Appetite is the desire to eat food items, usually due to hunger.
However, appealing food may provoke appetite even in the absence of hunger.
Appetite regulation is an immensely complex process involving the gastrointestinal tract, many hormones, and both the central and autonomic nervous systems.
Appetite includes the biological urge to eat as well as the interplay between senses, habits, past experiences, future expectations and available food.
The sensing of fuel and appetite are controlled by the hypothalamus.
The arcuate nucleus of the hypothalamus, a part of the brain, is the main regulatory organ for the human appetite.
Appetite and hunger are regulated by the hypothalamus in conjunction with other brain regions such as the striatum, the amygdala, insula, and orbitofrontal cortex.
The hypothalamus balances orexigenic and anorexigenic neurocircuits which tailor nutrient influx during meals by balancing appetite and satiation, and the functions vested in the brainstem are considered to be alarm responses that swiftly halt food intake.
Adjustments in feeding and energy expenditure ensure adequate balance matching bodily needs.
Eating satiates the appetite, provides feelings of gratification and stimulates the brain for reward and motivation and engages the limbic and paralimbic areas under the influence of neurotransmitters and releasing neuropeptides.
Increases in fructose increases insulin resistance.
Appetite can be greatly reduced by satiety.
Appetite serves to regulate adequate energy intake to maintain metabolic needs.
It is regulated by a close interplay between the digestive tract, adipose tissue and the brain.
Positive appetite behaviour (approach behaviour, and consummatory behaviour) are the only processes that involve energy intake, whereas all other behaviours affect the release of energy.
Appetite levels may increase as a result of stress with an increase of food intake.
Decreased desire to eat is termed anorexia, while polyphagia (or “hyperphagia”) is increased eating.
Dysregulation of appetite contributes to avoidance/restrictive food intake disorder, anorexia nervosa, bulimia nervosa, cachexia, overeating, and binge eating disorder.
A limited or excessive appetite is not necessarily pathological.
Abnormal appetite could be defined as eating habits that cause malnutrition and related conditions such as obesity and its secondary problems.
There are genetic and environmental factors may regulate appetite, and abnormalities in either may lead to abnormal appetite.
Poor appetite, or anorexia,can have numerous causes, but may be a result of physical problems of infectious, autoimmune or malignant disease, or psychological of stress, or mental disorders.
Hyperphagia or excessive eating, may be a result of hormonal imbalances, mental disorders and others reasons.
Dyspepsia, known as indigestion, can also affect appetite as one of its symptoms is feeling full soon after beginning a meal.
Taste, dysguesia, and smell, and bad taste or the lack thereof may also affect appetite.
Abnormal appetite may also be linked to genetic/chromosomal abnormalities: Prader–Willi syndrome, a type of obesity caused by chromosome alterations.
Anorexia nervosa and bulimia nervosa are more commonly found in females than males, suggesting the possibility of a linkage to the X-chromosome.
Dysregulation of appetite lies at the root of anorexia nervosa, bulimia nervosa, and binge eating disorder.
Anorexia nervosa is a mental disorder characterized as severe dietary restriction and intense fear of weight gain.
Individuals who have anorexia have high levels of ghrelin, a hormone that stimulates appetite, so the body is trying to cause hunger, but the urge to eat is being suppressed by the person.
Binge eating disorder, eating excessively or uncontrollably) between periodic time intervals can be present in children and most commonly manifests during adulthood.
The heritability of binge eating disorder in adults is approximately 50%.
Similarly to bulimia, some people with binge eating disordermay be involved in purging and binging.
The body dysmorphic disorder may involve food restriction in an attempt to deal with a perceived fault, and may be associated with depression and social isolation.
Some hereditary forms of obesity have been traced to defects in hypothalamic signaling, such as the leptin receptor and the MC-4 receptor.
Prader-Willi syndrome has a decreased response to satiety that may promote development of obesity.
It has been found that ghrelin-reactive IgG immunoglobulins affect ghrelin’s orexigenic response.
Ghrelin and leptin are released from the stomach and adipose cells, respectively, into the blood stream.
Ghrelin stimulates feelings of hunger, whereas leptin stimulates feelings of satisfaction from food.
Changes in production levels of these two hormones can lead to obesity.
The amount of leptin hormone production is stimulated by body fat percentage.
When body fat accumulates there is overproduction of leptin causing a resistant hypothalamus and eventually almost no leptin effect.
From then ghrelin production causes insatiable appetite.
Picky eating affects about 25% of children, but among children with development disorders this number may be significantly higher, which in some cases may be related to the sounds, smells, and tastes or a sensory processing disorder.
The glycemic index is thought to affect satiety; a high-glycemic food, potatoes, reduced appetite more than a low glycemic index food.