The Biochemistry of Eating Disorders

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An essay which pins down some of the latest scientific discoveries relating to the causes of behavioural illness, specifically eating disorders.

Submitted: December 29, 2011

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Submitted: December 29, 2011



The Biochemistry of Eating Disorders

By Niamh Jiménez


In a world where psychological illness is becominganirrefutablereality, this article aims to pin down the biochemical causes of behavioural disorders, with a special focus on eating disorders such as anorexia nervosa and obesity. Experts have discovered that lesions in the hypothalamus, leptin and abnormalities in levels of important neurotransmitters may be aiding and abetting psychological illness.

The Hypothalamus and Hunger

Experts postulate that the region of the brain known as the hypothalamus, comprising the lateral and ventromedial hypothalamus, plays a significant role in the manifestation of hunger and satiety. When we eat, glucose derived from our food is converted into fat by the liver and stored for later use. Stimulation of the lateral hypothalamus by the liver occurs in the absence of sufficient glucose levels; the lateral hypothalamus, now activated, initiates the responses our bodies have developed over time to signal hunger and thus trigger the act of consumption. These signals may manifest as stomach contractions or “hunger pangs”. The paraventricular hypothalamus governs our cravings for certain food types; hence it is responsible for alerting our bodies to the particular foods and nutrients it may require at any given time.

The ventromedial hypothalamus is responsible for the cessation of eating and feelings of satiety. Other factors, such as the distension of the stomach, are also involved in communicating the body’s need for nourishment. When food travels from the stomach to the intestines, a hormone known as CCK (Cholecystokinin) is secreted, causing a signal to be transmitted to the ventromedial hypothalamus, which in turn prompts the cessation of eating.

Suppression of appetite may be caused by a hormone called leptin, which is produced by the fat cells, and whose mechanism of action involves the hypothalamus.

Leptin and its Role in Appetite Suppression

Leptin plays an active role in appetite suppression via the hypothalamus. Leptin operates by stimulating the leptin sensitive cells, located in the medial hypothalamus, which are known as “anorectic” nerve cells. The term “anorectic” simply refers to substances which induce appetite loss. Once activated, these anorectic nerve cells secrete appetite suppressing neuropeptides, for example, POMC and CART. Neuropeptides consist of protein-like molecules, molecules comprising chains of amino acids, and play a significant role in brain activity and function. They are expressed and liberated by neurons which employ these molecules as a means of inter-communication. Examples of the different brain-related sensations governed by neuropeptides are reward, patterns of eating, and analgesia (numbness). Leptin stimulates the anorectic nerve cells, while simultaneously provoking an inhibition of the “orexigenic” cells, which regulate and encourage eating behaviour through the release of the neuropeptides NPY and AGRP.

Although scientists were aware of the hypothalamus’ active role in the regulation of eating behaviour and weight loss, the hormone leptin and its signals to the hypothalamus are relatively recent discoveries. Experiments involving lesions to the lateral and ventromedial hypothalamuses in rats have resulted in appetite suppression leading to eventual starvation, and compulsive eating, respectively. The lateral hypothalamus is believed to be the “eating centre”, as stimulation of this region causes compulsive eating and obesity, while damage to the region has been seen to induce appetite suppression.

Conversely, the ventromedial hypothalamus is said to be the “satiety centre” as its stimulation results in lack of appetite, while damage induces compulsive eating and obesity. These hypotheses have been corroborated by experiments which were conducted on the lateral and ventromedial regions of the lab rat’s brain. The neurotransmitters, norepinephrine, serotonin and dopamine, are believed to underlie these regulatory mechanisms. It can therefore be deduced that an abnormality in the activity or level of one of these neurotransmitters could negatively impinge upon the functioning of the satiety and eating centres, causing either appetite suppression in anorexics or appetite stimulation in the obese.

The net effect is that the leptin-sensitive cells send appetite-suppressing signals to key nerve cells in the lateral hypothalamus thought to control several behaviours including feeding, including a group that release the MCH neuropeptide.[1] Experiments on rats have shown that rats which lack the MCH gene were extremely thin and ate an insufficient diet, when compared with the intakes of their littermates.

The Brain-Thyroid Link

Abnormalities common amongst anorexics include a fall in the level of reproductive hormones, proliferation of stress-producing hormones, faulty appetite regulation and changes in thyroid function. These symptoms, while identified primarily as the outcome of developing an eating disorder, may also play a fundamental role in the perpetuation of the cycle of starvation. These abnormalities and biochemical changes are mainly centred on an area of the brain known as the limbic region.

In examining the effects of malnourishment, the pituitary gland is hugely important as it regulates thyroid function, the adrenal glands, growth and sexual development. Sexual maturation is often stunted in an anorexic due to a decrease in the levels of reproductive hormones; growth and adrenal function may also be affected, and the secretions of the thyroid gland, closely related to metabolism, may become diminished. Therefore, interference with or damage to the pituitary gland, a vital endocrine gland, gives rise to the hoard of hormone deficiencies commonly associated with the disorder. For example, damage to the hypothalamus or the pituitary gland affects the functioning of the thyroid, which in turn curbs its secretion of thyroid hormones influencing the metabolism. This accounts for an anorexic’s severe diminution of metabolic rate.

The amygdala is a region of the brain which is involved in the regulation of emotional response, including anxiety, stress, and depression. Sufferers of eating disorders experience a huge increase in stress and stress-stimulating hormones giving rise to prolonged states of depression and extreme anxiety. Anorexics and bulimics tend to have perpetually elevated levels of cortisol in their bloodstreams, a stress-inducing glucocoticoid; this hormone is involved in mobilizing body systems such as the heart, lungs and metabolism in the event of confronting a threat.

Neurotransmitters are chemicals secreted by nerve cells (neurons) which stimulate neighbouring neurons in the transmission of messages, in the form of electrical impulses, from one neuron to the next throughout the nervous system. Abnormalities in the levels and activity of three particular neurotransmitters, serotonin, norepinephrine, and dopamine, are prevailing trends in the malnourished. Serotonin is involved in the regulation of appetite, anxiety and general health, norepinephrine is a stress-related hormone, and dopamine stimulates reward-seeking behaviour. Dopamine receptors undergo a higher degree of stimulation and elevated activity in the brains of anorexics; the fact that these receptors are abnormally active may account for an anorexic’s inability to derive pleasure from the act of eating. Ghrelin, a hormone which increases hunger and reduces the rate of metabolism, has also been found to be present in elevated levels.

The production of crucial reproductive hormones is carried out by the HPA (hypothalamic-pituitary-adrenal axis). Studies show that these hormones are considerably depleted in anorexics. Although many may conceive of these abnormalities occurring as a result of developing the illness, 30 - 50% of anorexics experience aberrations in and disruptions to normal menstruation prior to any manifestation of severe malnutrition. Menstrual abnormalities may persist long after the restoration of normal weight gain and recovery. This appears to substantiate the theory that disturbances to the hypothalamic-pituitary system precede the development of the eating disorder and its physical symptoms.

Abnormalities in Neurotransmitters and Serotonin

Administration of serotonin to either the lateral or ventromedial hypothalamuses resulted experimentally in appetite suppression and eventual starvation. The administration of norepinephrine to lab animals induced a similar outcome. An increase in the body’s natural levels of serotonin was also found to generate sensations of restlessness and anxiety. One theory concerning anorexic behaviour is that an increase in serotonin activity, accompanied by elevated anxiety, may subconsciously prompt the sufferer to restrict his or her intake to combat the nervousness. Thus the overactivity of serotonin provokes the subconscious act of starvation in order to achieve an emotional sense of control and calm, something which is achieved by the brain’s physical response.

Abnormalities in serotonin levels may result in depression or anxiety, which are correlated not merely with malnutrition but also with behavioural disorders such as Obsessive Compulsive Disorder, Bipolar Disorder, Borderline Personality Disorder, and Attention Deficit/Hyperactivity Disorder (ADHD). The overproduction of serotonin or disruptions to its normal activity may also be caused by a genetic predisposition.


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