Reprinted from Eating Disorders Review
March/April 1999 Volume 10, Number 2
©1999 Gürze Books
Research into the sociocultural determinants of eating disorders has revealed a rich array of cultural and familial factors associated with anorexia nervosa and bulimia nervosa. In addition, a progression of new studies focusing on underlying biological processes can help answer the perennial question of why some individuals are more vulnerable than others to the cultural pressures toward thinness.
The surge in knowledge about the biology of eating disorders has come from a confluence of research in 8 areas: epidemiologic studies of risk factors, family studies, twin studies, genetic studies of eating disorders, studies on the neurobiology of feeding behavior and of eating disorders, studies on the genetics of obesity, and brain-imaging studies. Continued cross-fertilization of these areas will enrich our understanding of the underlying pathophysiology of eating disorders. These studies augment what is known about sociocultural aspects of eating disorders and will help provide a more comprehensive understanding of the development, maintenance, treatment, and prevention of these problems.
This article highlights the family and twin approaches and explores ways to integrate studies of biology with studies of environment.
Family studies provide unequivocal evidence that eating disorders run in families. In the two most methodologically sophisticated family studies to date, 1,2 family members of women with anorexia and bulimia nervosa were at markedly increased risk for eating disorders. However, one cannot determine the extent to which the familiality is due to environment or due to genetics from a family study alone, since both forces can lead to the familial aggregation of a trait. Instead, the question can be resolved by studies of twins.
The results of twin studies have been remarkably consistent. Given that monozygotic (MZ) twins share 100% of their DNA and dizygotic (DZ) twins share, on average, half of their DNA, if both members of MZ twin pairs display a disorder more frequently than both members of DZ twin pairs, then there is evidence of genetic transmission.
In addition to simple heritability estimates, twin studies allow one to determine the extent to which additive genetic effects (A), shared environmental effects (C), and unique environmental effects (E) contribute to liability to the disorder. Shared environmental effects refer to those environmental influences that are shared by members of a twin pair, such as socioeconomic status, the parents’ attitudes toward child-rearing, and school systems. Unique environmental effects are influences that are only experienced by one twin, such as being teased about weight or taking ballet lessons. Figure 1 illustrates how twin studies can decompose the variance in liability into these three factors.
A series of population-based twin studies from Virginia, Minnesota, and Australia provide valuable insight into the nature of the familiality of eating disorders.
First, research from Virginia has shown that bulimia nervosa is a highly heritable condition. Approximately 83% (95% confidence interval; 64%-100%) of the liability is due to additive genetic effects, with only a negligible contribution from shared environmental effects. The remaining variance in liability is attributable to unique environmental effects.3
Second, both the Australian and Minnesota studies have shown that heritability is not limited to the “disorder,” but that body dissatisfaction and other dimensional measures of disordered eating also appear to be heritable.4 Third, the genes that contribute to bulimia appear to be shared to some extent with the genes that contribute to panic disorder and phobias.5 This finding is consistent with clinical studies that have noted frequent comorbidity of anxiety and eating disorders. Fourth, the Minnesota studies indicate that the genetic effects on disordered eating may only emerge after puberty.6
Prior to puberty, shared environmental effects appear to be much more critical to eating and weight attitudes. This finding parallels those from studies of drug use, in which initial drug use is influenced more by family and social environment, while later dependence relies largely on genes.7 The same may hold true for eating disorders, in that early body dissatisfaction and dieting behavior are influenced by shared attitudes in the family, but the progression to an eating disorder is governed largely by genetic effects.
Although the findings from family and twin studies support the role of genes in the etiology of eating disorders, they do not exonerate the environment. In fact, eating disorders form an ideal setting for studying the interaction of genes and environment. A critical point to remember is that although the predisposing genes may exist in an individual, in the absence of exposure to certain environmental “releasers,” it may be less likely that she will develop the disorder. For example, if an individual is genetically predisposed to anorexia nervosa, yet has never been subjected to cultural pressures to be thin and has never gone on a diet, she may never develop the condition. An important extension of twin research is to understand how genes and environment interact to culminate in eating disorders.
Why should we support additional research on the psychobiology of eating disorders? There are several very sound reasons. First, dieting and eating-disordered behaviors are serious public health problems for young girls. Second, the mortality rate from anorexia nervosa—approximately 5% per decade is unacceptably high. Third, the “costs” of eating disorders include the loss of potential in afflicted individuals, the impact of eating disorders on fertility, reproduction, and offspring of women with eating disorders, and the drain on the collective potential of women caused by the constant preoccupation with weight and appearance.
Several fundamental questions about eating disorders remain unanswered. For example, how many eating disorders are there? Are anorexia nervosa and bulimia nervosa the only true eating disorders, or should binge eating disorder be considered to be an independent syndrome? To what extent are the various eating disorders distinct or overlapping? Where should we draw the line when determining clinical severity? Does a woman who binges and purges once a week differ in any meaningful ways from one who binges and purges twice a week?
Finally, how can we best account for the developmental progression of eating disorders? Can we predict who will develop bulimia nervosa after a course of anorexia nervosa and who will remain anorexic—and why?
Contributions of Biological and Genetic Research
How can research into the biology of eating disorders help? One answer is that this research can help de-stigmatize eating disorders for women and men. Many women I work with continue to encounter lack of understanding in the community and among some health-care professionals who view eating disorders as purely volitional. Too many professionals view these persons merely as individuals searching desperately for a thin ideal and taking weight loss behaviors to an extreme.
Our cognitive-behavioral and pharmacologic tools remain essential to help these people establish control over their biology. In addition, continued research in this area is likely to reveal underlying causal mechanisms, which will allow us to further refine our treatments.
We can also say with relative certainty that the children of women with eating disorders are themselves at increased risk of developing eating disorders. Although we do not yet know how best to approach the problem, interventions targeted toward these individuals and perhaps their mothers as well may help decrease their risk of developing problems with eating.
Finally, by using our present biological knowledge as a basis, we can begin to address which environmental factors confer greatest risk to the development of eating disorders and to understand the way in which genes and environment interact to result in anorexia nervosa, bulimia nervosa, and related eating disturbances.
- Lilenfeld L, Kaye W, Greeno C, Merikangas K, Plotnikov K, Pollice C, Rao R, Strober M, Bulik C, Nagy L. A controlled family study of restricting anorexia and bulimia nervosa: comorbidity in probands and disorders in first-degree relatives. Arch Gen Psychiatry 55:603, 1998.
- Strober M. A controlled family study of bulimia nervosa. Eating Disorders Research Society, Boston, MA, 1998.
- Bulik C, Sullivan P, Kendler K. Heritability of binge eating and bulimia nervosa. Biolog Psychiatry 44:1210, 1998.
- Wade T, Martin N, Tiggemann M. Genetic and environmental risk factors for the weight and shape concerns characteristic of bulimia nervosa. Psycholog Med 28:761, 1998.
- Kendler KS, Walters EE, Neale MC, Kessler RC, Heath AC, Eaves LJ. The structure of the genetic and environmental risk factors for six major psychiatric disorders in women: phobia, generalized anxiety disorder, panic disorder, bulimia, major depression and alcoholism. Arch Gen Psychiatry 52:374, 1995.
- Klump KL, McGue MK, Iacono WG. Age differences in genetic and environmental influences on eating attitudes and behaviors in adolescent female twins. Eating Disorders Research Society, Albuquerque, NM; 1997.
- Kendler KS, Prescott CA. Cannabis use, abuse, and dependence in a population-based sample of female twins. Am J Psychiatry 155:1016, 1998.
Plomin R, DeFries JC, McLearn GE, Rutter M (eds.) Behavioral Genetics. W.H. Freeman & Co., 1997.
Kendler K. Twin studies of psychiatric illness. Arch Gen Psychiatry 50: 905, 1993.
Kendler, K. Genetic epidemiology in psychiatry. Arch Gen Psychiatry 52:895,1995.