In a series of 67 twin probands, the concordance for restricting AN was markedly higher for monozygotic twins, 66%, than for dizygotic, 0%. A familial aggregation of AN and Bulimia Nervosa is present in AN probands (Treasure & Holland, 1989).
Agenomewide linkage analysis of 192 families with one AN member and another with any related eating disorder identified in the Diagnostic and Statistic Manual of Mental Disorders (fourth edition) showed a modest linkage on chromosome 4. When a subset of 37 families containing 2 with restricting AN was analyzed, a more robust linkage was found on chromosome 1p (Devlin et al., 2002; Grice et al., 2002).
A vulnerability for destabilization of the endocrine and metabolic mechanisms affecting eating behavior may cause the full-blown eating disorder under stresses such as severe dieting. Neurotransmitter serotonin pathways modulate feeding and inhibitory behaviors. There is evidence of aberrations in this neurotransmitter system in anorectic patients.
Because AN predominately starts during puberty (there is a bimodal peak for age onset at ages 14-15 and age 18), Crisp (1970) developed the hypothesis that AN reflects an attempt to cope with maturational problems through the mechanism of avoidance of biological maturity.
A genetic predisposition to develop AN could be a particular personality type. There is evidence that a rigid, inhibited, and perfectionistic personality may be at risk for developing AN-R (Halmi, 1999).
Two behavior variables, obsessionality and drive for thinness, showed high and concordant values in a cluster of AN pairs. These variables in the AN pairs showed suggestive linkages on chromosome 1, 2, and 13 (Devlin et al., 2002).
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