Post edited 11:32 pm – January 25, 2010 by odo
For those of you who like to read medical reviews – Cut & pasted from Medscape:
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.
Clinical Context
Consumption of high-fructose corn syrup, which is found in sweetened soda, has increased nearly 20-fold during the past 30 years, with average yearly intake of high-fructose corn syrup as an added sweetener approaching 62.4 pounds per person. The US Department of Agriculture estimates that regular soda and other sweetened beverages account for more than 70% of this intake.
In parallel with increasing rates of high-fructose corn syrup consumption, rates of obesity, metabolic syndrome, and chronic kidney disease have increased dramatically. Epidemiological surveys suggest an association between regular, but not diet, soda consumption and the frequency of hyperuricemia, and animal studies suggest that the metabolism of high-fructose corn syrup may lead to elevations in uric acid levels.
In the current study by Bomback and colleagues, the study authors assessed the effect of sugar-sweetened soda intake on the risk for hyperuricemia and reduced kidney function.
Study Highlights
- The objective of the study by Bomback and colleges was to examine whether drinking soda is associated with hyperuricemia and/or reduced renal function in a large biracial cohort.
- Chronic kidney disease was defined as estimated glomerular filtration rate less than 60 mL/minute/1.73 m2.
- The study cohort consisted of 15,745 patients in the Atherosclerosis Risk in Communities Study who completed a dietary questionnaire at baseline and who had measurements of serum creatinine and uric acid.
- At 3- and 9-year follow-up, the investigators calculated multivariate odds ratios from logistic regressions for binary outcome of hyperuricemia and chronic kidney disease.
- Prevalence rate of chronic kidney disease was 3% and incidence rate 8% in this cohort.
- There was no association between increased soda consumption and either microalbuminuria or macroalbuminuria.
- In cross-sectional analyses, drinking more than 1 soda per day was associated with increased odds of prevalent hyperuricemia and chronic kidney disease vs participants who drank less.
- In stratified analysis, the association between soda and kidney function became more pronounced as uric acid levels increased.
- Among participants who drank more than 1 soda per day and had serum uric acid levels higher than 9.0 mg/dL, odds ratio for chronic kidney disease significantly increased to 2.59.
- However, longitudinal analyses showed that drinking more than 1 soda per day was not associated with incident hyperuricemia or chronic kidney disease.
- The lack of association between soda drinking and incident chronic kidney disease was not affected by preexistent hyperuricemia or by development of hyperuricemia.
- Post hoc power analyses showed a greater than 80% power to detect a 6.5% higher incidence of hyperuricemia and a 3% higher incidence of chronic kidney disease in participants who drank more than 1 soda per day vs those who drank less than 1 soda per day.
- On the basis of these findings, the investigators concluded that high consumption of sugar-sweetened soda was associated with prevalent but not incident hyperuricemia and chronic kidney disease, adding to but not closing the ongoing debate regarding the potential dangers of sugar-sweetened soda.
- Limitations of this study include its reliance on dietary recall, observational design, unmeasured confounding, possible survival bias, and lack of detailed information on participants' medications and on heavy metal exposure.
Clinical Implications
- In the Atherosclerosis Risk in Communities Study, cross-sectional analyses showed that drinking more than 1 soda per day was associated with increased odds of prevalent hyperuricemia and chronic kidney disease vs participants who drank less. The association between soda intake and renal function became more pronounced as uric acid levels increased.
- Longitudinal analyses showed that drinking more than 1 soda per day was not associated with incident hyperuricemia or chronic kidney disease. The lack of association between soda drinking and incident chronic kidney disease was not affected by preexistent hyperuricemia or by development of hyperuricemia