Does TA-65 Cause Cancer? What the Research Actually Shows

No, it does not. That is the short answer. The rest of it requires me to get sciency on you, so read on at your own risk.

I want to be clear about what this article is. It is a review of the published research on telomerase activation and cancer risk. It is not a treatment claim, and nothing here says any supplement treats, prevents, or cures cancer. This is a doctor walking you through the biology so the fear in the back of your mind has somewhere to go besides your imagination.

Where the cancer fear comes from

Every so often I read another brilliant rocket scientist stating that telomerase is switched off in most of our cells “to protect us from cancer.” The implication is that turning it on must raise your cancer risk, which would make any telomerase activator dangerous. The authors making this claim tend to cite opinions from articles that are several years old.

In this field, research that is six months old is yesterday’s news, and over a year is the dark ages, unless it has been recently repeated. The link between cancer and telomerase is buried deep in old theory, not in current fact.

The “85 percent” statistic, explained properly

Here is the fact that gets misread. Roughly 85% of human cancers massively overexpress telomerase. People take that and conclude telomerase must drive cancer. That is backwards.

Short telomeres are definitively associated with cancer, not long ones. When telomeres get critically short and the cell’s regulatory machinery is intact, the cell triggers senescence or, if it shortens further, apoptosis. Both of those are protective. Both are mediated through the mitochondria and p53, but the telomeres rule the process.

For a normal cell to become cancerous, it has to take a minimum of four “escape” steps. Telomerase overexpression is often the very last step, the one that makes an already-cancerous cell line immortal. But telomerase is no more the cause of the cancer than anaerobic metabolism or angiogenesis are. The disease induces all of those changes. Fixing one downstream change without fixing the underlying cancer fixes nothing.

Blocking telomerase does not cure cancer either

If telomerase were the engine of cancer, shutting it off would stop cancer. It does not. Telomerase inhibitors like Imetelstat produced only temporary suppression followed by aggressive, treatment-resistant rebound, because the cancer figures out a way around the block. And here is the kicker: about 15% of cancers do not use telomerase at all. They lengthen their telomeres through the ALT mechanism instead. So telomerase is not even a prerequisite for cancer.

What the animal and human data actually show

The persistent “telomerase is oncogenic” myth traces back to early mouse studies that used known cancer-causing viruses to insert telomerase genes. The viruses caused the problem, not the telomerase. When non-oncogenic methods are used, there is no increase in cancer, and you see increased lifespan and healthspan instead. That is exactly what Maria Blasco’s telomerase gene therapy work in mice demonstrated.

The animal data on the cycloastragenol-class activator point the same way: in adult and old mice, TA-65 elongated short telomeres and increased health span without increasing cancer incidence. And in people, the human randomized controlled trial of TA-65 reported telomere effects without an increase in cancer. Consider the obvious, too: if telomerase were truly oncogenic, our species could not exist, because both stem cells and germ cells need extra telomerase to stay viable.

Cancer may use telomerase to stabilize its fragile genome, but it does not cause cancer. Cancer causes the overexpression of telomerase, the same way it warps and overexpresses many other enzymes.

So what should you actually take away from this?

Two things. First, the “telomerase protects us from cancer by staying off” story is a theory, not an established fact, and the evidence we have does not support it. Second, addressing your critically short telomeres is, by the biology, a reasonable thing to want to do. I cover the efficacy side of that in Does TA-65 Work, and the broader relationship in Telomeres and Cancer.

On the practical side, I no longer sell TA-65, though it is still on the market from its maker. The cycloastragenol-based telomere-support formula I formulate and take myself today is Telokynase, built in the same cycloastragenol family. For the full daily telomere system, most people pair it with the Immortality Edge Packs. As always, talk to your own physician before starting anything, especially if you have a personal cancer history.

We are stone-aged genes living in a space-aged time. For the first time in our history we have a measure of control over the cellular clock. Fear of an old, unsupported theory should not be the thing that keeps you from understanding it. For the full picture, start at the hub: Telomeres: The Crux of Aging.

To your lasting energy and vitality, Doc

References

• Short telomeres and cancer risk association (PubMed)
• Telomerase gene therapy in adult and old mice delays aging and increases longevity without increasing cancer (Bernardes de Jesus & Blasco, EMBO Mol Med 2012; mouse study)
• TA-65 telomerase activator elongates short telomeres and increases health span of adult/old mice without increasing cancer incidence (Aging Cell 2011; mouse study)
• Natural product telomerase activator (TA-65) in humans, randomized controlled trial (Salvador et al., Rejuvenation Res 2016)

Keep reading

• Telomeres: The Crux of Aging
• Telomeres and Cancer: The Real Relationship
• Does TA-65 Work? What I Found When I Tested It
• Telokynase: The Telomere-Support Formula I Make Now

— Doc