How was the study conducted?
The researchers used data from the US Health and Retirement Study. The mean age of the 5,065 participants without dementia at baseline was 67.5 years; 61.6% were women. 2,004 of the participants used vitamin D supplements. Cognitive performance was evaluated at two-year intervals for approximately six years, from 2014 to 2020.
What was the main finding?
The annual change in global cognitive score was statistically slightly more negative in those who used vitamin D supplements compared to non-users. A similar small difference was also reported for the executive function score. In the sensitivity analysis, this association was observed in those with normal baseline 25(OH)D levels, but was not observed in those with insufficient or deficient levels.
Does this result mean that “vitamin D harms the brain”?
No. In observational cohorts, supplement users and non-users may differ in many respects. For example, age, disease burden, health behaviors, other supplement use, physician recommendations, and the individual’s reason for starting supplementation can affect outcomes. Although the researchers adjusted statistically for numerous variables, unmeasured confounding factors cannot be completely ruled out.
What is the effect size?
Although the difference in the study was statistically significant, its magnitude was small: a difference of approximately -0.052 points/year in the rate of change of the global cognitive score and approximately -0.021 points/year in the executive function score was reported. Therefore, the result should not be interpreted as “everyone who takes supplements will experience clinically significant dementia.”
The researchers’ proposed mechanism hypothesis
The study discusses the hypothesis that excess vitamin D may affect signaling pathways and amyloid-beta biology in the brain. However, this mechanism is not proven in humans based on this cohort finding. Biological plausibility and clinical causality are not the same thing.
Why is it necessary to think in a U-shape for vitamin D?
As with many micronutrients, the primary goal is to prevent deficiency and maintain adequate levels. The fact that insufficiency is harmful does not mean that exceeding physiologically adequate levels will provide additional benefit. With vitamin D as well, requirements vary according to age, bone health, sun exposure, malabsorption disorders, the renal-parathyroid axis, and medications used.
Which measurement is the supplementation decision based on?
The primary biomarker used to evaluate vitamin D status is the serum 25(OH)D level. The result must be interpreted together with the clinical indication, bone mineral density, calcium-phosphorus balance, PTH, renal function, malabsorption, and the dose used. Rather than applying a single “ideal” target to everyone, the clinical context is what matters.
Are there other risks associated with high doses?
Unnecessarily high vitamin D intake can increase the risk of hypercalcemia, hypercalciuria, and, in some individuals, kidney stones or kidney damage. The risk generally becomes significant with uncontrolled high-dose or cumulative use rather than standard daily doses. Therefore, laboratory monitoring is required, especially if high-dose therapy is planned.
Where is the stronger evidence for protecting cognition?
In terms of cognitive aging, physical activity, hypertension and diabetes control, avoidance of smoking, treatment of sleep disorders, assessment of hearing loss, social-cognitive activity, and overall cardiovascular risk management have a broader evidence base. Vitamin D is a biological variable that should be corrected if a deficiency exists; it should not be viewed as a standalone “nootropic” or anti-aging solution.
Our approach at our Bodrum clinic
We address the supplementation decision not with a “the more, the better” logic, but through an approach of measurement, indication, and targeted correction. For vitamin D, the 25(OH)D level and clinical context are evaluated first; if necessary, an appropriate dose is selected, and follow-up is planned, especially for high-dose treatments. The goal is not to raise the laboratory value as high as possible, but to safely correct the deficiency and avoid unnecessary use.
Limitations of the evidence
The BMJ Open study is not a randomized controlled supplementation trial. The supplement dose, duration of use, and adherence level were not the same across all participants. The results pertain to an older US population and cannot be directly generalized to all age groups. This study generates a new safety signal and hypothesis; it is not the final word proving clinical causality.
References
- The Washington Post, September 10, 2026: Vitamin D supplements and the aging brain debate
- Hua R et al. Association between vitamin D supplement use and cognitive functioning: a longitudinal cohort study. BMJ Open. 2026.
- PubMed record: BMJ Open 2026;16:e106050.
Last medical review: September 18, 2026
