So, I asked him to tell me more. Out of that meeting came a follow-up interview and this article published on KurzweilAI.net. Please read that article as it describes well why we must prevent a "Global Aging Crisis".
And for anyone who wants to read the entire interview with Aubrey and the efforts of the SENS Foundation, here it is below:
Q. Would you give a brief summary of the new paper of which you are listed as a co-author in Science Translational Medicine?
The essence of this paper is that we argue for a more balanced approach to the quest for interventions to postpone age-related ill-health. Specifically, we highlight the fact that there are three general strategies to consider:
- promotion of healthy lifestyles (through reduction in environmental toxins, medical control of disease risk factors, etc);
- interventions to slow down the lifelong aging process, i.e. the accumulation of various types of molecular and cellular damage that eventually contribute to age-related pathology; and
- interventions to repair that damage using (broadly defined) regenerating medicine
and we highlight the features and limitations of each approach. Our main conclusion, as reflected in the paper's title, is that there is a atrong case for increasing the emphasis on the "damage-repair" style of intervention, which hitherto has received much less attention from gerontologists and policy-makers than the others.
Q. Who are the other authors on the review and why is it meaningful to have them come together with you to co-author this paper?
Five of the other authors - Butler, Campisi, Finch, Martin and Vijg - are among the absolute top tier of biogerontologists, whose views are universally respected within the field. They have never previously expressed the above conclusion (or not nerly so unequivocally), even individually. Therefore, their voice here will make a huge impact on thinking about this issue, both within the field and beyond. Another author, Gough, is a policy veteran with great influence in the corridors of power. The remaining authors - Rae, Perrott and Logan - are involved in organisations that have been promoting the case for repair-style interventions for some years.
Q. What impact will this paper have on the SENS Foundation? Do you expect the paper to raise more awareness and possible funding for research into "pre-disease interventions" and "human regenerative engineering"?
I feel very confident that this will be of great benefit to SENS Foundation, yes. SENSF is the global spearhead of the application of regenerative medicine to aging, and we intend to leverage this paper considerably.
Q. Could you briefly describe "pre-disease interventions" and "human regenerative engineering" as addressed in your paper?
We don't go into many details in this paper concerning the specifics of the interventions, but in my work over the past decade I have identified seven major categories of molecular and cellular "damage" that I believe we need to repair (or in some cases obviate) in order to rejuvenate the aged body comprehensively, and ways to implement that repair. Very briefly, the interventions consist of stem cell therapies to combat cell loss, suicide gene therapy against death-resistant cells, non-human enzymes against intracellular "molecular garbage", vaccination against extracellular "molecular garbage", small-molecule drugs against spontaneous crosslinks in the extracellular matrix, nuclear copies of the mitochondrial DNA to obviate mitochondrial mutations, and a complex combination therapy (involving suppression of telomere elongation together with a variety of stem cell therapies) to pre-empt cancer.
Q. Many gerontologists do not share your ideals about ending aging, how does the new paper seek to change paradigms? What paradigm is ideal in gerontology?
The ideal is not to have only one paradigm. Those gerontolgists who favour "optimising metabolism" to slow down the creation of these various types of molecular and cellular damage, rather than regenerative medicine to repair the damage, are not wrong: their approach is intrinsically less powerful, but it's also very likely to be far easier to implement. As such, it provides a "bridge" to the regenerative approach; the greatest benefit to humanity in terms of lives saved and suffering averted will occur if both approaches are pursued equally aggressively.
Q. What is human healthspan extension? How is this different than life extension?
For practical purposes there is no difference, and this is something that needs to be understood far better by the general public and by policy-makers. We simply cannot plausibly extend lifespans very much by keeping people alive in the diminished state of health that most people currently endure for the last year or three of their lives. Significant life extension will therefore occur only if we can postpone age-related ill-health, i.e. extend the healthy part of our lives. With regenerative medicine, I believe we have a realistic prospect of postponing ill-health so well that we simply never attain it - we postpone it faster than time is passing.
Q. Why do you think more people in general need to become familiar with new paradigms such as human healthspan extension? How will this new paper seek to break pre-conceived notions about aging?
The core reason is the obvious, boring one: funding. Serious public-purse resources to develop regenerative medicine against aging will emerge only when there is public support for it, and that will occur only by educating the respected, mainstream scientific community to take the concept seriously. This paper is directed mainly at those people - the biogerontologists who have hitherto presumed that this approach is too difficult to be worth even considering, or who have not appreciated its potential.
Q. What advice would you give to university students and scientists who are interested in performing research in line with goals for slowing or ending aging and human healthspan extension?
The main advice is simply to read up on the relevant experimental work that has already been done. Virtually all my conversations with scientists who initially doubt the feasibility of regenerative medicine against aging gravitate rapidly to the discovery that their pessimism arises from simply not knowing about the relevant published work. My book "Ending Aging" is a good place to start, since it is a single source for all this information with hundreds of references to the primary experimental literature.
Q. What projects is SENS working on? What lies ahead from the research?
SENS Foundation's research direction is based on two main principles: prioritise the SENS components that are not being adequately pursued through other funding sources, and prioritise those that are the most challenging. These two principles naturally overlap a lot, since difficulty is a disincentive to work on something. Accordingly, we are pursuing most of the seven SENS strands at this time. We anticipate that this will continue.
Q. How can more funding help SENS with their goals for the future?
There are no surprises there: it all about the fact that biology is irreducibly expensive. In particular, as more and more of our research programs move from the cell culture stage into live mice, the expense rises sharply.
Q. What can people look forward to in the near future from greater funding into aging research? What are a few concrete examples of near-future benefits?
I believe the main benefits we can expect to see in the coming few years will come from public health advances, and possibly from drugs to optimise metabolism. These will act, as I noted above, as a "bridge" to allow more people to survive in a healthy state for long enough to be able to benefit from the regenerative approach that SENS Foundation is pursuing.
