Can you lengthen or restore your telomeres?

Telomeres shorten a little with each cell division, and that shortening process has so far not proven to be fully reversible in humans. What does appear possible is slowing the rate of shortening. In the large VITAL study, a double-blind, placebo-controlled trial with more than a thousand participants followed for four years, the telomeres of white blood cells in people who took 2000 IU of vitamin D3 daily shortened on average 140 base pairs less than in the placebo group (p=0.039). The telomeres did not become longer, but they wore down more slowly. That difference of 140 base pairs over four years is measurable and statistically significant.

Omega-3 fatty acids from fish oil, also investigated in the same VITAL study at a dose of 1 gram per day over four years, had no measurable effect on the telomere length of white blood cells. Neither after two years nor after four years was there a significant difference from placebo. On the basis of this solid research, omega-3 therefore fails as a means of slowing telomere shortening.

The starting length of telomeres is largely determined at birth. Research using a new precise measurement method in 147 people showed that the relative ranking of telomere length per chromosome end remains stable as people age, with differences between chromosome ends potentially exceeding 6,000 base pairs. This indicates that genetics plays a major role in determining who has long or short telomeres, regardless of lifestyle.

Short telomeres are not only a marker of ageing but also a cause of disease. When stem cells have telomeres that are too short, they can no longer divide properly, which blocks tissue regeneration. People with mutations in genes that maintain telomeres develop conditions such as pulmonary fibrosis, aplastic anaemia, and liver fibrosis. Shorter telomeres are also associated with a higher risk of cardiovascular disease: endothelial cells in atherosclerosis display characteristics of aged, no-longer-dividing cells. In type 2 diabetes, telomere shortening proceeds more rapidly. In the case of cardiovascular disease, these are associations; direct causality in humans has not yet been fully proven.

Artificially lengthening telomeres sounds appealing, but it has a dark downside. In 416 children with neuroblastoma, it was found that tumour cells that actively maintain their telomeres are associated with worse survival. Tumours without this telomere maintenance had an excellent prognosis. Telomere lengthening therefore helps cancer cells remain immortal. This makes the idea of 'boosting telomeres as an anti-ageing strategy' risky as long as there is no way to treat cancer cells and normal cells separately.

Oxidative stress, caused by factors such as UV radiation or excessive alcohol use, can cause cells to age prematurely through a mechanism that is separate from the normal telomere shortening process. This has been demonstrated in laboratory studies with human cells. It means that lifestyle factors that increase oxidative stress accelerate cellular ageing, independently of genetically determined telomere length. As a practical guideline: limiting unnecessary oxidative stress (smoking, excessive alcohol, chronic UV exposure) is biologically plausible, although the direct translation from lab cells to the human body must be made with caution. Finally, telomere length alone is an incomplete picture of biological ageing. Scientists recommend assessing ageing through a combination of markers, including DNA methylation patterns and physiological measurements.