Hunger

Template:Dablink Hunger desribes the desire of animals to eat, and is activated by many different cues. The motivation to eat is controlled by the hypothalamus, and is generally strong in all animals when the energy expended by the animal exceed the energy consumed, and this imbalance is signalled to the brain in many different ways. Hunger can also be applied metaphorically to cravings of other sorts. The term is commonly used more broadly to refer to cases of widespread malnutrition or deprivation among populations, usually due to poverty, political conflicts or instability, or adverse agricultural conditions (famine). (See malnutrition for statistics and other information on hunger as a political and economic problem.)

Hunger as a condition

The term hungry is commonly used to mean having an appetite for food or to be ready for a meal. After a long period without food, the mild sensation of hunger associated with being ready for a meal becomes progressively more severe, until it is acutely painful. As hunger grows, most living things will experience some internal effects. In humans and other animals, hunger can cause a gurgling sound with a bubbling feeling in the small intestine (many mistakenly think the stomach does this), and can shrink the stomach. Prolonged hunger will drive people to eat substances with no nutritional value (such as grass and soil) simply to fill their stomachs, but doing so actually has an adverse effect on energy balance as energy is still required to digest these substances.

In contrast to hunger, which is involuntary, fasting is the practice of voluntarily not eating for a period of time. A hunger strike is fasting for the purpose of nonviolent resistance.

Physiology

The hypothalamus is a very complex part of the brain, which contains many different types of specialised nerve cell and controls many different physiological functions. One important role of the hypothalamus is to regulate food intake, and in this the 'hunger centres' and 'satiety centres' of the hypothalamus play a particularly important role. The most clearly identified hunger centre is in the lateral hypothalamus; this was first recognised when it was seen that after lesions to this area, animals do not eat spontaneously. Conversely lesions to the ventromedial hypothalamus, the main satiety centre, cause animals to overeat to excess, and become grossly obese.

Appetite for food is thus thought to be in part governed by a balance between hunger signals and satiety signals that converge at the hypothalamus. These signals converge at another part of the hypothalamus, the arcuate nucleus. The arcuate nucleus contains several different populations of nerve cells, one of which makes a peptide, neuropeptide Y, which is a very potent orixigen (when injected into the brain it causes animals to eat voraciously). These NPY neurons are activated by ghrelin, a hormone that is secreted from the empty stomach, and whose concentration in the blood falls after each meal and rises progressively until the next. Ghrelin is thus a major physiological hunger signal. Conversely, the NPY cells are inhibited by leptin, a hormone secreted from adipocytes (fat cells) that circulates in the blood in proportion to the energy stores of the body; leptin thus suppresses the desire to eat. There are some cases of humans born with leptin deficiency due to a genetic mutation - these individuals are grossly obese, but their body weight will return to normal if they recieve daily injections of leptin. However these cases are extremely rare, in most cases of obesity, the individuals have high circulating concentrations of leptin (as expected from the large fat mass) but appear to be insensitive to leptin - this "leptin resistance" appears to be similar to the "insulin resistance" seen in type 2 diabetes mellitus.

Leptin and ghrelin are not the only signals that reach the hypothalamus; cells in the ventromedial nucleus and some in the lateral hypothalamus are directly sensitive to glucose concentrations - some are inhibited when glucose concentrations are high, others are inhibited. The hypothalamus also contains neurons that are sensitive to insulin - insulin is secreted overall in amounts proportional to the size of the body fat stores, so is another signal that the brain can use to evaluate its energy reserves. Other hormones are also produced by the stomach and gastrointestinal tract, including PYY, which appears to act as a satiety signal.

These signals are only part of the complex systems regulating when and how much we eat. In humans as in many other animals, we eat at generally consistent times of the day, and we are conditioned to expect food and become hungry at these times. Experimental laboratory animals, even though food is freely available at all times will still tend to confine their eating to meal times, according to a circadian rhythm; rats for example generally become active and start to eat soon after the lights are switched off. Such rhythms are controlled by another nucleus in the hypothalamus - the suprachiasmatic nucleus. How much we eat is also affected by our levels of stress and anxiety - so called "comfort eating." Again, the hypothalamus is critically important - the paraventricular nucleus of the hypothalamus is the major control centre of the hypothalami-pituitary-adrenal axis (HPA axis) - the body systems that control our responses to stress.

Satiety

Painting by Carl von Bergen (1904).

Satiety, or the feeling of fullness and disappearance of appetite after a meal, is mediated by signals that arise from the stomach and gastrointestinal tract. These signals, which include signals arising from stretch receptors as the stomach is distended by food, and chemical signals arising in the stomach as the result of secretion from cells regulating digestion, activate afferent fibres of the vagus nerve. For example, the gut hormone cholecystokinin (CCK) is secreted in the stomach during a meal, and activates specific receptors (CCK-A receptors) on the nerve endings of the gastric vagus nerve. The vagally-mediated signals reach the hypothalamus via nuclei in the caudal brainstem - notably the nucleus of the solitary tract. Noradrenergic neurons in this area play a particularly important role in carrying these signals; these neurons project to many different parts of the hypothalamus.

Eating appears to stop when the satiety signals reaching the hypothalamus are sufficiently strong to activate particular populations of neurons that make "anorexigenic" peptides - peptides that when injected into the brain are potent at suppressing hunger. There are many diferent anorexigenic peptides just as there are many different orexigenic peptides - the neural circuitry that regulates appetite is extremely complex. However one of the most important anorexigenic peptides is alpha melanocyte stimulating hormone (alpha- MSH) which is made in another population of neurons in the arcuate nucleus. These neurons project to many diferent parts of the hypothalamus where alpha-MSH is released and acts on other neurons via specific melanocortin receptors.

Genetic disorders that prevent alpha-MSH being made or which prevent its normal actions result in individuals who are grossly obese as a result of chronic overeating.

See also

• Eating disorder
• Starvation
• Thirst
• Hypothalamus