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!



There are some serious issues with the way resveratrol is being marketed.

  1. A few years ago it was touted as a telomerase inhibitor and NOT to be taken with TA-65. Now there are claims that it is a telomerase activator and at least 1 study in vitro that suggests that this might be the case. However, the lab is a very distant realm from living human beings as I have often pointed out in support of TA-65. I personally sent four different brands of resveratrol to Bill Andrews at Sierra Sciences for testing before he affiliated with Isagenix and none of them tested positive for telomerase. Bill I think has tested other samples and found the same result. Thus, where the rubber meets the road, resveratrol has failed to activate telomerase. There are many reasons why this could be but one in particular is operator inexperience. This is why I went to Bill Andrews. No one on the planet has more experience with testing for telomerase activation.
  2. In addition you may be aware of the 750 million dollar acquisition of Sirtris Pharmaceuticals by GSK. The “super resveratrol” Dr Sinclair produced for them was removed from phase 2 trials due to hepatotoxicity. Another thing that reportedly happened was an inability to reproduce prior results for resveratrol.

The scientific community believes that resveratrol has been seriously over-hyped

I concur. It has pretty clearly been shown to work through adipokines and at best indirectly activates Sir 1, which has been proven to be a metabolic sensing gene and not a longevity gene, and that is at best.  Sir 6 shows some promise in humans but most of us in the field who are actually learned on the topic feel all the sittings are metabolic sensors and may exert some healthspan but not lifespan improvements, e.g. They are not true longevity genes in higher mammals and resveratrol is NOT a direct activator of any of them.

In my view, resveratrol is a good antioxidant that has merit, especially in the obese, diabetic and elderly. It is a mild mitochondrial poison, which decreases metabolism in the fashion calorie restriction does and doses should NOT exceed 300mg a day for this reason. At this point all my attempts to directly verify it has any direct actions as a telomerase activator or a Sirtuin stimulant has pointed in an opposite direction. The marketing machine, however, continues to present and represent it that way.

I would also add that I seriously doubt that resveratrol is the only natural compound that acts to improve metabolic sensing – it simply has had more money thrown at it because of its purported affiliation with Calorie Restriction (CR). CR has also been studied for 25 years now and in my opinion it has shown disappointing results in the longevity department unless you are a fruit fly, a round worm, or a very specific breed of mouse. The most common breed of mouse used in longevity experiments, known as “Black 6”, has not seen any life extension from CR.

The good news is

The CR society is putting their money where their mouth is (no pun intended!) and at least planning on participating in studies that will verify or vilify what they are doing for markers of longevity. I hope they follow through with it because it may help answer the questions about CR and longevity where it really counts: you and me!

In the meantime, I would remind you that there is very strong evidence that increased telomerase expression is much more likely to extend life and repair many of the defects associated with aging than any other therapy, especially in mammals. I would also remind you that the Immortality Edge Packs was, is and has been the only telomerase centric suppliment that I continue to take on a regular basis. You can draw any conclusions you’d like from that, however my testing has shown nothing but positive results.

Dr. Dave

telomeres photoI read an interesting article recently. Without going into all the gory scientific details, the gist of the article was as follows: even lean diabetics may have the same metabolic profile and telomere length shortening as non-diabetic obese people, if those lean diabetics have poor sugar control.

What is the big deal? Well, it means that, metabolically speaking, your telomeres really don’t know and certainly don’t care if you are fat with normal sugar levels, or skinny with bad sugar levels.

The central problem is a signaling molecule that comes from fat (yes, fat is very active!) called adiponectin.

In order to make sense of the opening statements, let’s take a brief simple look at this fat made hormone known as adiponectin.

Adiponectin is secreted in very high concentrations relative to other hormones, probably because it is so important to metabolic regulation.  It helps regulate appetite, sugar levels and fat levels in the bloodstream.  When it is present in high levels, blood sugar is reduced, appetite is reduced and fat synthesis is reduced.

All good things.

The problem arises when you get fat.  Then, adiponectin levels go down. This is part of what I refer to as the vicious cycle of obesity. Simply put, you getting fat supports you getting fatter and makes weight loss harder. If you’ve ever been fat or know someone who has been for a while, you know the struggles involved.

Here’s a tip: Being fat is inflammatory, and anti-inflammatory supplements can actually increase adiponectin (good!). This includes our old friend fish oil!

If you are not on fish oil, you should be.

Losing weight and reducing your blood sugar, even if you are not diabetic can also help.

Blood sugar control is another big one!  Poor blood sugar control with large excursions into high blood sugar levels can reduce adiponectin levels (bad).

High triglycerides (blood fats) can also lower adiponectin levels.  Remember, fish oil is good for that too! As a matter of fact, the only current FDA approved use for all the fish oil prescription “drugs” out there is to lower triglycerides.

OK, let’s look at this soon to be household word “adiponectin” and telomere shortening.  There is a linear relationship between adiponectin levels and telomere length.  Higher adiponectin levels equal longer telomeres, all other things being equal. Lower levels, as in obesity and poorly controlled diabetes, metabolic syndrome and most likely, low tissue Omega 3 levels, leads to more rapid shortening of telomeres, all other things being equal.

Now rest assured, Big Pharma is hard at work trying to create an “adiponectin-like” drug, which is bound to have horrendous side effects, the way they all do when you mess with Mother Nature.

Fortunately you can control your adiponectin and your telomere length with the following:

1)      Healthy telomeres*

2)      Healthy body weight

3)      Healthy blood sugar control.

In other words, all the things you already knew!

If you need added incentive let me add this:

Being overweight increases the risk of several cancers including breast, pancreas, and colon.

Being overweight shortens your telomeres and your health and lifespan.

Once you lose telomere length from obesity, studies suggest you do not “get it back”, even by weight loss, unless you actively pursue telomerase activation – see TA-65 below.

You do not need to wait until Big Pharma releases their next round of abominations with all the attendant side effects and problems that are bound to happen, when you isolate one receptor and slam it with a drug that is beyond anything the human body was designed to handle.

If you need help, here are a few suggestions:

1)      For weight loss, Ultra Strength Fat Furnace (I cannot tell you it will control blood sugars in disease states, but I will tell you I put some “healthy sugar support” compounds in there!).

2)      For telomere support/telomerase activation, TA-65, The Telomere Edge Packs or better yet, both!

3)      The world’s best cleanest fish oil.

If you can handle things with diet, exercise and lifestyle modifications and you can KEEP doing that day in and day out every day, you won’t need that help and more power to you.

For the rest of us humans, it doesn’t matter how you get there, just get there!

Dr Dave

frankensteinA recent German study has found an association between familial and non familial malignant melanoma and the telomerase gene.  I think we should talk about this because it shows where the seemingly unending association with telomerase and cancer came/comes from.

First concept: Cancer cells are not normal. They are the result not only of loss of growth control but of multiple other aberrations and mutations that change them into monsters. This most likely happens long before they hijack telomerase.

The monster is not born immortal.  The immortalization of any cell line appears to involve OVER EXPRESSION of telomerase. So when the monster that is cancer is born there are many places it can be stopped before it takes over the village. The problem is the village elders (in this case the immune system) are weak, old and disorganized.  Too weak, too old and too disorganized to stop it.

So it grows more powerful with every step (cell division) and eventually obtains the ability to hijack several processes including the ability to invade surrounding tissue (matrix metallo-proteinases), carry away its own anaerobic excrement (angiogenesis), and finally its own immortalization (telomerase).

Second concept: Telomerase is not oncogenic by itself. The enzyme telomerase does not cause cancer and may actually help prevent it (JAMA 2010 article showed association of short telomeres and poor type and prognosis of cancer).

The monster has to be “made” before telomerase gets involved and then it hijacks telomerase for its own purposes.  In the cell lines studied the hijacking of telomerase was the LAST step in the creation of an immortal cancer cell.

The amount of telomerase needed to sustain cancer growth in general is massive.  While I cannot assign an absolute number to it (telomerase expression is measured in arbitrary units and no one has done this comparison study) it could easily be 20 to 100X the amount present in those cell lines that actually express telomerase. This is far beyond the amount provided by TA-65, which is usually the next question I get asked.

When you add TA-65 to pre existing cancers (xerographs) there is no change in the cancer growth rate and as we have seen in mouse studies, no increase in the rate of cancer formation.

The same holds true for some genetic manipulations and also for Maria Blasco’s AAV-9 virus with regards to cancer formation.

Third concept: Telomerase inhibition as a sole or adjunctive agent to fight cancer is likely to fail for the following reasons:

a)      Most cancers are capable of using an alternate (ALT) method of preserving their telomere length. Destroying the telomerase dependent cells (the competition) allows the ALT cells to thrive and multiply. There are at least 2 studies where this has happened. ALT is often associated with cancers that are more deadly and more resistant to treatment.

b)      Inhibiting telomerase may weaken the already weakened immune system in the cancer patient which of course may be further weakened by chemo and radiation. It may also inhibit the growth of healthy tissues.

Forth concept: Mutations in the telomerase gene have been shown to be associated with super longevity.

Fifth concept: Increased Telomerase expression at sub cancer levels has been shown to improve the parameters of health and longevity. So far the only proven ways to have enough telomerase to actually affect telomere health are: TA-65, virosome expression, genetic “boosting” of telomerase.

Sixth concept: So far in humans the only safe way to affect telomere length (critically short telomeres) is TA-65. No ethics committee is going to allow a healthy human to be injected with a virus (ask me how I know!) and genetic boosting of telomerase still carries with it a risk of cancer.

The pharmacologic or more correctly nutraceutical approach (again TA-65) has the he advantage of being on then off and non constitutive (not continuous) and well below the threshold for cancer.

OK back to the German melanoma study before we wrap this up. After the researchers found a familial mutation that is associated with melanoma they looked at non familial cases.

Guess what! They found it was a frequent mutation in melanoma, although not the same mutation.

Honestly, guys, is that really a surprise given that cancer as a process hijacks telomerase?

My only hope is that other cancers will be studied this way. I am sure they will find similar situations there as well where the creation of cancer leads to a mutated form of telomerase.

Sadly the lead researcher in this team went on to talk about how telomerase inhibitors were already in Phase III clinical trials.

Yeah, I know of one for sure: Imetelstat and it made things worse. If people do not examine the literature and the results as a whole, then the myth that “telomerase causes cancer” will only propagate.

One other thing that is not a surprise: The researchers identified solar radiation as a common cause for melanoma-telomerase mutation.

Given the highly repetitive and highly vulnerable nature of the telomere (perhaps the most vulnerable chunk of DNA we have!) in particular the Thymidine residue which forms adducts with carcinogens with relative ease, and the Guanine which is super vulnerable to free radical damage it makes complete sense.

I hope the German study will lead to more help or even a cure for melanoma patients, but it will not be a telomerase inhibitor this I know for sure!

For all of us, the best policy is to keep our fragile telomeres long enough and healthy enough that we do not age prematurely and get these nasty diseases! Telomerase activation is one sure fire way to do that!

Dr Dave

PS as always I have over simplified some concepts here so they are easier to understand. It is not my intention to offend anyone involved in basic or clinical research but I do think Occam’s Razor applies here: the simplest explanation is usually the best!

twinkie pictureBottom line of this whole blog:  Supplemental Telomerase Activation is Required for increases in Longevity whether you calorie restrict or not.

There are probably three or four studies now that show one simple irrefutable fact: you must turn on and increase telomerase expression to improve longevity. Most of them have come from Maria Blasco’s lab in Madrid Spain but the first one actually came from a lab in Texas by a fellow I have had the good fortune to speak with as well: Jerry Shay.

There have been a couple of ways to do this. Originally it was done with oncogene (cancer) promoters attached to the telomerase gene to turn it on. Ironically in these cells the experiment ended not because of cancer but because of boredom and expense.  Basically the lab tech pleaded for mercy after the number doublings (effectively the replicative lifespan) exceeded 700% normal. At that point the cells were mercifully sent on into the great beyond since they had become immortal already and new studies with new cell lines were begun.

What is the take-home message from this study?

Add in enough telomerase to healthy cells and you will get healthy immortal cells without cancer.

Since that time others have replicated the data and found more or less the same thing: Telomerase activation improves healthspan and if you turn it up high enough (but not to high! Remember Goldilocks – JUST RIGHT!) you also get longevity improvements.

There have been other interesting finds that point to telomerase being one of the major keys to health and longevity.

Dr Blasco’s lab pioneered the use of a non-cancer-causing viral vector called AAV9 which has some special properties when coupled with telomerase. First, it is trophic, meaning it gets into lots of different cell and tissue types and next, it is “non-integrative” which means it does not insert itself into the DNA (genome). Two things happen because of this.

First, these little “virosomes” churn out telomerase like little telomerase factories. But with each cell division the effect is diluted out. This is important because in the past some integrative viral vectors (those that got into the genes) caused ongoing expression of telomerase from embryonic age on and did increase cancer incidence in measurable if not massive amounts. The dilutional aspect of the AAV9 virosomes allowed them to be added in mouse “middle age” and old age and the increases in telomerase were limited in amount and time compared to the mice that were genetically engineered.

The result of AAV9?

Middle aged mice lived 24% longer old mice lived 14% longer. So it does appear in mice at least that earlier treatment results in more effects. Now I have to tell you that is actually the opposite experience that I have seen with TA-65 because often the fastest and most dramatic effects are seen in older people who ostensibly would need it more. Keep in mind that younger and middle aged people also can benefit tremendously and there is value in “preventative” telomere maintenance.

The other critical thing to note is: unlike calorie restriction it appears that not only does the “average mouse” live longer than its non-telomerase-activated relative but also the oldest of the old mice gain in lifespan.

So you can no longer say that calorie restriction is the only way to lengthen life. In mice it does not seem to work that way UNLESS you add in telomerase.

That is the result of Dr Blasco’s most recent paper released just today.*

Calorie restriction did not lengthen life in her mice. It did improve neurologic parameters and decrease the incidence of cancer and metabolic disorders, but the mice still died at the typical age of mouse death.

When you added in telomerase by the genetic manipulation, which normally causes cancer, the calorie restriction appears to reduce the cancer risk associated with the ongoing high level telomerase expression back to baseline.  Only problem: the mice were only 3 months old when the calorie restriction started, which equates to about 18 years old in people.  That is a long time without Twinkies!

I hope you understand the importance of all of this work. These scientists have identified the level of telomerase, the ways it can and should be expressed and the direct effects on longevity without causing cancer.

In addition, Dr Blasco has found a way to extend mammalian life span with and without calorie restriction.

It’s called telomerase.

Dr Dave

*In case you are wondering how I got all this info the same day the info hit the presses, I spent an hour on the phone with Maria Blasco today – something I get to do more often than most!

I find myself saying the same thing over and over again and I still see the same baseless assumptions all over the internet. So, with my usual cut-through-the-BS attitude, I feel compelled to do what is necessary to protect the truth – YET AGAIN!

There are several misconceptions that continue to float around in the lay press/public about telomerase and cancer.  One is the mistaken assumption that telomerase somehow causes cancer, which arises from several seemingly viable sources, but fails under scrutiny. This is the danger of the internet. Someone who states something authoritatively becomes an authoritative expert and the misconceptions spread.

Simply, cancer makes telomerase, not vice versa. It makes it by gene amplification, mutation over promotion and all kinds of unnatural ways that are germane only to the process that creates cancerous transformation in the first place.  There are at least 3 cellular check points that have to be overcome, including the DDR (DNA damage response) P53/21 system and several others as well. Once that happens, in the presence of critically short telomeres, or processes that critically shorten the telomere, which are similar to the processes that cause cancer – mutations, oxidation, inflammation, etc. from all the various sources, telomerase can be massively over induced to sustain the already damaged genome of the cancer cell and allow it to divide far more rapidly than noncancerous cells.  Studies on villous adenoma have suggested that telomerase induction is the very last step in cancerous transformation. Inhibiting Telomerase will always fail as an anti-cancer measure, because in removing the telomerase positive cancer cell population, you either unmask or induce ALT telomere lengthening and the cancer comes back worse than ever. Imetelstat and other telomerase inhibitors have failed, probably because of that reason.

This must be the 1000th time I have said it, but telomerase is not oncogenic, unless it is constitutively massively over expressed. In 2002, Jerry Shay’s group created an immortal cell line with the worst possible vector – a RAS oncogene promoter.  The cell line doubled over 500X (normal cells quit after 70) with no evidence of cancer.  The cells died a quite death when the lab assistants got tired of feeding them – since they had effectively proved a point. Maria Blasco’s lab extended mammalian lifespan (mouse model) by 24% with the AAV9 non-integrating vector. No increase in cancer.  She also used the nutraceutical TA-65 in a different study for only 3 months and improved multiple measures of healthspan in a similar mouse model.  No increases in cancer.  Ron DePinho did a similar experiment reversing the phenotype of aging in his mouse model, using a tamoxifen trigger to express telomerase.  No increases in cancer.  A  JAMA study in late 2010, showed an association of short telomeres with more and worse cancers, and most of us feel that canonical activation of telomerase in cancer patients is a good thing, since things like TA-65 have been shown to improve the immune system, by restoring naïve active CD 28+ helper cells which fight viral infections and cancer to normal levels, reverse bone density abnormalities, reduce the markers of inflammation, restore collagen and elastin balance to the skin and many other biomarkers of aging. In a cancer patient especially, the immune function benefits would be huge, since this would be the way to fight off the ALT-based cancers and the amount of “extra telomerase”, expressed in the normal fashion pales in comparison to what the cancer is already doing without driving the cancer forward.

Now, here is the study I hope to fund soon.  We have extended mammalian lifespan as noted above. It is not rocket science to imagine that in doing so you must improve cellular repair processes, including mitochondrial function,  proteasome regulation, mTor, Sirtuins, intracellular junk, glycation, ubiquitination and so on and so forth – all the “theories of aging” or the organism could not possibly survive longer with all that dysfunction. Telomerase must reverse some of it, for at least a while. No one has done that particular study yet, but I am working on it.

You don’t need to genetically re-engineer the telomere to do this, unless you have a telomeropathy like IPF, one of the Progeriod syndromes (Lamellin has now been shown to critically damage or shorten telomeres) or aplastic anemia to begin with. To reduce the aging process and improve healthspan and lifespan, you need to genetically or pharmacologically improve the telomerase enzyme. It remains to be seen whether you can pass the Hayflick limit in humans this way, but it should be possible, since it has been done in mice, although no one has interviewed every mouse on the planet to see which one is the oldest!

Telomere erosion is based on two main things – cellular division and loss of telomere length (telomerase responsive) and toxicity to the telomere from lifestyle, environment, etc. (also telomerase responsive).  The inherent damage to the genome via defective repair from the DDR is always a concern, but as long as the cellular checkpoints are intact (also, you guessed it, telomere/telomerase dependent) those cells will be removed by your effective intracellular check points and your far more effective immune system. That is the current thinking, which is more than speculative, but not yet proven. Honestly, I think we should be glad we are alive now, because it is pretty promising.

Next:  Resveratrol’s action on SIRT1 is via adipokines – not direct action. The SIRT 1 protein is located in the mitochondria and its action is there – thus anything that depends directly or indirectly on SIRT1 effects mitochondrial function. The main regulators of mitochondrial function are the PPAR Co Factors, specifically PCR1 alpha. As was shown by both Passos and DePinho independently, these co factors are regulated by the P53/21 systems, which are in turn directly regulated by telomere length. Subsequently, they showed this regulation included the following mitochondrial behaviors: biogenesis, mtMutation rates, and ECT function, all of which “got worse” as the telomere shortened and apoptotic/senescent signals accrued. Ultimately, this was extended to include senstatic activation, now referred to as SASP (senescent activated secretory phenotype) resulting from mitochondrial dysfunction and ROS/NOS leakage with subsequent immune response.

Sirtuin expression has also been shown to be directly related to telomere length, so stop looking at resveratrol for longevity. It is a good antioxidant that has promise in treating -based disorders like diabetes, metabolic syndrome and obesity, all important. But, in spite of reports of telomerase activation, which cannot be reproduced by the best lab in the world for that sort of thing – Bill Andrews’ Sierra Sciences – it is not a telomerase activator and therefore not a longevity drug.

But if you are fat, by all means take it! Just don’t expect to live longer because of it.

I have never been accused of adopting the “Popular Opinion”. Moreover, I make it a point to try to disabuse people of false notions.  The problem is of course touched upon in the blog below, “The Connectivity Trap”, because we have created a totally open forum for human interaction. We have also created a totally open forum for BS.

No one is policing the comments, or stopping the nonsense. For better or worse, I occasionally try.  I thought you might enjoy a week in the life of Dr Dave, as he battles misconceptions and untruths, especially those that smack of “agendas”.  Agendas are fine, if they are based on fact, but otherwise…

The following was a response to what seems to come up endlessly on the internet.  ‘Turning on telomerase increases your cancer risk so TA-65 is dangerous.’  Simply put, this is nonsense.  Here is why:

Randall! Please stop automatically associating cancer with telomerase activation. The only time that has ever happened is when viral vectors are used to insert the telomerase gene into genomes, where it is not present, as in certain genetically engineered forms of mice. Long telomeres reduce cancer risk (JAMA Dec 2010).  Because cancer hijacks telomerase for its own purposes, people mistake telomerase activation as a de facto cancer risk.  It is not.  Studies with TA-65 and other non-commercial telomerase activators have not shown any increase in cancer. People are misconstruing the fact that cancer hijacks telomerase as a risk for cancer, when turning it on in non-cancer cells.  First off, cancer turns on telomerase by gene amplification, mutation, recombination and other methods that do not involve TA-65 or other “derepressors”.  Adding TA-65 to pre-malignant cells, or cancer xenografts (Perry, et. al), does not increase the speed or toxicity of the cancer. Basically, cancer is cancer and adding telomerase activation does not make it more cancerous.  In pre-malignant villous adenoma cultures, the same thing was found – no increase in the rate of cancerous transformation.  TA-65 does things no other single supplement can and has been proven in human trials, as well as cell cultures and animal studies (See Blasco, Maria in pub med). Is it expensive? What are your life and your health worth?  Has anyone else taken anything that can reduce hair loss, gray hair, improve the immune system, bone density, sex drive, eyesight, reduce skin damage, blood pressure, insulin and glucose levels and do so in a proven clinical human trial, not just someone out there claiming it does, in “their experience”. We look forward to even more potent telomerase activators in the future.  After 3+ years of taking TA-65, I will be in the line for the next one, and the next one etc., etc. I wish I could find a way to get people to do more research, before they volunteer their expert opinions on internet forums.  Dave Woynarowski MD, author The Immortality Edge

Next, we have a corollary statement: If turning on telomerase causes cancer (which of course it does not!) then short telomeres must be good.  This statement was extracted by someone who knows nothing about telomeres and is based on an internet hit citing anti-cancer therapy with telomerase inhibitors.  This was a real case of true, true and unrelated!

Statement: Short telomeres protect against cancer.

Short telomeres do not protect against cancer.  Nor do long telomeres or telomerase expression, when turned on in non-cancer cells, promote cancer. Telomeres shorten with each cell replication. Cancer cells are replicating at rates far above most non-cancer cells. They start with short telomeres and their telomeres get shorter as the cancer advances. Cancer hijacks telomerase to lengthen its own, already short telomeres, out of necessity.  Cancer cells would essentially commit suicide, if they were not able to recruit telomerase to maintain enough telomere length, to continue to survive and replicate. Studies have shown (JAMA Dec 2010) that long telomeres are protective against cancer and short telomeres are correlated both with incidence and severity of cancer.

The cancer telomere/telomerase association stems from the fact that 80+% of human cancers do hijack telomerase and use it for their own viability.  The other 15+% use a recombination known as ALT. Cancers can also use both, so the current research into telomerase inhibition as an “anti-cancer” therapy will likely be a temporizing measure at best. The effects of telomerase inhibition on the immune system and stem cell health are also issues.

Bottom line, long telomeres appear to protect against cancer, short telomeres appear to promote it. Shortening telomeres in pre-existing cancers may buy the victim some time but the consequences are not yet clear.  So far, telomerase activation (in the absence of viral vectors, which are known to increase cancer incidence on their own) has not shown any increase in cancer in cell culture animal studies and human studies (Rejuvenation Research Sept 2010). This does not stop people from propagating that myth, however.  Dave Woynarowski MD, author The Immortality Edge

And finally, an erudite internet doc has posted his attack on the Paleo diet while promoting, guess which agenda. His article is entitled “Epigenetics- the Death of the Paleolithic Human” and shows lack of even a basic understanding of the word epigenetics.  Personally, given this individual’s stature, I find that hard to believe and wonder if it was not deliberate! Perhaps this was the result of the infamous “copywriter intervention” that is so prevalent when people become internet superstars.

Epigenetics is the de facto reason for many papers and speculations. It is not, however, the creation of new genes. It is not the creation of altered pathways to handle the high loads of Omega 6 fatty acids in pure vegetarian vegan diets, as an example.  I recently tested Omega 6 to 3 ratios on 60 Vegans and found all were abysmally low on Omega 3 – dangerously so, if one believes Dr Land’s and Dr Simopoulos’  data. The gene for lactase persists a few months longer now than it did thousands of years ago. We have blue eyes in the population, as well as several blood dyscrasias thought to prevent death from malaria past reproductive age.

That is about it as far as mutations that could be cited as evolution. If there are not genes for altering fatty acid metabolism, processing phytic acid, keeping lactase far into adulthood and genetically controlled immune responses to the presence of gluten, then no manner of epigenetic silencing or expression shifting will make these healthy foods for humans.

Perhaps Dr Bland knows of these mutations and the rest of us do not. That would lend a lot more credulity to his “epigenetic” argument. These genes have not yet been sequenced in the human genome, so far as I know.  Interestingly, short term, both Paleo and Vegan style diets yield similar reductions in what are routinely considered unhealthy biomarkers and there are no conclusive long term studies to define the most “healthy” human diet. Ron Rosedale’s data was based on Paleo style eating, but his study was short term.

If one uses the epigenetics argument, then any information from the “China Study” is suspect, as is most population-based information, including that used to justify Paleo, since our American population clearly has different epigenetic expression than rural China or Kitaava for that matter.

We can toss the term epigenetics around to justify our agendas as much as we like, until we understand it better. These days, merely saying the words epigenetics, telomerase, stem cells and so forth, creates a “WOW” factor among the lay public and garners attention. I wish, before saying these words, we would be more cognizant of what we do and don’t know and admit that to the public. I suspect Dr Bland is very clear on what epigenetics really is. Personally, I am willing to admit I was not around 50,000 or 100,000 years ago, so there is still room for new information. Just because an argument sounds smart doesn’t mean it is.  Where are those new genes, Doc?  David Woynarowski MD

I want to personally thank Dr Mehment Oz’s research team for calling attention to things I have done for the past decade. Their attendance to raspberry ketone, Omega 3 testing and L Carnosine in the past few weeks and touting them as “new discoveries” has lent credence to my work!

Dr Dave

ta-65-and-bonus_256First off, if you need a quick update on what we are talking about in plain language, see me being interviewed on TV for a short segment on anti-aging and telomeres.

I am famous for debunking myths and in the process upsetting lots of people. So, why stop now?

Here are a few things you hear a lot, that are either way over-simplifications or simply not true.

1)  Telomeres protect the DNA from unraveling and as they shorten, the DNA unravels and this causes the cell to die or mutate.

While this is theoretically possible, it is probably not a real phenomenon in humans.  The length of the telomere is, however, intimately tied to a series of structural proteins that turn cell regulation on and off. In addition, the length of the telomere is directly related to certain cell signaling features that cause the cell’s mitochondria to behave like a nuclear reactor on overload (melt down) and autolyse, or explode, from the inside out.  The mitochondria release free radicals that are normally kept inside its own double walled membrane.  These free radicals go out into the rest of the cell and the cell dies.

This mechanism is the same, or very similar, to what happens when the cell experiences a double strand DNA break.

Thus, we see ties from “regular “ cell cycle regulation and the mitochondria to the telomere.  For the scientist and non scientist alike, this means the telomere tends to fit nicely in the center of several other “theories of aging.”

Remember free radicals, stress, and sleep deprivation are all related to shortening of the telomeres.

For more information on how you can help keep your telomeres longer remember this:

“The Immortality Edge” the definitive (and only) book on how to preserve and lengthen your telomeres will be out via John Wiley and Sons in January of 2011. Since I had a major hand in writing it, I can promise you there is almost no scientific jargon or confusing language.  There is just straightforward, no nonsense things you can do right this minute, to help keep your biologic time clocks ticking for a long, long time.

Please note my co-authors Greta Blackburn and Mike Fossel MD PhD are recognized experts in the field of anti-aging and longevity medicine.  Please note, there are a lot of people claiming to have expertise who are not authors of the book for the simple reason that they are not experts!

2)  Supplements can lengthen your telomeres.

There is only one supplement that turns on telomerase and has been shown to lengthen critically short telomeres (the exact way your natural telomerase works, if and when it is turned on!). That supplement is TA-65 and I am one of the few distributors.  If you have a serious interest in the only supplement that does what it says it does, then do this: contact our Customer Support Line at 866-654-7670 or send an email to [email protected] with a Subject line of “TA-65″. Serious inquires only please and let’s stick to the topic because there are tons of people calling already!

OK, what else works?

Pharmaceutical Grade Fish Oil: this is proven in a study of heart patients.  The higher the dose of Fish Oil, the longer the telomeres, with the highest dose group having the longest telomeres. Please note, no other form of Omega 3 was tested: specifically not krill, flax, chia, lyprinol or salba.

Vitamin D3 appears to have some action, but is not quantifiable yet.

There are other supplements that, by virtue of their anti-oxidant power, are reported to either slow down loss of telomeres, or actually lengthen them, but this has not been repeatable yet. We have a more complete list of natural telomerase activators compiled here.

What does not work?

I personally sent samples of a product called ASTRAGALOSIDE IV for testing at Sierra Sciences lab in Reno, NV.  It did nothing. (Please note this was one brand. There are a couple on the market).

Protein powder.  A large, well read internet organization is touting protein powder as a way to lengthen your telomeres, via glutathione. There is no proof that this powder  a) increases glutathione in the body b) does anything to telomerase or to telomeres. None whatsoever, but by virtue of “who” is saying “what”, people are not applying critical thinking.  Or, they’re not thinking at all!

Once again these and more claims and issues and myths and facts are all going to be revealed in our upcoming book “The Immortality Edge” – so make sure you put Jan 2011 on your calendar right now and listen to anyone, or anything else, with a jaundiced eye and a critical ear!

If someone claims to have a supplement that turns on telomerase, or lengthens telomeres, then they should be able to produce data from a reputable independent lab experienced in running these tests to prove it.

Sierra Sciences head scientist, Bill Andrews, has tested thousands of compounds for activity.  If you are interested in supporting his work contact him at Sierra Sciences.  When Bill wins humanity wins!

This post is going to be a little more scientific and detailed than I normally send, I hope that is ok, let me know what you think about this style of education and if you like it I’ll do more.

When we see people who are exceptionally fit or in incredibly good health in their later years we often blame it on having good genes.

And, that is partially true but the part that is true is the part of the genetic material we all share, it is the end of the chromosome called telomerase. Telomeres control how long and how well we live.

Let me explain.

The discovery of telomerase is a real Christmas miracle. It was on Christmas day that Greider and Blackburn finally proved their theory that an enzyme added telomeric DNA to the ends of chromosomes.  That was in 1984, and that enzyme was later named telomerase.

Telomerase is present and active in stem cells, germ cells and cancer cells which is one reason these cells never reach senescence (an endpoint where cells die or no longer divide and thus become inert).  Normal cells don’t express telomerase.  That gene is suppressed in them.  One key to immortality is turning that gene on.  Thanks to extensive scientific research, a natural activator TA-65 has been discovered and proven to successfully lengthen telomeres.

But every new discovery is initially feared, then embraced by pioneering spirits, and finally adopted by the hungry masses (or in the case of naturally occurring cures, co-opted by corporations to be patented and turned into expensive controlled medicine since they can’t patent nature).

When it comes to telomeres, many fear turning this gene on in healthy cells is unsafe and risky. Their concern stems from what incorrectly appears to be a similarity or link with cancer.

 So, what about cancer?  If telomerase is turned on in cancer cells and is the reason a cancer cell continuously replicates, would turning it on in normal cells increase the risk of these cells mutating and becoming cancerous? Specifically is there any evidence that TA-65 causes cancer?

The answer is no and I’ll tell you why.

Stimulating growth of telomeres on normal chromosomes does not cause them to become cancerous because cancer cells are by definition abnormal cells.  This bears repeating.  It DOES NOT cause normal cells to become cancer cells.

As I explained, cancer cells are abnormal cells.  When your genetic material (DNA) becomes damaged or is altered, it mutates and affects normal cell growth and division.  Activating telomerase to lengthen telomeres does not alter or damage our DNA.  Scientists have turned on the telomerase of normal cells ATTEMPTING to turn these cells into cancer cells and have been repeatedly unsuccessful. 

For the past few decades telomerase research was almost solely focused on creating a “telomerase inhibitor” that could be a potential cure for cancer.  Because 80% of all human cancers are immortalized by the turning on of telomerase it’s a logical conclusion that preventing the immortality of cancer cells would slow growth and allow chemotherapies to work more effectively.

I support this research, but when TA-65 was discovered a decade  ago and has been shown to be safe and effective as a telomerase activator in healthy cells then the research focus and possibilities expanded.  It’s with these new possibilities that I am most intrigued by and signal health and vitality for all long into our “golden years”.

We know that when cells approach senescence (their endpoint), the short telomeres stimulate the chromosome instability which can cause the mutations that are responsible for creating cancerous cells.  If we lengthen the telomeres and extend the life of the cell, we thereby reduce the risk of chromosome rearrangement (where tumor-suppressor genes can be shut off and cancer-causing genes turned on).  Telomerase has also been shown to extend the life span of our immune cells, which improves their ability to seek and destroy cancer cells. 

According to the American Cancer Society, 78% of all cancers are diagnosed in people 58 years and older.  Cancers are more likely to occur when signs of cellular senescence are present and when the immune system begins to be compromised with age and lose its ability to respond to threats.  It follows then that extending the period of time before normal cells reach senescence and before immune cells die, would help prevent the creation and spread of cancer in our bodies.

It’s important to note that the unbridled and aggressive way telomerase is activated in cancer cells is also very different from the gentle and mild activation of telomerase in stem-cell and germ-cell lines. TA-65 mimics the natural and gentle activation of telomerase in stem-cells and germ-cells. In 2002, testing and research began with TA-65 and to date there are no studies linking its use to cancer.  Rather studies showing its ability to increase the number of “good guys to fight off the bad guys”, gives hope that it will assist our bodies when fighting off cancerous mutations.

In addition adding TA-65 to human non immortal cancer cell lines, adding TA-65 to pre malignant cells ( cells on their way to becoming cancer), adding to-65 to highly cancer prone mice and of course giving TA-65 to people has shown no increases in cancer.  AS far as prevention that has not yet been thoroughly studied but many of us in the longevity field believe it holds promise for reducing the risk of cancer.

TA-65 is derived from the Astragalus root, a natural compound used and researched for its ability to measurably boost the immune system.  Before it was released as a supplement it was studied for effectiveness against various viruses and proved beneficial against HIV to CMV viruses, among others.  These viruses are associated with increased cancer rates, and because of this the question is often posed, “could a telomerase activator actually improve cancer outcomes and maybe even be a cancer preventative?”  Geron, the parent company that produces TA-65, is commencing tests and attempting to answer that question.

I believeTA-65 is currently offering cutting edge hope for those pioneering souls who want to explore the boundaries of living fully, healthfully, as long as possible.

A key to remember about living longer is that while the number of years you live is important, the number of years you live fully, with great brain and body function is the real measure of longevity. This is called health span. Most people, scientists, doctors and laymen alike agree, maximizing health span is more important than maximizing life span. Think of it this way, your life can be extended for quite some time with life support but most of us wouldn’t chose to live for months or years on life support.

With TA-65 and Telomerase activation increasing life and health span is now within the reach of almost everyone. I speak with people every day who are exploring ways of extending their health span. If you have specific questions around TA-65 and whether or not it might be effective for you, visit my website for info on contacting me, I’ll be happy to answer your questions.

And please do let me know in the comments below if you like these more technical, educational pieces, if so, I’ll get more of them out right away.


Dr. Dave