Eating disorders, including the diagnoses of anorexia nervosa, bulimia, binge-eating disorder, and atypical eating disorder, occur in 5-10 million females and 1 million males. Anorexia nervosa, with avoidance of high calorie foods, fear of gaining weight and distorted body image has the highest mortality rate, at 10% within ten years of diagnosis. Bulimia is self-induced vomiting. Athletes are at high risk for eating disorders, especially exercise-induced vomiting.
Anorexia in females causes weight loss and amenorrhea, diagnosed by the absence of at least three menstrual periods. In males, anorexia causes disorders of the hypothalamic-pituitary-gonadal axis with the loss of sexual motivation and impotency.
Genetic studies show that eating disorders are more common in people who have a family history of an eating disorder. Both twins are more likely to develop eating disorders in identical twins than in fraternal twins because of a genetic tendency.
Serotonin abnormalities seem to be involved in eating disorders. Tryptophan, which is necessary for serotonin production, is easily depleted by food restriction and can be studied easily. Insulin resistance, seen in anorexia and bulimia, reduces the production of serotonin from tryptophan. Low levels of serotonin are seen in low-weight anorexics.
Serotonin is necessary for the feeling of being full, a problem in bulimia. Bulimia studies consistently show problems with serotonin. Bulimics have poor responses to serotonin agonists (medications to increase serotonin). Binging and vomiting reduces serotonin synthesis.
Tryptophan depletion diets make the symptoms of bulimia worse. L-tryptophan given to bulimics reduced the size of meals eaten as compared to a pharmaceutical serotonin agonist that increases sertonin levels. A precursor of serotonin, 5-hydroxytryptophan (5-HTP), reduced prolactin production. This indicated that the patients most likely had low serotonin levels prior to dosage with the 5-HTP. Treatment of bulimics with 1 gram of L-tryptophan and 45 mg. of pyridoxine three times a day improved mood and decreased bulimic behavior.
Inositol was given at 18 grams a day to patients with bulimia and binge-eating disorder. After twelve weeks, there was significant improvement in binge eating and side effects of abdominal pain, gas, and soft stools were reduced by 12 grams of inositol per day.
Common complications of eating disorders include electrolyte abnormalities. Most commonly, patients with self-induced vomiting, diuretic use, and laxative abuse develop low levels of potassium (hypokalemia). Chronic hypokalemia can result in constipation, muscle wasting, and kidney damage. Patients commonly develop low magnesium levels along with the low potassium. The blood level of potassium can be normal even when the level within the body’s cells is low.
Low phosphate levels (hypophosphatemia) are the result of vomiting, diuretics, laxatives, and antacids used in eating disorders. Hypophosphatemia can be fatal or can be the cause of osteoporosis, often seen in low weight dancers with eating disorders.
Cardiovascular effects are due to electrolyte abnormalities and include bradycardia (low pulse), hypotension (low blood pressure) and blood pressure drop on standing (orthostatic hypotension). Irregular rhythms coming from the ventricles are a common cause of death in anorexia. Ipecac (a medication used to induce vomiting) abuse causes damage to the heart muscle.
There is evidence for thyroid shrinkage with eating disorders. This causes low thyroid hormone output, which contributes to mood depression. Gastrointestinal disorders are common with eating disorders, including pancreatitis and esophagitis.
Disorders of the hypothalamic-pituitary-gonadal axis can result in amenorrhea. Low levels of DHEA, DHEA sulfate and androstenedione are common. Elevated cortisol levels have been found to be predictive of major depression in eating disorders in adult females and in younger males and females. Serotonin regulation problems result in high cortisol levels (hypercortisolemia). There is some evidence that phosphatidylserine, a complexed amino acid found in the nervous system, can lower cortisol levels and relieve depression in bulimics.
Bone loss in eating disorders is the result of acidosis, low estrogen levels, malnutrition, and other factors. DHEA and insulin-like growth factor (IGF) treat the bone loss.
The incidence of eating disorders is increased in young females with type 1 diabetes as compared to young women without diabetes. Eating disorders should be suspected in young women with poorly controlled diabetes with repeated episodes of ketoacidosis.
Zinc may be involved with eating disorders because the symptoms of zinc deficiency are similar to the symptoms of eating disorders. Zinc is necessary to gain weight in anorexia. Serum zinc levels are a poor measure of the body’s total zinc status. Zinc helps correct many of the problems seen in eating disorders, such as prolactin problems, estrogen deficiency and low testerone levels. Zinc deficiency reduces levels of leptin, a peptide that helps regulate appetite in the hypothalamus.
Thiamine, riboflavin and magnesium deficiencies have been seen in eating disorders.
CONCLUSION: Treatment of eating disorders is quite complex and eating disorders are, potentially, fatal. Multiple nutrient deficiencies are seen in eating disorders and require treatment. Eating disorders cause endocrine, neurologic, bone density and gastrointestinal disorders. Further testing is needed to determine the effectiveness of inositol, zinc and serotonin precursors.
NOTE: Eating disorders are life threatening and, often, require extensive medical care.
To read the author’s abstract of the article click on the link to the author’s title of the article above.