Vitamin D supplementation is associated with slower epigenetic aging.
Level 3 - non-randomized controlled study
Prospective longitudinal cohort study with non-randomized (self-selected) intervention groups.
PubMed 35562603 · doi:10.1007/s11357-022-00581-9
What was done
Researchers used a quasi-interventional longitudinal design assessing 1,036 older adults from the Berlin Aging Study II (BASE-II) followed up an average of 7.4 years later in the GendAge study (mean age 75.6 years, range 64.9–94.1 years, 51.9% female). DNA methylation age acceleration (DNAmAA) was measured across five epigenetic clocks (7-CpG clock, Horvath, Hannum, PhenoAge, and GrimAge) via MS-SNuPE or Illumina MethylationEPIC arrays to compare participants who were vitamin D deficient and began supplementation versus those who remained untreated or were healthy controls.
What was found
Vitamin D-deficient participants who chose to start vitamin D supplementation showed a 2.6-year lower 7-CpG DNAmAA (p = 0.011) and a 1.3-year lower Horvath DNAmAA (p = 0.042) compared to untreated vitamin D-deficient participants. DNAmAA did not statistically differ between participants with successfully treated vitamin D deficiency and healthy controls (p > 0.16). The abstract did not report numerical values or results for the Hannum, PhenoAge, or GrimAge clocks.
Why it matters
This study provides longitudinal human evidence that correcting vitamin D deficiency via supplementation is linked to attenuated biological aging as measured by specific DNA methylation clocks.
Limits
Supplementation was self-selected rather than randomly assigned, introducing potential confounding and healthy-user bias. Statistically significant associations were reported for only two of the five evaluated epigenetic clocks, and exact dosages or formulations of vitamin D supplements were not detailed in the abstract.