The following questions were sent in concerning telomeres, telomerase, TA-65 and the Life Length assay as offered in the U. S. by adltests.com.
Question 1: Is the database mainly constructed in the US?
Answer: The database is worldwide but the bulk of the database comes from the U.S. The only lab currently offering the Life Length assay in the U.S. is adltests.com.
Question 2: Why is it that the average percent of short telomeres is roughly the same, and not rising, for the deciles 31-40, 41-50 and 51-60 of the results report?
Answer: The percentage of short telomeres required to drive disease/dysfunction is the same no matter what the age range of the participant. There is a threshold within each cell thus generating “old cells” that need to be removed in any biologic age population. Similarly “young cells” can exist in any age population as well. The threshold that confers senescence or apoptosis (self destruction/removal) of the cell is not dependent on chronologic age solely. It is dependent on number of replications, accrued damage (oxidation) and measures one might take to minimize or reverse that damage. The so-called Hayflick limit is an idealized maximum number of cellular divisions that can occur in more or less perfect conditions and implies that, no matter what, the cells will continue to “age” due to telomere loss. The actual human Hayflick limit is now 122 years as witnessed by Jean Calumet, the oldest documented human being who died fairly recently. It is important to understand that the Life Length assay is the only one reporting percent of short telomeres at this point, and one can have “normal” mean telomere length with a low or high percentage of short telomeres. The latter changes the meaning of telomere testing completely, as most people with “normal” mean telomere length have no idea if their cells are old or young biologically because this critical piece of information is missing.
Question 3: Have you found any evidence that the average percent of short telomeres may vary across different ethnic groups or by gender or any other grouping factor?
Answer: Since the Life Length Assay is still new I don’t think I can honestly answer that question until the database grows to a much larger size. Basing the answer on previous technologies may lead to false conclusions since they do not yield this kind of data. But the short answer and the one that is currently (and I stress the word “currently”) accepted is that there may be such ethnic and more likely gender differences. For instance there is a small subset of Ashkenazi Jews that have allelic “over expression” of telomerase which confers longer telomeres and longer life/healthspans.
But for most of us epigenetics which while heritable is also mutable is the most likely factor in telomere length and lifespan. Things like nutrition/supplementation stress handling, sleep, exercise habits etc are still far more likely to contribute to telomere health and length for the general population.
Question 4: Has there been any empirical test of the telomere hypothesis, i.e. that individuals with low percentages live longer?
Answer: There have been many such studies and it is generally agreed upon in the “telomere community” that, based on the studies, this is an immutable fact. Similarly evidence exists to show improved health parameters as well in humans mouse and human cell lines although this is a different line of questioning.
You will need to scroll to several pages to get the ones that specifically answer that question. In addition due to the failure of Calorie restriction over expression of telomerase to lengthen telomeres now exists as the ONLY method of extending life span in higher mammals. Maria Blasco was able to demonstrate a single isolated treatment with telomerase added 25% to the life span of middle aged mice and 13% to old mice. Her study on short telomere rate increase can be found here.
Please note: until the pharmaceutical industry jumps on this bandwagon, no one will have the money to do the study we all want: a longitudinal study of humans with random selection (not twins, etc.) in diverse populations over many decades to see the effects on human longevity when we turn on telomerase with supplements or other avenues. In other words “Can we make people live longer and healthier by lengthening their telomeres or more specifically decreasing the number (%) of short telomeres?” Even then it is likely they will not do that study; rather the answer will come from several generations of clinical observation and research into the results of drug therapy for telomerase when that actually happens. Surprisingly, human longevity and healthspan are not even on the radar of most governments!
TA-65 is currently the only telomerase activator that has been 1) evaluated for safe human consumptions 2) Proven to work in human beings. No other compound has that data.
One thing we know at this point is that, statistically speaking, diseases are fewer and lives are longer in those blessed with healthy long telomeres.
Please keep in mind one can still be hit by a bus!!!