Evidence of Food Addiction

Goal: The goal of this Handout is to briefly acquaint health professionals with key evidence that chronic overeating may be a kind of substance use disorder (SUD) manifesting as addiction to processed foods. 

Purpose: The purpose of the handout is to encourage health professionals to support patients and clients in efforts to abstain from processed foods in the same manner that drug addicts abstain from drugs of abuse.  In addition, it is hoped that the handout will help health professionals refrain from encouraging processed-food-addicted clients to use addictive foods. 

It is also hoped that the handout will help health professionals reconsider recommending ‘weight-loss’ regimens to food addicts. Through mechanisms of hunger and even, malnutrition, weight-loss regimens can make food addiction worse and should be avoided by food addicts.  Weight-loss has been observed in the course of treating food addiction by eliminating processed foods and establishing routines of well-balanced, fully portioned meals of unprocessed, high-fiber foods. 

This hand-out reviews key studies showing that the brains of obese people exhibit dysfunctional patterns that are similar to those of drug addicts. It summarizes how overeating behavior conforms to the DSM 5 SUD diagnostic criteria.  The handout briefly reviews the evidence that particular processed foods have addictive characteristics.  

Printable PDF

Addictive Properties of Specific Processed Foods

Research into processed foods shows addictive properties for sugar and sweeteners, flour, gluten, dairy, processed fats, excessive salt, and caffeine.  When combined, poly-substance characteristics can intensify the addictive properties of the food product. 

The addictive properties of sugar are perhaps the most studied.[1]  Rats have been shown to choose sugar, high fructose corn syrup, and saccharine over cocaine and heroin. Rats have shown a sugar withdrawal syndrome similar to that of morphine [2]. Sugar activates the dopamine pathway [3]. 

Gluten and flour made from gluten-grains contains a gluteomorphine that appears to activate the opiate pathways [4].  Salt has been observed to be used by morphine addicts in withdrawal, presumably as a replacement for morphine. [5] Processed fat appears to activate the opiate [6] and endocannabinoid [7] pathways in the brain. [8] Dairy contains a casomorphine which has been shown to bind to opiate receptors in the brain. [9] Caffeine has intoxication and withdrawal diagnoses in the DSM 5. [10] In the treatment of processed food addiction, these would all be classified as addictive or “trigger foods” which the food addict should abstain from.

The DSM 5 Addiction Diagnostic Criteria in Overeating

Application of the DSM 5 SUD Diagnostic Criteria to overeating shows that overeating meets the criteria for an addiction. The criteria and their manifestation in overeating are described below. 

  • Processed food is often taken in larger amounts or over a longer period than was intended. This criteria is reported in studies as the tendency to regain lost weight, presumably in a pattern of unintended overeating. [11]
  • There is a persistent desire or unsuccessful efforts to cut down or control processed food use. This behavior is seen in studies as an inability to lose weight. [12]
  • A great deal of time is spent in activities necessary to obtain processed food, use processed food, or recover from its effects. Food addicts report spending time too tired to exercise or do anything but watch television. This behavior is found in the overweight research. [13]
  • Craving, or a strong desire or urge to use processed food. Research shows a relationship between cravings responses and BMI. [14]
  • Recurrent processed food use resulting in a failure to fulfill major role obligations at work, school, or home. Lower productivity among the obese is established in the research literature. [15]
  • Continued processed food use despite having persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of processed food. Weight gain is documented in non-supportive marriages. [16
  • Important social, occupational, or recreational activities are given up or reduced because of processed food use. Isolation has been documented in the obese. [17] and human resource managers are seen to discriminate against the obese. [18]
  • Recurrent processed food use in situations in which it is physically hazardous. Eating is the most common distraction while driving. [19]
  • Processed food use is continued despite knowledge of having a persistent or recurrent physical or psychological problem that is likely to have been caused or exacerbated by processed food. Research shows non-compliance with diet in diabetics, for example. [20]
  • Tolerance, as defined by either of the following:   A need for markedly increased amounts of processed food to achieve intoxication or desired effect. The evidence for this phenomenon in overeaters comes from brain imaging research that shows the down-regulation of dopamine receptor fields characteristic of tolerance. [21] Or, A markedly diminished effect with continued use of the same amount of processed food.
  • Withdrawal, as manifested by either of the following: The characteristic withdrawal syndrome for the processed food. A morphine-like withdrawal from sugar has been observed in rats [22] and caffeine withdrawal is described in the DSM 5 [10]  Or, processed food is taken to relieve or avoid withdrawal symptoms.

There are observations and studies of loss of control over processed foods that meet the DSM 5 criteria for the diagnosis of an addiction.  Although processed foods are quite different from drugs and alcohol as they are perceived and used in our culture, nonetheless the eating patterns that result from their use are similar to addictive behavior. 


  1. Ahmed, S.H., K. Guillem, and Y. Vandaele, Sugar addiction: pushing the drug-sugar analogy to the limit. Curr Opin Clin Nutr Metab Care, 2013. 16(4): p. 434-9.
  2. Avena, N.M., et al., After daily bingeing on a sucrose solution, food deprivation induces anxiety and accumbens dopamine/acetylcholine imbalance. Physiol Behav, 2008. 94(3): p. 309-15.
  3. Avena, N.M., P. Rada, and B.G. Hoebel, Evidence for sugar addiction: behavioral and neurochemical effects of intermittent, excessive sugar intake. Neurosci Biobehav Rev, 2008. 32(1): p. 20-39.
  4. Fanciulli, G., et al., Gluten exorphin B5 stimulates prolactin secretion through opioid receptors located outside the blood-brain barrier. Life Sci, 2005. 76(15): p. 1713-9.
  5. Cocores, J.A. and M.S. Gold, The Salted Food Addiction Hypothesis may explain overeating and the obesity epidemic. Med Hypotheses, 2009. 73(6): p. 892-9.
  6. Avena, N.M., M.E. Bocarsly, and B.G. Hoebel, Animal models of sugar and fat bingeing: relationship to food addiction and increased body weight. Methods Mol Biol, 2012. 829: p. 351-65.
  7. DiPatrizio, N.V., et al., Endocannabinoid signaling in the gut mediates preference for dietary unsaturated fats. Faseb j, 2013. 27(6): p. 2513-20.
  8. Ziauddeen, H., et al., Effects of the mu-opioid receptor antagonist GSK1521498 on hedonic and consummatory eating behaviour: a proof of mechanism study in binge-eating obese subjects. Mol Psychiatry, 2013. 18(12): p. 1287-93.
  9. Blass, E.M., A.M. Jackson, and W.P. Smotherman, Milk-induced, opioid-mediated antinociception in rats at the time of cesarean delivery. Behav Neurosci, 1991. 105(5): p. 677-86.
  10. American, P.A., Diagnostic and Statistical Manual V. 2013.
  11. Dansinger, M.L., et al., Meta-analysis: the effect of dietary counseling for weight loss. Ann Intern Med, 2007. 147(1): p. 41-50.
  12. Kant, A.K., Weight-loss attempts and reporting of foods and nutrients, and biomarkers in a national cohort. Int J Obes Relat Metab Disord, 2002. 26(9): p. 1194-204.
  13. Must, A., et al., Activity, inactivity, and screen time in relation to weight and fatness over adolescence in girls. Obesity (Silver Spring), 2007. 15(7): p. 1774-81.
  14. Stice, E., et al., Relation of reward from food intake and anticipated food intake to obesity: a functional magnetic resonance imaging study. J Abnorm Psychol, 2008. 117(4): p. 924-35.
  15. Grieve, E., et al., The disproportionate economic burden associated with severe and complicated obesity: a systematic review. Obes Rev, 2013. 14(11): p. 883-94.
  16. Meltzer, A.L., J.K. McNulty, and B.R. Karney, Social support and weight maintenance in marriage: the interactive effects of support seeking, support provision, and gender. J Fam Psychol, 2012. 26(5): p. 678-87.
  17. Sarlio-Lahteenkorva, S. and E. Lahelma, The association of body mass index with social and economic disadvantage in women and men. Int J Epidemiol, 1999. 28(3): p. 445-9.
  18. Giel, K.E., et al., Stigmatization of obese individuals by human resource professionals: an experimental study. BMC Public Health, 2012. 12: p. 525.
  19. Stutts, J., et al., Driver's exposure to distractions in their natural driving environment. Accid Anal Prev, 2005. 37(6): p. 1093-101.
  20. Zilli, F., et al., The compliance of hypocaloric diet in type 2 diabetic obese patients: a brief-term study. Eat Weight Disord, 2000. 5(4): p. 217-22.
  21. Wang, G.J., N.D. Volkow, and J.S. Fowler, The role of dopamine in motivation for food in humans: implications for obesity. Expert Opin Ther Targets, 2002. 6(5): p. 601-9.
  22. Wideman, C.H., G.R. Nadzam, and H.M. Murphy, Implications of an animal model of sugar addiction, withdrawal and relapse for human health. Nutr Neurosci, 2005. 8(5-6): p. 269-76.
  23. Gearhardt, A.N., et al., Neural Correlates of Food Addiction. Arch Gen Psychiatry, 2011.
  24. Volkow, N.D., et al., Overlapping neuronal circuits in addiction and obesity: evidence of systems pathology. Philos Trans R Soc Lond B Biol Sci, 2008. 363(1507): p. 3191-200.
  25. Pelchat, M.L., et al., Images of desire: food-craving activation during fMRI. Neuroimage, 2004. 23(4): p. 1486-93.
  26. Batterink, L., S. Yokum, and E. Stice, Body mass correlates inversely with inhibitory control in response to food among adolescent girls: an fMRI study. Neuroimage, 2010. 52(4): p. 1696-703.
  27. Blum, K., et al., Reward circuitry dopaminergic activation regulates food and drug craving behavior. Curr Pharm Des, 2011. 17(12): p. 1158-67.

28. Kozak, A.T. and A. Fought, Beyond alcohol and drug addiction. Does the negative trait of low distress tolerance have an association with overeating? Appetite, 2011. 57(3): p. 578-81.


50% Complete

Two Step

Lorem ipsum dolor sit amet, consectetur adipiscing elit, sed do eiusmod tempor incididunt ut labore et dolore magna aliqua.