Dear Future Centenarian,
You know why the advice from a grizzled pro anti-aging medicine doctor is worth so much more than what you’d learn in a PhD program?

Because you don’t actually learn your lesson by reading about it.

That’s just too passive to be effective.

You learn it best by actually making the mistake, in real life, and dealing with the consequences.

Then doing a brutal deconstruction of what went wrong, and where you need to beef up your skills, mindset, resources and network…

… before going back out and getting into the same fight again.

This is why knowledgeable and experienced anti-aging docs can add YEARS to your healthspan.

And they do that process until they get it right. The lessons they learned by applying their continuing education to patient care are what puts them ahead of the curve in treating YOU.

Of course, continuing education helps, but only as prep aids. Patient feedback in the form of diagnostics and regular visits tracking and analyzing the data and anecdotal evidence
They still have to see how large numbers of patients respond (and it WILL be a surprise, if they’ve been relying too heavily on books for treatments).

Of course, continuing education helps, but only as prep aids. Patient feedback in the form of diagnostics and regular visits tracking and analyzing the data and anecdotal evidence are their real education.

They still have to see how large numbers of patients respond (and it WILL be a surprise, if they’ve been relying too heavily on books for treatments).

Of course there will always be failures. It’s extremely rare for someone to succeed in a straight line of victory after victory.

It just doesn’t happen in the real world.

Some patients won’t respond. Unfortunately, some will die. And except for the partial rejuvenation therapies we have today, we will all age, at least at some rate, until we can totally reverse your biological clock.
Humans are, basically, shaved apes with overloaded brains, suffering all sort of delusion and misconception about reality.

And that stuff needs to be field-tested and rejected through experience.

It’s how we get through the day in a hostile universe pretty much bent on our obliteration.

Beware of wet-behind-the-ears advice.

Go to the source, when possible and do continue your education… but APPLY that knowledge.

That goes for you as well as your physician. He or she can only advise, treat or prescribe. Hopefully they are the grizzled veterans (regardless of age) that partner with you on your road to super healthy longevity.

However, regardless of how good your physician is, it’s up to YOU to implement his or her advice.

If there’s not a good anti-aging physician in your area, there are certainly some good ones in your region. Alternatively, some excellent practitioners offer telemedicine services.

If you’re not one to see doctors for some reason, you can get excellent wellness and longevity advice from Life Extension Foundation, RAADfest and select books and videos.

Final caution: Resist becoming only an information junkie. Knowledge does you no good unless you put it to practice and track your results.

More Life,

David Kekich


Weekly News

Support Rejuvenation Research by Donating to the SENS Research Foundation Winter 2019 Fundraiser

Winter is upon us, and thus the yearly winter SENS Research Foundation fundraiser just recently started a few days ago. For those who don’t know, the SENS Research Foundation remains one of the most important and influential organizations working on advancing rejuvenation research to the point at which it can be moved into clinical development and funded by venture capital.

Through conferences and advocacy, the SENS Research Foundation staff also played a sizable role in ensuring that there is in fact an active venture capital community eager to back new companies working on the treatment of aging.

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Assessing Gene Therapy to Upregulate Three Longevity-Associated Genes in Mice

Today’s open access research materials report on results obtained in mice using gene therapy to upregulates protein production of several longevity-associated genes.

As expected from prior research into these genes and their influence on the operation of metabolism, health is improved in mouse models of age-related disease. As might also be expected based on past results, some combinations are not effective for reasons that remain to be explored: metabolism is complicated, and pulling on levers and turning dials rarely does exactly what was expected.

Evolution does not produce optimal organisms, as seen from the perspective of the individual. This is well illustrated in mice, where any number of single gene alterations, even just dialing up or down the amount of protein produced over time, leads to better health, less disease, longer lives.

Why haven’t any of these small alterations taken place via random mutation and thereafter prospered and spread through the species over the course of evolutionary time?

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GDF11 as a Calorie Restriction Mimetic

GDF11 was one of the first factors in blood identified as a possible explanation for the outcome of heterochronic parabiosis.

When a young and old mouse have their circulatory systems joined, some aspects of aging reverse in the old mouse, and some aspects of aging are accelerated in the young mouse.

GDF11 levels decline with age, and it was thought that increased levels of GDF11 provided by the young animal could act to improve function of cells and tissues in the older animal – though it was not well understood as to how GDF11 worked to produce these results.

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Cardiomyocytes Expressing SOX10 are Vital to Zebrafish Heart Regeneration

A few higher animal species, such as salamanders and zebrafish, are capable of regeneration of limbs and internal organs, regrowing lost and injured tissue without scarring or loss of function.

Numerous research groups are engaged in investigating the biochemistry of proficient regeneration, attempting to find the specific differences between species that might explain how it happens and why adult mammals are largely incapable of such feats of regrowth.

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TRIB1 Regulates Uptake of Oxidized Lipids into Macrophages, and thus Drives Atherosclerosis

Atherosclerosis is a condition of dysfunctional macrophages. Macrophages are responsible for clearing out lipids that end up in blood vessel walls, ingesting these misplaced lipid molecules and handing them off to HDL particles to be carried to the liver for excretion.

This works just fine in youth, in an environment of low oxidative stress and few oxidized lipids. Aging brings chronic inflammation, oxidative stress, and oxidized lipids, however. Macrophages cannot process oxidized lipids all that well, and so become pathological, turning into inflammatory foam cells packed with lipids, and unable to do more than send signals for help.

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Exercise is a Benefit at Any Age

In our modern societies of convenience and luxury, and the overwhelming majority of human societies today are exceedingly convenient and luxurious in comparison to the hunter-gatherer existence of our ancestors, it is the case that most people do not exercise to the degree needed to maintain function with advancing age.

If exercise is seen to produce benefits in near all patients of any later age, and it is, that is the case because those patients are not maintaining themselves sufficiently.

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Researchers Call for Rigorous Classifications of Aging to Assist Development of Therapies to Treat Aging

The first rejuvenation therapies exist, in the form of senolytic drugs that selectively destroy senescent cells, but no regulatory bodies yet recognize aging as a legitimate target for therapy.

A variety of efforts are underway to change this state of affairs, many of which focus on the contents of the International Classification of Diseases (ICD) maintained by the World Health Organization (WHO), which is presently in the process of revision to ICD-11. Incorporating aging into the ICD in a rigorous way would lead, in time, to medical service providers and regulatory bodies worldwide adopting the concept of aging as a condition that can be treated.

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An Investigation of Adverse Effects of Nicotinamide Riboside Supplementation

Nicotinamide riboside is so far the only approach to NAD+ upregulation for which there is published human trial data, though other trials for other approaches are underway at the present time.

NAD+ declines with age, for reasons that remain comparatively poorly understood, and this has a negative impact on mitochondrial function. Thus there is considerable enthusiasm at the moment for intervening in this known manifestation of aging by tackling the proximate causes, raising NAD+ levels, but without addressing underlying causes.

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Towards a Rigorous Definition of Cellular Senescence

The accumulation of lingering senescent cells is a significant cause of aging, disrupting tissue function and generating chronic inflammation throughout the body.

Even while the first senolytic drugs capable of selectively destroying these cells already exist, and while a number of biotech companies are working on the production of rejuvenation therapies based on clearance of senescent cells, it is still the case that much remains to be settled when it comes to the biochemistry of these errant cells.

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HDAC9 in Vascular Calcification

Researchers here show that HDAC9 plays a role in the calcification of blood vessel walls, a process that contributes to the stiffening of blood vessels that leads to hypertension and all of the damage that chronic raised blood pressure causes to delicate tissues throughout the body.

That mice lacking HDAC9 are more resistant to calcification suggests that there may be a mechanism here that can serve as the basis for a therapy to slow down the progression of calcification in human tissues.

That said, it is worth comparing effort such as this with the potential for senolytic drugs to achieve similar results, based on the evidence for senescent cells to contribute to vascular calcification.

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Modulating Gut Microbe Populations to Generate More Butyrate, thus Raising BDNF Levels and Improving Cognitive Function

The microbial populations of the gut have an influence on health and the progression of aging via the molecules that they generate, and which our cells react to.

It isn’t entirely clear as to the ordering of cause and effect in the detrimental changes that take place with aging in intestinal tissue, immune system, diet, and microbial populations. Studies have shown, however, that restoring more youthful populations can influence the function of tissues throughout the body, including the brain.

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Success for the MitoMouse Crowdfunding Project

The latest mitochondrial rejuvenation research project to be crowdfunded by the and SENS Research Foundation teams focused on proving out allotopic expression of mitochondrial gene ATP8 in mice with a loss of function mutation in that gene. I’m pleased to note that the community rallied around and the project was fully funded, including its stretch goals.

Mitochondria have their own small genome; allotopic expression is the process of placing a copy of a mitochondrial gene into the nuclear genome, suitably altered to enable the proteins produced to find their way back to the mitochondria where they are needed. This backup source of proteins allows mitochondria to function normally even when their own DNA is damaged.

The technique, when applied to single genes, allows for the treatment of inherited mitochondrial conditions, as demonstrated by Gensight Biologics. More importantly, however, when applied to all thirteen mitochondrial genes it will prevent mitochondrial DNA damage from contributing to the aging process.

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Extracellular Vesicles from Embryonic Stem Cells Make Mesenchymal Stem Cells More Effective in Therapy

Mesenchymal stem cell (MSC) is a category so broad as to be near meaningless, but many varieties are widely used for therapeutic purposes.

MSCs are taken from any one of a variety of sources, expanded in culture, and introduced to the patient.

Researchers here show that applying extracellular vesicles from embryonic stem cells to the cultured MSCs reduces the usual issues that arise when expanding cells in culture, such as senescence, and improves the effectiveness of MSCs as a therapy when tested in mice. On a practical basis, one would imagine that induced pluripotent stem cells would serve just as well as a source of extracellular vesicles with this capability.

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3-D Printing of Skin with Embedded Vasculature

Researchers continue to take incremental steps towards the creation of engineered living tissues containing the vascular networks needed to support it. Absent blood vessels, numerous varieties of functional tissue can be generated from cell samples: lung, liver, kidney, and so forth.

These organoids are limited in size to a few millimeters, however, the distance the nutrients and oxygen can perfuse. Generating blood vessel networks is a serious technical challenge, and the major obstacle to the production of entire organs for transplantation.

Consider that natural capillary networks exhibit a density of hundreds of vessels passing through every square millimeter of tissue cross-section. Even the best of present efforts are distant from that scale, though in laboratory demonstrations they suffice to produce essentially functional larger tissue sections.

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Reviewing Leucine Supplementation as a Treatment for Sarcopenia

Sarcopenia is the name given to the characteristic loss of muscle mass and strength that takes place with advancing age.

A surprisingly large fraction of this loss is self-inflicted: few people undertake the necessary exercise and strength training to maintain muscle in later life. But the rest of the losses are to some degree inevitable, a consequence of damage and disarray in muscle stem cells, neuromuscular junctions, and various processes necessary to muscle tissue maintenance.

There is evidence for one those issues to be a growing inability to process leucine, an essential amino acid. Leucine supplementation may thus slow the onset of sarcopenia, even while being a compensatory approach that in no way addresses the underlying causes of this form of age-related degeneration.

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