Appetite

Source: Wikipedia, the free encyclopedia.
For other uses, see Appetite (disambiguation).
Not to be confused with apatite or hunger.

Appetite is the desire to eat food items, usually due to

consummatory behaviour, are the only processes that involve energy intake, whereas all other behaviours affect the release of energy. When stressed, appetite levels may increase and result in an increase of food intake. Decreased desire to eat is termed anorexia, while polyphagia (or "hyperphagia") is increased eating. Dysregulation of appetite contributes to anorexia nervosa, bulimia nervosa, cachexia, overeating, and binge eating disorder
.

Role in disease

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 (

smell ("dysgeusia", bad taste) or the lack thereof may also affect appetite.[3]

Abnormal appetite may also be linked to genetics on a chromosomal scale, shown by the 1950s discovery of Prader–Willi syndrome, a type of obesity caused by chromosome alterations. Additionally, anorexia nervosa and bulimia nervosa are more commonly found in females than males – thus hinting at a possibility of a linkage to the X-chromosome.[4]

Eating disorders

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. Furthermore, persons with anorexia nervosa may exercise ritualistically. 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.[5] 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%.[6] Similarly to bulimia, some people may be involved in purging and binging. They might vomit after food intake or take purgatives. 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.[7]

Obesity

Various hereditary forms of obesity have been traced to defects in hypothalamic signaling (such as the leptin receptor and the

orexigenic response.[9]

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 adipose cells, respectively, into the blood stream. Ghrelin stimulates feelings of hunger, whereas leptin stimulates feelings of satisfaction from food.[10] Any changes in normal 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 all ghrelin production causes insatiable appetite.[11]

Pediatric eating problems

Eating issues such as "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 (sensory processing disorder).[12]

Pharmacology and treatment

The

satiety; a study investigating the effect of satiety found that a high-glycemic food, potatoes, reduced appetite more than a low glycemic index food.[13]

Suppression

Mechanisms controlling appetite are a potential target for weight loss drugs. Appetite control mechanisms seem to strongly counteract undereating, whereas they appear weak to control overeating. Early

PYY 3-36 suggest that this agent may contribute to weight loss
by suppressing appetite.

Given the epidemic proportions of obesity in the Western world and the fact that it is increasing rapidly in some poorer countries, observers[who?] expect developments in this area to snowball in the near future.

Stimulation

Weight loss or loss of appetite ("cachexia") is an effect of some diseases, and a side effect of some prescription drugs. Stimulants such as methylphenidate commonly reduce appetite in patients,[14] and have been prescribed off-label for weight loss.[15] Three agents are approved for appetite stimulation in the United States: megestrol acetate - a progesterone available as an oral tablet, oxandrolone - an oral anabolic steroid, and dronabinol - a cannabinoid available in an oral capsule.[16]

Ghrelin, a gut hormone recognized as affecting appetite, is under investigation.[17] Ghrelin itself must be delivered parenterally[17]: 2178  and research has therefore focused on substances that can be taken orally. Rikkunshito, a traditional Japanese Kampo medicine, is under preliminary research for its potential to stimulate ghrelin and appetite.[17]

See also

Wikiquote has quotations related to Appetite.
Look up appetite in Wiktionary, the free dictionary.

References

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  2. ^ "Indigestion". Digestive.niddk.nih.gov. National Digestive Diseases Information Clearinghouse (NDDIC). Archived from the original on 2014-11-05. Retrieved 2011-12-04.
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  8. doi:10.1002/pdi.1960100105
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  9. PMID 24158035
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  10. ^ "How The Hormones Ghrelin and Leptin Affect Appetite". The Monterey Diet.
  11. PMID 12912793. Open access icon
  12. PMID 22937249
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  13. S2CID 24129879
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  14. ^ "Ritalin LA Prescribing Information" (PDF). Novartis. 2011-07-20. Archived (PDF) from the original on 2011-07-20. Retrieved 2020-06-04.
  15. ^ "How ADHD Medication Can Affect Your Weight". WebMD. Retrieved 2020-06-04.
  16. ^ Archer M, Steinvoort C, Larson B, Oderda G (2014). "Agents used as appetite stimulants: Drug class review" (PDF). University of Utah College of Pharmacy. Archived from the original (PDF) on 9 October 2016. Retrieved 19 April 2019.
  17. ^
    PMID 30110683
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