It's early. First, I don't have any money. We're always in need of much more money to do what we do. So, um, today I am not going to talk about the stuff that I do, most of my time, because I know that most of you know about that already. I have this foundation that is focused on aging, and who are particularly in the possibility of applying rejuvenating tech to the problem of aging, and not just slowing down the molecular damage, but actually repairing and reversing that damage. Most of you know that I have historically divided the problem into seven sub-problems, or highlighted, potential solutions for these things. I don't claim that this will be a complete solution to aging, but we do have a respectable chance in the next three decades to give us extra life. This might also work for middle-aged people, which has implications: if we continue to improve these therapies at a modest rate, termed longevity escape velocity, we'll get the functional equivalent of complete repair of aging, even though the tech we have will never be perfect. I always make sure to emphasize that the longevity consequences are a side-benefit. The purpose is to keep people healthy, and disease free from the pathologies of aging. I am not going to talk about this today.

I am going to be talking about what I see as an important issue, for people who are self-trained, who do not work within the regular academic system, who do know about different areas of science, like areas that have momentous consequences for the future. I am going to focus on areas of relevance to the biology of aging. The essential message of aging. We need more accurate understanding on behalf of the general public and policy makers, as to what breakthroughs are important and which ones are not. In what ways are they important? I am going to focus on telomeres. Probably a lot of you know that the end of the chromosomes, the telomeres, get shorter as a side-effect of cell division and replication, just as a consequence of the way that DNA replication works. If you make cells divide really often, unless something happens to combat this, enough chromosome is lost that the cell doesn't work any more. Hailflick called this "replicative senescence". Telomerase combats this process in some cells. Because of the problem of replicative senescence, telomerase has gained reputation as something relevant to the defeat of aging.

The problem with the term "replicative senescence", is that it refers to DNA replication and cell division. Therefore, it sort of confuses the issues. The way that cell works, and aging, are conflated. This has caused a few problems about this over the years. There's a general belief that telomerase is the fountain of youth. Here's a friend of mine, Mike West, he ran Geon (?) a while back. And because it was a company, ahead of anything else, he had to have subtle self-promotion. Here's one of the low key paper:

Extension of Life-Span by Introduction of Telomerase into Normal Human Cells

And the resulting avoidance of the phenomonon of replicative senescence. You need to read the title carefully. It doesn't say extension of replicative stuff, but rather it's talking about in vitro cells, not just cells in humans. So, this confuses it. It gets worse than this. Here's a paper which also refers to replicative senescence, it's recent.

Feedback between p21 and reactive oxygen production is necessary for cell senescence.

It identifies just one small part that cells get into and maintain the state of replicative senescence. Here's the press release for that paper. "Scientists solve ageing puzzle". They don't go into anything outrageous. It was sufficiently cloudy that when the mainstream media got into it, it became somewhat more. "Scientists discover the secret of ageing". Just from you know, a really minor piece of work- a good one, but overall minor. This is a bit of a problem. It's not just hype, it's also anti-hype.

Here's another good friend: Shoal Shansky. He's known for his vocal and frequent, and vocal skepticism about aging. He says things like that: "Don't age, don't grow old, and don't die- that's what they promise you- how ridiculous is that? The one common characteristic of all anti-aging practicioners of the past is that they're all dead." Olshensky.

Why is this a problem? I don't think it's really a problem that scientists are engaged in self-promotion. You've got to do that, sure. It's really easy to engage in the biology of aging self-rpomotion. You have to do that to get money, sure, it's so close to self-preservation. You have to carry on and get funding. The real problem is the last of these things: the short-sightedness. You may gain in the short term, like the prestige of one's work. In the overall long-term, people may fretter.

Gerontologists say that "aging is not a disease". I have a problem with this. If aging isn't a disease, then why should we throw any money at it? Well, there's some small wins, and stuff. That's the mantra- aging is not a disease. Everyone who works on the biology of aging knows that it's ridiculously vastly underfunded, given that the intervention into aging constitutes preventive medicine. There are other preventive medicines that are vastly over-funded. So, this mantra has been a crippling effect, the distinction between aging and diseases of aging.

Craig Venter was recently heavily in the news because he produced a new real tour-de-force version of DNA synthesis via creating a genome of a small bacterial cell with a cytoplasm, and he inserted it into the vicerated shadow of another cell, which was a similar but not identical species, and the new DNA altered the old cell into the new cell, and demonstrating that the DNA was where we thought it was. It was definitely interesting. It got publicized interestingly, like in reasonably respectable magazines, like "scientists create synthetic life". Creating life is a pretty ridiculous thing for this. Craig Venter is not any less public than I am I guess. You had plently of media coverage in the mainstream press, in which it was pointed out that it was a big deal, and some people said it wasn't a big deal. This was fine. You had scientists actually tempering each other's enthusiasm or lack of enthusiasm for a piece of work that was very important, but had been distorted and described as much more important by people who weren't thinking very hard.

I had a similar thing happen to me, because in 2005 there was an article called "Do you want to live forever?". Some people describe my work as pseudoscience. The MIT Tech Review did a rather nice feature on me in February of 2005 which, um, with some editorials that were down-right insulting, and they were allowed to do this by some careless remarks off the record remarks by some of my colleagues. A lot of people like you didn't like that, said this was superficial treatment, and nobody was being told what was wrong with Aubrey's ideas. They ran a prize competition called the Life Extension Pseudoscience and SENS Plan, which is where they described why they thought that SENS is pseudoscience. They were forced to write it down, because I was able to write a response. A lot of real interesting and very prominent technologists and biotechnologists- including Craig Venter- were asked to evaluate whether or not my ideas were worth discussing. They came to the review that they were discussing, and the pseudoscience claims were just ad hominen. So that was a success. SENS is now much more perfected within the scientific world tahn 5 years ago. The evaluation of it has been improved as a result of interventions like this.

In closing, citizen scientists can make an enormous difference in the rate of tech. They can do it by the improving the accuracy of media coverage of scientific advancements, and the quality of public and policy maker's understanding. Look out for hype and anti-hype, and figure out how to articulate in an authorative way, in what's wrong, when people engage in it. If you do that, in just as the SENS challenge, you can make a difference as to what happens, and speed up progress. Thank you very much.