Food addiction

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Addiction and dependence glossary[1][2][3][4]
addiction – a brain disorder characterized by compulsive engagement in rewarding stimuli despite adverse consequences
addictive behavior – a behavior that is both rewarding and reinforcing
addictive drug – a drug that is both rewarding and reinforcing
dependence – an adaptive state associated with a withdrawal syndrome upon cessation of repeated exposure to a stimulus (e.g., drug intake)
drug sensitization or reverse tolerance – the escalating effect of a drug resulting from repeated administration at a given dose
drug withdrawal – symptoms that occur upon cessation of repeated drug use
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)
reinforcing stimuli – stimuli that increase the probability of repeating behaviors paired with them
rewarding stimuli – stimuli that the brain interprets as intrinsically positive and desirable or as something to be approached
sensitization – an amplified response to a stimulus resulting from repeated exposure to it
substance use disorder - a condition in which the use of substances leads to clinically and functionally significant impairment or distress
tolerance – the diminishing effect of a drug resulting from repeated administration at a given dose
(edit | history)

A food addiction or eating addiction is a behavioral addiction that is characterized[jargon] by the compulsive consumption of palatable (e.g., high fat and high sugar) foods – the types of food which markedly activate the reward system in humans and other animals – despite adverse consequences.[5][6]

Psychological dependence has also been observed with the occurrence of withdrawal symptoms when consumption of these foods stops by replacement with foods low in sugar and fat.[5] Professionals address this by providing behavior therapy.[7]

Sugary 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;[5] 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.[5]

Description[edit]

"Food addiction" refers to compulsive overeaters who engage in frequent episodes of uncontrolled eating (binge eating). The term binge eating means eating an unhealthy amount of food while feeling that one's sense of control has been lost.[8] People who engage in binge eating may feel frenzied, and consume a considerable[jargon] amount of calories before stopping. The after effects of bingeing in this way is generally followed by feelings of guilt and depression; for example,[9] some will cancel their plans for the next day because they "feel fat."[10] Binge eating also has implications on physical health, due to excessive intake of fats and sugars, which can cause numerous health problems.

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 binge eating and experience feelings of guilt after their binges, they can be said to have binge eating disorder (BED).[8]

In addition to binge eating, compulsive overeaters may also engage in grazing behavior, during which they continuously eat throughout the day.[8] 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 (far more than is healthy), resulting in a temporary release from psychological stress through an addictive high not unlike that experienced through drug abuse.[9] Compulsive overeaters tend to show brain changes similar to those of drug addicts, a result of excessive consumption of highly processed foods.[11]

For the compulsive overeater, ingesting trigger foods causes the release of the chemical messengers serotonin and dopamine in the brain.[9] 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.[9] The resulting decreased levels of serotonin in the individual may trigger higher levels of depression and anxiety.[12]

Eventually, compulsive overeaters continuously think about food. Food is in the preeminent[jargon] positions of their minds; when deprived of it, the person may engage in actions similar to those of hard drug addicts, including an uncontrollable search for the substance, and in devious behaviour, such as stealing or lying.[13][14][15] The problem of obesity is becoming a worldwide problem. A sugar tax is set to be introduced in Ireland to minimise the consumption of harmful foods and drinks.[16]

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, and eating to the point of feeling sick to the stomach. Other signs include significantly decreased mobility[jargon] 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.[9][17]

Hiding consumption is an emotional indicator of other symptoms that could be a result of having a food addiction. Hiding consumption of food includes eating in secret; late at night while everybody else is asleep, in the car, and hiding certain foods until ready to consume in private. Other signs of hiding consumption are avoiding social interactions to eat the specific foods that are craved. Other emotional indicators are Inner guilt; which includes making up excuses to why the palatable food would be beneficial to consume, and then feeling guilty about it shortly after consuming.[18]

Sense of loss of control is indicated in many ways which includes, going out of the way to obtain specific foods, spending unnecessary amounts of money on foods to satisfy cravings. Difficulty concentrating on things such as a job or career can indicate sense of loss of control by not being to organize thoughts leading to a decrease in efficiency. Other ways to indicate the sense of loss of control, are craving food despite being full. One may set rules to try to eat healthy but the cravings over rule and the rules are failed to be followed. One big indicator of loss of control due to food addiction is even though one knows they have a medical problem caused by the craved foods, they cannot stop consuming the foods, which can be detrimental to their health.[19][18]

Food addiction has some physical signs and symptoms. Decreased energy; not being able to be as active as in the past, not being able to be as active as others around, also a decrease in efficiency due to the lack of energy. Having trouble sleeping; being tired all the time such as fatigue, oversleeping, or the complete opposite and not being able to sleep such as insomnia. Other physical signs and symptoms are restlessness, irritability, digestive disorders, and headaches.[19][18]

In extreme cases food addiction can result in some suicidal thoughts.[19]

Potential negative effects[edit]

A Food addiction, especially long-term, can result in negative consequences to all aspects of a person’s life, creating damaging and chronic symptoms.[18]

Physical consequences:[18][edit]

The short-term physical effect associated with dopamine and endogenous opiate release in the brain reward center is low level euphoria, a decrease in both anxiety and emotional pain also known as a “food coma.” The long-term physical effects may vary. The health consequences can be severe.

If a food addict has obesity, it can be associated with the following:

  • diabetes
  • high blood pressure
  • high cholesterol and triglycerides
  • osteoarthritis in the knees
  • hips and back
  • fungal infections in skin folds that are hard to clean
  • congestive heart failure
  • shortness of breath
  • coronary artery disease
  • death.

Psychological consequences[edit]

The psychological and mental effects can prove intense and plague an individual for years. These include hopelessness, powerlessness, isolation, shame, depression, self-loathing, guilt, suicidal thoughts, suicide attempts, and/or self-injurious behaviors.[18]

Relational consequences[edit]

Food addiction impacts relationships, especially those within the family. This is because the person with the addiction is vastly more involved with food than with people – it becomes their safest, most important and meaningful relationship. Other connections to friends and family take a back seat. This often leads to a deep sense of isolation from others.[20]

Management[edit]

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.[21][22]

Lisdexamfetamine is an FDA-approved appetite suppressant drug that is indicated[jargon] for the treatment of binge eating disorder.[23] The antidepressant fluoxetine is a medication that is approved by the Food and Drug Administration (FDA) for the treatment of an eating disorder, specifically bulimia nervosa. This medication has been prescribed off-label for the treatment of binge eating disorder (BED). Off-label medications, such as other selective serotonin reuptake inhibitors (SSRIs), have shown some efficacy, as have several atypical[jargon] agents, such as mianserin, trazodone and bupropion.[24][25] Anti-obesity medications[26] have also proven very effective. Studies suggest that anti-obesity drugs, or moderate appetite suppressants, may be key to controlling binge eating.[27]

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[jargon] obstacles need to be resolved.[28] 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".[29] 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.[30]

As well, several twelve-step programs exist to help members recover from compulsive overeating and food addiction,[9] such as Overeaters Anonymous and others.

Prognosis[edit]

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%.[5]

Summary of addiction-related plasticity[edit]

Form of neuroplasticity
or behavioral plasticity
Type of reinforcer Sources
Opiates Psychostimulants High fat or sugar food Sexual intercourse Physical exercise
(aerobic)
Environmental
enrichment
ΔFosB expression in
nucleus accumbens D1-type MSNs
[5]
Behavioral plasticity
Escalation of intake Yes Yes Yes [5]
Psychostimulant
cross-sensitization
Yes Not applicable Yes Yes Attenuated Attenuated [5]
Psychostimulant
self-administration
[5]
Psychostimulant
conditioned place preference
[5]
Reinstatement of drug-seeking behavior [5]
Neurochemical plasticity
CREB phosphorylation
in the nucleus accumbens
[5]
Sensitized dopamine response
in the nucleus accumbens
No Yes No Yes [5]
Altered striatal dopamine signaling DRD2, ↑DRD3 DRD1, ↓DRD2, ↑DRD3 DRD1, ↓DRD2, ↑DRD3 DRD2 DRD2 [5]
Altered striatal opioid signaling No change or
μ-opioid receptors
μ-opioid receptors
κ-opioid receptors
μ-opioid receptors μ-opioid receptors No change No change [5]
Changes in striatal opioid peptides dynorphin
No change: enkephalin
dynorphin enkephalin dynorphin dynorphin [5]
Mesocorticolimbic synaptic plasticity
Number of dendrites in the nucleus accumbens [5]
Dendritic spine density in
the nucleus accumbens
[5]

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 3898681Freely accessible. PMID 24459410. Despite the importance of numerous psychosocial factors, at its core, drug addiction involves a biological process: the ability of repeated exposure to a drug of abuse to induce changes in a vulnerable brain that drive the compulsive seeking and taking of drugs, and loss of control over drug use, that define a state of addiction. ... A large body of literature has demonstrated that such ΔFosB induction in D1-type [nucleus accumbens] neurons increases an animal's sensitivity to drug as well as natural rewards and promotes drug self-administration, presumably through a process of positive reinforcement ... Another ΔFosB target is cFos: as ΔFosB accumulates with repeated drug exposure it represses c-Fos and contributes to the molecular switch whereby ΔFosB is selectively induced in the chronic drug-treated state.41. ... Moreover, there is increasing evidence that, despite a range of genetic risks for addiction across the population, exposure to sufficiently high doses of a drug for long periods of time can transform someone who has relatively lower genetic loading into an addict. 
  3. ^ "Glossary of Terms". Mount Sinai School of Medicine. Department of Neuroscience. Retrieved 9 February 2015. 
  4. ^ Volkow ND, Koob GF, McLellan AT (January 2016). "Neurobiologic Advances from the Brain Disease Model of Addiction". N. Engl. J. Med. 374 (4): 363–371. PMID 26816013. doi:10.1056/NEJMra1511480. Substance-use disorder: A diagnostic term in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) referring to recurrent use of alcohol or other drugs that causes clinically and functionally significant impairment, such as health problems, disability, and failure to meet major responsibilities at work, school, or home. Depending on the level of severity, this disorder is classified as mild, moderate, or severe.
    Addiction: A term used to indicate the most severe, chronic stage of substance-use disorder, in which there is a substantial loss of self-control, as indicated by compulsive drug taking despite the desire to stop taking the drug. In the DSM-5, the term addiction is synonymous with the classification of severe substance-use disorder.
     
  5. ^ a b c d e f g h i j k l m n o p q r Olsen CM (December 2011). "Natural rewards, neuroplasticity, and non-drug addictions". Neuropharmacology. 61 (7): 1109–1122. PMC 3139704Freely accessible. PMID 21459101. doi:10.1016/j.neuropharm.2011.03.010. 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"
  6. ^ Hebebrand J, Albayrak Ö, Adan R, Antel J, Dieguez C, de Jong J, Leng G, Menzies J, Mercer JG, Murphy M, van der Plasse G, Dickson SL (November 2014). ""Eating addiction", rather than "food addiction", better captures addictive-like eating behavior". Neurosci Biobehav Rev. 47: 295–306. PMID 25205078. doi:10.1016/j.neubiorev.2014.08.016.
    • Evidence for addiction to specific macronutrients is lacking in humans.
    • 'Eating addiction' describes a behavioral addiction. ...
    We concur with Hone-Blanchet and Fecteau (2014) that it is premature to conclude validity of the food addiction phenotype in humans from the current behavioral and neurobiological evidence gained in rodent models. ... To conclude, the society as a whole should be aware of the differences between addiction in the context of substance use versus an addictive behavior. As we pointed out in this review, there is very little evidence to indicate that humans can develop a 'Glucose/Sucrose/Fructose Use Disorder' as a diagnosis within the DSM-5 category Substance Use Disorders. We do, however, view both rodent and human data as consistent with the existence of addictive eating behavior.
     
  7. ^ 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. PMID 8556026. doi:10.1002/1098-108X(199511)18:3<291::AID-EAT2260180312>3.0.CO;2-Y. 
  8. ^ 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. 
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  11. ^ Nolen-Hoeksema, Susan (2014). (ab)normal Psychology. New York, NY: McGraw-Hill Education. p. 348. ISBN 9781308211503. 
  12. ^ 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]
  13. ^ Sheppard, Kay (1993). Food Addiction: The Body Knows. ISBN 978-1-55874-276-5. [page needed]
  14. ^ "Are You a Food Addict?". Food Addicts Anonymous. Retrieved 2014-02-01. 
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  16. ^ http://www.irishtimes.com/search/search-7.1213540?q=sugar%20tax
  17. ^ "Food Addiction Signs and Treatments". WebMD. Retrieved 2017-02-28. 
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  19. ^ a b c "About Food Addiction: Signs, Symptoms, Causes & Articles For Treatment Help". www.eatingdisorderhope.com. Retrieved 2017-02-28. 
  20. ^ "Food Addiction Information & Treatment - Timberline Knolls Residential Treatment Center". www.timberlineknolls.com. Retrieved 2017-02-28. 
  21. ^ "Binge-eating disorder Treatment at Mayo Clinic - Diseases and Conditions". Mayo Clinic. 2012-04-03. Retrieved 2014-02-01. 
  22. ^ 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. PMID 24132249. doi:10.1001/jamapsychiatry.2013.2295. Lay summaryScienceDaily (October 25, 2013). 
  23. ^ "Vyvanse Prescribing Information" (PDF). United States Food and Drug Administration. Shire US Inc. January 2015. Retrieved 24 February 2015. 
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  25. ^ 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. PMID 21927936. doi:10.1007/s11126-011-9192-0. 
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  28. ^ "Factors That May Contribute to Eating Disorders". NEDA. Retrieved October 27, 2014. 
  29. ^ 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. doi:10.14219/jada.archive.2010.0075. 
  30. ^ 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]