Investors Business Daily is running a profile of entrepreneur turned longevity science advocate Dave Kekich, who you might recall was one of the first wave of donors to support the Methuselah Foundation back when it was getting starting. If you'd like to know more about the driving force behind the Maximum Life Foundation and the recent Manhattan Beach Project activities, then take a look.

Dave Kekich Seeks The Fountain Of Youth:

Told that he would never walk again, Kekich sank into hopelessness. "I felt my life had pretty much ended because I was much into the physical aspect of life," he told IBD.

...

Having regained a great deal of lost confidence, Kekich started a venture capital firm in his bedroom. He raised money for entrepreneurs from angel investors and took a few companies public. Over 10 years, he closed about $22 million in venture capital deals. He pocketed millions in income but declines to say exactly how much.

After raising $300,000 for paralysis research over 12 years, Kekich realized that even if he could walk again, he'd "still be faced with all the horrible (side effects) of aging - cancer, heart disease, Alzheimer's," he wrote in his 2009 book, "Life Extension Express."

He figures that 150,000 people in America suffer from spinal cord injuries, but they're dwarfed by the 6.5 billion people who will one day have to contend with old age. So with a few hundred thousand dollars of his own money, he founded the Maximum Life Foundation and moved back to California.

His nonprofit is dedicated to raising money for biotechnology research that will lead to medicine and therapies to reverse aging.

It is an illustrative lesson for those folk who wonder what it is they can contribute to the future of human longevity. Never let it be said that you can't succeed, or can't contribute, or can't find a way to do what you want to do in life. It won't be easy - nothing worthwhile ever is - but what you achieve is almost entirely up to you.

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I notice some thoughts from Colin Farrelly, who came to support as much progress as possible in longevity science from a very different original position to my own:

As a political theorist interested in aging and longevity science, I am in a minority among researchers in the field. The literature on distributive justice, multiculturalism, equality, liberty, deliberative democracy etc. is voluminous and detailed. Little has been written on science and justice, let alone a marginal field of scientific inquiry like biogerontology.

And thus I suspect many theorists think my interest in aging is odd, if not frivolous. When there are so many pressing problems in the world today the idea of fixating on aging has little, if any, intuitive appeal. A fews ago I use to think this same way. But after pondering these questions, learning some biology and following the pace of scientific discovery in the field of aging research, I have come to now hold the view that the stakes at risk in these debates are very important indeed. I would go so far as to suggest that tackling global aging is one of this century's most important challenges. And because very few people see aging as a problem the challenge of tackling aging is an even bigger problem than it would otherwise be if we all saw it for the problem it really is.

We live in a world in which most people don't give much thought to degenerative aging until it happens to them, and once in that unfortunate position, they don't give much thought to what might be done to stop this from happening to everyone. Consider how easy it is for a state-level politician in the US to raise a million dollars from the public at large (done in under a week in some cases that spring to mind) versus how hard it is for even a noted researcher in the field of aging research to do the same. Yet that politician doesn't matter in the grand scheme of things; he cannot create new technology, he will be fat on bribes and gone in a few years, and all his actions will be unimportant in comparison to the daily toll of death and suffering caused by aging:

While you were reading this sentence, a dozen people just died, worldwide.

But people have their hobbies, their sports teams, their politicians. The hundred pressing distractions from grander matters. Beyond the more valid daily concerns relating to putting bread on the table, so very many motivated folk throw themselves into things that will never change the world - which is their choice, and a free society is founded upon the right to choose as you will. But persuade even a fraction of these people to see the scope of age-related death and suffering, and the great potential of medical technology to alleviate these harms within a few decades ... well, then we'd be off to the races. No barrier or limitation can long withstand the attentions of a large and motivated group of humans.

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Fight Aging! was inaugurated at the end of January 2004, a dark age of the distant past that we shining folk of this new era barely recall. Tempus fugit. For all this great passage of time, the Fight Aging! mission remains as I have described it in past years. Constancy is still regarded as a virtue in some quarters, I am told.

A conversation is presently taking place on the topic of healthy life extension, although it may not always look like a conversation in the traditional sense. It wends its way throughout human interactions and publications; articles, magazines, websites, blogs, actual physical conversations, letters public and private. It is a single pathway in the great marketplace of ideas and culture.

Sometimes our conversation is hard to find, however. ... someone has to be talking on topic to keep the conversation growing, to avoid lapses in which newcomers might miss the party - hence the existence of Fight Aging!

Somewhere along the way, I started to use Fight Aging! as a part of my own efforts to better educate myself on the biochemistry of aging, the state of modern biotechnology, and work taking place on longevity science. If the earlier posts contained more advocacy than science, the last couple of years have been fairly evenly divided between those two topics. But the archives have grown large indeed - somewhere in the vicinity of 1800 posts - and almost every topic related to engineered longevity that I consider useful or interesting has been touched on in some way. Indeed, six years of writing has generated more than enough material to surprise me on a regular basis by what turns up in the Fight Aging! archives. Memory is the first thing to go, or so they say.

So is all this effort getting us anywhere? That is an interesting question, and one that is a challenge to answer. My visibility into the reach of Fight Aging! is limited to what I hear and the statistics on traffic I gather, neither of which are particularly reliable in and of themselves. From what I know, however, I am reasonably certain that readership has remained constant over the past couple of years. On the one hand, talking in detail about fairly complex scientific research is an excellent way to drive people away. On the other hand it seems as though there should be an increasing level of interest in engineered longevity - even if only from those folk who are looking for age-slowing pills and drugs as a result of increased publicity for the search for calorie restriction mimetics.

My analysis is that Fight Aging! has ossified a little as a pillar (one of many modest pillars) of a forward-looking longevity science community that is not growing very fast. I'm starting to lean towards the present Methuselah Foundation view that working to greatly expand the community of supporters is presently as important as fundraising initiatives.

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If you wend your way back through the Fight Aging! archives, you'll find a lot of material on mitochondria, mitochondrial DNA, and how accumulated damage to mitochondrial DNA contributes greatly to aging. The short version is this:

Mitochondria are the cell's power plants, important in the operation of metabolism, central to the mechanisms by which metabolism determines life span, and implicated as the culprit in many age-related diseases. As described in the mitochondrial free radical theory of aging, a small number of mitochondrial genes are known to be crucial to its operation as the cell's power plant. Damage to those genes is unfortunately a natural consequence of the operation of a mitochondrion, and leads to a Rube Goldberg sequence of events in which is a healthy cell is turned into a damaged cell that spews forth damaging biochemicals into your body. As these errant cells accumulate, their actions collectively give rise to many of the unwelcome forms of change and damage that come with age: systems failing, organs shutting down, and important biochemical processes running awry because their component molecules are corrupted.

But you should certainly read one of the longer versions, as that will provide a better introduction to the mitochondrial free radical theory of aging. You should also look into some of the early stage work presently taking place to either replace damaged mitochondrial DNA throughout the body, replace just the few relevant damaged genes, or make all such damage irrelevant and harmless. We can hope that these lines of research will gain the funding and support needed to produce therapies capable of reversing mitochondrial damage and its contribution to degenerative aging. Knowledge is power.

I noticed a paper today that might be taken as evidence that working to repair mitochondrial DNA is an idea slowly gaining popularity in the scientific community. These researchers note that a range of natural repair mechanism exist (but are clearly overwhelmed by damage over a human life span), and that improving upon these mechanisms is only a matter of time:

Mitochondrial DNA (mtDNA) directs key metabolic functions in eukaryotic cells. While a number of mtDNA mutations are known causes of human diseases and age-related dysfunctions, some mtDNA haplotypes are associated with extreme longevity. Despite the mutagenic mitochondrial environment naturally enhancing somatic mtDNA mutation rates, mtDNA remains grossly stable along generations of plant and animal species including man. This relative stability can be accounted for by the purging of deleterious mutations by natural selection operating on growing cells, tissues, organisms and populations

...

In the adult multicellular organism, however, mtDNA mutations accumulate in slowly dividing cells, and, to a much higher degree, in postmitotic cells and tissues. [The following processes:]

1) Dynamic mitochondrial fusion and fission, by redistributing polymorphic mtDNA molecules;

2) mitophagy, by clearing defective mitochondria and mutated mtDNA;

3) compensatory mutations and mtDNA repair

can compensate for the accumulation of mtDNA mutations only to a certain extent, thereby creating a dysfunctional threshold. Here we hypothesize that this threshold is naturally up-regulated by both vertical and horizontal transfers of mtDNA from stem cells or cell types which retain the capacity of purging deleterious mtDNA through cell division and natural selection in the adult organism. When these natural cell and tissue mtDNA reserves are exhausted, artificial mtDNA therapy may provide for additional threshold up-regulation.

Replacement of mtDNA has been already successfully accomplished in early stage embryos and stem cells in a number of species including primates. It is thus simply a matter of refinement of technique that somatic mtDNA therapy, i.e., therapy of pathological conditions based on the transfer of mtDNA to somatic eukaryotic cells and tissues, becomes a medical reality.

You'll notice the reference to mitophagy there. This is one aspect of autophagy, or recycling of cellular components - here the interest is in that recycling process when it operates to tear down damaged mitochondria before they can cause harm. Recall that it is plausible that much of the benefit to health and longevity derived from increased autophagy, such as occurs in calorie restriction, administration of calorie restriction mimetic drugs, and in most of the life-extending genetic manipulations examined to date, is due to cells more aggressively clearing out mitochondrial damage.

Dani MA, & Dani SU (2010). Improving upon nature's somatic mitochondrial DNA therapies. Medical hypotheses PMID: 20116178

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For many years, up until fairly recently, life science researchers who talked in public about altering or reversing the course of aging found that this was a quick and effective way to destroy fundraising prospects. The mainstream institutions involved in grants are conservative indeed. So next to nobody said anything - in public at least. But times are changing. It has to be said that scientists involved in aging research are now becoming noticeably more comfortable about talking in public on the topic of extending life span. Perhaps a little too comfortable here in the choice of title, but the science is sound:

Spermidine: A novel autophagy inducer and longevity elixir:

Spermidine is a ubiquitous polycation that is synthesized from putrescine and serves as a precursor of spermine. Putrescine, spermidine and spermine all are polyamines that participate in multiple known and unknown biological processes. Exogenous supply of spermidine prolongs the life span of several model organisms including [yeast, nematodes, and flies] and significantly reduces agerelated oxidative protein damage in mice, indicating that this agent may act as a universal anti-aging drug.

Spermidine induces autophagy in cultured yeast and mammalian cells, as well as in nematodes and flies. Genetic inactivation of genes essential for autophagy abolishes the life span-prolonging effect of spermidine in yeast, nematodes and flies. These findings complement expanding evidence that autophagy mediates cytoprotection against a variety of noxious agents and can confer longevity when induced at the whole-organism level.

We hypothesize that increased autophagic turnover of cytoplasmic organelles or long-lived proteins is involved in most if not all life span-prolonging therapies.

I've mentioned spermadine in the context of longevity and autophagy in the past, and the authors of the paper quoted above are far from the only folk who think that all roads lead to autophagy when it comes to altering metabolism to increase life span.

The better known life extension mechanisms in lesser animals are all driven by changes in autophagy - or so say the autophagy specialists. It's true that the various hyperspecialized communities of modern biology are overly cloistered and ignorant of one another's research, but the autophagy researchers are assembling compelling evidence for this position.

You might notice the similarity between the longevity-enhancing effects of calorie restriction and those of spermadine: both stop working if researchers eliminate autophagy in lower animals.

Madeo F, Eisenberg T, Büttner S, Ruckenstuhl C, & Kroemer G (2010). Spermidine: A novel autophagy inducer and longevity elixir. Autophagy, 6 (1) PMID: 20110777

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