Eating Disorders : DNA or MTV?

(Les troubles de l’alimentation : Société ou héredité?)

Howard Steiger, Ph.D.
Director, Eating Disorders Program, Douglas University Institute
Professor, Psychiatry Department, McGill University

We used to take it for granted that Eating Disorders (like Anorexia and Bulimia Nervosa) were caused by social pressures to have a slim, fit appearance. We called these disorders “culture-bound syndromes” and “social epidemics” (Gordon, 1990), viewing them as extreme versions of our society’s obsession with dieting—sort of “diets gone wild”. Of course it’s likely that eating and body-image disturbances have a lot to do with social emphasis on dieting and slimness. A study by Anne Becker (2004) provides a striking example of this, showing that when American television was introduced in Fiji (during the 90s) it had an amazing impact—Fijian women and girls who were initially pretty happy with their body image became dissatisfied with their appearance! In a similar vein, evidence confirms that Bulimia Nervosa has been on the rise during past decades, in a fashion that seems quite in synch with the rise of the Culture of Thinness (Keel & Klump, 2003). In this respect, bulimia seems to be a pretty direct result of society placing too much pressure on people to diet—susceptible people starting to lose control of their suppressed appetites, and beginning to binge eat. However, even if Bulimia Nervosa depends upon the incentive to diet, it seems to occur especially often in people who are susceptible for other reasons—people who often show problems of mood, anxiety, impulsivity or substance misuse. Separating eating disorders even further from cultural pressure to be thin, cross-cultural and historical data have revealed that Anorexia Nervosa has existed throughout the history of civilization, and indeed, in societies that are not even brushed by the pressure to be thin. It starts to look like another type of explanation is needed: So what other factors might be involved in the vulnerability to developing an eating disorder?
For the past 15 years or so, researchers and theorists concerned with eating disorders have been speaking more and more about the role of heredity and genetics (Bulik, 2005; Collier & Treasure, 2004; Steiger & Bruce, 2007). New evidence had made it clear that EDs run in families, and especially in families in which members show either eating disorders, or symptoms that frequently accompany eating disorders (like anxiety, compulsivity, depression, or impulsivity). Eating disorders are 3 to 10 times more common in the blood relatives of people who themselves have an eating disorder. Reinforcing the idea that heredity is involved, twin studies have shown identical twin sisters to show very striking match (or concordancy) for EDs (in the 50% to 70% range)—in other words, at levels consistent with genetic transmission. And some studies (especially very-recent ones) have provided clues as to what genes might contribute to risk. Good candidates may be genes influencing brain serotonin and dopamine systems, or a brain chemical called “brain-derived neurotropic factor” (BDNF)--all of which influence eating behavior, mood, impulsivity, and other things associated with eating disorders (Steiger & Bruce, 2007; Ribases et al, 2004). Likewise, research has pointed to certain locations on Chromosomes 1 and 10 as possible loci of risk for an eating disorder (Bulik, 2004; Collier & Treasure, 2004). If you are surprised, don’t be. Many things we normally assume to be “learned” emerge as being quite hereditary. Things like perfectionism, religiosity--even political conservatism!—turn out to be about 50% explained by genetic effects (Alford et al, 2005; Hamer, 2004). Not to be outdone, EDs also emerge as being about 50% explained by genetic effects. So, does this mean that you INHERIT an ED?
Most mental-health problems involve heredity. But this doesn’t mean that you just “get” them. It’s more interesting to think about the possibility that environmental factors can actually “switch on” inherited susceptibilities (that are genetically transmitted in people “at risk”). The idea here is that genetic factors are involved, but don’t mean much until the environment “turns them on”. For EDs, we have begun to think of the ways in which factors (like social pressures to diet, family conflicts, stresses to achieve and perform) could activate genetic susceptibilities towards anxiety, mood, and appetite-regulation problems, that are carried by hereditary factors (genes) influencing the functioning of certain brain systems—the serotonin, dopamine and BDNF systems, for example. Or, we are thinking of ways in which genes may actually determine the extent to which people, because of hereditary traits, put themselves at risk--by being perfectionistic, body image conscious, and so on. Such traits may cause people to be especially sensitive to social pressures to diet, and then to become “perfect dieters” when in social contexts that encourage them to diet!
Some people find it disturbing to think that aspects of our behavior are hereditary, as though this implies that we’re “pre-programmed” or “lacking free will”. This view, of course, is not well-informed. Let me dispel some of the myths:

Myth no.1: “If genetic factors act in eating disorders, then I’m stuck. I’ll have my eating disorder always”.

Answer: Not at all. Genetic theory has us understand that the environment (in this case one that encourages lots of dieting) “switches on” genetic vulnerabilities that might, otherwise, lie dormant in people carrying them. Too much dieting activates biological risks carried by some people. One obvious example (for which there’s a lot of support from research) is that eating, mood and anxiety problems may involve shared alterations in brain serotonin activity (Steiger, 2004)—which we know to be very sensitive to effects of dieting. Studies show that 3 weeks of MODEST dieting alters brain serotonin activity quite substantially….and more so in women than in men! (Cowen et al, 1996). Not only does this help explain why it is that EDs often occur in people who are prone to mood or anxiety problems (all three linked to serotonin activity) and often in females (whose serotonin systems are more sensitive to becoming unbalanced after dieting). It says that recovery will often involve backing up and doing things that “switch off” the biological risks. First on this list will be to STOP DIETING! A related point is that people do not develop an ED because of some kind of “moral weakness” or “problem with character”. They didn’t ASK to have an eating disorder, and it isn’t their FAULT. Rather, EDs develop in people who are vulnerable to them—people for whom biological susceptibilities make dieting an especially dangerous thing!

Myth 2: “If I have an ED, and EDs are hereditary, then my children will get one too”.

Answer: Not at all. The same factors that promote vulnerability to an ED (e.g., traits of perfectionism, compulsivity) often underlie peoples’ strengths (e.g., ability to get jobs done well or to accomplish a lot). So the real issue is to “use traits well”. We have to help children learn to use their traits to best advantage, being able to commit to projects and work hard, but also being able to set reasonable limits and value being “good-enough” (rather than perfect). In the same way, children need to learn balanced attitudes about body-image and weight control, and ideas favoring moderation in dieting and exercise. In this way, we hope that even biologically susceptible kids won’t fall prey to eating disorders that result when excessive dieting “switches on” biological vulnerabilities in specifically vulnerable people.

Myth 3: “If EDs involve biology, then there will no longer be a place for psychotherapy, or attention to emotional needs or family factors in treatment”.

Answer: Although awareness of biological influences in the Eating Disorders has increased, Eating Disorder treatment still depends upon an interpersonal process—A RELATIONSHIP--that unfolds between the person in treatment, her therapist(s), and the other people with whom she may share the task of recovery. In fact, emphasis on the role had by biology may, paradoxically, have “humanized” therapy: When we understand that biological susceptibilities to anxiety, to liking things to be orderly or controllable, or to appetite dysregulation play in the risk of developing an eating disorder, and become amplified by the effects of malnutrition during an active eating disorder, we become less prone to criticizing the eating-disordered person for being “obstinate”, “resisting change” or “bringing about her own problems” when she (or he) has trouble getting eating symptoms under control. More realistically, hereditary traits and temperaments, exaggerated by effects of malnutrition and environment--and not “obstinacy”, explain peoples’ apparent rigidity or excessive needs for control while under the influence of an active eating disorder. Likewise, although family functioning can be a factor, eating disorders are not “caused” by anxious or overprotective mothers, or by emotionally unavailable fathers. We no longer point fingers at parents for causing their children’s eating disorders. Rather, there has been a shift—a huge benefit in my mind—towards therapeutic interventions that shame and blame people less, and that assist and guide more—helping eating-disorder sufferers and their relatives recognize and manage the influence in their lives of inherited behavioral traits, emotional sensitivities, and thinking styles that sometimes explain unique vulnerabilities to ED development.
In the end, people don’t develop eating disorders because they are weak or stupid or “asked for it”. I believe that when someone develops an eating disorder, it’s because there has been an unfortunate, but usually unavoidable “collision” of factors—psychological, social and biological. It’s sort of like you were walking along the sidewalk when the movers dropped the piano from the rooftop. You didn’t ask to be hit. But if you were, you have the job of repairing the damage. In other words, you can’t always avoid what happens when your own genetic susceptibilities (to anxiety, perfectionism, preference for order or control) become amplified by family and social stresses (e.g., overprotection, neglects, separations, failure experiences, criticisms), and then finally triggered by the effects of dieting. What is possible, though, is to undo the damage. Usually, this means learning to live well with ones traits (using them to good effect, while limiting tendencies towards excess)--and when we’re talking about eating disorders—invariably, to stop the dieting that is the final factor that puts a lit match to the fuse.

August 31, 2007

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