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Sugar Addiction

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Dopaminergic Pathways’ Role in Addiction: Sugar and Drugs of Abuse Researchers are hesitant to claim sugar to be addictive, however, many studies have been performed showing how sugar has the ability to produce addictive symptoms similar to those of addictive drugs (1). The Diagnostic and Statistical Manual of Mental Disorders (2004) does not define addiction, but rather, has criteria for substance dependence. The first two criteria relate to the “physiological dependence” of drugs of abuse- tolerance: a need for markedly increased amounts of the substance to achieve intoxication or desired effect, and withdrawal: the removal of the drug of choice and its subsequent feelings of anxiety and depression. Often the same (or a closely related) substance is taken to relieve or avoid these symptoms. Sugar consumption has increased because it is ubiquitous- it’s everywhere and in everything. Popular literature claims sugar to be addictive, and mounting scientific evidence is substantiating this concept (2). Research has shown that addiction emerges in the part of the brain known as the Mesolimbic pathway, referred to as the “Reward Center”, which is one part of the dopaminergic pathway (3). This brain system, which reinforces natural behaviors such as sex and feeding, has adapted to synthetic reinforcement (4). Drugs of abuse activate neurons in the ventral tegmental area (VTA). Neurons originating in the VTA project axons into multiple areas of the limbic system including the nucleus accumbens (NAc). Vesicles containing dopamine in the neuronal axons within the VTA fuse with the plasma membrane and release dopamine into the synaptic cleft where it binds to its receptors located on dendrites in the NAc (5). There are several subtypes of dopamine receptors, D1, D2, D3, that are implicated in addiction. D1 and D3 receptors are up regulated in the presence of cocaine, whereas D2 receptors are down regulated (4,6). Drugs of abuse also block the dopamine reuptake transporter, which is located on the transmitting neuron, causing increased levels of dopamine in the synaptic cleft. The increased levels of this dopamine continually stimulate the receiving neuron, thereby prolonging the feeling of pleasure. Tolerance occurs when over stimulation of dopamine to its receptors desensitizes the receiving neuron creating a change in the amount of receptors. These neurons develop tolerance to dopamine and become less responsive, thereby causing the drug user to use more of the substance to receive the same effect (7) Studies using animal models have shown that sugar dependency develops and has similar symptoms as those of drugs of abuse. Rats have been observed for their responses to sugar and have shown signs of binging, withdrawal, and craving after intermittent exposure to sugars (4,6,8,9). The effects of sugar on the neurochemical mechanisms of the mesolimbic pathway are very similar to drugs of abuse, e.g. cocaine (4,10, 11). Sugar has been shown to increase dopamine levels in the synaptic cleft after ingestion and it increases dopamine receptors D1 and D3 binding in the NAc, as well as dopamine transporter binding in the midbrain and has been shown to decrease D2 receptors binding similar to cocaine use (4,6). Many other neuromodulators and neurotransmitters play an important role in addiction. Endogenous opioids released into the NAc have been found to stimulate the desire for sucrose and have developed into addiction in animal models (9). Excessive sugar consumption was shown to sensitize mu-opioid receptors as shown with drugs of abuse (12). The feeling of satiation is due to the release of acetylcholine (ACh) in the NAc, and increased levels of Ach have been found in animal models both on sugar binging diets and being administered methamphetamines (4,9). This is by far not an extensive list of neurochemicals, their pathways, and receptors associated with addiction, however, the similarities of their actions on both drugs of abuse and sugar show much evidence for the concept of sugar addiction.

References
(1) Irene Rumbaum-Keller. Is Sugar Addictive? Huff Post: Healthy Living. Feb. 22nd 2012 http://www.huffingtonpost.com/irene-rubaumkeller-/is-sugar-addictive_b_217115.html
(2) The Diagnostic and Statistical Manual of Mental Disorders, (Fourth Edition) 2004
(3) Zhang TA, Maldve RE, Morrisett RA. 2006. Coincident signaling in mesolimbic structures underlying alcohol reinforcement. Biochemical Pharmacology 72:919-27
(4) Nicole M. Avena, Pedro Rada, and Bartley G. Hoebel. 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) Margolis EB, Lock H, Hjelmstad GO, Fields HL. 2006b. The ventral tegmental area revisited: Is there an electrophysiological marker for dopaminergic neurons? J. Physiol. 577(Pt. 3):907–24
(6) Nicole M. Avena, Kristin A. Long, Bartley G. HoebelT. Sugar-dependent rats show enhanced responding for sugar after abstinence: Evidence of a sugar deprivation effect. Physiology & Behavior 84 (2005) 359 – 362
(7) Carl Erickson. Dopamine - A Sample Neurotransmitter. http://www.utexas.edu/research/asrec/dopamine.html
(8) Drake Morgan* and Glen M. Sizemore. Animal Models of Addiction: Fat and Sugar. Current Pharmaceutical Design, 2011, 17, 1168-1172

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