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The People Who Will Keep You From Aging

Longevity News Digest

Funding Aging Research

The People Who Will Keep You From Aging

Dear Future Centenarian, 

Once we solve aging, if you look deeply enough behind the curtain, you would be shocked to see what a diverse and surprising group of individuals had a hand in your œsecond chance.

Last week, I attended and spoke at the most incredible conference I ever saw. There was a sold out overflow crowd of approx. 250 attendees. Actually, I should say œparticipants, since it was an interactive experience.

No, it wasn™t a biotech conference. Not an anti-aging or medical conference either. Attendees were a group of high-powered marketing oriented entrepreneurs. You know, the kind of people who make the world go around. As you may know, nothing happens till someone sells something. (And ironically, salesman get a bad rap.)

My good friend, Joe Polish, held the event in Newport Beach, CA, and people lined up with $10,000 checks in hand for the privilege of being there. The information was groundbreaking, inspiring¦ and worth every dime to the attendees. The consensus was that on average, the experience will translate to $250,000 extra profit to each attendee.

And that™s borne out by the 150 people who pay Joe $25,000 annually to meet three times a year to exchange ideas. Most original members have renewed for 6-7 years running.

Some of the speakers were: Kevin Harrington and Daymond John from Shark Tank; Peter Diamandis, X-Prize founder; Arianna Huffington, founder of the Huffington Post and Tim Ferris, author of œ4 Hour Work Week.

Surprising to me was how well represented the health and wellness industry was.

My topic of course¦ was extreme life extension.

More about this event in another newsletter, including why some of the lessons learned will make your longevity œsatisfyingly happy. For now, let™s take a look at how the people there will contribute to YOUR longevity.

The primary contribution is they (or others like them) will accelerate research.

They™re not researchers, so how is that possible? (I actually did spend time there with two biophysicists with a breakthrough stem cell technology.)

For a long time, I™ve been saying progress is held back more to the lack of marketing than from solid science.

Some of these and other marketing genius entrepreneurs will apply their marketing skills, directly or indirectly, to raising the capital needed to push research forward. And some will contribute management expertise to new startups in this field as well.

The two most important ingredients to companies in general are innovation and marketing. In fact, all or nearly all revenue is spawned by those two. Tons of innovation now is screaming to be funded.

Here™s a link to one of the more fascinating, educational, productive¦ and FUN groups on the planet. It™s already changing the world.

More Life,
David Kekich

Latest Headlines from Fight Aging!
Calico Website Launched - Monday, August 11, 2014
Google's California Life Company has launched a stub website. The sparse information presented there is supportive of the view that Calico will be taking the Longevity Dividend path of focusing on genetics, metabolic manipulation, and standard issue drug discovery.

This will look a lot like a continuation of sirtuin research, which is to say that they will spend a lot of money, generate a lot of data, and utterly fail to produce ways to meaningfully extend healthy human life. That is a fairly safe prediction for the outcome of any well-funded project that is not trying to build repair-based technologies to revert the causes of aging, but rather intends to alter the operation of metabolism to gently slow aging.

(My note: I understand Calico has contacted Aubrey de Grey for possible consultation. So repair-based technologies MAY be part of their plan)

Metabolism is immensely complex and poorly understood, and there is no well-defined course towards results that is analogous to the SENS plans for repair-based approach. A billion dollars and fifteen years has been spent on simply trying to reproduce a fraction of the most understood form of natural metabolic alteration that enhances longevity, the response to calorie restriction, with no good results. For that time and money we could have a demonstration of rejuvenation in mice via SENS therapies already.

Genetics is hot and drug discovery is safe and understood by investors. So as interest in treating aging is rising, we see funds raised and ventures started for groups trying to perform drug development based on genetic studies of aging and longevity. This is not because it has a hope of meaningful results, but because it is where funds can be raised, and where money can be made in the traditional Big Pharma fashion even without achieving any great extension of human longevity.

In the Longevity Dividend viewpoint an ambitious goal is to add seven years of life expectancy over the next two decades through new drugs that alter metabolism - which is a miserable failure and a grand missed opportunity when compared to the indefinite extension of healthy life that might be attained by realizing comprehensive repair therapies for the damage that causes aging.

This is all disappointing, but that has been the signal all along as to where things were going with Calico: it is a project that may turn out to look a lot like a more highly publicized version of the Ellison Medical Foundation, in that it is simply adding more of the work already taking place at the NIA and elsewhere that is destined from the start to fail to advance human longevity. Its existence helps those elsewhere who are trying to raise funds to tackle aging, as it shifts conservative funding institutions in a direction of supporting such work, but that is about it.

To my eyes all of this reinforces the need to demonstrate beyond a doubt that repair approaches to reverse aging do in fact work, and work very much better and for far less cost of development than metabolic alteration. The way in which repair-based approaches will take over the mainstream of research is by showing that they produce compelling results at a time in which the other approaches are failing to do anything other than generate data and consume resources.

The nearest approach to that point for the purposes of convincing people who support slowing aging but are not on board with aiming for rejuvenation is probably the targeted destruction of senescent cells, but even there it has been hard to raise funding for continued work and the reliance is on philanthropy to run the present study in normal rather than accelerated aging mice.

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Genetic Studies of Longevity Leading to Drug Development - Monday, August 11, 2014
The research linked below is an example of work in the Longevity Dividend model: study the comparative genetics of longevity in humans to find epigenetic patterns and genetic variants that correlate with membership of long-lived families.

From there proceed to identify underlying mechanisms and undertake drug development to find ways to recreate those differences. This mainstream, well-supported research is absolutely the wrong path to take if the aim is to producing meaningful extension of healthy life, however.

Aging occurs because we accumulate damage as a side-effect of metabolism within and around our cells. Outside of a few rare and devastating genetic mutations, we all suffer exactly the same types of damage for exactly the same reasons. Genetic and epigenetic variants have a limited effect on our interaction with this growing damage until very old age, so we should ignore them: researchers should focus instead on repairing and reverting these known forms of damage that cause aging. The resulting treatments built for this purpose will be applicable to everyone, and thus can be mass produced cheaply.

Given a choice between spending vast sums on building age-slowing drugs that help maintain people for longer in a state of being old and damaged, or building repair biotechnologies that help maintain people in a youthful, undamaged state, I know in which direction my money is heading.

Drugs to slow aging will never be particularly helpful for those already old and damaged, while repair biotechnologies will aid those in greatest need of repair. It seems fairly self-evident to me where the focus should be. Yet the vast majority of research funding for the comparatively young field of longevity science is aimed at the inferior goal of slowing aging. This must change.

Note: Except for the supplements and drugs that could add healthy years to average lifespans. This buys us more time and improves the quality of our lives

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Studying Calorie Restriction and Rapamycin - Tuesday, August 12, 2014
Here is an example of the sort of work presently taking place in many of the labs interested in aging and longevity, consisting of exploration of existing drugs shown to have some effect on life span in animal studies, alongside continued research into the details of the calorie restriction response.

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Building Brain Tissue for Research and Testing - Tuesday, August 12, 2014
A lot of the early applications of tissue engineering are focused on aiding research: the small amounts of tissue created are using for testing and investigation.

That is a stepping stone for the various companies and labs involved, a way to generate revenue and interest while steadily improving their capabilities. It is worth keeping an eye on these efforts, because it is from here that later applications in clinical medicine will arise.

Read More

A Twist in the Progression of Atherosclerosis - Wednesday, August 13, 2014
Atherosclerosis is a dangerous condition caused by molecular damage to certain proteins circulating in the blood and then spurred on by growing chronic inflammation in aging.

Where it takes root, the walls of your arteries corrode, malform, and expand inward into soft plaques of degenerative material. This is largely formed of macrophage cells attracted to the area by dysfunctional signaling and then choked by the debris. Ultimately this leads to serious vascular dysfunction, but more importantly if a large enough chunk of plaque material breaks away it will cause a heart attack or stroke.

Here researchers suggest that the immune system is not the dominant origin for the macrophages that make up plaque debris, and a more important and unusual source is actually closer at hand.

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Aging is the Cost of Species Adaption and Survival - Wednesday, August 13, 2014
A small number of species have exceedingly long life spans and show few signs of degenerative aging, so clearly biology is up to the task of continual repair and vigor. Yet the vast majority of species consist of individuals who age, and who will die because of aging should they survive the many other causes of mortality in the wild.

Why do we age to death? The present consensus is that the prevalence of aging is the result of an evolutionary arms race to the bottom. Species that age better adapt to changing conditions and thus will take over most evolutionary niches. In effect we age because the world changes. Some thoughts here from a researcher in the field.

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Being Overweight or Obese Raises the Risk of Cancer - Thursday, August 14, 2014
This recent study provides yet another reason to make lifestyle choices that better manage your weight. If nothing else cancers thrive in an inflammatory environment, and metabolically active visceral fat tissue generates chronic inflammation. More of it is definitely worse for your long-term health in a range of ways.

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Working Towards a Way to Clear Cytomegalovirus - Thursday, August 14, 2014
Like other herpes viruses, cytomegalovirus (CMV) cannot be effectively naturally cleared from the body as it has evolved the means to hide from the immune system. It is harmless for most people in the short term, but over the long term it causes ever more of the limited supply of immune cells to become uselessly devoted to fighting it.

Since near everyone is exposed to CMV by the time they are old, this appears to be an important contribution to the age-related decline of the immune system.

One possible approach to dealing with this issue is to selectively destroy CMV-specialized immune cells. They will be replaced naturally and fairly quickly, or that replacement can be hurried along with an infusion of immune cells grown from a sample of the patient's tissues. The cancer research community is a fair way along in the development of highly selective cell destruction technologies that identify targets based on their distinctive surface chemistry, and this work can be adapted for use in winnowing the immune system.

Another approach is to find ways to clear out CMV, but that isn't so helpful for people who have lived with it for a long time and are therefore already suffering the consequences in the form of a distorted balance of immune cells. Nonetheless, here is a look at research into how CMV hides from the immune system. This is a starting point on the path towards disabling these molecular mechanisms to enable immune cells to clear CMV from the body.

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12-Lipoxygenase is Critical in Type 2 Diabetes - Friday, August 15, 2014
For the overwhelming majority of sufferers, type 2 diabetes is a lifestyle disease. It is something that they did to themselves, and which could be turned back at near any point with a suitable (albeit increasingly drastic) change in diet and lifestyle.

Giving yourself the highest chance of avoiding type 2 diabetes is easy: stay active and stay thin. Nonetheless, the medical research community spends a lot of time and effort on finding ways for people to remain fat and indolent while still avoiding diabetes - though of course these efforts also apply to the much smaller population unfortunate enough suffer the condition regardless.

Here researchers find a way to protect the small population of insulin generating beta cells impacted by the mechanisms of type 2 diabetes, but by the sounds of it this will not affect any of the numerous other consequences of becoming fat, such as a raised risk of suffering all of the other common age-related conditions.

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Daumone as Calorie Restriction Mimetic - Friday, August 15, 2014
In this open access paper researchers present the evidence for daumone to be a calorie restriction mimetic in mammals.

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DISCLAIMER:  News summaries are reported by third parties, and there is no guarantee of accuracy. This newsletter is not meant to substitute for your personal due diligence and is not to be taken as medical advice. For originating report, please see

David A. Kekich
Maximum Life Foundation

"Where Biotech, Infotech and Nanotech
     Meet to Reverse Aging by 2033"


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