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Soda and Stroke Risk: A Pop Connection?
Abstract & Commentary
By Susan T. Marcolina, MD, FACP, Internist and Geriatrician, Issaquah, WA. Dr. Marcolina reports no financial relationships relevant to this field of study.
Synopsis: Two large, well-known, U.S. prospective cohort studies, the Nurses' Health Study and the Health Professionals Follow-up Study, evaluated both sugar-sweetened and diet (low-calorie, also called artificially sweetened) soda consumption over 20 years and found one or more daily servings to be associated with a significantly higher risk of stroke. Conversely, alternative beverage choices of either skim milk, caffeinated coffee, or decaffeinated coffee were associated with diminished stroke risk. This association appeared to be stronger for women than men and independent of established dietary and nondietary cardiovascular disease risk factors, including body mass index and energy intake. Beverage choice may be a modifiable risk factor for cerebrovascular events.
Source: Bernstein AM, et al. Soda consumption and the risk of stroke in men and women. Am J Clin Nutr 2012;95:1190-1199.
This epidemiologic study evaluated beverage types and amounts consumed by two large representative male and female populations of health professionals over more than two decades in detail via biennial validated food frequency questionnaires (FFQs) in addition to their health status questionnaires. The types of sodas included on the FFQs included low-calorie, caffeinated, and decaffeinated colas; other low-calorie, non-cola carbonated beverages; sugar-sweetened colas with and without caffeine; and other carbonated, caffeinated, and decaffeinated beverages with sugar. Soda was categorized as sugar-sweetened or low-calorie, and then participants were divided into categories of cumulative average serving intake of each type (sugar-sweetened and low-calorie soda consumption), which included none, up to once per week, once per week up to once per day, and once per day or more.
The investigators evaluated the associations between sugar-sweetened and low-calorie soda intake and total stroke (hemorrhagic and ischemic) incidence in both populations. In multivariable analyses adjusted for dietary risk factors (intakes of alcohol, fruit and vegetable servings, cereal fiber, fish, red meat, trans fats) and non-dietary cardiovascular disease risk factors (exercise, smoking, family history, menopausal status [women], aspirin, and multivitamin use), increased consumption of both sugar-sweetened and low-calorie colas and non-cola carbonated beverages was associated with a greater risk of overall stroke. For men, one or more daily servings of sugar-sweetened soda was associated with an insignificant relative risk (RR) of total stroke of 1.08 (95% confidence interval [CI], 0.82-1.41; P = 0.43); whereas in women, the statistically significant RR was 1.19 (95% CI, 1.00-1.42; P = 0.02). For men who consumed one or more daily servings of low-calorie soda, the RR for total stroke was 1.10 (95% CI, 0.92-1.32; P = 0.13) and in women was 1.18 (95% CI, 1.05-1.33; P = 0.003). The pooled multivariable risk of stroke among both sexes was 1.12 (95% CI, 1.02-1.24; P = 0.02) for one or more daily servings of sugar-sweetened soda and 1.09 (95% CI, 1.04-1.15; P = 0.0001) for one or more daily low-calorie soda servings.
Interestingly, compared with men and women who did not consume sugar-sweetened soda, those who consumed one or more daily servings had higher rates of hypertension, hypercholesterolemia, and lower physical activity. Greater consumption of low-calorie soda was associated with higher body mass indices (BMIs) and rates of chronic disease.
The authors evaluated the pooled risk ratios for consumption of alternative beverages in regard to stroke risk and found that compared with one daily serving of sugar-sweetened soda, daily servings of decaffeinated and caffeinated coffees were associated with modest reductions of 10% and 9% in stroke risk, respectively. When compared with one daily serving of low-calorie soda, consumption of one daily serving of skim milk, caffeinated coffee, or decaffeinated coffee was associated with decreases in stroke risk of 11%, 11%, and 13%, respectively. Although the 95% CIs suggested a modest benefit with the water for soda substitution, the authors suggest that the chlorogenic acids, lignans, and magnesium content of coffee and the potassium magnesium and calcium content of milk act both as antioxidants and mediators of glucose metabolism and blood pressure, which may be associated with the reduced stroke risk result seen with these beverages.1
Stroke is the third major cause of death and the leading cause of functional impairment, with 15-30% of survivors left with permanent disability and lost independence. It is a major public health concern in the United States. Effective primary prevention remains the optimal way to reduce the burden of disease and disability, since more than 70% of strokes occur as first-time events.2
The benefit of information obtained from large, long-term cohort studies such as this one is that it prompts us to consider ways in which individuals, in conjunction with their health care providers in the medical home context, can mitigate risk by virtue of dietary and lifestyle interventions that are low-cost, effective, and achievable.
Over the past 25 years, sugar-sweetened and diet soda consumption has increased 135% in the United States in parallel with the prevalence of obesity.3 The temporal association has a scientific basis in view of the fact that sodas are nutrient-poor beverages consumed in lieu of potentially nutrient-rich beverages such as enriched nondairy milks, milk, calcium-fortified juices, or just plain water, which provides necessary hydration without additional cost or calories. Additionally, the caramel coloring in sugar-sweetened and low-calorie colas has advanced glycation endproducts, which have been linked to inflammatory processes that enhance initiation, growth, and destabilization of atherosclerotic plaques.4
Another factor in the soda-stroke linkage may be the fructose content of soda either as sucrose (the "sugar" disaccharide composed of 50% fructose and 50% glucose) or high-fructose corn syrup (55% fructose and 45% glucose). Due to this high volume and content of rapidly absorbable carbohydrates, sodas may increase the risk of metabolic syndrome and type 2 diabetes by increasing dietary glycemic load, leading to insulin resistance, weight gain, beta cell dysfunction, and inflammation. Ingested fructose is metabolized almost entirely in the liver; this hepatic metabolism favors lipogenesis, which increases triglyceride levels and reduces low-density cholesterol lipoprotein particle size. Such alterations in the lipoprotein profile increase atherogenicity. Hepatic metabolism of fructose also increases serum uric acid, which reduces endothelial nitric oxide and can result in blood pressure elevation, a known risk factor for stroke.5
Additionally, fructose has different metabolic effects than glucose. It does not increase postprandial insulin and leptin (satiety hormone) or suppress ghrelin (appetite-stimulating hormone) levels, thus suggesting another means by which it promotes weight gain.6
Several other epidemiologic studies have shown an association between consumption of sugar-sweetened beverages and the development of metabolic syndrome and type 2 diabetes, both of which contribute to risk of stroke.7
Although deKoning et al found no association between low-calorie soda intake and diabetes risk,8 low-calorie soda consumption of two or more daily servings has been associated with albuminuria and progression of kidney disease.9
Another consideration is that many carbonated beverages contain a large amount (> 10 mg in a 12 fluid-ounce serving) of inorganic phosphorus (P) in the form of additives such as phosphoric acid or monosodium phosphate. These P salts readily dissociate and are absorbed to a much greater extent compared to the more tightly protein-bound organic P present in natural sources such as beef, chicken, and egg yolks (> 90% absorption vs 40-60% intestinal absorption, respectively). Such additional bioavailable P increases serum P levels and urinary P excretion and decreases serum and urine calcium concentrations. These changes induce a secondary hyperparathyroidism, with its negative consequences for bone health.10
The pitfalls with this study, as with any observational study, is that the soda-stroke association cannot confer causality due to confounding from as yet unidentified and unmeasured factor(s). The association may also be an indirect one, linked by other disease processes that may be mitigated by dietary beverage choice including inflammation, endothelial dysfunction, and dyslipidemia. Further information regarding whether, what type, and how much soda consumption can affect stroke risk will depend upon randomized, controlled trial results.
In the meantime, we can all drink to our health by following the advice offered by Dr. William Osler in his 1893 Principles and Practices of Medicine text that "the sugar should be kept to a minimum."11
1. Ding EL, Mozaffarina D. Optimal dietary habits for the prevention of stroke. Semin Neurol 2006;26:11-23.
2. American Stroke Association. A Division of American Heart Association. AHA/ASA Guidelines for the Primary Prevention of Ischemic Stroke. Available at: http://stroke.ahajournals.org/content/37/6/1583.full.pdf+html. Accessed May 1, 2012.
3. Nielsen SJ, Popkin BM. Changes in beverage intake between 1977 and 2001. Am J Prev Med 2004;27:205-210.
4. Malik VS, et al. Sugar-sweetened beverages, obesity, type 2 diabetes mellitus, and cardiovascular disease risk. Circulation 2010;121:1356-1364.
5. Johnson RJ, et al. Potential role of sugar (fructose) in the epidemic of hypertension, obesity and the metabolic syndrome, diabetes, kidney disease, and cardiovascular disease. Am J Clin Nutr 2007;86:899-906.
6. Havel PJ. Dietary fructose: Implications for dysregulation of energy homeostasis and lipid/carbohydrate metabolism. Nutr Rev 2005;63:133-157.
7. Malik VS, et al. Sugar-sweetened beverages and risk of metabolic syndrome and type 2 diabetes: A meta-analysis. Diabetes Care 2010;33:2477-2483.
8. de Koning L, et al. Sugar-sweetened and artificially sweetened beverage consumption and risk of type 2 diabetes in men. Am J Clin Nutr 2011;93:1321-1327.
9. 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;6:160-166.
10. Sullivan CM, et al. Phosphorus-containing food additives and the accuracy of nutrient databases: Implications for renal patients. J Ren Nutr 2007;17:350-354.
11. Osler W. The Principles and Practices of Medicine. 2nd edition. Appleton NY: 1893:287-295.