Framingham Heart Study Offspring cohort does not find similar association for sugar-sweetened drinks.
Just last week, we saw how artificial sweeteners in soda are associated with high risk of stroke and dementia. This association was not seen with sugar-sweetened drinks.
This study should not be taken as suggesting that sugar-sweetened beverages are okay. We know that too much sugar is associated with many negative outcomes, including obesity, dysbiosis, and metabolic dysfunction. But the study should lend some caution as to the safety of artificial sweeteners. One that has had the most controversy is aspartame.
Aspartame is composed of 50% phenylalanine, 40% aspartic acid, and 10% methanol. One of several potentially toxic byproducts of aspartame is formaldehyde. P. Humphries et al summarized the potential cellular mechanisms aspartame has on the brain in the European Journal of Clinical Nutrition. They state that aspartame disturbs integrity of neuronal function, causes nerves to fire excessively, depletes ATP function in mitochondria, and causes dysfunction of the endothelium, leading to a compromised blood–brain barrier. The literature has mentioned concern for aspartame in relation to headaches, malignancies, and learning disabilities.
This was an observational study and thus causation cannot be made. An additional caveat to keep in mind when interpreting the results of this study is that participants with diabetes, who are more likely to develop stroke and dementia, also consumed more artificially sweetened beverages. While the authors adjusted for diabetes in supplementary analyses, it is likely that residual confounding in both primary and supplementary analyses has not been eliminated.
Sugar- and artificially-sweetened beverage intake have been linked to cardiometabolic risk factors, which increase the risk of cerebrovascular disease and dementia. We examined whether sugar- or artificially sweetened beverage consumption was associated with the prospective risks of incident stroke or dementia in the community-based Framingham Heart Study Offspring cohort.
They studied 2,888 participants age >45 years for incident stroke (mean age 62 [SD, 9] years; 45% men) and 1,484 participants age >60 years for incident dementia (mean age 69 [SD, 6] years; 46% men). Beverage intake was quantified using a food-frequency questionnaire at cohort examinations 5 (1991-1995), 6 (1995-1998), and 7 (1998-2001). Researchers quantified recent consumption at examination 7 and cumulative consumption by averaging across examinations. Surveillance for incident events commenced at examination 7 and continued for 10 years. They observed 97 cases of incident stroke (82 ischemic) and 81 cases of incident dementia (63 consistent with Alzheimer’s disease).
After adjustments for age, sex, education (for analysis of dementia), caloric intake, diet quality, physical activity, and smoking, higher recent and higher cumulative intake of artificially sweetened soft drinks were associated with an increased risk of ischemic stroke, all-cause dementia, and Alzheimer’s disease dementia. When comparing daily cumulative intake to 0 per week (reference), the hazard ratios were 2.96 (95% confidence interval, 1.26-6.97) for ischemic stroke and 2.89 (95% confidence interval, 1.18-7.07) for Alzheimer’s disease. Sugar-sweetened beverages were not associated with stroke or dementia.
From the results it was concluded that artificially sweetened soft drink consumption was associated with a higher risk of stroke and dementia.
This study is a reminder that nature is smarter than we are. We are likely better off eating whole foods artfully combined by a good chef than a processed food put together by a biochemist.
- After adjusting for multiple confounders, both recent intake and cumulative intake of artificially sweetened drinks were associated with significantly greater risks for ischemic stroke and dementia.
- Similar associations were not found for sugar-sweetened drinks.
Humphries P, Pretorius E, Naude H. Direct and indirect cellular effects of aspartame on the brain. Eur J Clin Nutr. 2008;62(4):451-462. http://www.nature.com/ejcn/journal/v62/n4/full/1602866a.html