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.

Physiological factors

There is no neurological explanation as to why chocolate fudge cake evokes more appetite than porridge, but rats are like humans in their preference for sweet and/or fatty foods.[1] Rats show a preference for sucrose over sucralose, suggesting the importance of calories in reward from food.[2] Nonetheless, although glucose and fructose have the same caloric content, fructose stimulates appetite more than glucose.[3]

Cannon and Washburn (1912) proposed that eating begins when we have an empty stomach. They suggested 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' stomachs had been 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, tobacco smokers and women ovulating experienced a lower appetite than their counterparts.[4]

Regulation

The regulation of appetite (the appestat) has been the subject of much research in the last decade. 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.[5] 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.[5] The circulating gut hormones that regulate many pathways in the body can either stimulate or suppress appetite.[6] For example, ghrelin stimulates appetite, whereas cholecystokinin and glucagon-like peptide-1 (GLP-1) suppress appetite.[6]

Effector

The arcuate nucleus of the hypothalamus, a part of the brain, is the main regulatory organ for the human appetite. Many brain neurotransmitters affect appetite, especially dopamine and serotonin.[7] Dopamine acts primarily through the reward centers of the brain,[7] whereas serotonin primarily acts through effects on neuropeptide Y (NPY)/agouti-related peptide (AgRP) [stimulate appetite] and proopiomelanocortin (POMC) [induce satiety] neurons located in the arcuate nucleus.[8] Similarly, the hormones leptin and insulin suppress appetite through effects on AgRP and POMC neurons.[9]

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 affect the palatability of foods.[10]

The nucleus accumbens (NAc) is the area of the brain that coordinates neurotransmitter, opioid and endocannabinoid signals to control feeding behaviour. The few important signalling molecules inside the NAc shell modulate the motivation to eat and the affective reactions for food. These molecules include the DA, Ach, opioids and cannabinoids and their action receptors inside the brain, DA, muscarinic and MOR and CB1 receptors respectively.[11]

Sensor

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 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 (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.[12] Taste and smell ("dysgeusia", bad taste) or the lack thereof may also effect appetite.[13]

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.[14]

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.[15] 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%.[16] 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.[17]

Obesity

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.[18] It has been found that ghrelin-reactive IgG immunoglobulins affect ghrelin's orexigenic response.[19]

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.[20] 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.[21] This will produce a perpetual cycle for those that are obese.

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).[22]

Pharmacology

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.[23]

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 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 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 overwhelmingly put weight back on afterwards.

Stimulation

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.[24] Direct ghrelin administration increases appetite as well.[25]

Rikkunshito, a traditional Japanese Kampo medicine, has been found to stimulate ghrelin and appetite.[26]

In rats, appetizers including a ginger or karpurvalli (Coleus aromaticus) beverage were found to improve food consumption.[27] A subsequent study in human volunteers found that, depending upon the concentration, karpurvalli decreased or increased leptin.[28]

Visual influence

Blue tableware

There may also be some visual influence on appetite. According to some research, the colour red increases appetite.[29]

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.[30]

See also

References

  1. 1 2 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. ↑ de Araujo IE, Oliveira-Maia AJ, Sotnikova TD, Gainetdinov RR, Caron MG, Nicolelis MA, Simon SA (2008). "Food reward in the absence of taste receptor signaling". Neuron. 57 (6): 930–941. doi:10.1016/j.neuron.2008.01.032. PMID 18367093.
  3. ↑ Luo S, Monterosso JR, Sarpelleh K, Page KA (2015). "Differential effects of fructose versus glucose on brain and appetitive responses to food cues and decisions for food rewards". Proceedings of the National Academy of Sciences of the United States of America. 112 (20): 6509–6514. doi:10.1073/pnas.1503358112. PMC 4443321. PMID 25941364.
  4. ↑ Gregersen, NT; Møller, BK; Raben, A; Kristensen, SRT; Holm, L; Flint, A; et al. (2011). "Determinants of appetite ratings: The role of age, gender, BMI, physical activity, smoking habits, and diet/weight concern". Food & Nutrition Research. 55: 7028. doi:10.3402/fnr.v55i0.7028. PMC 3160809. PMID 21866221.
  5. 1 2 Wynne, K; Stanley, S; McGowan, B; Bloom, S (February 2005). "Appetite Control". Journal of Endocrinology. 184: 291–318. doi:10.1677/joe.1.05866. PMID 15684339.
  6. 1 2 Suzuki, K; Jayasena, CN; Bloom, SR (2011). "The Gut Hormones in Appetite Regulation". Journal of Obesity. 2011: 1–10. doi:10.1155/2011/528401. PMC 3178198. PMID 21949903. Article id:528401.
  7. 1 2 Bojanowska E, Ciosek J (2016). "Can We Selectively Reduce Appetite for Energy-Dense Foods? An Overview of Pharmacological Strategies for Modification of Food Preference Behavior". Current Neuropharmacology. 14 (2): 118–142. doi:10.2174/1570159x14666151109103147. PMC 4825944. PMID 26549651.
  8. ↑ Wyler SC, Lord CC, Lee S, Elmquist JK, Liu C (2017). "Serotonergic Control of Metabolic Homeostasis". Frontiers in Cellular Neuroscience. 11: 277. doi:10.3389/fncel.2017.00277. PMC 5611374. PMID 28979187.
  9. ↑ Varela L, Horvath TL (2012). "Leptin and insulin pathways in POMC and AgRP neurons that modulate energy balance and glucose homeostasis". EMBO Reports. 13 (12): 1079–1086. doi:10.1038/embor.2012.174. PMC 3512417. PMID 23146889.
  10. ↑ 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 (30): 12512–12517. doi:10.1073/pnas.0905874106. PMC 2718390. PMID 19597155.
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  12. ↑ "Indigestion". Digestive.niddk.nih.gov. National Digestive Diseases Information Clearinghouse (NDDIC).
  13. ↑ 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.
  14. ↑ 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.
  15. ↑ Schacter, D. T.; Gilbert, D. T.; Wegner, D. M. (2011). Psychology (2nd ed.). New York, NY: Worth Publishers.
  16. ↑ 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.
  17. ↑ "Anorexia nervosa | University of Maryland Medical Center". Umm.edu. 2013-05-07. Retrieved 2014-03-08.
  18. ↑ Lawton, CL (1993). "Obesity: a disorder of appetite". Practical Diabetes International. 10 (1): 10–12. doi:10.1002/pdi.1960100105.
  19. ↑ 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.
  20. ↑ "How The Hormones Ghrelin and Leptin Affect Appetite". The Monterey Diet.
  21. ↑ 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.
  22. ↑ 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.
  23. ↑ 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.
  24. ↑ 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.
  25. ↑ 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.
  26. ↑ 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: 519035. doi:10.1155/2014/519035. ISSN 1741-427X.
  27. ↑ 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.
  28. ↑ Wadikar, Dadasaheb Dattatraya; Premavalli, Kunigal Srinivasaiah. "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.
  29. ↑ Color Control: Curb Appetite and Eat Less Shape Magazine
  30. ↑ 青色の食欲減退効果に関する研究 小島みなみ Kyoto Gakuen University
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