In this issue, the review by Lustig, “Fructose: Metabolic, Hedonic, and Societal Parallels with Ethanol” (
1), contains a juxtaposition of information on metabolic, inflammatory, and hormonal pathways from which the author suggests “parallelism” between fructose and ethanol. The major premise of the review is that neither ethanol nor fructose provokes a satiety signal (insulin or leptin), so feedback on the consumption of these nutrients is lacking, leading to hedonic and societal consequences. The author further draws the parallel between alcoholic fatty liver disease (AFLD) and nonalcoholic fatty liver disease (NAFLD). He suggests the metabolic consequences of fructose and ethanol are also “parallel” based on similarities in signaling pathways associated with the steatohepatitis that results from excess intake of these nutrients. Similar arguments have been advanced in another recently published review by Lustig's group (
- Lustig R.H.
Fructose: Metabolic, hedonic, and societal parallels with ethanol.
J Am Diet Assoc. 2010; 110: 1307-1321
- Lim J.S.
- Mietus-Snyder M.
- Valente A.
- Schwarz J.M.
- Lustig R.H.
The role of fructose in the pathogenesis of NAFLD and the metabolic syndrome.
Nat Rev Gastroenterol Hepatol. 2010; 7: 251-264
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- Fructose: Metabolic, hedonic, and societal parallels with ethanol.J Am Diet Assoc. 2010; 110: 1307-1321
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L. O. Byerley is an associate professor, research, Department of Physiology, Louisiana State University Health Science Center, New Orleans.
W.-N. P. Lee is a professor, Department of Pediatrics, Endocrinology and Metabolism, Harbor-UCLA Medical Center, Torrance, CA.
Accepted: May 20, 2010
© 2010 American Dietetic Association. Published by Elsevier Inc. All rights reserved.