Eating Disorders - Causes

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In one study, female athletes who consumed a high-fat diet (35% of daily calories) performed longer and with greater intensity than those with a standard athletic low-fat diet (27% of daily calories). And such a diet appeared to be more estrogen-protective.

Hormonal Abnormalities

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Hormonal problems are rampant in eating disorders and include chemical abnormalities in the thyroid, the reproductive regions, and areas related to stress, well-being, and appetite. Many of these chemical changes are certainly a result of malnutrition or other aspects of eating disorders, but they also may play a role in perpetuating or even creating susceptibility to the disorders.

The primary setting of many of these abnormalities originate in a small area of the brain called the limbic system. A specific system called hypothalamic-pituitary-adrenal axis (HPA) may be particularly important in eating disorders. It originates in the following regions in the brain:

• Hypothalamus. The hypothalamus is a small structure that plays a role in controlling our behavior, such as eating, sexual behavior and sleeping, and regulates body temperature, emotions, secretion of hormones, and movement.

Click the icon to see an image of the hypothalamus.

• The pituitary gland. The pituitary gland develops from an extension of the hypothalamus downwards. It is involved in controlling thyroid functions, the adrenal glands, growth, and sexual maturation.
• Amygdala. This small almond-like structure lies deep in the brain and is associated with regulation and control of major emotional activities, including anxiety, depression, aggression, and affection.

Click the icon to see an image of the brain-thyroid link.

Stress Hormones. The HPA systems trigger the production and release of stress hormones called glucocorticoids, including the primary stress hormone cortisol. Chronically elevated levels of stress chemicals have been observed in patients with anorexia and bulimia. Cortisol is very important in marshaling systems throughout the body (including the heart, lungs, circulation, metabolism, immune systems, and skin) to deal quickly with any threat.

Release of Neurotransmitters. The HPA system also releases certain neurotransmitters (chemical messengers) that regulate stress, mood, and appetite and are being heavily investigated for a possible role in eating disorders. Abnormalities in the activities of three of them, serotonin, norepinephrine, and dopamine, are of particular interest. Serotonin is involved with well-being, anxiety, and appetite (among other traits), and norepinephrine is a stress hormone. Dopamine is involved in reward-seeking behavior. Recent research suggests that people with anorexia have increased activity in the brain’s dopamine receptors. This overactivity may explain why people with anorexia do not experience a sense of pleasure from food and other typical comforts.

Ghrelin. High levels of ghrelin, a hormone that increases the feeling of hunger and slows metabolism, have been noted in patients with anorexia and bulimia.

Low-Leptin Levels. Leptin is a hormone that appears to trigger the hypothalamus to stimulate appetite, and low levels have been observed in people with anorexia and bulimia.

Low Reproductive Hormones. The hypothalamic-pituitary system is also responsible for the production of important reproductive hormones that are severely depleted in anorexics. Although most experts believe that these reproductive abnormalities are a result of anorexia, others have reported that in 30 - 50% of people with anorexia, menstrual disturbances occurred before severe malnutrition set in and remained a problem long after weight gain, indicating that hypothalamic-pituitary abnormalities precede the eating disorder itself.

Compensating for Mood Swings during Binge-Purging Cycles

Low levels of serotonin have been observed not only in eating disorders but also in depression. One theory for the persistence of the binge-purge cycle in bulimia involves restoring serotonin imbalances and so improving mood. It involves the following:

• Bingeing elevates tryptophan, a compound found in food, particularly carbohydrates, which is essential to the production of serotonin in the brain. People may binge in order to produce serotonin, thereby improving their mood. An initial increase in tryptophan, however, produces depression in some people. Both events are consistent with a study on young people with bulimia who reported negative moods before bingeing and even worse moods right after bingeing.
• Such depression may become associated with guilt over bingeing and the need to purge. Right before and after a purge cycle, however, studies report an improvement in mood, which might indicate the delayed increase in serotonin triggered by the tryptophan. The heightened mood after the purge cycle may be due to stimulation of natural opioids that occur during this process.
• The binge-purge cycle might then be stimulated by chemical changes and perpetuated by feelings of guilt and depression after bingeing and release from guilt and euphoria during and after purging.

Infections

In some cases, infection has been associated with anorexia. In such cases, immune factors released to fight these infections may cause inflammation and injury in the areas of the brain that affect appetite and behavior.

Streptococcal Infection. The bacteria responsible for strep throat and rheumatic fever -- called group A beta-hemolytic streptococcal (GABHS) -- is now a suspect in some cases of anorexia. Some children who have been infected with these bacteria develop a syndrome that includes obsessive-compulsive disorder (OCD), tics, and anorexia nervosa. The syndrome is called PANDAS (Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcus). More research is needed to confirm this as an actual cause of anorexia and to determine if it may be treatable with antibiotics.

Epstein Barr Virus. Epstein Barr, the virus that causes mononucleosis, has also been associated with the development of anorexia.

Click the icon to see an image of infectious mononucleosis.

Review Date: 12/13/2006
Reviewed By: Harvey Simon, MD, Associate Professor of Medicine, Harvard Medical School; Physician, Massachusetts General Hospital.