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說明

食欲好的人，對于食物的需求十分多以及頻繁；食欲不好的人，則只會吃很少的食物，同時不太容易感覺到餓。食欲跟一個人腸胃的消化吸收以及運(yùn)動消耗有很大關(guān)系。

疾病

食欲的好壞，在很多程度上，也能反應(yīng)出一個人的健康程度。如果食欲旺盛，容易感覺到饑餓，身體卻日漸消瘦，伴有口渴、多飲、多尿，則可能是患了糖尿?。蝗绻秤?，但體重下降，并伴有乏力、怕熱、易出汗、易激動等癥狀，則有可能是患了甲亢。

Appetite is the desire to eatfood, sometimes due to hunger. Appealing foods can stimulate appetite even when hunger is absent. Appetite exists in all higher life-forms, and serves to regulate adequate energy intake to maintainmetabolicneeds. It is regulated by a close interplay between the digestive tract, adipose tissue and thebrain. Appetite has a relationship with every individual"s behavior. Appetitive 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

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.

Regulation

The regulation of appetite (the appestat ) has been the subject of much research in the last decade . Breakthroughs included the discovery, in 1994, ofleptin, a hormone produced by the adipose tissue that appeared to provide negative feedback. Leptin is a peptide hormone that affects homeostasis and immune responses. 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. The circulating gut hormones that regulate many pathways in the body result in appetite stimulation.

Effector

The hypothalamus, a part of the brain, is the main regulatory organ for the human appetite. The neurons that regulate appetite appear to be mainlyserotonergic, although neuropeptide Y (Y) 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 thethyroid(thyroxineregulates 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.

The nucleus accumbens (NAc) is the area of the brain that coordinatesneurotransmitter, 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.

Sensor

The hypothalamus senses external stimuli mainly through a number of hormones such asleptin, ghrelin, PYY 3-36,orexinand 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.

在疾病中的作用

有限或過多的食欲不一定是病態(tài)的。食欲異?？梢员欢x為飲食習(xí)慣導(dǎo)致營養(yǎng)不良和相關(guān)條件如肥胖及其相關(guān)問題。

遺傳和環(huán)境因素都可能調(diào)節(jié)食欲，異?？赡軐?dǎo)致食欲不振。食欲不振可能有很多原因，但可能是身體的結(jié)果（感染性，自身免疫性或惡性疾?。┗蛐睦恚▔毫?，精神障礙）因素。 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. Tasteand smell ("dysgeusia", bad taste) or the lack thereof may also effect appetite.

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 at a possibility of a linkage to the X-chromosome.

Eating disorders

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 limiting of food consumption. Furthermore, anorexics might do excessive exercise. Individuals who 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. 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%. Similarly to bulimia some 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.

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. It has been found that ghrelin-reactive IgG immunoglobulins affect ghrelin"s orexigenic response.

Other than genetically-stimulated appetite abnormalities, there are physiological ones that do not require genes for activation. For example, ghrelin andleptinare 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. 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 pancreas is producing leptin, the body will not understand that it should stop eating. 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).

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.

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 increasesserotoninand 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. Progestagens such as medroxyprogesterone acetate (MPA) and megestrol acetate (MA) are approved as a treatment in Europe, along withcorticosteroids for short-term use. Direct ghrelin administration increases appetite as well.

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

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

Visual influence

  Blue tableware

Not only olfaction, There is some visual influence of appetite. Some research has,Red(de:Warme Farbe) sharpens appetite. (regarding Hot food)

Actually, Many inexpensive restaurants (It includes Fast food) use red signs or interior furniture (walls, counters). Complementary colors Red and green combination can be often seen (an example: Tabasco sauce packaging).

Blue(de:Kalte Farbe) is the opposite influence.

See also

Specific appetite

Orexigenic

References

Neary, NM; Goldstone, AP; Bloom, SR. Appetite regulation: from the gut to the hypothalamus. Clin Endocrinol (Oxford). 2004, 60 (2): 153–60. PMID 14725674 . doi:10.1046/j.1365-2265.2003.01839.x .

Wynne, K; Stanley, S; Bloom, S. The gut and regulation of body weight. J Clin Endocrinol Metab. 2004, 89 : 2576–82. PMID 15181026 . doi:10.1210/jc.2004-0189 .

Olsen, Anne; van Belle, C; Meyermann, K; Keller, KL. Manipulating fat content of familiar foods at test-meals does not affect intake and liking of these foods among children. Appetite. 2011, 57 (3): 573–7. PMID 21801772 . doi:10.1016/j.appet.2011.07.007 .

Orrell-Valente, JK; Hill, LG; Brechwald, WA; Dodge, KA; Pettit, GS; Bates, JE. " Just three more bites": An observational analysis of parents" socialization of children"s eating at mealtime. Appetite. 2007, 48 (1): 37–45. PMC 2045650 . PMID 17000028 . doi:10.1016/j.appet.2006.06.006 .

Carlson, Neil R.; Donald, Heth C.; Miller, Harold; Donahoe, John W.; William, Buskist; Martin, Neil G.; Schmaltz, Rodney M. Psychology: the science of behavior. Toronto: Pearson. 2010.

Suzuki, K; Jayasena, CN; Bloom, SR. The Gut Hormones in Appetite Regulation. Journal of Obesity. 2011, 2011 : 1–10. PMC 3178198 . PMID 21949903 . doi:10.1155/2011/528401 . Article id:528401.

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