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In addition, sugar consumption has been shown to increase reward seeking, impulsivity to feed and compulsivity in rats willing to endure noxious stimuli such as extreme cold, heat and foot-shock to procure sugar and highly palatable foods ( Cabanac and Johnson, 1983 Avena et al., 2005 Foo and Mason, 2005 Oswald et al., 2011).
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In rats, intermittent consumption of 10% (w/v) sucrose or 25% (w/v) glucose solution) elicits hallmark signs of addictive behavior such as binging, tolerance, craving ( Rada et al., 2005), cross-sensitization ( Avena and Hoebel, 2003b) and symptoms of withdrawal ( Colantuoni et al., 2002 Avena et al., 2008) such as anxiety-( Colantuoni et al., 2002 Avena et al., 2008 Parylak et al., 2012 Eudave et al., 2018 Gueye et al., 2018 Xu and Reichelt, 2018) and depressive-like behaviors ( Vollmayr et al., 2004 Iemolo et al., 2012 Harrell et al., 2015 Santos et al., 2018). High sugar and/or high fat diets have been shown to precipitate addiction-like psychiatric phenotypes in a number of rodent studies ( Avena et al., 2009 Avena, 2010 Criscitelli and Avena, 2016). In humans, sugar and sweetness can induce dopamine release, reward and craving that are comparable in magnitude to those induced by addictive drugs, suggesting that sugar changes brain reward signaling and circuitry similar to other drugs of abuse ( Avena and Hoebel, 2003b Rada et al., 2005 Lenoir et al., 2007 Klenowski et al., 2016 Shariff et al., 2016, 2017). This hedonistic desire for palatable food is reward-driven and overeating may result in maladaptive/negative neuroplasticity that overrides homeostatic regulation ( Kenny, 2011). Humans consume sugar and food to regulate homeostatic energy balance, but also for pleasure and comfort. There is, however, increasing evidence of overlap in the brain circuitry and molecular signaling pathways involved in sugar consumption and drug abuse (for recent review see Jacques et al., 2019). The concept of “sugar addiction” and the classification of sugar as a substance of abuse are still debated. This suggests that long-term overconsumption of sugar, as that which occurs in the Western Diet might contribute to an increased risk of developing persistent hyperactivity and neurocognitive deficits in adulthood. The deficits in hippocampal-dependent learning and memory were accompanied by altered hippocampal neurogenesis, with an overall decrease in the proliferation and differentiation of newborn neurons within the dentate gyrus. Our results are similar to those reported in attention deficit and hyperactivity disorders. Using a well-validated mouse model of sugar consumption, we found that long-term sugar consumption, at a level that significantly augments weight gain, elicits an abnormal hyperlocomotor response to novelty and alters both episodic and spatial memory. The long-term effects on cognitive processes and hyperactivity from sugar overconsumption, beginning at adolescence are not known. Recent evidence suggests that obesity and impulsivity from poor dietary habits leads to further overconsumption of processed food and beverages.
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This has led to overconsumption of sugar in children, adolescents, and adults, with more than 60 countries consuming more than four times (>100 g/person/day) the WHO recommendations (25 g/person/day). Sugar has become embedded in modern food and beverages.