“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.
Insufficient telomerase activity, stemming from low telomerase reverse transcriptase (TERT) gene transcription, contributes to telomere dysfunction and aging pathologies. Besides its traditional function in telomere synthesis, TERT acts as a transcriptional co-regulator of genes pivotal in aging and age-associated diseases. Here, we report the identification of a TERT activator compound (TAC) that upregulates TERTtranscription via the MEK/ERK/AP-1 cascade. ***In primary human cells and naturally aged mice, TAC-induced elevation of TERT levels promotes telomere synthesis, blunts tissue aging hallmarks with reduced cellular senescence and inflammatory cytokines, and silences p16 *** INK4aexpression via upregulation of DNMT3B-mediated promoter hypermethylation. In the brain, TAC alleviates neuroinflammation, increases neurotrophic factors, stimulates adult neurogenesis, and preserves cognitive function without evident toxicity, including cancer risk. Together, these findings underscore TERT’s critical role in aging processes and provide preclinical proof of concept for physiological TERT activation as a strategy to mitigate multiple aging hallmarks and associated pathologies.
Telomeres lenghts have to be appreciated per species and per person
Indeed, its the only viable answer we can make to date because: ALL studies that genetically induced telomerase in mamals proved drastic lifespan extension : liz parrish, blasco…
Long telomere due a certain condition, is not the same as long telomere from a young person. So someone old that will restore his lenght via telomerase therapy, will most probably NOT face any harm and “encapsulate” error code.
My telomere length has been increasing consistently since I started with NR - Nov, 2022, I then switched to NMN In June, 2023 and it has continued to increase.
That’s a good question. I don’t know if it is statistically significant.
For now I am interested in the trend over time, in this case over 3 years. In general, as we age telomeres often get shorter. Measuring a trend over time is all I have for now
From the 2024 test;
If we were to estimate your biological age strictly from your telomere measurement, we would anticipate your age to be: 61.86
This puts you in the: 71.82st Percentile
When I go back to the 2021 test result, it is reported like this;
If we were to use the data from our sample subjects to predict your biological age from your telomere measurement we would anticipate your age to be 72.86
In a span of 3 years, going from a telomere “age” of 73 to 62, a reduction of 11 “years”, seems relevant to this 68 year old but who knows for sure
For reference, newborns have 8,000 base pairs (8 Kb), I’m currently close to 7 Kb and my wife is at 7.2 Kb and her telo “age” is 42 (chrono age of 66 at time of last test)
She beats me in almost all the test
At your chronological age of 66.72, your telomeres are longer than 98.97th% of people
its nice to know thanks. But beware Mike lustgarten made a video to say his other biomarker was worst once in niacin / nmn (aged faster…).
The telomere lenghts of the leukocytes are not good measure… we would need cell type such as fibroblast, myocite etc even the “6-panel Flow FISH assay” is not good enough.
I believe the only real deal would be genetic manipulation such as the one Liz Parrish did
ABC7 Exclusive: New study reveals promising results for age reversal pill on dogs
Zeus was granted access to the medication due to his dire situation. In April, Marsha was instructed to give him one pill a day and she said she saw results almost immediately.
“We have watched him get better and better and better,” Marsha said.
A recent scan on Zeus showed the cancer in his body was completely gone. […]
I think Dr. Roizen is a reputable doctor, but I’m not sure how much he knows about telomere science…the view he’s espousing in this article is in conflict with what many geoscientists in the field believe. Michael Roizen, MD | Cleveland Clinic
The CEO of Telomir Pharmaceuticals, Dr. Christopher Chapman partnered with Dr. Michael Roizen from the Cleveland Clinic to test a new drug aimed at lengthening telomere caps on human stem cells.
“If you can increase telomeres, you can reproduce stem cells and keep repairing things so you can literally get younger,” Dr. Roizen said.
Dr. Roizen said the drug’s pre-clinical data from a previous in vitro human cell study showed that telomeres lengthened by 200%.
