide or monoamine activity could be secondary to dietary abnormalities or premorbid traits that contribute to a vulnerability to develop anorexia nervosa or bulimia nervosa. One way to tease apart cause and effect is to study