Pitavastatin may slow the quickening pace of biological aging in people with HIV

People with HIV, even when well treated with antiretroviral therapy, have higher cardiovascular risk and appear to age biologically faster than people without HIV. The REPRIEVE trial showed that pitavastatin lowered major adverse cardiovascular events in this population. Whether statins also influence the underlying biology of aging has been unknown.

This pilot substudy used stored blood samples from 99 randomly selected US REPRIEVE participants (65 pitavastatin, 34 placebo), with a median age of 57. DNA methylation was measured in peripheral blood mononuclear cells at baseline and 24 months. The primary outcomes were two epigenetic clocks: PCGrimAge, which was trained to predict mortality risk, and DunedinPACE, which estimates the pace of multi-organ decline.

At entry, all participants showed epigenetic age acceleration, with PCGrimAge a median of about 7 years above chronological age. Over 24 months, PCGrimAge stayed accelerated and did not differ between arms (P = .89). DunedinPACE, however, rose in the placebo group (median change 0.036, P = .021) but not in the pitavastatin group (0.001, P = .77). The between-group difference was marginal (P = .049).

These findings suggest pitavastatin might prevent an increase in the pace of biological aging in people with HIV, adding a possible non-cardiovascular benefit to its established role. They also fit the idea that statins have anti-inflammatory and other pleiotropic effects.

Caveats are substantial. The sample was small and unevenly split, the effect was borderline significant, and PCGrimAge showed no benefit. Epigenetic clocks are surrogate markers whose clinical meaning is still being established, and there was no HIV-negative comparison. This analysis is based on the abstract only, so details such as multiplicity handling and sensitivity analyses could not be evaluated. The results need replication in larger samples.