Hunger (physiology)

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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. [1] There are several theories about how the feeling of hunger arises. [2] The desire to eat food, or appetite, is another sensation experienced with regard to eating. [3]

Contents

The term hunger is also the most commonly used 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. A healthy, well-nourished individual can survive for weeks without food intake (see fasting), with claims ranging from three to ten weeks. [4]

Satiety is the opposite of hunger; it is the sensation of feeling full. [5]

Hunger pangs

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.[ citation needed ]

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. [6] 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. [7] [8]

Short-term regulation of hunger and food intake

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 tract

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. [9]

Hormone signals

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. [10]

Psychological factors

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 [11] [12] and may be due to change in memory-related processes. [13] 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. [14]

Long-term regulation of hunger and food intake

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. [15] 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. [15] The circulating gut hormones that regulate many pathways in the body can either stimulate or suppress appetite. [16] For example, ghrelin stimulates appetite, whereas cholecystokinin and glucagon-like peptide-1 (GLP-1) suppress appetite. [16]

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, [17] especially dopamine and serotonin. [18] Dopamine acts primarily through the reward centers of the brain, [18] 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. [19] Similarly, the hormones leptin and insulin suppress appetite through effects on AgRP and POMC neurons. [20]

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. [21]

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. [22]

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.

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:

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. [9]

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.

Set point theories of hunger and eating

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. [23] 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. [24]

Positive-incentive perspective

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. [28] 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. [29] 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. [25]

Premeal hunger

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. [30] [31] [32]

Similar conditions

A food craving is an intense desire to consume a specific food, as opposed to general hunger. Similarly, thirst is the craving for water. [33]

A concept of food noise or food chatter has gotten more attention in the early 2020s since the advent of antiobesity indications for a class of medications called GLP1 agonists (such as semaglutide). Food noise is a mental preoccupation with food in general (as opposed to one specific food) that is largely independent from physiological hunger but nonetheless is distracting for many people; it includes recurring thoughts about what one has or hasn't eaten in recent hours, what one would like to eat right now or "shouldn't" eat right now, and what one might be eating (or "should" avoid eating) in upcoming hours. Among people for whom these medications are effective in helping with weight loss, most express that the level of food noise in their mind is noticeably reduced. [34] Even without these medications, some people may be able to reduce food noise by modifying their dietary patterns and exercise; [34] this is more effective for some people than others. [34]

See also

Related Research Articles

<span class="mw-page-title-main">Anorexia (symptom)</span> Loss of appetite

Anorexia is a medical term for a loss of appetite. While the term outside of the scientific literature is often used interchangeably with anorexia nervosa, many possible causes exist for a loss of appetite, some of which may be harmless, while others indicate a serious clinical condition or pose a significant risk.

<span class="mw-page-title-main">Hypothalamus</span> Area of the brain below the thalamus

The hypothalamus is a small part of the vertebrate brain that contains a number of nuclei with a variety of functions. One of the most important functions is to link the nervous system to the endocrine system via the pituitary gland. The hypothalamus is located below the thalamus and is part of the limbic system. It forms the basal part of the diencephalon. All vertebrate brains contain a hypothalamus. In humans, it is about the size of an almond.

<span class="mw-page-title-main">Eating</span> Ingestion of food

Eating is the ingestion of food. In biology, this is typically done to provide a heterotrophic organism with energy and nutrients 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.

<span class="mw-page-title-main">Leptin</span> Hormone that inhibits hunger

Leptin, also known as obese protein, is a protein hormone predominantly made by adipocytes. Its primary role is likely to regulate long-term energy balance.

<span class="mw-page-title-main">Appetite</span> Desire to eat food

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 ARFID, anorexia nervosa, bulimia nervosa, cachexia, overeating, and binge eating disorder.

<span class="mw-page-title-main">Arcuate nucleus (hypothalamus)</span>

The arcuate nucleus of the hypothalamus (ARH), or ARC, is also known as the infundibular nucleus to distinguish it from the arcuate nucleus of the medulla oblongata in the brainstem. The arcuate nucleus 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.

<span class="mw-page-title-main">Ghrelin</span> Peptide hormone involved in appetite regulation

Ghrelin is a hormone primarily 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.

<span class="mw-page-title-main">Agouti-related peptide</span> Mammalian protein found in Homo sapiens

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.

<span class="mw-page-title-main">Ventromedial nucleus of the hypothalamus</span> Nucleus of the hypothalamus

The ventromedial nucleus of the hypothalamus is a nucleus of the hypothalamus. In 2007, Kurrasch et al. found that the ventromedial hypothalamus is a distinct morphological nucleus involved in terminating hunger, fear, thermoregulation, and sexual activity. This nuclear region is involved in the recognition of the feeling of fullness.

The gastrointestinal hormones constitute a group of hormones secreted by enteroendocrine cells in the stomach, pancreas, and small intestine that control various functions of the digestive organs. Later studies showed that most of the gut peptides, such as secretin, cholecystokinin or substance P, were found to play a role of neurotransmitters and neuromodulators in the central and peripheral nervous systems.

<span class="mw-page-title-main">Lateral hypothalamus</span>

The lateral hypothalamus (LH), also called the lateral hypothalamic area (LHA), contains the primary orexinergic nucleus within the hypothalamus that widely projects throughout the nervous system; this system of neurons mediates an array of cognitive and physical processes, such as promoting feeding behavior and arousal, reducing pain perception, and regulating body temperature, digestive functions, and blood pressure, among many others. Clinically significant disorders that involve dysfunctions of the orexinergic projection system include narcolepsy, motility disorders or functional gastrointestinal disorders involving visceral hypersensitivity, and eating disorders.

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.

<span class="mw-page-title-main">Growth hormone secretagogue receptor</span> 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.

<span class="mw-page-title-main">Central melanocortin system</span> System involved in the regulation of weight and peripheral tissue such as hair and skin

The central melanocortin system is defined anatomically as a collection of central nervous system circuits which include:

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.

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. Disruptions in these ingestive regulatory mechanisms can result in eating disorders such as obesity, anorexia, and bulimia.

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.

The Cannon-Washburn Hunger Experiment was conducted in 1912 by American physiologist Walter Cannon and his colleague, graduate student A.L. Washburn. This experiment investigated the physiological mechanisms of hunger by examining the relationship between stomach contractions and the sensation of hunger. The results of the study provided early evidence for the role of the stomach in hunger regulation and helped establish a foundation for modern research on appetite control. The findings continue to influence current studies on the physiological mechanisms that underlie metabolism and eating behavior.

<span class="mw-page-title-main">Pathophysiology of obesity</span> Physiological processes in obese people

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.

<span class="mw-page-title-main">Hyperpalatable food</span> Food that triggers the brains reward system

Hyperpalatable food (HPF) combines high levels of fat, sugar, sodium, and/or carbohydrates to trigger the brain's reward system, encouraging excessive eating. The concept of hyperpalatability is foundational to ultra-processed foods, which are usually engineered to have enjoyable qualities of sweetness, saltiness, or richness. Hyperpalatable foods can stimulate the release of metabolic, stress, and appetite hormones that play a role in cravings and may interfere with the body's ability to regulate appetite and satiety.

References

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