Monday, June 2, 2008

The Biology of Bulimia

The binge-and-purge addiction.

By 2000, the biological substrate unifying alcoholism, addiction, depression, and certain eating disorders had become irrefutable. Population surveys had shown that nearly half of alcoholic patients had a long history of coexisting depression and/or anxiety disorders. Overall, about a third of patients with depression or panic disorder have had lifelong problems with drug abuse. These are estimates, best clinical guesses, but associating depression and addiction is no longer a speculative venture.

As with more familiar forms of addiction, bulimia was coming to be seen as another serotonin/dopamine-mediated medical condition. As noted, serotonin is involved in both the binge and the purge. Once researchers began performing the necessary double blind, placebo-controlled studies, it became clear that serotonin-boosting drugs dramatically lessened bulimic behavior in general, and associated carbohydrate binging in particular, in a large number of diagnosed bulimics. (Anorexia nervosa, another eating disorder, does not show the same serotonin affinities in action.)

Bulimics often maintain a normal weight, but can suffer serious physical consequence—heart rhythm irregularities, electrolyte imbalances, low blood pressure, and damage to the esophagus. Once the binge-purge cycle has been established, some researchers believe, drug-like changes in serotonin 5HT receptor distributions help reinforce the pattern. It is not surprising to learn that Prozac and other serotonin reuptake inhibitors such as dexfenfluramine were prominent among the drugs being tested against bulimia in the 1990s. By 1995, a paper presented at the National Social Science Association Conference in San Diego stated: “The serotonin hypothesis of bulimia nervosa suggests that bulimia is the behavioral manifestation of functional underactivity of serotonin in the central nervous system.”

In 1997, Prozac became the first drug ever licensed by the Food and Drug Administration (FDA) for the treatment of bulimia nervosa, as this chronic disorder is officially known. The drug’s formal approval was based on three clinical studies showing median reductions in binging of as much as 67 per cent for Prozac, compared with 33 per cent for placebo. Vomiting was reduced by 56 per cent, compared to 5 per cent for female placebo users. (About 10 per cent of diagnosed bulimics are males.) There is often a family history of alcoholism and/or eating disorders. The locus of “serotonergic dysfunction” appears to be the hypothalamus. Low levels of serotonin and dopamine metabolites have been documented in the cerebrospinal fluid of bulimic patients. Evidence exists for the involvement of norepinephrine as well.

Bulimia, like alcoholism and other drug addictions, has its psychosocial side, but twins studies show that there is very probably a genetics of bulimia to be pursued. In one influential study, an identical twin stood a one-in-four chance of developing bulimia, if the other twin was diagnosed with the disorder. A combination of SSRI drugs and some form of structured cognitive therapy is the recommended approach.

--Excerpted from
The Chemical Carousel: What Science Tells Us About Beating Addiction © Dirk Hanson 2008, 2009

Photo Credit: Graham Menzies Foundation

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