The essence of the articles to which you linked is that telomerase is found in most cancer cells. That doesn’t mean it causes cancer. Water is found in cancer cells, too. Take away all the water in your body, you will no longer have cancer. Of course you’ll be dead, too.

An even better analogy is that you could similarly argue that insulin is the cause of type 2 diabetes because people with that disease have high insulin levels, just like many cancer cells lines are found to have higher than normal levels of telomerase. But take away all the insulin, and you will probably severely harm or even kill the patient. In reality, the root cause of the type 2 diabetes condition isn’t the insulin itself, just as telomerase is not the root cause for cancer.

It’s overly simplistic to argue that elevated telomerase leads to cancer. While it is true that most human cancer cell lines depend upon telomerase to maintain indefinite replication and often have higher than normal telomerase expression, there are cancer cell lines that do not.

Approximately 8 or 9 out of 10 cancer tumors depend upon telomerase to continue replication. This is why Geron Corporation and many others are interested in finding a way to block the activity of telomerase, particularly in cancer cells themselves. It could slow down the cancer growth enough for other treatments to be more effective, or even for the body’s own defenses to be more capable of reversing the cancer.

But none of that means that telomerase causes cancer. If presence of higher then zero or near zero levels of telomerase were by itself evidence that there is a tumor, then your reproductive cells (germ line cells) and stem cells (including adult stem cells) must be tumors because they also have telomerase levels that are higher than normal somatic cells.

There is an argument that one of the factors that contributes to the development of cancer is DNA damage from cellular replication that goes haywire because of telomeres getting too short and important genes being dropped, cross-linked, or otherwise damaged leading to cancer. When telomeres become too short, the odds of DNA damage goes up. So by this argument, you could say that telomerase helps to prevent cancer.

There’s another argument that goes that cancer develops in part because of the immune system being inadequate to kill off malfunctioning cells. One of the reasons why this may occur is because of chronic viral infections that force rapid reproduction of certain immune cells to the point that the immune system develops senescent decay, meaning new immune cells cannot be readily reproduced because the telomeres have become too short. Much of the research on TA-65 has involved watching immune system telomere length and it has been noted that people with shorter than normal immune system telomeres often have chronic viral infections such as cytomegalovirus or one or more of the herpes virus family.

Boosting telomerase levels in healthy cells would likely counteract both of these problems, preventing some cells from becoming cancerous and boosting the immune system to help clean up cells that still become cancerous by some other process (e.g., radiation induced DNA damage).

You also have top scientists who have been working with telomerase activators and inhibitors in cancer research taking TA-65 or other telomerase activators. If these highly educated specialists are doing this, does that mean they are trying to kill themselves with cancer? No, actually some of them (Bill Andrews is a prime example) argue that boosting telomere length is likely to prevent some cancers. That’s because there is research that shows that people with longer telomeres are less likely to get cancer:

(from Does the length of someone’s telomeres predict their risk of cancer?)

Now, in a study just published in the Journal of the American Medical Assn., Austrian researchers reported that people with shorter telomeres are more likely to develop cancers.

The researchers measured telomere length in the leukocytes (a type of white blood cell) of 787 people in 1995. The scientists sorted the people into three groups based on their blood cells’ telomere length: longest, middle and shortest.

Over the next 10 years, 92 developed cancer. The researchers found that the risk of cancer was twice as high in the middle-length group compared with the longest-length group. It was three times higher in the shortest-length group compared with the longest-length group.

This makes sense, the authors wrote, given that telomeres keep chromosomes stable and cancer is associated with rearrangements of chromosomes that can result in some genes working overtime and others not at all — causing cells that shouldn’t proliferate to begin multiplying out of control.

Bill Andrews believes that when all risks are considered, pumping up telomere length may help avoid cancer and isn’t likely to do a lot to help cancer grow as most cancer cells already have plentiful supplies of telomerase. It’s a calculated gamble, one that this expert thinks he understands well enough to make the choice to use TA-65 on himself.

Alison

http://www.sciencemag.org/content/266/5193/2011.short

http://www.sciencedirect.com/science/article/pii/S0959804997000622

http://cancerres.aacrjournals.org/content/57/3/549.short

http://www.sciencedirect.com/science/article/pii/S0092867400805383

http://cytognomix.org/LeukDown/cancerarticles/HahnNatMed5_1999.pdf

http://www.pnas.org/content/91/8/2900.short

http://cancerres.aacrjournals.org/content/55/15/3258.short

English version:
TA-65 does not appear to have any significant short-term side effects. Some speculate that it could trigger cancer because many cancer cells use telomerase to proliferate out of control. However, there is no actual evidence of TA-65 posing a cancer risk. Moreover, many cancers get started from DNA damage that occurs when telomeres get too short and celllular replication starts to make mistakes that damage the DNA. But without long-term studies in large groups of humans, it’s too early to know for sure what the long-term side effects of TA-65 may be.

You can buy TA-65 from various doctors or from TA Sciences directly. See the TA Sciences contact page to contact them or call 888-360-8886 or 212-588-5805. If you look on the upper right hand corner that page, you’ll also see a “find a doctor” control that can help you locate a doctor in your area that can provide TA-65.

Hope this helps, and keep in mind that TA-65 addresses just one piece of the aging puzzle. Be sure to also read TA-65 Telomere Lengthening Just One Part of Anti-Aging Healthcare.

Alison

I heard that we can get the treatment apart from USA, in Sydney and Singapore. If that is correct, please provide me with all the details. I can act as your agent and might get myself the treatment.

There are very few telomerase activating compounds and all are expensive at this time.

The cost of TA-65 has some down somewhat, as low as $200 per month from TA Sciences for dosages that are apparently higher than what they were using in early usage. Also look into the contents of their additional supplement packs to get an idea of what nutrients they consider important. They sell something they call the “TA Support Pack” which is apparently $300 of additional supplements for each 30 day period. I don’t see the current list of what is included readily visible on their website, but recall that they used to have this information available and it included things like antioxidants, vitamins, alpha lipoic acid, L-carnosine, EPA and DHA omega-3 fatty acids, DMAE, etc. that were pretty standard stuff for anybody seriously into using supplements.

I did a little more digging and found a PDF document containing the label for the TA Support Pack that might be of help. There is also a more comprehensive manual on using TA-65 that might be of some help. In particular, this document mentions that “telomerase inhibitors” such as resveratrol, curcumin, garlic, etc. that are being discussed by some competitors may really not be that big of a deal as their inhibition properties are claimed to have been identified in cancer cell lines outside the human body and may not be relevant to normal cells inside the human body:

(from Chapter 7: TA Support Packs, Resveratrol, And Other Nutritional Supplements)

Common sense tells us that commonly taken supplements do not inhibit telomerase. However there is some confusion because of misinformation on the internet. A series of potentially helpful supplements including fish oil, curcumin, milk thistle, vitamin E, green tea extract, cacao, garlic, quercetin, and resveratrol have been identified as potential telomerase inhibitors.

The tests that showed telomerase inhibition properties for the supplements mentioned above are not applicable to live humans. These tests were done using cancer cell lines in petri dishes and thus are not valid in normal or even senescent human cell lines that have not undergone cancerous transformation.

I’ve mentioned some good supplement options in my article TA-65 Telomere Lengthening Just One Part of Anti-Aging Healthcare, but none of these are telomerase activators. It does appear, however, that such supplements do help maintain longer telomeres. It may be they work not by telomerase activation but simply by preventing oxidation and inflammation damage and thereby reducing the need for cell replication. This would have the long-term effect of keeping your telomeres longer as you age. While I am not aware of any definitive conclusions on this yet, it appears to me that a rationale hypothesis is that simply keeping your health up means your cells divide less often to replace damaged cells and thereby avoid many extra telomere-sapping cell divisions.

The TA Support Packs roughly combine the nutrients you’d find in premium-brand multi-nutrient supplements like those featured in Life Extension’s Top Ten Supplement List minus a few things such as the hormone DHEA and some of the newer ingredients like pterostilbene, a compound found in blueberries somewhat similar in action to resveratrol and thought to be complementary and/or synergistic with it.

Alison

It appears that the evidence for TA-65 causing lengthening of the telomeres is substantial. However, keep in mind that this is reversing just one aspect of aging. There are many other components of aging, including oxidation, glycation, mitochondrial damage, hormonal imbalances, and many other common aging problems. While there are strong reasons to believe that increasing telomere length will allow healthy cells to replicate for years or even decades longer, if the other aging factors are not addressed then it may not be enough to make much difference in the lifespan of an entire organism even if individual cells can live much longer.

TA-65 is not the only compound found to increase telomere length. There is some evidence that supplementation with high levels of antioxidants and B vitamins may have similar effects.

When telomeres shorten over the aging of individual cells, eventually the cells become senescent and cannot replicate further. It appears that there may be a way around this besides the TA-65 approach of activating the telomerase enzyme to grow the telomeres. There is a drug call rapamycin (brand name Sirolimus) that may help cells with short telomeres continue to function. The problem is that it is an immunosuppressant typically used for transplant patients. A 2009 study of rapamycin on mice showed that there was a significant increase in lifespan:

(from Sirolimus aka Rapamycin mouse lifespan extension)

In a 2009 study, the lifespans of mice fed rapamycin were increased between 28-38% from the beginning of treatment, or 9-14% in total increased maximum lifespan. Of particular note, the treatment began in mice aged 20 months, the equivalent of 60 human years. This suggests the possibility of an effective anti-aging treatment for humans at an already-advanced age, as opposed to requiring a lifelong regimen beginning in youth. However, because it strongly suppresses the immune system, the drug cannot be easily used by humans. While the mice in the study were housed in pathogen-free facilities, people taking rapamycin are very susceptible to life-threatening infections, and require constant medical supervision.

Another research paper on rapamycin effects of preventing cell death from short telomeres suggests that the effects are entirely separate from a telomere lengthening effort seen in other research such as on TA-65 and in cancer research. This paper suggests that rapamycin may have this effect because of a strong antioxidant action.

I hope this helps put TA-65 in perspective. I’d view it as one means to help reverse some of the effects and components of aging.

Alison