Hunger is a sensation that motivates the consumption of food.
Hunger sensation typically manifests after only a few hours without eating and is generally considered to be unpleasant.
It has complex and redundant pathways involving all five senses that regulate it.
Thst there is a relative stability of body weight overtime in any given person suggests a sophisticated metabolic machinery, capable of regulating a multitude of variables, including metabolic rate, quality, and quantity of food ingested, thermic effects of food, macronutrient composition, and physical activity.
There is a distinction between hunger, which is the physiological impulse to eat, that is triggered by starvation with acute energy deprivation to maintain energy balance-and appetite, which referred to as hedonic hunger with food intake, driven by pleasure rather than metabolic necessity.
Hunger can be categorized by three interconnected mechanisms: homeostatic, hedonic, and microbiota-driven.
Homeostatic hunger involves the brain gut access, specifically, the hypothalamus-gut access:Hunger is a passive process, triggered by nutrient depletion and alleviated by nutrient absorption.
The hypothalamic circuitries controlling hunger are regulated by sensory signals stemming from the G.I. tract.
An empty stomach stimulates, the vagus nerve, and the secretion of gherlin considered the appetite hormone.
Therefore, eating requires a sophisticated coordination between the brain and the gut (gut-brain axis) cross talk.
Satiety occurs between 5 and 20 minutes after eating.
The term hunger is also the most commonly used 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.
Afferent vagal stimulation and endocrine signals are relayed to the hypothalamus conveying the need to eat.
A healthy, well-nourished individual can survive for weeks without food intake, with claims ranging from three to ten weeks.
Satiety is the opposite of hunger; it is the sensation of feeling full.
The physical sensation of hunger is related to contractions of the stomach muscles.
Hunger pangs 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.
Hunger related stomach contractions can be especially severe and painful and children and young adults.
Hunger pangs can be made worse by irregular meals.
Following food intake, hunger repression is initiated by gastric distention as detected by mechanical receptors of tension, stretch, and volume, and then relaying signals to the hindbrain through vagal and spinal nerves.
Satiety signals are reinforced by amino acids and fatty acids in the G.I. tract, also lead to hunger suppression.
Gastric emptying, and osmotic load within the G.I. tract contribute to early satiety.
Gastrointestinal hormones, including glucagon like peptide one (GLP-1), cholecystokinin, and peptide YY are secreted in the presence of digested food within the proximate small intestine and lead to satiety by generating inhibitory signals in the brain.
Late satiety is reached when a completion of digestive processes, plasma levels of amino acids, glucose, and insulin increase along with sensory signals and integration of all processes in the CNS completes the cycle of homeostatic hunger control.
Older people may feel less severe stomach contractions with hunger, but still suffer the secondary effects resulting from low food intake: these include weakness, irritability and decreased concentration.
Prolonged inadequate nutrition causes increased susceptibility to disease and reduced ability for the body to heal.
Short-term regulation of hunger and food intake is multifactorial, involving neural signals from the GI tract, blood levels of nutrients, GI tract hormones, and psychological factors.
Gut content is also evaluated through vagal nerve fibers that carry signals between the brain and the gastrointestinal tract (GI tract).
Stretch receptors work by inhibiting 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.
Cholecystokinin suppresses 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.
Hypoglycemia triggers hunger by regulating the activity of specific hypothalamic neurons that respond to serum glucose levels.
Motilin induced interprandial phase III gastrointestinal, contractions control hunger, and regulation of food intake in both healthy and disease states, through a cholinergic pathway.
Luminal stimuli (bitter tastes) modulate motilinrelease affecting hunger and food intake.
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.
Wanting is the motivation to consume the food.
Both are reduced by the repeated consumption of foods.
Wanting food may be due to change in memory-related processes, and can be triggered by a variety of psychological processes.
The regulation of appetite is referred to as the appestat.
Leptin, a hormone produced by the adipose tissue provides negative feedback.
Leptin, 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.
Appetite regulation is an immensely complex process involving the gastrointestinal tract, many hormones, and both the central and autonomic nervous systems.
Gut hormones regulate many pathways in the body can either stimulate or suppress appetite.
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.
Serotonin primarily acts through effects on neuropeptide Y (NPY)/agouti-related peptide (AgRP) to stimulate appetite and proopiomelanocortin (POMC) to 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 neurologic projections contribute to the awareness of hunger.
The somatic processes controlled by the hypothalamus include vagal tone, the activity of the parasympathetic autonomic nervous system, stimulation of the thyroid’s thyroxine that regulates the metabolic rate, and the hypothalamic-pituitary-adrenal axis along with 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 behavior.
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, dopamine, 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.
These hormones all modify the hypothalamic response, and
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, explaining 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.
Leptin functions: Suppresses 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.
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.
Insulin effects long-term hunger and food intake regulation.
The biological clock, which is regulated by the hypothalamus, stimulates hunger.
Cerebral loci, as from the limbic system and the cerebral cortex, project on the hypothalamus and modify appetite, explaining why with depression and stress, energy intake can change quite drastically.
Homeostatic hunger is typical of people who experience food deprivation.
Hedonic or pleasure driven hunger is characterized by desire to eat in the absence of acute caloric need.
In homeostatic hunger, there is a tightly regulated, satiety balance that is adjusted to maintain metabolic homeostasis that prevents excessive caloric intake.
Hedonic hunger that occurs in the presence of substantial food availability when reward cortical circuitries supersede hypothalamic control of energy balance, leading to the ingestion of energy, dense, high fat, and high sugar foods not out of necessity, but for pleasure.
Hedonic hunger is influenced by emotions, resulting in individual differences in eating behavior; anger, fear, sadness, and depression are often associated with excessive consumption of sweet food.
Babies are prone to favor sweet and salty taste as compared with bitter and sour taste, and adapt to consume safe foods such as human milk, which is sweet and favors better satiety control than baby formulas.
Western parents are more prone to let their children eat palatable, energy dense food, despite their detrimental effects on health, and maybe partly responsible for the obesogenic trends, particularly among children.