Appetite

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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. [1] 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 (or "hyperphagia") is increased eating. Dysregulation of appetite contributes to anorexia nervosa, bulimia nervosa, cachexia, overeating, and binge eating disorder.

Contents

Role in disease

A limited or excessive appetite is not necessarily pathological. Abnormal appetite could be defined as eating habits causing malnutrition and related conditions such as obesity and its related problems.

Both genetic and environmental factors may regulate appetite, and abnormalities in either may lead to abnormal appetite. Poor appetite (anorexia) can have numerous causes, but may be a result of physical (infectious, autoimmune or malignant disease) or psychological (stress, mental disorders) factors. Likewise, hyperphagia (excessive eating) may be a result of hormonal imbalances, mental disorders (e.g., depression) and others. Dyspepsia, also known as indigestion, can also affect appetite as one of its symptoms is feeling "overly full" soon after beginning a meal. [2] Taste and smell ("dysgeusia", bad taste) or the lack thereof may also affect appetite. [3]

Abnormal appetite may also be linked to genetics on a chromosomal scale, shown by the 1950s discovery of Prader–Willi syndrome, a type of obesity caused by chromosome alterations. Additionally, anorexia nervosa and bulimia nervosa are more commonly found in females than males – thus hinting at a possibility of a linkage to the X-chromosome. [4]

Eating disorders

Dysregulation of appetite lies at the root of anorexia nervosa, bulimia nervosa, and binge eating disorder. Anorexia nervosa is a mental disorder characterized as severe dietary restriction and intense fear of weight gain. Furthermore, persons with anorexia nervosa may exercise ritualistically. Individuals who have anorexia have high levels of ghrelin, a hormone that stimulates appetite, so the body is trying to cause hunger, but the urge to eat is being suppressed by the person. [5] Binge eating disorder (commonly referred to as BED) is described as eating excessively (or uncontrollably) between periodic time intervals. The risk for BED can be present in children and most commonly manifests during adulthood. Studies suggest that the heritability of BED in adults is approximately 50%. [6] Similarly to bulimia, some people may be involved in purging and binging. They might vomit after food intake or take purgatives. Body dysmorphic disorder may involve food restriction in an attempt to deal with a perceived fault, and may be associated with depression and social isolation. [7]

Obesity

Various hereditary forms of obesity have been traced to defects in hypothalamic signaling (such as the leptin receptor and the MC-4 receptor) or are still awaiting characterization Prader-Willi syndrome  – in addition, decreased response to satiety may promote development of obesity. [8] It has been found that ghrelin-reactive IgG immunoglobulins affect ghrelin's orexigenic response. [9]

Other than genetically stimulated appetite abnormalities, there are physiological ones that do not require genes for activation. For example, ghrelin and leptin are released from the stomach and adipose cells, respectively, into the blood stream. Ghrelin stimulates feelings of hunger, whereas leptin stimulates feelings of satisfaction from food. [10] Any changes in normal production levels of these two hormones can lead to obesity. The amount of leptin hormone production is stimulated by body fat percentage. When body fat accumulates there is overproduction of leptin causing a resistant hypothalamus and eventually almost no leptin effect. From then all ghrelin production causes insatiable appetite. [11]

Pediatric eating problems

Eating issues such as "picky eating" affects about 25% of children, but among children with development disorders this number may be significantly higher, which in some cases may be related to the sounds, smells, and tastes (sensory processing disorder). [12]

Pharmacology and treatment

The glycemic index is thought to affect satiety; a study investigating the effect of satiety found that a high-glycemic food, potatoes, reduced appetite more than a low glycemic index food. [13]

Suppression

Mechanisms controlling appetite are a potential target for weight loss drugs. Appetite control mechanisms seem to strongly counteract undereating, whereas they appear weak to control overeating. Early anorectics (appetite suppressants) were fenfluramine and phentermine. A more recent addition is sibutramine which increases serotonin and noradrenaline levels in the central nervous system, but had to be withdrawn from the market when it was shown to have an adverse cardiovascular risk profile. Similarly, the appetite suppressant rimonabant (a cannabinoid receptor antagonist) had to be withdrawn when it was linked with worsening depression and increased risk of suicide. Recent reports on recombinant PYY 3-36 suggest that this agent may contribute to weight loss by suppressing appetite.

Given the epidemic proportions of obesity in the Western world and the fact that it is increasing rapidly in some poorer countries, observers[ who? ] expect developments in this area to snowball in the near future.

Stimulation

Weight loss or loss of appetite ("cachexia") is an effect of some diseases, and a side effect of some prescription drugs. Stimulants such as methylphenidate commonly reduce appetite in patients, [14] and have been prescribed off-label for weight loss. [15] Three agents are approved for appetite stimulation in the United States: megestrol acetate - a progesterone available as an oral tablet, oxandrolone - an oral anabolic steroid, and dronabinol - a cannabinoid available in an oral capsule. [16]

Ghrelin, a gut hormone recognized as affecting appetite, is under investigation. [17] Ghrelin itself must be delivered parenterally [17] :2178 and research has therefore focused on substances that can be taken orally. Rikkunshito, a traditional Japanese Kampo medicine, is under preliminary research for its potential to stimulate ghrelin and appetite. [17]

See also

Related Research Articles

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

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.

An eating disorder is a mental disorder defined by abnormal eating behaviors that negatively affect a person's physical or mental health. Types of eating disorders include binge eating disorder, where the patient eats a large amount in a short period of time; anorexia nervosa, where the person has an intense fear of gaining weight and restricts food or overexercises to manage this fear; bulimia nervosa, where individuals eat a large quantity (binging) then try to rid themselves of the food (purging); pica, where the patient eats non-food items; rumination syndrome, where the patient regurgitates undigested or minimally digested food; avoidant/restrictive food intake disorder (ARFID), where people have a reduced or selective food intake due to some psychological reasons; and a group of other specified feeding or eating disorders. Anxiety disorders, depression and substance abuse are common among people with eating disorders. These disorders do not include obesity. People often experience comorbidity between an eating disorder and OCD. It is estimated 20–60% of patients with an ED have a history of OCD.

<span class="mw-page-title-main">Bulimia nervosa</span> Type of eating disorder

Bulimia nervosa, also known as simply bulimia, is an eating disorder characterized by binge eating followed by purging or fasting, and excessive concern with body shape and weight. This activity aims to expel the body of calories eaten from the binging phase of the process. Binge eating refers to eating a large amount of food in a short amount of time. Purging refers to the attempts to get rid of the food consumed. This may be done by vomiting or taking laxatives.

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

Eating is the ingestion of food. In the natural biological world, this is typically 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.

Binge eating disorder (BED) is an eating disorder characterized by frequent and recurrent binge eating episodes with associated negative psychological and social problems, but without the compensatory behaviors common to bulimia nervosa, OSFED, or the binge-purge subtype of anorexia nervosa.

<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.

Polyphagia or hyperphagia is an abnormally strong, incessant sensation of hunger or desire to eat often leading to overeating. In contrast to an increase in appetite following exercise, polyphagia does not subside after eating and often leads to rapid intake of excessive quantities of food. Polyphagia is not a disorder by itself; rather, it is a symptom indicating an underlying medical condition. It is frequently a result of abnormal blood glucose levels, and, along with polydipsia and polyuria, it is one of the "3 Ps" commonly associated with uncontrolled diabetes mellitus.

<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.

Night eating syndrome (NES) is an eating disorder, characterized by a delayed circadian pattern of food intake. Although there is some degree of comorbidity with binge eating disorder, it differs from binge eating in that the amount of food consumed in the night is not necessarily objectively large nor is a loss of control over food intake required. It was originally described by Albert Stunkard in 1955 and is currently included in the other specified feeding or eating disorder category of the DSM-5. Research diagnostic criteria have been proposed and include evening hyperphagia and/or nocturnal awakening and ingestion of food two or more times per week. The person must have awareness of the night eating to differentiate it from the parasomnia sleep-related eating disorder (SRED). Three of five associated symptoms must also be present: lack of appetite in the morning, urges to eat at night, belief that one must eat in order to fall back to sleep at night, depressed mood, and/or difficulty sleeping.

Purging disorder is an eating disorder characterized by the DSM-5 as self-induced vomiting, or misuse of laxatives, diuretics, or enemas to forcefully evacuate matter from the body. Purging disorder differs from bulimia nervosa (BN) because individuals do not consume a large amount of food before they purge. In current diagnostic systems, purging disorder is a form of other specified feeding or eating disorder. Research indicates that purging disorder, while not rare, is not as commonly found as anorexia nervosa or bulimia nervosa. This syndrome is associated with clinically significant levels of distress, and that it appears to be distinct from bulimia nervosa on measures of hunger and ability to control food intake. Some of the signs of purging disorder are frequent trips to the bathroom directly after a meal, frequent use of laxatives, and obsession over one's appearance and weight. Other signs include swollen cheeks, popped blood vessels in the eyes, and clear teeth which are all signs of excessive vomiting.

<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.

An orexigenic, or appetite stimulant, is a drug, hormone, or compound that increases appetite and may induce hyperphagia. This can be a medication or a naturally occurring neuropeptide hormone, such as ghrelin, orexin or neuropeptide Y, which increases hunger and therefore enhances food consumption. Usually appetite enhancement is considered an undesirable side effect of certain drugs as it leads to unwanted weight gain, but sometimes it can be beneficial and a drug may be prescribed solely for this purpose, especially when the patient is suffering from severe appetite loss or muscle wasting due to cystic fibrosis, anorexia, old age, cancer or AIDS. There are several widely used drugs which can cause a boost in appetite, including tricyclic antidepressants (TCAs), tetracyclic antidepressants, natural or synthetic cannabinoids, first-generation antihistamines, most antipsychotics and many steroid hormones. In the United States, no hormone or drug has currently been approved by the FDA specifically as an orexigenic, with the exception of Dronabinol, which received approval for HIV/AIDS-induced anorexia only.

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.

<span class="mw-page-title-main">Anorexia nervosa</span> Type of eating disorder

Anorexia nervosa (AN), often referred to simply as anorexia, is an eating disorder characterized by low weight, food restriction, body image disturbance, fear of gaining weight, and an overpowering desire to be thin.

The differential diagnoses of anorexia nervosa (AN) includes various types of medical and psychological conditions, which may be misdiagnosed as AN. In some cases, these conditions may be comorbid with AN because the misdiagnosis of AN is not uncommon. For example, a case of achalasia was misdiagnosed as AN and the patient spent two months confined to a psychiatric hospital. A reason for the differential diagnoses that surround AN arise mainly because, like other disorders, it is primarily, albeit defensively and adaptive for, the individual concerned. Anorexia Nervosa is a psychological disorder characterized by extremely reduced intake of food. People with anorexia nervosa have a low self-image and consider themselves overweight.

<span class="mw-page-title-main">Eating disorders and memory</span> Memory impairments linked to eating disorders

Many memory impairments exist as a result from or cause of eating disorders. Eating disorders (EDs) are characterized by abnormal and disturbed eating patterns that affect the lives of the individuals who worry about their weight to the extreme. These abnormal eating patterns involve either inadequate or excessive food intake, affecting the individual's physical and mental health.

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.

<span class="mw-page-title-main">Pathophysiology of obesity</span>

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.

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