The Science Behind Food Addiction

by Bashar Khiatah, MD

We have written before about the balance of hunger and satiety and some of the hormones associated with these systems. Staying in tune with these cues and listening to the body when it talks to us is key in maintaining good health. But unfortunately, the food industry has worked hard to understand the biochemistry of food addiction, and has used this knowledge to create products that cause intense cravings, without regard to the foods that optimize healthspan and longevity. In this post, we’re diving deeper into the science behind why we eat and the mechanisms behind food addiction.

The brain controls our daily food intake and eating behavior with a very complex system that mainly consists of the homeostatic and reward systems (1). While the homeostatic system regulates the balance of the energy levels (hungry or full), the rewards system manages the liking, wanting and learning systems (appetite) (2). The homeostatic systems are located in the hypothalamus in the arcuate nucleus and consist of two cortical groups of neurons, the orexigenic and anorexigenic neurons. This system receives signals from the intestines, pancreas, adipose tissue and brainstem. Leptin and insulin play a significant role in this system. Any increase in each one of these hormones leads to negative feedback to the homeostatic system with a superior effect of leptin, meaning an increase in satiety. On the other hand, any decrease will provide the opposite effect (1). This system is very sensitive to satiety signals, which result in switching to stop mode (3). These signals are provided directly by leptin/insulin or indirectly from the brainstem and hypothalamus controlled by Glucagon-Like Peptide 1 GLP-1, Cholecystokinin and peptide YY which serves as satiety signals in the hypothalamus and the brainstem(4-5).

Beside the hypothalamus, the critical nodes of the rewards system reside in the ventral striatum consisting of the ventral pallidum (VP), ventral tegmental area (VTA) and the nucleus accumbens (NAcc). They receive signals from the prefrontal cortex and orbitofrontal cortex (6). As mentioned previously, the rewards system consists of three components: liking, wanting, and learning systems. The liking system refers to the hedonic impact of the reward, whereas the wanting system refers to the motivation for the reward. The association with the reward and the anticipation for it are influenced by the learning system (7). Many studies have reported the implication of opioid and cannabinoid use in the hedonic experience, and dopamine’s role in the wanting and learning systems. Both of these systems have many hotspots in the hypothalamus, VP, VTA and NAcc, which if stimulated provide either liking or wanting experiences (8-10). Now, while satiety signals in the liking and wanting systems may cause attenuation, it does not result in switching to ‘stop status’ because these two systems are ‘go systems’, which means that they override the satiety signals and continue to promote food intake signals (3).

Whenever the individual experiences dysfunction in this circuit for any reason, he or she falls into food addiction. These days, addiction is a very popular word, referring to many different substances that can cause addiction. Addiction is defined by the American Society of Addiction Medicine as a chronic disease that is caused by a dysfunction in the brain reward, memory, motivation and related circuit which manifest on biological, psychological, social and spiritual levels and if left without treatment will lead to many health complications, disability or early death (13). The characteristics of addiction in relation to food are brain reward dysfunction, preoccupation, risky use, impaired control, tolerance/withdrawal, social impairment, chronicity, and relapse as reported in a systematic review study (14). While it is not as acute, dramatic, or illegal like drugs, food addiction can be a serious lifetime addiction and it has many consequences including, but not limited to obesity and overweight.

In the pre-industrial era, the human diet was minimally processed, high in protein, grains, and produce, and relatively low in salt. As an adaptation to motivate consumption of calorically dense foods, we evolved to find foods high in sugar and fat more hedonically rewarding (15). In the industrial era, the previously limited access to calorie-dense foods became an abundance of it, with artificially elevated levels of fat, sugar, salt, caffeine and flavor enhancers (16). This highly processed food is referred to as hyperpalatable food (17). Hyperpalatable, processed foods, like drugs of abuse, are proven to trigger strong cravings(18,19) and are associated with compulsive overuse. Additionally, there is evidence of chronic relapse and an inability to cut down consumption of these foods, as is true of substance abuse (20-22). It has also been reported to induce tolerance, specifically, a research group in Florida found that rats who overate highly palatable food showed a reward dysfunction that worsened as the rats gained more weight. These rats showed downregulated dopamine D2 receptors and elevated reward thresholds which altogether resulted in a reward dysfunction (23). In this way, since the development of food science, hyperpalatable food has become an addictive substance.

The level of addiction of hyperpalatable food is significantly associated with higher levels of depression, anxiety, and stress as reported by a group at Yale University. They studied 408 patients with type 2 diabetes and investigated the relationship between the level of processed food addiction and the level of anxiety, depression, and stress. Their findings in the majority of those participants who met the severe-PFA classification (5 or more symptoms) had extremely severe levels of depression and anxiety, 59% and 70% respectively (24). In another clinical study among 593 adolescent participants in China, they found that food addiction was associated with depression, low self-esteem, and loneliness (25).

Between 2013–2016, approximately 37% of adults consumed fast food on any given day (26). Worldwide we have incredibly easy access to many highly rewarding food that unfortunately, is providing little nutritional value, while pushing our rewards system. The decision to eat or not to eat, as well as the decision of what to eat, is critical to our physical and mental health. Despite the intent of people to live longer and healthier, not all individuals are willing to change their food habits or their diet pattern, since for some people a source of pleasure or happiness, and for someone else an addiction, or a way to treat psychological issue whether it’s depression or anxiety.


  1. Morton GJ, Meek TH, Schwartz MW. Neurobiology of food intake inhealth and disease. Nat Rev Neurosci 2014;15:367–78.
  2. Berridge KC et al. Affective neuroscience of pleasure: re-ward in humans and animals. Psychopharmacology (Berl) 2008;199:457–80
  3. Berridge KC et al. The tempted brain eats: pleasure and desire circuits in obesity and eating disorders.Brain Res 2010;1350:43–64
  4. Anini Y, Hansotia T, Brubaker PL. Muscarinic receptors control post-prandial release of glucagon-like peptide-1: in vivo and in vitro studiesin rats. Endocrinology 2002;143:2420–6.35.
  5. Williams KW, Elmquist JK. From neuroanatomy to behavior: central integration of peripheral signals regulating feeding behavior. Nat Neu-rosci 2012;15:1350–5
  6. Berthoud H-R. Multiple neural systems controlling food intake andbody weight. Neurosci Biobehav Rev 2002;26:393–428.
  7. Berridge KC, Robinson TE, Aldridge JW. Dissecting components ofreward:’liking’,“wanting,”and learning. Curr Opin Pharmacol2009;9:65–73
  8. Peciña S, Berridge KC. Hedonic hot spot in nucleus accumbens shell:where do mu-opioids cause increased hedonic impact of sweetness?J Neurosci 2005;25:11777–86.21.
  9. Peciña S. Opioid reward’liking’and“wanting”in the nucleus accum-bens. Physiol Behav 2008;94:675–80.22.
  10. Mahler SV, Smith KS, Berridge KC. Endocannabinoid hedonic hot-spot for sensory pleasure: anandamide in nucleus accumbens shell en-hances“liking”of a sweet reward. Neuropsychopharmacology 2007;32:2267–78
  11. Miller EK, Cohen JD. An integrative theory of prefrontal cortex func-tion. Annu Rev Neurosci 2001;24:167–202.77.
  12. Heatherton TF, Wagner DD. Cognitive neuroscience of self-regulationfailure. Trends Cogn Sci 2011;15:132–9
  13. Corwin, R.L.; Hayes, J.E. Are sugars addictive? Perspectives for practitioners. InFructose, High Fructose CornSyrup, Sucrose and Health, 1st ed.; Rippe, J.M., Ed.; Humana Press: New York, NY, USA, 2014; pp. 199–215.ISBN 978-1-4899-8076-2
  14. Gordon EL, Ariel-Donges AH, Bauman V, Merlo LJ.What Is the Evidence for “Food Addiction?” A Systematic Review.Nutrients. 2018 Apr 12;10(4). pii: E477. doi: 10.3390/nu10040477.PMID: 29649120
  15. Eaton BS. The ancestral diet: what was it and should it be a paradigm for contemporary nutrition? Proc Nutr Soc 2006; 65: 1-6.
  16. Gearhardt AN, Grilo CM, DiLeone RJ, et al. Can food be addictive? Public health and policy implication. Addiction 2011; 106(7): 1208-12.
  17. Gearhardt AN et al. The addiction potential of hyperpalatable foods.Curr Drug Abuse Rev. 2011 Sep;4(3):140-5. PMID: 21999688
  18. Pelchat ML, Johnson A, Chan R, et al. Images of desire: food craving activation during fMRI. Neuroimage 2004; 23: 1486-93.
  19. White MA, et al. Development and validation of the food-craving inventory. Obes Res 2002; 10: 107-14.
  20. Gearhardt AN et al. Food addiction: an examination of the diagnostic criteria for dependence. J Addict Med 2009; 3: 1-7.
  21. Pickering, C et al. Withdrawal from free-choice high-fat high-sugar diet induces craving only in obesity-prone animals. Psychopharmacology 2009, 204, 431–443.
  22. McGee, H.M. et al. Behavioral effects of withdrawal from sweetened vegetable shortening in rats. Brain Res. 2010, 1350, 103–111.
  23. Johnson, P.M.; Kenny, P.J. Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats. Nat. Neurosci. 2010, 13, 635–641.
  24. Raymond KL et al. A graduated food addiction classifications approach significantly differentiates depression, anxiety and stress among people with type 2 diabetes.Diabetes Res Clin Pract. 2017 Oct;132:95-101. Doi: 10.1016/j.diabres.2017.07.028.
  25. Zhao Z, Ma Y, Han Y, Liu Y, Yang K, Zhen S, Wen D. Psychosocial Correlates of Food Addiction and Its Association with Quality of Life in a Non-Clinical Adolescent Sample. Nutrients. 2018 Jun 28;10(7). pii: E837. doi: 10.3390/nu10070837.
  26. Cheryl D. Fryar, et al. Fast Food Consumption Among Adults in the
    United States, 2013–2016. NCHS Data Brief, No 322, October 2018