Less Inflammation, Longer Telomeres in Centenarian Offspring

Researchers have in the past demonstrated that the children of very long-lived individuals tend to themselves have greater longevity. Thus is isn't surprising to see evidence of better measures of health as well, such as in thus study where the offspring of centenarians have less inflammation and longer telomeres. Aging is a process of accumulating damage to cells and tissues, and both chronic inflammation and telomere shortening are largely or completely a reflection of that damage and its direct consequences, and in turn go on cause their own further consequences. Rising levels of inflammation, for example, are in part caused by immune system dysfunction and the effects of cross-link forming advanced glycation end-products on cell activities.

"Centenarians and supercentenarians are different - put simply, they age slower. They can ward off diseases for much longer than the general population." In groups of people aged 105 and over (semi-supercentenarians), those 100 to 104 (centenarians), those nearly 100 and their offspring, the team measured a number of health markers which they believe contribute towards successful ageing, including blood cell numbers, metabolism, liver and kidney function, inflammation and telomere length.

Scientists expected to see a continuous shortening of telomeres with age, however what they found was that the children of centenarians, who have a good chance of becoming centenarians themselves, maintained their telomeres at a 'youthful' level corresponding to about 60 years of age even when they became 80 or older. "Our data reveals that once you're really old, telomere length does not predict further successful ageing. However, it does show that those who have a good chance to become centenarians and those older than 100 maintain their telomeres better than the general population, which suggests that keeping telomeres long may be necessary or at least helpful to reach extreme old age."

Centenarian offspring maintained lower levels of markers for chronic inflammation. These levels increased in everybody with age including centenarians and older, but those who were successful in keeping them low had the best chance to maintain good cognition, independence and stay alive for longer. "It has long been known that chronic inflammation is associated with the ageing process in younger, more 'normal' populations, but it's only very recently we could mechanistically prove that inflammation actually causes accelerated ageing in mice. "This study, showing for the first time that inflammation levels predict successful ageing even in the extreme old, makes a strong case to assume that chronic inflammation drives human ageing too. Our study showed that over a wide age range, including unprecedentedly large numbers of the extremely old, inflammation is an important driver of ageing that might be something we can develop a pharmacological treatment for. Accordingly, designing novel, safe anti-inflammatory or immune-modulating medication has major potential to improve healthy lifespan."

I think that there are some cart and horse issues in the conclusions drawn here by the researchers involved. This is the case in much of modern medicine for age-related conditions: development focuses on addressing proximate causes and consequences of root causes rather than on the root causes themselves. It is trying to clean up the spill from a broken pipe without fixing the pipe, or trying to make an old, worn car run more effectively by being very diligent in changing the oil. Present research and development strategies result in expensive treatments that do comparatively little, and this must change if we are to see greater progress towards effective treatments for aging.

Link: http://www.ncl.ac.uk/press.office/press.release/item/scientists-crack-the-secret-of-the-centenarians


Telomere attrition leads to increasingly poorer gene expression and is also a driver of NF-KB inflammation in age. It makes sense to maintain telomeres (and thus youthful gene expression profiles in stem cells) in order to reduce this issue and to maintain repair and regenerative systems.

Telomeres do not cause aging (though TPE mediated changes to gene expression contribute to aging) but they are a suitable intervention point. DNA double strand breaks, stem cell mobilization, greatly improved gene expression profile and other benefits come from rejuvenated telomeres. Fix them and see what else is left to repair. We will see soon enough anyway.

Posted by: Steve H at August 11th, 2015 8:29 AM

@Steve H - given Telomere lengthening is implicated in cancer, wouldn't it be simpler and quicker to simply go after the proposed seven classes of damage proposed by the SENS foundation?

Posted by: Jim at August 11th, 2015 4:28 PM

Jim the Cancer argument is unfounded and various papers have shown lengthening telomeres to optimum (not just making them really long) in fact offers a level of cancer protection due to improved cellular stability. The whole cancer link was started back in the 2000s and in fact some of the very people who suggested the risk eg, Maria Blasco have since then revised their position on the matter.

Yes Cancer does hijack telomerase and lengthens the telomeres (we see this in lung cancer where telomeres become very long, beyond their normal length) but telomerase as correctly asserted by Cal Harley is not an oncogene nor have we seen an increase in cancer incidence when it is transiently activated making it a viable way to regenerate cells and tissue.

Sure it is not quite SENS (not the only game in town) and it beats playing about with dozens of pathways further downstream. It also fixes some of damage types eg, double strand breaks, some data to suggest it helps ECM too and it helps stabilize the genome as well as mobilizes the stem cells to boost regeneration. Mobilized stem cells as demonstrated by Conboy are almost as good as young cells too.

Use it and see what else is left to fix, got to be worth trying it just in case it simplifies the damage that SENS needs to repair. It is also something we can do right now via AAV transient delivery too.

Posted by: Steve H at August 12th, 2015 6:52 AM

It makes you wonder if a drug going to be discovered that will enable radical life extension, but it will also cause eventual cancer at the same time. A couple of decades from now I think we will have ways to cure or at lease live with cancer for a long time without it ever becoming fatal. Maybe in the future a person could be 150 years old and also have seven different types of cancer occurring in their body, but all are manageable. Some might say that the FDA would never approve a drug that causes cancer, but 30 years from now we might accept that trade-off.

Posted by: Deleo77 at August 12th, 2015 8:34 PM

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