High Fructose Intake Linked to Metabolic Syndrome, Kidney Disease

Anthony J. Brown, MD

January 15, 2010

January 15, 2010 — Excessive intake of fructose, a common sweetener in soft drinks, can induce features of metabolic syndrome and may be a risk factor for chronic kidney disease, according to the findings from two studies.

The results of both studies suggest that these adverse effects are mediated, at least in part, through elevations in uric acid levels.

"Excessive fructose intake causes metabolic syndrome in animals and can be partially prevented by lowering the uric acid level," Dr. S. E. Perez-Pozo, lead author of the first study, and colleagues note. "We tested the hypothesis that fructose might induce features of metabolic syndrome in adult men and whether that is protected by allopurinol."

The researchers' study, reported in the December 22nd online issue of the International Journal of Obesity, featured 74 adult men who were randomized to receive 200 g fructose daily for 2 weeks without or without allopurinol. Primary endpoints included changes in ambulatory blood pressure, lipid levels, glucose and insulin, homeostatic model assessment (HOMA) index, body mass index, and criteria for metabolic syndrome.

Fructose intake was associated with an average increase in systolic and diastolic blood pressure of 7 and 5 mm Hg, respectively (p < 0.004 and p < 0.007, respectively), Dr. Perez-Pozo, from Son Llatzer Hospital–Palm of Majorca, Spain, and colleagues report.

Mean fasting triglyceride levels rose by 0.62 mmol/L (p < 0.002), while high-density lipoprotein cholesterol levels fell by 0.06 mmol/L (p < 0.001).

Although plasma glucose levels did not change, a significant increase in fasting insulin and HOMA indices was observed. Depending on the criteria used, the prevalence of metabolic syndrome increased by 25% to 33%.

Allopurinol treatment reduced uric acid levels and prevented the increase in blood pressure. In addition, it reduced levels of low-density lipoprotein cholesterol. Although allopurinol did not reduce HOMA or fasting triglyceride levels, it did help stave off newly diagnosed metabolic syndrome (p = 0.009).

The results "suggest that the primary effect of lowering the uric acid level on the metabolic syndrome induced by fructose is to reduce the blood pressure elevation," the authors conclude. "It remains possible that the lowering of uric acid level might be beneficial on lipids and insulin resistance if postprandial levels were targeted as opposed to fasting levels," they add.

In the second study, published in the December 23rd online issue of Kidney International, Dr. Andrew S. Bomback, from Columbia University College of Physicians and Surgeons, New York, and colleagues assessed the impact of sugar-sweetened soda intake on the risk of hyperuricemia and reduced kidney function. They analyzed data from 15,745 patients in the Atherosclerosis Risk in Communities Study who completed dietary questionnaires at baseline and had levels of creatinine and uric acid measured.

On cross-sectional analysis, consumption of more than 1 soda per day increased the odds of hyperuricemia by 31% relative to intake of less than 1 soda per day. Likewise, such intake was associated with 46% increased risk of chronic kidney disease, defined as an estimated glomerular filtration rate of <60 mL/min per 1.73 meters-squared. In subjects with uric acid levels over 9.0 mg/dL, intake of more than 1 soda per day increased the risk of kidney disease by 159%.

By contrast, on longitudinal analysis, high soda intake was not linked with hyperuricemia or chronic kidney disease at either 3 years or 9 years, the findings indicate.

Given that only the cross-sectional analysis showed a significant association between soda intake and hyperuricemia/chronic kidney disease, "our findings add to but in no way close the heated discussion over the potential dangers of sugar-sweetened soda," the authors conclude.

Int J Obesity. Published online December 22, 2009.

Kidney Int. Published online December 23, 2009.


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