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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.

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Role in diseaseEdit

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 disordersEdit

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]

ObesityEdit

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 problemsEdit

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]

PharmacologyEdit

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]

SuppressionEdit

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 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.

StimulationEdit

Weight loss and loss of appetite ("cachexia") is an effect of some diseases, and a side effect of some drugs. Certain progestins such as medroxyprogesterone acetate (MPA) and megestrol acetate (MGA) are used at very high dosages as a treatment, along with corticosteroids for short-term use.[14] Direct ghrelin administration increases appetite as well.[15]

Rikkunshito, a traditional Japanese Kampo medicine, has been found to stimulate ghrelin and appetite.[16]

In rats, appetizers including a ginger or karpurvalli (Coleus aromaticus) beverage were found to improve food consumption.[17] A subsequent study in human volunteers found that, depending upon the concentration, karpurvalli decreased or increased leptin.[18]

Visual influenceEdit

 
Blue tableware

There may also be some visual influence on appetite. According to some research, the colour red increases appetite.[19]

Many restaurants and fast food chains use red signs or interior furniture. Complementary colors such as the combination of red and green combination are also common (for example, Tabasco labelling).

Blue is theorised to have the opposite influence.[20]

See alsoEdit

ReferencesEdit

  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.  
  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: 1–8. 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. ^ Tazi, EM; Errihani, H (2010-01-01). "Treatment of Cachexia in Oncology". Indian Journal of Palliative Care. 16 (3): 129–137. doi:10.4103/0973-1075.73644. ISSN 0973-1075. PMC 3012235. PMID 21218002.
  15. ^ Garin, Margaret C.; Burns, Carrie M.; Kaul, Shailja; Cappola, Anne R. (2013-05-01). "Clinical review: The human experience with ghrelin administration". The Journal of Clinical Endocrinology and Metabolism. 98 (5): 1826–1837. doi:10.1210/jc.2012-4247. ISSN 1945-7197. PMC 3644599. PMID 23533240.
  16. ^ Mogami, Sachiko; Hattori, Tomohisa (2014-01-01). "Beneficial effects of rikkunshito, a Japanese kampo medicine, on gastrointestinal dysfunction and anorexia in combination with Western drug: a systematic review". Evidence-Based Complementary and Alternative Medicine: ECAM. 2014: 1–7. doi:10.1155/2014/519035. ISSN 1741-427X. PMC 3979068. PMID 24778703.
  17. ^ Wadikar, D. D.; Premavalli, K. S. (2011-08-01). "Appetizer administration stimulates food consumption, weight gain and leptin levels in male Wistar rats". Appetite. 57 (1): 131–133. doi:10.1016/j.appet.2011.04.001. ISSN 1095-8304. PMID 21510990.
  18. ^ Wadikar, Dadasaheb Dattatraya; Premavalli, Kunigal Srinivasaiah (2014). "Beverage from Coleus aromaticus reduces leptin levels and improves appetite rating in human volunteers". Nutrition. 30 (6): 702–705. doi:10.1016/j.nut.2013.11.025. PMID 24800669.
  19. ^ Color Control: Curb Appetite and Eat Less Shape Magazine
  20. ^ 青色の食欲減退効果に関する研究 小島みなみ Kyoto Gakuen University

BibliographyEdit