You can find the transcript and audio of that interview here:
http://100isnew50.com/?sta1
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I will quote directly from the transcript:

Q: “Hi Bill, are there any supplements that you recommend not taking because you’ve discovered that they actually reduce telomerase expression in your lab screens?”

A: “There are none that I know of that aren’t safe. Of course you don’t want to take gasoline or something like that. There’s been a few publications suggesting that there are supplements that can interfere with telomerase activity. We have checked every one of them in our labs here, and we have not been able to find that any of them have any significant effect on telomerase activity.”

In my opinion, it’s very foolish to avoid taking these compounds if you’re also taking a telomerase activator. They have very strong anti-cancer properties. The question of whether or not telomerase activation increases/decreases the risk for cancer is still very much being debated. I’ve seen some crazy ideas advocated: for example, that foods rich in dietary polyphenols should be restricted because they inhibit telomerase. This is nonsense.

The fact that compounds like curcumin, resveratrol, EGCG, etc. inhibit telomerase in cancer cell lines simply reinforces the fact that they have strong antineoplastic activity, and likely prevent cancer through telomerase mechanisms and well as many other mechanisms. It has very little bearing on whether these same compounds have any effect whatsoever on the repressor protein in healthy somatic cells. In fact, I strongly suspect that several botanicals that inhibit telomerase in cancer cells do in fact bind to the repressor protein and activate the protein component of hTERT in somatic cells — thus simultaneosly inhibiting telomerase in cancer cells and activating it in somatic cells. Several such compounds are likely in Product B.

The mechanism that activates telomerase in healthy somatic cells is well-defined and well-understood. There’s a repressor protein bound to a regulator element controlling the expression of hTERT. You introduce a small molecule that attaches to the repressor protein and this dislodges it from its DNA binding site. The hTERT gene then starts expressing the protein component of telomerase which combines with plenty of available RNA component to form the telomerase enzyme.

Botanicals like curcumin, green tea, boswellia, resveratrol, etc. only cause a problem in somatic cells if they somehow prevent the small molecule in question from coaxing the repressor protein off its binding site. (A good screen finds the small molecules that coax the repressor protein off the DNA, and simulatneously weeds out the molecules that encourage it to hang on tighter.)

In contrast, the mechanisms that activate telomerase in cancer cells are poorly-defined and poorly-understood. There’s no one mechanism. Cancer cells have figured out a plethora of diiferent ways to do it, and no one is close to understanding how many ways there really are — let alone how each individual mechanism works. For example, some cancer cells seem to replicate the telomerase gene over and over again, making many different copies. Others rely on a virus to insert itself upstream of the promoter. The list goes on and on. It varies greatly from one cancer cell line to another.

Suppose you expose some cancer cell line to some random molecule (say curcumin, green tea, boswellia, etc), and then discover via a TRAP assay that telomerase expression has been reduced. What can you then conclude about healthy somatic cells? Very little. There’s a whole series of intermediate mechanisms that occur in the cancer cell in between exposure to the compound and the reduction of telomerase, which the experiment tells you nothing about — and which, as I said, are very poorly understood to begin with. All of this has very little to do with whether or not this particular molecule (curcumin, green tea, boswellia, resveratrol, etc) will make it harder to coax the repressor protein off its binding site in a healthy somatic cell.

In summary, my view is that studies that show reduced telomerase expression in cancer cells lines have little to no relevance in deciding which supplements to take along with a telomerase activator.

Is the citation you are concerned with at http://www.ncbi.nlm.nih.gov/pubmed/17312453 ? Thanks for tracking thus down. It was the reference I had intented to point to in the blog entry. Not only does Ginko Biloba activate telomerase according to the work cited, but also EPC progenitor cell senescence is delayed. The really interesting question of course is whether the same effect happens in-vivo at the usual doses of Ginko Biloba supplementation. I strongly suspect that nobody has looked at this. I do regularly take Ginlo supplements, however, and they are in my firewalls regimen along with resveratrol of course.

Vince

Welcome to this blog! And thanks.

Vince

VG that has been the conventional wisdom for many years.&

We can convert a health cell into a transformed pre-cancerous cell by over expressing telomerase in that cell. I have done this with Breast epithelial cells.

VG Possibly true. However the complete transformation involves acticvation/inactivation of a substantial number of other genes as well

So I dont really think that taking substances which activates telomerase is a very good idea.

VG I am not sure what the literature says about this, whether there is any research that showed telomerase activation actually leading to cancers. I have not seen any although I have often heard the concern expressed. And as I have discussed in several blog entries including this one, certain research studies say that many innocent substances like resveratrol and vitamin C mildly activate telomerase. Cancers use quite different mechanisms to activate telomerase.

However, if we start thinking about telomere health, things change a bit. A normal cell has a limited lifespan, as it ages the telomeres shortern and the cells eventually go into senescence and die (aging). If you can titrate in just enough telomerase to maintain the telomeres then the cell will not go into senescence and it will stay young.

VG That was my thinking for many years. However there now seems to be a body of research and thinking out there that says the process of cell senescence is very complicated and that shortened telomeres is just one aspect of senescence, a downstream consequence instead of a driver. On the other hand the recent “age reversal” mouse experiment suggests that restoring telomerase expression can restore relative youth though not extemd normal aging. I think the important factor to focus on is telomerase expression rather than absolute telomere lengths as long as they are not critically short. Telomerase does a lot more than extending telomeres.

If you express too much telomerase, the telomeres will elongate and a pre-cancerous state may arise. So the balance is critical.

VG Possibly, possibly not. Many factors regulate telomere length homeostasis in addition to telomerase expression. And I don’t fully buy the pre-cancerous state argument. Have you seen the part of my treatise that deals with the telomere shortening theory of aging? At http://www.vincegiuliano.name/Antiagingfirewalls.htm#Telomereshorteningtheory. And I have written a number of additional blog entries relevant to the topic.

Vince

We can convert a health cell into a transformed pre-cancerous cell by over expressing telomerase in that cell. I have done this with Breast epithelial cells.

So I dont really think that taking substances which activates telomerase is a very good idea.

However, if we start thinking about telomere health, things change a bit.

A normal cell has a limited lifespan, as it ages the telomeres shortern and the cells eventually go into senescence and die (aging). If you can titrate in just enough telomerase to maintain the telomeres then the cell will not go into senescence and it will stay young. If you express too much telomerase, the telomeres will elongate and a pre-cancerous state may arise. So the balance is critical.