Open main menu
Home
Random
Recent changes
Special pages
Community portal
Preferences
About Wikipedia
Disclaimers
Incubator escapee wiki
Search
User menu
Talk
Dark mode
Contributions
Create account
Log in
Editing
Appetite
(section)
Warning:
You are not logged in. Your IP address will be publicly visible if you make any edits. If you
log in
or
create an account
, your edits will be attributed to your username, along with other benefits.
Anti-spam check. Do
not
fill this in!
==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 (symptom)|anorexia]]) can have a number of 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., [[clinical depression|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.<ref>{{cite web |publisher=National Digestive Diseases Information Clearinghouse (NDDIC) |url=http://digestive.niddk.nih.gov/ddiseases/pubs/indigestion/ |title=Indigestion |website=Digestive.niddk.nih.gov |access-date=2011-12-04 |archive-url=https://web.archive.org/web/20141105001458/http://digestive.niddk.nih.gov/ddiseases/pubs/indigestion/ |archive-date=2014-11-05 |url-status=dead }}</ref> [[Taste]] and [[Olfaction|smell]] ("[[dysgeusia]]", bad taste) or the lack thereof may also affect appetite.<ref>{{cite journal | vauthors = Henkin RI, Levy LM, Fordyce A | title = Taste and smell function in chronic disease: a review of clinical and biochemical evaluations of taste and smell dysfunction in over 5000 patients at The Taste and Smell Clinic in Washington, DC | journal = American Journal of Otolaryngology | volume = 34 | issue = 5 | pages = 477–89 | date = 2013-09-01 | pmid = 23731850 | doi = 10.1016/j.amjoto.2013.04.006 }}</ref> 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.<ref name="pmid16837373">{{cite journal | vauthors = Owen JB | title = Weight control and appetite--a genetic perspective | journal = Clinical Nutrition | volume = 9 | issue = 5 | pages = 291–3 | date = October 1990 | pmid = 16837373 | doi = 10.1016/0261-5614(90)90039-U }}</ref> === 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.<ref>{{cite book | vauthors = Schacter DT, Gilbert DT, Wegner DM |year=2011 |title=Psychology |url=https://archive.org/details/psychology0000scha |url-access=registration |edition=2nd |place=New York, NY |publisher=Worth Publishers|isbn=9781429237192 }}</ref> 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%.<ref>{{cite journal | vauthors = Tanofsky-Kraff M, Bulik CM, Marcus MD, Striegel RH, Wilfley DE, Wonderlich SA, Hudson JI | title = Binge eating disorder: the next generation of research | journal = The International Journal of Eating Disorders | volume = 46 | issue = 3 | pages = 193–207 | date = April 2013 | pmid = 23354950 | pmc = 3600071 | doi = 10.1002/eat.22089 }}</ref> 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.<ref>{{cite journal | vauthors = Phillips KA | title = Body dysmorphic disorder: the distress of imagined ugliness | journal = The American Journal of Psychiatry | volume = 148 | issue = 9 | pages = 1138–49 | date = September 1991 | pmid = 1882990 | doi = 10.1176/ajp.148.9.1138 }}</ref> === Obesity === Various hereditary forms of obesity have been traced to defects in hypothalamic signaling (such as the leptin receptor and the [[melanocyte-stimulating hormone|MC-4]] receptor) or are still awaiting characterization – [[Prader-Willi syndrome]] – in addition, decreased response to [[satiety]] may promote development of [[obesity]].<ref>{{cite journal | vauthors = Lawton CL |title=Obesity: a disorder of appetite |journal=Practical Diabetes International |year=1993 |volume=10 |issue=1 |pages=10–12 |doi=10.1002/pdi.1960100105}}</ref> It has been found that ghrelin-reactive [[Immunoglobulin G|IgG]] immunoglobulins affect ghrelin's [[orexigenic]] response.<ref>{{cite journal | vauthors = Takagi K, Legrand R, Asakawa A, Amitani H, François M, Tennoune N, Coëffier M, Claeyssens S, do Rego JC, Déchelotte P, Inui A, Fetissov SO | display-authors = 6 | title = Anti-ghrelin immunoglobulins modulate ghrelin stability and its orexigenic effect in obese mice and humans | journal = Nature Communications | volume = 4 | pages = 2685 | date = 2013-10-25 | pmid = 24158035 | pmc = 3826639 | doi = 10.1038/ncomms3685 | bibcode = 2013NatCo...4.2685T }}</ref> 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 [[Adipocyte|adipose cells]], respectively, into the blood stream. Ghrelin stimulates feelings of hunger, whereas leptin stimulates feelings of satisfaction from food.<ref>{{cite web |url=http://www.montereydiet.com/ghrelin_and_leptin.html |title=How The Hormones Ghrelin and Leptin Affect Appetite |publisher=The Monterey Diet |date=<!--not specified--> |access-date=2013-03-09 |archive-date=2020-05-13 |archive-url=https://web.archive.org/web/20200513062423/http://www.montereydiet.com/ghrelin_and_leptin.html |url-status=usurped }}</ref> 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.<ref>{{cite journal | vauthors = Sader S, Nian M, Liu P | title = Leptin: a novel link between obesity, diabetes, cardiovascular risk, and ventricular hypertrophy | journal = Circulation | volume = 108 | issue = 6 | pages = 644–6 | date = August 2003 | pmid = 12912793 | doi = 10.1161/01.CIR.0000081427.01306.7D | doi-access = free }} {{open access}}</ref> === Pediatric eating problems === Eating issues such as "[[Avoidant/restrictive food intake disorder|picky eating]]" affects about 25% of children, but among children with [[Developmental disorder|development disorders]] this number may be significantly higher, which in some cases may be related to the sounds, smells, and tastes ([[sensory processing disorder]]).<ref>{{cite journal | vauthors = Nadon G, Feldman DE, Dunn W, Gisel E | title = Association of sensory processing and eating problems in children with autism spectrum disorders | journal = Autism Research and Treatment | volume = 2011 | pages = 541926 | date = 2011-09-22 | pmid = 22937249 | pmc = 3420765 | doi = 10.1155/2011/541926 | doi-access = free }}</ref>
Edit summary
(Briefly describe your changes)
By publishing changes, you agree to the
Terms of Use
, and you irrevocably agree to release your contribution under the
CC BY-SA 4.0 License
and the
GFDL
. You agree that a hyperlink or URL is sufficient attribution under the Creative Commons license.
Cancel
Editing help
(opens in new window)