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Telomeres - The fountain of longevity?

Telomeres are a specific structure located at the end of DNA chromosomes. They protect DNA from degradation and fusion or entanglement with each other.

Every time a cell in the body is replicated (creates a copy of itself), telomeres undergo erosion (shortening). We can think of telomeres as shoelaces on our shoes. Every time we need to adjust the shoe, we need to untie the laces first and tie them back. And every time we do that, the laces get a tiny little bit more fragile.

Human cells are replicating all the time. This process ensures the functionality of a tissues (because all tissues are made of cells) and serves as a replacement for older, dying or damaged cells. Some cells such as bone cells, joint cells or nervous system cells have a slow and low level of replication. Other cells such as skin cells and cells of the digestive tract undergo more frequent replication because they are exposed to more mechanical friction and pressure.


Whenever a cell replicates, the DNA structure is opened (unwrapped) and copied onto a messenger protein called mRNA (this process is called Transcription, see picture below). Every single protein in the body is coded by mRNA, which copies particular information from the DNA of a cell. Imagine in the old days, when films were not digital but tied around these huge coils presenting pictures one after another at such a speed that a continuous stream was created. If you wanted to find a specific picture, you would have to keep uncoiling the whole thing until you found that specific shot.

DNA replication by mRNA works the same way. DNA opens up and keeps unwrapping until a particular section is found. Whenever the body requires a new molecule (for example serotonin) it needs to go back to the base DNA, find the particular section (blueprint), copy it on mRNA and send it to another unit called Ribosome (see picture), where the process of building a new molecule starts. It is much more complicated than that, but this is as far as we go.

Every time a DNA is opened in this way, the telomere at the end of the chromosome gets shortened (wear & tear from constant usage), and over decades, it shrinks to the point that the cell can no longer replicate – this is how ageing happens. Loss of the ability to replicate means tissues starts shrinking and become more vulnerable, unable to repair themselves. (e.g. wrinkles caused by gradual loss of skin elasticity and self-maintenance ability caused by loss of skin cells to telomere attrition).

However, telomeres can sometimes regain some size by a work of 2 enzymes hTERT (human Telomerase Reverse Transcriptase) and of hTERC (human Telomerase RNA Component). You may think, “awesome, so the more of these enzymes I have, the longer I’ll live”. Well, technically, yes and no. Can you guess which cells have the highest activity of hTER & hTERC enzymes? …Cancer cells. This is (among other reasons) why they can just replicate endlessly. Somehow they have hijacked this biological process in their favour and are replicating without the loss of telomere length obstructing other cells and forming tumours. As to why this is happening, billions of research dollars are being invested in finding out. A healthy cell should have a natural balance between natural telomere shortening with age and elongation without either action becoming excessively dominant.



In rare genetic disorders, some individuals are born with shorter telomeres or are predisposed to more rapid telomere shortening . Telomeres also naturally shorten with ageing, and this is something that cannot be stopped. Accelerated shortening of telomeres has been seen in people with cardiovascular disease, stroke, diabetes, osteoporosis (bone loss), psychiatry disorders and obesity.

Telomere shortening may be caused by exposure to certain chemicals, heavy metals and excessive exposure to molecules called free radicals in process called oxidative stress. [Oxidative stress is caused when the amount of free radicals exceeds the body’s ability to cope with them, and they start causing damage. Free radicals can come from the environment (e.g. toxins and pollutants), from the diet (e.g. fried food, burned food, oxidised fats) and from internal processes and metabolic functions. The body uses antioxidants to get rid of free radicals, but in this process, antioxidants are depleted and need to be recharged (for example, glutathione) or re-consumed (for example, vitamin C or selenium)]

Overall, the individuals with the shortest telomeres have a higher incidence of premature mortality. It has also been found that patients who sought medical advice for infertility had significantly shortened telomeres. It is hard to say whether this was the cause of infertility or a consequence of something else going on in the body such as systemic inflammation. A worrying factor is that the shorter the telomeres become, the more “unstable” DNA molecules become as well, and there is a greater chance of genomic instability, which may lead to mutations and cancer.


Smoking accelerates telomere shortening at a dose-dependent rate. The more, the worse it is. In fact, telomere length can be a reasonably reliable indicator of how much damage smoking is causing to the body and how depleted antioxidants in the body have become.

Both current and past smokers have statistically shorter telomere lengths compared to non-smokers when observed in research. A year of smoking can induce up to 10% in single telomere shortening. Naturally, some of that will be repaired by the two enzymes (hTER & hTERC), but perhaps that is why smokers often appear aged and wrinkled – a gradual loss of cellular integrity through loss of function to repair and replicate.

Likewise regular consumption of alcohol may increase the speed of cellular ageing and telomere degradation because alcohol is a systemic toxin. Alcohol increases oxidative damage in the body (↑ production of free radicals, see above).


A study on 1122 women found that those with the highest BMI had the most profound telomere shortening. Obese people often have low levels of a hormone called leptin that induces a feeling of satiety and high levels of another hormone called ghrelin that induces hunger. In fact, there is often a state called “leptin resistance” where the brain is unable to “hear” the chemical signal that says, “I’ve had enough, stop eating NOW!”

In summary, those with the lowest levels of leptin and those with the highest BMI (body-mass index) had the most accelerated telomere shortening. In addition, obese people usually have an increased rate of systemic inflammation which leads to the formation of previously mentioned free radicals. Free radicals have been shown to damage DNA molecules and accelerate telomere shortening and ageing.


We don’t have a lot of research on this, but it appears toxins & common pollutants may indeed accelerate telomere shortening. Theoretically, it makes a lot of sense. Chemicals such as pesticides, herbicides, environmental pollutants, heavy metals, food chemicals etc. increase oxidative stress in the body and this raises the production of free radicals. As mentioned previously, we know with pretty good certainty that free radicals are one of the main causes of rapid telomere shortening

The following environmental pollutants have been associated with the increased rate of telomere shortening in a small amount of human studies.

  • Heavy metals - lead, arsenic, cobalt, cadmium and mercury. People with higher content of heavy metals in urine & tissues have consistently been found with shorter telomeres and reduced ability to repair them.

  • Polycyclic Aromatic Hydrocarbons (PAH)– produced during grilling, flaming and barbecuing of animal food but also by the process of coal and wood burning. Burned food is exceptionally high in PAHs and should never be eaten. Vehicular emissions, especially from diesel engines, are a significant source and people living in large crowded cities have an increased urine content of PAHs. Living in proximity of mine, fracking station, highway, or a very busy road also raises PAH levels in the body. Smoking of tobacco and marihuana also exposes people to PAHs from tar.

  • Persistent Organic Pollutants (POP)

  • > Polychlorinated biphenyls (PCB) – found in farmed salmon (nearly 15times more than in wild Alaskan salmon), can be found in meat, especially the more fatty ones as PBs tend to stick to fat tissue. In the USA, from 1979 the use of PCBs in a variety of electronics is banned; however, older electronic equipment, paints, oils, hydraulic fluids, floor tiles etc. may still be contaminated.

  • > Polybrominated diphenyl ethers (PBDE) – found in flame retardants, household dust (chemicals from outside often stick to household dust when brought inside home) fish (highest in sardines and farmed salmon), meat, dairy. Content in meat and dairy is very diversified across the world and in some countries may be a hundredfold of what it would be in another country.

  • > Organochlorine pesticides – primary sources being meat, fish, dairy and some heavily sprayed vegetables but mostly in animal products as they also hang around in fat tissue.

The best advice, in this case, is to spend some time and effort to familiarise yourself with the most common pollutants in food, air and water and do your best to protect yourself. Because some of my readers come from different continents, I am not able to provide general advice; however, I intend to look into toxins, heavy metals and systemic detoxification more in the future, so stay tuned for those future articles.


While we have a lot of research looking at the relationship between diet & telomere shortening, the results of these studies are very inconsistent. It appears the Mediterranean diet showed the most promising results.

A large Korean cohort study following a group of people for 10 years found that those with the greatest adherence to what resembled the Mediterranean diet had the longest telomeres on average. However, in other observational studies, this effect was not replicated, and many have not shown any difference between the Mediterranean and other, more western diets.

Despite the inconsistency in research outcomes, we know that the Mediterranean type of diet has a huge amount of research showing beneficial effects for heart health, cancer and inflammation, and we also know that inflammation is in the core of accelerated telomere shortening, so it is safe to claim that despite lack of scientific evidence, adhering to a mostly whole-food, plant-based diet with small amount of fish, dairy and eggs (not necessary) will be fairly protective for our health including telomere length.


Unfortunately no. This is still an unanswered question, and I will leave you with the conclusion of one study that summarised it nicely:

"Is Telomere Length (TL) a biomarker of aging? Coronary artery disease? Breast cancer?”..are the common questions that scientists tried to answer. Despite all hard work, so far, TL has not fulfilled all of the conditions for being considered as a “biomarker” for diagnostics of disease conditions or in predicting the “biological age” of individual. The reasons for this are many individual factors that are influencing TL and are preventing the identification of a clear casual relation between condition itself and telomeres. TL should not be tested as a biomarker of the single disease condition, but as a general state of organism that reveals potential susceptibility for all-disease risk" (Gorenjak et al. 2018)


  • Telomeres are a protein structure at the end of our chromosomes (clusters of DNA) which protect the DNA from damage, degradation and end-to-end fusion.

  • Every time a cell replicates, the telomere is shortened. Once the full length of the telomere is lost, the cell stops replicating, and the tissue starts degrading.

  • Increased rate of telomere shortening has been associated with many diseases such as cardiovascular disease, dementia, cancer and psychiatric disorders

  • Smoking, obesity, inflammation and many environmental toxins & pollutants may accelerate the rate of telomere degradation.

  • Avoidance of known toxins where possible, reducing excessive consumption of alcohol, meat, farmed fish and tobacco/marihuana smoking is a good practice for toxin exposure reduction. I will release more content on toxin awareness and avoidance in the future.

  • In terms of diet and telomere length preservation, the studies are very inconsistent, but it seems the diet based around a more whole-food Mediterranean type made of primarily plants with small amounts of fish, dairy & eggs (unless eating a vegan diet) is helpful and protective.

DISCLAIMER: Nothing in this article is to be mistaken for a medical advice


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Cinegaglia, N. et al. (2019) ‘Shortening telomere is associated with subclinical atherosclerosis biomarker in omnivorous but not in vegetarian healthy men’, Aging, 11(14), pp. 5070–5080.

Cong, Y.-S., Wright, W. E. and Shay, J. W. (2002) ‘Human Telomerase and Its Regulation’, Microbiology and Molecular Biology Reviews, 66(3), pp. 407–425.

Furukawa, S. et al. (2004) ‘Increased oxidative stress in obesity and its impact on metabolic syndrome’, Journal of Clinical Investigation, 114(12), pp. 1752–1761.

Gorenjak, V. et al. (2018) ‘The future of telomere length in personalised medicine’, Frontiers in Bioscience - Landmark, 23(9), pp. 1628–1654.

Gu, Y. et al. (2015) ‘Mediterranean diet and leukocyte telomere length in a multi-ethnic elderly population’, Age, 37(2).

Lee, J. Y. et al. (2015) ‘Association between dietary patterns in the remote past and telomere length’, European Journal of Clinical Nutrition, 69(9), pp. 1048–1052.

Liu, J. et al. (2019) ‘Replicative and Chronological Ageing’, Cells, pp. 1–10.

Louzon, M. et al. (2019) ‘Telomere dynamic in humans and animals: Review and perspectives in environmental toxicology’, Environment International, 131

Pérez, L. M. et al. (2018) ‘Effects of diet on telomere length: Systematic review and meta-analysis’, Public Health Genomics, 20(5), pp. 286–292.

Rafie, N. et al. (2017) ‘Dietary patterns, food groups and telomere length: A systematic review of current studies’, European Journal of Clinical Nutrition, 71(2), pp. 151–158.

De Rooij, S. R. et al. (2015) ‘Prenatal undernutrition and leukocyte telomere length in late adulthood: The Dutch famine birth cohort study1’, American Journal of Clinical Nutrition, 102(3), pp. 655–660.

Valdes, A. M. et al. (2005) ‘Obesity, cigarette smoking, and telomere length in women’, Lancet, 366 (9486), pp. 662–664.

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