Bill Andrews of Sierra Sciences Announces Collaboration with BioViva
At a recent conference, Bill Andrews of Sierra Sciences announced a forthcoming collaboration with BioViva, currently pushing regulatory boundaries to develop gene therapies as treatments for aging. A new company will be formed, BioViva Fiji, to offer gene therapies that can compensate for some of the aspects of degenerative aging via medical tourism in Fiji. The principle focus, given that this is Sierra Sciences we are talking about here, is telomerase gene therapy, but BioViva is also working on a follistatin gene therapy, and it is worth bearing in mind that in this age of CRISPR rolling out any single target gene therapy that has some background work in the research community isn't the huge technical undertaking it would have been in past years. All of the time and cost goes into a reasonable level of testing, and the only real hurdle left from a technical point of view is proving that a therapy can reliably introduce genes into a large enough number of cells to produce benefits. We're going to see a lot of work on gene therapies in the next few years - this is just the start and the tip of the iceberg.
Fiji, like many countries in the Asia-Pacific region, has been taking steps in recent years to make itself attractive as a destination for medical tourism, and thereby encourage the growth of high-end local industries that benefit from the wealth of larger and more prosperous countries. It makes a lot of sense as a long-term plan, and competition between regions for medical tourism will hopefully prevent these countries from falling into the overregulated repression of medical development found in the US and Europe, a state of affairs that slows development and that gave rise to medical tourism in the first place. Fiji is the destination for this particular effort, but it could equally have been any of a number of other choices.
"Sierra Sciences and BioViva - Liz Parrish - have now joined forces. We have started a new company, called BioViva Fiji, on Fiji island, and we are now building a large-scale production facility and a clinic to soon be able to provide a gene therapy approach towards curing aging."
Bill Andrews is, as many of you will recall, an enthusiast for telomerase and telomere length as a key to aging, and he is in full sales mode above. The goal of Sierra Sciences before the company floundered was to build a viable treatment along these lines, but they ran out of funding and then turned to selling herbal nonsense. That was a sad end for a group that was at the outset working on interesting science. Interesting, yes, but from where I stand age-related reduction in average telomere length is a marker of aging, not a cause of aging. Telomerase gene therapies most likely extend life in mice through increased stem cell activity, counteracting some of the decline in stem cell populations that occurs with advancing age. It was surprising to find that this doesn't raise the risk of cancer, as those stem cell populations become damaged by age, and their decline is generally through to be an evolved defense against cancer in later life. It may be that the general enhancement of cell activity extends to the immune system, and better immune surveillance and clearance of cancerous cells is enough to offset that raised risk due to pushing damaged cells back to work. This or any other thesis is far from proven at this point, and telomerase gene therapies in humans still seem overly risky on this count to my eyes.
I believe based on the evidence to date that telomerase gene therapy should be classed as a compensatory treatment. It is pushing a damaged engine to do more, and it may well be the case that in humans as well as mice the balance of factors brings a net improvement in the same way as do stem cell therapies, another field associated with a prospering medical tourism industry, but that is yet to be nailed down and proven. Follistatin or myostatin gene therapies are similarly compensatory. They do not address the damage that causes aging, but they compensate partially for one its effects, in this case by adding extra muscle tissue to offset that lost over time to the mechanisms of aging. Is this all useful? Yes - if you think that stem cell therapies are worth it, then you should also think that this sort of gene therapy is worth it. I'm pleased to see Bill Andrews working on something that doesn't make me sad for the waste of potential it signifies, as was the case for the end of Sierra Sciences as a legitimate scientific venture.
We should not forget, however, that telomerase therapies cannot cure aging. A lot of people would like to think that they do, but it simply isn't the case. They don't treat the causes of aging, they instead adjust a lot of factors to paper over those causes just a little bit better than the papering over that the present mainstream of medicine can achieve. Undergo a telomerase gene therapy and you may benefit in a very similar way to a stem cell treatment, but in both cases you are still aging and still damaged. You still have mitochondrial DNA damage, lipofusin in your long-lived cells, cross-links stiffening your arteries, and so on and so forth, and all those things are still killing you.
"We should not forget, however, that telomerase therapies cannot cure aging. A lot of people would like to think that they do, but it simply isn't the case. They don't treat the causes of aging, they instead adjust a lot of factors to paper over those causes just a little bit better than the papering over that the present mainstream of medicine can achieve. Undergo a telomerase gene therapy and you may benefit in a very similar way to a stem cell treatment, but in both cases you are still aging and still damaged. You still have mitochondrial DNA damage, lipofusin in your long-lived cells, cross-links stiffening your arteries, and so on and so forth, and all those things are still killing you."
Hold up for a second. Although I am also of the opinion that telomeres are only one part of the aging puzzle, I feel like you've overstepped the mark here and are acting like your opinion is fact.
Are you a doctor? Or a scientist? Because there are several doctors and scientists who would disagree with your statement that telomerase therapies don't treat the causes of aging. Michael Fossel, Bill Andrews, Maria Blasco, Jason Williams, Ronald DePinho all spring to mind.
@qt3.14: I probably should have qualified that statement with something about who believes what. I did say "cure aging" not "treat aging" - a response to the Bill Andrews quote. Treat and cure are two different things. Clearly you can treat aging with therapies that compensate for rather than address its causes. It just isn't anywhere near as good as addressing root causes, and cannot possibly bring aging under control to the point of being called a cure because the damage is still there, causing havoc. Telomerase gene therapy can't be one of the necessary parts of a toolkit that cures aging unless telomere length or loss of telomerase expression is a cause of aging. I'm in the camp of those who think it isn't.
I'd say exactly the same things about present stem cell therapies. Nice to have, but not a part of the toolkit to control aging as presently constituted. A SENS approach to stem cell populations is to replace the existing population with undamaged cells, but that isn't what current stem cell therapies do.
I've read both books (Bill Andrews and Michael Fossel) which argue that telomere shortening is the cause of aging. They are rather convincing. Nevertheless, I agree with you, Reason, that the processes that SENS aims to treat are the actual causes of aging and that telomere shortening is a biomarker, not a cause.
I just came over this new study in the NEJM: http://www.nejm.org/doi/full/10.1056/NEJMoa1515319
Any thoughts?
Methods
In a phase 1-2 prospective study involving patients with telomere diseases, we administered the synthetic sex hormone danazol orally at a dose of 800 mg per day for a total of 24 months. The goal of treatment was the attenuation of accelerated telomere attrition, and the primary efficacy end point was a 20% reduction in the annual rate of telomere attrition measured at 24 months.
Conclusions
In our study, treatment with danazol led to telomere elongation in patients with telomere diseases.
I fully agree with the views of Reason that telomerase and stem cells treat, but not cure aging. Aging is the continuation of human development and the only way to cure is to loop the program of human development. Prevents, interferes to make it: irreversible programmed changes in the extracellular matrix, deposition of lipofuscin and programmed "оpinion" of cell niche community. Any rejuvenated cell will be met by such a niche as a stranger. So, it either has to submit "opinion" and become how they are - also old or turn into unruly - a cancer cell.
I also think that telomere length is a hallmark of aging but not a way to cure it. In the end, all hallmarks of aging need to be addressed. What I like about current developments including BioViva is that we start to address these problems, not all of them, but some. Gene therapy or even danazol should be able to positively influence telomere length and inhibition of myostatin should counter the effects of age-related muscle wasting. These therapies could enable us to extend our lives a few important years until we find new treatments for other hallmarks of aging.
I think far more animal data is needed to draw concrete conclusions about aging. I do not dismiss telomerase as a potential therapy nor do I fall for the stuff Bill Andrews peddles, though Michael Fossell is another matter.
Our lab intends to explore telomerase and seek the answers to questions about telomerase that are not known and help end the debate one way or the other.
Our current focus however is senolytics.
I have nightmares about Aubrey de Grey and the SENS Foundation winding up like Sierra Sciences, out of money and selling out with herbal rubbish. Hopefully they'll be able to get enough of their programs across the valley of death before that happens.
@Jim: It wouldn't happen. Sierra Sciences went to that endpoint because of the incentives and obligations operating on the leadership of startup companies, none of which apply to a non-profit like the SENS Research Foundation. If the SRF runs out of money, which will hopefully be avoided before the primary goals are achieved, then it would continue as a much less active advocacy and volunteer hub of connections, much as it did back before raising funds.
Even if telomere attrition is downstream of more fundamental causes of aging, and I agree it is, it is still probably a valid intervention point in stopping or reversing aging - I applaud Bill Andrews and Co on working on this.
For those asserting that sufficiently expressing telomerase in human cells such that telomere shortening is entirely halted would not cure aging, how do you reconcile that with animals such as lobsters whose remarkable longevity has been directly linked to ubiquitous telomerase expression? I realize that humans differ from crustaceans, however it's a compelling argument none the less.