Eating Disorders 235anorexia (9 out of 16) whereas only 7 percent of nonidentical twins were
(1 out of 14) (Holland et al., 1984; Crisp, Hall, and Holland, 1985).
Further studies show concordance rates for identical twins of 57 percent
(Schepank, 1992) and 45 percent (Treasure and Holland, 1989), and only
0 percent and 7 percent respectively for nonidentical twins. This difference
was even greater when the definition of anorexia was limited to restricting
anorexia, thereby excluding those who showed bingeing behavior. For
bulimia, the evidence for genetic factors is much weaker. For example,
studies of bulimia have reported concordance rates for identical twins of
26 percent (Kendler et al., 1991) and 35 percent (Treasure and Holland,
1989), and 16 percent and 25 percent for nonidentical twins respectively.
Therefore, the twin data provide some support for a genetic influence
on anorexia, particularly restricting anorexia, but a much weaker role, if
any, on the development of bulimia. How a genetic predisposition expresses
itself remains unclear. Some researchers have addressed this issue and have
pointed to the role of obsessive-compulsive disorder, perfectionism, and
body dissatisfaction as vulnerability traits (Treasure and Holland, 1995).
This suggests that the genetic predisposition expresses itself in a greater
tendency towards these factors, which then trigger anorexia. This conclusion
remains tentative and as yet unsupported by an evidence base.
A neural model of ANThe role of neurotransmitters in explaining food intake was outlined in
chapter 3, where it was suggested that food intake is influenced by cate-
cholamines, serotonin, and peptides, which can either increase or decrease
eating. Much of the research evidence comes from studies on rats, and some
examines humans with specific brain lesions. The hypothalamus has been
identified as the center of the neural regulation of food intake. If applied
to AN, it could be argued that those suffering from AN are not hungry
and have no appetite, and that that is why they do not eat. In particular,
it could be argued that they have low levels of chemicals, such as nore-
pinephrine, neuropeptide Y, and galanin, and high levels of cholecystokinin
and serotonin (Leibowitz, 1986; Rowlan, Li, and Morien, 2001).
There are, however, several problems with this approach. First, it neglects
the social context of AN and the ways in which it is clearly located within
a modern world. Second, even if such levels of brain chemicals were
identified in those with AN, they may be the consequence of starvation
rather than the cause of it (i.e., not eating causes a shift in the levels of