How Real is Radical Life Extension?

Healthy Life Extension

Funding Aging Research

How Real is Radical Life Extension?

posted on March 13th, 2012

Dear Future Centenarian,

As you may know, I project the demonstrated capability of reversing the human aging process by as early as 2033¦ if we raise the modest amount of funding for the Manhattan Beach Project. That™s the good news. Not as good news is¦ the original target was 2029.

What happened?

Next to nothing.

In other words, we didn™t raise the money on time. Sadly, that will cost lives. Possibly over 100 million. We are acutely aware of that and work tirelessly to hit the 2033 mark. Reason at Fighting Aging is knocking himself out on this mission as well.

As he recognizes, outside the scientific community, and again despite tremendous progress in advocacy over the past decade, there remains a great deal of work to do:


"At the end of a post on the science of aging, filmmaker Robert Kane Pappas says the following on the goal of greatly extending human life:

'Actual age reversal was something - that, when I first heard of it 5 years ago - I put in the category of time travel and ghosts. [But] after 5 years of interviewing the researchers and poking around labs with my camera, it is not a question of if but when. The general population has little idea of what is about to befall them.'

"Which is both true and a problem. From an advocate's point of view, I'd say that unless a much larger portion of the public gains an understanding of longevity, the level of support will not rise far enough to generate the large sums of money needed for meaningful progress within the next 20 to 30 years.™

˜Outside of stem cell medicine and cancer research, the necessary research programs to build rejuvenation biotechnology are somewhere between fringe, anemic, and non-existent, relatively speaking - and it's only the dedicated efforts of groups like the Methuselah Foundation and SENS Foundation that have boosted these research projects to be more than non-existent. The present few million dollars a year is a lot in one sense, but a drop in the bucket in comparison to the hundred of millions that are necessary for real progress.

"Given that, I feel I can say that if the first fruits of longevity science come as a surprise to the world at large, to the average fellow in the street, then those advances will likely be faltering and far less imposing than might have been possible. On the large scale progress in science and medical technology is a numbers game: the more public support there is, the easier it becomes to raise funding, the more researchers become interested in working in the field, and the more entrepreneurs step forward... and the wheel turns faster as a result. To gain that greater public support requires persuasion, communication, and education - informal and otherwise - are thus it is these line items that are the roots of progress when looking at breadth of society and a length of decades."


What are you going to do this year to help ensure your longevity?

Long Life,
David Kekich


The immune system falls apart with age in ways that are as much a matter of configuration as wear and tear - it is a machine in which the programming runs awry, leading it to do the wrong things at the wrong time, or just do nothing when it should be doing something. This activity leads to damage, which in turn accelerates aging:

"Immune aging is associated with loss of critical immune functions, such as host protection from infection and malignancy. Unexpectedly, immunosenescence also renders the host susceptible to inflammation, which may translate into tissue-damaging disease as the senescent immune system loses its ability to maximize inflammatory protection while minimizing inflammatory injury. On the other hand, chronic inflammation associated with immune-mediated disease represents a profound stress factor for the immune system, affecting cellular turn-over, replication and exhaustion.

Immune cell longevity is tightly connected to the functional integrity of telomeres which are regulated by cell multiplication, exposure to oxidative stress and DNA repair mechanisms. Lymphocytes are amongst the few cell types that can actively elongate telomeres through the action of telomerase. In patients with the autoimmune disease rheumatoid arthritis (RA), telomerase deficiency is associated with prematurity of immune aging.

Patients with RA have other defects in DNA repair mechanisms, including the kinase Ataxia telangiectasia mutated (ATM), critically involved in the repair of DNA double strand breaks. ATM deficiency in RA shortens lymphocyte survival. Dynamics of telomeric length and structure are beginning to be understood and have distinct patterns in different autoimmune diseases, suggesting a multitude of molecular mechanisms defining the interface between chronic immune stimulation and progressive aging of the immune system."

Via EurekAlert!: "Alzheimer's disease is characterized by abnormal deposits in the brain of the protein Amyloid-ß, which induces the loss of connections between neurons, called synapses. Now, scientists [have] discovered that specific antibodies that block the function of a related protein, called Dkk1, are able to completely suppress the toxic effect of Amyloid-ß on synapses.

Dkk1 is elevated in the brain biopsies of people with Alzheimer's disease but the significance of these findings was previously unknown. Scientists [have] found that Amyloid-ß causes the production of Dkk1, which in turn induces the dismantling of synapses (the connections between neurons) in the hippocampus, an area of the brain implicated in learning and memory.

Scientists conducted experiments to look at the progression of synapse disintegration of the hippocampus after exposure to Amyloid-ß, using brain slices from mice. They were able to monitor how many synapses survived in the presence of a specific antibody which targets Dkk1, compared to how many synapses were viable without the antibody. The results show that the neurons that were exposed to the antibody remained healthy, with no synaptic disintegration."

You'll find some thoughts on incentives, politicians, and longevity science over at h+ Magazine. I don't agree with all of them, but then my views on the state as a millstone hung upon the neck of medical progress are known: "After finding out I was an economist, [Aubrey de Grey] effectively challenged me to work out what we should want politicians to do.

With over 150,000 people dying every day, I hope governments would respond to the animal experiments by accelerating our journey to [actuarial] escape velocity through massively increasing funding for longevity medical research, because the cost of dying this year goes way up if it causes you to just miss out on the chance to live long enough to live forever. But since a rational world would already make abolishing death a top priority, we can't count on politicians automatically doing this.

Still (as I will explain at the end of this article) people will likely be made aware of any inevitable approach to escape velocity which should cause at least some voters to reward politicians who increase taxpayer support for medical research. Once we actually reach escape velocity, U.S. politicians would face enormous political pressure to make the necessary medical treatments available to all Americans, regardless of income. The U.S. government might well do this by limiting how much companies could charge for the needed medicines. Predicting this, pharmaceutical companies would have fewer incentives to develop the cures in the first place."

Most known cancer suppression genes and mutations shorten life in laboratory mice, as they suppress the mechanisms of cell replication needed to maintain tissues. There are exceptions that have emerged as researchers find more sophisticated methods of genetic engineering to work around these limitations, but this life-extending example of gene engineering seems to be more straightforward than most:

"Mice with an extra dose of a known anti-cancer gene lose weight even as their appetites grow. Not only that, but [the] animals also live longer, and that isn't just because they aren't getting cancer, either. One of the animals' youthful secrets is hyperactive brown fat, which burns energy instead of storing it. The findings add to evidence that tumor suppressors aren't designed only to protect us against cancer, the researchers say. They also point to new treatment strategies aimed to boost brown fat and fight aging.

Tumor suppressors are actually genes that have been used by evolution to protect us from all kinds of abnormalities. In this case, the researchers studied a tumor suppressor commonly lost in human cancers. Mice with an extra copy of the gene known as Pten didn't get cancer, but that's not the half of it. Those mice were also leaner, even as they ate more than controls. That suggested that the animals were experiencing some sort of metabolic imbalance - and a beneficial one at that. Cancer protection aside, the animals lived longer than usual. They were also less prone to insulin resistance and had less fat in their livers. Those benefits seem to trace back to the fact that those Pten mice were burning more calories thanks to overactive brown fat."

The stifling regulation attending medical research and development ensures that veterinary medicine is years ahead of human medicine:

"Products in the veterinary medical space can be brought to market more rapidly, iterated upon more rapidly, and therefore improved more rapidly. With owners eager to try new treatments, lower barriers to entry for new products, and far less risk of lawsuits dogs and other pets offer great advantages for development of therapies. Owners of pets who try assorted stem cell therapies, gene therapies, and the like have information that is now not being collected systematically.

That's a great lost opportunity and the opportunity will grow with each new treatment that reaches the veterinary market. If vets could also report information then test results could be combined with owner observations (e.g. did Fido start running again after stem cells injected into joints?) then the efficacy (or lack of efficacy) of therapies could be discovered much more rapidly. This ties into a bigger problem: As things stand today truly objective medical research is much rarer than generally appreciated.

We need basically open source medical research with large amounts of data collected independent of companies that develop drugs and other treatments. Given enough software and some group (could be mostly volunteers) to manage a web site to collect pet medical histories many others could analyze the data. Pets are also great for research information collection because with pets privacy isn't a big consideration. My guess is most people won't mind having their pet's medical history made public if they can see a benefit for their current and future pets and for humans as well. Given public availability of the data a far larger number of people with requisite training in statistics, medicine (veterinary or otherwise), and biological sciences could do analyses and discover patterns in the data."

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