“It can actually reverse aging and age-related diseases.” — Telomir Pharmaceuticals Co-Founder Frank O’Donnell
“Telomir Pharmaceuticals Co-Founder Frank O’Donnell joined Steve Darling from Proactive to share what the company believe is groundbreaking potential of their new drug designed to extend telomeres, which could reverse aging and age-related diseases. During a recent interview, O’Donnell elaborated on the drug’s potential, supported by extensive research in mice and successful trials in larger animals like a German shepherd.” […]
”The shortening of telomeres is one of the primary causes of aging, and the action of telomerase is a way to prevent it.” — María Blasco, Director of CNIO and researcher.
I’m not convinced that telomeres are the limiting factor for most of us in terms of lifespan… but its interesting to follow the work. I hope they do some lifespan studies on model organisms to validate their approach.
Studies show Gotu Kola extract (centella asiatica) to be a potent activator of telomerase:
A meta-analysis of published data noted that it has substantial anti-aging effect on the skin, and is a possible candidate for replacing tretinoin:
“From the reported data, it is possible to conclude that C. asiatica improved lip and periocular wrinkles, and may replace retinoids if its long-term safety is established and C. asiatica is standardized.”
Is the are based on that other things will break down / go bad first? What if/when other longevity pillars start working so that we can start living to 120 or longer, would telomeres kick in an be a remaining bottleneck then in your framework?
Trying to visualize where the field of longevity research needs to go for these long, long lives behind helping us go from 78-80s to 90s or so.
I’m not sure what the critical path items are in terms of longevity… I’ve just seen a lot of discussions on telomeres over the past 15 years and not much in the way of mouse or other model organism studies that would demonstrate significant lifespan improvement with longer telomeres.
From an editorial last year:
There are many important questions remaining to address telomere length and species lifespans. For example, how can one explain the large variation in mouse species telomere lengths, and the lack of large variation in the lifespan of those species? For example, the Mus musculus castaneus mouse species has a telomere length of 18–20 kb (Hemann and Greider, 2000), and yet the lifespan of Mus musculus castaneous (≈681 days (Hemann and Greider, 2000)) is similar to the lifespan of other mouse species such as C57BL/6J (≈767 days (Hemann and Greider, 2000)) which can have telomere lengths of 40–50 kb (Zijlmans et al., 1997; Hemann and Greider, 2000; Vera et al., 2012; Varela et al., 2016). A thorough investigation comparing initial telomere length, telomere shortening rate, percentage of short telomeres, the length of the shortest telomeres, and other aging markers such as DNA methylation may provide insights. Another caveat is that telomeres are often measured from circulating lymphocytes in the blood, which may not be the best cell type for these measurements (Fossel, 2012). Additional Research Topics of interest are more thorough investigations of outlier species which have much longer lifespans than expected such as the naked mole rat which can live 31 years (Buffenstein, 2005) compared to the mouse which lives about 2 years (Hemann and Greider, 2000), or the bat, which can live up to 37 years in some species (de Magalhães et al., 2007) even though a bat is about the same size as a mouse. Overall, a complete understanding of telomere dynamics and species lifespan requires further studies and discoveries.
Very little of anything of what I’ve seen in general or above is in context of what happens to an otherwise maximally longevity enhanced / optimized organism.
An analog is perhaps that most men did not have to worry about AD historically as they died of heart attack, stroke or cancer before AD processes started to manifest symptomatcally. But men that start living into their 90s and 100s will likely suffer AD to very high degrees if not solving AD risks.
Similarly it seems that at some point telomere shortening/ “hayflick limits” would mechanistically just have to start to kick in as a longevity bottleneck if not fixed as we succeed in living longer in other ways if nothing is done to avoid them shortening out.
