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The appetite is the desire to eat food, felt as hunger. Appetite exists in all higher lifeforms, 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. Decreased desire to eat is termed anorexia, while polyphagia (or "hyperphagia") is increased eating. Disregulation of appetite contributes to anorexia nervosa, bulimia nervosa, cachexia, overeating, and binge eating disorder.

In its wide meaning appetite can refer to the desire tosatisfy any physicalo craving [1].

Physiological factors=Edit

The reasons for beginning a meal must somehow be related to the fact that the body needs nourishment: Physiological factors are clearly involved in eating. Cannon and Washburn (1912) proposed that eating begins when we have an empty stomach. They suggest that the walls of an empty stomach rub against each other to produce what are commonly called "hunger pangs". Some skeptics called Cannon's explanation of hunger "the rumble theory". However, observations of surgical patients indicated that there was more to the onset of eating than hunger pangs. Removal of the stomach did not abolish hunger pangs, and these patients reported the same feelings of hunger and satiety that they had experienced before surgery (Inglefinger, 1944). (The patients had had their stomachs removed because of cancer or large ulcers, and their esophagi had been attached directly to their small intestines). Although the patients ate small, frequent meals because they had no stomachs to hold food, their reports of feelings of hunger and their total food intake were essentially normal. Depletion of the body's store of nutrients is a more likely cause of hunger. The primary fuels for the cells of our body are glucose (a simple sugar) and fatty acids (compounds produced by the breakdown of fats). If the digestive system contains food, these nutrients are absorbed in the blood and nourish our cells. But the digestive tract is sometimes empty; in fact, it is empty when we wake up every morning. There must be a reservoir that stores nutrients to keep the cells of the body nourished when the gut is empty. Indeed, there are two reservoirs: a short-term reservoir and a long-term reservoir. The short-term reservoir stores carbohydrates and the long-term reservoir stores fat. A number of variables have been found to relate to appetite sensation in individuals. The most influential of these is gender and age, with females experiencing greater appetite satisfaction than males and a decrease in appetite with age. Although BMI was not found to influence appetite,smokers and women ovulating experienced a lower appetite than their counterparts.[2]


RegulationEdit

The regulation of appetite (the appestat) has been the subject of much research in the last decadeTemplate:Dated maintenance category. Breakthroughs included the discovery, in 1994, of leptin, a hormone produced by the adipose tissue that appeared to provide negative feedback. Leptin is a peptide hormone that affects homeostasis and immune responses.[3] Lowering food intake can lower leptin levels in the body, while increasing the intake of food can raise leptin levels. Later studies showed that appetite regulation is an immensely complex process involving the gastrointestinal tract, many hormones, and both the central and autonomic nervous systems.[3] The circulating gut hormones that regulate many pathways in the body result in appetite stimulation.[4]

EffectorEdit

The hypothalamus, a part of the brain, is the main regulatory organ for the human appetite. The neurons that regulate appetite appear to be mainly serotonergic, although neuropeptide Y (NPY) and Agouti-related peptide (AGRP) also play a vital role. Hypothalamocortical and hypothalamolimbic projections contribute to the awareness of hunger, and the somatic processes controlled by the hypothalamus include vagal tone (the activity of the parasympathetic autonomic nervous system), stimulation of the thyroid (thyroxine regulates the metabolic rate), the hypothalamic-pituitary-adrenal axis and a large number of other mechanisms. Opioid receptor-related processes in the nucleus accumbens and ventral pallidum effect the palatability of foods.[5]

The nucleus accumbens (NAc) is the area of the brain that coordinates neurotransmitter, opioid and endocannabinoids signals to control feeding behaviour. The few important signalling molecules inside the NAc shell modulates the motivation to eat and the affective reactions for food. These molecules include the DA, Ach, oipoids and cannabinoids and their action receptors inside the brain, DA, muscarinic and MOR and CB1 receptors respectively.[6]

SensorEdit

The hypothalamus senses external stimuli mainly through a number of hormones such as leptin, ghrelin, PYY 3-36, orexin and cholecystokinin; all modify the hypothalamic response. They are produced by the digestive tract and by adipose tissue (leptin). Systemic mediators, such as tumor necrosis factor-alpha (TNFα), interleukins 1 and 6 and corticotropin-releasing hormone (CRH) influence appetite negatively; this mechanism explains why ill people often eat less.

In addition, the biological clock (which is regulated by the hypothalamus) stimulates hunger. Processes from other cerebral loci, such as from the limbic system and the cerebral cortex, project on the hypothalamus and modify appetite. This explains why in clinical depression and stress, energy intake can change quite drastically.

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.[7]

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.[8]

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.[9] 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%.[10] 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.[11]

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.[12]

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.[13] 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.[14] This will produce a perpetual cycle for those that are obese.

PharmacologyEdit

Drugs may be either appetite depressing drugs or appetite stimulating drugs.

Mechanisms controlling appetite are a potential target for weight loss drugs. Appetite control mechanisms seem to strongly counteract under eating, whereas, they appear weak to control over-eating. 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[attribution needed] expect developments in this area to snowball in the near future. Dieting alone is ineffective in most obese adults - and even obese adults who successfully lose weight through dieting, often put weight back on afterwards.



See alsoEdit

ReferencesyEdit

  1. Coleman,A F (2006). Oxford Dictionary of Psychology, 2nd ed. Oxford:OUP.
  2. Gregerson, T.N., Møller, B.K., Raben, A., Kristensen, S.T., Holm, L., Flint, A., Astrup, A. (2011). Determinants of appetite ratings: the role of age, gender, BMI, physical activity, smoking habits, and diet/weight concern. Food Nutr Res:55.
  3. 3.0 3.1 Wynne, K., Stanley, S., McGowan, B., & Bloom, S. (2005). Startling Review: Appetite Control. "Journal of Endocrinology, 184", 291-318.
  4. Suzuki, K., Jayasena, C.N., & Bloom, S. (2011). The Gut Hormones in Appetite Regulation. "Journal of Obsesity", 1-10.
  5. Wassum KM, Ostlund SB, Maidment NT, Balleine BW. (2009). Distinct opioid circuits determine the palatability and the desirability of rewarding events. Proc Natl Acad Sci U S A. 106:12512–12517 PMID 19597155 DOI:10.1073/pnas.0905874106
  6. Fulton, "Appetite and Reward", "Frontiers in Neuroendocrinology", (2010)
  7. National Digestive Diseases Information Clearinghouse (NDDIC). Indigestion.
  8. Owen JB (October 1990). Weight control and appetite--a genetic perspective. Clin Nutr 9 (5): 291–3.
  9. Schacter, D.T., Gilbert, D.T., Wegner, D.M. (2011). "Psychology (2nd ed.)." New York, NY: Worth Publishers.
  10. Marian Tanofsky‐Kraff, Cynthia M. Bulik, Marsha D. Marcus, Ruth H. Striegel, Denise E. Wilfley, Stephen A. Wonderlich, James I. Hudson. "Binge eating disorder: The next generation of research" International Journal of Eating Disorders (April 2013), 46 (3), pg. 193-207
  11. [1]
  12. Lawton, Clare.L. (January 1993). A disorder of Appetite. Obesity 10 (Practical Diabetes International): 10–12.
  13. "How The Hormones Ghrelin and Leptin Affect Appetite." The Monterey Diet, n.d. Web. http://www.montereydiet.com/ghrelin_and_leptin.html
  14. Sader, Sawsan, Min Nian, and Peter Liu. "Leptin." Leptin. American Heart Association. http://circ.ahajournals.org/content/108/6/644.full

Further readingEdit

Key textsEdit

BooksEdit

  • Neary NM, Goldstone AP, Bloom SR. Appetite regulation: from the gut to the hypothalamus. Clin Endocrinol (Oxford) 2004;60:153-60. PMID 14725674.

PapersEdit

Additional materialEdit

BooksEdit

  • Wynne K, Stanley S, Bloom S. The gut and regulation of body weight. J Clin Endocrinol Metab 2004;89:2576–82. PMID 15181026.

PapersEdit

External linksEdit

Further readingEdit

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