Consumption of sugar-sweetened beverages (SSBs) is associated with an increased risk of hypertension in cross-sectional studies. However, prospective data are limited.
To examine the associations between SSBs and artificially sweetened beverages (ASBs) with incident hypertension.
DESIGN AND SETTING
Prospective analysis using Cox proportional hazards regression to examine the association between SSBs and ASBs with incident hypertension in three large, prospective cohorts, the Nurses' Health Studies I (n = 88,540 women) and II (n = 97,991 women) and the Health Professionals' Follow-Up Study (n = 37,360 men).
Adjusted hazard ratios for incident clinically diagnosed hypertension.
Higher SSB and ASB intake was associated with an increased risk of developing hypertension in all three cohorts. In a pooled analysis, participants who consumed at least one SSB daily had an adjusted HR for incident hypertension of 1.13 (95 % CI, 1.09–1.17) compared with those who did not consume SSBs; for persons who drank at least one ASB daily, the adjusted HR was 1.14 (95 % CI, 1.09–1.18). The association between sweetened beverage intake and hypertension was stronger for carbonated beverages versus non-carbonated beverages, and for cola-containing versus non-cola beverages in the NHS I and NHS II cohorts only. Higher fructose intake from SSBs as a percentage of daily calories was associated with increased hypertension risk in NHS I and NHS II (p-trend = 0.001 in both groups), while higher fructose intake from sources other than SSBs was associated with a decrease in hypertension risk in NHS II participants (p-trend = 0.006).
Residual confounding factors may interfere with the interpretation of results.
SSBs and ASBs are independently associated with an increased risk of incident hypertension after controlling for multiple potential confounders. These associations may be mediated by factors common to both SSBs and ASBs (e.g., carbonation or cola), but are unlikely to be due to fructose.
This is a preview of subscription content, log in to check access.
Buy single article
Instant access to the full article PDF.
Tax calculation will be finalised during checkout.
Subscribe to journal
Immediate online access to all issues from 2019. Subscription will auto renew annually.
Tax calculation will be finalised during checkout.
Dhingra R, Sullivan L, Jacques PF, Wang TJ, Fox CS, Meigs JB, et al. Soft drink consumption and risk of developing cardiometabolic risk factors and the metabolic syndrome in middle-aged adults in the community. Circulation. 2007;116(5):480–8.
de Koning L, Malik VS, Rimm EB, Willett WC, Hu FB. Sugar-sweetened and artificially sweetened beverage consumption and risk of type 2 diabetes in men. Am J Clin Nutr. 2011;93(6):1321–7.
Choi JW, Ford ES, Gao X, Choi HK. Sugar-sweetened soft drinks, diet soft drinks, and serum uric acid level: the Third National Health and Nutrition Examination Survey. Arthritis Rheum. 2008;59(1):109–16.
Ouyang X, Cirillo P, Sautin Y, McCall S, Bruchette JL, Diehl AM, et al. Fructose consumption as a risk factor for non-alcoholic fatty liver disease. J Hepatol. 2008;48(6):993–9.
Nguyen S, Choi HK, Lustig RH, Hsu CY. Sugar-sweetened beverages, serum uric acid, and blood pressure in adolescents. J Pediatr. 2009;154(6):807–13.
Jalal DI, Smits G, Johnson RJ, Chonchol M. Increased fructose associates with elevated blood pressure. J Am Soc Nephrol. 2010;21(9):1543–9.
Fowler SP, Williams K, Resendez RG, Hunt KJ, Hazuda HP, Stern MP. Fueling the obesity epidemic? Artificially sweetened beverage use and long-term weight gain. Obesity (Silver Spring). 2008;16(8):1894–900.
Lin J, Curhan GC. Associations of sugar and artificially sweetened soda with albuminuria and kidney function decline in women. Clin J Am Soc Nephrol. 2011;6(1):160–6.
Willett WC, Sampson L, Stampfer MJ, Rosner B, Bain C, Witschi J, et al. Reproducibility and validity of a semiquantitative food frequency questionnaire. Am J Epidemiol. 1985;122(1):51–65.
Rimm EB, Giovannucci EL, Stampfer MJ, Colditz GA, Litin LB, Willett WC. Reproducibility and validity of an expanded self-administered semiquantitative food frequency questionnaire among male health professionals. Am J Epidemiol. 1992;135(10):1114–26. discussion 27–36.
Feskanich D, Rimm EB, Giovannucci EL, Colditz GA, Stampfer MJ, Litin LB, et al. Reproducibility and validity of food intake measurements from a semiquantitative food frequency questionnaire. J Am Diet Assoc. 1993;93(7):790–6.
Appel LJ, Moore TJ, Obarzanek E, Vollmer WM, Svetkey LP, Sacks FM, et al. A clinical trial of the effects of dietary patterns on blood pressure. DASH Collaborative Research Group. N Engl J Med. 1997;336(16):1117–24.
Wolf AM, Hunter DJ, Colditz GA, Manson JE, Stampfer MJ, Corsano KA, et al. Reproducibility and validity of a self-administered physical activity questionnaire. Int J Epidemiol. 1994;23(5):991–9.
Rimm EB, Stampfer MJ, Colditz GA, Chute CG, Litin LB, Willett WC. Validity of self-reported waist and hip circumferences in men and women. Epidemiology. 1990;1(6):466–73.
Colditz GA, Martin P, Stampfer MJ, Willett WC, Sampson L, Rosner B, et al. Validation of questionnaire information on risk factors and disease outcomes in a prospective cohort study of women. Am J Epidemiol. 1986;123(5):894–900.
Ascherio A, Rimm EB, Giovannucci EL, Colditz GA, Rosner B, Willett WC, et al. A prospective study of nutritional factors and hypertension among US men. Circulation. 1992;86(5):1475–84.
Sanchez-Lozada LG, Tapia E, Jimenez A, Bautista P, Cristobal M, Nepomuceno T, et al. Fructose-induced metabolic syndrome is associated with glomerular hypertension and renal microvascular damage in rats. Am J Physiol Renal Physiol. 2007;292(1):F423–9.
Singh AK, Amlal H, Haas PJ, Dringenberg U, Fussell S, Barone SL, et al. Fructose-induced hypertension: essential role of chloride and fructose absorbing transporters PAT1 and Glut5. Kidney Int. 2008;74(4):438–47.
Glushakova O, Kosugi T, Roncal C, Mu W, Heinig M, Cirillo P, et al. Fructose induces the inflammatory molecule ICAM-1 in endothelial cells. J Am Soc Nephrol. 2008;19(9):1712–20.
Forman JP, Choi H, Curhan GC. Fructose and vitamin C intake do not influence risk for developing hypertension. J Am Soc Nephrol. 2009;20(4):863–71.
Ghanim H, Mohanty P, Pathak R, Chaudhuri A, Sia CL, Dandona P. Orange juice or fructose intake does not induce oxidative and inflammatory response. Diabetes Care. 2007;30(6):1406–11.
de Carvalho Sales-Peres SH, Magalhaes AC, de Andrade Moreira Machado MA, Buzalaf MA. Evaluation of the erosive potential of soft drinks. Eur J Dent. 2007;1(1):10–3.
Remer T, Manz F. Potential renal acid load of foods and its influence on urine pH. J Am Diet Assoc. 1995;95(7):791–7.
Schulze MB, Manson JE, Ludwig DS, Colditz GA, Stampfer MJ, Willett WC, et al. Sugar-sweetened beverages, weight gain, and incidence of type 2 diabetes in young and middle-aged women. JAMA. 2004;292(8):927–34.
Nettleton JA, Lutsey PL, Wang Y, Lima JA, Michos ED, Jacobs DR Jr. Diet soda intake and risk of incident metabolic syndrome and type 2 diabetes in the Multi-Ethnic Study of Atherosclerosis (MESA). Diabetes Care. 2009;32(4):688–94.
Lutsey PL, Steffen LM, Stevens J. Dietary intake and the development of the metabolic syndrome: the Atherosclerosis Risk in Communities study. Circulation. 2008;117(6):754–61.
The authors wish to thank Elaine Coughlin-Gifford for her help with the statistical programming in this manuscript. This work was funded by AHA Grant-in-Aid #2009A050171 (JF). The funding source did not influence the study design, conduct, or reporting. This work was presented as a poster at the 2011 American Society of Nephrology (ASN) meeting on November 4, 2011 in Philadelphia, PA.
Conflict of Interest
The authors declare that they do not have a conflict of interest.
We ascertained fructose intake from sugar-sweetened beverages by multiplying the frequency of consumption of a particular SSB by the sugar content (in grams) per beverage serving, derived from US Department of Agriculture Research Service nutritional data (http://www.ars.usda.gov/SP2UserFiles/Place/12354500/Data/SR23/reports/sr23fg14.pdf). The fructose derived from each type of SSB was then computed as 55 % of the sugar total obtained from that beverage, since the high-fructose corn syrup used to sweeten all sugary beverages contains 55 % fructose. The fructose intakes from each individual type of SSB were then summed to determine the fructose intake from all SSBs for each participant (in grams). Next, fructose intake obtained from sugar-sweetened beverages was subtracted from their total fructose intake to obtain the fructose intake from other sources (such as apples, bananas, raisins, etc.). Grams of fructose from SSBs and fructose from other sources were then multiplied by 4 calories/gram to obtain energy derived from that source of fructose, and divided by the participant’s total daily energy intake to obtain the following variables: percent of total daily calories from fructose from SSBs; and percent of total daily calories from fructose from other sources. In the NHS I at baseline, SSBs contributed 16 % of all fructose consumed by the cohort. In NHS II at baseline, SSBs accounted for 20 % of fructose intake. In HPFS at baseline, SSBs made up approximately 17 % all fructose consumed.
About this article
Cite this article
Cohen, L., Curhan, G. & Forman, J. Association of Sweetened Beverage Intake with Incident Hypertension. J GEN INTERN MED 27, 1127–1134 (2012). https://doi.org/10.1007/s11606-012-2069-6
- sweetened beverages
- artificial sweetener