Appetite is another sensation experienced with eating; it is the desire to eat food. There are several theories about how the feeling of hunger arises. A healthy, well-nourished individual can survive for weeks without food intake (see fasting), with claims ranging from three to ten weeks. The sensation of hunger typically manifests after only a few hours without eating and is generally considered to be unpleasant. Satiety occurs between 5 and 20 minutes after eating.
Hunger is also the most commonly used term in social science and policy discussions to describe the condition of people who suffer from a chronic lack of sufficient food and constantly or frequently experience the sensation of hunger, and can lead to malnutrition.
The physical sensation of hunger is related to contractions of the stomach muscles. These contractions—sometimes called hunger pangs once they become severe—are believed to be triggered by high concentrations of the ghrelin hormone. The hormones Peptide YY and Leptin can have an opposite effect on the appetite, causing the sensation of being full. Ghrelin can be released if blood sugar levels get low—a condition that can result from long periods without eating. Stomach contractions from hunger can be especially severe and painful in children and young adults.
Hunger pangs can be made worse by irregular meals. People who cannot afford to eat more than once a day sometimes refuse one-off additional meals, because if they do not eat at around the same time on the next days, they may suffer extra severe hunger pangs. Older people may feel less violent stomach contractions when they get hungry, but still suffer the secondary effects resulting from low food intake: these include weakness, irritability and decreased concentration. Prolonged lack of adequate nutrition also causes increased susceptibility to disease and reduced ability for the body to heal.
Short-term regulation of hunger and food intakeEdit
Short-term regulation of hunger and food intake involves neural signals from the GI tract, blood levels of nutrients, GI tract hormones, and psychological factors.
Neural signals from the GI tractEdit
One method that the brain uses to evaluate the contents of the gut is through vagal nerve fibers that carry signals between the brain and the gastrointestinal tract (GI tract). Stretch receptors work to inhibit appetite upon distention of the GI tract by sending signals along the vagus nerve afferent pathway and inhibiting the hunger center.
The hormones insulin and cholecystokinin (CCK) are released from the GI tract during food absorption and act to suppress the feeling of hunger. CCK is key in suppressing hunger because of its role in inhibiting neuropeptide Y. Glucagon and epinephrine levels rise during fasting and stimulate hunger. Ghrelin, a hormone produced by the stomach, is an appetite stimulant.
Two psychological processes appear to be involved in regulating short-term food intake: liking and wanting. Liking refers to the palatability or taste of the food, which is reduced by repeated consumption. Wanting is the motivation to consume the food, which is also reduced by repeated consumption of a food and may be due to change in memory-related processes. Wanting can be triggered by a variety of psychological processes. Thoughts of a food may intrude on consciousness and be elaborated on, for instance, as when one sees a commercial or smells a desirable food.
Long-term regulation of hunger and food intakeEdit
The regulation of appetite (the appestat) has been the subject of much research; 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. 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 can either stimulate or suppress appetite. For example, ghrelin stimulates appetite, whereas cholecystokinin and glucagon-like peptide-1 (GLP-1) suppress appetite.
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. Dopamine acts primarily through the reward centers of the brain, 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. Similarly, the hormones leptin and insulin suppress appetite through effects on AgRP and POMC neurons.
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.
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 dopamine (DA), acetylcholine (Ach), opioids and cannabinoids and their action receptors inside the brain, DA, muscarinic and μ-opioid receptor (MOR) and CB1 receptors respectively.
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.
Leptin, a hormone secreted exclusively by adipose cells in response to an increase in body fat mass, is an important component in the regulation of long term hunger and food intake. Leptin serves as the brain's indicator of the body's total energy stores. When leptin levels rise in the bloodstream they bind to receptors in ARC. The functions of leptin are to:
- Suppress the release of neuropeptide Y (NPY), which in turn prevents the release of appetite enhancing orexins from the lateral hypothalamus. This decreases appetite and food intake, promoting weight loss.
- Stimulate the expression of cocaine and amphetamine regulated transcript (CART).
Though rising blood levels of leptin do promote weight loss to some extent, its main role is to protect the body against weight loss in times of nutritional deprivation. Other factors also have been shown to effect long-term hunger and food intake regulation including insulin.
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.
The set-point theories of hunger and eating are a group of theories developed in the 1940s and 1950s that operate under the assumption that hunger is the result of an energy deficit and that eating is a means by which energy resources are returned to their optimal level, or energy set-point. According to this assumption, a person's energy resources are thought to be at or near their set-point soon after eating, and are thought to decline after that. Once the person's energy levels fall below a certain threshold, the sensation of hunger is experienced, which is the body's way of motivating the person to eat again. The set-point assumption is a negative feedback mechanism. Two popular set-point theories include the glucostatic set-point theory and the lipostatic set-point theory.
The set-point theories of hunger and eating present a number of weaknesses.
- The current epidemic of obesity and eating disorders undermines these theories.
- The set-point theories of hunger and eating are inconsistent with basic evolutionary pressures related to hunger and eating as they are currently understood.
- Major predictions of the set-point theories of hunger and eating have not been confirmed.
- They fail to recognize other psychological and social influences on hunger and eating.
The positive-incentive perspective is an umbrella term for a set of theories presented as an alternative to the set-point theories of hunger and eating. The central assertion to the positive-incentive perspective is the idea that humans and other animals are not normally motivated to eat by energy deficits, but are instead motivated to eat by the anticipated pleasure of eating, or the positive-incentive value. According to this perspective, eating is controlled in much the same way as sexual behavior. Humans engage in sexual behavior, not because of an internal deficit, but instead because they have evolved to crave it. Similarly, the evolutionary pressures of unexpected food shortages have shaped humans and all other warm blooded animals to take advantage of food when it is present. It is the presence of good food, or the mere anticipation of it that makes one hungry.
Prior to consuming a meal, the body's energy reserves are in reasonable homeostatic balance. However, when a meal is consumed, there is a homeostasis-disturbing influx of fuels into the bloodstream. When the usual mealtime approaches, the body takes steps to soften the impact of the homeostasis-disturbing influx of fuels by releasing insulin into the blood, and lowering the blood glucose levels. It is this lowering of blood glucose levels that causes premeal hunger, and not necessarily an energy deficit.
- Oxford University Press. "satiety, n." OED Online. Retrieved 14 March 2017.
- Taylor, Chase, Holman, Ira Carelton (1918). "Texas Medicine, Volume 13". Texas Medical Association, 1918. 3: 341.
- Ravilious, Kate (27 December 2005). "How long can someone survive without water?". The Guardian. London. Retrieved 12 August 2007.
"People can last a few days without water depending on the environment in which they find themselves and whether [they are] injured or not," says Jeremy Powell-Tuck, professor of clinical nutrition at Barts and the London Queen Mary school of medicine, who supervised Blaine's recovery.
- Lieberson (MD), Alan. "How long can a person survive without food?". Scientific American. Retrieved 12 November 2012.
- Steen, Juliette (10 November 2016). "We Found Out If It Really Takes 20 Minutes To Feel Full". The Huffington Post. Retrieved 20 April 2017.
- David Model (30 October 2012). "Britain's hidden hunger". BBC. Retrieved 4 November 2012.
- Howard Wilcox Haggard (1977). Diet and Physical Efficiency. Arno Press. ISBN 0405101716.
- Carol Kop (11 February 2009). "The Hunger Hormone". CBS News. Retrieved 7 November 2012.
- Marieb, E., & Marieb, E. (2010). Human anatomy & physiology. (8th ed. ed., pp. 945-947). San Francisco: Pearson Benjamin Cummings.
- Marieb, E., & Marieb, E. (2013). Human anatomy & physiology. (9th ed.). San Francisco: Pearson Benjamin Cummings.
- Berridge, Kent C. (1 January 1996). "Food reward: Brain substrates of wanting and liking". Neuroscience & Biobehavioral Reviews. 20 (1): 1–25. doi:10.1016/0149-7634(95)00033-B. PMID 8622814. S2CID 18707849. [needs update]
- Andrew J., Lynn D., John E., Hill, Magson, Blundell (1984). "Hunger and palatability: Tracking ratings of subjective experience before, during and after the consumption of preferred and less preferred food". Appetite. 5 (4): 361–371. doi:10.1016/S0195-6663(84)80008-2. PMID 6529262. S2CID 2048152.CS1 maint: multiple names: authors list (link)
- Epstein, Leonard H.; Temple, Jennifer L.; Roemmich, James N.; Bouton, Mark E. (2009). "Habituation as a determinant of human food intake". Psychological Review. 116 (2): 384–407. doi:10.1037/a0015074. PMC 2703585. PMID 19348547.
- Kavanagh, David J.; Andrade, Jackie; May, Jon (April 2005). "Imaginary Relish and Exquisite Torture: The Elaborated Intrusion Theory of Desire" (PDF). Psychological Review. 112 (2): 446–467. doi:10.1037/0033-295x.112.2.446. PMID 15783293.
- Wynne, K; Stanley, S; McGowan, B; Bloom, S (February 2005). "Appetite Control". Journal of Endocrinology. 184 (2): 291–318. doi:10.1677/joe.1.05866. PMID 15684339.
- 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.
- M.F., Roitman (2006). "Persistent hunger for sodium makes brain stimulation not so sweet: Theoretical comment on Morris et al. (2006)". Behavioral Neuroscience. 120 (3): 744–747. doi:10.1037/0735-7044.120.3.744. PMID 16768628. S2CID 28651962.
- 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.
- 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.
- 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.
- Wassum, KM; Ostlund, SB; Maidment, NT; Balleine, BW (2009). "Distinct opioid circuits determine the palatability and the desirability of rewarding events". Proceedings of the National Academy of Sciences of the United States of America. 106 (30): 12512–12517. Bibcode:2009PNAS..10612512W. doi:10.1073/pnas.0905874106. PMC 2718390. PMID 19597155.
- Fulton, S (2010). "Appetite and Reward". Frontiers in Neuroendocrinology. 31 (1): 85–103. doi:10.1016/j.yfrne.2009.10.003. PMID 19822167. S2CID 9863116.
- Wenning, A (1990). "Sensing effectors make sense". Trends in Neurosciences. 22 (12): 550–555. doi:10.1016/s0166-2236(99)01467-8. PMID 10542435. S2CID 9775553.
- De Castro, J.M.; Plunkett, S. (2002). "A general model of intake regulation". Neuroscience & Biobehavioral Reviews. 26 (5): 581–595. doi:10.1016/s0149-7634(02)00018-0. PMID 12367591. S2CID 1729679.
- Pinel, J. P. J., Biopsychology, 6th ed. 293–294. ISBN 0-205-42651-4
- Pinel, J. P. J.; Assanand, S.; Lehman, D. R. (2000). "Hunger, eating, and ill health". American Psychologist. 55 (10): 1105–1116. doi:10.1037/0003-066x.55.10.1105. PMID 11080830.
- Lowe, M. R. (1993). "The effects of dieting on eating and behavior: A three-factor model" (PDF). Psychological Bulletin. 114 (1): 100–121. doi:10.1037/0033-2909.114.1.100. PMID 8346324.
- Berridge, K. C. (2004). "Motivation concepts in behavioral neuroscience". Physiology and Behavior. 81 (2): 179–209. doi:10.1016/j.physbeh.2004.02.004. PMID 15159167. S2CID 14149019.
- Booth, D. A. (1981). "The physiology of appetite". British Medical Bulletin. 37 (2): 135–140. doi:10.1093/oxfordjournals.bmb.a071690. PMID 7032646.
- Woods, S. C. (1991). "The eating paradox: How we tolerate food". Psychological Review. 98 (4): 488–505. doi:10.1037/0033-295x.98.4.488. PMID 1961770.
- Woods, S. C. (2004). "Lessons in the interaction of hormones and ingestive behavior". Physiology & Behavior. 82 (1): 187–190. doi:10.1016/j.physbeh.2004.04.050. PMID 15234611. S2CID 23128604.
- Woods, S. C.; Ramsay, D. S. (2000). "Pavlovian influences over food and drug intake". Behavioural Brain Research. 110 (1–2): 175–182. doi:10.1016/s0166-4328(99)00194-1. PMID 10802313. S2CID 21810492.
- Ronzio RA (2003). "Craving". The Encyclopedia of Nutrition and Good Health (2nd ed.). Facts on File. p. 176. ISBN 978-0-8160-4966-0.