Everyone eats, and to some extent almost everyone has eating issues. From a public health perspective, secular prophets besiege us with stern warnings and commandments related to eating and weight (1). We know that increasing percentages of Americans are now overweight or obese, and also that an increasing number are dangerously underweight. During that past golden era, when we weren’t so sedentary or so preoccupied with thinness, more people successfully cleaved closer to the golden mean, we are told. Now, on the scale, many of us come up short (or fat, or thin). Individuals who take this too seriously worry about health matters, become self-deprecating for dietary misbehaviors, and find justification for poor self-esteem. Some people manage to modify their weight through effective lifestyle change, but many turn repeatedly to drastic, short-term, and ultimately ineffectual weight loss methods or to self-inflicted serious semistarvation with its attendant negative physical and psychological consequences. Lucky individuals for whom overeating or undereating, or overexercising or underexercising, aren’t especially big deals find it hard to fathom those people at either extreme of the weight spectrum who can’t seem to control their eating behaviors. Those suffering from weight- and eating-related maladaptive behaviors may seem morally inferior. Health professionals as well as laypersons easily fall into blaming and scolding modes when confronting those whose eating patterns lead, in one direction or the other, to visually obvious deviance (2).
Two reports in this issue of the Journal detail emerging findings from the weight and eating disorders research front that reflect the wide scope of the biopsychosocial approach.
Devlin and colleagues provide a masterful overview of information about the causes, consequences, and treatment of obesity. Their presentation underscores that obesity, or better perhaps, the obesities, are medical conditions, not psychiatric disorders listed in the DSM. Obesity becomes psychiatrically relevant because it is a prominent health issue for many of our patients and because some obese patients have concurrent psychiatric issues of considerable importance to their treatment. Patients with extremely dangerous and disabling morbid obesity are often severely self-disparaging and often have other comorbid psychiatric problems as well.
As Devlin et al. describe, various physiological propensities, through a myriad of genetic influences, contribute to becoming overweight or obese. More than 200 distinct genes that contribute to appetite, hunger, satiety, metabolic efficiency, fat storage, and/or activity tendencies have already been identified (3, 4). For example, genetic factors may contribute to the extent to which humans "fidget" and expend calories through nonexercise activity thermogenesis (NEAT) (5), only one way in which some thinner individuals differ from those of a stockier persuasion. Animal models for genetically induced obesity abound.
But it’s clear that nurture and environment play important roles in shaping our shapes. Animal models for environmentally induced obesity also abound (6). Although genes may set tendencies and determine limits in biological and psychological growth and development, for humans, the cultures of family, peers, and community fashion the play-by-play actions that determine how we shape up. The story of the Pima Indians told by Devlin et al. shows how environments interact with genes to produce phenomenological realities. Given a genetic package geared toward maximal energy efficiency in the harsh world of hunter-gatherers in Southwestern deserts, if you are a Pima Indian who lives in Mexico and your environment requires that you be physically active for more than 20 hours a week to obtain your daily bread, you stay slim. If you have the same genetic package, live north of the border in Arizona, find that highly palatable food is easily obtainable, and can get along by doing no more than a few hours of physical activity a week, you are much more likely to become fat and develop diabetes (7).
For the mental health field, one obesity-related issue requiring special mention is that many effective medications—including typical and atypical antipsychotics, lithium, valproic acid, and certain antidepressants—are notorious for inducing weight gain (8, 9). Many patients, especially younger women, have great difficulty accepting obesity as a cost of taking these medications, and so medication adherence suffers. Better designer psychopharmacology is sorely needed.
As for anorexia nervosa and related eating disorders, genetic-environmental interactions also rule. In this issue of the Journal, Bulik and coworkers describe the many different combinations, permutations and sizes of eating disorders-related concerns, attitudes, and behaviors reported by a large community sample. It is noteworthy that 1,071 of the 2,163 Caucasian female subjects who constituted their study group responded positively to at least one question screening for eating disorders. This result accents the astonishing prevalence of these concerns in the population at large. The substantial psychiatric comorbidity they report as accompanying eating disorder syndromes is eye-catching and suggests that psychiatrically burdened, weight-preoccupied individuals may be most vulnerable to clinical eating disorders. Notably, the monozygotic twins in their study were more likely to resemble one another in class membership in eating disorder subtypes than were the dizygotic twins.
Studies searching for candidate genes that may contribute to the etiology of eating disorders are actively underway. (If you know of a family in which several members have a clinical eating disorder, please call 1-888-895-3886 for information about how the family may be enrolled in a multicenter study hosted at the University of Pittsburgh.) At least one genetically interesting animal model exists: in herds bred to produce leaner pork, veterinarians have observed the emergence of some hyperactive sows that eat little and waste away. This disorder, called "thin sow disease" and bearing some phenotypic resemblance to anorexia nervosa, has captured the interest of geneticists studying eating disorders (10). Other potential genetic factors in these disorders may contribute to tendencies to eat in the face of emotional arousal or frustration or may relate to temperamental tendencies such as perfectionism, compulsivity, impulsivity, "neuroticism," and other salient behavioral, cognitive, and emotional propensities. Still, the answer is unlikely to be all in the genes. In an environmentally induced animal model of anorexia nervosa, so-called activity anorexia, rats who are both underfed and put on running wheels may run themselves to death. Studies of brain pathophysiology and of the potential benefits of selective serotonin reuptake inhibitors are now being conducted using this model (11).
What about treatment? Here clinicians must approach with great humility. For treatment of obesity, given professional caution in the wake of the "fen-phen" debacle, standard fare is still largely based on nutritional modification together with behavioral and psychological change—and compassion. Medications and, in the case of morbid obesity, surgery are reserved for medically high-risk, less tractable cases. Results are mixed at best. With the potential for bringing multibillion-dollar profits and with data on pertinent genes and receptors briskly rolling off research benches, the number of promising antiobesity agents looming on the biotech horizon is huge. In care of patients with anorexia nervosa, bulimia nervosa, and binge-eating disorder, we’re getting a little better, but we haven’t yet achieved real success. Reasonable treatments exist for bulimia nervosa, and they may be emerging for binge eating disorder. Clinical research on human anorexia nervosa is very difficult to do, so treatment remains a mix of compassionate understanding, common sense, clinical experience from leading centers, and interventions informed by evidence-based medicine (12). We’re pounding away, but still have a long way to go.
Address reprint requests to Dr. Yager, Department of Psychiatry, University of New Mexico School of Medicine, 2400 Tucker NE, Albuquerque, NM 87131-5326; firstname.lastname@example.org (e-mail).