Dear Future Centenarian,
Due to unforeseen circumstances, I missed this year’s RAADfest. But I’m watching the videos now… and they are fabulous!

If you attended, you saw how you could get around $10,000 worth of life extending products and services just about FREE. Bill Faloon at Life Extension made this possible.

But more importantly, you saw how to put yourself on the path to an open-ended youthful lifespan with what we learned in just the past few years, much of which is new this year.

What an exciting time to be alive! Hardly anyone would have guessed how close we are in 2019. I can’t wait to see what 2020 will bring.

I started my quest informally over 40 years ago when I predicted we would never have to die from aging if we could make it to my 100th birthday. Almost everyone I shared that with back then laughed at me. As it looks now though, I might have been conservative.

Was I ahead of my time? Did I have great insights into the future of medical technology? I’d like to think I was that smart, but the truth is, although I did know a little about where research was heading, it was probably just wishful thinking.

In June of 2000, Maximum Life Foundation sponsored our first longevity conference in Manhattan Beach, CA. It was a weekend roundtable brainstorm session among around a dozen of the top aging researchers from around the world.

Our objective was to generate a strategy to reverse aging. Aubrey de Grey attended, and that’s where he formulated his SENS strategy to control aging.

We did create a roadmap to “cure” aging which taught us what we thought would have to be accomplished for full rejuvenation.

One of the attendees posed a question. “In the future, when aging is a non-issue, what year would people of the future say aging was cured?”

Responses were all over the board, from something like 2025 to never. I threw out some highs and lows and settled on 2029 as a rough average. This was predicated on enough money being raised over the next few years… which didn’t happen.

Therefore, I adjusted my prediction to 2033.

Recently however, money has been increasingly invested in that initiative. If this trend continues, and I’m certain it will, it could be closer to 2029… or even sooner… depending on how you define a cure.

Will it be periodic temporary rejuvenation? Longevity Escape Velocity? Of full cell-by-cell rejuvenation, using nanomedicine for example, to make and keep all of our cells young and disease resistant?

Time will be the judge. But we do know this: We can already partially rejuvenate ourselves today. If you attended RAAD, you know what I mean.

Whether you were there or not, I recommend you get the videos at

More Life,
David Kekich


Weekly News

Kelsey Moody Presenting on the LysoClear Program at Ending Age-Related Diseases 2019

Kelsey Moody of Ichor Therapeutics presented on the LysoClear development program at the Ending Age-Related Diseases conference organized by the Life Extension Advocacy Foundation earlier this year.

LysoClear is an example of the commercial development of a rejuvenation therapy, taken all the way from the starting point of the discovery of microbial enzymes capable of breaking down certain forms of harmful age-related molecular waste that contribute to aging and age-related diseases.

The actual research is largely done, and the task now is to focus on manufacture, regulatory approval, and entry into the clinic.

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Cycles of DNA Damage and Repair as a Cause of Age-Related Epigenetic Drift

Researchers have recently proposed that the normal operation of DNA repair contributes to the epigenetic change that is observed to occur with age.

This is an interesting concept, and we’ll see how it progresses in the years ahead, particularly as therapies based on alteration of epigenetic markers emerge as an area of active medical research and development.

Epigenetic decorations to DNA are a part of the complex regulatory system controlling the amounts and timing of protein production carried out by a cell.

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Increased Insulin Sensitivity is Not Required for Extension of Healthy Life Span in Mice via Calorie Restriction

The biochemistry surrounding insulin and insulin signaling is very well studied in the context of aging. A number of ways to slow aging in laboratory species involve directly manipulating these signaling pathways.

Calorie restriction, like a number of other methods of slowing aging, improves insulin sensitivity, and the consensus in the research community has been that some fraction of the benefits to health and longevity that result from a restricted calorie intake are derived from this change to insulin metabolism.

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Autoimmunity Against AT1 Receptor Spurs Endothelial Cellular Senescence and Vascular Aging

The presence of antibodies against the angiotensin II receptor (AT1 receptor) has been noted in a number of conditions involving raised blood pressure, from preeclampsia during pregnancy to the hypertension associated with aging.

These antibodies induce dysfunction in vascular smooth muscle, preventing appropriate contraction and dilation in response to circumstances. That in and of itself is enough to produce hypertension, chronically raised blood pressure.

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We Still Have a Long Way to Go in Telling the World that the Longevity Industry Exists

I have been slacking on conference reports these past few months, but largely because the conferences I was attending were not wholly dedicated to longevity science or the longevity industry.

I was at BASEL Life in Switzerland, where Alex Zhavoronkov and the In Silico Medicine crew had taken over a section of the broader conference to talk about aging, at the Founders Forum events in New York and Boston, where one will find a handful of influential people from outside our community who are interested in longevity, and LSX USA, a Boston biotech industry gathering.

This week I was attending Giant Health in London, where the Aikora Health principals and Liz Parrish of BioViva Science organized a longevity-focused gathering within the much larger event.

Once one steps out of the circle of events dedicated to our community, such as Undoing Aging, Ending Age-Related Diseases, Longevity Therapeutics, and so forth, it is quite striking to see just how much more work there is left to do in terms of telling people that we exist.

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Chronic Inflammation as a Contributing Cause of B Cell Decline in Aging

B cells are important to the coordination of the immune response. Dysfunctional B cells emerge with age, however, leading to autoimmunity and contributing to immunosenescence, the name given to the general age-related decline in effectiveness of the immune system.

Animal studies have shown that selective destruction of the entire B cell population is beneficial in older individuals, improving the immune response: the cells are quickly replaced, but the harmful portion will take much longer to reemerge.

Setting all of this to one side, the open access review here is largely focused on more subtle changes in the B cell population and its production in the bone marrow, driven by the effects of age-related chronic inflammation on stem cells and progenitor cells.

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Many Longevity Enhancing Interventions Work via Upregulation of Autophagy

Many, possibly even most, longevity enhancing interventions tested to date in short lived species produce their effects on aging and life span via an increase in the cellular maintenance processes of autophagy.

The major focus of the research community over the past few decades in the matter of aging has been to replicate some of the calorie restriction response, or other responses to cellular stress. Cells responds to lack of nutrients, excessive heat, and so forth, by undertaking greater maintenance efforts for an extended period of time.

If the stress is mild and transient, the result is a net benefit. Unfortunately this class of approach doesn’t have sizable effects on life span in long-lived species such as our own: if we want to live significantly longer in good health, then we need to look at other strategies, such as rejuvenation biotechnologies after the SENS model that repair the forms of cell and tissue damage that causes aging.

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A Small Clinical Trial of Transcranial Electromagnetic Stimulation Shows Benefits in Alzheimer’s Patients

Researchers here report on a small clinical trial of a form of electromagnetic stimulation, claiming reduction in amyloid burden and improvement in cognitive function in Alzheimer’s patients. Other approaches to electromagnetic stimulation have been tested in human trials for Alzheimer’s disease and failed; the authors here argue that the details of the methodology used matter greatly.

It is not unreasonable to expect electromagnetic fields to have effects on cellular metabolism, and there are a range of efforts to try to affect everything from neurodegeneration to wound healing via this class of approach. There is always the question of mechanisms, however: determining how exactly it might be working to affect amyloid levels and cellular behavior, after an effect is confirmed, is a challenging task.

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How Much of Sarcopenia Lies in the Nervous System Rather than in Muscle?

Sarcopenia is the name given to the characteristic age-related loss of muscle mass and strength that manifests in all older individuals. A sizable fraction of this decline is self-inflicted, as demonstrated by the gains that can be obtained via resistance training in older individuals.

Nonethless, there are inexorable processes of decline, such as the loss of stem cell function in muscle tissue. Researchers have suggested that when it comes to loss of strength, damage and decline in neuromuscular junctions may be to blame, the point of integration between nervous system and muscle tissue. Researchers here suggest that contributing factors could emerge anywhere in the nervous system, including the brain, however.

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A Mechanism for Mammalian Cartilage Regrowth is Discovered

A theme of recent years is the discovery of processes of regrowth that operate in mammalian tissues long thought to be non-regenerative.

In this case, researchers have found a mechanism of regeneration that operates in cartilage, albeit not to the degree that would be helpful for recovery from more serious injury or the wear of aging. Still, where a mechanism exists at all, it should be possible to find ways to enhance its operation.

This work is interesting for the resemblance that this regenerative process bears to the way in which salamanders regrow lost organ tissue. Finding ways to bring that sort of exceptional regenerative capacity into mammals is the subject of numerous research programs.

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Becoming Overweight Raises the Risk of Many Cancers

People who become overweight at younger adult ages have significantly greater cancer risk than their slimmer peers. Visceral fat tissue is very active, producing chronic inflammation through a range of mechanisms including the production of greater numbers of lingering senescent cells.

This sort of tissue environment is more hospitable to the development of cancer. Cancer risk is far from the only downside of carrying excess visceral fat tissue, of course: one can expect a shorter, less healthy life on all fronts, accompanied with a raised lifetime medical cost.

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Business Analysts Start to Pay Attention to the Longevity Industry

Larger business analysis concerns are starting to notice that the longevity industry exists.

I point out this press release not because the contents are all that interesting or useful – it is very much business as usual in the white paper production community, and the people creating these materials typically have a poor understanding of the biology and the biotechnology – but rather as an indication of progress towards a broader appreciation of the potential to treat aging as a medical condition. Slowly, the eyes of the world are opened.

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Why Does Reduced Grip Strength Correlate with Chronic Lung Disease in Aging?

In this open access paper, researchers speculate on the common mechanisms underlying the correlation between reduced grip strength and chronic lung disease in old age.

The many, complex, and diverse manifestations of aging emerge from a much smaller, simpler set of root causes. Simple forms of damage applied to a very complex system necessarily produce very complex outcomes. Nonetheless, the incidence of many of those outcomes, even when very different from one another, will correlate because they depend to a sizable degree on the same forms of underlying damage.

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CDK5 as a Target to Reduce Cell Death Following Ischemic Stroke

A great deal of effort goes towards methods of reducing the damage caused by ischemic stroke, the cell death in the brain that occurs in response to even a temporary loss of blood supply.

Altering cellular reactions to this ischemia can greatly reduce this cell death response, and a number of different approaches to this goal have been demonstrated in mice over the years. Progress towards the clinic is, as ever, slow and uncertain, however.

Ultimately what should be developed are not ways to make a stroke less traumatic, or to improve the presently all too limited degree to which recovery can take place, but rather the means to prevent stroke from occurring at all – therapies that aid in maintenance and periodic repair of the vascular system, preventing it from degenerating into a state in which stroke is possible.

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A Brief History of Oisin Biotechnologies

This article includes a brief history of how the senolytic suicide gene therapy company Oisin Biotechnologies came about. Oisin Biotechnologies was one of the first senolytics biotech startups, of which there are now many, one of the first longevity industry companies, and launched at a time in which it was still quite hard to persuade investors that treating aging as a medical condition was a legitimate line of work.

That was actually just a few years ago now, 2015 as seen in the rear view mirror, and matters have changed rapidly since then. At the present time there are perhaps 50 to 100 startup biotech companies that we might categorize as being in the longevity industry, and there is enough interest from investors for it to be comparatively easy to raise funds for any credible approach. Still, this is only the very first stage of what will grow to be a truly massive industry in the years ahead.

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