Choices · Telomeres

Telomeres and longevity: the caps on our chromosomes, the gene therapies and the natural habits

Marek and Liz Parrish walking on a forest path among tall trees and ferns, with a dog.
Marek Piotrowski and Liz Parrish on a forest walk near Seattle, June 2024 — a Live Beyond interview on gene therapy, including telomerase.

Telomeres were the first thing I ever heard about aging that made it feel fixable. Every time a cell divides, the caps at the ends of its chromosomes get a little shorter, like a fuse burning down. Make the fuse longer, the idea went, and you make life longer. On our quest, Alek and I met the woman who, by her own account, was the first to try it on herself, and the scientists who told us why the story is more complicated, and more interesting.

By Marek Piotrowski · Updated 2026-11-06

In short

Telomeres are the protective caps at the ends of our chromosomes, and the discovery of how they protect our chromosomes won a Nobel Prize. They shorten as cells divide, and people with shorter telomeres have, on average, more heart disease. In mice, a gene therapy that switches on telomerase, the enzyme that rebuilds telomeres, made older animals live longer without more cancer.

In people, the picture is more complex: genetically longer telomeres also come with a higher risk of some cancers, and the telomere tests sold to the public are too imprecise to guide your life.

The good news: the habits that protect the whole body, moving, sleeping, managing stress and eating real food, are linked to healthier telomeres too, and they are already in your hands. [1][2][3][4]

This is not medical advice.

This page shares experiences from our quest and what scientists told us. It does not recommend any medicine, peptide, supplement or treatment, and it knows nothing about you.

Never start, stop or change any medicine, peptide, supplement or treatment without your own doctor, who knows your health and can check your blood work. That matters even more if you are pregnant or planning a pregnancy, live with a health condition, or take other medicines.

Longevity, as we mean it: more healthy, joyful years. What we mean →

What telomeres are

Our DNA is packed into 46 long strands, the chromosomes. At both ends of each one sits a cap called a telomere: a short piece of DNA repeated thousands of times, which protects the rest from fraying, a little like the plastic tip on a shoelace. In 2009, three scientists received the Nobel Prize for discovering how telomeres, and telomerase, the enzyme that can rebuild them, protect our chromosomes.

Infographic: three chromosomes drawn as bars with orange caps that get shorter, from a young cell, to a cell after many divisions, to a cell that stops dividing; four numbers: 2009, the Nobel Prize for how telomeres and telomerase protect chromosomes; 40 to 60 divisions before an ordinary human cell in a dish stops; 54% higher risk of coronary heart disease with the shortest telomeres; 24% longer median life in mice given a telomerase gene therapy, not yet shown in people.
Telomeres in four numbers — a Live Beyond infographic from the Nobel Prize 2009, Leonard Hayflick's work on cell division, a review of 24 heart studies (BMJ 2014) and the telomerase study in mice (EMBO Molecular Medicine 2012).

Why they get shorter

In London, in July 2024, Patrick Sewell, a doctor who works on gene therapy, explained it to us as a story about a cell:

Patrick Sewell in a light blue shirt, gesturing as he speaks, with a piano behind him.
Patrick E. Sewell in London, July 2024 — a Live Beyond interview with Marek Piotrowski on gene therapy and telomeres.
“And telomerase is an enzyme which lengthens telomeres on cells. […] going through that process shaves a little bit of the telomere off every time. […] I’m gonna quit doubling. I’m just gonna sit here, and I’m gonna wait till I die.”
Patrick Sewell · regenerative medicine and gene therapy doctor · London, July 2024

In plain words: Each time a cell divides, it can’t copy the very end of its chromosomes, so the telomeres get a little shorter. When they become too short, the cell stops dividing and becomes a senescent, “retired” cell. In most of our body, telomerase is switched off, so the shortening adds up over a lifetime.

A limit on cell division

In the 1960s, Leonard Hayflick showed that ordinary human cells in a dish divide only a limited number of times, roughly 40 to 60, before they stop. Shortening telomeres turned out to be one of the main reasons.

Based on: Laboratory studies [5]

Words worth knowing

Three words behind the caps

From our glossary. Tap a card to turn it over: the science on the back, and the people we met who explained it to us.

No. 44 / 66Inside the body

Telomeres

The plastic tips on a shoelace. When they fray past a point, the cell retires.

Hallmark 02Telomere attrition
No. 44 / 66Inside the body

Telomeres

What helps

Length is mostly inherited, and lengthening it on purpose is not something to chase — the same machinery is what cancers exploit. What is well supported: sleep, exercise, not smoking, and lower chronic stress track with slower shortening. Be sceptical of anything sold as a telomere lengthener.

It came up most in our conversations with: Liz Parrish, Patrick Sewell, Vadim Gladyshev

See it in the 12 hallmarks of ageing →
No. 45 / 66Inside the body

Telomerase

Telomerase is the enzyme that puts length back on the ends of our chromosomes.

Hallmark 02Telomere attrition
No. 45 / 66Inside the body

Telomerase

Most adult cells keep it switched off; stem cells keep it on.

What helps

Nothing you can buy switches it on safely: most cancers use the same machinery to keep dividing, which is why it is watched so closely. What is well supported is slowing the wear — sleep, exercise, not smoking and lower chronic stress. As a gene therapy it is experimental. Read more →

It came up most in our conversations with: Liz Parrish, Patrick Sewell

See it in the 12 hallmarks of ageing →
No. 59 / 66Inside the body

Cellular senescence

Cells that retired but stayed in the building, complaining loudly enough to make everyone else worse at their jobs.

Hallmark 08Cellular senescence
No. 59 / 66Inside the body

Cellular senescence

What helps

Clearing them extends healthy life in mice, which is why senolytics attracted so much attention. Human trials so far have been small and the results mixed. This is a genuinely promising area that is not yet a thing you should be dosing yourself for.

It came up most in our conversations with: Boris Djordjevic, Alessandra Zonari, Carolina Reis Oliveira

See it in the 12 hallmarks of ageing →

What short telomeres are linked to

Heart disease

In a review of 24 studies with more than 43,000 people, those with the shortest telomeres in their white blood cells had about a 54% higher risk of coronary heart disease than those with the longest.

Based on: Review of observational studies [2]

But telomere length is not the clock of aging people once hoped for. At Harvard, in November 2024, Vadim Gladyshev, who studies aging across many species, told us why:

“There was so much variability, like telomeres, for example, you measure length of the telomeres, but mice, which are shorter lived, they have longer telomeres than humans, for example.”
Vadim Gladyshev · scientist who studies aging, Harvard Medical School · Boston, November 2024

In plain words: Telomere length differs a lot from person to person, and even between species, without matching how long they live. Mice live two or three years and have longer telomeres than we do. So telomeres are one piece of aging, not the whole story.

The cancer question

There is a reason our bodies keep telomerase switched off in most cells. Most cancers switch it back on, because it lets their cells divide forever. Liz Parrish, who took a telomerase gene therapy herself in 2015, knew that worry well:

“Because I was the first person to take telomerase reverse transcriptase, that’s a gene that lengthens the caps at the ends of the chromosomes, but there’s worry that that gene is also associated with cancer.”
Liz Parrish · founder of BioViva · Dublin, August 2023

Longer is not always better

A large genetic study looked at people born with variants that give them naturally longer telomeres. They had a lower risk of coronary heart disease and of three other conditions (a swelling of the main artery in the belly, celiac disease and a scarring lung disease), but a higher risk of several cancers, including melanoma, lung adenocarcinoma, glioma and kidney cancer.

Based on: Genetic (Mendelian randomization) study [4]

Patrick Sewell has a different view: he thinks well-protected chromosomes may actually be less likely to turn cancerous. He was honest about where that view stands:

“I can’t prove that yet, but that’s my theory.”
Patrick Sewell · regenerative medicine and gene therapy doctor · London, July 2024

In plain words: Scientists don’t agree yet. Short telomeres seem to raise some risks, long telomeres raise others. That is why any therapy that lengthens telomeres has to be tested for years, with cancer watched very carefully.

Telomere tests

What a test measures

Commercial tests usually measure the average telomere length in white blood cells. Results vary with the lab method and between labs: when ten laboratories measured the same samples, their absolute numbers differed widely, and even in one lab the same sample gives somewhat different numbers from run to run. A single result says little about your own future health.

Based on: Comparison of ten laboratories [6]

Before you pay for a test

Ask how the lab measures, how precise the result is, and what you would do differently with the number. If the honest answer is “nothing”, the money may be better spent elsewhere. Aging clocks look at many markers at once instead of one: biological age and aging clocks.

Telomerase gene therapy

In mice

In 2012, scientists in Madrid gave one- and two-year-old mice a gene therapy carrying telomerase. The treated mice lived longer, 24% and 13% at the median, stayed healthier on several measures, and did not develop more cancer.

Based on: Study in mice [3]

Liz Parrish didn’t want to wait for human trials. In Dublin, in August 2023, she told us how it began:

“When we first did the first gene therapy that I took, I took two different genes. One was called telomerase reverse transcriptase that lengthens the caps at the ends of your chromosome, and the other one is called follistatin […] And at that point, that was 2015, we were super excited. […] It was vastly held that telomerase reverse transcriptase might reverse all of aging itself.”
Liz Parrish · founder of BioViva · Dublin, August 2023
“Then five years later in 2020, I took four gene therapies, repeating the first two and then adding PGC-1alpha and klotho […] And I think that it showed us the complexity of the problem.”
Liz Parrish · founder of BioViva · Dublin, August 2023

In plain words: Liz says she was the first person to take a gene therapy aimed at aging, and she did it in public, on herself. The results she has shared are her own measurements, not a clinical trial. Her biggest lesson, in her own words, is that aging is more complex than one gene.

What is not known in people

No clinical trial has yet shown that a telomerase gene therapy is safe and makes people live longer or healthier. Treatments offered outside trials are experimental. More on gene therapy for longevity.

What everyday life does

Lifestyle and telomeres

In a small five-year study of men with early prostate cancer, the ten who chose to follow a program of plant-based food, moderate exercise, stress management and social support had longer telomeres on average at the end, while in the 25 men without the program they got shorter on average. The study was small and not randomized, so it is a hopeful sign, not a proof.

Based on: Small pilot study [7]

The same habits protect the heart, the brain and the muscles, so even if telomeres were not part of the story, they would be worth it. Our pages on walking, sleep, stress and strength training show how simple they can be.

Before you try anything

Where the joy is

Walking with Liz through the forest near Seattle, I felt what I love most about this field: people brave enough to go first, and scientists honest enough to say “we don’t know yet”. Telomeres taught us both lessons.

And the joy is that the best-proven way to care for every cell in your body costs nothing: move, sleep, eat real food and spend time with the people you love. Your telomeres will be grateful too. Caring for your cells is caring for your healthspan, the years you live healthy and active, and that is longevity. What we mean by longevity.

Telomeres on the Longevity Map

Longevity BasicsMovement, sleep, real food, managing stress and good relationships: the everyday habits linked to healthier telomeres, and to almost everything else.Biohacking UpgradesTelomere tests sit here: interesting to some, but too imprecise to guide your life.Radical Life ExtensionTelomerase gene therapy belongs here: promising in mice, tried by brave pioneers, still unproven in people.

Not medical advice, and not a recommendation for or against any test or therapy. We describe what the studies say and what the people we met told us.

This is not medical advice.

This page shares experiences from our quest and what scientists told us. Telomerase gene therapy is experimental and not approved anywhere as a treatment for aging; telomere tests are not a diagnosis. Every body is different: what works for one person may not work the same way for another.

Never start, stop or change any medicine, peptide, supplement or treatment without your own doctor, who knows your health and can check your blood work. In an emergency, call your local emergency number.

Sources

Every number on this page, by the number in square brackets. Quotations come from Live Beyond’s own recorded interviews, cleaned only of “um” and “uh”. Not medical advice. Talk to your doctor before you change anything.

  1. The Nobel Prize in Physiology or Medicine 2009: Elizabeth H. Blackburn, Carol W. Greider, Jack W. Szostak, “for the discovery of how chromosomes are protected by telomeres and the enzyme telomerase”. NobelPrize.org.
  2. Haycock PC, Heydon EE, Kaptoge S, et al. Leucocyte telomere length and risk of cardiovascular disease: systematic review and meta-analysis. BMJ. 2014;349:g4227. doi:10.1136/bmj.g4227
  3. Bernardes de Jesus B, Vera E, Schneeberger K, et al. Telomerase gene therapy in adult and old mice delays aging and increases longevity without increasing cancer. EMBO Mol Med. 2012;4(8):691-704. doi:10.1002/emmm.201200245
  4. Telomeres Mendelian Randomization Collaboration; Haycock PC, Burgess S, Nounu A, et al. Association between telomere length and risk of cancer and non-neoplastic diseases: a Mendelian randomization study. JAMA Oncol. 2017;3(5):636-651. doi:10.1001/jamaoncol.2016.5945
  5. Hayflick L. The limited in vitro lifetime of human diploid cell strains. Exp Cell Res. 1965;37:614-636.
  6. Martin-Ruiz CM, Baird D, Roger L, et al. Reproducibility of telomere length assessment: an international collaborative study. Int J Epidemiol. 2015;44(5):1673-1683. doi:10.1093/ije/dyu191
  7. Ornish D, Lin J, Chan JM, et al. Effect of comprehensive lifestyle changes on telomerase activity and telomere length in men with biopsy-proven low-risk prostate cancer: 5-year follow-up of a descriptive pilot study. Lancet Oncol. 2013;14(11):1112-1120. doi:10.1016/S1470-2045(13)70366-8