Appetite

Appetite is the desire to eat food, sometimes due to hunger. Appealing foods can stimulate appetite even when hunger is absent, although appetite can be greatly reduced by satiety.[1] Appetite exists in all higher life-forms, and 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. Appetite has a relationship with every individual’s behavior. Appetitive behaviour also known as approach behaviour, and consummatory behaviours, 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[edit]

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.[2] Taste and smell (“dysgeusia“, bad taste) or the lack thereof may also effect 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[edit]

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. However, the person may still believe they are overweight.[7]

Obesity[edit]

Various hereditary forms of obesity have been traced to defects in hypothalamic signaling (such as the leptin receptor and the MC-4 receptor) or are still awaiting characterization – Prader-Willi syndrome – in addition, decreased response to satiety may promote development of obesity.[8] It has been found that ghrelin-reactive IgG immunoglobulins affect ghrelin’s 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. 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 adipose cells are producing leptin, the body will not understand that it should stop eating.[11] This will produce a perpetual cycle for those that are obese.

Pediatric eating problems[edit]

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[edit]

Glycemic index has been thought to effect satiety; however, a study investigating the effect of satiety found that a high-glycemic food, potatoes, reduced appetite more than a high glycemic index food.[13]

Suppression[edit]

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 anorectics (appetite suppressants) were fenfluramine and phentermine. A more recent addition is sibutramine which increases serotonin and noradrenaline levels in the central nervous system, but had to be withdrawn from the market when it was shown to have an adverse cardiovascular risk profile. Similarly, the appetite suppressant rimonabant (a cannabinoid receptor antagonist) had to be withdrawn when it was linked with worsening depression and increased risk of suicide. Recent reports on recombinant 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[edit]

Weight loss or loss of appetite (“cachexia“) is an effect of some diseases, and a side effect of some prescription drugs. Three agents are approved for appetite stimulation in the United States: megestrol – a progesterone available as an oral tablet, oxandrolone – an oral anabolic steroid, and dronabinol – a cannabinoid available in an oral capsule.[14]

Ghrelin, a gut hormone recognized as affecting appetite, is under investigation.[15] Ghrelin itself must be delivered parenterally[15]: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.[15]

See also[edit]

References[edit]

  1. ^ Egecioglu E, Skibicka KP, Hansson C, Alvarez-Crespo M, Friberg PA, Jerlhag E, Engel JA, Dickson SL (2011). “Hedonic and incentive signals for body weight control”. Reviews in Endocrine & Metabolic Disorders. 12 (3): 141–151. doi:10.1007/s11154-011-9166-4. PMC 3145094. PMID 21340584.
  2. ^ “Indigestion”. Digestive.niddk.nih.gov. National Digestive Diseases Information Clearinghouse (NDDIC).
  3. ^ Henkin, Robert I.; Levy, Lucien M.; Fordyce, April (2013-09-01). “Taste and smell function in chronic disease:: A review of clinical and biochemical evaluations of taste and smell dysfunction in over 5000 patients at The Taste and Smell Clinic in Washington, DC”. American Journal of Otolaryngology. 34 (5): 477–489. doi:10.1016/j.amjoto.2013.04.006. PMID 23731850.
  4. ^ Owen JB (October 1990). “Weight control and appetite—a genetic perspective”. Clin Nutr. 9 (5): 291–3. doi:10.1016/0261-5614(90)90039-U. PMID 16837373.
  5. ^ Schacter, D. T.; Gilbert, D. T.; Wegner, D. M. (2011). Psychology (2nd ed.). New York, NY: Worth Publishers.
  6. ^ Tanofsky‐Kraff, M; Bulik, CM; Marcus, MD; Striegel, RH; Wilfley, DE; Wonderlich, SA; et al. (April 2013). “Binge eating disorder: The next generation of research”. International Journal of Eating Disorders. 46 (3): 193–207. doi:10.1002/eat.22089. PMC 3600071. PMID 23354950.
  7. ^ “Anorexia nervosa | University of Maryland Medical Center”. Umm.edu. 2013-05-07. Retrieved 2014-03-08.
  8. ^ Lawton, CL (1993). “Obesity: a disorder of appetite”. Practical Diabetes International. 10 (1): 10–12. doi:10.1002/pdi.1960100105.
  9. ^ Takagi, Kuniko; Legrand, Romain; Asakawa, Akihiro; Amitani, Haruka; François, Marie; Tennoune, Naouel; Coëffier, Moïse; Claeyssens, Sophie; do Rego, Jean-Claude (2013-10-25). “Anti-ghrelin immunoglobulins modulate ghrelin stability and its orexigenic effect in obese mice and humans”. Nature Communications. 4: 2685. doi:10.1038/ncomms3685. PMC 3826639. PMID 24158035.
  10. ^ “How The Hormones Ghrelin and Leptin Affect Appetite”. The Monterey Diet.
  11. ^ Sader, S; Nian, M; Liu, P (2003). “Leptin: a novel link between obesity, diabetes, cardiovascular risk, and ventricular hypertrophy”. Circulation. 108 (6): 644–46. doi:10.1161/01.CIR.0000081427.01306.7D. PMID 12912793. open access
  12. ^ Nadon, Geneviève; Feldman, Debbie Ehrmann; Dunn, Winnie; Gisel, Erika (2011-09-22). “Association of Sensory Processing and Eating Problems in Children with Autism Spectrum Disorders”. Autism Research and Treatment. 2011: 541926. doi:10.1155/2011/541926. ISSN 2090-1925. PMC 3420765. PMID 22937249.
  13. ^ Kaplan, Randall J.; Greenwood, Carol E. (2002-07-01). “Influence of dietary carbohydrates and glycaemic response on subjective appetite and food intake in healthy elderly persons”. International Journal of Food Sciences and Nutrition. 53 (4): 305–316. doi:10.1080/09637480220138160. ISSN 0963-7486. PMID 12090026.
  14. ^ Archer, Melissa; Steinvoort, Carin; Larson, Bryan; Oderda, Gary (2014). “Agents used as appetite stimulants: Drug class review” (PDF). University of Utah College of Pharmacy. Retrieved 19 April 2019.
  15. ^ a b c Khatib, Mahalaqua Nazli; Gaidhane, Abhay; Gaidhane, Shilpa; Quazi, Zahiruddin Syed (2018). “Ghrelin as a promising therapeutic option for cancer cachexia”. Cellular Physiology and Biochemistry. 48 (5): 2172–2188. doi:10.1159/000492559. ISSN 1015-8987.