ABSTRACT: Rates of fructose consumption continue to rise worldwide, and have been linked to rising rates of obesity, type-2 diabetes mellitus, and metabolic syndrome. Elucidation of fructose metabolism in liver and fructose action in brain demonstrate three parallelisms with ethanol. First, hepatic fructose metabolism is similar to ethanol in that by accelerating the process of de novo lipogenesis, both promote hepatic insulin resistance, dyslipidemia, and hepatic steatosis. Second, fructosylation of proteins with resultant superoxide formation can result in inflammation similar to acetaldehyde, an intermediary metabolite of ethanol. Lastly, by stimulating the “hedonic pathway” of the brain both directly and indirectly, fructose creates habituation, and possibly dependence; also paralleling ethanol. On a societal level, the treatment of fructose as a commodity on the open market exhibits similarities to ethanol. Fructose induces alterations in both hepatic metabolism and central nervous system energy signaling, leading to a “vicious cycle” of excessive consumption and disease consistent with metabolic syndrome. These dose-dependent actions of fructose on the liver and on the hedonic pathway of the brain recapitulate the effects of ethanol.