Reprinted from Eating Disorders Review
May/June 2007 Volume 18, Number 3
©2007 Gürze Books
The arrival of puberty produces significant surges in disordered eating, including increased preoccupation with weight, elevated body dissatisfaction, and binge eating. Many studies have focused on the psychosocial impact of physical changes that occur during puberty, particularly increased body fat in girls. These theories postulate that additional adiposity leads to negative affect and body dissatisfaction, which in turn increase risk for eating disorders.
Kelly L. Klump, PhD, of Michigan State University, and colleagues at Cornell University and the University of Minnesota investigated whether puberty moderates genetic influences on disordered eating (Psychol Med 2007;37:627). This is the first study to examine the effects of puberty on disordered eating. Three years before, using data from the Minnesota Twin Family Study, the authors found that the heritability of disordered eating symptoms increases during puberty. In the earlier study, most twins were 11 years old (age range: 10-13 yrs). Dr. Klump and colleagues found little genetic influence in twins before puberty but a substantial genetic effect (more than 50%) among twins who had begun puberty. At about the same time, a study by another group found no significant effects on puberty on the heritability of disordered eating (Biolog Psychol 2002;51:172).
The authors revisited the twins in the original study, who were now 13 to 16 years of age, to see if increases in heritability were influenced by puberty. The study included 510 adolescent female twins. The researchers used the Minnesota Eating Behavior Survey (MEBS), which was adapted from the Eating Disorders Inventory (EDI 1 and EDI 2). The MEBS total score includes items that assess body dissatisfaction, binge eating, weight preoccupation and the use of inappropriate compensatory means to lose weight. The Pubertal Development Scale was used to assess pubertal development; the subjects themselves rated their development on a 4-point scale, beginning with “Development has not yet begun” to “Development seems to be completed.”
Dr. Klump and her colleagues found that genetic effects on disordered eating emerge during puberty and these effects increase linearly as development continues. Most of the twins were in mid-to-late puberty, although the scores showed considerable variability in disordered eating and pubertal development. The heritability of disordered eating was found to increase from 0% to 44% across the four pubertal stages. The authors stress that their findings show that puberty moderates genetic influences on disordered eating, not increases in the incidence of disordered eating.
Ovarian hormones are suspected causal agents
The most likely causal agents are ovarian hormones activated during puberty in girls. Although other biological systems are also involved in puberty, such as stress hormones and the hypothalamic pituitary axis, ovarian hormones drive pubertal changes in girls. Ovarian hormones are known to affect food intake and body weight, and are also known to change with pubertal development. Decreased levels of estrogen and increased levels of progesterone are associated with increased food intake and body weight in adult women—these findings appear to extend to disordered eating patterns as well, according to Dr. Klump and colleagues.
The researchers wondered if individual differences in the activation of ovarian hormones during puberty might account for the moderation of genetic effects seen in their study. Although promising early results have been found for an estrogen receptor beta gene (Psychol Med 2006;36:539), replications are lacking and no studies have examined candidate genes for progesterone. Another possibility, according to Dr. Klump and colleagues, is that ovarian hormones may influence the congenital predisposition to eating pathology indirectly through their regulation of gene transcription. Future studies will help examine the role of ovarian hormones in regulation of serotonin, and the direct effects of ovarian hormone receptor genes on food intake, mood, and risk during puberty.