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!

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

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!



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.

broken dna strandA couple of questions have been nagging at those of us who study telomeres and telomerase closely.

The first is – what is the correlation, if any, between tissue types? Typically we measure telomere length in the granulocyte line of White Blood Cells. These cells are typically responsible for fighting off viral infections and the immune surveillance against cancer.  How do the lengths that we measure correlate with other tissues? Limited studies have pointed to a good correlation with telomere behavior but not necessarily length. In other words, when someone has short telomeres in one type of tissue they will have short telomeres in another type relative to that type.  The numbers will not be the same but the tendencies will be.

Next, why is there variation in the speed at which telomeres are lost? It seems most of us lose a lot of telomere length relatively early in life and then sometime around late-middle age we slow down that loss. In old age there is a steady slow loss of telomere length unless you provoke it.

Finally, what is the major stress for telomere loss and how does it explain what happens to us when we get sick and/or age rapidly?

A most recent study has pointed to the following very important answers:

1)      The White Blood Cell Line we measure is probably the most important for two reasons. First, it does indeed correlate well with other tissues’ telomere behavior even though the absolute lengths are different.  The white blood cell line is capable – and actually required – to have tremendous ability to replicate because of the short lives of these cells and their high demand. This results in a line of cells that actually have the shortest telomeres among the cell types tested. The other lines had increasingly longer telomere lengths in this order: skin, fat, muscle. Once again it is important to understand that once you have established a relative “normal length” for the telomeres in each specific tissue type, you do see a correlation between “long” or “short” telomeres in each tissue type, basically making the White Blood Cell (WBC) measurement a reasonable surrogate for what is happening elsewhere.

2)      The variation in the speed of loss during life seems to depend on the need for each tissue to replicate.  The WBC are constantly replicating their entire volume throughout life. Early in life the amount of cells actually has to grow to meet the growth of the person from infant to adult. All the while there are immune challenges that have to be met for that child to reach a healthy adult state. That means lots of replication. Muscle cells, on the other hand, need far fewer replications to go from childhood to adult. They do not die off at nearly the rate WBC’s do and once they are there they simply grow larger rather than replicate to make more cells.  Skin cells turnover a lot so they behave more like WBC’s and fat cells behave more like muscle. The variation in the need for replication in each tissue accounts for the rapid telomere loss early in life and a slowing down later in life, since once the person is mature, only maintenance is required.

3)      The major stress for telomere loss is replication but here is the absolute super important fact. It affects the stem cells most. Recall stem cells are the parts bags we use to rebuild our bodies. Stem cells have only a small amount of telomerase (the enzyme that lengthens telomeres) to keep them young for a time, but they do age like other cells as we get older. This means they cannot keep pace with the need for replication and we start to age and get sick because of the combined loss of non-stem cell mass (typical cells) and the loss of our repair parts (stem cells).  When damage exceeds repair we get into trouble and age and get sick.

A couple of very interesting things also were backed up by this new study. First, inflammation is absolutely critical in accelerating the loss of both our typical cells and our stem cells, especially in the WBC line. Since they are part of the immune system, low grade inflammatory stuff like obesity, sedentary behavior, poor diet, smoking, lack of sleep and stress all accelerate their demise and burn out the stem cell lines. This is particularly true if you have high Omega 6 levels and low Omega 3 (fish oil) levels. So take enough fish oil to make a difference!

Next, certain specific behaviors can accelerate telomere loss in tissues that normally don’t see a lot of it.  We know that the cartilage cells in basketball players tend to have short telomeres.  The repeated jumping undoubtedly stresses the replication capacity of the stem cells of those tissues and burns them out faster. Similarly the muscles of long distance runners have shorter telomeres for the same reason – burned out stem cells.

There are two other things you can intuit from these findings. 1) Things that stimulate telomerase not only benefit regular cells but, in particular, stem cells.  This would mean that the natural telomerase activator TA-65 is a true stem cell stimulator. I’ve often said it has to be, but now we know why.

On the flip side, it is already known that EGF-1 one of the main ingredients in RG-Cell Super Stem Cell Activator have been shown to be telomerase activators. We are not making this claim for RG-Cell yet since it has not been specifically tested, but it is highly likely.

In summary, the above strongly support Fish oil, TA-65 and RG-Cell as the ultimate anti-aging combination! These are the telomere supplements you have been looking for!

Big Stuff!!! And speaking of Big Stuff, keep your eyes on my newsletters for a huge announcement any day now!

Things are getting really exciting!


Reference study: Telomeres shorten at equivalent rates in somatic tissues of adults

  • Lily Daniali, Athanase Benetos, Ezra Susser, Jeremy D Kark, Carlos Labat, Masayuki Kimura, Kunji Desai, Mark Granick, Abraham Aviv, Affiliations Contributions, Corresponding author

Nature Communications

4, 19 March 2013

Warning: this blog is not just regurgitation or rewording of a press release from somewhere else. It contains original content and original commentary.

Since February is National Heart Health Month, I thought I would update you on some recent advances in how telomere length interacts with the health of your heart.

Telomeres and the heart is a touchy subject for some.  There are still many doctors out there who just skim headlines and don’t read articles. When I am speaking to doctors, I still get asked this question, usually in a hostile tone: “Doctor (there is a certain way they say it that usually indicates they are cardiologists and I am just a lowly internist!), we know that the heart is postmitotic. How can telomere shortening account for dysfunction in a tissue that is not dividing and therefore not losing telomere length?”

Now, since you are probably not a cardiologist, let me tell you what that little paragraph means.

Certain tissues in the body do not divide and have extremely limited capacity to divide once they are fully grown. I say fully grown instead of “reach adulthood” because when you say adulthood it implies you are an adult and some tissues stop “growing” long before that.  And some continue to “grow” with their cells dividing into your twenties.  No matter how you define the above, the word postmitotic clearly means ‘stop dividing’.  This means that the tissue (heart and brain are the two best examples) cannot repair damage by cellular replication the way say skin and blood cells can.  Skin turns over every 72 hours and blood cells, depending on whether they are white or red, can turn over in hours or a few months.

The ability to divide gives the tissue a large repair capacity since it can make new cells to replace old damaged ones.  The postmitotic state of the heart and brain means they cannot repair the damage of say a heart attack or a stroke, and you are likely stuck with something permanent and bad if those tissues are damaged.

This is a huge oversimplification but the ability to divide and repair relies primarily on telomerase expression and a stem cell reservoir.  It turns out that heart and brain, like most other organs in the body, have them both but in smaller numbers, amounts and with an increased suppression of telomerase.  This means that unlocking those things — telomerase and stem cells — could potentially regenerate even these “non-repairable tissues”.

Here is where my cardiology colleagues usually blow it.  They actually forget what they are treating.

The Best Source of CoQ10 on the Planet

I ask, “What are you treating in a heart attack?”  The answer is usually something like, “The heart muscle, you idiot!”

Wrong! Other than the few cardiologists who actually use Coenzyme Q10 in their patients, there is not one drug for long term treatment of heart muscle.  Luckily, the heart muscle is not the problem. The blood supply to it is, so you are actually treating the blood supply to the heart muscle, the coronary arteries. And no one debates that blood vessel health function and aging is very much telomere dependent. So as the blood supply to the heart and the heart ages, gets damaged and dies.

Case closed?  Well sort of!

That is only half of the story. You see, God, the universe or Mother Nature if you prefer, gave the human cardiomyocyte (heart muscle cell that does the pumping) longer than average telomeres, at least in those cases where we’ve been able to look at them.  This means that the heart might be more resistant to telomere loss than other tissues. Why would that be the case?

Well, oxygen, the essential element in air that keeps us alive, is a dangerous friend. Why?  Because it can oxidize biologically active molecules by forming free radicals.  The heart is the very first tissue to see that most highly oxygenated blood – so having longer telomeres would be a good thing, giving the heart a little extra mileage in terms of longevity.

Unfortunately we humans have figured out many ways to shorten those telomeres faster than normal.

Here are the usual suspects: a diet rich in inflammatory Omega 6 fats and low in Omega 3 fats, lack of sleep, stress, lack of or too much exercise, a nutritionally poor diet lacking vitamins minerals and antioxidants.  All of this helps speed up the loss of our telomere biologic time clocks in all cells, not just the heart.

But there is still one more piece of the puzzle and this is the really cool part.  Over the past decade or so a huge project looking at the human genome, called ENCODE, has been going on. This is part of the reason why epigenetics has become a hot topic.  But just as epigenetics was hitting its stride as the du jour household word, information came out about a bunch of other “factors” that influence how our genes are read.   As a reminder, we age not because of changes in our genes, but how our genes are read, so pay attention here.

One of several “new” (new here meaning not commonly known by the public!) messengers have been discovered. One of them is call miRNA short for micro RNA. If you remember high school biology, RNA is the stuff that you make from “reading DNA, the genetic blue print”. That RNA usually goes along and gloms on to some protein factory somewhere and some enzyme or other messenger protein is made.

Not so with miRNAs. Their function is strictly to turn something on and off. As far as we know, they don’t ‘make’ anything.

OK, now back to the heart. An miRNA was recently discovered called miR-34a.  MiR-34a is associated with two big things: an aging heart, which makes more of it and MI’s, more commonly known as heart attacks. Once again, this is a gene off/on signal that rises with aging and changes which genes are read and how.

If you block the production of this particular miRNA or its target called PNUTS, you reduce heart cell death rate following heart attack and you reduce scarring. You also reduce the age-related decline in heart function.* How?  By reducing the end point of all this, which is telomere shortening in the heart.  So all this great new stuff points once again to our old friend the telomere as the central actor in determining who lives and who dies in the heart and otherwise!

Another why: because the telomere governs the damage response of the cell and whether it lives, senesces (slow death) or explodes from the inside out (apoptosis). And heart telomeres get shorter just like any other telomere! And because they normally express absolutely no telomerase, they are even more susceptible to telomere loss even if they start out with longer telomeres than other tissues.**

That is enough science for today but let me sum it up even more simply for you.

Heart disease is the number one cause of death in this country.

Telomeres rule!

Take care of your telomeres.

Don’t forget your fish oil and TA-65.

Happy Healthy Heart Month!


* This is still at the laboratory level and has not been tested in living people!

**Well established norms for telomere length in various tissue types have not yet been explored fully.


MicroRNA-34a regulates cardiac aging and function

There has been a lot of focus on “Long slow distance” (LSD) exercise and telomere health.  I have oft quoted the “German Runners Study” which was actually a paper presentation and not a fully published work at the time that it got so much press.  That study showed that men who ran at high levels (50 miles a week) had telomere length comparable to 25-year-olds.

It did not, however, address what other exercises they were doing, their supplementation habits, their family genetics and their overall lifestyles. More importantly it did not look at what their actual favorite distance was. If you run everyday, 50 miles a week boils down to about 6.7 miles a day.  Five days a week and you are at 10 miles a run.  These are not marathons, nor are they marathon training distances in most cases. Yet every marathon blog on the planet was saying “SEE! Marathons can make you live longer!” In point of fact, serious long term high level marathon training doesn’t even start until you hit about 70 miles a week and there is an association with cardiac dilatation, valvular dysfunction and potentially fatal cardiac arrhythmias, probably causing some of the famous “runners deaths” we read about from time to time. By the way, this is also seen in endurance cycling. I remind you, I have run ultra-marathons, which are often 3x marathon distance, but I have not done that my whole life and currently limit myself to 6 miles a run, maximum.

On the opposite end of the spectrum

Telomere length and weight training have not been adequately evaluated with a large well controlled study. There is, however, data on grip strength, leg strength and overall power generation and longevity, all of which suggests you need some muscle and especially power (max force x min time = max power) to live longer.

Additionally, there is a published study showing the benefits of “interval style” training for telomerase activation and telomere health.

For most people I still like this for getting in shape. In my practice, the LSD preselects out “people who can take it” because the only ones left standing are those with the genetics (and joints!) to tolerate the LSD. In addition, two other things to consider:

  1. People will want to generalize this to “fit” their sport. I guarantee you this will wind up on marathon blogs as proof of the “healthiness” of running marathons or some other thing. It will also wind up on gym blogs as proof that “exercise is good for longevity and come buy a membership to our gym!” This study was about cross country skiing and while it was endurance, it is a very different exercise than long distance running. Remember as you get out your Dr Dave Voodoo dolls that I am an ultra-runner and am telling you I do not think it is healthy for most! This is one reason I take high dose TA-65!
  2. The study does not address causality and we have no way of knowing that the long distance skiers do not do a lot of other healthy things that essentially preselect for longer telomeres and a better healthspan.  Finally, the fastest way to improve your cardiac fitness and VO2 max is interval-style training. This will help any LSD work you do if you do that because, contrary to popular belief, LSD does not raise VO2 max much at all! I run ultras because I like what it does for my brain and I enjoy the solitude of moving through miles of territory most people avoid – not because it is good for my telomeres!  Take your fish oil, Take TA-65 if you can, and absolutely consider getting on this. Have a rigorous regular exercise routine that includes mobility, strength and endurance. And keep your eyes open for my two books that should come out towards the end of this year.

Thanks to Andy Newman for asking this question!

I’ve also written extensively on lengthening your telomeres with your food choices as well as natural telomerase activators outside of just exercise. Remember good health takes a broad spectrum of attention, don’t just focus on lengthening your telomeres with exercise, get the complete picture


Dr. Dave

Let me be clear.  I am a supplement guy; have been for years.  I take supplements.  I make supplements and I sell supplements, which have unequivocally improved the lives of a lot of people.

As a supplement guy, the most exciting thing to come along ever, has been TA-65, the Astragalus derived compound that lengthens critically short telomeres.  I am certain that it is the first true bridge to real longevity and health span for people.

But not everyone agrees.

Thea Singer, a journalist who writes for The Beast, published a scathing article about TA-65.  It was a cleverly written, thinly veiled attempt to discredit TA-65 and many of the scientists that have worked on it.
The former issue does not bother me.  TA-65 is controversial, because of what it does and how it does it.  The concept that something may actually lengthen life and the cellular mechanisms by which it may do so, are so radical to human thinking, that it will take a while for people to catch on and readjust to a new reality.

That reality is coming no matter what.

Typical agendas to discredit TA-65 include: ‘aging is not a disease, just do normal things like your parents told you, eat right, destress and exercise and you’ll be fine – until you hit 80 and die.’ Then my personal favorite; ‘those greedy doctors are just trying to make a buck out of people who are getting older.’  Since TA-65 is an expensive supplement, many people claim they cannot afford it or simply won’t.

All of that is understandable and typical.

But there are the obvious flaws with the Beast article.

1)     While the mouse model of human aging is very useful, mice do not age by telomere shortening alone and the scientists interviewed in the article know that.  They are also aware, I am sure, of the human published trial with TA-65 showing similar results, to what has been found in mice.

2)     Lack of statistical significance means any finding that does not reach statistical significance is likely to be chance – and the scientists know that too. No doubt they have used that term hundreds of times with that exact meaning in their own studies.

3)     The oral absorption of TA-65 and/or TAT 2, is both well documented by Dr Harley and Co. and the scientists know that as well.  They have no doubt seen the same data and same slides I have that date back to prior to 2007, showing marked improvements in the immune function and reduction in various viral loads in early testing.  I guess all that happened because of the world’s biggest placebo effect and had nothing to do with the compound being absorbed orally.

Again, this kind of stuff is pretty much par for the course for writers who have an anti-anti-aging agenda.

But then they started picking on the individual scientists.

Thea Singer mentioned Cal Harley’s age of 58.  She did not say how old anyone else was, just Cal.  Then came the insinuation that Dr Harley was looking for a soft place to land and some financial gain from TA-65, etc.  I forgot that scientists are not supposed to make money.  They are supposed to grovel for grant money instead.  Money is bad, unless you are a journalist! My bad!

Still, I and thousands and probably soon millions of people, will be in debt in a non-financial way to Dr Harley for his seminal work in the field of telomerase activation and human health and longevity.

Also, somehow Singer forgot to mention that Dr Elizabeth Blackburn, who is one of the Nobel Laureates from 2009, is now in business with Dr Harley.  Care to comment on that Ms. Singer? Does that also make her a 50 something scientist looking for a big financial score?  I doubt it!

Then came the attack on poor (or maybe soon to be not so poor!) Maria Blasco, whose work on the specifics of telomerase activation and its longevity effects is second to none.

I wondered what got everyone so upset at Maria?  After all, she worked for and with one of the Nobel Laureates as well.

Then it dawned on me.

She basically invented short telomere testing, which is the single most important thing for individual results and small group studies, despite the protestations against its use.  Recent articles have shown that the short telomeres are the critical ones in terms of the results of what happens to and inside a cell.

  • The shortest telomere (not average telomere length) is critical for cell viability and chromosome stability. Hemann et al. Cell 107(1): 67-77

Incidentally, this paper is not new; it was published in 2001 from Carol Greider’s lab!

Ultimately the work on short telomeres means that mean telomere length (MTL), long the standard of studies on telomeres, is of marginal use when following an individual’s telomere therapeutics, especially over such a short time frame as one year.

It also means that we should be using that test and not the MTL for such studies, since the MTL is a pretty sloppy test.  I have read studies using a Q-PCR MTL analysis, claiming a near miraculous telomere lengthening after 90 days.  Given that the Q-PCR varies by a standard deviation of 1,000 base pairs, I find those results questionable.  Same with the FLO-FISH, which while twice as good, still has a huge variability gap.

Clearly MTL is very useful but only in the right situations. It only takes one short telomere to send a cell into senescence, crisis or worse.

In vivo telomerase finds the short telomeres first and fixes them first and in many cases exclusively.  That is the natural order of things.  It may be speculation, but it seems that any meaningful improvements in MTL come from the lengthening of short telomeres in the first place.

More outrageous was the insinuation that Maria Blasco’s TA-65 study deliberately coincided with the launch of her new company, Life Length, which is devoted to measuring short telomeres.  Anyone with even a tiny bit of business sense knows that starting a biotech company requires investors and venture capitalists.  I highly doubt Dr. Blasco was able to conveniently arrange for her investments to coincide with the exact date of the TA-65 study.  I highly doubt that was even a consideration.  Still, I am glad it happened.

Then again, I am just a dumb doctor – not a brilliant researcher.  But I can see why people are upset with Maria Blasco for changing the rules of the game and ushering in a really meaningful way for those of us who individually want to follow what is happening to our telomeres.

For the record, I think all of the scientists involved in the “Blasco Fiasco” are brilliant.  But of course Dr. Harley and Dr. Blasco were not asked to comment.  Neither was another brilliant scientist, Dr Bill Andrews, who discovered the human telomerase gene.

I found Ms. Singer’s article pretty repugnant on many levels, but not surprising I guess.  It made me wish scientists would concentrate on being scientists.  It made me wish all of the scientists in this field would get the professional courtesy, recognition and yes, money they deserve for ushering what must surely become the biggest discovering in the history of human health and longevity.

Finally, I wondered why Thea Singer would take such a stance, other than what has already been mentioned.

Maybe her book is not selling.

Ours is doing great.

Dave Woynarowski, MD – co-author The Immortality Edge

I have been seeing this headline circulating a lot lately – “Telomeres are the new cholesterol”. I actually know where it came from and the people who are responsible for its creation and circulation.

These people are very smart and well meaning.  But in their attempts to educate the public as to the very real importance of telomere length and its predictive value for overall health, I think they have inadvertently created a misconception.

The standard measurement of telomere length is called WBC MTL. It stands for white blood cell mean telomere length. The two ways of doing this test are called QPCR and FLO-FISH. The QPCR has an agreed inaccuracy of about 1000 base pairs of telomere DNA. This translates into about 5 to 10 years of aging or aging reversal just as a function of the test. In other words there is a pretty big error.  The FLO-FISH is a bit better with an inaccuracy of about 500 base pairs.  One way to get a more meaningful value is to wait longer to do the test.  Like 2 or 3 years!  Often studies show tests done in a few weeks or a few months after the initial intervention was begun.  They pronounce gigantic leaps in longevity in 6 weeks for things like green tea.

This is simply not possible and is a function of the inaccuracies of the test.  In other words it’s absolutely meaningless! Yet there are some pretty big names in the field still using this test to make positive pronouncements.

One of the most appealing things about TA-65 is that a group of people were tested using what is, in my opinion, the only meaningful test there is for telomere length: short telomere testing.

Studies have shown that the shortest telomere is the one that does the damage and therefore the most important- maybe the only important one in the bunch so to speak.

This is yet another reason why TA-65 is really the only thing that has been proven to work for addressing telomere length. It transcends the errors in testing and works exactly where it needs to to combat aging!

Sadly, until short telomere testing becomes a widely available test, which it is not (only one lab does it in Spain!), testing telomere length the current way will mean waiting 2 or 3 years before seeing meaningful results in the typical MTL tests.


For those of us in the field, the recent slew of articles that show an age-independent link between telomere length and cancer comes as no surprise.

When I say age-independent I mean your age, not the age of your individual cells.

Cells age independently of the organism in some cases and the oldest cells have the shortest telomeres and are at the greatest risk of cancerous transformation.

As Dr Dave has said in talks at the A4M and the AMMG “cancer is a disease of short telomeres.”

So it would be wise for this and many other reasons to keep your telomeres longer.

Again to review, slowing down shortening and lengthening telomeres are two very different things.

You can slow them down with the right kinds of exercise (come to to learn all about this) proper sleep, a good diet (Paleolithic), and supplements like fish oil, Vitamin D, and others.

The only way we know to lengthen them at this point is TA-65 a telomerase activator which you should contact us directly about if you are interested.

As more research is done, more and more disease will be linked to short telomeres.  Keep in mind the shortest telomere is the weakest link and that is exactly where TA-65 seems to work.

P.S., Be on the lookout for the first and only book on how YOU can do all the right things to keep those telomeres as healthy as possible.  It’s called “The Immortality Edge” by Greta Blackburn  Mike Fossel and Dave Woynarowski and is due out in January of 2011, but you’ll be able to get advanced reserved copies here soon!