Telomeres are repeating DNA caps that protect the ends of your chromosomes and shorten each time a cell divides. Short telomeres track with ageing and disease. But genetics shows the relationship runs both ways: inheriting longer telomeres lowers heart disease risk and raises the risk of several cancers. There is no length to aim for.
What are telomeres?
Every chromosome is a long double strand of DNA with two ends, and an end is a problem. The repair machinery in a cell is built to recognise a broken DNA end and stick it back to something. Left unmarked, the natural ends of your chromosomes would be fused together, which is catastrophic. That machinery is not free either: the PARP enzymes that repair broken DNA consume NAD+ every time they work, which is part of why the coenzyme ended up in ageing research at all.
The solution is a telomere: several thousand base pairs of the same six letter sequence, TTAGGG, repeated over and over, wrapped in a six protein complex called shelterin and tucked into a lasso shaped structure known as the t-loop. The repeats carry no gene. Their entire function is to be recognised as a chromosome end rather than as damage.
They also solve a second problem. DNA polymerase, the enzyme that copies DNA, cannot finish the very end of one strand. Every replication therefore loses a small stretch. Because that stretch is telomere, no genetic information is lost. It is a buffer, and it is consumed. This is the end replication problem, and it is why telomere shortening happens whether or not you look after yourself.
When telomeres in a cell get short enough, shelterin can no longer hide the end. The cell reads it as damage and stops dividing permanently, a state called replicative senescence. Leonard Hayflick showed in 1961 that cultured human fibroblasts divide roughly 50 times and then stop, a ceiling that still carries his name. Telomeres are its molecular clock.
Telomerase, and why most of your cells switch it off
Telomerase is the enzyme that rebuilds telomeres. It carries its own RNA template and adds TTAGGG repeats back onto the end. Elizabeth Blackburn, Carol Greider and Jack Szostak shared the 2009 Nobel Prize in Physiology or Medicine for working this out. Greider and Blackburn found the enzyme in 1984, in a pond dwelling single celled organism called Tetrahymena, so 25 years passed between the discovery and the prize.
Here is the part that gets skipped. If telomerase can undo the clock, why do your cells not run it? Because a cell that can divide indefinitely is the definition of the problem. Telomerase stays active in germ cells, stem cells and some immune cells, and is silenced almost everywhere else. Telomere shortening is not a design flaw. It is a brake on runaway division, and the great majority of human cancers work by releasing it, reactivating telomerase so the tumour cells become effectively immortal.
Any product promising to activate your telomerase is proposing to release that brake across your whole body. That is a serious proposition, and it deserves to be stated rather than sold as a wellness feature.
What destroys telomeres?
Age is the largest single factor and the one you cannot negotiate. On top of that sits everything that raises the rate of cell turnover or the local oxidative load, because the guanine rich telomere sequence is unusually vulnerable to oxidative damage.
- Smoking. The most consistently reproduced lifestyle association in the literature.
- Obesity and visceral fat, through chronic low grade inflammation and higher immune cell turnover.
- Chronic psychological stress, particularly long running caregiving stress, in the work that first linked the two fields.
- Chronic infection and inflammatory disease, for the same reason: white blood cells that divide more, more often.
- Air pollution and heavy alcohol, with weaker and less consistent data.
Blackburn, Epel and Lin summarised the state of this field in Science in 2015. Their framing is worth keeping: telomere maintenance is set partly by genetics and partly by non genetic influences accumulated across a whole life, and the two interact. It is a cumulative record, not a dial.
The inflammation route is the one most people can act on, and it is the same terrain as joint and tendon problems. If that is why you are reading, a formulation aimed at the inflammatory background belongs in a conversation about symptoms rather than in a conversation about chromosome ends.
Why longer telomeres are not a target
Observational studies show short telomeres alongside disease. The obvious reading is that shortening causes the disease. The obvious reading may also be backwards, because being ill makes cells divide more.
Mendelian randomisation settles the direction. You inherit variants that set your telomere length at birth, before any illness, so comparing people by those variants gives you a natural experiment. The Telomeres Mendelian Randomization Collaboration, led by Haycock, did exactly that in JAMA Oncology in 2017, pooling 420 081 cases and 1 093 105 controls across 35 cancers and 48 non-neoplastic diseases. The typical disease in that set contributed 2 526 cases, so this is not one large study but 83 of them read together.
The result is not the one the anti-ageing market expects. Genetically longer telomeres were associated with a higher risk of many site specific cancers, and the effects were large.
RISK PER STANDARD DEVIATION OF GENETICALLY LONGER TELOMERES
The associations were stronger for rarer cancers and at tissue sites with lower rates of stem cell division. For most psychiatric, autoimmune, inflammatory and diabetic conditions there was little evidence of any association at all. Blackburn and colleagues had already put the same point more carefully: genetically caused variation in telomere maintenance raises or lowers cancer risk in a highly cancer type specific way.
ONE TRAIT, TWO DIRECTIONS
What longer telomeres buy you
- Lower coronary heart disease risk, odds ratio 0.78.
- Lower abdominal aortic aneurysm risk, odds ratio 0.63.
- At 40, longer than average leukocyte telomeres track with more years of life.
What they cost
- Glioma risk more than five times higher per standard deviation.
- Lung adenocarcinoma more than three times higher.
- Melanoma, bladder, kidney, testicular and endometrial cancer all raised.
What UK Biobank added
The largest single analysis of telomere length in people is British. Codd and colleagues at Leicester measured leukocyte telomere length in 472 174 participants of UK Biobank and published the result in Nature Genetics in 2021. They identified 197 independent sentinel variants at 138 genomic loci, 108 of which were new, and linked genetically determined telomere length to traits ranging from height to bone marrow function and to diseases across cancer, vascular and inflammatory categories.
of lower life expectancy at age 40 for people whose leukocyte telomere length is more than one standard deviation below the population mean, compared with those more than one standard deviation above it.
Codd et al., Nature Genetics, 2021, UK Biobank, 472 174 participants
Two and a half years is real and it is modest. Put next to the cancer findings, it describes a trade-off rather than a target. And note what the figure is: a population average across a genetically defined group, not a prediction for an individual. Nothing in that paper supports measuring your own telomeres and drawing a conclusion from the number. It is the same limitation every biological age estimate runs into: informative across a population, too noisy on one person, with different clocks disagreeing about the same blood sample by several years.
Can food lengthen your telomeres?
The best evidence for a dietary pattern comes from the Nurses’ Health Study. Crous-Bou and colleagues published it in the BMJ in 2014, using 4 676 women free of disease who had both a measured leukocyte telomere length and a completed food frequency questionnaire, drawn from a cohort of 121 700 nurses enrolled in 1976. Greater adherence to the Mediterranean diet was associated with longer telomeres after adjustment for confounders.
Now the size. The least squares mean telomere length z score was -0.038 in the lowest adherence group and 0.072 in the highest, with a P value for trend of 0.004. That gap is about a tenth of a standard deviation. It is a real, statistically solid, biologically small difference, measured in an observational cohort, in women, mostly nurses, in the United States. It is not evidence that changing your diet lengthens your telomeres, because nobody randomised anyone.
No single food does anything measurable here. The pattern is the unit: vegetables, fruit, pulses, nuts, whole grains, fish, olive oil in place of butter, and not much red or processed meat. It is also the wholegrain and pulse heavy pattern behind the mortality gap in the Bruneck spermidine cohort, where the molecule and the diet it arrives in could not be separated. That is also, and not by coincidence, the pattern behind most of the cardiovascular evidence.
Does lifestyle activate telomerase? What the five year follow-up showed
One study is quoted more than any other on this question, usually at second hand and usually wrongly. In 2008 Dean Ornish and colleagues reported that three months of intensive lifestyle change was associated with increased telomerase activity in immune cells. That single finding became the foundation of an entire genre of writing about foods that switch on telomerase.
The same group followed the participants for five years and published the result in The Lancet Oncology in 2013. Read it carefully, because it says the opposite of what the genre claims.
| Measured at 5 years | Lifestyle group (n = 10) | Controls (n = 25) | Result |
|---|---|---|---|
| Relative telomere length | +0.06 T/S units | -0.03 T/S units | Difference p = 0.03 |
| Telomerase activity | -0.25 units | -1.08 units | p = 0.64 |
| Telomerase and adherence | No association | RR 0.93, p = 0.57 | |
Telomerase activity fell in both groups, and the difference between them was not significant. It was not related to how well anyone stuck to the programme. What did move, modestly, was telomere length itself. So the honest summary is that a comprehensive lifestyle change was associated with a small increase in telomere length over 5 years in 10 men with low risk prostate cancer, compared with 25 men used as external controls and not randomised, in what the authors themselves call a small pilot study calling for larger randomised trials.
There is no food that activates telomerase in a person. That claim is a misreading of a 2008 measurement that the same team could not reproduce at five years.
Telomere tests and telomerase supplements
Direct to consumer telomere tests are sold in the United Kingdom, usually as a cell age or biological age reading. The decisive study here is an international collaboration led from Newcastle and published by Martin-Ruiz and colleagues in 2014. Ten laboratories, using Southern blotting, STELA and quantitative PCR, measured the same blinded human DNA samples twice.
Rankings correlated well between laboratories, with coefficients from 0.63 to 0.99, so the methods agree about who has longer telomeres than whom. Absolute results differed so widely that they could not be compared directly. Inter-laboratory coefficients of variation averaged about 10% for Southern blotting and STELA, and more than 20% for quantitative PCR, the cheap method commercial tests use. The authors concluded that this variation severely limits data pooling and excludes any shared reference range.
No shared reference range means there is nothing to compare your number with. A telomere result from a commercial laboratory tells you where you sit in that laboratory’s own distribution on that day, and it will not match the number the laboratory next door would have produced from the same tube.
As for telomerase activating supplements, the best known is a cycloastragenol preparation derived from astragalus, published in 2011 by Harley and colleagues as part of a health maintenance programme. The authors included people associated with the company that sells it, there was no randomised placebo group, and the design mixed the compound with other interventions. Nothing in the Great Britain health claims register permits any statement about telomeres or telomerase on a food supplement.
The practical conclusion is dull and defensible. Stop smoking, keep visceral fat down, sleep, move, eat the Mediterranean pattern, and treat persistent inflammation rather than accepting it. Those things have evidence behind them for outcomes you can feel. If stiffness and joint pain are what you are actually managing, a supplement made for osteoarthritis plus a proper assessment from your GP will do more for you this year than any chromosome measurement.
Frequently asked questions
Can you improve your telomeres?
You can plausibly slow the rate at which they shorten by not smoking, keeping weight and inflammation down and staying active. Lengthening them on purpose is a different claim, and the only human study to report it involved ten men, no randomisation and a five year follow-up in which telomerase activity did not rise.
What destroys telomeres?
Cell division itself, which is unavoidable, plus anything that speeds it up or raises oxidative load. Smoking, obesity, chronic inflammation, chronic infection and long running psychological stress are the associations that reproduce most consistently across cohorts.
Do people with long telomeres look younger?
There is no reliable evidence for that. Telomere length is usually measured in white blood cells, which say little about skin. Visible ageing tracks far more closely with sun exposure and smoking, both of which also shorten telomeres, which is probably where the impression comes from.
Do longer telomeres mean a longer life?
On average, and only slightly. In UK Biobank, being more than one standard deviation below the mean at age 40 corresponded to about 2.5 fewer years of life expectancy than being more than one standard deviation above it. The same genetic data show longer telomeres raising the risk of several cancers, so it is a trade-off rather than a score.
Is a telomere test worth buying?
For a healthy adult, no. Different laboratories produce different absolute values from the same DNA, inter-laboratory variation exceeds 20% for the PCR method commercial tests use, and no shared reference range exists. There is also nothing you would do differently on the basis of the result.
Does exercise lengthen telomeres?
Physically active people tend to have longer telomeres in observational studies, and the association survives adjustment for smoking and weight in most of them. Whether exercise causes it has not been shown by a randomised trial. Train for the outcomes that are proven instead.
Does telomerase cause cancer?
Telomerase does not cause cancer on its own, but its reactivation is one of the steps most human cancers take, because a cell that cannot rebuild its telomeres eventually stops dividing. That is why the enzyme is silenced in most adult tissues, and why activating it deliberately is not a straightforwardly good idea.
Sources
Haycock P.C., Burgess S., Nounu A., et al., Telomeres Mendelian Randomization Collaboration. Association between telomere length and risk of cancer and non-neoplastic diseases: a Mendelian randomization study. JAMA Oncology, 2017. DOI: 10.1001/jamaoncol.2016.5945
Codd V., Wang Q., Allara E., et al. Polygenic basis and biomedical consequences of telomere length variation. Nature Genetics, 2021. DOI: 10.1038/s41588-021-00944-6
Ornish D., Lin J., Chan J.M., 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. The Lancet Oncology, 2013. DOI: 10.1016/S1470-2045(13)70366-8
Blackburn E.H., Epel E.S., Lin J. Human telomere biology: a contributory and interactive factor in aging, disease risks, and protection. Science, 2015. DOI: 10.1126/science.aab3389
Crous-Bou M., Fung T.T., Prescott J., et al. Mediterranean diet and telomere length in Nurses’ Health Study: population based cohort study. BMJ, 2014. DOI: 10.1136/bmj.g6674
Martin-Ruiz C.M., Baird D., Roger L., et al. Reproducibility of telomere length assessment: an international collaborative study. International Journal of Epidemiology, 2014. DOI: 10.1093/ije/dyu191
Harley C.B., Liu W., Blasco M., et al. A natural product telomerase activator as part of a health maintenance program. Rejuvenation Research, 2011. DOI: 10.1089/rej.2010.1085
This article is general information, not medical advice. No food or supplement carries an authorised health claim about telomeres in Great Britain. Speak to your GP about symptoms that persist.
