Mental Health
Eating Disorders
Causes of Eating Disorders - Biochemistry
To understand eating disorders, researchers have studied the neuroendocrine system, which is made up of a combination of the central nervous and hormonal systems.
The neuroendocrine system regulates multiple functions of the mind and body. It has been found that many of the following regulatory mechanisms are, to some degree, disturbed in people with eating disorders:
- sexual function
- physical growth and development
- appetite and digestion
- sleep
- heart function
- kidney function
- emotions
- thinking
- memory
Eating disorders and depression:
Many people with eating disorders also appear to suffer from depression, and is believed that there may be a link between these two disorders. For example:
- In the central nervous system, chemical messengers known as neurotransmitters control hormone production. The neurotransmitters serotonin and norepinephrine, which function abnormally in people who have depression, have been discovered to also be decreased in both acutely-ill anorexia and bulimia patients, and long-term recovered anorexia patients.
- Research has shown that some patients with anorexia may respond well to antidepressant medication that affects serotonin function in the body.
- People with anorexia, or certain forms of depression, seem to have higher than normal levels of cortisol, a brain hormone released in response to stress. It has been shown that the excess levels of cortisol in both persons with anorexia and in persons with depression are caused by a problem that occurs in or near the hypothalamus of the brain.
- Biochemical similarities have been discovered between people with eating disorders and obsessive-compulsive disorder (OCD), and patients with OCD frequently have abnormal eating behaviors.
- The hormone vasopressin is another brain chemical found to be abnormal in people with eating disorders and OCD. Levels of this hormone are elevated in patients with OCD, anorexia, and bulimia.
This page was last updated on: February 5, 2008.
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