Researchers have attempted to explain eating disorders through neurological abnormalities and biochemical imbalances. The hypothalamus acts as a form of control centre which sends messages to various parts of the brain affecting the behaviours that control eating. There are two parts, the lateral hypothalamus (LH) and the ventromedial hypothalamus (VMH). The former supposedly produces hunger when activated whilst the latter depresses the appetite when it is activated. Keesey and Corbett (93) found that these two parts of the brain act as a weight thermostat. The LH is activated if the weight falls lower than the set point in order to produce hunger however if it weight continues to fall the VMH is activated.
If the hypothalamus is not functioning adequately, this could provide an explanation for eating disorders. This malfunctioning of the hypothalamus may cause a primary problem such as Amenorrhea which sometimes takes place before weight loss due to low endocrine levels.
The major problem with this theory however is that there is no conclusive evidence from post-mortems that anorexia and bulimia are caused by neurological damage as they have not found any damage to the hypothalamus.
Research has been carried out more recently investigating the effects of some neurotransmitters such as norepinephrine, dopamine and serotonin due to evidence that sufferers of anorexia and bulimia have abnormalities in their levels of neurotransmitters. Jimerson et al (97) compared the serotonin function in patients with bulimia with a control group of healthy participants and found significant differences. They concluded that impaired serotonin responsiveness may provoke the onset of bulimia and maintain the disorder. Binge eating is linked with low levels of serotonin therefore Walsh et al (97) developed a serotonin-active antidepressant which has proven to be the most effective biological treatment for bulimia as it decreases binge eating.
Fava et al...