Dear Future Centenarian,

Here’s a sizzling tip that helped me leapfrog my way up the extreme longevity ladder:

Don’t start reading your next diet or exercise book…

… until you’ve put at least one thing into action from the last book.

Don’t attend or watch another wellness conference or seminar…

… until you’ve put at least one thing into action from the last one.

Idea junkies seldom make actual improvements. They fill up their brains with theory and wish lists…

… but end up having a miserable reputation for not following through. (Which is where the big advancements live.)

Don’t be that person.

Read, act, repeat. That’s the key to healthy longevity beyond the dreams of most.

There are only a handful of fundamental ideas required to get or stay on the path to radical life extension, anyway. Most of the books out there just rehash the same rigamarole over and over. You’re storing up recycled info.

If you want to stay on the cutting edge, attend every RAADfest. If you missed the last one, order the videos.

Do read. A lot.

Just USE the stuff you learn from attending, watching and reading. Immediately, to cement it into your system.

Putting the good ideas you have into action requires proactivity (rather than just thinking about how well or lean you’ll be). And you master those skills through real-world application.

Which requires a steady diet of doing or eliminating stuff. Not just thinking about doing it.

Movement beats “coulda, woulda, shoulda” excuses every time.

(Special thanks to John Carlton for this inspiration.)

More Life,

David Kekich


Weekly News

Data on Exercise as a Treatment for Age-Related Arterial Stiffness

In addition to its effect on muscle growth, exercise upregulates a range of maintenance processes, such as autophagy, that improve tissue function when maintained over the long term.

Lack of exercise in later life accelerates the decline in muscle mass and strength, an issue that appears reversible to a degree that might surprise most people. A similar situation occurs with respect to stiffening of blood vessels, in that while much of this depends on mechanisms such as cross-linking and presence of senescent cells, some of the decline is a matter of being sedentary.

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The Many Roles of Senescent Cells

Long-lived senescent cells accumulate with age, initially quite slowly as they are efficiently removed by the immune system when their own programmed cell death processes fail, but once the immune system starts to decline with age, the burden of cellular senescence ramps up dramatically.

Senescent cells secrete a potent mix of signals known as a senescence-associated secretory phenotype (SASP). It spurs chronic inflammation, destructively remodels nearby tissue, encourages nearby cells to also become senescent, and causes all sorts of other issues as well. It is very harmful, and the more senescent cells there are, the worse the consequences.

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The SENS Research Foundation on the Beneficial Nature of Senolytic Therapies

The SENS Research Foundation should need no introduction to this audience, but, just in case, this is one of the few non-profit organizations dedicated to advancing the state of the art in rejuvenation research and development.

The focus of the SENS Research Foundation staff is on unblocking lines of research that are presently moving too slowly, rather than on reinforcing success. The co-founder, Aubrey de Grey, assembled the Strategies for Engineered Negligible Senescence (SENS) going on twenty years ago. It was, and is, a synthesis of what is known in the research community regarding the root causes of aging.

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Lipid Metabolism in Aging and Age-Related Disease

Lipids are everywhere in our biochemistry. Where they are present in cell structures and molecular mechanisms that are important to any specific age-related disease, or are among the underlying root causes of aging, it will tend to be the case that differences between species (and possibly individuals) can lead to changes in the pace of aging and disease.

For example, lipid composition determines resistance to oxidative damage to cell membranes. A range of evidence supports the membrane pacemaker hypothesis of aging, in that longer-lived species tend to have more resilient cell membranes, based on their lipid composition.

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Is Displaced Nuclear DNA a Meaningful Cause of Chronic Inflammation in Aging?

Sterile inflammation arises without external cause, such as infection or injury, and chronic sterile inflammation is a characteristic of aging.

Inflammatory signaling becomes constant and pronounced in tissues, and the immune system is constantly roused to action. Processes, such as regeneration from injury, that depend upon a clear cycle of inflammation that starts, progresses, and resolves are significantly disrupted.

It is no exaggeration to say that the downstream consequences of chronic inflammation accelerate the progression of all of the common age-related conditions.

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An Interview with Sergey Young of the Longevity Vision Fund

The Longevity Vision Fund is the third of the sizable pools of venture funding to emerge of late, after Juvenescence and Life Biosciences, that are dedicated to the new longevity industry.

Unlike the other two, the Longevity Vision fund is initially focused on what I would say are initiatives that don’t much matter and won’t much move the needle on human aging. Only in their second phase do they intend to invest in classes of biotechnology and therapy that may include high value approaches.

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Combining Strategies to Slow Aging to Increase Life Span in Flies by 48%

The research and development communities have little incentive to try combinations of approaches when it comes to intervening in the aging process, or indeed to treat any medical condition.

There is little funding and large barriers stand in the way of any effort to combine either existing or novel therapies, such as issues with intellectual property rights. Thus, few groups undertake such work.

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Deletion of p38? in Neurons Slows Neural Stem Cell Decline and Loss of Cognitive Function in Mice

Researchers here provide evidence for p38? to be involved in the regulation of diminished neural stem cell activity with age. It is thought that the loss of stem cell activity with age, throughout the body and not just in the brain, is an evolved response to rising levels of damage that serves to reduce the risk of cancer that arises from the activity of damaged cells.

The cost, however, is a slow decline into dysfunction and tissue failure.

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Mitochondrial Mutator Mice May be a Poor Model

Mitochondrial dysfunction and mitochondrial DNA damage are significant features of aging. One of the tools used to investigate the role of mitochondria in aging is the lineage of mitochondrial mutator mice.

These mice accumulate mutations in mitochondrial DNA quite rapidly, and exhibit accelerated aging.

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An Interview with Amutha Boominathan of the SENS Research Foundation

Amutha Boominathan leads the mitochondrial research program at the SENS Research Foundation, focused on achieving allotopic expression of mitochondrial genes.

This is the process of placing mitochondrial genes into the nuclear genome, suitably altered sot the proteins produced are transported back to mitochondria where they are needed.

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Investigating the Superior DNA Defenses of Tardigrades

Tardigrades are extremely resilient to radiation induced DNA damage, and here researchers delve into some of the mechanisms involved. Mining other species for potential improvements to our own biochemistry, or the basis for therapies, is an expanding line of work in the life science community.

Possible ways to improve mammalian defenses against damage to nuclear DNA are of interest for a range of reasons, not least of which is that it is the present consensus that stochastic mutation to nuclear DNA contributes to both cancer risk and aging itself, as mutations in stem cells or progenitor cells can spread throughout tissues via clonal expansion.

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