Role in disease appetite

Role in disease  appetite

A limited or excessive appetite is not necessarily pathological. Abnormal appetite could be defined as eating habits causing malnutrition and related conditions such as obesity and its related problems.
Both genetic and environmental factors may regulate appetite, and abnormalities in either may lead to abnormal appetite. Poor appetite (anorexia) can have numerous causes, but may be a result of physical (infectious, autoimmune or malignant disease) or psychological (stress, mental disorders) factors. Likewise, hyperphagia (excessive eating) may be a result of hormonal imbalances, mental disorders (e.g. depression) and others. Dyspepsia, also known as indigestion, can also affect appetite as one of its symptoms is feeling "overly full" soon after beginning a meal.^[6]
Abnormal appetite may also be linked to genetics on a chromosomal scale. In the 1950s, the discovery of the Prader Willi Syndrome, a type of obesity, displayed a causation at a gene locus. Additionally, anorexia nervosa and bulimia nervosa are more commonly found in females than males - thus hinting a possibility of a linkage to the X-chromosome.^[7]
Dysregulation of appetite lies at the root of anorexia nervosa, bulimia nervosa and binge eating disorder. Anorexia nervosa is an eating condition categorized by a penetrating fear of being fat and severe limit of food consumption. Furthermore, they might do excessive exercise. Individuals that have anorexia have high levels of ghrelin, a hormone that stimulates appetite, so the body is trying to cause hunger, but it is being suppressed by the person.^[8] Binge eating disorder (commonly referred to as BED,) is described as eating excessively (or uncontrollably) between periodic time intervals. The risk for BED can be present in children and most commonly manifests during adulthood. Studies suggest that the heritability of BED in adults is approximately 50%.^[9] Likewise to bulimia, several people may be involved in purging and binging. They might puke after food intake or take purgatives. However, the person may still believe they are overweight.^[10]
Various hereditary forms of obesity have been traced to defects in hypothalamic signalling (such as the leptin receptor and the MC-4 receptor), or are still awaiting characterisation – Prader-Willi syndrome – in addition, decreased response to satiety may promote development of obesity.^[11]
Other than genetically-stimulated appetite abnormalities, there are physiological ones that do not require genes for activation. For example, ghrelin and leptin are released from the stomach and pancreas, respectively, into the blood stream at the signal of the hypothalamus. Ghrelin stimulates feelings of hunger, whereas leptin stimulates feelings of satisfaction from food.^[12] Any changes in normal production levels of these two hormones will lead to obesity. Looking at leptin, the more cells present in a body, the more adipose tissues there are, and thus, the more leptin would be produced. This overproduction of leptin will cause the hypothalamus to become resistant to leptin and so, although the pancreas is producing leptin, the body will not understand that it should stop eating.^[13] This will produce a perpetual cycle for those that are obese.

Pharmacology