Longer Lipid Chains Identified as a Shared Aging Marker in Worms, Flies, Mice and Humans
Increasing fatty acid chain length is an aging feature conserved across species, and reversing it extended lifespan in worms.

The chain length of lipids, which handle cell membranes and energy storage, has been observed to grow longer with age in many organisms. Researchers at Amsterdam University Medical Centers (Amsterdam UMC) in the Netherlands proposed in Nature Aging that this "lipid elongation" is an aging feature conserved across species.
Analyzing several tissues from four species at once
The researchers integrated and compared lipidomics data from many tissues of the roundworm C. elegans, fruit flies, mice and humans. They found a repeated shift in ratios with age: lipids with long acyl chains increased and lipids with short chains decreased. Similar lengthening was seen as human heart disease progressed, and conversely, dietary restriction in mice shortened heart lipids.
The researchers focused on Plb1, a lipid-remodeling enzyme that regulates this process. In mice, Plb1 expression levels correlated with lifespan, and in human genome analysis, a causal link with frailty was suggested. When Plb1 was suppressed in worms, lipid lengthening was reversed and lifespan was extended, and this effect depended on lipid length.
However, the lifespan extension was confirmed only in worms, and the abstract does not give the number of human samples or the effect size. Whether lipid lengthening is a cause or a result of aging also needs further verification.
- Multi-tissue lipidomics in worms, flies, mice and humans showed lengthening of lipid acyl chains with aging in all of them
- Similar changes as human heart disease progressed; dietary restriction in mice shortened heart lipids
- Suppressing the lipid-remodeling enzyme Plb1 reversed lipid lengthening and extended lifespan in worms
Limitations Lifespan extension was confirmed only in worms, and the abstract gives no human sample size or effect size, so a causal interpretation for human aging is premature.
Original Research
- Li W, et al. · Amsterdam UMC (University of Amsterdam). Longer lipids mark aging and constrain lifespan. Nature Aging. DOI: 10.1038/s43587-026-01223-x
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