28/01/2026
Vitamin D3 slows biological aging primarily by protecting the genetic stability of cells and reducing age-related cellular decline. Research published in 2025 from the VITAL clinical trials suggests that daily supplementation with 2,000 IU of Vitamin D3 can slow biological aging by nearly three years at the cellular level. The core mechanisms identified are:
🗂️Preservation of Telomere Length:
🗒️Telomeres are protective caps at the ends of chromosomes that naturally shorten during cell division. Vitamin D3 reduces this attrition.
🗒️Measurable Impact: In a 4-year study, participants taking Vitamin D3 lost roughly 140 fewer base pairs of DNA compared to a placebo group.
🗒️Telomerase Activation: Vitamin D increases the activity of telomerase, the enzyme responsible for rebuilding and extending telomeres.
🗂️Epigenetic Regulation:
🗒️Biological Clock Deceleration: Supplementation has been shown to slow epigenetic aging (changes in how DNA is expressed as measured by DNA methylation “clocks” like the Horvath and Hannum methods.
🗒️Gene Expression Modulation: Vitamin D binds to the Vitamin D Reception (VDR), which regulates hundreds of genes involved in DNA repair and genomic maintenance.
🗂️Reduction of Cellular Stress:
🗒️Anti-Inflammatory Action: Chronic inflammation (often called “inflammaging”) is a major driver of biological aging. Vitamin D inhibits inflammatory pathways helping to lower cellular stress.
🗒️DNA Repair Support: It enhances the body’s ability to repair DNA damage and reduces oxidative stress, which can otherwise accelerate telomere loss and cellular decay.
🗒️Senescence Prevention: By maintaining cellular health, Vitamin D may delay the onset of cellular senescence - a state where cells stop dividing and instead release harmful inflammatory molecules. These are also sometimes called “zombie cells”.
See S T Rahman et al. J Nutr Health Aging. 2023