New insights into the epidemiology of gout

Editor, Rheumatology

RE: New insights into the epidemiology of gout



The recent article by Michael Doherty [1] lists three dietary risk factors for gout: higher intakes of red meat, beer and fructose. Benjamin Franklin’s celebrated meaty diet and love for Madeira wine [2] aptly illustrates a historical recognition of meat and alcohol as legitimate risk factors for gout. The addition of fructose to this list by Doherty is completely unwarranted, however, because it lacks adequate justification and proof in real-world diets.

First, all USDA-defined macronutrient categories — added sugars, added fats, flour/cereal, vegetables, fruit, dairy and milk/eggs/nuts — have increased more or less in parallel with total energy intake (+24%) since the introduction of high fructose corn syrup (HFCS) 35 years ago [3]. Because all macronutrients contribute energy to the diet, a focus on fructose is misleading because it cavalierly dismisses other macronutrients and misses the greater issue that we eat too much of everything.

Second, Doherty’s speculation about fructose differences in sucrose vs. HFCS is completely unnecessary and ignores mainstream consensus on sugars. There is now general agreement that sucrose and HFCS are metabolically equivalent among scientific experts, expert scientific panels like those convened by the Center for Food Safety and Nutrition (University of Maryland) [4], Experimental Biology (FASEB) [5] and ILSI-USDA [6], and professional organizations like the American Medical Association [7] and the American Dietetic Association [8]. Recent human studies by Melanson [9], Angelopoulos [10] and Havel [11] directly comparing HFCS and sucrose for metabolic markers of obesity confirm no substantive differences in serum glucose and insulin, ghrelin and leptin, hunger and satiety, triglycerides and uric acid.

And finally, experimental data used in support of fructose as a dietary risk factor is inappropriately applied from extreme diets that do not resemble real-world human exposures. Rat studies commonly use fructose at 60-66% of energy [see ex., 12]; human studies use fructose at 20-50% of energy [13,14]. The most recent estimate for fructose intake [15] reports the mean whole-population value at 9.1% of energy and the 95th percentile (males and females, 19-22 y) value at 16.1% of energy. Human studies thus test unrealistic fructose levels, while animal studies use highly exaggerated exposures that not only don’t remotely resemble human intakes, but may well approach toxic conditions. It is likely that the experimental diet is itself inducing a variant of normal human metabolism not in evidence at typical fructose levels.

At the current state of scientific understanding, it is decidedly premature and unjustified to include fructose on the same list of dietary risk factors for gout as red meat and beer.

  • Doherty M. New insights into the epidemiology of gout. Rheumatology (Oxford) 2009;48:ii2-ii8.
  • Finger S, Hagemann IS. Benjamin franklin’s risk factors for gout and stones: From genes and diet to possible lead poisoning. Proc Am Philos Soc 2008;152:189-206.
  • White JS. Straight talk about high-fructose corn syrup: What it is and what it ain’t. Am J Clin Nutr 2008;88:1716S-21S.
  • Forshee RA, Storey ML, Allison DB, et al. A critical examination of the evidence relating high fructose corn syrup and weight gain. Crit Rev Food Sci Nutr 2007;47:561-82.
  • Fulgoni V, 3rd. High-fructose corn syrup: Everything you wanted to know, but were afraid to ask. Am J Clin Nutr 2008;88:1715S.
  • Jones JM. Dietary sweeteners containing fructose: Overview of a workshop on the state of the science. J Nutr 2009;139:1210S-3S.
  • American Medical Association. Ama finds high fructose syrup unlikely to be more harmful to health than other caloric sweeteners. Chicago: American Medical Association, 17 June 2008.
  • American Dietetic Association. High fructose corn syrup and weight status. Hot Topics, 2009.
  • Melanson KJ, Zukley L, Lowndes J, Nguyen V, Angelopoulos TJ, Rippe JM. Effects of high-fructose corn syrup and sucrose consumption on circulating glucose, insulin, leptin, and ghrelin and on appetite in normal-weight women. Nutrition 2007;23:103-12.
  • Angelopoulos TJ, Lowndes J, Zukley L, et al. The effect of high-fructose corn syrup consumption on triglycerides and uric acid. J Nutr 2009;139:1242S-5S.
  • Stanhope KL, Griffen SC, Bair BR, Swarbrick MM, Keim NL, Havel PJ. Twenty-four-hour endocrine and metabolic profiles following consumption of high-fructose corn syrup-, sucrose-, fructose-, and glucose-sweetened beverages with meals. Am J Clin Nutr 2008;87:1194-203.
  • Nakagawa T, Hu H, Zharikov S, et al. A causal role for uric acid in fructose-induced metabolic syndrome. Am J Physiol Renal Physiol 2006;290:F625-31.
  • Reiser S, Powell AS, Scholfield DJ, Panda P, Ellwood KC, Canary JJ. Blood lipids, lipoproteins, apoproteins, and uric acid in men fed diets containing fructose or high-amylose cornstarch. Am J Clin Nutr 1989;49:832-9.
  • Emmerson BT. Effect of oral fructose on urate production. Ann Rheum Dis 1974;33:276-80.
  • Marriott BP, Cole N, Lee E. National estimates of dietary fructose intake increased from 1977 to 2004 in the united states. J Nutr 2009;139:1228S-35S.
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