HIGH consumption of artificial sweeteners is associated with accelerated global cognitive decline over an eight-year study period.
Longitudinal Findings on Artificial Sweeteners and Cognitive Decline
In a prospective longitudinal cohort evaluation of 12,772 civil servants over a median follow up of eight years, investigators evaluated dietary exposure to seven low and no calorie sweeteners. Participants in the highest tertile of total sweetener consumption demonstrated a 32 percent higher rate of memory decline and a 62 percent higher rate of global cognitive decline compared to those in the lowest intake tier. This accelerated trajectory was equivalent to approximately 1.6 additional years of cognitive aging. Further domain specific testing revealed that high consumers experienced a 110 to 173 percent faster reduction in verbal fluency scores over time.
Differential Risk Profiles Across Age and Diabetes Status
Age and metabolic status significantly influenced these neurocognitive outcomes. Stratified analyses indicated that the heightened risk of cognitive decline associated with high artificial sweetener consumption was particularly pronounced in adults younger than 60 years. In contrast, older adults did not demonstrate significant associations between sweetener tertiles and cognitive trajectories. Furthermore, diabetes status served as an important effect modifier. Among individuals with diabetes, high intake of total sweeteners, as well as individual agents such as aspartame, acesulfame k, and saccharin, was strongly associated with accelerated memory and global cognitive impairment.
Clinical Implications for Sweetener Selection and Patient Guidance
When examining individual non-nutritive agents, higher intake of aspartame, saccharin, acesulfame k, erythritol, sorbitol, and xylitol each independently correlated with faster global cognitive decline. Daily frequency of sweetener intake was similarly associated with cognitive deterioration in memory and verbal fluency domains. Notably, tagatose was the only investigated sweetener that was not associated with accelerated decline, showing potential protective associations in younger adults. Proposed biological mechanisms include microglial neuroinflammation, hippocampal cellular apoptosis, and gut dysbiosis induced by sweetener metabolites. Physicians should consider these findings when counseling patients, particularly younger adults and patients with diabetes, regarding dietary sugar substitutes.
Reference
Gomes Gonçalves N et al. Association Between Consumption of Low- and No-Calorie Artificial Sweeteners and Cognitive Decline: An 8-Year Prospective Study. Neurology. 2026;105(7):e214023.
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