Increase Your Longevity

How Ten Obscure Scientists Paved the Way to Your Longevity

posted on May 18, 2010

Last Friday, I was invited to a dedication of a new $100 million stem cell research center. Eye opening in a couple of ways.

A prominent billionaire and his wife, Bill and Sue Gross, were the primary donors, and they were honored at the event. I got to reconnect with Bob Klein, the initiator and moving force behind California’s Proposition 71, the $3 billion stem cell bond issue initiative. It was also fun seeing old friends and making some new ones.

But here is one of the two most impactful happenings (at least to me).

When the speeches started, I heard what sounded like cheerleaders practicing. It was at the University of California at Irvine (UCI) campus, and I was surprised at the lack of coordination between the athletic department and the event organizers.

But then I realized it was not a cheerleading squad at all. It was a rude group of protestors who were determined to disrupt the proceedings. It was annoying at first, and it was irritating to have a group of people demonstrate their rights of free speech, while at the same time interrupting others expressing their opinions, on their turf, and at their expense.

The protests finally faded into the background, but not before I was reminded how nearly every great idea is first ridiculed, then opposed and finally widely accepted and supported. Here were some of the more productive and brilliant minds on the planet, kicking off a program that will someday positively impact almost everyone’s life, directly or indirectly, while some of those future beneficiaries were trying to tear it down. Ironic, huh?

The second happening was much more positive and impactful.

Not long ago, Bob Klein had a revolutionary idea. Motivated by one of his children’s disease, he decided to raise $3 billion for stem cell research at a time when stem cell science was politically incorrect. So he was ridiculed. Then he ran into major opposition. And now his idea is helping change the world. Millions of people will benefit from his and his associates efforts without ever giving a second thought as to who made it possible for them or how it ever happened. They’ll just take their cures for granted. But the important thing is, they will benefit, and many will dodge death sentences.

Bob told a story about how ten scientists in Italy started the modern scientific revolution. Their meeting gave birth to the Royal Society in England in 1660, then the French Academy of Science and then the ripple effect that led to the medical miracles we see happening all around us. Billions benefited.

You and I are witnessing and are part of a similar event. We are launching the Manhattan Beach Project which will some day help allow millions, and perhaps billions avoid death from aging. Can you think of anything more gratifying? Imagine the thrill of being able to help save just one life, let alone millions.

Long Life,
David Kekich
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SOME ADVICE FROM REASON

Live healthily not because you think it will let you survive into the far outskirts of present human longevity, but because it will increase your chances of living in good health to benefit from future developments in medical science. The older we get, the more our remaining life span and health is determined by progress in advanced medical technologies - which suggests that we should all be doing more now to support the best and most promising research.
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LATEST HEALTHY LIFE EXTENSION HEADLINES

MICROMASONRY IN TISSUE ENGINEERING (May 14 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4725
A new technique for tissue engineering: "Tissue engineering has long held promise for building new organs to replace damaged livers, blood vessels and other body parts. However, one major obstacle is getting cells grown in a lab dish to form 3-D shapes instead of flat layers. To obtain single cells for tissue engineering, researchers have to first break tissue apart, using enzymes that digest the extracellular material that normally holds cells together. However, once the cells are free, it's difficult to assemble them into structures that mimic natural tissue microarchitecture. Some scientists have successfully built simple tissues such as skin, cartilage or bladder on biodegradable foam scaffolds. That works, but it often lacks a controlled microarchitecture. You don't get tissues with the same complexity as normal tissues. Researchers [have] come up with a new way to overcome that challenge, by encapsulating living cells in cubes and arranging them into 3-D structures, just as a child would construct buildings out of blocks. The new technique, dubbed 'micromasonry,' employs a gel-like material that acts like concrete, binding the cell 'bricks' together as it hardens. You can reproduce this in any lab. It's very simple. The short-term next step is really looking at different cell types and the viability of tissue growth."

CREATING INNER-EAR CELLS (May 14 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4724
Via EurekAlert: "Humans are born with 30,000 cochlear and vestibular hair cells per ear. (By contrast, one retina harbors about 120 million photoreceptors.) When a significant number of these cells are lost or damaged, hearing loss occurs. The major reason for hearing loss and certain balance disorders is that - unlike other species such as birds - humans and other mammals are unable to spontaneously regenerate these hearing cells. After years of lab work, researchers [have] found a way to develop mouse cells that look and act just like the animal's inner-ear hair cells - the linchpin to our sense of hearing and balance - in a petri dish. If they can further perfect the recipe to generate hair cells in the millions, it could lead to significant scientific and clinical advances along the path to curing deafness in the future. While researchers will ultimately need human hair cells, the mouse version is a good model for the initial phases of experimentation, he said. In addition to using mouse embryonic stem cells, the researchers used fibroblasts that had been reprogrammed to behave like stem cells: These are known as induced pluripotent stem cells, or iPS cells."

CR MIMETICS AND THE DEFINITION OF INSANITY (May 13 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4723
From the SENS Foundation: "To date, all successful interventions into the biological aging process in experimental animals have entailed modulation of basic metabolic pathways, generally through genetic or dietary manipulation. Of these, the earliest, most well-studied, and arguably the most robust, is Calorie restriction (CR): the reduction in dietary energy intake, without compromise of essential nutrients. With few exceptions, CR retards the biological rate of aging in nearly every species and strain of organisms in which it has been tested, ranging from rotifers, through small multicellular invertebrates, and most extensively to laboratory rodents; and although inconclusive, recent evidence also supports its effectiveness in dogs and nonhuman primates. Moreover, while necessarily preliminary, a growing body of human research has reported that rigorous CR, when practiced by previously normal-weight adults, results in physiological, functional, and perhaps even structural changes consistent with its translation to the human case. But despite the initial attractiveness of the notion; its strong theoretical basis; the high level of scientific interest that it has garnered; the launching of biotech startups originating in CR mimetic research; and the popularization and commercial exploitation of the concept by the dietary supplement industry - despite all of these drivers, the ensuing decade and a half or more of CR mimetic research have thus far been fruitless. Initially-promising compounds have failed to extend lifespan, while surprising findings have preempted the further investigation of what might otherwise have been novel targets for CR mimetics."

THE CHALLENGE OF LONGEVITY (May 13 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4722
From QFinance: "Big business and governments are already grappling with the uncomfortable side effects of increasing longevity. According to actuaries, the present generation has gained the equivalent of 12 minutes an hour or a 20% increase in average lifespan by comparison with the previous generation. The impact of this is felt first and foremost in the pensions arena, with businesses having to run harder just to stand still as far as their pension scheme deficits are concerned. But it is felt too by governments across Europe as they struggle to pay out meaningful state pension benefits against the headwind imposed by the fact that the ratio of those in work to those on pension is getting more and more out of balance.

The impact of increased longevity is felt too in the health systems, where the diseases and ailments of old age take an increasing toll on a country's medical resources. These problems might seem fairly intractable, or at least extremely difficult and challenging in their own right, but it could be just the tip of the iceberg, according to the renowned longevity specialist Dr Aubrey de Grey, Chief Scientist at the charity SENS, which specializes in promoting research that aims to 'defeat ageing.' Dr de Grey is famous for asserting that the first person to enjoy a four-digit lifespan is probably already in his or her middle years. Before I give a rapid summary of his reasoning - those interested in learning more can watch a video of one of his presentations at the SENS website - it is worth saying that if de Grey is right, then instead of exacerbating the pensions problem, as I suggested earlier, it will probably make the problem vanish like a puff of smoke. Provided society stays reasonably open, people will have more than enough time to acquire independent means. The magic of compound arithmetic will be very much in their favor. Start small, watch it grow, where's the hurry?"

INSULIN RESISTANCE ACCELERATES ATHEROSCLEROSIS (May 11 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4719
Another consequence of the overeating and lack of exercise that leads to metabolic syndrome and diabetes: "In people with insulin resistance or full-blown diabetes, an inability to keep blood sugar levels under control isn't the only problem by far. A new report [shows] that our arteries suffer the effects of insulin resistance, too, just for entirely different reasons. Earlier studies showed that in the context of systemic insulin resistance, blood vessels become resistant, too. Doctors also knew that insulin resistance and the high insulin levels to which it leads are independent risk factors for vascular disease. But it wasn't clear if arteries become diseased because they can't respond to insulin or because they get exposed to too much of it. Now comes evidence in favor of the former explanation. Mice prone to atherosclerosis fare much worse when the linings of their arteries can't respond to insulin. The animals' insulin-resistant arteries develop plaques that are twice the size of those on normal arteries. Insulin-resistant blood vessels don't open up as well, and levels of a protein known as VCAM-1 go up in them, too. VCAM-1 belongs to a family of adhesion molecules [which sit on the endothelium and bind] white blood cells. Those cells can enter the artery wall, where they start taking up cholesterol, and an early plaque is born. The results provide definitive evidence that loss of insulin signaling in the endothelium, in the absence of competing systemic risk factors, accelerates atherosclerosis."

ARRESTIN AND NEMATODE LONGEVITY (May 10 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4717
From ScienceDaily: researchers "have found that the level of a single protein in the tiny roundworm C. elegans determines how long it lives. Worms born without this protein, called arrestin, lived about one-third longer than normal, while worms that had triple the amount of arrestin lived one-third less. Arrestin interacts with several other proteins within cells to regulate longevity. The human version of one of these proteins is PTEN, a well-known tumor suppressor. The links we have found in worms suggest the same kind of interactions occur in mammals although human biology is certainly more complicated. We have much work to do to sort out these pathways, but that is our goal. We don't know at this point if human arrestins regulate PTEN function or if anything happens to arrestin levels during the development of cancer. Do increasing levels turn off more PTEN, thus promoting cancer, or do levels decrease and allow PTEN to be more active? If it turns out to be the first scenario - that increasing amounts of arrestin turn off the tumor suppressor activity of PTEN, then it may be possible to selectively inhibit that process. We have some interesting work ahead."

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