Eating Disorder – Anorexia nervosa – Factors,Causes
It is clear that there is no single cause for anorexia and that it stems from a mixture of social, psychological and biological factors. Current research is commonly focused on explaining existing factors and uncovering new causes. However, there is considerable debate over how much each of the known causes contributes to the development of anorexia. In particular, the contribution of perceived media pressure on women to be thin has been especially contentious.
Family and twin studies have suggested that genetic factors contribute to about 50% of the variance for the development of an eating disorder and that anorexia shares a genetic risk with clinical depression.This evidence suggests that genes influencing both eating regulation, and personality and emotion, may be important contributing factors.
Several rodent models of anorexia have been developed which largely involve subjecting the animals to various environmental stressors or using gene knockout mice to test hypotheses about the effects of certain genes on related behaviour. These models have suggested that the hypothalamic-pituitary-adrenal axis may be a contributory factor, although the models have been criticised as food is being limited by the experimenter and not the animal, and these models cannot take into account the complex cultural factors known to affect the development of anorexia nervosa.
There are strong correlations (but not proven causation) between the neurotransmitter serotonin and various psychological symptoms such as mood, sleep, emesis (vomiting), sexuality and appetite. A recent review of the scientific literature has suggested that anorexia is linked to a disturbed serotonin system, particularly to high levels at areas in the brain with the 5HT1A receptor – a system particularly linked to anxiety,
mood and impulse control. Starvation has been hypothesised to be a response to these effects, as it is known to lower tryptophan and steroid hormone metabolism, which, in turn, might reduce serotonin levels at these critical sites and, hence, ward off anxiety.
In contrast, studies of the 5HT2A serotonin receptor (linked to regulation of feeding, mood, and anxiety), suggest that serotonin activity is decreased at these sites. One difficulty with this work, however, is that it is sometimes difficult to separate cause and effect, in that these disturbances to brain neurochemistry may be as much the result of starvation, than continuously existing traits that might predispose someone to develop anorexia. There is evidence, however, that both personality characteristics (such as anxiety and perfectionism) and disturbances to the serotonin system are still apparent after patients have recovered from anorexia, suggesting that these disturbances are likely to be causal risk factors.
Zinc deficiency causes a decrease in appetite that can degenerate in anorexia nervosa (AN), appetite disorders and, notably, inadequate zinc nutriture. The use of zinc in the treatment of anorexia nervosa has been advocated since 1979 by Bakan. At least five trials showed that zinc improved weight gain in anorexia. A 1994 randomized, double-blind, placebo-controlled trial showed that zinc (14 mg per day) doubled the rate of body mass increase in the treatment of AN. Deficiency of other nutrients such as tyrosine and tryptophan (precursors of the monoamine neurotransmitters norepinephrine and serotonin, respectively), as well as vitamin B1 (thiamine) could contribute to this phenomenon of malnutrition-induced malnutrition.