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We’ve all experienced it; that intense craving for a piece of chocolate, lolly or anything sweet and calorie dense. Called sugar cravings, or in more severe cases, sugar addiction; the term refers to the intense desire to consume something sweet. Although many joke about sugar cravings as a means of justifying their binge on a chocolate bar or biscuit, recent research suggests that in certain individuals, sugar cravings can be compared to drug-like cravings and that they are one of the primary causes of the current obesity epidemic1.

The Neurochemical Link Between Sugar Cravings and the Brain

As far back as 2007 in the American Journal of Psychiatry, researchers by the name of Volkow and O’Brien were the first to suggest that obesity may in fact be a brain disorder undermined by an addiction to sugar2. Since that time the idea has gained significant momentum in research circles. Numerous studies have now been published showing that the specific chemicals (i.e. dopamine and opiods) in the brain which reward us with good feelings after consuming a sweet food are the exact same chemicals that lead to feelings of reward and pleasure when say a heroin addict is administered heroin3. The catch, however, is that these symptoms of full blown addiction to sugar only manifest in 10-20% of people4, 5 – which is actually similar to the proportion of cocaine or heroin users who go on to develop addiction6.

Explaining Sugar Cravings and Food Addiction

All this adds up to the notion that in certain individuals, continued consumption of high sugar foods can result in development of a range of behavioral and neurochemical symptoms that resemble those that occur after repeated exposure to addictive drugs. The same pattern is said to occur with consumption of high fat foods and together, the theory is collectively referred to as “food addiction”7.  The worrying aspect about this notion of sugar or food addiction is its inherent cyclical and reinforcing nature. Whenever susceptible individuals consume a high sugar food it produces a rewarding effect that strengthens the action-outcome associations and reinforces future behaviour directed at obtaining these foods. This is really just a fancy way of saying food junkies end up seeking out food to get a ‘high’ or prevent them from becoming ‘low’ or depressed.

Genetic Predisposition of Sugar Cravings

It’s important to highlight the role that genetics are thought to play in sugar cravings and food addiction. Just as everyone who is exposed to drugs does not become an addict, similarly, not every person exposed to high-risk foods goes on to compulsively over eat. It’s thought that the difference in susceptibility can be attributed in part to underlying genetic predispositions. One proven example of a genetic link with food addiction is that of dopamine receptors; more specifically a subtype of dopamine receptors called D2 receptors. Obese individuals and those addicted to substances of abuse have decreased dopamine receptor D2 availability in the brain8, 9. In obese individuals, this level of decrease is proportional to the body mass index10, which makes intuitive sense in the case of food addiction, as dopamine is the primary reward transmitter in the brain’s reward circuitry11. Therefore, it has been postulated that food-addicted individuals are driven to eat either because they obtain a very high reward from the food itself (too much dopamine) or because they are not satisfied by normal amounts of food (too little dopamine)12-14.

Obestiy Epidemic and Food Addiction

These rewarding effects of ‘energy-dense’ foods are thought to play a major role in overeating and the current epidemic of obesity. As a result, further research is being carried out to explore the link between the genes, molecules and neural circuitry that mediate food reward. It is hoped that such research may be able to uncover promising avenues of pharmaceutical, dietary, exercise or psychotherapy treatment15.

Losing Weight May be a Battle of the Mind for Some

In closing, it can be stated that sugar and food addiction in humans is an evolving theory, which still requires more research to uncover it’s precise aetiology, however, work in animal models and humans thus far suggests that consumption of highly palatable or sugar-rich food is regulated, in part, by the same brain regions that are activated in response to drugs of abuse. As such, circuitry exists within the human brain for certain foods to have addictive potential. Therefore some of the modern-day fast food and confectionary that so many enjoy may well have reinforcing abilities similar to alcohol or other drugs of abuse7.

On the flip side, this research tells us that obese individuals who desire to lose weight and break their cycle of binge eating might need to be prepared to endure significant withdrawal symptoms from some of the energy-dense foods they regularly enjoy. This research also provides some validation for obese individuals battling to lose weight by means of significant diet modification. Studies show that such dietary changed are hard to maintain in the long term, with obese individuals often reverting back to their normal diet. These type of individuals may find comfort in the knowledge that breaking their sugar addiction can be akin to a heroin addict coming off heroin.

1. Fulton S. Appetite and reward. Frontiers in Neuroendocrinology. 2010;31:85-103.
2. Volkow ND & O'Brien CP. Issues for DSM-V: should obesity be included as a brain disorder? Am J Psychiatry.2007;164:708–710.
3. Avena NM & Gold MS. Food and addiction - sugars, fats and hedonic overeating. Addiction. 2011;106:1214–1215.
4. Gearhardt AN, et al. Preliminary validation of the Yale Food Addiction Scale. Appetite. 2009; 52:430–436.
5. Meule A. How Prevalent is ‘Food Addiction’? Front Psychiatry. 2011;2:61.
6. Sussman S, Lisha N, Griffiths M. Prevalence of the addictions: a problem of the majority or the minority? Eval Health Prof. 2011;34:3–56.
7. Avena NM, et al. Further developments in the neurobiology of food and addiction: update on the state of the science. Nutrition. 2012;28(4):341-343.
8. Volkow ND, et al. Overlapping neuronal circuits in addiction and obesity: evidence of systems pathology. Philos Trans R Soc Lond B Biol Sci. 2008;363:3191–3200.
9. Noble EP, et al. Allelic association of the D2 dopamine receptor gene with receptor-binding characteristics in alcoholism. Archives of General Psychiatry. 1991;48:648–654.
10. Wang GJ, et al. Brain dopamine and obesity. Lancet. 2001;357:354–357.
11. Kirsch P, et al. Imaging gene-substance interactions: the effect of the DRD2 TaqIA polymorphism and the dopamine agonist bromocriptine on the brain activation during the anticipation of reward. Neurosci Lett. 2006;405:196–201.
12. Stice E, et al. Weight gain is associated with reduced striatal response to palatable food. J Neurosci. 2010;30:13105–13109.
13. Stice E, et al. Relation between obesity and blunted striatal response to food is moderated by TaqIA A1 allele. Science. 2008;322:449–452.
14. Taghva A, et al. Obesity and brain addiction circuitry: implications for deep brain stimulation. Neurosurgery. 2012;71:224–238.
15. Yarnell S, et al. Pharmacotherapies for overeating and obesity. Journal of Genetic Syndrome and Gene Therapy. 2013;4(3):131.

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