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It is helpful to look at some examples of EDNOS. The criteria for anorexia nervosa call for patients to weigh less than 85% of their ideal body weight (IBW) (1). Some individuals meet all the parameters for anorexia except that, despite profound weight loss, they are above 85% IBW. Suppose, for instance, that a patient presents at 87% IBW; her symptom profile would pose a significant risk to her health and well-being and would be classified as an eating disorder not otherwise specified. Similarly, amenorrhea (absent menses) is an official criterion for anorexia; for women who menstruate but meet every other determinant of the illness, the EDNOS diagnosis would be appropriate (1).

Narrowly missing all the criteria for anorexia or bulimia is associated with substantial impairment and comorbidity (4-7). Individuals who present with all but one of the official determinants of anorexia or bulimia often go on to develop full criteria (8-10). Low bone density occurs not only in women who meet the full anorexia classification but also in those who fulfill all the criteria except amenorrhea (7, 11). On tests of eating disorder severity, depression and self-esteem no differences were found between adolescents with full-fledged anorexia and adolescents with EDNOS who narrowly missed strict criteria for anorexia (3).

Other EDNOS types overlap with bulimia nervosa, which is characterized by recurrent binge eating and inappropriate compensatory behaviors (such as self-induced vomiting, misuse of laxatives or diuretics, fasting, excessive physical activity) to prevent weight gain. One of the official determinants of bulimia is binge eating twice a week (1). For a patient who binges once a week but meets all other parameters for bulimia, EDNOS would be the appropriate diagnosis. Like individuals who meet all criteria for the illness, many who miss the bulimia diagnosis only because of the binge frequency criterion are prone to depression and are unduly concerned about body size and weight (4, 12).

Over the last decade, increased research has focused on the EDNOS called binge eating disorder (BED). This illness spreads across different ethnic groups (13), striking an estimated 3.2% of females and 2% of males between the ages of 18 and 65 in the United States (13, 14). There is mounting evidence that BED also afflicts adolescents (3, 15, 16). The hallmark of BED is recurrent binge eating in the absence of compensatory behaviors to prevent weight gain. Individuals with this illness are often overweight or obese and experience marked distress regarding their eating behaviors (13).

BED impacts all aspects of a patient’s life, compromising health and leading to impaired occupational and social functioning (13,17,18). Obesity, which has become increasingly prevalent in America over the last three decades, is associated with heightened risk for Type 2 diabetes, cardiovascular disease and some kinds of cancer (19). When asked about their health, obese binge eaters often acknowledge major disorders such as high blood pressure, visual impairment, asthma or other respiratory illness, cardiac problems, diabetes, or arthritis (20). In addition, obese individuals who binge eat are prone to sleep disturbances, chronic muscle pain, low back pain and increased neck-shoulder pain (21). Due to their physical health problems, many patients with this illness find it very difficult, if not impossible, to participate in usual activities (22).

The fact that such physically infirmed individuals also suffer from psychiatric symptoms makes their lives all the more trying. People with BED place inordinate emphasis on body weight or shape and often measure their self-worth based on these factors (13, 23, 24). In comparison to the nonbingeing obese, obese individuals who binge eat have lower self-esteem (17) and experience significantly greater disturbance in eating attitudes and behavior as well as higher distress regarding body size and shape (25, 26). And, relative to obese controls, patients with BED are substantially more likely to suffer from a co-existing brain disorder such as major depression (25, 26).

Family and twin studies have been invaluable in teaching us about the genetic aspects of eating disorders. Recent research has demonstrated that BED runs in families. Relatives of individuals with BED are more likely to develop the illness than relatives of control subjects (27-29). A study conducted in 2008 estimated BED’s heritability at 57%, which is similar to those of bulimia nervosa (60%) and anorexia nervosa (56%) and higher than that of major depression (38%) (references 29-33).

BED is polygenic, meaning that its development is influenced not by a single gene but rather by the combined effects of many. Efforts are underway to locate the specific genes that confer vulnerability to this illness. In order to appreciate the complexity of such a search, it helps to think of the genome (the entirety of a person’s DNA) as a code of over 3 billion molecular bases across 23 pair of chromosomes (34). Genetic makeup is largely determined by the order in which these bases occur. This sequence is very much the same from one person to another, but there are millions of individual differences along the way that can serve as indicators of disease vulnerability (34). Determining whether people with a particular illness share the same areas of abnormal genetic activity is a huge challenge that is driving exciting advances in technology (34).

Scientists are learning more about the potential roles of the neurotransmitters serotonin and dopamine in the biology of BED and such knowledge is helping to inform the search for specific vulnerability genes (35, 36). There is also interest in the hormone ghrelin, one of several neuropeptides (molecular messengers) involved in appetite regulation. Recent evidence of unusually low concentrations of ghrelin in the plasma of BED sufferers (37) raises interesting possibilities. Are variant (abnormal) ghrelin genes more common in individuals with BED than in those without the illness? Do such genes contribute to susceptibility to BED? Research is addressing these questions (38).

To put the question of biological basis in perspective, it is helpful to look at what is known about the psychiatric illnesses that often accompany eating disorders. For example, studies of major depression have generated valuable clues—particularly about neurotransmitter systems—and called attention to several genes as potential contributors to the illness; yet understanding of the neurochemical and genetic underpinnings of major depression is incomplete (39). Disturbance in neurotransmitters is also implicated in the biology of anxiety disorders, such as obsessive compulsive disorder (40), social anxiety disorder (41) and panic disorder (41) and though research to identify the specific genes that influence the development of these conditions has moved forward, there is still a long way to go.

With professional treatment, the majority of individuals with BED improve and many recover (13, 42). A multidisciplinary, team approach to treatment is most effective due to the disease’s complex combination of genetic, neurochemical, psychological and sociocultural factors. Recommended services for individuals with BED generally include nutritional counseling (43), individual or group psychotherapy, and medication.

For many patients, psychotherapy unlocks the door to recovery. Of the short-term psychological approaches to the treatment of BED, cognitive behavioral therapy (CBT) is the most effective, though other models, such as interpersonal therapy (which focuses on relationships) and dialectical behavior therapy (which focuses on affect) can also be useful (13, 44). In CBT, patients learn to monitor their eating problems and to restructure their negative self- and body- thoughts into positive ones as a foundation for behavior change. Though not particularly effective in promoting weight loss (13), CBT typically leads to reductions in binge eating and depression and these improvements are often maintained over a one-year follow-up period (13, 45).

Another exciting development in the quest for successful treatments for BED is the potential role of medication. Antidepressants are the most widely studied drugs for this illness (13). The class of antidepressant known as Selective Serotonin Reuptake Inhibitors (SSRIs) includes the well-known Prozac (fluoxetine), as well as similar medications, which help regulate neurotransmitter activity in the brain and are well-tolerated in most cases. Short-term treatment with SSRIs can help cut down on binge eating episodes and give patients a sense of overall improvement, but does not necessarily result in weight loss (44, 46).

Other medications are now under study for the treatment of BED, and results sound promising. One is the anticonvulsive drug Topamax (topiramate), which helps suppress binge eating and promotes weight loss (47), and may also be helpful to individuals with bulimia nervosa (48). Another is Meridia (sibutramine), an appetite suppressant approved in 1997 by the U.S. Food and Drug Administration for the treatment of obesity. Recent testing of Meridia as a potential medication for BED showed reductions in binge eating and body weight (49). A third drug of interest is Strattera (atomoxetine), which is used for the treatment of attention-deficit hyperactivity disorder. A short-term trial of Strattera in patients with BED demonstrated decreases in body weight and in binge eating (50). Future testing will help shed light on the effectiveness of each of these three medications (Topamax, Meridia, Strattera) when prescribed in combination with CBT for the treatment of BED (13).

For eating disorders not otherwise specified – just as for full-criteria anorexia and bulimia – the importance of early diagnosis and intervention cannot be emphasized enough. Patients who enter treatment early in the course of these illnesses are more likely to achieve positive outcomes (2,8). Comprehensive, individualized treatment programs that address the multiple dimensions of eating disorders and provide conscientious follow-up go a long way in restoring patients to health and in preventing relapse of these potentially disabling illnesses.

Click to view:
The Biological Basis of Anorexia Nervosa
The Biological Basis of Bulimia Nervosa

References: The Biological Basis of Eating Disorder Not Otherwise Specified (EDNOS)

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This page was posted on May 14, 2008.