Design a site like this with
Get started

Which foods cause food addiction

In this blog I’ll be publishing excerpts from my dissertation on food addiction and research that supports using a whole-food plant-based diet to conquer food addiction for good.

In previous posts, I discussed that food addiction is not only real, but can be more accurately characterized as a substance use disorder (such as a drug addiction) than a behavioral addiction (like gambling disorder). The resulting implication is that certain types of food have addictive properties. In other words, the common saying that “there are no good foods or bad foods” is most likely incorrect because there are foods that, for some people at least, can precipitate an addiction.

The most relevant characteristics of foods that have been shown scientifically to exhibit addictive properties are their “palatability” (how pleasant to the taste buds they are) and high energy density (in other words, high calorie concentration). Since the term palatable is defined as “pleasant to taste,” we can say that palatable foods generally produce a very pleasurable experience. This is because they actually stimulate the reward pathways in the brain, that is, the parts of the brain in charge of helping us feel pleasure.

Food processing generally increases the palatability and energy density of foods in a significant way by concentrating the sugar, salt and fat content to an extent beyond what is found in unprocessed foods. By removing the fiber and extracting purified components such as sugars, starch and oil, the production process results in foods that are far from what we find in nature. The consumption of these processed foods results in an accelerated absorption (since the fiber has been mostly removed), and an artificially increased release of naturally occurring endorphins. Endorphins are “feel good” substances that are normally produced in the brain but, when produced in excess, they can intensify the impact on the reward pathways of the brain.1  

For example, intense sweetness (either with artificial sweeteners or sugar) has been found to produce an effect similar to that of addictive drugs. Laboratory rats were found to have a preference for intense sweetness over intravenous cocaine even when the rats had been previously drug sensitized and addicted to cocaine.2 The rats in this study were also more willing to work to obtain the intense sweet solution than to obtain cocaine, even in the face of increased effort necessary to obtain it (i.e., the number of lever presses required to obtain the reward). Therefore, intense sweetness can surpass the reward from cocaine, which led the study authors to conclude that sugar-rich diets provide a “supranormal stimulation” of sweet receptors. This stimulation in turn provides a “supranormal reward signal in the brain, with the potential to override self-control mechanisms and thus lead to addiction.”67

Foods that are energy dense, poor in nutrients, and high in both sugar and fat also appear to have addictive properties.3 In particular, foods that have either high amounts of fat or refined carbohydrates (or both) have been shown to result in higher levels of food cravings4 and are the most commonly consumed items during bingeing episodes.5 Specifically, these items include foods such as bread and pasta, sweets, high fat meats, and salty snacks.5 The Nurses’ Health Study found something similar and reported that food addiction was associated with consumption of hamburger and other red or processed meats, French fries, pizza, and other palatable foods high in refined carbohydrates and fat, such as snacks, desserts and candy bars.6  

Chocolate is an example of a high-fat, high-sugar food that has been shown to have addictive properties. Chocolate’s effect may involve the endogenous opioid peptide system since the use of an opioid antagonist (naloxone) reduced consumption and diminished the size of binge-eating bouts in bulimics.7 Individuals who considered themselves “chocoholics” reported having lack of control around chocolate, and those who ate it secretly reported a higher degree of aberrant eating.8

The addictiveness of chocolate and its opiate effects are probably due to the fact that it contains several potentially addictive substances such as caffeine, theobromine, phenylethylamine (or PEA) and anandamide. A one ounce serving of dark chocolate with 70-85% cacao solids, has 22.7 mg of caffeine. 9 Therefore, a typical 3.5 oz. bar has about 80 mg of caffeine, which is only slightly less than a cup of coffee. A bar of dark chocolate also contains about 800 mg of theobromine, which is a chemical related to caffeine but milder in its stimulating effect. Theobromine has been found to be about 10 times milder than caffeine,10 but since chocolate contains about ten times as much theobromine as caffeine, the psychoactive effect of both theobromine and caffeine combined could be significant. Phenylethylamine (PEA) is a small molecule that, like its alpha-methylated derivative, amphetamine, has stimulating effects which lead to the release of biogenic amines such as dopamine and serotonin. PEA is broken down into phenylacetic acid which has been described as having an effect similar to the activity of natural endorphins (known as the “runner’s high”).11 Lastly, anandamide is a brain lipid that binds to cannabinoid receptors and mimics the psychoactive effects of plant-derived cannabinoid plants. Chocolate contains three substances (the N-acylethanolamines N-oleoylethanolamine, N-linoleoylethanolamine, and anandamide) that can act as cannabinoid mimics either directly (by activating cannabinoid receptors) or indirectly (by increasing anandamide levels in the brain).12 One study compared self-identified “chocolate addicts” with “non-chocolate addicts” and found that exposure to chocolate cues led to affective changes (i.e., anxiety, restlessness) similar to those seen in substance addiction.13

High-fat savory foods may also be addictive.14 Rats fed a high-fat diet showed resistance to “outcome devaluation,” a sign of compulsive habitual eating behavior.15 Another study showed that rats fed a high-fat diet had blunted circulating levels of cholecystokinin (CCK), a satiety peptide.16 Some of the foods that have been shown to be the most addictive are high-fat savory foods, such as pizza, French fries, cheeseburgers and chips.17 In general, the most highly addictive foods are also highly processed, and it is theorized that the processing of foods increases the amount, or dose, of fat and/or refined carbohydrates that are absorbed in the human body, beyond what one may find in natural foods (such as fruits or nuts). This increases the food’s addictive potential just like in other addictive substances (i.e., grapes processed into wine, poppies processed into opium, coca leaves processed into cocaine).17  It is important to note also that fat and simple carbohydrates such as sugar are rarely found in the same foods in nature, whereas processed foods are routinely manufactured to have high amounts of both.

Although there is no empirical evidence that refined flour in particular is addictive, it has been theorized that due to the fact that flour is a processed product that does not exist in nature, and has been stripped of its fiber and nutrients, it can become as addictive as sugar.18 Flour products like bread (both white and whole grain) have a high glycemic index compared to a low glycemic index for intact grains such as wheat berries.19 In other words, the calories from flour products are absorbed faster and the glucose levels in the blood increase more rapidly when consuming flour products compared to consuming grains in their intact form. This is due to the fact that the grain’s cellular structure is disintegrated in the milling process. Therefore, the plant cells are no longer encapsulated in a cellular wall made up of fiber, which causes the flour particles to be much smaller and the starch to be much more digestible than in intact grains.20,21 Unless labeled as “stone-ground,” most of the modern “whole-wheat” flour products available on retail stores shelves are made of “recombined or reconstituted” white flour to which the bran and germ have been added back.22,23 Therefore, they might still produce very similar effects to white flour products. On the other hand, intact grains such as rye berries have been shown to have a “second meal effect,” which means that there is a reduction in the consumption of calories in a subsequent meal after consuming them.24 This increased satiety effect was seen even twelve hours after consuming a meal with intact grains. The effect has been attributed to the fermentation of the intact fibers by the gut microflora which positively altered appetite sensation.24

Other foods that have been suggested to have an addictive effect are cheese and meat. The main protein in cheese, casein, is broken down into casomorphins upon digestion. Casomorphins are opioid peptides which cross the blood-brain barrier27 and bind to endogenous opioid receptors.25 Human breast milk also contains casein, but the composition of bovine milk is quite different from that of human breast milk since its casein content is many times higher.26 While dairy milk has a ratio of 80% casein and 20% whey, human breast milk has a ratio of roughly 60% whey to 40% casein. Additionally, cheese has much higher concentrations of casein than milk, since in the manufacturing process most of the whey is discarded leaving the casein behind. This makes cheese the food with the highest casein concentration in the human diet. Milk- and cheese-derived opioid peptides have been described as able to elicit pharmacological properties similar to, although milder than, opium and morphine.27 

The mechanisms which might make meat addictive are less clear. It has been theorized that meat’s addictive effects come from the stimulating properties of hypoxanthine, which is found in the muscle cells of meat.28 Hypoxanthine is a naturally occurring purine derivative, chemically related to caffeine and theobromine.29,30 Other similar substances found in meat are inosinic acid and guanylic acid.28 Their combined action might explain the stimulating effect of meat and its potential addictiveness, but this has not been shown empirically. What researchers have found, however, is that meat might have an opiate-like effect since the administration of an opiate antagonist caused a decrease in the consumption of ham, salami and tuna when these foods were tested.31   

In summary, many different types of food have been scientifically shown to produce addictive behaviors. These foods are typically highly processed and high in calorie concentration. Addictive foods can have an effect in the brain similar to addictive drugs. These brain adaptations usually can only be reversed by adopting a “abstinent” food plan, which doesn’t mean staying away from all foods, but only abstaining from foods known to be addictive.

By Maria Jose Hummel, PhD (c), MPH, MS


  1. Ifland, J. & Peeke, P. (2018). Overlap between Drug and Processed Food Addiction. In Ifland, J., Marcus, M. T., & Preuss, H. G., Processed food addiction: Foundations, assessment, and recovery (pp. 3-25). Boca Raton, FL: CRC Press.
  2. Lenoir, M., Serre, F., Cantin, L., & Ahmed, S. H. (2007). Intense sweetness surpasses cocaine reward. PloS one2(8), e698.
  3. Pursey, K. M., Davis, C., & Burrows, T. L. (2017). Nutritional Aspects of Food Addiction. Current Addiction Reports, 4(2), 142–150. doi:10.1007/s40429-017-0139-x 
  4. White, M. A., Whisenhunt, B. L., Williamson, D. A., Greenway, F. L., & Netemeyer, R. G. (2002). Development and Validation of the Food-Craving Inventory. Obesity Research, 10(2), 107–114. doi:10.1038/oby.2002.17 
  5. Allison, S., & Timmerman, G. M. (2007). Anatomy of a binge: Food environment and characteristics of nonpurge binge episodes. Eating Behaviors, 8(1), 31–38. doi:10.1016/j.eatbeh.2005.01.004 
  6. Lemeshow, A. R., Rimm, E. B., Hasin, D. S., Gearhardt, A. N., Flint, A. J., Field, A. E., & Genkinger, J. M. (2018). Food and beverage consumption and food addiction among women in the Nurses’ Health Studies. Appetite121, 186–197.
  7. Drewnowski, A., Krahn, D. D., Demitrack, M. A., Nairn, K., & Gosnell, B. A. (1992). Taste responses and preferences for sweet high-fat foods: evidence for opioid involvement. Physiology & behavior, 51(2), 371–379.
  8. Hetherington, M. M., & Macdiarmid, J. I. (1993). “Chocolate Addiction”: a Preliminary Study of its Description and its Relationship to Problem Eating. Appetite, 21(3), 233–246. doi:10.1006/appe.1993.1042 
  9. FoodData Central Search Results. Retrieved from
  10. Baggott, M. J., Childs, E., Hart, A. B., de Bruin, E., Palmer, A. A., Wilkinson, J. E., & de Wit, H. (2013). Psychopharmacology of theobromine in healthy volunteers. Psychopharmacology228(1), 109–118.
  11. Irsfeld, M., Spadafore, M., & Prüß, B. M. (2013). β-phenylethylamine, a small molecule with a large impact. WebmedCentral4(9), 4409.
  12. di Tomaso, E., Beltramo, M., & Piomelli, D. (1996). Brain cannabinoids in chocolate. Nature382(6593), 677–678.
  13. Tuomisto, T., Hetherington, M. M., Morris, M.-F., Tuomisto, M. T., Turjanmaa, V., & Lappalainen, R. (1999). Psychological and physiological characteristics of sweet food “addiction.” International Journal of Eating Disorders, 25(2), 169–175. doi:10.1002/(sici)1098-108x(199903)25:2<169::aid-eat6>;2-b 
  14. Markus, C. R., Rogers, P. J., Brouns, F., & Schepers, R. (2017). Eating dependence and weight gain; no human evidence for a “sugar-addiction” model of overweight. Appetite, 114, 64–72. doi:10.1016/j.appet.2017.03.024 
  15. Tantot, F., Parkes, S. L., Marchand, A. R., Boitard, C., Naneix, F., Layé, S., … Ferreira, G. (2017). The effect of high-fat diet consumption on appetitive instrumental behavior in rats. Appetite, 108, 203–211. doi:10.1016/j.appet.2016.10.001 
  16. Covasa, M., Grahn, J., & Ritter, R. C. (2000). High fat maintenance diet attenuates hindbrain neuronal response to CCK. Regulatory Peptides, 86(1-3), 83–88. doi:10.1016/s0167-0115(99)00084-1 
  17. Schulte, E. M., Avena, N. M., & Gearhardt, A. N. (2015). Which Foods May Be Addictive? The Roles of Processing, Fat Content, and Glycemic Load. PLOS ONE, 10(2), e0117959. doi:10.1371/journal.pone.0117959 
  18. Ifland, J. R., Preuss, H. G., Marcus, M. T., Rourke, K. M., Taylor, W. C., Burau, K., … Manso, G. (2009). Refined food addiction: A classic substance use disorder. Medical Hypotheses, 72(5), 518–526. doi:10.1016/j.mehy.2008.11.035 
  19. Atkinson, F. S., Foster-Powell, K., & Brand-Miller, J. C. (2008). International tables of glycemic index and glycemic load values: 2008. Diabetes care31(12), 2281–2283.
  20. Edwards, C. H., Grundy, M. M., Grassby, T., Vasilopoulou, D., Frost, G. S., Butterworth, P. J., Berry, S. E., Sanderson, J., & Ellis, P. R. (2015). Manipulation of starch bioaccessibility in wheat endosperm to regulate starch digestion, postprandial glycemia, insulinemia, and gut hormone responses: a randomized controlled trial in healthy ileostomy participants. The American journal of clinical nutrition102(4), 791–800.
  21. Grundy, M. M., Carrière, F., Mackie, A. R., Gray, D. A., Butterworth, P. J., & Ellis, P. R. (2016). The role of plant cell wall encapsulation and porosity in regulating lipolysis during the digestion of almond seeds. Food & function7(1), 69–78.
  22. Slavin, J., Tucker, M., Harriman, C., Jonnalagadda, S.S. (2013). Whole Grains: Definition, Dietary Recommendations, and Health Benefits. Cereal Foods World. 58: 191–198. 
  23. Seal, C. J., Nugent, A. P., Tee, E.-S., & Thielecke, F. (2016). Whole-grain dietary recommendations: the need for a unified global approach. British Journal of Nutrition, 115(11), 2031–2038. doi:10.1017/s0007114516001161 
  24. Ibrügger, S., Vigsnæs, L. K., Blennow, A., Škuflić, D., Raben, A., Lauritzen, L., & Kristensen, M. (2014). Second meal effect on appetite and fermentation of wholegrain rye foods. Appetite, 80, 248–256. doi:10.1016/j.appet.2014.05.026 
  25. Meisel, H., & FitzGerald, R. J. (2000). Opioid peptides encrypted in intact milk protein sequences. British Journal of Nutrition, 84(S1). doi:10.1017/s000711450000221x 
  26. Shah, N. P. (2000). Effects of milk-derived bioactives: an overview. British Journal of Nutrition, 84(S1). doi:10.1017/s000711450000218x 
  27. Peuhkuri, K., Sihvola, N., & Korpela, R. (2011). Dietary proteins and food-related reward signals. Food & nutrition research55, 10.3402/fnr.v55i0.5955.
  28. Pamplona-Roger, G. (2004). Foods that heal. Hagerstown, MD: Review and Herald Pub. Association.
  29. Benoit, R. L., & Fréchette, M. (1985). Protonation of hypoxanthine, guanine, xanthine, and caffeine. Canadian Journal of Chemistry, 63(11), 3053–3056. doi:10.1139/v85-506 
  30. Suzuki, T., & Takahashi, E. (1975). Metabolism of xanthine and hypoxanthine in the tea plant (Thea sinensis L.). The Biochemical journal146(1), 79–85.
  31. Yeomans, M. R., Wright, P., Macleod, H. A., & Critchley, J. A. J. H. (1990). Effects of nalmefene on feeding in humans. Psychopharmacology, 100(3), 426–432. doi:10.1007/bf02244618 

Published by Maria Jose Hummel

Nutritionist, health educator

Leave a Reply

Fill in your details below or click an icon to log in: Logo

You are commenting using your account. Log Out /  Change )

Twitter picture

You are commenting using your Twitter account. Log Out /  Change )

Facebook photo

You are commenting using your Facebook account. Log Out /  Change )

Connecting to %s

%d bloggers like this: