Calorie Control Council Response to Jalal et al.

Increased Fructose Associates with Elevated Blood Pressure

Jalal DI, Smits G, Johnson RJ, Chonchol M. Increased fructose associates with elevated blood pressure.
J Am Soc Nephrol. 2010; 21: 1543-1549.

Jalal et al. investigated whether increased fructose consumption from added sugars is associated with an increased risk for higher blood pressure levels in U.S. adults without a history of hypertension. The researchers conducted a cross-sectional analysis using data from the National Health and Nutrition Examination Survey (NHANES 2003-2006) involving 4,528 adults. Jalal et al. reportedly found that an increased fructose intake of >74 grams/day was “independently and significantly associated with higher odds of elevated blood pressure levels” 1 .

Jalal et al. correlate the rising prevalence of hypertension in the U.S. population with the increase in fructose consumption in recent years. While fructose consumption has increased since the 1970s, it has not been found to increase disproportionately to the rest of the diet. In a 35-year nutrient intake study, average calorie intake from added sugars, flour/cereal and fats increased 50, 190 and 300 calories/day, respectively. The consumption of added sugars, including the principal fructose-containing sweeteners, sucrose and high fructose corn syrup, increased at nearly the identical rate (23%) as total calories (24%) 2 . In fact, most of the calorie-dense nutrient categories (added fats, flour/cereal, added sugars) increased proportionately with total calories. Targeting one nutrient, in this case fructose, as the cause of hypertension or any other health condition does not seem as prudent when considering the welldocumented health effects of obesity due to excess calories.

No reliable data exist asserting that fructose poses a specific health risk at typical intake levels (9.1% of calories) 3 . The fructose intake required to provoke hypertension (>74 grams/day) is high – equivalent to the 95 th percentile of fructose consumption – and does not reflect fructose use patterns of the vast majority of Americans 4 . It should be noted that this level corresponds not to 2.5 sugary soft drinks per day as the authors claim, but rather nearly four 12-ounce cans per day (sucrose and high fructose corn syrup sweeteners both contain nearly equivalent amounts of glucose, which must be considered in the calculation).

It is not widely known that an approximately 50:50 glucose to fructose ratio is common in all caloric sweeteners (sucrose, high fructose corn syrup, honey and fruit juice concentrates) and most fruits and vegetables 5 . Every increment of dietary fructose is thus accompanied by equivalent glucose. As noted earlier, fructose consumption has not increased disproportionately to other sugars. Jalal et al. do not provide monosaccharide control data for comparison with fructose to prove the unique effect they claim. Though the authors acknowledge high dietary glucose could have contributed to their findings, they did not calculate glucose intakes or report their association with hypertension.

The broader literature regarding an association between fructose and hypertension is mixed. For example, Dhingra et al. reported that consumers of >1 soft drink/day had a higher risk for incidence of individual metabolic traits except hypertension 6 . Forman et al. found no association between fructose intake and hypertension in three large cohort studies: The Nurses Health Studies I and II, and the Health Professional Follow up Study 7 . In the present study, Jalal et al. reports an association between fructose and hypertension but none with uric acid, triglycerides, BMI, waist circumference or diabetes. The lack of an association between uric acid and fructose intake is especially significant, since it decouples co-author Johnson’s recent hypothesis that uric acid is the causal link between fructose and hypertension 8.

By discounting Forman’s inability to find an association between higher fruit intake with hypertension as an anomaly, the authors are suggesting the unlikely scenario that fructose from added sources poses a greater health risk than naturally occurring fructose fruits and vegetables.

The points made here suggest the authors’ conclusion that fructose is associated with hypertension is weakly established based on current science and the attendant recommendation for decreased fructose intake is premature.

References
1. Jalal DI, Smits G, Johnson RJ, Chonchol M. Increased fructose associates with elevated blood pressure. J Am Soc Nephrol. 2010; 21: 1543-1549.
2. Marriott BP, Cole N, Lee E. National estimates of dietary fructose intake increased from 1977 to 2004 in the United States. J Nutr. Jun 2009;139(6):1228S-1235S.
3. White JS. Misconceptions about high-fructose corn syrup: is it uniquely responsible for obesity, reactive dicarbonyl compounds, and advanced glycation endproducts? J Nutr. Jun 2009;139(6):1219S-1227S.
4. Dhingra R, Sullivan L, Jacques PF, et al. Soft Drink Consumption and Risk of Developing Cardiometabolic Risk Factors and the Metabolic Syndrome in Middle-Aged Adults in the Community. Circulation. July 23, 2007 2007;116:480-488.
5. Forman JP, Choi H, Curhan GC. Fructose and vitamin C intake do not influence risk for developing hypertension. J Am Soc Nephrol. Apr 2009;20(4):863-871.
6. Johnson RJ, Perez-Pozo SE, Sautin YY, et al. Hypothesis: could excessive fructose intake and uric acid cause type 2 diabetes? Endocr Rev. Feb 2009;30(1):96-116

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