Food addiction

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Addiction glossary[1][2][3]
addiction – a state characterized by compulsive engagement in rewarding stimuli despite adverse consequences
reinforcing stimuli – stimuli that increase the probability of repeating behaviors paired with them
rewarding stimuli – stimuli that the brain interprets as intrinsically positive or as something to be approached
addictive drug – a drug that is both rewarding and reinforcing
addictive behavior – a behavior that is both rewarding and reinforcing
sensitization – an amplified response to a stimulus resulting from repeated exposure to it
drug tolerance – the diminishing effect of a drug resulting from repeated administration at a given dose
drug sensitization or reverse tolerance – the escalating effect of a drug resulting from repeated administration at a given dose
dependence – an adaptive state associated with a withdrawal syndrome upon cessation of repeated exposure to a stimulus (e.g., drug intake)
physical dependence – dependence that involves persistent physical–somatic withdrawal symptoms (e.g., fatigue and delirium tremens)
psychological dependence – dependence that involves emotional–motivational withdrawal symptoms (e.g., dysphoria and anhedonia)
(edit | history)

A food addiction is a behavioral addiction that is characterized by the compulsive over-consumption of high fat or sugary foods – the two types which markedly activate the reward system in humans and other animals – despite adverse consequences.[4] Sugar and high fat food have both been shown to increase the expression of ΔFosB, an addiction biomarker, in the D1-type medium spiny neurons of the nucleus accumbens;[4] however, there is very little research on the synaptic plasticity from compulsive food consumption, a phenomenon which is known to be caused by ΔFosB overexpression.[4] Psychological dependence has also been observed with the occurrence of withdrawal symptoms when consumption of these foods stops by replacement with low fat or sugar food. Professionals address this disorder by means of behavior therapy.[5]

Description[edit]

Food addicts obsess about eating food by indulging in fantasies over it. Also, compulsive overeaters engage in frequent episodes of uncontrolled eating (binge eating). The term binge eating means eating an abundance of food while feeling that one's sense of control has been lost.[6] People who engage in binge eating may feel frenzied, and consume 5,000 to 15,000 calories before stopping. The after effects of bingeing in this way is generally followed by feelings of guilt and depression; for example,[7] some will cancel their plans for the next day because they "feel fat."[8]

Unlike individuals with bulimia nervosa, compulsive overeaters do not attempt to compensate for their bingeing with purging behaviors, such as fasting, laxative use, or vomiting. When compulsive overeaters overeat through bingeing and experience feelings of guilt after their binges, they can be said to have binge eating disorder (BED).[6]

In addition to binge eating, compulsive overeaters may also engage in grazing behavior, during which they return to pick at food throughout the day.[6] These actions result in an excessive overall number of calories consumed, even if the quantities eaten at any one time may be small.

During binges, compulsive overeaters may consume between 5,000 and 15,000 food calories daily, resulting in a temporary release from psychological stress through an addictive high not unlike that experienced through drug abuse.[7] Compulsive overeaters tend to show brain changes similar to those of drug addicts, a result of excessive consumption of highly processed foods.[9] Researchers have speculated that binge eaters have an abnormality of endorphin metabolism in the brain that triggers the addictive process. In this line of thought, other theories explain addictive behaviors as primarily involving an anomaly in the reward centers of the brain.

For the compulsive overeater, ingesting trigger foods causes the release of the neurotransmitters serotonin and dopamine.[7] This could be another indicator that neurobiological factors contribute to the addictive process. Conversely, abstaining from addictive food and food eating processes causes withdrawal symptoms for those with eating disorders.[7] The resulting decreased levels of serotonin in the individual may trigger higher levels of depression and anxiety.[10]

Eventually, compulsive overeaters continuously think about what the next meal will be. Food is in the preeminent positions of their minds; when deprived of it, the person may engage in actions similar to those of cocaine addicts, including an uncontrollable search for the substance, and in extreme cases, stealing or lying.[11][12][13]

Signs and symptoms[edit]

A food addiction features compulsive overeating, such as binge eating behavior, as its core and only defining feature. There are several potential signs that a person may be suffering from compulsive overeating. Common behaviors of compulsive overeaters include eating alone, consuming food quickly, and gaining weight rapidly. Other signs include significantly decreased mobility and the withdrawal from activities due to weight gain. Emotional indicators can include feelings of guilt, a sense of loss of control, depression and mood swings.[7]

Potential negative effects[edit]

Left untreated, compulsive overeating can lead to serious medical conditions. For example, compulsive overeating usually results in weight gain and obesity, although it is not the only cause thereof. In addition, compulsive overeating could potentially lead to high cholesterol, diabetes, heart disease, hypertension, sleep apnea, and major depression. Additional long-term side effects of the condition include kidney disease, arthritis, bone deterioration, and stroke. In severe cases, compulsive overeating can result in death.

Other negative effects may include the amount of money that is wasted on food and the feelings of low self-esteem that usually accompany bingeing.

Management[edit]

See also: Jaw wiring

Compulsive overeating is treatable with nutritional assistance and medication. Psychotherapy may also be required, but recent research has proven this to be useful only as a complementary resource, with short-term effectiveness in middle to severe cases.[14][15]

The antidepressant fluoxetine is the only medication approved by the Food and Drug Administration (FDA) for the treatment of an eating disorder, specifically bulimia nervosa. This medication has been prescribed for the treatment of BED. Off-label medications, such as other selective serotonin reuptake inhibitors (SSRIs), have shown some efficacy, as have several atypical agents, such as mianserin, trazodone and bupropion.[16][17] Anti-obesity medications[18] have also proven very effective. Studies suggest that anti-obesity drugs, or moderate appetite suppressants, may be key to controlling BED.[19]

Many eating disorders are thought to be behavioral patterns that stem from emotional struggles; for the individual to develop lasting improvement and a healthy relationship with food, these affective obstacles need to be resolved.[20] Individuals can overcome compulsive overeating through treatment, which should include talk therapy and medical and nutritional counseling. Such counseling has been recently sanctioned by the American Dental Association in their journal article cover-story for the first time in history in 2012: Given “the continued increase in obesity in the United States and the willingness of dentists to assist in prevention and interventional effort, experts in obesity intervention in conjunction with dental educators should develop models of intervention within the scope of dental practice”.[21] Moreover, Dental appliances such as conventional jaw wiring and orthodontic wiring for controlling compulsive overeating have been shown to be “efficient ways in terms of weight control in properly selected obese patients and usually no serious complications could be encountered through the treatment course.[22] Finally, several twelve step programs exist to help members recover from compulsive overeating and food addiction.[7]

Epidemiology[edit]

A review on behavioral addictions listed the estimated the lifetime prevalence rate (i.e., the proportion of individuals in the population that developed the disorder during their lifetime) for food addiction in the United States as 2.8%.[4]

Summary of addiction-related plasticity[edit]

Part of this section is transcluded from FOSB. (edit | history)
Form of neural or behavioral plasticity Type of reinforcer Sources
Opiates Psycho­stimulants High fat or sugar food Sexual reward Physical exercise
(aerobic)
Environmental
enrichment
ΔFosB expression in
nucleus accumbens D1-type MSNs
[4]
Behavioral plasticity
Escalation of intake Yes Yes Yes [4]
Psychostimulant
cross-sensitization
Yes Not applicable Yes Yes Attenuated Attenuated [4]
Psychostimulant
self-administration
[4]
Psychostimulant
conditioned place preference
[4]
Reinstatement of drug-seeking behavior [4]
Neurochemical plasticity
CREB phosphorylation
in the nucleus accumbens
[4]
Sensitized dopamine response
in the nucleus accumbens
No Yes No Yes [4]
Altered striatal dopamine signaling DRD2, ↑DRD3 DRD1, ↓DRD2, ↑DRD3 DRD1, ↓DRD2, ↑DRD3 DRD2 DRD2 [4]
Altered striatal opioid signaling μ-opioid receptors μ-opioid receptors
κ-opioid receptors
μ-opioid receptors μ-opioid receptors No change No change [4]
Changes in striatal opioid peptides dynorphin dynorphin enkephalin dynorphin dynorphin [4]
Mesocorticolimbic synaptic plasticity
Number of dendrites in the nucleus accumbens [4]
Dendritic spine density in
the nucleus accumbens
[4]

See also[edit]

References[edit]

  1. ^ Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 15: Reinforcement and Addictive Disorders". In Sydor A, Brown RY. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 364–375. ISBN 9780071481274. 
  2. ^ Nestler EJ (December 2013). "Cellular basis of memory for addiction". Dialogues Clin. Neurosci. 15 (4): 431–443. PMC 3898681. PMID 24459410. 
  3. ^ "Glossary of Terms". Mount Sinai School of Medicine. Department of Neuroscience. Retrieved 9 February 2015. 
  4. ^ a b c d e f g h i j k l m n o p q Olsen CM (December 2011). "Natural rewards, neuroplasticity, and non-drug addictions". Neuropharmacology 61 (7): 1109–1122. doi:10.1016/j.neuropharm.2011.03.010. PMC 3139704. PMID 21459101. Functional neuroimaging studies in humans have shown that gambling (Breiter et al, 2001), shopping (Knutson et al, 2007), orgasm (Komisaruk et al, 2004), playing video games (Koepp et al, 1998; Hoeft et al, 2008) and the sight of appetizing food (Wang et al, 2004a) activate many of the same brain regions (i.e., the mesocorticolimbic system and extended amygdala) as drugs of abuse (Volkow et al, 2004). ... As described for food reward, sexual experience can also lead to activation of plasticity-related signaling cascades. ... In some people, there is a transition from “normal” to compulsive engagement in natural rewards (such as food or sex), a condition that some have termed behavioral or non-drug addictions (Holden, 2001; Grant et al., 2006a). ... the transcription factor delta FosB is increased during access to high fat diet (Teegarden and Bale, 2007) or sucrose (Wallace et al, 2008). ...To date, there is very little data directly measuring the effects of food on synaptic plasticity in addiction-related neurocircuitry. ... Following removal of sugar or fat access, withdrawal symptoms including anxiety- and depressive-like behaviors emerge (Colantuoni et al, 2002; Teegarden and Bale, 2007). After this period of “abstinence”, operant testing reveals “craving” and “seeking” behavior for sugar (Avena et al, 2005) or fat (Ward et al, 2007), as well as “incubation of craving” (Grimm et al, 2001; Lu et al, 2004; Grimm et al, 2005), and “relapse” (Nair et al, 2009b) following abstinence from sugar. In fact, when given a re-exposure to sugar after a period of abstinence, animals consume a much greater amount of sugar than during previous sessions (Avena et al., 2005).
     "Table 1"
  5. ^ Ho, Karen S. I.; Nichaman, Milton Z.; Taylor, Wendell C.; Lee, Eun Sul; Foreyt, John P. (1995). "Binge eating disorder, retention, and dropout in an adult obesity program". International Journal of Eating Disorders 18 (3): 291–4. doi:10.1002/1098-108X(199511)18:3<291::AID-EAT2260180312>3.0.CO;2-Y. PMID 8556026. 
  6. ^ a b c Saunders, Ronna (January 1, 2004). ""Grazing": A High-Risk Behavior". Obesity Surgery 14: 98–102. doi:10.1381/096089204772787374. Retrieved October 27, 2014. 
  7. ^ a b c d e f Goldberg, Joseph (August 21, 2014). "Food Addiction". WebMD. WebMD. Retrieved October 27, 2014. 
  8. ^ Goldsmith, Toby D. (2013-01-30). "Bulimia: Binging and Purging". Psych Central. Retrieved 2014-02-01. 
  9. ^ Nolen-Hoeksema, Susan (2014). (ab)normal Psychology. New York, NY: McGraw-Hill Education. p. 348. ISBN 9781308211503. 
  10. ^ Kriz, Kerri-Lynn Murphy (May 2002). The Efficacy of Overeaters Anonymous in Fostering Abstinence in Binge-Eating Disorder and Bulimia Nervosa (PhD Thesis). Virginia Polytechnic Institute and State University. [page needed]
  11. ^ Sheppard, Kay (1993). Food Addiction: The Body Knows. ISBN 978-1-55874-276-5. [page needed]
  12. ^ "Are You a Food Addict?". Food Addicts Anonymous. Retrieved 2014-02-01. 
  13. ^ "Food Addiction - Signs, Symptoms & Treatment". Addictions.com. Retrieved 2014-02-01. 
  14. ^ "Binge-eating disorder Treatment at Mayo Clinic - Diseases and Conditions". Mayo Clinic. 2012-04-03. Retrieved 2014-02-01. 
  15. ^ Johnson, Bankole A.; Ait-Daoud, Nassima; Wang, Xin-Qun; Penberthy, J. Kim; Javors, Martin A.; Seneviratne, Chamindi; Liu, Lei (2013). "Topiramate for the Treatment of Cocaine Addiction". JAMA Psychiatry 70 (12): 1338–46. doi:10.1001/jamapsychiatry.2013.2295. PMID 24132249. Lay summaryScienceDaily (October 25, 2013). 
  16. ^ White, Marney A.; Grilo, Carlos M. (2013). "Bupropion for Overweight Women with Binge-Eating Disorder". The Journal of Clinical Psychiatry 74 (4): 400–6. doi:10.4088/JCP.12m08071. PMC 4021866. PMID 23656848. 
  17. ^ Calandra, Carmela; Russo, Rina Giuseppa; Luca, Maria (2011). "Bupropion Versus Sertraline in the Treatment of Depressive Patients with Binge Eating Disorder: Retrospective Cohort Study". Psychiatric Quarterly 83 (2): 177–85. doi:10.1007/s11126-011-9192-0. PMID 21927936. 
  18. ^ "Obesity Treatment at Mayo Clinic - Diseases and Conditions". Mayo Clinic. 2013-06-07. Retrieved 2014-02-01. 
  19. ^ McElroy, Susan L.; Guerdjikova, Anna I.; Mori, Nicole; O'Melia, Anne M. (May 7, 2012). "Pharmacological management of binge eating disorder: Current and emerging treatment options". Therapeutics and ClinicalRisk Management: 219–41. doi:10.2147/TCRM.S25574. PMC 3363296. PMID 22654518. Retrieved October 31, 2014.
  20. ^ "Factors That May Contribute to Eating Disorders". NEDA. Retrieved October 27, 2014. 
  21. ^ Curran, Alice E.; Caplan, Daniel J.; Lee, Jessica Y.; Paynter, Lauren; Gizlice, Ziya; Champagne, Catherine; Ammerman, Alice; Agans, Robert (November 2010). "Dentists' Attitudes about Their Role in Addressing Obesity in Patients: A national survey". Journal of the American Dental Association 141 (11): 1307–1316. 
  22. ^ K. Al-Dhubhani, Mohammed; M. Al-Tarawneh, Ahmad (November 2014). "The Role of Dentistry in Treatment of Obesity—Review". Saudi Journal of Dental Research. doi:10.1016/j.sjdr.2014.11.005. 

Further reading[edit]

  • Brownlee, Christen (2009). "Food fix: Neurobiology highlights similarities between obesity and drug addiction". Science News 168 (10): 155–6. doi:10.1002/scin.5591681012. INIST:17072118. 
  • "Eating Awareness Training" Molly Gregor, copyright 1983 "...reclaim (your) 'birthright', the right to eat without compulsion, obsession, or suffering. ...what the body wants, as much as it wants, whenever it wants." From the Preface by Thomas Lebherz, M.D.