Healthy Life Extension

Funding Aging Research

Critical Health/Longevity Technology

posted on January 10th, 2012

Dear Future Centenarian,

I™m sure you heard about the $10 million Ansari X Prize that was awarded to Burt Rutan in 2004.

It was a space competition in which the X Prize Foundation offered a $10 million prize for the first private enterprise to launch a reusable manned spacecraft into space twice within two weeks. It was aimed to spur development of low-cost spaceflight.

Created in May 1996 and initially called just the “X Prize,” it was renamed the “Ansari X Prize” on May 6, 2004 following a multi-million dollar donation from entrepreneurs Anousheh and Amir Ansari.

The prize was won on October 4, 2004 by the Tier One project designed by Burt Rutan and financed by Microsoft co-founder Paul Allen, using the experimental spaceplane SpaceShipOne. Although $10 million was awarded to the winner, more than $100 million was invested in new technologies in pursuit of the prize.

Several other X Prizes have since been announced, promoting further development in space exploration and other technological fields including the X PRIZE for Organ Cryopreservation.

The global need for breakthroughs in the availability and access to organs has never been greater. The potential value of organ cryopreservation is immense on several levels. First, the technology could obviously have potential for the preservation of internal organs that currently have only a brief window of viability after being removed from a donor. This could substantially increase the effectiveness and decrease the cost of organ replacement by reducing the geographical and time constraints on organ transplantation.

Second, thanks to burgeoning advances in tissue engineering, cryopreservation could also provide a way for people to store and manage replacement organs grown from their own stem cells instead of waiting on a compatible donor. Storing your stem cells, at an early age as possible, should be an important part of your personal health and longevity program.

The X PRIZE envisions the Cryopreservation X PRIZE as A $10 million prize for the first team to transplant a human or animal vital organ (heart, lung, liver, kidney) into five animals that lacks their own, with 3 months’ post-transplant survival, having stored each organ below -120 degrees C for at least a week before transplantation. 

Once perfected, you will be able to freeze your own stem-cell regenerated organs for a time when you need them and that of increasing the window of viability of organs for transplant. However, more conveniently and much less expensively, you can store your blood stem cells now in anticipation of needing them to grow your organs in the future. See the many advantages of of doing so now by clicking here: .

Long Life,
David Kekich


From CTV News: “Researchers say they have discovered a new source of stem cells at the back of the eye, which they hope may one day provide a way to repair the damage from age-related macular degeneration, or AMD. [Researchers] identified the central nervous system stem cells in a single layer called the retinal pigment epithelium, or RPE, which lies behind the retina. The researchers salvaged the stem cells from the RPE layer in the eyes of more than 100 deceased donors, who ranged in age from 22 to 99. But the cells can also be isolated from the fluid surrounding the retina at the back of the eye, meaning they’re also accessible in living people.

You can literally go in and poke a needle in the eye and get these cells from the sub-retinal space. It sounds awful, but retinal surgeons do it every day. In culture dishes in the lab, the researchers were able to coax about 10 per cent of the RPE-derived stem cells to grow in the lab. Further prodding caused the cells to differentiate into, or give rise to, a variety of cell types – those that make bone, fat or cartilage. [The researchers] also generated a progenitor cell that carries some characteristics of one type of nervous system cell, although it was not fully differentiated. But the fact that we could make these cells that were part-way, that were immature, indicates to us that if we keep on manipulating them, going forward in the future, we should be able to find ways to create other types of central nervous system cells.”

ALZHEIMER’S STARTS EARLY Thursday, January  5, 2012
The onset of Alzheimer’s is not a sudden thing, which reinforces the view of it as a lifestyle disease: “The first changes in the brain of a person with Alzheimer’s disease can be observed as much as ten years in advance – ten years before the person in question has become so ill that he or she can be diagnosed with the disease. [Researchers] are studying biomarkers – substances present in spinal fluid and linked to Alzheimer’s disease. The group has studied close to 140 people with mild memory impairment, showing that a certain combination of markers (low levels of the substance beta-amyloid and high levels of the substance tau) indicate a high risk of developing Alzheimer’s disease in the future.

As many as 91 per cent of the patients with mild memory impairment who had these risk markers went on to develop Alzheimer’s within a ten-year period. In contrast, those who had memory impairment but normal values for the markers did not run a higher risk of getting Alzheimer’s than healthy individuals. This is a very important finding with regard to the development of new therapies against the disease. All prospective therapies have so far shown to be ineffective in stopping the disease, and many people are concerned that the pharmaceutical companies will give up their efforts in this field. But these failures may depend on the fact that the new therapies were initiated too late. When a patient receives a diagnosis today, the damage has already gone too far.” I’m not sold on this last comment, given the evidence suggesting that Alzheimer’s symptoms are reversible.

TOWARDS LIMB REGROWTH IN MAMMALS Wednesday, January  4, 2012
From Big Think: “The loss of a human limb is a tragedy. We know that once they’re gone, mammalian arms and legs can’t ever be restored. But if you cut off a salamander’s leg – or tail – it will reappear in just a few weeks. … Now, a new generation of longevity-seekers hopes to apply the power of amphibians like the salamander, the axlotl, and the worm to human medicine. In the future, if we had the ability to grow a brand new heart or parts of hearts with that person’s very own adult stem cells, then when we know that they have heart disease, we could just replace the heart. All of those [costly] visits to the hospital, all of the drugs, won’t be required.

Better tools will enable us to repair people rather than just sort of patching them up for a little while until they get sicker and sicker. Over the past few decades, scientists have begun to understand exactly how the regeneration process works in nature. When a salamander is injured, a clump of cells called a blastomea forms at the site of the wound. Like embryonic stem cells, the blastomea are especially plastic. These cells are then triggered to de-differentiate and re-initiate growth. Debate remains over whether they’re fully pluripotent, meaning that they have the ability to form any type of tissue, or whether the cellular dynamics merely have to be reprogrammed. The trick, of course, is applying this knowledge to human anatomy.”

Two supercentenarian genomes have been sequenced, and suggest that – as always – the roots of variations in human longevity are more complex than we’d like them to be: “Supercentenarians (age 110+ years old) generally delay or escape age-related diseases and disability well beyond the age of 100 and this exceptional survival is likely to be influenced by a genetic predisposition that includes both common and rare genetic variants. In this report, we describe the complete genomic sequences of male and female supercentenarians, both age >114 years old.

We show that: (1) the sequence variant spectrum of these two individuals’ DNA sequences is largely comparable to existing non-supercentenarian genomes; (2) the two individuals do not appear to carry most of the well-established human longevity enabling variants already reported in the literature; (3) they have a comparable number of known disease-associated variants relative to most human genomes sequenced to-date; (4) approximately 1% of the variants these individuals possess are novel and may point to new genes involved in exceptional longevity; and (5) both individuals are enriched for coding variants near longevity-associated variants that we discovered through a large genome-wide association study. These analyses suggest that there are both common and rare longevity-associated variants that may counter the effects of disease-predisposing variants and extend lifespan. The continued analysis of the genomes of these and other rare individuals who have survived to extremely old ages should provide insight into the processes that contribute to the maintenance of health during extreme aging.”

Researchers are applying the most modern tools of biotechnology in efforts to better understand the evolution of longevity: “The genetic basis of the large species differences in longevity and aging remains a mystery. Thanks to recent large-scale genome sequencing efforts, the genomes of multiple species have been sequenced and can be used for cross-species comparisons to study species divergence in longevity. By analyzing proteins under accelerated evolution in several mammalian lineages where maximum lifespan increased, we identified genes and processes that are candidate targets of selection when longevity evolves.

We identified several proteins with longevity-specific selection patterns, including COL3A1 that has previously been related to aging and proteins related to DNA damage repair and response such as DDB1 and CAPNS1. Moreover, we found that processes such as lipid metabolism and cholesterol catabolism show such patterns of selection and suggest a link between the evolution of lipid metabolism, cholesterol catabolism, and the evolution of longevity. Lastly, we found evidence that the proteasome-ubiquitin system is under selection specific to lineages where longevity increased and suggest that its selection had a role in the evolution of longevity. These results provide evidence that natural selection acts on species when longevity evolves, give insights into adaptive genetic changes associated with the evolution of longevity in mammals, and provide evidence that at least some repair systems are selected for when longevity increases.”

RAGING AGAINST AGING Monday, January  2, 2012
One of the needed shifts in our culture is to move away from the dominant themes of apologism and acceptance of aging – this is a necessary precursor for widespread support of longevity science, to the level needed to raise up rejuvenation biotechnology research to match cancer research or regenerative medicine in funding and enthusiasm. So more of this sort of thing is welcome: “In 1981, five days before cancer killed him, the life-loving writer William Saroyan told the Associated Press: ‘Everybody has to die, but I always believed an exception would be made in my case. Now what?’ There it is: ‘Now what?’ That is the great question growing all the greater for being asked by the biggest, most self-conscious and possibly most self-deluded generation in American history, the baby boomers.

The youngest of them are middle-aged now, taking a hard-headed look at old age and asking: Now what? Some are also taking a soft-headed look, as if they were already demented beyond grappling with reality. Some of them like to think of old age as ‘elderhood,’ which is thinking of old age as just another stage of life, like childhood or adulthood. But then what? Surely not deathhood. Or afterhood, or oblivionhood. No, a lot of people are making a lot of money promising immortality. But I digress. Then again, digression is the essence of William Ian Miller’s book about old age. It answers the question of ‘Now what?’ with its title: ‘Losing It.’ The point, if I may dare to sum up: Old age is an annoying, ridiculous and pathetic decline toward the state of a turnip softening in a compost heap, if death is not kind enough to intervene first. But why write a book about it? Mr. Miller wants to express his contempt for the positivity crowd that echoes ‘grow old along with me, the best is yet to be,’ in the words of Robert Browning, one of the softer turnips of 19th-century English poetry.”

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