Competing Paradigms for Anorexia Nervosa

The contributors to the April 2007 American Psychologist special issue on eating disorders are to be commended for acknowledging lack of progress in understanding, classifying, and treating anorexia nervosa (AN). They highlighted the acute need to refine diagnosis (Wonderlich, Joiner, Keel, Williamson, & Crosby, 2007), understand comprehensive causal mechanisms to tune treatments and transcend “hodgepodge diagnoses” (Striegel-Moore & Bulik, 2007, pp. 181–182), study functional neural circuits and link behavior with “genomic, cellular, and systems data” (Chavez & Insel, 2007, p. 164), and develop effective treatments (Wilson, Grilo, & Vitousek, 2007, p. 201). Specifically, Chavez and Insel (2007) wrote that “present-day treatments are significantly limited” and that identifying underlying pathophysiology “will be critical for developing more effective treatments and preventive strategies” (p. 160). This state of the field could suggest that a new paradigm is needed, but new paradigms are often resisted by the established scientific community (Kuhn, 1962), of which the contributors to the special issue are internationally recognized leaders.

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Guisinger AP Comment 2008

Guisinger, S. (2008). Competing paradigms for anorexia nervosa. The American Psychologist, 63(3), 199-200.

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Modeling the heritability of Anorexia Nervosa


Shan Guisinger, Ph.D

David Schuldberg, Ph.D.

The University of Montana– Missoula

Growing genetic evidence indicates that symptoms of anorexia nervosa (AN), representing illness today, were selected in the past. Eight genes have been identified in AN individuals that decrease appetite and increase activity, triggered by falling weight. The adapted-to-flee-famine hypothesis (Affh) has proposed that abilities to ignore hunger, deny starvation, and move energetically are remnants of archaic adaptations that helped some in starving hunter-gatherer bands lead others from depleted home range. Yet, only 1-2% carrying the genes develop the disorder, which also exhibits sex differences. Maynard Smith clarified when natural selection results in stable polymorphisms; density-dependent selection describes how net individual benefit depends on behavioral strategies of others. We model effects of a variety of variables — including number of potential leaders, survival of those leaving home, refeeding success, reproductive outcomes for “successful” anorectics, and syndrome lethality — evaluating effects on the prevalence and sex distribution of AN.

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Monitor on Psychology

An evolutionary explanation for anorexia?

by Karen Kersting

Monitor, Vol. 35, No. 4, page 22 | April 2004

Modern anorexia may stem from an adaptation that helped ancient nomadic people find food, according to a recently proposed theory.

An evolutionary instinct that told members of migrating populations to move along when their food supply ran out may be a major contributor to modern anorexia nervosa, according to a new theory.

When food is scarce and starvation begins, most animals and people demonstrate intense hunger, low activity levels and a single-minded search for food. But, when starved, individuals with a genetic tendency toward anorexia feel sated, full of energy and unfazed by starvation–a set of symptoms described in the DSM-IV, says psychologist and Missoula, Mont. private practitioner Shan Guisinger, PhD, in an article published last year in Psychological Review (Vol. 110, No. 4).

“In treating anorexics, I started to wonder if their symptoms could be something that was useful in the past,” Guisinger explains. “When nomadic foragers were starving, it wouldn’t make sense to hunker down and just not eat. If you’re starving it means that there’s no food there, and so you should move on–normal adaptations to starvation would get in the way.”

A problematic adaptation

In the nomadic groups that preceded modern civilization, members who were undeterred by hunger may have become leaders and moved the group to places where food was plentiful, Guisinger says. She argues that this ancient adaptation, which was likely an advantage at the time, today continues to cause anorexia in people who have a genetic predisposition to it.

But whereas food scarcity may have been the original catalyst for anorexia–which kicks in when genetically susceptible people lose 15 percent of their normal body weight through lack of food–intentional dieting related to societal fear of being fat is most often the cause in modern cases, Guisinger says.

“A lot of people have trouble with this theory because they think now, in modern times, when there’s so much food around, why don’t anorexics just start eating again?” she notes. “But the thing about the brain is that it simply responds to body fat levels, making automatic adjustments to hunger and satiety signalers. Evolution is not very elegant sometimes, and adaptations persist where they are not needed. In this case, the adaptation turns off hunger in modern women who diet.”

Making the case through research

Guisinger backs up her theory with evidence from myriad studies pieced together to show that the core symptoms of the disease make adaptive sense. For example, she references research by psychologists Nicholas Mrosovsky, PhD, and David F. Sherry, PhD, that describes food-restriction behavior across species when animals must migrate.

She also cites research by Leo Kron, MD, that illustrates anorexic patients’ tendency toward hyperactivity and compulsions to move. And she points to research by historian Rudolph Bell, PhD, that documents anorexia in medieval people who lost weight through religious fasting. They, too, demonstrated distorted body images, hyperactivity and food refusal.

Though Guisinger’s theory is carefully constructed through her presentation of such evidence, proving an evolutionary cause for a modern illness is tricky, says psychologist Jeanine Cogan, PhD, founder of the Eating Disorders Coalition for Research, Policy and Action. Because Guisinger is looking to the past for causation, proving her hypothesis through research is impossible, she adds.

“She’s made an interpretation that’s compelling,” Cogan says. “And what I found most useful is she raised some excellent points about the physiological and psychological effects of food restriction that may play an important role in causing anorexia.”

Guisinger, who has never published a research article on anorexia before, says she came to her evolutionary conclusion after years of observing patients who wanted to eat, but claimed to be stopped by their bodies. Now, she says the most important step in helping patients is getting their weight back to normal, which, she believes, will turn off their genetically programmed anorexic response. The hypothesis can serve as a basis for cognitive behavioral therapy and for enlisting the aid of loved ones to help keep body weight up, she adds.

“It doesn’t make psychotherapy irrelevant, but it means that more than anything, people are going to need all the help they can get from their therapist, family, doctor and dietician to fight against their body’s signals in, what is to them, a very unnatural way,” she says.

Find a copy of the article here.

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Adapted to Flee Famine: Adding an Evolutionary Perspective

Psychological Review 2003

Anorexia nervosa (AN) is commonly attributed to psychological conflicts, attempts to be fashionably slender, neuroendocrine dysfunction, or some combination of these factors. Considerable research reveals these theories to be incomplete. Psychological and societal factors account for the decision to diet but not for the phenomenology of the disorder; theories of biological defects fail to explain neuroendocrine findings that suggest coordinated physiological mechanisms. This article presents evidence that AN’s distinctive symptoms of restricting food, denial of starvation, and hyperactivity are likely to be evolved adaptive mechanisms that facilitated ancestral nomadic foragers leaving depleted environments; genetically susceptible individuals who lose too much weight may trigger these archaic adaptations. This hypothesis accounts for the occurrence of AN-like syndromes in both humans and animals and is consistent with changes observed in the physiology, cognitions, and behavior of patients with AN.

View the PDF version of this paper here .

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