The repeating sequence of the Telomere-TTAGGG has proven to be a gold mine for determining biologic age ( how old your body is acting!) and disease prognosis ( how bad you are likely to get something) as well as the effects of stress.

A recent study on the effects of racism on the telomere length of black men was the latest to show how social stress can affect longevity.  I have concerns about how the study was done but I think it makes sense to say that this kind of stress is detrimental to anyone’s health no matter what race or color.

This study builds on previous studies done in orphans who grew up with universally shorter telomeres than non orphans,  and the effects of stress on caregivers responsible for sick children.  All of these situations lead to more rapid aging and faster decline.  You can bet being sick in general can shorten your telomeres and your life.

This was shown by another study involving men between 50 and 75 who were admitted with ACS, acute coronary syndrome. Basically they were on their way to having a heart attack and no doubt some of them did.  The ones with the shortest telomeres did worse.

This study echoes the now famous Farezeneh Far, Blackburn study that showed that Omega 3 (fish oil) levels were protective of telomeres in heart disease.

So it seems everyone is linking just about everything bad that can happen to you to short telomeres and everything good to long telomeres.

It would be a good time for me to mention that other diseases of aging like Cancer and Alzheimer Disease ( yes they dropped the ‘s!) are also linked to telomere length in terms of incidence and severity.

Now there is still a lot of disagreement among researching scientists as to whether telomere loss is actually all that important in aging.  This pretty much depends on what their pet project is and where their grant money comes from.

I have a simple ( my PhD colleagues would say simplistic!) way of explaining this. My friend Maria Blasco did a study recently that showed that turning on telomerase extends life span in adult and old adult mice.  That was the end point of the study.  There are many other people out there looking at things like intracellular junk (lipofuscin) mitochondrial function, calorie restriction, sirtuin proteins and mTOR inhibitors.  None of these strategies have been shown by themselves to lengthen life although some of them seem to improve health.

I am certain that ALL of these things were improved by telomerase activation or the mice would not have lived longer.  You can’t live longer with declining mitochondria, abnormal proteins and increasing intracellular junk.  It’s simply not possible.  But because these things were not specifically measured common sense takes a back seat to scientific skepticism.

Here’s the thing: They would rather remain skeptical than investigate these questions probably because their grand money does not include answering these questions.  It does involve protecting their source of income for their pet project however.

Here’s another thing: as I said above Telomerase Activation seems to be the only current feasible way to extend life in mammals.  The folks spending time on all that other stuff have been unable to demonstrate increased longevity AND healthspan.

Want it to be even more simple?

I will quote that bastion of American Health who brought us the great Dr Oz.

Yes, I am talking about Oprah who said “I want long telomeres!” She should be on TA-65!

You probably should too!

I am entering year 5 with nothing but positive improvements in both telomere length and % of short telomeres. Both are going the right way for decreasing biologic age.

What is youth worth to you?


PS what I have said here is especially important if YOU are under constant or severe stress, get sick a lot or have a family history of one of those nasty diseases above!

Drum roll and trumpets please!  A new cancer causing pathway has been found. It involves telomeres of course.

I bring it to your attention though, not for what it has shown us, but for how it its marketed. You see even scientists know they stand a better chance of getting recognition if they blow the trumpets and role the drums.  That means press releases and social media nonsense that is written by non scientists.

Now don’t misunderstand me. I give them the same “get out of jail pass” I often claim: “I didn’t make this world, I just live in it!”

Still as your source of the truth about all things telomere related, especially when it comes to your health and your understanding, I consider it my calling in life to make sure you are not blown all over the map by media hype and internet nonsense.

So let’s go over a few facts:

1)      Fact one: Telomerase does NOT CAUSE CANCER. Every time I write this I hope it is my last but that is never the case it seems.  85% of human cancers turn on telomerase somewhere in the process of becoming cancer. In the one or two cases we are clear on its actually one of the last steps ( villous adenoma to colon cancer) but cancer genetics are a diverse thing and no one knows the exact sequence that mutations happen in all cancers. There is a growing contingent of people out there who feel that contrary to 65 years of research, cancer may not even be a genetic disease. When telomerase is expressed in cancer it can be a) mutated, b) amplified c) transposed d) any other genetic abnormality that can lead to over expression! The key is to understand that things happen to cause cancer long before telomerase expression shows up to immortalize the cells, and that those things lead to the loss of normal control of many genes and their end products. Telomerase over expression does not seem to cause cancer by itself in the absence of other major changes.

2)      Telomerase is required for ultra long longevity and gene integrity in cells. Two of the best examples are germ cells (the things that become sperm and eggs) where there is a large amount of telomerase expression and stem cells where there is less. The later fact is probably one of the main reasons stem cells age albeit at a slower rate than the rest of our cells.

3)      There are normal “cell cycle check point” mechanisms that have been known for some time now that need to be bypassed in order for cancer to take hold.

4)      Longer telomeres are associated with a cleaner genome (fewer mutations) cleaner mitochondrial cell powerhouses (fewer mutations better function and better ability to make new mitochondria) and a lower and less sever incidence of cancer.

5)      While most cancers turn on telomerase there is another way for cancer cells to lengthen their telomeres and survive that does not involve telomerase.  This generally is reserved for the badest of the bad in terms of genetic instability (actually if I am being scientifically correct its “genomic instability” but you know what I mean!). This mechanism is called ALT.

6)      The ability to divide endlessly either using telomerase or ALT is one of the hallmarks of human cancer.

That brings me to the “latest findings”.

One Dr Jan Karlseder of the Salk institute discovered one of the mechanisms behind the ALT method of lengthening telomeres. Dr Karlseder found a protein called ASF-1 that drops down to zero and triggers cells in culture to use the ALT mechanism to lengthen their telomeres.

All well and good but here are my gripes.

Cancers in real life have measurable levels of that protein. It does not drop to zero in ALT driven cancers.

The super irritating insinuation that I see in all such articles “This will help us develop drugs to fight cancer”  is present here. Cancer drugs are expensive, Cancer drugs are deadly, Cancer drugs divert research away from, gasp, cancer prevention which no scientists is willing to admit they believe in. And there is no money in prevention. If you think this is a joke mark my words a cancer preventative treatment that is not a patentable drug will not be released until a drug company owns it. At least not over their dead bodies. That said most of the quacks who claim to have cured cancer and have been jailed for such statements actually do belong there!

Next, the press release is entitled “Cancer Causing Pathway Explained”.

Now I bet this was the sole concoction of the press release company. I do not think that such smart scientists would allow their discovery to be called named this way. The ALT pathway does not cause cancer, it is probably one of the last or later pieces in the puzzle.  By naming it this way they are propogating the myth that telomeres are responsible for cancer.

Next there is the usual talk of “balancing cell aging with risk of cancer” . This implies that we get old and die to prevent cancer from killing us. After I am done with the LOL ing I want to remind everyone that old cells, senescent cells seem to excrete inflammatory and yes cancer causing signals. For this reason it seems nonsensical to propose that getting old protects us from cancer. Especially when cancer is a disease of aging in 95% of all cases!

Summing it up, I would say it this way: We are barking up the wrong tree. Telomerase and telomere lengthening are cancer protective under normal circumstances. Guys you have to keep looking for the chicken that is laying the egg not examining the ingredients in the omelet!   This is also the reason I am intrigued if not convinced of the metabolic cause/component of cancer.  The genetic stuff leads nowhere but to an ever increasingly large ‘room full of pathways’ that has no end. Great for researchers and crappy for people who have or want to prevent getting cancer.

In 12+ years of research I can tell you two things with surety. Walk around with “high” omega 3 levels and keep your telomeres long anyway you can.

There are quite a number of famous scientists who are doing just that even though they will not say it in front of their peers for fear of ridicule. Me? I don’t care who ridicules me. I refuse to sit on my ass and get old when there are real answers to slowing and eventually stopping the process.

I will make this prediction. Classic science just like classic medicine will not make major breakthroughs in aging and health span. They will trumpet their findings just like the article above but the real breakthroughs will come from people who are actively seeking the answers and doing something about it every day .

That is you and me my friend!

Best, Dr Dave

ta-65-and-bonus_256I am not going to rehash all of the things I have said about telomerase activation and cancer in the past because there is too much new stuff to tell you about.

But I will remind you that cancer has a nasty and unique ability to amplify telomerase expression in just about every way you could imagine, recombination, gene amplification, mutation and more. This is “cancer’s fault”! It does not mean that telomerase causes cancer as I have said a thousand different ways and a thousand different times.

I will also remind you that this has absolutely nothing to do with TA-65!

Currently studies from Maria Blasco’s lab suggest that we can amplify telomerase more or less continuously for at least a year at a 10 fold level without increasing the incidence of cancer. That particular study showed a 25% increase in the life span of middle aged subjects (mice) and 13% in geriatric mice that were basically already hitting their maximum life span. Remember Dr Blasco disabused the world of a myth- that mice do not age like people e.g. they do not age by telomere loss. That in fact is not true as she showed- they DO age by telomere loss specifically the accumulation of higher and higher percentages of short telomeres.

Her studies were ground breaking because they showed mice as ideal models for human aging surrogates and, that telomerase activation was the only current way to extent life span in mammals.

This came in the wake of the calorie restriction studies in monkeys being shown as flawed which ultimately undermined the stance that CR works in mammals at least for the moment. And of course there was the DePinho study where mouse aging was actually reversed by telomerase activation.

Because Dr DePinho used a common trigger, the drug tamoxifen as the off on switch some anti-aging docs wrongly interpreted this to mean that bioidentical hormone replacement lengthens your telomeres. There is not one study that shows that although there are lots of reasons to consider hormone replacement! Same thing for men and testosterone.

Earlier( 2010) there was the peer reviewed TA-65 study in Rejuvenation Research which showed multiple improvements in health parameters in real live free living people, and as I have mentioned before there is a study that was started this past May in Barcelona which is randomized double blinded placebo controlled in people taking TA-65.

There is some interesting research though on telomerase and cancer, sort of. By sort of I mean that it is not directly relating to telomerase but to cancer.

First a study identified the specific region or “protein motif” where telomerase binds to the telomere. This is for all intents and purposes the “gate keeper” portion of telomerase that allows it to bind directly to the telomere and start making it longer. Of course the first words out of the researchers mouths had to do with the Big Pharma payday they expect to get if they can exploit this by “making a drug that might inhibit cancer”.

I will say this much: That drug better be very very specifically targeted to cancer cells only or its going to play havoc with the rest of the immune system and the stem cell population. Geron’s drug Imetelstat while brilliantly conceived by some very smart people has not panned out and actually looked like it made the cancer worse. Now a lot of this may have been due to poor patient selection when choosing who got the treatment but the sad fact is cancer figures out lots of ways to tenaciously survive these kinds of things while non cancerous normal cells do not. I stand by my original statements: non targeted telomerase inhibition is a bad idea!

The good news is that it (the  telomerase binding domain) can be used in the reverse and when the enough momentum and public desire for anti-aging telomerase activation happens and the profit margin gets big enough without the financial risk ( in other words when someone else does the hard work) Big Pharma will surely swoop in and capitalize. Then we will have the world’s first telomerase activating drug. Unless Google’s new anti-aging company beats them to it!

Another thing that you may be aware of is that some viruses cause cancer.  Recently an inherited Herpes Virus (HHV6A +B) was found to integrate into the telomere. When it “comes out” it apparently destabilizes the telomere and the rest of the genome and at the very least shortens the life span of the affected cells.

This is the first time I have ever seen documentation of a specific virus integrate directly into telomere DNA which is very different than the rest of the genome where other viruses often hide. While no one is sure what this means and there is not a direct relationship to cancer, there is a spectrum of associations of HHV6 with childhood Roseola or “6th disease” being the most common. There is speculation about Chronic Fatigue and MS as well.

The bottom line is something you already knew: destruction of telomeres and shortening thereof can have serious consequences.  Sickness aging and death are among them!

That is why I am constantly harping on you to “Take Care of Your Telomeres!”


Citation: Michael Harkisheimer, Mark Mason, Elena Shuvaeva, Emmanuel Skordalakes, ‘A Motif in the Vertebrate Telomerase N-Terminal Linker of TERT Contributes to RNA Binding and Telomerase Activity and Processivity’, Structure September 19 2013 DOI:10.1016/j.str.2013.08.013

Ok you’ve seen me beat up on the QPCR as a tool for accurate assessment of telomere length in the recent Ornish study. To my mind that was the absolute worst use of that technology and it invalidates much of what the authors concluded primarily because the study was so small and did not correlate well with telomerase activity. If you haven’t read that blog it’s here .

But another recent study that used this technology was exactly the kind where QPCR might actually be useful… sort of. You’ll see why I am qualifying it.

Keep in mind as you read this that the vagaries of these studies are not even in the consciousness of the people writing about them. They just look at the study and parrot back the conclusions as if they were fact. Apparently most people want exactly that with very little consideration for “the truth” because if the study supports their agenda, they are not going to want to hear anything that raises questions. Again if you read my blog on the Ornish study you will see that is not my way either.

Now onto this new study out of Holland. The gist of it is: if you are significantly neurotic you are shortening your telomeres and probably your lifespan and your health span more rapidly than you should be and more rapidly than someone who is better emotionally balanced!

This study had all the things the “Ornish” study did not. It had an “n” of over 3300 people. It used the telomere measurement over long periods of time between measurements, 1, 3, and 6 years. The combination of the large number of participants and the long delay between assays especially the 3 and 6 year gaps helps make up for some of the inaccuracies in this kind of test because the numbers give it more ability to predict trends and the time gives more chance for REAL changes in telomere length that are within the detection of the tests ability to actually happen. To the statisticians in the audience you know I just simplified the heck out of that explanation but most of the folks reading this will understand it and would not get the terminology you like to use!

Now would have HTQFISH been a better choice? Absolutely! It would have actually looked at the telomeres and seen the percentage of short telomeres as well as mean telomere length.  And it would have delivered the data in almost exactly the same time frame with more accuracy allowing the authors to have a shorter and potentially cheaper cost to the study while giving more information.

Why didn’t they do that instead? I can only guess but they weren’t looking for individual information only large group and mostly because scientists have not caught on yet to this technology!  You can experience it yourself if you want to at ADL Tests.

Now comes the critique part of the study e.g. what is wrong with it. Mainly that they had to use a questionnaire to access neuroticism. Questionnaires are a necessary evil in things like nutrition, exercise/injury study and psychiatry but they are fraught with potential errors mainly because people don’t always tell the truth when they talk about themselves!

Still if you look at some of the better studies that Epel and Blackburn have done in the past it fits with the findings. Mental stress whether self inflicted or related to “the others” in one’s life shortens our lives and can wreck our health almost as surely as some physical disease.

So what can you do if you are stressed, neurotic or carrying around harmful mental wounds?

Well you can start by forgiving yourself and valuing yourself. Then you can forgive and value others!

In the process you might read our little book The Immortality Edge – but hurry even Amazon is running out of them! You will find there several ways to achieve physical and mental balance that have worked for many people. Some are expensive (TA 65) and some cost nothing.

Only YOU can decide how much you are worth!



A recent study out of Italy links statin drugs to increased telomerase activity and slower shortening of telomeres.

If you read my blogs you know this is not the first time such an association has been found.  Back in March of this year I reviewed another article predicting we would see more of this. And now we have!

The gist of this study is that statins appear to have a mild effect on white blood cell telomerase activity. They do not lengthen telomeres but they could be put into the broad category of “things that slow down telomere loss”.

The authors make a rather prophetic remark in that they suggest that some of the increased survival that may be seen with statin therapy may be due to improved stabilization of the telomere. They do not go so far as to say that ALL of it may be due to this. They also still mention the cholesterol lowering effect of statins as a survival mechanism.

Let’s look at that a bit more.  Statin drug therapy started when Merck took the “active” molecule from red yeast rice and patented as Mevacor. This first statin drug was much like TA-65 in that it was all natural- a small molecule purified and concentrated that came from a Chinese plant!

Soon after “semi-synthetic” statins arrived and Rosuvastatin or Crestor tm represents the new generation of totally synthetic computer generated molecules. In the process an industry and test was created to support Big Pharma to the tune of $20 billion a year.

In spite of all of this the drug companies are still having to do studies that “justify the use of statins”. As a matter of fact the JUPITER study was done a few years back providing highly funded and perfectly credentialed evidence ( American Journal of Cardiology and researchers from Mass General aka the New England Journal of Medicine folks) that basically everyone on the planet should get a statin drug.

Of course the facts are not all that clear cut. Statins are costly, have a very high cost per prevention of second heart attack let alone first, work mostly in high risk men, don’t work well in women, have side effects profiles that include memory loss, impotence, diabetes, and have failed to provide the much vaunted anti-cancer and anti-Alzheimer’s benefits Big Pharma was hoping for.

Simply put if we applied the same standards to statin use as we did to mammograms, pap smears and PSA for prostate cancer we would not be using statins because they are too costly. And yet they are still much beloved by allopathic doctors like me and almost universally recommended. They even feature heavily on the Cardiology section of the Internal Medicine Boards!

I think you get the picture. Statins are too big and too profitable to be gone anytime soon. But this whole association between statins and telomeres does have a very positive side. Sort of.

If Big Pharma gets involved in the anti-aging market things will move much faster. Then again they will own it which is not necessarily a good thing for all of us. Then again it may not be preventable.

My friend what you are really watching hear is a “product cycle” in development. The association between a drug company drug and the anti-aging market will blossom when enough people like me have done enough work and educated enough people to support the desire in Big Pharma to capitalize on the market need and desire that has been created. Then when the social moral and economic risks are the lowest, and someone else has incurred the cost and risk of developing the answer, Big Pharma will swoop in, use their gigantic advertising resources to saturate the market, buy off the actual pioneers in the industry ( don’t worry they won’t pick me! I am far too controversial!) and be the hero of all humanity thus cementing our dependency on them forever more. Or so they hope.

The truly good thing is that telomeres and the association of telomeres with disease and disease prevention and treatment will become a real thing with a real agenda instead of just a fascinating research tool like it is now. Finally the field will get some of its due even if there is a terrible price to pay.

So here is some food for thought. If you are on TA-65 or the Telomere Edge Pack you are actually in the fringe-pioneer group that is forging the new future for humanity RIGHT NOW.

While we cannot link TA-65 to disease prevention just yet it is a real possibility in the not too distant future. Remember it is the only compound on the market that actually has real human data.

This brings up another point. TA Sciences had the foresight to use the Life Length assay before it was even commercially available. Unlike the Italian study just released which used the inaccurate Q-PCR assay to measure people’s telomeres (which makes the data suspect in the first place!) their data is real, repeatable and in the process of being expanded as we speak.

The Life Length test is the ONLY test that can give you an accurate biologic age.

And I have to be honest. For a lot of people only drugs will do. This is true of most doctors who do not understand how severely and tactically they have been marketed to become the mouth pieces of the pharmaceutical industry.

But for guys like me- I feel a lot safer and better about using an all natural product that I have proven in repeated personal testing using the Life Length Assay has reversed my biologic age by 7 years.

So the only question is: are you a pioneer?!





PS as an aside my telomere research buddies tell me that statins may actually work better in people who have shorter telomeres because they may have a more demonstrable effect on their telomeres. This means that Big Pharma could and should do some stratification work on their respective statin drugs to see who will benefit most. This will cost money and reduce the risk of statins so don’t look for it any time soon!




Parallel_telomere_quadrupleI am not sure how many times I’ve said that longer telomeres protect against cancer. Probably almost as many times as I’ve had to refute someone saying “telomerase causes cancer therefore TA-65 might cause cancer.”

Back in December 2010 JAMA a very drug centric Big Pharma supported journal published a study that associated short telomere lengths with more cancer and worse cancer and vice versa. Conclusion: short telomeres are associated with cancer and long ones are not.  Then came the attacks

“What about those tumors that have longer telomeres like glioblastoma?”

Answer: those tumors use the ALT mechanism to lengthen their telomeres which does not involve telomerase. This mechanism, ALT, is however associated with the same genetic (or if you prefer genomic) instability that is caused by short telomeres because the recombination of ALT ruins the integrity of the genome, similar to the way short telomeres allow the genome to become unstable.

The common pathway is genome instability.

So over the past 5 years or so I’ve been fighting a slowly winning battle to convince more and more people that having longer telomeres or more specifically fewer critically short ones is a good thing associated with better health and potentially longer life.

Along with this I have been saying that because the immune stimulation, something TA-65 does really well, having healthier telomeres may turn out to be cancer protective.

I have also been asked, “If you got cancer would you keep taking TA-65?” My answer is: I would take more!!! Or more specifically I would take high dose (4 a day) more frequently that once a day.”

Now here is the disclaimer part:

I am telling you what I would do, not what you should do. If you are worried about cancer or have cancer, the usual advice must apply- talk to YOUR doctor! Do not interpret what I have said here to mean that TA-65 is in any way cancer protective or a cancer treatment, and know clearly that what I have said here is contrary to the advice 99.99% physicians in advanced countries with advanced Pharmaceutical Industries would tell you.

But while you are at it read this:

It basically says that cancer cells try to keep their telomeres short because it facilitates their “cancer like” behavior. It also says that lengthening telomeres would increase the differentiation of the cell into a less cancer like form that may not have the immortal and aggressive characteristics of a cancer.

And finally think about what I’ve been telling you for the past 5 years and watch for more and more supporting evidence.

Stay well and have fun!



broken dna strandThe following questions were sent in concerning telomeres, telomerase, TA-65 and the Life Length assay as offered in the U. S. by

Question 1:  Is the database mainly constructed in the US?

Answer:  The database is worldwide but the bulk of the database comes from the U.S. The only lab currently offering the Life Length assay in the U.S. is

Question 2:   Why is it that the average percent of short telomeres is roughly the same, and not rising, for the deciles 31-40, 41-50 and 51-60 of the results report?

Answer: The percentage of short telomeres required to drive disease/dysfunction is the same no matter what the age range of the participant. There is a threshold within each cell thus generating “old cells” that need to be removed in any biologic age population. Similarly “young cells” can exist in any age population as well. The threshold that confers senescence or apoptosis (self destruction/removal) of the cell is not dependent on chronologic age solely. It is dependent on number of replications, accrued damage (oxidation) and measures one might take to minimize or reverse that damage. The so-called Hayflick limit is an idealized maximum number of cellular divisions that can occur in more or less perfect conditions and implies that, no matter what, the cells will continue to “age” due to telomere loss.  The actual human Hayflick limit is now 122 years as witnessed by Jean Calumet, the oldest documented human being who died fairly recently. It is important to understand that the Life Length assay is the only one reporting percent of short telomeres at this point, and one can have “normal” mean telomere length with a low or high percentage of short telomeres. The latter changes the meaning of telomere testing completely, as most people with “normal” mean telomere length have no idea if their cells are old or young biologically because this critical piece of information is missing.

Question 3:   Have you found any evidence that the average percent of short telomeres may vary across different ethnic groups or by gender or any other grouping factor?

Answer:  Since the Life Length Assay is still new I don’t think I can honestly answer that question until the database grows to a much larger size. Basing the answer on previous technologies may lead to false conclusions since they do not yield this kind of data. But the short answer and the one that is currently (and I stress the word “currently”) accepted is that there may be such ethnic and more likely gender differences. For instance there is a small subset of Ashkenazi Jews that have allelic “over expression” of telomerase which confers longer telomeres and longer life/healthspans.

But for most of us epigenetics which while heritable is also mutable is the most likely factor in telomere length and lifespan. Things like nutrition/supplementation stress handling, sleep, exercise habits etc are still far more likely to contribute to telomere health and length for the general population.

Question 4: Has there been any empirical test of the telomere hypothesis, i.e. that individuals with low percentages live longer?

Answer: There have been many such studies and it is generally agreed upon in the “telomere community” that, based on the studies, this is an immutable fact. Similarly evidence exists to show improved health parameters as well in humans mouse and human cell lines although this is a different line of questioning.

You will find large scale studies to validate that longer telomeres equate to longer life starting here.

You will need to scroll to several pages to get the ones that specifically answer that question. In addition due to the failure of Calorie restriction over expression of telomerase to lengthen telomeres now exists as the ONLY method of extending life span in higher mammals. Maria Blasco was able to demonstrate a single isolated treatment with telomerase added 25% to the life span of middle aged mice and 13% to old mice. Her study on short telomere rate increase can be found here.

Please note: until the pharmaceutical industry jumps on this bandwagon, no one will have the money to do the study we all want: a longitudinal study of humans with random selection (not twins, etc.) in diverse populations over many decades to see the effects on human longevity when we turn on telomerase with supplements or other avenues. In other words “Can we make people live longer and healthier by lengthening their telomeres or more specifically decreasing the number (%) of short telomeres?” Even then it is likely they will not do that study; rather the answer will come from several generations of clinical observation and research into the results of drug therapy for telomerase when that actually happens. Surprisingly, human longevity and healthspan are not even on the radar of most governments!

TA-65 is currently the only telomerase activator that has been 1) evaluated for safe human consumptions 2) Proven to work in human beings. No other compound has that data.

One thing we know at this point is that, statistically speaking, diseases are fewer and lives are longer in those blessed with healthy long telomeres.

Please keep in mind one can still be hit by a bus!!!

Dr Dave

chronic painA new study has linked the pain syndrome known as Fibromyalgia to shortened telomeres (biologic time clocks). I have already begun to get emails asking me if TA-65 will help this, due to the most recent information.

Before I answer that question, a little background is in order. As you hopefully know already, the telomere is a small segment of non-coding DNA at the end of the chromosome.  Originally thought to be junk, it was found to be intimately involved in “cell cycle” regulation.  Things like the ability of the cell to replicate and make more of itself, as well as many functions associated with cellular (and organismal) aging, were eventually tied to telomere length.

Things like overall longevity, healthspan, and the associations of all kinds of diseases of aging, including heart disease, Alzheimer’s, cancer, depression and stress, were seen with shortened telomeres*. In some cases, they are clearly biomarkers of aging and disease. In some cases, they drive aging and disease.

In all cases that we know of so far, longer, healthier telomeres are associated with improved prognosis in the middle and older age groups that get these diseases. And of course, they are part of living longer.  In populations that have “allelic variations”, which are basically mutations, in most cases that express increased amounts of telomerase (the enzyme that lengthens telomeres), there is a significant likelihood you will find the extremely long-lived and more healthy individuals.

Fibromyalgia (FM) is a vexing, chronic pain syndrome that seems to have many causes and just as many treatments. In addition to antidepressants and numerous dietary and exercise prescriptions, there is a growing feeling among many people who have treated it, that it is a mitochondrial disorder.

The mitochondria, the cellular powerhouses, appear to become dysfunctional in this syndrome and facilitate pain transmission via the effects of the toxic metabolites they produce and can no longer handle. Basically, a free radical trigger like oxygen or nitrogen accumulates and is not appropriately balanced or handled, and a series of events result that cause pain transmission to occur at a lower threshold.  The attendant illness, Chronic Fatigue Syndrome (CFS), is even easier to explain by this mechanism, since decreased mitochondrial function is associated with lowered energy output and fatigue.  This is what you see as your parents age and slow down as well!

If you live in Europe or Japan and have CFS or FM and seek treatment, you will most likely receive Coenzyme Q10 in its reduced form, in doses of around 400mg a day as starters.  This is also the dose I give my elderly patients complaining of fatigue (200mg 2X a day or 400mg at once). Here in the US, most doctors avoid using supplements for treatment, still clinging to anti-depressants and lifestyle modifications, which if they work at all, are the result of the person slowly healing themselves by avoiding excess energy expenditure and healing their mitochondria!

So, the question comes around to treatment.  I always started with Coenzyme Q10 and then moved into B Vitamins.  When TA-65 came along much later (2009), its energizing properties were of great use to some of my patients with CFS.  I never did an official study though, and it was not part of our soon-to-be-released TA-65 survey questions.

Still, the telomere seems to have some major sway over mitochondrial behavior.  Dr Ron DePinho, now at MD Anderson Cancer Center, has shown the likely involvement of telomere length directly affecting mitochondrial energy generation, biogenesis, and mutation rate.  So, it’s highly likely that anything that improves the health and length of the telomeres like TA-65 should be of great help in CFS.

The other thing to keep in mind is the modification of the way the body deals with stress.  Our Nobel Laureate, Liz Blackburn and her colleague Elisa Epel, have done several studies that show telomere length correlates with perceived stress levels.  Others have shown the association with depression.

The key word here is “perception”. We all know people who have had what most of us would term a hard life, physically and mentally, but live long and happy lives. We all know people who fall apart at the slightest provocation and respond poorly to minimal stresses. Often referred to as a person’s “nature” (happy, sad, stoic, etc), these correlations with biologic changes have made doctors uncomfortable since they are not easily quantifiable. Liz Blackburn used urinary excretions of stress metabolites to give this kind of perception a quantifiable and valid number. They also found cortisol drops over time, instead of rising, giving credence to the concept of “adrenal burnout”. Lowered cortisol or inappropriate cycles of cortisol secretion can allow the chronic, low grade, self-targeting inflammation we know is associated with many diseases of “aging” to rise and run rampant.

If you’ve gotten this far in this blog with me, then you will probably not be surprised by the following comment: Candice Pert, Bruce Lipton and Abraham Hicks are right! How you handle things and what you think about has a lot to do with what goes on inside your body!!!

I am now in my 4th year of taking TA-65. There have been a few times when I stopped it for a week or two. No More! I cannot afford anything less than maximum drive and energy in my life!


*One final comment on the article:

Since the article mentions “biologic age”, I would hope the method used to determine telomere length included both median and percentage short telomeres, since the latter is really the only assay that can comment on biologic age. Short telomeres drive aging and cellular dysfunction and currently the “cut off” is in the 3KB range. Short telomeres are unseen in typical QPCR and FLO FISH assays, which also have poor accuracy and reproducibility. They can easily be at a critical value, buried within the data of median telomere length and often do not correlate well with median or mean telomere length at all. The veracity of small studies especially, could be markedly improved by using HT-QFISH technology developed by Maria Blasco that has been commercially available for over three years now. In its absence, the findings of any telomere study that is looking at individuals in small numbers, is questionable. The median telomere length is also obtained by this technique and it correlates well with other technologies.

If you are serious about telomere length measurements for your own personal use, then go to and get the life length assay done. If you are already on TA-65, any future telomere tests you do should be done with this test.

Reference quote from the article which appeared in Anesthesiology News on-line: “Patients were categorized as experiencing high levels of pain (BPI ≥5; n=30) or lower levels of pain (BPI<5; n=31). Women who scored at least a 5 on the BPI—the cutoff for “high” levels of pain—were more likely to have shorter telomeres regardless of their chronological age (F=5.39;P=0.024). “This difference,” Dr. Hassett said, “represents approximately five years of aging.” That estimate is based on a previous study that linked the deterioration of telomeres to time (Proc Natl Acad Sci USA 1998;95:5607-5610).”

MitochondriaWe got this question through our book site.  The answer, of course, is in the book reference section, but I have long ago given up on people doing anything more than wanting us to do all the work for them!

“In your book, under ‘why is Co Q10 so important,’ you state, ‘some studies that used various forms of Co Q10 suggest that it can actually stop shortening altogether.’ Where can I get this info?” – R

Hi, R. In every cell in the human body, there are many small powerhouses called mitochondria. The purpose of the mitochondria is primarily to burn fat and oxygen (think of a carburetor that burns air and fuel, with fat being the fuel). The source of fat is a combination of dietary fats, carbs and proteins that are all funneled through specific intermediates, into these powerhouses.  Energy is released in stepwise fashion, down a cascade of energy donors and acceptors so that ATP, the ultimate energy currency of the cell is generated.  In the mitochondria, there are 5 major energy exchange complexes named I-V. The very first and the one most susceptible to damage, is the one that relies on reduced Co Q to accept and release energy.

Co Q not only accepts the energy, but it buffers the mitochondrion (singular) from the potential oxidation that this energy can cause. For reasons that are not 100% clear, we begin to develop measurable drops in mitochondria Co Q levels around age 40 and this progresses as we age. Ultimately, our mitochondria become dysfunctional and at least two things happen. They begin to trigger other mechanisms that age the cell and march it towards its demise, and they begin to leak free radicals, through their own protective membranes, out into the rest of the cell, which circles back and a) damages the cell and b) triggers more “I’m getting old” signals in the cell.

The combination of all of this is intimately involved in how fast the telomere shortens and of course, the telomere then can activate other signals that say, “This cell is getting old and needs to die, or be removed from the active cell pool”. Finally, telomere length also accelerates the aging process of the mitochondria by accelerating the generation and leakage of free radicals from it, which causes internal damage to the cell and to the mitochondria.

This is a textbook worth of material in one paragraph, but it gives you an idea of the vicious cycle of telomere/mitochondrial aging as we understand it, at this moment.

Bottom line: the use of reduced CO Q10 ( look for ubiquinol, not ubiquinone) can slow down and in some cases, reverse this decline and help save the telomeres from this type of “internal” free radical damage. Along with Fish Oil and the Telomere Edge Packs, it’s a great way to support the actions of TA-65.

Thank you for this interesting question!

At least this one was interesting and this person seemed genuinely interested. Lots of people write in with “accusatory” questions that are really them venting their own personal agendas. I welcome genuinely interested, open minded people like “R”!

All the best,

Dr Dave

spittingI published this in response to a blog touting the benefits of salivary testing from a company called TeloMe. I will use the same phrase I did when comparing the efficacy of other telomerase activators to TA-65. It went like this, “How much will people spend on something worthless to “save money”?  Answer: About a hundred bucks.

Here is what I wrote in response to that blog.

Sir, there are a few things that need to be addressed in your blog.

First, the analogy between 23andMe and TeloMe is stretched, because 23andMe measures genes, not telomeres. The accuracy and reproducibility of the salivary genetic testing is improved when the gene is fairly large. In most cases, the genes commented on by 23andMe are in excess of 200,000 base pairs.

The average newborn has a telomere length of 10,000 base pairs, the average middle aged adult, 6,800 base pairs – far shorter and far more likely to be misinterpreted by a salivary test, where DNA degradation is inevitable. Most people are not forensic scientists and will not use the careful collection and processing needed to preserve salivary samples.  In addition, salivary cells completely leave out the important WBC component tested in blood telomere testing. You mention immunosenescence. Nothing about salivary testing tells you anything about this.

Next, biologic age can only be interpreted by the percentage of short telomeres present, not by mean or average telomere length. Those values in the individual case are worthless and say nothing of the biologic age. I have seen numerous cases where people had ‘normal’ average telomere length and very different (higher or lower) percentage of short telomeres, which would have been missed by a mean telomere length test. In the same vein, a mean telomere test has huge gaps in accuracy and reproducibility that are not found in HT Q-FISH short telomere testing. In all cases, two or more tests done at 1 year intervals will be much more useful. I would be very curious to see how close your 1 year values will be with this test. If they vary greatly, which is highly likely, the results will be meaningless.

Next, careful what you say about calorie restriction. Like sirtuins and resveratrol, this has been a banner for large amounts of money research dollars and even a society dedicated to its enactment. But the data are extremely thin, as one moves up the biologic ladder from invertebrates to mammalian forms. There are only a very few strains of mice that respond to calorie restriction with extended lifespans.  Recently, Maria Blasco tested the effects of CR on wild type and telomerized mice. CR did not extend lifespan in either. Increasing telomerase expression did. The recent debacle in monkeys, surrounding the horrible diet fed to the controls and the optimal diet fed to the CR monkeys, abrogated any response from CR in what had been the flagship species, to prove the efficacy of CR in higher mammals. Increased expression of telomerase is, at this point, the only broadly applicable way to increase lifespan in many higher species. For it to work the way it does, it must improve mitochondrial function de facto, as well as a whole host of other things, including protein cross linking, sirtuin expression, AGE’s, mutation rates, etc. etc.

The mitochondrial theory of aging is most likely false for many reasons. The simplest of which is that mitochondrial diseases do not present with accelerated aging. Telomeropathies do. Next, the work of Passos and DePinho, in the past 2 years, points out the likely way that short telomere length controls the behavior of mitochondria, which frankly have too few genes that regulate even their own function, to be a true central controller of aging.

While telomere testing varies greatly in price and accuracy, people spend more on their cell phones and TV’s than on an accurate telomere test, that gives them true biologic age and other information. Not a good use of funds. You mention various price points for testing. At this point, there is no good, cheap way to get meaningful information from a cheap test. People are better off ponying up if they want a real answer, or saving their money and waiting until prices on better tests come down. In similar fashion, if you actually want to ‘take a telomerase activator to do something for your telomeres’ you are better off investing in the only product that has a human track record of safety and efficacy, TA-65.

At a most recent conference, Dr Maria Blasco, one of today’s premier telomere scientists, certified that there are some food supplements, such as TA-65, that activate telomerase and contribute to natural rejuvenation and life extension, without causing cancer.

And there you have it, from a person who I would bet on for a future Nobel Prize!


Dr Dave – author, The Immortality Edge– Wiley 2010.