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Sugar addiction is a term popularly applied to individuals who express difficulty controlling intake of sweet foods or beverages. Although the term itself is not generally used to refer any scientific construct, mounting evidence suggests that under certain conditions, consumption of sweets or sugar may indeed become addiction-like.[1]

Scientific evidence

Any concept of sugar addiction is complicated by a lack of consensus on the actual definition of addiction.

There has been reference to the idea of sugar addiction in the popular literature for a number of years. In 1998, Kathleen DesMaisons[2] outlined the concept of sugar addiction as a measurable physiological state caused by activation of mu opioid receptors in the brain. Her work extracted data from studies done by Blass[3] showing that sugar acted as an analgesic drug whose effects could be blocked by a morphine blocker. Acting on years of anecdotal evidence from her work in the field of addiction, DesMaisons noted that dependence on sugar followed the same track outlined in the DSM IV for other drugs of abuse.

Since that time, a growing body of laboratory evidence[who?] has corroborated DesMaisons' hypothesis.[citation needed] Bart Hoebel at Princeton began showing the neurochemical effects of sugar, noting that sugar might serve as a gate drug for other drugs.

In 2008, Nicole Avena published data[4] stating that sugar affects opioids and dopamine in the brain, and thus might be expected to have addictive potential. She references "Bingeing," "withdrawal," "craving" and "cross-sensitization" are each given operational definitions and demonstrated behaviorally with sugar bingeing as the reinforcer. These behaviors are then related to neurochemical changes in the brain that also occur with addictive drugs. Neural adaptations include changes in dopamine and opioid receptor binding, enkephalin mRNA expression and dopamine and acetylcholine release in the nucleus accumbens.

"Recent behavioral tests in rats further back the idea of an overlap between sweets and drugs. Drug addiction often includes three steps. A person will increase his intake of the drug, experience withdrawal symptoms when access to the drug is cut off and then face an urge to relapse back into drug use. Rats on sugar have similar experiences. Researchers withheld food for 12 hours and then gave rats food plus sugar water. This created a cycle of binging where the animals increased their daily sugar intake until it doubled. When researchers either stopped the diet or administered an opioid blocker the rats showed signs common to drug withdrawal, such as teeth-chattering and the shakes. Early findings also indicate signs of relapse. Rats weaned off sugar repeatedly pressed a lever that previously dispensed the sweet solution." (Leah Ariniello, Brain Briefings, October 2003)

The sugar industry claims that similar effects have been reported for rats given solutions that tasted sweet, but contained no calories. [1] However, caloric value may not be the issue. Sugar and the taste of sweet stimulate the brain by activating beta endorphin receptor sites. These are the same chemicals activated by heroin and morphine.[citation needed]

Some psychologists maintain that results of this type may indeed provide a new way of looking at overeating, but that much caution should be exercised about using them to effectively put sugar in the same category as drugs. They believe there is some overlap between the systems that control food intake and addiction but this cannot yet unambiguously be said to necessarily make certain foods addictive.[citation needed]

Some animals, and some people, may become overly dependent on sweet food, particularly if they periodically stop eating and then binge. This may relate to eating disorders such as bulimia. It would probably be more correct to refer to the laboratory rats referred to above as "sugar-dependent" rather than "addicted." In general, to be classified as an addiction, reproducible "double blind" experiments would have to show that the experimental subjects exhibited all three elements that make up the definition of this term: a behavioral pattern of increased intake and changes in brain chemistry; then signs of withdrawal and further changes in brain chemistry upon deprivation; and third, signs of craving and relapse after withdrawal is over.

In 2003, a report was commissioned by two U.N. agencies, the World Health Organization and the Food and Agriculture Organization, compiled by a panel of 30 international experts. It stated that sugar should not account for more than 10% of a healthy diet.[2] In contrast, the US Sugar Association [3] insists that other evidence indicates that a quarter of our food and drink intake can safely consist of sugar. However, this contradicts the sugar industry's criticism of the research discussed above:

Research into sugar addiction was initiated at one research group at Princeton University where they fed rats chow as well as a 25% sugar solution - similar to the sugar concentration of soda-pop. In just 1 month the rats became dependent on their daily dose of sweet stuff, they gradually chose to eat less chow but increased their intake of the sugary drink until it doubled." Tufts University Health & Nutrition Letter.New York:OCT 2002. Vol.20, Iss. 8; Pg.1,3 pgs. [4]

"The rats were given a drug to block their opiate-receptors and showed withdrawal signs typical of drug-addicted rats- teeth chattering, paw tremors, and head shakes."

Since the preliminary work at Princeton, a number of studies have continued and expanded the assertion for the evidence of sugar addiction.[citation needed]

Fatty foods may cause cocaine-like addiction. Taking drugs such as cocaine and eating too much junk food both gradually overload the so-called pleasure centers in the brain, according to Paul J. Kenny, Ph.D., an associate professor of molecular therapeutics at the Scripps Research Institute, in Jupiter, Florida. Eventually the pleasure centers "crash," and achieving the same pleasure—or even just feeling normal—requires increasing amounts of the drug or food, says Kenny, the lead author of the study.[5]

See also


  1. Hoebel BG; Rada P; Avena NM (2008). "Evidence for sugar addiction: behavioral and neurochemical effects of intermittent, excessive sugar intake". Neuroscience and Biobehavioral Review 32 (1): 20–39. doi:10.1016/j.neubiorev.2007.04.019. PMC 2235907. PMID 17617461.
  2. Kathleen DesMaisons, Ph.D. (1998). "Potatoes Not Prozac." Simon & Schuster. ISBN 141655615X
  3. Blass, E., E. Fitzgerald, and P. Kehoe, Interactions between sucrose, pain and isolation distress. Pharmacol Biochem Behav, 1987. 26(3): p. 483-9.
  4. Avena NM, Rada P, Hoebel BG. Evidence for sugar addiction: behavioral and neurochemical effects of intermittent, excessive sugar intake. Neurosci Biobehav Rev. 2008;32(1):20-39. Epub 2007 May 18.
  5. "Fatty foods may cause cocaine-like addiction". CNN. March 30, 2010.

Further reading

  • Kathleen DesMaisons, Ph.D. (2000). The Sugar Addict's Total Recovery Program. Ballantine Books. ISBN 0-345-44132-X.
  • Kathleen DesMaisons, Ph.D. (2008). "Potatoes Not Prozac." Simon & Schuster. ISBN 141655615X
  • Avena NM, Rada P, Hoebel BG.

Evidence for sugar addiction: behavioral and neurochemical effects of intermittent, excessive sugar intake. Neurosci Biobehav Rev. 2008;32(1):20-39. Epub 2007 May 18.

  • Avena NM, Hoebel BG.

A diet promoting sugar dependency causes behavioral cross-sensitization to a low dose of amphetamine. Neuroscience. 2003;122(1):17-20.

  • Avena NM, Long KA, Hoebel BG.

Sugar-dependent rats show enhanced responding for sugar after abstinence: evidence of a sugar deprivation effect. Physiol Behav. 2005 Mar 16;84(3):359-62.

  • Blass, E., E. Fitzgerald, and P. Kehoe, Interactions between sucrose, pain and isolation distress. Pharmacol Biochem Behav, 1987. 26(3): p. 483-9.
  • Blass, E.M. and A. Shah, Pain-reducing properties of sucrose in human newborns. Chem Senses, 1995. 20(1): p. 29-35.
  • Carlo Colantuoni, Pedro Rada,, Joseph McCarthy, Caroline Patten, Nicole M. Avena, Andrew Chadeayne and Bartley G. Hoebel. Evidence That Intermittent, Excessive Sugar Intake Causes Endogenous Opioid Dependence. Obesity Research 10:478-488 (2002)
  • Cleary, J., et al., Naloxone effects on sucrose-motivated behavior. Psychopharmacology (Berl), 1996. 126(2): p. 110-4.
  • Colantuoni C, Schwenker J, McCarthy J, Rada P, Ladenheim B, Cadet JL, Schwartz GJ, Moran TH, Hoebel BG.

Excessive sugar intake alters binding to dopamine and mu-opioid receptors in the brain. Neuroreport. 2001 Nov 16;12(16):3549-52.

  • Czirr, S.A. and L.D. Reid, Demonstrating morphine's potentiating effects on sucrose-intake. Brain Res Bull, 1986. 17(5): p. 639-42.
  • D'Anci, K.E. and R.B. Kanarek, Naltrexone antagonism of morphine antinociception in sucrose- and chow-fed rats. Nutr Neurosci, 2004. 7(1): p. 57-61.
  • d'Anci, K.E., R.B. Kanarek, and R. Marks-Kaufman, Duration of sucrose availability differentially alters morphine-induced analgesia in rats. Pharmacol Biochem Behav, 1996. 54(4): p. 693-7.
  • Drewnowski, A. and M.R. Greenwood, Cream and sugar: human preferences for high-fat foods. Physiol Behav, 1983. 30(4): p. 629-33.
  • Drewnowski, A., et al., Taste responses and preferences for sweet high-fat foods: evidence for opioid involvement. Physiol Behav, 1992. 51(2): p. 371-9.
  • Drewnowski, A., et al., Naloxone, an opiate blocker, reduces the consumption of sweet high-fat foods in obese and lean female binge eaters. Am J Clin Nutr, 1995. 61(6): p. 1206-12.
  • Erlanson-Albertsson, C., [Sugar triggers our reward-system. Sweets release opiates which stimulates the appetite for sucrose—insulin can depress it]. Lakartidningen, 2005. 102(21): p. 1620-2, 1625, 1627.
  • Fantino, M., J. Hosotte, and M. Apfelbaum, An opioid antagonist, naltrexone, reduces preference for sucrose in humans. Am J Physiol, 1986. 251(1 Pt 2): p. R91-6.
  • Fullerton, D.T., et al., Sugar, opioids and binge eating. Brain Res Bull, 1985. 14(6): p. 673-80.
  • Kampov-Polevoy, A.B., et al., Sweet preference predicts mood altering effect of and impaired control over eating sweet foods. Eat Behav, 2006. 7(3): p. 181-7.
  • Kanarek, R.B., S. Mandillo, and C. Wiatr, Chronic sucrose intake augments antinociception induced by injections of mu but not kappa opioid receptor agonists into the periaqueductal gray matter in male and female rats. Brain Res, 2001. 920(1-2): p. 97-105.
  • Laeng, B., K.C. Berridge, and C.M. Butter, Pleasantness of a sweet taste during hunger and satiety: effects of gender and "sweet tooth". Appetite, 1993. 21(3): p. 247-54.
  • Leventhal, L., et al., Selective actions of central mu and kappa opioid antagonists upon sucrose intake in sham-fed rats. Brain Res, 1995. 685(1-2): p. 205-10.
  • Levine, A.S., C.M. Kotz, and B.A. Gosnell, Sugars and fats: the neurobiology of preference. J Nutr, 2003. 133(3): p. 831S-834S.
  • Levine, A.S., et al., Opioids and consummatory behavior. Brain Res Bull, 1985. 14(6): p. 663-72.
  • Rada P, Avena NM, Hoebel BG.

Daily bingeing on sugar repeatedly releases dopamine in the accumbens shell. Neuroscience. 2005;134(3):737-44.

  • Schoenbaum, G.M., R.J. Martin, and D.S. Roane, Relationships between sustained sucrose-feeding and opioid tolerance and withdrawal. Pharmacol Biochem Behav, 1989. 34(4): p. 911-4.
  • Spangler R, Wittkowski KM, Goddard NL, Avena NM, Hoebel BG, Leibowitz SF.

Opiate-like effects of sugar on gene expression in reward areas of the rat brain. Brain Res Mol Brain Res. 2004 May 19;124(2):134-42.

External links

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