In a groundbreaking advancement for aging and disease prevention research, a new study derived from the Vitamin D and Omega-3 Trial (VITAL) has demonstrated that daily vitamin D3 supplementation reduces leukocyte telomere length (LTL) attrition, a pivotal marker of biological aging. A recent study, published and registered under NCT04386577, provides long-anticipated data from a large randomized controlled trial supporting the potential role of vitamin D in maintaining cellular integrity.
The aim of this study was to determine whether long-term use of vitamin D or omega-3 fatty acids preserves telomere length. Telomere length naturally shortens with each cell division and during the aging process, making it a critical biomarker of biological aging and a key public health concern. Critically short telomeres lead to cellular senescence, a state linked to increased risk for chronic conditions such as cancer and cardiovascular disease.
Researchers evaluated a sub-cohort of participants from the larger VITAL trial. A total of 1031 participants were followed for over four years. Participants were randomized into one of four groups: daily dosage of 2000 IU/day of vitamin D3, daily dosage of 1g/day of marine omega-3 fatty acids, vitamin D + omega-3, and placebo. Telomere lengths were measured at baseline, two years, and four years using a quantitative polymerase chain reaction (qPCR) method.
Participants receiving vitamin D3 supplementation exhibited significantly less loss of LTL compared to the placebo group, a difference of 0.14 kilobase pairs (kb) over four years (95% CI: 0.01 to 0.27; P = 0.039). Additionally, trend analysis indicated that LTLs were on average 0.035 kb longer each year of follow-up in the vitamin D3 group compared to the placebo group (95% CI: 0.002 to 0.07; P = 0.037). In contrast, marine omega-3 fatty acid supplementation did not show a significant impact on LTL at either the two- or four-year time points.
Telomeres function as protective caps on the ends of chromosomes, preserving genetic stability. Their progressive shortening of telomeres predicts many age-related diseases and thus attracts researchers to consider telomere length as a promising biomarker for healthy aging.
Few observational studies have shown a relationship between vitamin D and telomere length, but until now, not much research has provided more robust evidence from a randomized controlled trial. The findings suggest that vitamin D, already known for its important role in bone health and immune modulation processes, may also contribute to the prevention of cellular aging.
The VITAL Telomere sub-study cohort had a mean age of 64.9 years, with approximately half of the participants being women. The majority of participants were White (84%), with 9% identifying as Black. Baseline characteristics were well-balanced across all groups, and randomization ensured that there was no demographic bias in treatment allocation.
Previous evidence from the broader VITAL trial has suggested that vitamin D’s systemic benefits extend beyond telomere maintenance, showing associations with lower risks of advanced cancers and autoimmune diseases. In contrast, omega-3 fatty acids, which have been promoted for their cardiovascular benefits, did not substantially impact telomere attrition in this analysis.
In conclusion, this four-year study contributes to the growing evidence that daily vitamin D3 supplementation may reduce the rate of cellular aging by preserving telomere length. While omega-3 fatty acids did not demonstrate a similar benefit, the findings position vitamin D as a low-cost, low-risk approach with the potential to slow biological aging. As aging populations seek strategies to extend health span, vitamin D may prove to be a critical component in combating aging-related cellular decline.
Reference: Zhu H, Manson JE, Cook NR, et al. Vitamin D₃ and marine ω-3 fatty acids supplementation and leukocyte telomere length: 4-year findings from the VITamin D and OmegA-3 TriaL (VITAL) randomized controlled trial. Am J Clin Nutr. 2025. doi:10.1016/j.ajcnut.2025.05.003
