Frequently Asked Questions about Telomeres

Question 1:  Are telomeres just indicators of disease or are they causal?

First clues but inconclusive evidence:

Telomeres predict disease onset in observational studies. However, that does not mean they are causal. 

People with extremely short telomeres from having genetic mutations in their telomere or telomerase genes develop early disease and mortality.  This does not mean it applies to aging in people with normal variations in their telomere related genes

Then a smoking gun:

New studies show that people with normal variations in their telomere genes that make them longer tend are less likely to get diseases of aging (cardiovascular disease, dementia).

These types of studies, linking genetics to disease outcomes, are the most causal type of evidence we can have in humans.  They show that telomeres play a causal role in creating statistical likelihood of getting diseases earlier.  These genetic studies are something that many researchers in aging are not yet aware of.  Cutting edge experts in telomere biology are beginning to understand the complexity of telomeres in long lived humans – how telomeres play a causal role, and how short telomeres protect from cancer but promote heart disease, and vice versa.   


Question 2:  Can long telomeres or high telomerase cause cancer?

Having long telomeres, as measured (which is a combination of life experience and genetics) typically predicts protection from most types of cancer including breast cancer. (Zhang et al, 2015Ennour-Idrissi et al, 2016)

However, having one or more genes that create high telomere or long telomeres predicts greater likelihood of getting certain cancers (adult glioma, melanoma, leukemia, non-smoknig lung cancer), including during childhood (neuroblastoma, leukemia).  It seems genes for long telomeres have potent effects on cancer that can show up early in life. (Walsh et al, 2016,  Ojha et al, 2016 )


Question 3:  Do telomeres predict longevity, or just disease?

Telomeres are pretty reliable predictors of early disease onset in meta-analyses (so they predict it in most of the studies, when averaged), across most of the major diseases of aging.  In the largest study on mortality so far, in a sample of 65,000, shorter TL did predict earlier mortality. (Rode et al, 2015)

When it comes to mortality, the results are more diverse, with some studies finding effects and some not finding effects, maybe around 50/50 across studies.  However, It is not the case that longer telomeres predict earlier death, except in the case of some rare cancers.  Therefore, if half of the studies find that shorter TL predicts mortality, and the other half do not find a relationship at all, then there is likely a relationship.  

Because humans are so long lived, telomeres play a larger role in our health than in the health of most animals.  In animal species, telomeres tend to matter less, depending on the species. Rodents do not die of short telomeres (unless genetically engineered to have very short telomeres), because they start out with enormous telomeres.   In birds, telomere length early in life predicts longevity.

Time of death in humans is determined by many things besides sickness.  Regardless, It is logical that if you are sicker, you are more likely to die early.  But what we can say with confidence is that healthy telomeres predict healthspan (longer period of life without disease), which is what matters most in the end! 

Question 4:  Is sugared soda linked to shorter telomeres? 

There are now four studies, below, linking sugared soda/ sugary beverage consumption to shorter telomeres, two by Dr. Cindy Leung, a nutrition epidemiologist at UCSF.   There is one study (Nettleton et al, 2008) that does not show a relationship.  Thus, there appears to be a relationship in observational studies, and of course experimental evidence would be the way to test this causally.  We do have an experimental study ongoing.

A note on our first study on soda/telomeres, from NHANES (Leung et al, 2014):

The study showed that sugared soda was associated with shorter telomeres, after adjusting for age, race/ethnicity, and other important individual characteristics and health behaviors. However, in unadjusted analyses, it appeared that telomere length was longer with higher intakes of sugared soda. This suggests that there were several individual characteristics influencing this association and the descriptive data should not be interpreted as the real association. For example, Black race has been associated with higher soda consumption and shorter telomeres. Researchers often report both unadjusted and adjusted associations to show the magnitude of the confounding by how they differ. In this case, because the unadjusted and adjusted associations appeared very different, it was important to show them both, and to understand the adjusted association reflects the real association between sugared soda consumption and telomere length.