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In 2002 research at Princeton began showing the neurochemical effects of sugar, noting that sugar might[weasel words] serve as a gateway drug for other drugs.[non-primary source needed] The research group fed chow to the rats as well as a 25% sugar solution similar to the sugar concentration of soft drinks. After one month the rats became "dependent" on the sugar solution, ate less chow and increased their intake of the sugary drink to 200%. The sugar industry asserts that similar effects have been reported for rats given solutions that tasted sweet, but contained no calories. However, some scientists say that caloric value may not be the issue. Researchers say that sugar and the taste of sweet is said to stimulate the brain by activating beta endorphinreceptor sites, the same chemicals activated in the brain by the ingestion of heroin and morphine.
In 2003, a report commissioned by two U.N. agencies at the World Health Organization and the Food and Agriculture Organization was compiled by a panel of 30 international experts. It recommended that sugar not account for more than 10% of a person's diet. However, the U.S. Sugar Association asserted that other evidence indicates that a quarter of our food and drink intake can safely consist of sugar.
Finally, a 2008 study noted that sugar affects opioids and dopamine in the brain, and thus might[weasel words] be expected to have addictive potential. It referenced" bingeing, withdrawal, craving and cross-sensitization", and gave each of them operational definitions in order to demonstrate behaviorally that sugar bingeing is a reinforcer. These behaviors were said to be related to neurochemical changes in the brain that also occur during addiction to drugs. Neural adaptations included changes in dopamine and opioid receptor binding, enkephalinmRNA expression and dopamine and acetylcholine release in the nucleus accumbens.[non-primary medical source needed]
^ abcAvena, Nicole M.; Rada, Pedro and Hoebel, Bartley G. "Evidence for sugar addiction: behavioral and neurochemical effects of intermittent, excessive sugar intake". Neuroscience & Biobehavioral Reviews, 2008;32(1):20-39. Epub 2007 May 18. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2235907/
^Blass, E., E. Fitzgerald, and P. Kehoe, Interactions between sucrose, pain and isolation distress. Pharmacol Biochem Behav, 1987. 26(3): p. 483-9.
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. PMID 14596845.
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. PMID 15763572.
Blass, E., E. Fitzgerald, P. Kehoe, Interactions between sucrose, pain and isolation distress. Pharmacol Biochem Behav, 1987. 26(3): p. 483-9. PMID 3575365.
Blass, E.M., A. Shah, Pain-reducing properties of sucrose in human newborns. Chem Senses, 1995. 20(1): p. 29-35. PMID 7796057.
Colantuoni,Carlo and Rada,Pedro and McCarthy, Joseph and Patten, Caroline and Avena, Nicole M. and Chadeayne, Andrew and Hoebel, Bartley G. Evidence That Intermittent, Excessive Sugar Intake Causes Endogenous Opioid Dependence. Obesity Research 10:478-488 (2002) PMID 12055324.
Cleary, J., et al., Naloxone effects on sucrose-motivated behavior. Psychopharmacology (Berl), 1996. 126(2): p. 110-4. PMID 8856829.
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. PMID 3801926.
Czirr, S.A., L.D. Reid, Demonstrating morphine's potentiating effects on sucrose-intake. Brain Res Bull, 1986. 17(5): p. 639-42. 15085560.
D'Anci, K.E., R.B. Kanarek, Naltrexone antagonism of morphine antinociception in sucrose- and chow-fed rats. Nutr Neurosci, 2004. 7(1): p. 57-61. PMID PMID 8853191.
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.
DesMaisons, Kathleen, Ph.D. (2000). The Sugar Addict's Total Recovery Program. Ballantine Books. ISBN 0-345-44132-X.
DesMaisons, Kathleen, Ph.D. (2008). "Potatoes Not Prozac." Simon & Schuster. ISBN 1-4165-5615-X
Drewnowski, A., M.R. Greenwood. Cream and sugar: human preferences for high-fat foods. Physiol Behav, 1983. 30(4): p. 629-33. PMID 6878464.
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. PMID 1313591.
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. PMID 15962882.
Fantino, M., J. Hosotte, M. Apfelbaum. An opioid antagonist, naltrexone, reduces preference for sucrose in humans. Am J Physiol, 1986. 251(1 Pt 2): p. R91-6. PMID 3728712.
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. PMID 16843219.
Kanarek, R.B., S. Mandillo, 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. PMID 11716815.
Laeng, B., K.C. Berridge, 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. PMID 8141596.
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. PMID 7583248.
Levine, A.S., C.M. Kotz, B.A. Gosnell. Sugars and fats: the neurobiology of preference. J Nutr, 2003. 133(3): p. 831S-834S. PMID 12612162.
Levine, A.S., et al., Opioids and consummatory behavior. Brain Res Bull, 1985. 14(6): p. 663-72. PMID 2992720.
Rada P, Avena NM, Hoebel BG. Daily bingeing on sugar repeatedly releases dopamine in the accumbens shell. Neuroscience. 2005;134(3):737-44. PMID 15987666.
Schoenbaum, G.M., R.J. Martin, D.S. Roane. Relationships between sustained sucrose-feeding and opioid tolerance and withdrawal. Pharmacol Biochem Behav, 1989. 34(4): p. 911-4. PMID 2623045.
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. PMID 15135221.