Telomerase Therapies?

Note added 2018 March

Below is the article I wrote 6 years ago, but the evidence has changed in the interim, and my thinking has become more nuanced.

My 2012 thinking was based on theory and epidemiology.  Theory: Replicative senescence (based on rationing telomerase) is one of the oldest modes of programmed death in protozoans, long before there was multi-celled life.  It is natural to imagine that it is a conserved evolutionary pathway of programmed aging in humans. Epidemiology: People with shorter telomeres have shorter life expectancies and higher mortality risk than people the same age with longer telomeres.

Since that time, there is new epidemiology and new biochemistry.  The epidemiology, much to my surprise, has linked longer telomeres with some cancers—notably melanoma and lung cancer.  New biochemistry has linked telomerase to the Horvath Aging Clock in the wrong direction.  Telomerase accelerates aging, according to observed methylation patterns.

I still believe that longer telomeres are a net benefit, potentially adding 3 to 5 years to our lives.  Longer telomeres are a major protection against cardiovascular disease.  I no longer believe that telomeres are the primary aging clock, or that major gains in life expectancy can be achieved through telomere extension.

Telomere biology has the potential to extend human life span, to dramatically lower rates of the great remaining killer diseases: heart disease, stroke, and Alzheimer’s.  All three diseases increase exponentially with age, and their toll will be slashed as we we learn how to address the body’s aging clocks.

You would think that the 2009 Nobel Prize might have done more to raise the profile of research in telomere biology, but the field remains a specialized backwater of medical research, and few biologists (fewer doctors) take it seriously as a panacea for the diseases of old age.  If the National Institute of Health has money to put into heart disease and cancer and Alzheimer’s and Parkinson’s diseases, there is no better place to invest than in telomere biology.  Research on these diseases commands multi-billion dollar budgets, because they are considered “medicine”, funded by NIH, while telomere biology is considered “science” and is funded by NSF.  The total NSF budget for all cell biology is only $123 million, and the portion devoted to telomere biology is a few million. The private sector is doing a little better – there are several companies selling herbs that stimulate our own bodies to liberate telomerase.  But this is short-sighted venture capital, and what we need is focused research with a ten-year vision.

There is good reason to think that telomere length is a primary aging clock in the human body.  The body knows perfectly well how to lengthen telomeres, but chooses not to.  All we have to do is to signal the body to activate the telomerase genes that are already present in every cell.   Of course, there is no guarantee that this will work, but compared to the sluggish rate of progress on individual diseases, it’s a pretty good bet, and the target is rather simple.  IMHO, it’s worth a crash research effort.

Three objections raised against telomerase research

1.  “Aging is inevitable because Physics tell us that nothing can last forever.”  This statement refers to the Second Law of Thermodynamics, which says that closed systems, evolving in isolation, must become more disordered over time.  But living systems are open, taking in free energy in the form of food or sunlight, dumping their entropy out into the environment.  There is no reason that such systems cannot maintain themselves indefinitely.  Indeed, growth and maturation would not be possible if this law of physics applied to open thermodynamic systems. Since the 19th Century when the laws of thermodynamics were formulated, it has been understood that aging cannot be explained from physics, and therefore commands an explanation from evolution.

2. “Evolution has been working to maximize animal life spans in order to increase fitness.  It is unlikely that any simple adjustment to physiology that humans can discover will do better than evolution has done over millions of years.”  In fact, evolution has not worked to maximize life span, but only to make it sufficient to assure time for reproduction.  Aging is a form of programmed death, on a flexible but finite schedule.  It is fixed in our genes.  There are mechanisms of aging that have been programmed into living things since the first eukaryotic cells.  Telomere attrition has been used to time the life cycle and form a basis for programmed death for at least a billion years.  Many species of protozoans do not express telomerase during mitosis (but only during conjugation), so their telomeres shorten with each reproduction, leading to a limit of a few hundred reproductions per cell line.  This mechanism is the precursor to telomeric aging that exists to the present day in humans and many other higher animals.

3.  “Expressing telomerase will increase the risk of cancer.” There is a great deal of theoretical concern in this direction, which I think is entirely misguided.  It is true that cancer cells express telomerase.  It is not true that expressing telomerase causes a cell to become cancerous.  This relationship is clearly explained by two seasoned experts (Shay and Wright 2011)

In early studies, the only way of increasing telomerase activity in lab animals was to add extra genes for telomerase.  Technology in the early 2000s did not permit a gene to be added at a targeted location, but only inserted randomly into a chromosome.  Tampering with the structure of DNA in this way is known to increase cancer risk no matter what gene is added or subtracted.  In three of these early studies, cancer rates in mice were increased [123].

There are no lab studies to my knowledge in which activating the native telomerase has increased the risk of cancer.  The modern view is that “while telomerase does not drive the oncogenic process, it is permissive and required for the sustain growth of most advanced cancers.”  Recent perspectives from both Harvard lab of de Pinho and the Spanish lab of Blasco focus on the potential for telomerase to decrease cancer risk, and these were the very people who produced the three studies suggesting caution a decade earlier.

And there are many studies showing that (a) telomerase expression does not increase cancer risk in lab animals, and (b) short telomeres are a very strong cancer risk.  I believe that telomerase activators will greatly reduce the cancer rate, first by eliminating cells that are pro-inflammatory and potentially carcinogenic because their telomeres have become short, and second by rejuvenating the immune system, which is our primary defense against cancer.  I published an article on this subject last year.

Why we might expect big life expectancy gains from extending telomeres

This is the affirmative question, then: what makes me think that telomere extension will have such a powerful effect on diverse aspects of aging biology?

A)    Telomere attrition is an ancient mechanism of aging.

Protists were the first eukaryotic cells, and they appeared on earth a billion years ago (they were a leap up in complexity from bacteria, which had been around 3 billion years before).  In protists, DNA is linear and hence there are telomeres and a need for telomerase.  Since protists reproduce by simple cell division, you would not expect that the cells would “age” or even that the concept of aging could have any meaning for their life cycle.  But a protist cell lineage can age, and indeed some do.  This is the oldest known mechanism of aging, and it is implemented through withholding telomerase.

Paramecia are an example.  When paramecia reproduce, their cells simply fission, the DNA replicates, and telomerase is expressed.  Hence, telomeres get shorter with each cell division. Paramecia can conjugate, which is a primitive form of sexual gene exchange.  Two paramecium cells merge, mingle their DNA, and then separate.  It is only in the conjugation process that telomerase is expressed.  Therefore, any cell lineage that does not conjugate will die out after a few hundred generations.  This prevents cell colonies from becoming too homogeneous.  Thus aging is a billion years old, and some of the genetic mechanisms of aging have been conserved and passed on through all the transformations of multicellular life (William R Clark has written two accessible books [12] on this topic.)

B)    Telomeres shorten with age in humans.

This has been known for twenty years.

C)    People with shorter telomeres have a much higher risk of mortality.

This was established by Richard Cawthon (2003) in a paper which took the field by surprise.  Researchers before then had assumed on erroneous theoretical grounds that telomere attrition, which was known to occur, could not have anything to do with human aging.  It was assumed that the number of cell replications, though limited, must be sufficient to last through the longest lifetime that humans normally experience.  After all, if aging were as simple as telomere attrition, then the body could solve the problem merely by expressing telomerase.  This would enhance individual fitness.  Why would not evolution have found such a simple expedient?  (The answer, of course, is that natural selection favors aging, for the sake of the demographic stability – an evolutionary force not recognized by most evolutionary biologists.)  In Cawthon’s study, the top ¼ of 60-year-olds in terms of telomere length had half the overall mortality risk as the bottom ¼.  Cawthon had access to a unique database of 20-year-old blood samples, and to my knowledge his study has not been replicated or refuted these 11 years.


D)     People with short telomeres have a higher risk of diseases, especially CVD, after adjusting for age.  The association with cardiovascular disease has been consistent, not just in Cawthon’s original study, but also several other studies [Ref Ref Ref].  There are also associations with dementia [RefRef] and with diabetes [RefRef].

E)    Animals with short telomeres also have a higher risk of mortality, after adjusting for age.

This has been established in several bird species [Ref Ref Ref], and in baboons.  In 2003, it was already known that long-lived species tend to lose telomere length more slowly, and short-lived species lose telomeres more rapidly.

F)    In limited studies with mice, telomerase enhancers have led to rejuvenation.  (Mice are expected to be a much less effective target for this strategy than humans, because to all appearances, aging in humans relies on telomere attrition much more so than in mice.)

The first experiment of this type was done in 2008.  In the Spanish lab of Maria Blasco, Tomas-Loba engineered mice that were both cancer-resistant and contained an extra telomerase gene, expressed in some tissues where, even in mice, it would not normally be found.  Cancer-free mice with the extra telomerase lived 18% longer than cancer-free mice with only the normal gene for telomerase.

But soon it was discovered that all the experimental precautions around cancer may not have been necessary.  The same lab Bernardes de Jesus (2011) reported that they could increase health span in mice with the commercial product called TA-65 (widely rumored to be cycloastragenol) with no increase in the incidence of cancer.  Cycloastragenol is a weak telomerase activator compared to man-made chemicals discovered at Sierra Sciences, and even compared to some other herbal extracts.  Nevertheless, the Blasco lab was able to show that the shortest telomeres in the mice were elongated, and that markers of health including insulin sensitivity were improved by short-term treatment with TA-65.

Blasco’s lab then worked with a more potent (though more dangerous) method of telomerase induction: infection with a retrovirus engineered to introduce telomerase into the nuclear DNA of the infected cell.  “Treatment of 1- and 2-year old mice with an adeno associated virus (AAV) of wide tropism expressing mouse TERT had remarkable beneficial effects on health and fitness, including insulin sensitivity, osteoporosis, neuromuscular coordination and several molecular biomarkers of aging.” (Bernardes  de Jesus, Vera et al. 2012)  The mice lived 13% longer when AAV treatment began at age 2 years, and 24% longer when treatment began at 1 year.  There was no increase in cancer incidence.

The most dramatic example of rejuvenation is from the Harvard laboratory of Robert de Pinho.  Normally, mice (unlike people) express telomerase freely through their lifetimes.  These scientists engineered a mouse without the normal (always on) gene for telomerase, but instead had a telomerase gene that could be turned on and off at will by use of a chemical signal that the experimenters could feed to the mice.  As these mice grew older, they developed multiple, severe symptoms of degeneration in the testes, spleen, intestine, nervous system and elsewhere.  All these symptoms were not just halted but reversed when telomerase was turned on late in the animals’ lives. The effect on the nervous system is particularly interesting because nerve cells last a lifetime and do not depend on continual regeneration from stem cells, the way blood and intestinal and skin cells do.  Nevertheless, these mice with telomerase turned off suffered sensory deficiencies and impaired learning that was reversed when the experimenters administered the chemical signal to turn telomerase back on.

Stanford/Geron research group worked with “skin” grown from human cells in a lab setting.  They found they were able to restore youthful elasticity, softness and texture to the cultured “skin” by infecting the cells with an engineered retrovirus that inserted the gene for telomerase.

G)     In addition to its function in lengthening telomeres, telomerase also acts as a kind of growth hormone.

This fact was suspected as early as the 1990s, and confirmed definitively in a Stanford experiment [RefRefRefRef].  In this experiment, mice were engineered with “denatured” telomerase that lacked the RNA template for creating telomeres.  Still, the telomerase was shown to induce hair growth.  Telomerase has been shown to affect a hormonal signaling pathway called Wnt. Other functions for telomerase are reviewed by Cong and Shay (2008).

H)        In one human case, huge doses of herbal telomerase activators has led to rejuvenation.

I am recently in touch with a physicist from Kansas who has been taking super-high doses of telomerase-activating herbs and supplements for six years and claims to look and feel younger, with improved athletic performance.  He may be an interesting case study.  Jim Green has commented on this blog site.

 The Bottom Line

In my opinion, telomerase activation is a field that offers the most potential for human life extension in the next few years.  This research is languishing for lack of funds, and for lack of attention.

160 thoughts on “Telomerase Therapies?

  1. Thanks for this great article. I’ve been trying to find information about telomerase and just have to believe that there is something in nature that does not require all this high processing to extract the essence of what we need. I’ve seen supplements claiming that animal glandulars activate this enzyme, certain vitamins will activate it and so forth. Could be something as simple as exercise, fresh air, or even “grounding” to the earth. Whatever it is, it’s probably right under our noses.

  2. Hi there, I discovered your web site via Google while searching for a similar subject, your web site got here up, it seems great. I’ve added to favourites|added to bookmarks.

  3. Hi Josh,

    I’ve enjoyed reading your blog and also your essay in “Lynn Margulis – the life and legacy of a scientific rebel”. I have a (genuine) question:

    Why are you (and others) so focussed on prolonging and preserving human life?

    Many thanks


    • Thanks, Chris.
      Your question is about fundamental values and not about science.

      On the one hand, human overpopulation has been a bane on the earth’s bounty, disruptive to the ecosystems created over many millions of years. Overpopulation is a result of lowering birth rates chasing lowering death rates, but not quite fast enough…

      On the other hand, our society spends huge sums of money on medical care, and most of this is tending to diseases of old age. If we as a society are already pouring resources into medical research into cancer and heart disease and diabetes, if treatment of these diseases costs us hundreds of billions of dollars a year and a great deal of suffering, then it would seem to be worthwhile to forestall all of these diseases at once with a generalized program of life extension.


      • Awesome truth…but the fact is the big pharmaceutical companies receive big benefits from our illnesses…so sad!!! I want to have a productive life…not one filled with sickness..and also most people enjoy working… this would also help people to work and contribute taxes to a much longer date.

  4. First of all, my sincere compliments for the blog.

    I am not a life scientist (I am a mathematician), but I have been a bit puzzled by this post.

    Telomerase is highly expressed in many human tumors (that’s why cancer cells are mostly immortal, namely they bypass Hayflick limit). Suppressing telomerase is considered a target for cancer therapy.
    Moreover, while it is true that mice have highly expressed telomerase, it is also true that most of them die of cancer (I think it is the 80% in lab) where telomerase is expressed in somatic cells. This does not happen with larger animals where telomerase is expressed only in the embryo and in some pluripotent cells, but not in somatic cells. So turning off telomerase seems to be a protective mechanism against cancer.
    It seems that the problem is that cancer cells know how to unlock the key.

    • “This does not happen with larger animals where telomerase is expressed only in the embryo and in some pluripotent cells, but not in somatic cells. So turning off telomerase seems to be a protective mechanism against cancer.
      It seems that the problem is that cancer cells know how to unlock the key.”

      Lobsters are said to express telomerase throughout and are said to have low cancer incidence. Regards cancer, it is said there is a telomerase free alternate method of extending telomeres.

      • And lobsters do grow quite large, in fact they never actually stop growing. Native americans and fisherman of the late 19th century reported catching lobsters off NewFoundland coast up to 6 ft. long. Today’s lobsters are mere fingerlings of their great, great grandparents. I mention this to point attention to possible relationship between telomerase and growth hormone.

  5. Found TA-65 at $2000 a bottle! Seems like only the wealthy will be able to stay young!
    Hopefully a telomerase inducer will be found cheap enough for an old maths teacher like me! I’d love to keep my mind intact for a few more decades.

    • It’s bad, but it’s not that bad. TA-65 costs a few hundred dollars a bottle, not $2000. You can find it on EBay or Amazon Market.

      TA-65 is widely rumored to be cycloastragenol. You can find cycloastragenol from China far cheaper at these same sources.

      Product B is based on different herbs from different sources. On the one hand, it’s stronger than TA-65 in lab tests. On the other hand, there’s actual clinical data for TA-65 showing its effectiveness, and there is none for Product B. Product B is about $75/month.

      The first ingredient in Product B is Silymarin. You can find Silymarin for much less than Product B. Here’s a web page with other ingredients in Product B:

      • A big seller of TA65, claims that milk thistle extract which has Silymarin does not activate telomerase. But given that this is a competing product, an independent test and claim would be more reliable than one from entities vested in outcomes.

  6. Your article was fascinating in an opposing way and your blogs are truly interesting, but I disagree with your premise!

    Isn’t the increase in telomerase, the potential for a longer cell life, and the increase in the number of cell divisions in its life time going to increase the chance for cancer, not provide youth? As the cell division increases, the oppertunity for an error in cell division to occur increases as well and the chance for cancer goes up? Isn’t that what cancer is, an “error” in cell division? If more time is alotted for an error to occur, it most likely will? If you have read, the scientific world has noted that an increase presence of telomerase has occured in many cancer patients and could be used as a future alert for people who might have cancer. Telomerase is the cause, not the solution. The increase in telomerase allows the cancer immortality. Your article, naive, is written on the pretense of a perfect world where if the protein causes immortality in cancerous cell, then it must do the same for healthy ones. The thing is were not in a perfect world and the effects and complications were not considered. Where both of us are standing, cancer by regulation of telomerase and cancer by an over production of telomerase, cancer is still occuring and nothing seemed to happen, except one life was focused on living and the other was focused on prolonging life.


    • Alexandra –
      You are correct that there is a widespread assumption among biologists that “it can’t be that easy” – that if evolution had such an easy path to a longer life span, then we would have evolved to express telomerase. So the view you express is quite traditional. Judith Campisi has written on this subject.
      However, the actual evidence does not indicate that turning on telomerase increases cancer risk. There have been experiments with mice in which telomerase is turned on, the mouse lives longer, and cancer risk is not increased. Furthermore, people with short telomeres have much higher risk of cancer. I have written a paper on the subject, to be published next month.

      • I may be naïve, but germ cells express telomerase throughout life; yet germ cell cancers are far less common than epithelial cancers, which argues against the correlation between telomerase/tert expression and cancer. Also, I hazard to guess that telomerase activation is not the “cause” for cancer, but it is necessary for cancer cells to turn on telomerase to escape the Hayflicks limit similar to several other pathways that it turns on (or off) to achieve immortality. If the argument is true, then activating telomerase is necessary for cancer cells to achieve immortality, but activation of telomerase may not automatically induce cells to become cancerous. Besides there are many cancers where there is no activation of TERT and uses other mechanism to overcome the Hayflick limit. I would also guess that for those how already have the sub-type of cancers that are more dependent on telomerase activation for survival, activating telomerase by telomerase activators may be bad. In this vein, one has to acknowledge that telomerase inhibition does not kill all cancer cells that have increased telomerase activity. It seems that a lot of things about telomerase is not understood due to the lack of research and the hypothesis that cancer will be automatically induced upon activation of telomerase is more conjecture than based on scientific fact and on experiments where activation of telomerase by recombinant viral vectors carrying copies of TERT increases incidence of cancer in mice, which in itself cannot be extrapolated to increased incidence of cancer in humans upon activation of telomerase by mild activators of telomerase.

        • I agree with Josh Telomerase activation does not cause Cancer, if anything short Telomeres allow Cancer to hijack cells. It has been observed in studies that Telomere length falls until the cell is hijacked then the Telomerase rises again as Cancer takes over. Cancer progression is a multi faceted situation and Telomerase is only one component.

          Also of interest is this new study from CNIO where Blasco et al have managed to effectivly turn cancer off by attacking the Telomeres via a different method and it is looking very promising. This is the same research facility that has made so much progress with Telomerase rejuvenation.

          • Ed Park, MD is a telomerase activation specialist in Costa Mesa, CA. Recently he published statistics on cancer in his patients and in a matched population of people not on a telomerase activator. The medium was one of his “podcasts.” This one was titled “Prostate Cancer” and is available on UTube.

            If I understand Park correctly, his patient-population provides between 3000 and 4000 person-years of experience with telomerase activation. The expected number of new cancer diagnoses in a population with similar characteristics but without telomerase activation is 66. The observed number among his patients is 2-3. Being on a telomerase activator reduced one’s probability of getting a diagnosis of cancer by a factor of between 22 and 33.

  7. I used ta-65 for a little over a year, while deployed in Afghanistan (as a contractor, I could afford it, though only 1/2 dose). It did more for me, particularly mentally, than anything I had ever used. I’ve had lasting effects in the reduction of bad anxiety and depression, not a miracle but definitely noticeable.
    I can’t afford it with a stateside job, but I did try the crack aging cycloastrenegol for about 60 days. It just didn’t seem at all to be the same; especially the deep sleep and active dreaming produced by the ta-65. I’d always feel so extremely rested; I get a similar, though not as pronounced effect by taking n-acetyl-cysteine before bed.
    Other effects, my chest hair (I’m 52 but have little grey hair on my head) turned from grey to a mixture of dark brown and some grey. I’ve been off it for 1.5 years now and the grey is coming back again. 🙁

    Sure wish I could keep taking the ta-65!!

  8. Well, I think I’ve put Death In Chains with ,
    but it takes quite a while to roll through it, and then you have to start
    all over again, to refresh yourself. Ergo it mirrors the Myth of Sisyphus,
    by Albert Camus, which resembles Albert Caw-“mu”s, which reminds me of
    my work on the gravitational coupling constant mu in classical general
    relativity and in electromagnetic-like gravitation, described at . Furthermore,
    the Myth of Sisyphus seems to roll by each year up on the celestial sphere,
    in the constellations. Each year the rock reaches the perihelion of its orbit
    as Orion chases Perseus-Pleiades-Aries across the sky, but there is a phase
    where the Hero of the Stars seems to fall like Bootes perched on the
    Handle of the Big Dipper back into Summer heat.
    For an extensive list of telomerase activators that are being examined, see .
    I don’t think any more extensive list is available online.

  9. Josh, I might have missed this in the comments, but I’m wondering what avenue you have taken? Do you pay the $100’s or do you take one of the cheaper alternatives and still feel the effects, if that question isn’t too personal? I feel I could benefit but definitely don’t have money to waste.

    • I’m always experimenting as I learn. I’m hesitant to share my own practices until they become more consistent. Lately, I’ve discovered that astragalus root is sold by the pound in Chinese groceries, about 100 times cheaper than the pills. I’ve been taking silymarin and ashwaghanda and horny goat weed rather than Product B, also to save money.

      As for “feeling the effects”, this is not why I’m taking these supplements. I’m hoping that they have their effect in the long run. I hope to slow aging over a period of years and decades. Anything I feel today from taking a pill today is a distraction at best.

  10. Com relação a telomerase e câncer, talvez se possa associar a relação que se fazia equivocadamente ao câncer de próstata e testosterona. Se a testosterona fosse a responsável pelo câncer de próstata, a incidência maior seria na juventude quando a testosterona é mais alta. Ao contrario, o câncer de próstata atinge pessoas mais velhas.

    Google translate from Portuguese:
    With respect to telomerase and cancer, perhaps one can associate the relationship that was mistakenly to prostate cancer and testosterone. If testosterone were responsible for prostate cancer, the incidence was higher in youth when testosterone is highest. Rather, prostate cancer affects older people.

  11. I’m grateful for this website Josh, and I am surprised at how little scientific work there is on the “aging problem.”

    I’ve recently started a regimen of NR (4000mg) and astragalus (2500mg) at 42 years old and we’ll see how it goes. I have noticed that since starting the NR that my strength in the gym has noticeably increased. I’m now benching more weight than I was when I stopped weight lifting 10 years ago… No, nothing dramatic like sci-if, but only by a few pounds, but still a noticeable amount to myself.

    I’m also a physicist by degree so I’m watching my own experiment and trying to be objective. I applaud your work here, and will keep reading up on your work here.

  12. Just an update and a correction… I am actually taking 25gr of astragalus, not 2.5gr. I’ve not had any bad side effects since beginning this “experiment”. My strength at the gym has definately and noticeably increased. Again, we’re not talking sci-if. I injured my Achilles’ tendons working on my calves with 160lbs (over extended and stretched) and I thought I was going to be sidelined for months and have to see a doctor. It completely healed up within 3 weeks. Not saying it’s because of the supplements, but typically those injuries take 6 weeks to heal.

    All I can really report is that concurrent with beginning NR I experience some gains at the gym that have since plateaued. I hope the astragalus staves off the effects aging and senescence to keep myself healthy and fit in the very long run.

  13. …oh, and yes, I am taking about 1/2 a bottle a day of NR. The same is true of the astragalus. No negative side effects to report. I’ve also added alt-711 to my list last week at about 50mg in the morning, and at night. Being 42, the idea of preventing stiffness in the heart muscle due to old age before becoming old seems like a no-brainier to me. If only there were something for the AGE accumulation in the skin.

  14. Great article! Regarding to your comment on neurons:
    “The effect on the nervous system is particularly interesting because nerve cells last a lifetime and do not depend on continual regeneration from stem cells, the way blood and intestinal and skin cells do. Nevertheless, these mice with telomerase turned off suffered sensory deficiencies and impaired learning that was reversed when the experimenters administered the chemical signal to turn telomerase back on.”

    Nerve cells do regenerate, especially glial cells, which form the supportive infrastructure for neurons, so telomerase effects on the nervous system do make sense:

      • It’s also now known that stem cells in the hippocampus (and possibly other areas) generate thousands of new neurons every day throughout adult life.

    • See also The Other Brain by R. D. Fields. Glial cells have turned out to be a lot more than just “the supportive infrastructure for neurons”.

      Regarding neuron growth, the text we used in a 2011 course in Abnormal Psychology (Abnormal Psychology, 2nd ed, Hansell & Damour, 2008, pp. 559-560) mentioned that continual life long learning, whether academic or otherwise, creates new dendrite arbors (tree-like clusters of neural dendrites). In fact continued learning and the frequent solving of difficult mental problems (i.e., really exercising the brain) are one preventative method suggested for dementias resulting from reduced number of interneuronal connections, Alzheimer’s being one. Of course that is far too simplistic to be a full solution to brain degeneration with aging, but it adds one more tool to the kit for fighting the mental effects of aging. I would add that of course the intracellular crud (neuritic plaques) needs to be prevented and/or reduced as much as possible, and supplementation and chelation therapies could be beneficial in that regard. There is plenty of info here on the former, and unfortunately I only have anecdotal information with regard to the latter.

      BTW, that psych course was during my last semester of completing an old outstanding psychology degree, which I left dangling after I diverged to a 35+ year (and still going) career in electronics. I received that BS in psychology 12-17-2011, exactly 2 weeks after my 61st birthday. I am now (at age 64) pursuing another bachelors degree in physics, and I will add as much biochemistry as possible, with the long range goal of a PhD in biophysics. Bionics and advanced prosthetics are my areas of interest, as replacement hands, arms, legs, etc, need to be surgically integrated with full peripheral nervous system connectivity and feedback, so they feel and function like the originals. The current art is getting there, but it has a way to go yet, and I would like to be involved. The biochem will, as an added benefit, give me better insight into some of the life extension technologies currently being pursued. My ex-wife was a a natural healer and herbalist, so I picked up some background with herbal supplements. I take a basic range of supportive items, but not nearly the number or quantities some people mention here. It is interesting to read these comments, and it gives me some ideas to research. And it is good to see other people pursuing life extension techniques. I may make my goal or I may not, but it won’t be for want of trying. I have no intention of shutting down, retiring, and dying as some of my peers think I should. Besides, as we age and do not have the historical grace to diminish and die, we need to periodically reinvent ourselves.

  15. My understanding of relationship between cancer and telomerase is: Lack of telomeres on chromosomes can lead to cancer by allowing corruption of genetic data at or near those ends; rapid cancer cell reproduction triggers telomerase but it is to late. Teomerase should have been triggered before cancer to stop the corruption befoe it happened. I’m not saying this is the only way cancer starts but could be one of them, that allows genetic corruption.
    I made a comment here after reading the research:

  16. Your expression in this blog is logical therefore I see no reason to discount any of the points you raised indeed I share your views,

    As a simple side note AAV’s(in the experiment discussed they are rAAV-because they are recombinant) used by Blasco in 2012(in the experiment discussed) are naturally a double-stranded DNA virus with very stable behavior in mammalian cell-lines, they insert themselves in only a specific location in chromosome 19 but in the case of rAAV they will be episomal(they do not integrate into the DNA, but can be used to express the gene in them – this IS ideal to prevent any risk of random integration which doesn’t occur normally with AAV’s anyway).
    What can be said about retroviruses(or indeed recombinant retroviral vectors is that they are RNA not DNA and may integrate themselves randomly – this IS NOT ideal and may lead to cancer…

  17. Any Updates? Especially any more news from (H), the physicist that was taking massive doses of telomerase activators. Do we know what they are and is this person willing to let the rest of us in on it?

  18. If world society manages to educate as big a proportion as possible of the population(and also paradoxically raise the life expectancy) humanity will have actually achieved strict replacement rates as soon as possible, possibly as soon as 2050, beyond that if humanity doesn’t find a way to prolong life expectancy in a dramatic way we will be facing a slow decline in demographics,.. Hans Rosling explains it best, look him up on youtube.

    • Thanks for the reference, Alex. I’m not worried about population decline. If it ever happens, it will be far in the future, and there will be lots of time to plan around it. I am worried about overpopulation, and the strain that humans put on the world’s ecosystems and physical resources.

      • Am pus si eu aceeasi problema a factorului demografic, in discutia cu Michael Fossel, iar raspunsul a fost ca trebuie sa gasim modalitati sa creem fiecare in parte noi locuri de munca si nu sa asteptam sa primim locuri de munca si altii sa le creeze pentru noi… dar acest lucru e foarte greu de gasit…. a zis ca pot sa apara probleme mari in unele tari, daca speranta medie de viata va fi dublata …. dar a spus ca fiecare vom avea de ales intre a avea o pensie si de a mai trai cam vreo 5 ani…. sau sa ne creem locuri de munca si sa mai traim fara pensie inca 50 ani….

        • Google translation of the above:
          I put myself the same issue of the demographic factor, in discussion with Michael Fossel, and the answer was that we must find ways to create each of new jobs and did not expect to get jobs and others to create for us … but this is very hard to find …. he said that big problems can occur in some countries, if the average life expectancy will be doubled …. but said each will have to choose between have a pension and live a little longer about five years …. or we create jobs and longer live without pension since 50 years ….

  19. Hiroyuki Seimiya et al, Telomere length influences cancer cell differentiation, Mol. Cell. Biol. doi:10.11.1128/MCB.00136-13, May 28, 2013

  20. Spot on Josh. Telomere activation therapy (eg Htert) once approved should massively boost lifespan and health. There are a significant number of companies now researching the technology ie, Andrews INC etc…

    Coupled with Senescent cell deletion methods also being developed should boost lifespan a great deal. It will also buy time to develop the other therapies associated with age decline. We live in exciting times.

  21. I can recommend subscribing to health,,, by dr. David williams,, healthandhealing.comby dr. Julian whittaker, dr.,, and by dr. Shallenberger.I look and read books and literatures in all directions and then compare them.

  22. Good Evening,

    Josh, thank you so much for what you do. This article was so insightful and helpful to people like us……Progressives and of like minds. I/we appreciate what you do. 🙂

  23. Yes this is very promising on top of the work by M.Blasco, I am convinced that restoration of Telomere length would be a considerable boost to the body in restoring itself to a younger state.

  24. Josh,
    Any thoughts on the announcement of approach to lengthening Telomeres using a modified RNA that encodes a telomere-extending protein? Even avoids the immune response!

  25. In vivo to a human, may mean either specific tissue targeted for delivery of TERT mRNA, or whole body – but given current technical progress or forseable that would be prohibitively expensive probably in the tens of millions$ figure for 1000 bp telomere elongation.

  26. Have anybody looked into Low Level Laser therapy to induce telomerase?

    I found couple things on the internet:

    “He:Ne laser irradiation induced survival and cell cycle progression effects on human circulating mononuclear cells in vitro”

    and another similar paper:

    “Human Telomerase Reverse Transcriptase (hTERT) Gene Expression in Rheumatoid
    Arthritis (RA) Patients after Usage of Low Level Laser Therapy (LLLT)”

    These studies I believe, shows that there is a path to activate telomerase via Low Level Laser stimulation, technology that is actually within our grasp. So create a device that does that, doesn’t require huge financial investment. I’m wondering if Michael Fossel, Bill Andrews, etc. have tried this?

  27. Salve Adrian Crisan,

    Hello Adrian nice to see other Romanians interested in this, I am currently trying to develop a relatively cheap way to make a viral vector to deliver the TERT transgene directly to a human cell. I am aware that Michael Fossel is currently trying to develop a repeatable and relatively cheap way to deliver transgene TERT to the human cell using a non-viral liposome(basically fat bubbles that can inglobate DNA withing them) method. He should soon be having results soon. I have never heard of this method that you speak about: TERT(the catalytic component of telomerase) through lasers, please tell us more.

    Salut si numai bine.

    • @Alexandru Dumitru – very nice that other Romanians are helping by doing research in this field of longevity/reverse aging. Unfortunately, I’m not a “professional” in the field, I’m just an enthusiast, so I cannot tell much more. I do have a background in physics though, and that connection between lasers and telomerase activation caught my eye. I’m researching this on my spare time – which you can approximate how much I have, by how long took me to post back here on Josh’s blog … – so I cannot add much more to what I have read in these articles. However, I think would be interesting (re)searching this path for telomerase activation, since it goes hand in hand with nano-technologies. I have a feeling that far infrared light, also could play a role into this. I do believe that nano-technologies implementation into biology of (reverse) aging will play a huge role, and as of now, we just see the tip of the iceberg. For example see Google’s patent for Nanoparticle Phoresis:
      From a simple physics stand point, we know that energy can be transformed in mass and vice-versa, so in theory any (adequate) energy stimulation at a cellular level, can lead to interesting and promising results. Somehow, could be a lot easier to yield some results this way, than the other mentioned paths.
      Anyway, meanwhile Josh published some very interesting news about Michael Fossel’s activity with newly formed BioViva. Let’s hope that the results with their work will be as most of us hope: great.
      BTW: do you do your research across the ocean in EU or here in US? Does your research group have a web site we can look at? or a LinkedIn profile?
      Numai bine! All the best!

  28. Josh,

    I’m really enjoying your site. I noticed your mention of the fact that cycloastragenol is a relatively weak telomerase activator compared with some other man made chemicals and herbal extracts. Could you please tell me where I might find more information on these other substances, especially the herbal extracts, particularly how they relate to cycloastragenol as telomerase activators?
    Thank you very much in advance.

    • This is not published information. I heard it from Sierra Sciences, which does the telomerase-activation assays for several of the companies that sell these products. They say the best is TAM-818, which was actually developed at Sierra, now marketed by OneTruth, New Zealand, but only as a skin cream.

  29. I tend to disagree with one of the previous correspondent’s assertion that the delivery of hTERT into cells in the body would be extremely expensive.
    Perhaps I could refer all to the Blasco et al patent (Telomerase reverse transcriptase for protection against ageing – EP 2402038 A1).

    When one sums the actual cost of the materials used they come to far less than a year’s salary. The catches of course are many in number. One needs primarily to understand the language and terminology used (molecular biology), the relative safety of the procedure as related to the relative safety of various alternatives, the efficacy of the procedure, and then take an estimate on the unknowns. Many of these issues are already covered in the patent (for that particular procedure).

    I am not suggesting replicating the patent and selling the result but what I am saying is that there is a whole raft of information there in educating one about the procedure.

    Further, this happens to be the age of the “Wet Garage”. I will leave that one for the site to ponder.

    In my opinion, what is needed is a dedicated few (apparently there are some corresponding on this site) to begin/continue some “wet work” in order to push the “peoples’ solution” to this aging problem to a conclusion, as those writers and thinkers before us have already pioneered (Blackburn, de Grey, Blasco, Jaskelioff, Blau, et al). T’would be quite a coup.

    I have read extensively on this subject including the cancer risk associated with telomere lengthening. The area is vastly written about in various scientific journals. Let me know if you require specific enlightenment. I may be able to assist.


    • Thanks for your interesting thoughts, Frank.

      I know of someone who has put together a credible team to do hTERT gene therapy abroad, looking for patients/subjects at a few hundred thousand dollars per treatment.

      And I would like to learn from your readings on telomerase and cancer. I am writing about that subject, and would like to ask for the strongest lab evidence you have encountered suggesting that telomerase might increase cancer risk. (My belief is that extending telomeres is likely to decrease cancer risk.

      – Josh

      • Hi Josh,

        I have given some thought to your request and cannot recall lab evidence, or envisage the likelihood, that telomerase would increase cancer risk or increase cancer occurrence. It sounds a little like the impossibility of proving a negative. One never knows.

        There are perhaps exceptions which I could envisage one of which could be an appearance of precancerous cells which have not yet learned how to harness telomerase production. But even then it would be a currently indeterminate matter whether the extended telomeres would silence the (or one) cancer promoting active gene in the particular DNA string. Perhaps a very small chance of cancer. But even then there are so many cancer solutions appearing (in R&D of course) that most of those cells could be picked up in tests.

        Another exception may be a cancer with a preponderance of double strand breaks. Who knows just what telomerase (or any other enzyme) would be doing in those extraordinarily complex situations.

        And another instance would be that which would happen in germ and stem cells which appear to have their own adequate supply of telomerase. What happens if a greater amount is supplied?

        And all of the above does not exclude the unknown reactions (and possible molecular biological necessity) of (naturally) having and using telomerase for other purposes in the cell.

        Proceeding along the lines of the preponderance of lab studies which indicate startlingly positive outcomes for telomerase use in somatic cells and the perhaps almost zero evidence for the opposite, one would presently feel quite justified in using telomerase for improved health.

        But there again, as I have mentioned previously it appears to be a simple matter of risk/benefit analysis. I feel that such a risk/benefit approach in the Western world is not in vogue at this time. I won’t go into the reasons, real or suspected, for such a state of affairs. Nevertheless it seems to be quite a valid approach and a possible set of criteria to many human situations.

        So perhaps you are suggesting an avenue for justification of pursuing such a promising therapy (such as telomeric therapy) which simply cannot be totally (100%) vindicated at the current level of technology. One could probably feel that there might be dozens of hazardous outcomes including cancer for a cell with this type of intervention, but it seems that all of them could be minor and eliminated by the cell itself on early recognition.

        This does not answer your implied question as there is no answer. However I hope that such an opinion might assist in seeing that there is probably a better method of analysis for the therapy’s envisaged future (current?) use.


        • Frank – I think it’s simpler than this. There are experimental results indicating that telomerase therapies will DECREASE risk of cancer. What we observe is the difference between known mechanisms that facilitate cancer, and larger known mechanisms that prevent cancer.
          – Josh

    • Dear frank6,

      I did not obtain the explicit approval of the authors of the patent Blasco et al patent (Telomerase reverse transcriptase for protection against ageing – EP 2402038 A1), so I cannot post the figure which shows the method used in the patent(a well known but far from cheap or cost-effective in any way) to deliver the hTERT gene. The figure is titled figure 1A and 1B at Arama Raporu (5) – the fifth picture from left to right. The method discussed in the patent you mentioned is also called tri-plasmid rAAV(AAV=adeno-associated virus) method and it is best explained at this site:

      The product of the patent you mentioned was used in the article:
      Telomerase gene therapy in adult and old mice delays aging and increases longevity without increasing cancer – Bruno Bernardes de Jesus, Elsa Vera, Kerstin Schneeberger, Agueda M. Tejera, Eduard Ayuso, Fatima Bosch, Maria A. Blasco.

      The method is far from cheap because for even a small number of viral genomes(carrying the transgene – in this case hTERT) three different sets of plasmids need to be generated through the usual molecular biology methods and then purified…

  30. I am currently working on my Master’s thesis ( at Bucharest University) which will explore the way in which the TERT gene(the molecular machine may be delivered using adeno-associated virus(AAV for short). TERT actually does the extending of telomeres using TERC RNA component – a sort of “matrix” if you see what it spells out it spells out 5′-TTAGGG-3′ in reverse and in RNA (of course) so it would be 5′-CCCUAA-3′ ). But it appears that the TERT component is what is missing in adult somatic cells, where telomere extension does not take place.
    In the near future I plan to pursue this venture , perhaps in the US with Michael Fossel.

  31. Thank you Josh for the reassurance on the telomere lengthening question. Nice to get input from a professional source.
    Perhaps you could help me with something that’s been on my mind for quite a while and that is the very large differences in rejuvenation results of Jaskelioff and Blasco on mice. They both use essentially the same method ie. adding telomeres to the chromosomes for rejuvenation.
    What is the reason for this large discrepancy?

  32. Your statement about entropy and life is unfortunately, or fortunately wrong.

    Entropy of Life can be considered as decreasing since it is not a closed system.

    • I think we have no disagreement.
      When I look at what I said, it seems clear to me, and consistent with what you are saying.
      Living systems are able to reduce their internal entropy by increasing the entropy of their environment. That is the essence of not being a closed system.
      Where is the misunderstanding?

  33. “there has been one heart patient who has received the AAV/myostatin treatment it with excellent results. ”


      • Oh please, NOT Parrish again. You can read about Liz Parrish here, written by an ACTUAL scientist with a PhD in Microbiology as opposed to Liz who has NO advanced degrees in medicine whatsoever. None in Microbiology, Neurobiology, Chemistry, Molecular Biology, Genetics, Genomics, RN, LPN, or even Phlebotomist, however we have been able to verify she held one license, to cut hair, but that has since been revoked or expired

        Additionally, I was cc’d on an e-mail written to you Josh by Dr. Michael Fossel M.D. PhD, Dr. Fossel stated: “I am not and have not been on Liz Parrish or BioViva’s board of directors, nor she on mine. Liz’s main motivation is MONEY, where our own intent is to ensure safety, efficacy, and credibility by pursuing FDA-sanctioned human trials aimed at Alzheimer’s disease, this is where our philosophies and protocols differ by 180 degrees. Liz once placed my name on her board of directors without permission, (Hmmnn, sounds trustworthy, NOT!) and I requested that she remove it, which (as far as I know) she did. Neither I nor our biotech company, Telocyte, are in any way associated with Liz, BioViva, or their “board”, nor will we be. To be clear, we are not associated with her in any manner and I would appreciate if you would help spread that word Josh.

        Lastly, on Liz’s well press released “experiment,” If it was a real gene therapy, it’s hard to see how it could have such clear results because of the numbers problem with gene therapies in general. There could be some cells with telomerase, but all or most leukocytes? I would want to be extremely sure that the data was true before accepting that.
        It’s not so hard to fake it by culturing her leukocytes, transfecting them, then taking a blood sample, separating the leukocytes and adding cultured ones back in.
        In mice that had an mTert system transfected, the life span gain wasn’t that big. In older mice, it gave a median gain of 13%, and a 90th percentile gain of 15.6%. There are more effective ways of extending life span with lower probable risk. I have methods in my pipeline that have much greater effect on life and health span than this telomerase should if it works. This first one has unknown extension, but should be relatively easy to get through FDA. I’m doing the GHRH because it should be relatively easy to get through FDA, it’s meaningful for health-span, and I don’t want to blow up like a Theranos if I do get serious investment. When I do something, it’s got a solid basis.

        Kekich FTC actions past
        I don’t know how to obtain FTC actions served on companies, but there must be a public record. One of David’s companies is Piranha Marketing. Grapevine is pretty strong on Kekich faking results for his supplements.

        Faking it
        A friend of mine who knows the crew involved with Liz well suggested a very simple method of faking those telomerase results. This scientist is more suspicious than I am, which is hard to do. Just submit a sample from someone else as sample 1 or sample 2. The article claims she had shorter than normal telomeres for her age, 44. So I thought that perhaps she had submitted an old person’s sample first, and then her own. But digging into it, that’s not the case. If this was faked, it was done with sample 2.
        This sounds like it would be difficult, but we’ve confirmed that commercial labs don’t check to make sure that a sample of blood is actually from the person that is claimed on the label. Afterward, it is disposed of.

        The article states Liz went from “6.71kb to 7.33kb” in the test results from Spectracell. It also says that her telomeres were short for her age. “SpectraCell‘s … revealed that Parrish’s telomeres were unusually short for her age.”

        According to Spectracell’s posted chart, 6.71kb is significantly high for her age, although possibly within the range of normal variation. So the article makes a false claim that she had unusually short telomeres.
        But look at this chart. Instead, hers were longer than normal for her age in the first sample. The first sample could be from a 32 year old if their chart is correct.
        I looked to see if their chart is correct and this 2013 paper says cells lose on average about 24 bp per year in adults. Starting at 8,000 at 18 gives 7.8kb for a 25 year old. At 44, that would be 7.4kb, which is what Liz’ second results show. But there is literature saying different assay methods show different telomere lengths, and 8,000 may be long for an 18 year old. If we assume 8,000 is a 12 year old, then a 25 year old would be 7.7kb and a 44 year old would be 7.2kb. So, if we adjust the starting value downward to what Spectracell’s chart shows at 25, and start at 7.4kb, then a 44 year old would have 6.9kb. That’s close enough to believe Spectracells chart.

        Questions on the protocol as claimed
        First, this PR doesn’t tell us about her somatic cells as a whole because of the numbers and access problem. She may have transfected a fraction of cells in her body, but it is less than 0.0026882% of cells in her body.
        Not knowing the vector, capsid count, or anything else about the treatment, I can’t be sure. I can estimate, because it is certainly a viral vector, probably AAV because that was used in mouse studies. Her injections contained no more than 10^12 viral capsids unless they are doing something unusual. Jesse Gelsinger died from 3.8×10^13 viral capsids, and the standard is to use 10^10 – 10^12 in humans. Approximately 1 in 1000 of those transfect a cell. So the useful range is 10^7 to 10^9 viral capsids. That seems like a lot of transfected cells with 10 million to 1 billion viral capsids accomplishing transfection. But this is a probabilistic thing, and the most accessible cells will be transfected multiple times. Leukocytes circulating in blood will take up a lot of them. A large number will end up off-target, transfecting cells in vascular walls. And bone marrow cells will have varying degrees of transfection.
        If you model it as random with all cells having equal access, you get a poisson distribution. To get 90%+ of all cells transfected at least once, you need at least a 5X multiplier, and probably 100X if mouse is any guide. That would mean that to be really meaningful, they would need to inject ~4×10^15 to 4×10^17 capsids. But it’s believed to be skewed toward first-contacted cells.
        Humans have 37 trillion cells (3.72×10^13). – “An estimation of the number of cells in the human body.” Mice have about 1.2×10^10 cells. A mouse will be injected with 10^12 or more viral capsids in one of these gene therapies. This is because mice are able to take 3000 times more per kg of immune stimulants without generating sepsis-like syndromes. So you can see that transfection is proportionally far lower in humans. You have more cells in your hand than a mouse does in its body.

        Second, to the extent that the report is true, what it means is that she should have made some population of stem cells in her bone marrow more susceptible to cancer, which means increased lymphoma or leukemia. – “Telomeres and telomerase in leukaemia and lymphoma”
        Hematopoetic stem cells are the fastest dividing cells in the body. That’s why they are so susceptible to radiation. We know that when iPSCs are cultured beyond the Hayflick limit of 40-50 times, pathology shows up in chromosomes. – “Genetic instability of modified stem cells – a first step towards malignant transformation?”
        The effectiveness of our stem cells at dying off when something isn’t right is what determines our later life resistance to lymphoma and leukemia. A super-centenarian was down to two apparent clonal populations for all of her leukocytes. – “Somatic mutations found in the healthy blood compartment of a 115-yr-old woman demonstrate oligoclonal hematopoiesis”
        So, far from being something to celebrate, seeing this in her blood is reason for great concern. If this is true, then she has uncontrolled super-activation of telomerase. So she’s added 20 years of length to some cells? That took what, 6-7 months? What will be the outcome of this? We can’t exactly be sure, but we do know that without secondary genes added to telomerase, cancer is an expected primary result.
        There is a paper that did not appear to show cancer in mice from Blasco. – “Telomerase gene therapy in adult and old mice delays aging and increases longevity without increasing cancer” But others used anti-cancer genes together with telomerase to prevent it.
        Will she get cancer? We shall see. Let’s hope not because it’s pretty nasty to die of lymphoma.

        Faking it by laboratory methods.
        Last, there are ways to fake this that don’t cost too much. Take her blood, use a Ficoll spin to separate her leukocytes, culture them by standard techniques, apply telomerase transfection to them, take a blood sample, separate the leukocytes, then add the cultured cells and send it off to the lab.

        • December 27, 2016

          Dr. Chris Roberts
          on May 17, 2016 at 1:05 am said:
          Oh please, NOT Parrish again.

          Avi Discussion: Thanks to Dr. Chris Roberts for a rather knowledgable discussions on BioVIva CEO +.

          But if we are really interesed in “Telomerase/Telomeres” knowledge based medical intervention development, it would be great help to discuss Dr. Michael Fossel, Md. Ph..D, and his initative , start-up company, called Telocyte. He has also written a rather well regarded book recently (2015) called “The Telomerase Revolution”, outlineing his optimistic “revolutionary” expectations, and his company’s focus on doing “Human Trials” for Telomerase based human trials in the United States , when all the “safety issues’ are addressed. Can anyone make comments or critique Dr. Fossle’s book , “The Telomerase Revolution (BenBella, 2016) ?

  34. Hello
    I signed up to receive notifications for your blog today. I am very interested in anti-ageing research and try to stay abreast of it. The Bioviva company sounds so cutting edge. I totally want to go get myself injected with telomerase bottleneck thing and the other thing but I just don’t have a couple hundred thou to spare currently. I am 66. Everyone says I look younger. I feel fine and I eat right and take a handful of supplements three times a day to keep myself fit. I did get the TA 65 ( concentrated astragalus) product and took that at the recommended dose for 2 yrs. Not sure what that did. I THINK it helped but I do so many things, not sure what really did help. I still take the TA 65 at a lower dose.
    What do you think is realistic for a person my age to hope for as far as being able to avail myself of anything that will make a big difference? If I follow my family’s typical trajectory, we start to fall apart pretty bad in our late 80’s. Up until then both my parents were active and healthy. So that gives me about 20 years til I am ready for the nursing home. Do you think in the next 20 years there will be something meaningful to push that back? I sincerely hope so and I know a lot of other “boomers” my age do too.
    What say you?
    By the way, I love the tapestry picture of the lion and the stag playing chess on your home page. So Game of Thrones!

    • @Sabra: For what it’s worth I am following Bioviva’s progress and I can tell you for certain that a pilot test in a person is being planned and can be ready in six weeks. The caveat in this is funding as this is not a paid for therapy by the patient given it is a purely experimental first pass attempt at rejuvenation.

      The plan is it will be crowdfunded, hopefully via which launches in August and is the only life extension and rejuvenation crowd sourcing platform to bring research like this to the public. A first pass attempt is going to be administered to a patient targeting the skin and sub dermal layers to confirm rejuvenation occurs as it has in animals and Human cells treated in-vitro.

      Back in 2000 Cal Harley conducted this very relevant experiment in human cells showing considerable benefits from Telomerase treatment including reversal of cell age, improved function and repair of the Dermal matrix and a return of collagen production to youthful levels. This is an example of the “Free Lunch” Josh is talking about.

      The Pilot study should be announced soon and if Bioviva can get the funds together will be pushing ahead and proving once and for all Telomerase has huge potential. I will update once details are agreed.

      Dr Michael Fossel plans to bring the same gene therapy to the FDA under a IND request and Bioviva will share data with him. If the offshore test therapy works as hoped this should considerably help justify Dr Fossels request for it to go to clinical trials in the US. His initial aim is to use Telomerase to cure AL under the “Telocyte” project.

        • December 27, 2016

          Steve H
          on June 16, 2015 at 9:22 am said:

          Back in 2000 Cal Harley conducted this very relevant experiment in human cells showing considerable benefits from Telomerase treatment including reversal of cell age, improved function and repair of the Dermal matrix and a return of collagen production to youthful levels. This is an example of the “Free Lunch” Josh is talking about.

          Avi Discussion: This company Geron who did this favorable study back in 2000, is mentioned in various places in Dr. Michael Fossel’s recent book, “The Telomerase Revolution”. But so far I have not seen any “pilot study” announced by Geron as follow up to their 2000 Study. I have to go back and check what Fossel said in his book about his link to Geron. But it’s end of 2016 , almost 2 decades later. Why hasn’t Geron announced any clincal study since then ?

      • Does anyone have information how uniformly AAV infects cells in the body. Most viruses have some level of tissue specificity (although this can be altered through clever genetic engineering to some extent). Would it be necessary to infect all cells uniformly? Or would infecting just stem cells (again in all organs) be adequate. If so how would one do it? Does anyone possess any scientific information on this? The same may be true also for TA65. The tissue distribution may be not uniform thereby reducing the effectiveness of a telomerase activator. I haven’t seen any studies on this. Hopefully, these issues will be addressed as the research progresses.

        • The problem is that TA-65 is the only substance for which there is data on the record for telomerase activation. But Bill Andrews is head of the company that does the assays (Sierra, which has now been renamed Andrews, Inc) and he has told me off the record that there are much better substances.
          – Josh

  35. By the way Josh I have sent you this privately but I thought it was such an interesting study involving TERT/Telomerase and its potential role in AL and how Dr Fossel’s proposed Telocyte project or the Bioviva therapy which is the same may well work against AL that I thought I would share it on here. The “Free Lunch” you are talking about seems to be increasingly likely.

    I am growing increasingly more confident that Telomerase is going to be a huge step towards addressing the dysfunction and consequences of aging.

  36. Hi Josh:

    You have mentioned that “Cycloastragenol is a weak telomerase activator compared to man-made chemicals discovered at Sierra Sciences, and even compared to some other herbal extracts”. What are these herbal extracts that are more potent than cycloastragenol? I have found some plants extracts have purported hTERT activating property, but the science does not seem solid. If you know of some proven extracts that are more potent in activating telomerase I’d be very interested in learning about them. Thanks

  37. So what are the telomerase activators better than TA 65??? Cycloastrogenol? something else? And please where can you get the eye drops that help you regain your vision without glasses? I went to the Russian site for Vizmotin (spelling?) but did not see anywhere to purchase the product in the US.

        • Thanks for answering. Very cool. read the info about the peptides and how they are supposed to work. why are organs set at 42%? I didn’t get that. Has anyone here tried the peptide combinations for anything? they sound a bit too good to be true but worth a try. Russian research is certainly “out there”. One thing to keep in mind when ordering products made from beef and these seem to be, is what is the source? Creutzfeldt Jacob disease is around and can be in products like this. but it would be rare.
          thanks for info about the eye drops Josh. the 10 dollar thing was only a DEPOSIT on 150 dollars. I got the one for 139 I will report on its efficacy here.

          • Sabra – You’re welcome. My comment may have been too cryptic. The antiaging systems website is a great place for product information.

            One Russian peptide that you might reconsider is described at Read the product information there and then read user reviews at Typically, I read reviews at Amazon before I purchase. The price is $40 plus postage at both sites.

    • It’s not necessarily true that the first ingredients are the most potent. All these ingredients have been tested in cell cultures, but not in the human body. So it may be that Isagenix is hedging their bets by including more of the less potent ingredients. For example, the first ingredient is silymarin (milk thistle) which is poorly absorbed from the stomach into the bloodstream.

      • Thank you David PS and Josh. So much to think about. New things to try. So glad I stumbled on this website.

  38. I have to admit that I’m a little confused. This article talks about how telomerase activators are good for life extension, but I was just reading about berberine, which is supposed to mimic metformin, and it was called a telomerase inhibitor. Is metformin both a telomerase activator and inhibitor?

    • I had missed this…Thanks for pointing this out.
      My first guess is that it makes little difference unless we are simultaneously taking berberine and a telomerase activator; but many people might want to do exactly that.
      So there are potential tradeoffs with berberine as well as metformin.

    • There is a new publication (Aug 2015) from Wayne Alexander’s lab in Cell Reports that alpha lipoic acid activates the function PCC-1-alpha which induces transcriptional activation of hTERT in cardiac myocytes reversing vascular aging and atherosclerosis. There is a lot more science on how ROS inhibits hTERT (which can be relieved by N-acetyl carnitine).. PGC-1-alpha also activates the cytoprotective Nrf-2-mediated antioxidant/electrophile response element (ARE-ERE) preventing high fat-induced myopathy of the artery. It is indeed a fascinating paper and it will be worthwhile translating it into simple language for those who have difficulty understanding the paper.. It also fortifies the fact that activating telomerase may not be all that bad as the sceptics predict (without solid evidence)

  39. This has to be the most informative blog on telomere therapy.
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    This may help save thousands of lives! Has anyone been using Al Sear’s Telo-Essence?
    This could be the most portent telomere formula to date., A 3 month supply
    will cost a whopping $597 after discount! For more infor goto
    For those of you who want to make it more affordable, you can check the ingredients at
    Most of the ingredients can be bought a any supplement store at very affordable prices.
    We now have the means to live a much better quality of life for much longer than we ever dreamed possible!
    All it needs is action on our part.

    • I have bee reading about Trichostatin-A and telomere lengthening, GDF11 activation, and it’s benefits to progeria. Interesting, and available for purchase from several labs.

    • After researching for months on Telomerase and the available potential activators, my friend and I decided on Dr. Sear’s Ultra-Essence (which was originally Essence and now advanced to Telo-Essence) over Product B and TA-65, the other big names out at the time. Multiple researchers and/or blogs had been recently suggesting that Astragalus may be a “weak” activator of telomerase and that the clinical results from TA-65 trials/usage may better be attributed to other ingredients in Telomerase Activating Supplements. Telo-Essence contained many ingredients in that category and that are thought to have telomere maintenance (ability to reduce shortening) or lengthening effects. My friend, being a couple decades older (chronologically) than me began immediately and has been taking Ultra-Essence (and more recently Telo-Essence) for around a year now. I decided to wait to get my Telomeres tested/measured through LifeLength to have a baseline for determining the efficacy of the supplements/therapy. My friend has noted increased mood and sometimes energy and sleep but isn’t really keeping a scientific record of changes and didn’t even do any before/after facial photos to determine if hair or skin is “youth-ening” in any way. I plan on making a much more comprehensive study of the supplement and a few other friends are likely to jump on board when I get my baselines established and start my protocol. Will be sure to keep Josh/this blog updated on our results.

  40. Certified Nutraceuticals has developed a product to halt Telomere shortening. The product is Telos95® which is highly purified Polyphenols isolated from Grapevine and Olive Leaf. Clinical study by Life Length of Madrid, Spain world experts on Telomere testing was performed. Objective: To assess the potential effect of Astragalus root extract P.E. and Telos95® on telomere length in a cell line.

    The present study was aimed at assessing any potential effect of the compounds called Austragalus root extract P.E. and Telos95® (Certified Nutraceuticals) on telomere length.
    By using Life Length proprietary TAT technology and the lymphoblastoid line C0126, we measured both median telomere length and the percentage of short telomeres (< 3kb) in these cells daily supplemented with these compounds up to ten days.
    Astragalus root extract P.E. showed no demonstrable effect on telomere length in any of the conditions of the study.
    On the other hand, Telos95® had shown positive results to halt telomere shortening when cells are supplemented during 10 days with this compound at a concentration of ~0.4mg/ml. We believe the measured effect does not involve telomerase activation because the change in median telomere length is only significant against untreated cells incubated during 10 days (i.e. cells which telomeres get progressively shorter) but not against untreated cells at time 0.

    As a final conclusion, Telos95® clinical responses shown positive results for Telomeres health maintenance and support. The implications of Telos95® for longevity are a leap forward in the science of aging. Telos95® is a new invention of highly purified proprietary natural ingredients – it is the only affordable scientifically validated ingredient for Telomere health support. Certified Nutraceuticals continues to stay on the forefront of research and innovation and is always at least 5 years ahead of its time with new anti-aging ingredients.

    Telomeres and Ageing Additional Science: Check this PDF file

    • Abdul –
      I can’t find this article in Google Scholar. Can you send a link please?
      It’s hard to draw conclusions from such a limited account. It may be, for example, that Telo95 simply inhibits cell replication, which would be sufficient to slow telomere shortening.
      – Josh

      • Josh I know you are aware of this news and will be in contact with Liz soon but for the interest of the readers I will leave this here.

        Finally after seven months hard work bioviva moves into the first human telomerase therapy. Even more interesting is its a twin therapy with htert and a proprietary myostatin inhibitor. The therapy is whole body induction using a broad serotype.

        Let’s hope the initial data is positive but so far patient is doing well two weeks after deployment.

      • Hello Josh,

        I have tried several times to submit a reply, but always came back. Let see this time if it works. Please see this link:

        I also have more information to share with you. You may know that there is a lawsuit against TA65 for claiming their products activate Telomerase. Life Length of Madrid that made our clinical study also looked at Austragalus which TA65 isolated the root. The present study was aimed at assessing any potential effect of the compounds called Austragalus root extract P.E. and Telos95™ (Certified Nutraceuticals) on telomere length. Astragalus root extract P.E. showed no demonstrable effect on telomere length in any of the conditions of the study. On the other hand, Telos95™ had shown positive results to halt telomere shortening when cells are supplemented during 10 days with this compound at a concentration of ~0.4mg/ml. We believe the measured effect does not involve telomerase activation because the change in median telomere length is only significant against untreated cells incubated during 10 days (i.e. cells which telomeres get progressively shorter) but not against untreated cells at time 0.

  41. I saw a You Tube video that Liz Parrish,CEO of Bioviva, made about her recent involvement with an experiment about a month ago, in which she was injected with the adenovirus? containing the gene to activate Telomerase. This is such an amazing experiment. Why is there not more coverage of this? In the video she said that the doctor who injected her had done himself a few years ago with good results, i.e., he has virtually no arterial plaque. More info please! Ms. Parrish herself looks pretty youthful so unless she reverts to a 15 year old it will be hard to tell if there is any phenotype change.

    • Because it’s an offfshore tourism scam run by a hairdresser and her compadre, a US Dr who was fined and ordered to cease and desist this activity or lose his license. It’s a scam aimed ich naive people who think they can buy their way to living forever. Most egregious scam in the world sans the catholic church.

  42. This is a very good question and I have also wondered why there is not too much publicity about it. For one, I saw an unconfirmed statement in a blog that it costs $180,000 a pop. But the main reason why there is scepticism is because (1) there has been some doubts cast more recently about telomarase most likely because TA65 – the face of telomerase activation therapy — may not extend life (reports from a Spanish lab showed no improvement in life-span of mice, but did show improvement in certain other biochemical parameters. This is not to say telomerase activation has no role in extending life-span — it just tells us that TA65 may not be what it is touted to be (I wish they would do a proper double blind clinical trial to monitor changes in some biochemical parameters associated with aging) (2) the Biovia people are relying on some mouse data as the basis for the therapy. No clinical trial has been done. We don’t know how many tissues are infected by the virus and how many express telomerase. Even if all tissues express telomerase, does it stabilize or lengthen telomere in these tissues. No one knows. They need to do some better clinical science before they put something out in the market.
    Regarding reduction of arterial plaques, alpha lipoic acid may be able to do the same trick and does not cost $180,000. Again no clinical proof, but neither does AAV delivered hTERT. The Sr author in the paper was Wayne Alexander and it appeared in Cell Reports (2015) 12, Pg 1-9. To quote verbatim “Xiong et al. show that PGC-1a disruption drives telomerase TERT downregulation, telomere malfunction, and DNA damage, thereby developing vascular aging and atherosclerosis. Ectopic expression and induction of PGC-1a by ALA activate TERT and ARE/ERE signaling and ameliorate aging related pathology”. The studies were quite elegant and the experiments prove an association of hTERT expression and reversal of vascular aging.

  43. From Geron website – see especially last sentence. Are they then against telomerase activators in cancer?
    Telomerase is upregulated in many tumor progenitor cells, which enables the continued and uncontrolled proliferation of the malignant cells that drive tumor growth and progression. Telomerase expression has been found to be present in approximately 90% of biopsies taken from a broad range of human cancers. Our non-clinical studies, in which the telomerase gene was artificially introduced and expressed in normal cells grown in culture, have suggested that telomerase does not itself cause a normal cell to become malignant. However, the sustained upregulation of telomerase enables tumor cells to maintain telomere length, providing them with the capacity for limitless proliferation. We believe that sustained upregulation of telomerase is critical for tumor progression as it enables malignant progenitor cells to acquire cellular immortality and avoid apoptosis, or cell death.

    • So is what your saying: telomere is upregulated by tumor cells anyway regardless of weather the normal cells are activated with a gene to produce telomerase. Does it look possible that a tumor would produce more telomerase, for upregulation of telomers, if normal cells that it may possibly spring from or tumors are less likely to come from treated normal cells in the first place.

  44. The implication of playing around with telomerase activators/inhibitors is clearly not fully understood at this point. The long term implications even less so.

    I agree with Josh, that in order to drastically add years to lifespan, we need to use a drastically different approach.

    However, a pharmaceutical approach seems unlikely to work out in the near future. The biological complexity of aging is just too overwhelming IMO. It is true that every day we get a more complete picture of the biological processes involved in aging, but at the same time complexity increases. The number of variables is simply overwhelming.

    With simple, well-documented practices like CR/IF, exercise, healthy diet, we can get rid of most cardiovascular diseases, AD and some cancers. It will add life to years, but not many years to life, unfortunately.

    • >>The biological complexity of aging is just too overwhelming
      Why would you say this in light of the fact that so many simple interventions are known that substantially extend life span in test animals. There are small molecules, single genes, and such things as CR and hormesis, all causes for optimism.

  45. Because humans are not mice and commonsense dictates otherwise.

    Aubrey keeps saying we just needs to fix 7 key issues. Just get rid of old garbage inside cells. Just get rid of garbage outside cells. Just fix mutations, just fix cancer, just fix, just fix….. We just need an enzyme and so on.. He keeps talking about the human body, as if it was a car sent for maintenance at the local garage.

    His SENS team needs to orchestra a “one-size-fits-all” pill (still taking into account each of us have a unique genetic setup), which addresses all 7 areas at the same time.

    I hope he will succeed, but I have my doubts…

  46. Your theory and approach seems more nuanced and realistic compared to Aubrey’s, which I quite frankly think belongs in a fantasy world. Especially the timeframe he has given for eternal life.

    The signalling approach is especially appealing, and if we can get to a point where we can rejuvenate the body to a somewhat younger state, at least we have achieved something. I don’t think everybody necessarily wants to live a thousand years. If I could reach 120 in a not too bad shape, I’d be more than happy. Let’s be realistic…..

    Here, Dr. Tyrell in the act of evolution and Roy Batty as his imperfect creation in the epic science fiction “Blade Runner” (warning: not for the faint hearted):

  47. Have tried most if not all of the supplements listed on this blog. Thanks all for input. So far, my personal favorite, feel better with it almost right away, is SYSTEMA by Gematria products. It’s inventor is an interesting character, Dr. Todd Ovakaitis. A Johns Hopkins trained physician who has abandoned medicine to make nutritional supplements and work on something he calls the Qi Laser. I find his work fascinating with the right blend of science and out there ness. Dr. Todd, as he is called, has some pretty persuasive arguments to bolster his products.
    Report on the Vismotin eye drops: not much change. Too expensive to continue without better results. I gave it many months. BUT I did start to see better after starting SYSTEMA.
    Also, those of you with bad backs, joints etc., really hyped about a very affordable product called the Micro-pulse. Look at the guys website, he says it best:

  48. Hi Josh, what are the most potent herbal telomerase activators? I have taken TA-65 before and didn’t notice a huge difference. Thank you for this article, it was great!

    • Daphne –
      Don’t expect any noticeable changes from telomerase activators. Their action continues over years, and there are no short-term benefits. We don’t know which of them work best because data is proprietary. Sometimes, even ingredients are proprietary. TA-65 is the only one with published data behind it, but that doesn’t mean it’s the most effective.
      – Josh

    • I may have mentioned this somewhere in this or another blog, but I read Xiong et al from Wayne Alexander’s lab at Emory University that alpha lipoic acid is an activator of telomerase (hTERT). The authors showed that PGC1 alpha downregulation leads to ROS production as well as hTERT inhibition in ApoE knockout mice, which can be reversed by alpha lipoic acid at moderate doses in these animals. However, they looked at endothelial cells only (the study was focused on atherosclerosis) so we don’t know if this is true for other cell types. The data is very convincing and was published in Cell Reports. I could not find any comparable studies in humans or in other cell types, so whether ALA will work as an hTERT activator in humans in most or all cells is an open questions. It will be interesting to see if anyone else has done studies since the above publication linking ALA with telomerase activation (they also show PGC1 alpha and Sirtuin 1 activation by ALS in these cells). Remember, the alpha lipoic acid we purchase commercially is usually a recemic mixture, so only 50% of the dose is effective.

  49. I am a small animal holistic veterinarian. Four years ago I did a liposuction stem cell procedure on a Great Dane. I took fat from the dog, the fat was mixed with platelet rich plasma and sent to a lab to have stem cells cultured and multiplied. We then injected the stem cell product back into the dog for its condition. The lab that did the stem cell enrichment had a way of giving a count of the stem cells. The count was a certain number, I forget what it was exactly. However, I do remember that we repeated the procedure after a year. This time we prefaced the harvesting of the fat with feeding the dog six weeks of 3 capsules a day of a preparation made by Gematria Nutraceuticals. It was the precursor to the product they carry now called SYSTEMA. This time when we did the stem cell harvesting the cell count was hundreds of times higher. The lab said they had never seen such a high stem cell count. So I know this product does that. It would seem logical that it lengthens telomeres as well. I take it and I think better, eyesight better, more energy, lots of things better. Things that I noticed. Not just, gee I think maybe this is better. It was very clear. So that is my testimonial.

  50. Has anyone here tried Telos95 from Certified Neutraceuticals? Outside of this site and a few companies selling it I am unable to find any information or reviews on this product. Thanks in advance for any pointers.

  51. Could you please recommend me the most effective Astragalus root extract supplement for immunity booster and telomeres extension?
    Thank you

  52. Michael Fossel told me that the best telomerase activators, on this very present moment, available on market, are not doing age reversal, are not fading wrinkles, are not make you younger… although a lot of advanced skin related cosmetics had been invented but yet thay all failed to reverse the aging of the entire body… But the new activators, invented by Michael Fossel using his new technology, are now on trial for toxicity on lab rats and later on, in the second half of this year, human tests will begin in 12 Alzheimer patients. Then, I’ll have a new interview with Michael Fossel in december.

  53. Dear Josh,
    I came across your name after reading a book dedicated to Lynn Margulis to which you contributed a nice article. Enjoyed reading it! The reason I am writing is to comment on the telomerase story. Actually, I do research on telomeres and telomerase. It seems that reality is always more complex than we anticipate. The story of telomerase and life extension would be nice if there is no biological alternative to it. And also alternative to alternative and so on. The alternative mechanism is called ALT (alternative lengthening of telomeres). I would also caution optimism about the fact that stimulating telomerase is not potentially carcinogenic. Again, the story here is more complex than you suggest in your blog post. The origin of telomerase is very interesting. Telomerase is similar to ancient retrotransposons. I have written recently about the role of telomeres including telomerase and ALT in chromosome evolution (

    • I agree that there is some evidence that telomerase can promote carcinogenesis in some cell types, but longer telomeres also prevent those cell types from forming in the first place. It remains a controversial issue, but the evidence as I see it points to the conclusion that telomerase prevents more cancers than it causes.

  54. Hi Josh, after quite a lot of excitement over telomere gene therapy a few years ago, it seems to have all gone quiet. Perhaps this is simply because so many people are now focused on Senolytics. But surely telomerase therapy is still a valid intervention against aging and is likely to be produce additional benefit when combined with other treatments? Have you any news and do you still consider this approach valid?

    • The reason the “excitement” as you put it has severely subsided is Liz Parrish and Bioviva began her financing by receiving one investment/donation and funds she misappropriated from another. I’ve seen the documents, canceled checks, 1st class flight receipts, 5 star hotel suite receipts, etc. From day one her entire plan for Bioviva was structured as a medical tourism scam. In short; use herself as “patient zero” thereby giving her complete control over every phase of the “experiment. The procedure (if there was one), the Dr. ((if there was one), the results ((if there were any), the “documentary film crew” which allegedly amounted to one man with a camera ((if there was one), Where’s the documentary? What’s it entitled? Did it premiere at Sundance, Tribeca, Cannes or TIFF ((if there was one), and finally report perfect results, hang with the Aubrey de Grey Quack Crew and find a country willing to allow a lab to be utilized (for pay) to hustle scared, naive, wealthy, elderly people into paying exorbitant sums of money in hopes of curing their ills and / or lengthen their life. The reason why you’ve heard nothing is Colombia said no, Fiji said no, Guatemala said no, Panama said no and any reputable scientist remotely involved backed off, far off. No location, no approval, no lab, no name Dr, no scam. This began in 2012 long before anyone here ever heard of it when the initial funds were misappropriated and reached its height when she had the alleged “treatment” in late 2015, lots of talk for a year and since N O T H I N G exactly where it began and exactly where it’s ended. Read the Bioviva Wikipedia page which we’re confident was originally written by Ms. Parrish herself (a Wikipedia no no) and once the Wikipedia editors began looking into the facts now it had appeared on their site things went downhill quickly. Have a look and form your own opinion;

  55. Hi Josh,
    Nice article and lots of good comments. I am obviously a few years late to the party (this thread). It seems that most are concerned with supplementing.
    My plan is to increase length or at least slow things down by eating a ketogenic and Fasting Mimicking Diet (FMD).
    I am using Teloyears to do my lab work.

    My baseline: 52 years old and 40 in teloyears.

    For the FMD I am planning to use prolon to help with the fasting.
    So in about 6 months I will be sending another blood sample to teloyears to see if the effort was worth it. I’ll post my results when I get them.


    • So you are increasing autophagy which is a very powerful anti-aging tool. Perhaps there is a synergy to combining telomerase production with an increase in autophagy.

  56. sylibinin, which increases telomerase three fold in liver, in earlier findings on methylation patterns (before Horvath clock) was observed to stop these methylations in liver. So… what method of inducing of telomerase you refer to and what tissue it was observed in? Because your claim that telomerase speeds aging is exactly opposite to what was observed and confirmed before.

  57. Hi Josh,

    I would like to share a human clinical study on Telomeres. We have just finished a one year study that showed Telos95 “decreases TeloYear Cellular age by 8.52 years”. In other words, Telos95 halts the shortening of our Telomeres by 8.52 years.

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