Fifth SENS Conference

August 31 to September 4, 2011 I attended fifth biannual SENS Conference (SENS5, Strategies for Engineered Negligible Senescence) at Cambridge University in the United Kingdom.

People who attend SENS conferences are the demographic that is the most receptive to cryonics of any identifiable group I have yet found. They are mostly scientists interested in intervening in the aging process. Quite a number of attendees are already cryonicists, including Aubrey de Grey, the originator of SENS and the organizer of the conference. But cryonicists are nonetheless a distinct minority. In previous years I brought a few Cryonics Institute brochures, which were soon taken. This year I brought enough brochures for as many of the 240 attendees as might want one (there were many left over).  I also brought a few copies of my “Scientific Justification of Cryonics Practice” (the published write-up of my SENS3 cryonics presentation) which I gave to a few attendees who seemed most receptive.

In addition to my oral presentation on cryonics I also had a poster. Scientific conferences usually have poster sessions where scientists present research, reviews, or ideas in the form of a poster. Poster presenters stand by their posters at scheduled times to discuss their work on a one-to-one basis with individuals rather than to an audience. My poster dealt with challenging the concept of biological age and denying the possibility of a biomarker of aging that could determine biological age. I contended that biological age and biomarkers of aging assume a singular underlying aging process, which I denied on the grounds that aging is multiple forms of damage. I sought to make maximum use of the one-to-one interaction by preparing Socratic questions to stimulate thinking and discussion with the attendees. The process also gave me another means of meeting and speaking to those attending. One interesting person I met was a Torontonian who is currently studying for his PhD at University of Glasgow. His work involves developing gene vectors that can precisely target and modify genes on chromosomes. I consider gene therapy to be an essential tool for the ultimate implementation of SENS, and a deficiency of SENS that there is so little attention paid to this technology. I don’t see how SENS can be implemented by any means other than genetic re-programming. LysoSENS, for example, would require new genes to create new, more effective enzymes for the lysosomes. MitoSENS would require all mitochondrial proteins be made in the nucleus and imported into the mitochondria.

Partly in this connection, was my aggressive lobbying of Aubrey de Grey to have Argentinian biogerontologist and Cryonics Institute member Rodolfo Goya as an invited speaker at SENS5. I began lobbying in January when Dr. de Grey was at ConFusion 2011. Aubrey was initially reluctant based on the first batch of Dr. Goya’s papers that I sent, but a later batch in which Dr. Goya was principle investigator proved to be effective. In Dr. Goya’s presentation at SENS5 he described his use of viral vectors attached to magnetic nanoparticles to deliver IGF-1 genes to senescent female rats to rejuvenate dopamine-producing cells in the hypothalamus. He injects the particles into the venticles, so the technique is somewhat invasive. Another speaker, Matthew Wood, described exosome nanoparticles which can cross the blood-brain barrier so I am hopeful that Dr. Goya can adopt this technique. Dr. Goya ended his presentation with a short pitch for cryonics (showing CI’s cryostats), which even I found embarrassingly awkward. I introduced Dr. Goya to a number of other cryonicists attending SENS5, including Igor Artyuhov, who is the scientific advisor for KrioRus, and Alcor Member Maria Entraigues, who is the SENS volunteer co-ordinator, and a native of Argentina (now living in Los Angeles).

Russian biogerontologist Alexey Moskalev reported on decreasing the number of single-strand DNA breaks and increasing the maximum lifespan in fruit flies by overexpressing the stress response/DNA repair gene GADD45 in the nervous system. That such a presentation would be included in SENS5 was of special interest to me insofar as I have contended that (and debated with Aubrey de Grey concerning) nuclear DNA damage possibly being a significant cause of aging damage that is missing from SENS:

Alexey later told me that he had read my paper in REJUVENATION RESEARCH, and I’d like to think that I helped inspire his work.

Alexey announced that there will be a genetics of aging conference in Moscow in April 2012. I entertained the thought of going, partly because of my desire to see KrioRus, but I would rather go later when KrioRus is established in its new building, and has a research program in full swing.

Alexey’s research was partly funded by the Science for Life Foundation (the organization of the wealthy life-extensionist Russian Mikhail Batin). Maria Konovalenko (who was featured in LONG LIFE magazine) reported on her work at the Science for Life Foundation to build an open web-based database of age-related changes (molecular and phenotypic). Maria has her own blog.

I am not going to attempt to describe the other very excellent SENS5 presentations other than to say that great progress has been made in starting research programs on each of the SENS strategies, and by 2012 research on all the strategies is expected to be in progress.

Alcor President Max More was an invited speaker, which means that he had a half-hour time-slot immediately preceding my 15-minute time-slot near the end of the program. Max gave an overview of cryonics, whereas I concentrated on technical and scientific issues associated with vascular and neuronal injury from ischemia and reperfusion. During the question period I was asked if we are interacting with hospital staff to limit pre-mortem ischemia in cryonics patients. I said that the current legal environment limits such interactions, but that pre-mortem anti-oxidant protocol has been recommended and used.

I arranged to send more information to a few people in the audience, including a man who was interested in hydrogen sulfide to limit ischemic injury in cryonics, and an Italian neuroscientist who is interested in neurophysiology studies of vitrified brain tissue as well as contact information for Italian cryonicists.

At the final banquet I sat with CI Member Dr. Gunther Kletetschka, who is now living in the Czech Republic and is pursuing a number of imaginative cryonics-related research projects. One of these involves carbon nanotubes to deliver non-toxic metals to cells to use magnetocaloric cooling. Such a technique could cool tissues uniformly rather than externally, thereby eliminate the thermal stress that causes cracking when vitrified cryonics patients are cooled at cryogenic temperatures.

The last day was spent punting on the Cam River, with dinner in the evening. This provided an opportunity for more networking and information exchange, although most of this was in connection with biogerontology.

There was much biogerontology to be learned at SENS5. What I learned at SENS5 can potentially extend my life and that of others. To postpone cryopreservation by life extension is to benefit from technical advances, to extend the time in which I can contribute to technical advancement, and to enjoy more present life. In the best case, rejuvenation will become a reality in my lifetime and I won’t need to be cryopreserved at all. I work for this possibility as well as for improved cryopreservation. Moreover, in doing research for my cryonics presentation at SENS5 — and in giving the presentation — I learned many things that can help me make more informed choices in directing the research that Aschwin and Chana de Wolf do for the Cryonics Institute.

A video of my presentation may eventually be placed on the SENS5 YouTube site.

Ben Best on nuclear DNA damage and aging

The June 2009 issue of Rejuvenation Research features an article by Cryonics Insitute President Ben Best about the involvement of nuclear DNA damage in the aging process:


This paper presents evidence that damage to nuclear DNA (nDNA) is a direct cause of aging in addition to the effects of nDNA damage on cancer, apoptosis, and cellular senescence. Many studies show significant nDNA damage with age, associated with declining nDNA repair, and this evidence for the decline of nDNA repair with age is also reviewed. Mammalian lifespans correlate with the effectiveness of nDNA repair. The most severe forms of accelerated aging disease in humans are due to nDNA repair defects, and many of these diseases do not exhibit increased cancer incidence. High rates of cellular senescence and apoptosis due to high rates of nDNA damage are apparently the main cause of the elderly phenotype in these diseases. Transgenic mice with high rates of cellular senescence and apoptosis exhibit an elderly phenotype, whereas some strains with low rates of cellular senescence and apoptosis show extended lifespan. Age-associated increases of nDNA damage in the brain may be problematic for rejuvenation because neurons may be difficult to replace and artificial nDNA repair could be difficult.

HT Longevity Meme