Ingestive behaviors

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Ingestive behaviors encompass all eating and drinking behaviors. These actions are influenced by physiological regulatory mechanisms; these mechanisms exist to control and establish homeostasis within the human body. [1] Disruptions in these ingestive regulatory mechanisms can result in eating disorders such as obesity, anorexia, and bulimia.

Contents

Research has confirmed that physiological mechanisms play an important role in homeostasis; however, human food intake must also be evaluated within the context of non-physiological determinants present in human life. [2] Within laboratory environments, hunger and satiety are factors that can be controlled and tested. Outside of experiments though, social constraints may influence the size and number of daily meals.

Initiating ingestion

Body weight regulation requires a balance between food intake and energy expenditure. Two mechanisms are required to maintain a relatively constant body weight: one must increase motivation to eat if long-term reservoirs are being depleted, and the other must restrain food intake if more calories than needed are being consumed.

Signals from environment

The environment of early humans shaped the evolution of ingestive regulatory mechanisms, starvation used to be a greater threat to survival than overeating. [3] Human metabolism evolved to store energy within the body to prevent death from starvation. Today, the environment now has an opposite effect on humans eating behaviors. With the widespread availability of food in today's society, concern has shifted from starvation to overeating. As food scarcity and availability have become less and less of a problem, food intake has increased. [4] The increase of food intake by so many people is due primarily to a number of environmental factors. Main social environmental factors include:

  • People who eat in groups tend to eat more than when they are by themselves
  • When people eat in the presence of models who eat a lot or a little, they are likely to eat similarly to the model
  • Individuals who eat in the presence of others who they think are watching them, tend to eat less than they do when they are by themselves [5]

Along with social environmental factors, ingestive behaviors are also influenced by atmospheric environmental factors. Atmospheric factors include:

  • Package sizing: the size of the packaging tends to influence what an individual thinks is the norm for consumption
  • Food odor: unpleasant odors are likely to decrease ingestion, while pleasant odors are likely to increase ingestion
  • Temperature of environment: people tend to eat more in cold climates and tend to drink more in warmer climates
  • Lighting of environment: people are more likely to stay put and eat in an environment with dim lighting rather than harsh bright lighting [6]

Signals from stomach

The gastrointestinal system, particularly the stomach, releases a peptide hormone called ghrelin. [7] In 1999 [8] experiments have revealed that hunger is communicated from the stomach to the brain via this hormone peptide. This peptide can stimulate thought about food, [9] and is suppressed after food is ingested. Nutrient injection into the blood stream does not suppress ghrelin, so the release of hormone is directed by the digestive system and not by nutrient availability in the blood. [10] These blood levels of ghrelin increase with fasting and are reduced after a meal. Ghrelin antibodies or ghrelin receptor antagonists inhibit eating. [11] Ghrelin also stimulates energy production and signals directly to the hypothalamus regulatory nuclei that control energy homeostasis. [12]

Metabolic signals

Hunger is the result of a fall in blood glucose level or depriving cells of the ability to metabolize fatty acids—glucoprivation and lipoprivation, respectively, stimulate eating. [13] Detectors in the brain are only sensitive to glucoprivation; detectors in the liver are sensitive to both glucoprivation and lipoprivation outside the blood–brain barrier. However, no single set of receptors is solely responsible for the information the brain uses to control eating.

Satiety signals

There are two primary sources of signals that stop eating: short-term signals come from immediate effects of eating a meal, beginning before food digestion, and long-term signals, that arise in adipose tissue, control the intake of calories by monitoring the sensitivity of brain mechanisms to hunger and satiety signals received.

Short-term signals

Head factors

There are several sets of receptors located in the head: eyes, nose, tongue, and throat. The most important role of head factors in satiety is that taste and odor can serve as stimuli that permit learning about caloric contents of different foods. Tasting and swallowing of food contributes to the feeling of fullness caused by the presence of food in the stomach. [14]

Gastric and intestinal factors

The stomach contains receptors that can detect the presence of nutrients, but there are detectors in the intestines as well, and the satiety factors of the stomach and intestines can interact. [15] [16] [17] Cholecystokinin (CCK) is a peptide hormone secreted by the duodenum that controls the rate of stomach emptying. CCK is secreted in response to the presence of fats, which are detected in by receptors in the duodenum. Another satiety signal produced by cells is peptide YY3-36 (PYY), which is released after a meal in amounts proportional to the calories ingested.

Liver factors

The last stage of satiety occurs in the liver. The liver is also the first organ to detect that nutrients are being received from the intestines. When the liver receives nutrients, it then sends a signal to the brain that produces satiety; [18] but essentially, it is continuing the satiety that was already started by signals that arose from the stomach and upper intestine.

Long-term signals

Signals arising from the long-term nutrient reservoir of the body may alter the sensitivity of the brain to hunger signals or short-term satiety signals. [19] A peptide, leptin, has profound effects on metabolism and eating. It is secreted by adipose tissue and it increases metabolic rate while decreasing food intake. Its discovery has stimulated interest in finding ways of treating obesity.

Brain mechanisms

Neural circuits in the brain stem are able to control acceptance or rejection of sweet or bitter foods, and can be modulated by satiation or physiological hunger signals. [20] Signals from the tongue, stomach, small intestine and liver are received by the area postrema and nucleus of the solitary tract, which then send information to many regions of the forebrain that control food intake. The lateral hypothalamus contains two sets of neurons that increase eating and decrease metabolic rate by secreting the peptides orexin and melanin concentrating hormone (MCH). Neuropeptide Y (NPY) in the lateral hypothalamus induces ravenous eating; neurons that secrete NPY are targeted by ghrelin in the hypothalamus. Leptin desensitizes the brain to hunger signals and inhibits NPY-secreting neurons.

Related Research Articles

Digestion Biological process of breaking down food

Digestion is the breakdown of large insoluble food molecules into small water-soluble food molecules so that they can be absorbed into the watery blood plasma. In certain organisms, these smaller substances are absorbed through the small intestine into the blood stream. Digestion is a form of catabolism that is often divided into two processes based on how food is broken down: mechanical and chemical digestion. The term mechanical digestion refers to the physical breakdown of large pieces of food into smaller pieces which can subsequently be accessed by digestive enzymes. Mechanical digestion takes place in mouth through mastication and in small intestine through segmentation contractions. In chemical digestion, enzymes break down food into the small molecules the body can use.

Eating Ingestion of food

Eating is the ingestion of food, typically to provide a heterotrophic organism with energy and to allow for growth. Animals and other heterotrophs must eat in order to survive — carnivores eat other animals, herbivores eat plants, omnivores consume a mixture of both plant and animal matter, and detritivores eat detritus. Fungi digest organic matter outside their bodies as opposed to animals that digest their food inside their bodies. For humans, eating is an activity of daily living. Some individuals may limit their amount of nutritional intake. This may be a result of a lifestyle choice, due to hunger or famine, as part of a diet or as religious fasting.

Appetite is the desire to eat food items, usually due to hunger. Appealing foods can stimulate appetite even when hunger is absent, although appetite can be greatly reduced by satiety. 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 behaviour, 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 is increased eating. Dysregulation of appetite contributes to anorexia nervosa, bulimia nervosa, cachexia, overeating, and binge eating disorder.

Cholecystokinin Hormone of the gastrointestinal system

Cholecystokinin is a peptide hormone of the gastrointestinal system responsible for stimulating the digestion of fat and protein. Cholecystokinin, officially called pancreozymin, is synthesized and secreted by enteroendocrine cells in the duodenum, the first segment of the small intestine. Its presence causes the release of digestive enzymes and bile from the pancreas and gallbladder, respectively, and also acts as a hunger suppressant.

Paraventricular nucleus of hypothalamus

The paraventricular nucleus is a nucleus in the hypothalamus. Anatomically, it is adjacent to the third ventricle and many of its neurons project to the posterior pituitary. These projecting neurons secrete oxytocin and a smaller amount of vasopressin, otherwise the nucleus also secretes corticotropin-releasing hormone (CRH) and thyrotropin-releasing hormone (TRH). CRH and TRH are secreted into the hypophyseal portal system and act on different targets neurons in the anterior pituitary. PVN is thought to mediate many diverse functions through these different hormones, including osmoregulation, appetite, and the response of the body to stress.

Arcuate nucleus

The arcuate nucleus of the hypothalamus is an aggregation of neurons in the mediobasal hypothalamus, adjacent to the third ventricle and the median eminence. The arcuate nucleus includes several important and diverse populations of neurons that help mediate different neuroendocrine and physiological functions, including neuroendocrine neurons, centrally projecting neurons, and astrocytes. The populations of neurons found in the arcuate nucleus are based on the hormones they secrete or interact with and are responsible for hypothalamic function, such as regulating hormones released from the pituitary gland or secreting their own hormones. Neurons in this region are also responsible for integrating information and providing inputs to other nuclei in the hypothalamus or inputs to areas outside this region of the brain. These neurons, generated from the ventral part of the periventricular epithelium during embryonic development, locate dorsally in the hypothalamus, becoming part of the ventromedial hypothalamic region. The function of the arcuate nucleus relies on its diversity of neurons, but its central role is involved in homeostasis. The arcuate nucleus provides many physiological roles involved in feeding, metabolism, fertility, and cardiovascular regulation.

Ghrelin Peptide hormone involved in appetite regulation

Ghrelin is a hormone produced by enteroendocrine cells of the gastrointestinal tract, especially the stomach, and is often called a "hunger hormone" because it increases the drive to eat. Blood levels of ghrelin are highest before meals when hungry, returning to lower levels after mealtimes. Ghrelin may help prepare for food intake by increasing gastric motility and stimulating the secretion of gastric acid.

Agouti-related peptide

Agouti-related protein (AgRP), also called agouti-related peptide, is a neuropeptide produced in the brain by the AgRP/NPY neuron. It is synthesized in neuropeptide Y (NPY)-containing cell bodies located in the ventromedial part of the arcuate nucleus in the hypothalamus. AgRP is co-expressed with NPY and acts to increase appetite and decrease metabolism and energy expenditure. It is one of the most potent and long-lasting of appetite stimulators. In humans, the agouti-related peptide is encoded by the AGRP gene.

Neuroendocrinology is the branch of biology which studies the interaction between the nervous system and the endocrine system; i.e. how the brain regulates the hormonal activity in the body. The nervous and endocrine systems often act together in a process called neuroendocrine integration, to regulate the physiological processes of the human body. Neuroendocrinology arose from the recognition that the brain, especially the hypothalamus, controls secretion of pituitary gland hormones, and has subsequently expanded to investigate numerous interconnections of the endocrine and nervous systems.

Peptide YY Peptide released from cells in the ileum and colon in response to feeding

Peptide YY (PYY) also known as peptide tyrosine tyrosine is a peptide that in humans is encoded by the PYY gene. Peptide YY is a short peptide released from cells in the ileum and colon in response to feeding. In the blood, gut, and other elements of periphery, PYY acts to reduce appetite; similarly, when injected directly into the central nervous system, PYY is also anorexigenic, i.e., it reduces appetite.

Nesfatin-1 is a neuropeptide produced in the hypothalamus of mammals. It participates in the regulation of hunger and fat storage. Increased nesfatin-1 in the hypothalamus contributes to diminished hunger, a 'sense of fullness', and a potential loss of body fat and weight.

Gastrointestinal physiology is the branch of human physiology that addresses the physical function of the gastrointestinal (GI) tract. The function of the GI tract is to process ingested food by mechanical and chemical means, extract nutrients and excrete waste products. The GI tract is composed of the alimentary canal, that runs from the mouth to the anus, as well as the associated glands, chemicals, hormones, and enzymes that assist in digestion. The major processes that occur in the GI tract are: motility, secretion, regulation, digestion and circulation. The proper function and coordination of these processes are vital for maintaining good health by providing for the effective digestion and uptake of nutrients.

Growth hormone secretagogue receptor Protein-coding gene in the species Homo sapiens

Growth hormone secretagogue receptor(GHS-R), also known as ghrelin receptor, is a G protein-coupled receptor that binds growth hormone secretagogues (GHSs), such as ghrelin, the "hunger hormone". The role of GHS-R is thought to be in regulating energy homeostasis and body weight. In the brain, they are most highly expressed in the hypothalamus, specifically the ventromedial nucleus and arcuate nucleus. GSH-Rs are also expressed in other areas of the brain, including the ventral tegmental area, hippocampus, and substantia nigra. Outside the central nervous system, too, GSH-Rs are also found in the liver, in skeletal muscle, and even in the heart.

In biology, energy homeostasis, or the homeostatic control of energy balance, is a biological process that involves the coordinated homeostatic regulation of food intake and energy expenditure. The human brain, particularly the hypothalamus, plays a central role in regulating energy homeostasis and generating the sense of hunger by integrating a number of biochemical signals that transmit information about energy balance. Fifty percent of the energy from glucose metabolism is immediately converted to heat.

Hunger is a sensation that motivates the consumption of food. 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. There are several theories about how the feeling of hunger arises. The desire to eat food, or appetite, is another sensation experienced with regards to eating.

The nervous system, and endocrine system collaborate in the digestive system to control gastric secretions, and motility associated with the movement of food throughout the gastrointestinal tract, including peristalsis, and segmentation contractions.

Weight management Techniques for maintaining body weight

Weight management includes the techniques and physiological processes that contribute to a person's ability to attain and maintain a certain weight. Most weight management techniques encompass long-term lifestyle strategies that promote healthy eating and daily physical activity. Moreover, weight management involves developing meaningful ways to track weight over time and to identify ideal body weights for different individuals.

Hedonic hunger or hedonic hyperphagia is "the drive to eat to obtain pleasure in the absence of an energy deficit." Particular foods may have a high "hedonic rating" or individuals may have increased susceptibility to environmental food cues. Weight loss programs may aim to control or to compensate for hedonic hunger. Therapeutic interventions may influence hedonic eating behavior.

Pathophysiology of obesity

Pathophysiology of obesity is the study of disordered physiological processes that cause, result from, or are otherwise associated with obesity. A number of possible pathophysiological mechanisms have been identified which may contribute in the development and maintenance of obesity.

The food-entrainable oscillator (FEO) is a circadian clock that can be entrained by varying the time of food presentation. It was discovered when a rhythm was found in rat activity. This was called food anticipatory activity (FAA), and this is when the wheel-running activity of mice decreases after feeding, and then rapidly increases in the hours leading up to feeding. FAA appears to be present in non-mammals (pigeons/fish), but research heavily focuses on its presence in mammals. This rhythmic activity does not require the suprachiasmatic nucleus (SCN), the central circadian oscillator in mammals, implying the existence of an oscillator, the FEO, outside of the SCN, but the mechanism and location of the FEO is not yet known. There is ongoing research to investigate if the FEO is the only non-light entrainable oscillator in the body.

References

  1. ↑ Carlson, Neil R. (2010). Physiology of Behavior. Allyn & Bacon. ISBN   9780205666270.
  2. ↑ Bellisle, France (2009). "How and why should we study ingestive behaviors in humans?". Food Quality and Preference. 20: 539–544. doi:10.1016/j.foodqual.2009.03.005.
  3. ↑ Savage, J.; Fisher, J.; Birch, L. (2007). "Parental influence on eating behavior". J Law Med Ethics. 35: 22–34. doi:10.1111/j.1748-720x.2007.00111.x. PMC   2531152 . PMID   17341215.
  4. ↑ Kearney, J. (2010). "Food consumption trends and drivers". Philosophical Transactions of the Royal Society 365.
  5. ↑ Herman, C. Peter (2003). "Effects of the presence of others on food intake". Psychological Bulletin. 129: 873–86. doi:10.1037/0033-2909.129.6.873. PMID   14599286.
  6. ↑ Wansink, B. (2004). "Environmental factors that increase the food intake and consumption volume of unknown consumers". Annu. Rev. Nutr. 24: 455–479. doi:10.1146/annurev.nutr.24.012003.132140. PMID   15189128.
  7. ↑ Carlson, Neil R. (2012). "Ingestive behavior". Physiology of Behavior. Pearson. p. 407.
  8. ↑ Inui, Akio (2001). "Ghrelin: An orexigenic and somatotrophic signal from the stomach". Nature Reviews Neuroscience. 2: 551–60. doi:10.1038/35086018. PMID   11483998.
  9. ↑ Schmid, D.; Held, K.; Ising, M.; Uhr, M.; et al. (2005). "Ghrelin stimulates appetite, imagination of food, GH, ACTH, and cortisol, but does not affect leptin in normal controls". Neuropsychopharmacology. 30 (6): 1187–1192. doi: 10.1038/sj.npp.1300670 . PMID   15688086.
  10. ↑ Schaller, G.; Schmidt, A.; Pleiner, J.; Woloszczuk, W.; et al. (2003). "Plasma ghrelin concentrations are not regulated by glucose or insulin: A double-blind, placebo-controlled crossover clamp study". Diabetes. 52: 16–20. doi: 10.2337/diabetes.52.1.16 .
  11. ↑ Carlson, Neil R. (2012). "Ingestive behavior". Physiology of Behavior. Pearson. p. 407.
  12. ↑ Inui, Akio (2001). "Ghrelin: An orexigenic and somatotrophic signal from the stomach". Nature Reviews Neuroscience. 2: 551–60. doi:10.1038/35086018. PMID   11483998.
  13. ↑ Carlson, Neil R. (2010). Physiology of Behavior. Allyn & Bacon. ISBN   9780205666270.
  14. ↑ Cecil, J.E.; Francis, J.; Read, N.W. (1998). "Relative contributions of intestinal, gastric, oro-sensory influences and information to changes in appetite induced by the same liquid meal". Appetite. 31: 377–390. doi:10.1006/appe.1998.0177.
  15. ↑ Davis, J.D.; Campbell, C.S. (1973). "Peripheral control of meal size in the rat: Effect of sham feeding on meal size and drinking rate". Journal of Comparative and Physiological Psychology. 83: 379–387. doi:10.1037/h0034667.
  16. ↑ Deutsch, J.A.; Gonzalez, M.F. (1980). "Gastric nutrient content signals satiety". Behavioral and Neural Biology. 30: 113–116. doi:10.1016/s0163-1047(80)90989-9.
  17. ↑ Feinle, C.; Grundy, D.; Read, N.W. (1997). "Effects of duodenal nutrients on sensory and motor responses of the human stomach to distension". American Journal of Physiology. 273: G721–G726.
  18. ↑ Tordoff, M.G.; Friedman, M.I. (1988). "Hepatic control of feeding: Effect of glucose, fructose, and mannitol". American Journal of Physiology. 254: R969–R976.
  19. ↑ Carlson, Neil R. (2010). Physiology of Behavior. Allyn & Bacon. ISBN   9780205666270.
  20. ↑ Carlson, Neil R. (2010). Physiology of Behavior. Allyn & Bacon. ISBN   9780205666270.
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