Healthy Life Extension

The Importance of Improvement

posted on May 17, 2011

Dear Future Centenarian,

Some time back, I read an enlightening article by Reason at www.FightAging.org. He described how important the debate over human enhancement is in ongoing efforts to persuade people of the merits of engineered human longevity.

The faster we progress, the louder institutional voices in Western culture with an aversion to human enhancement become. Instead, the ideal of equality runs rampant. Many intellectuals seem to support equality by leveling down to the lowest denominator and preventing new heights from being achieved. I found this to be true during Army basic training. It was geared to the weakest getting through. This was the kind of mindset that lost the Viet Nam War. This is the mindset that governs our economics as well, and you can see where that is getting us.

This rejection of human enhancement is in essence a rejection of the urge to improve, and it is one of a number of important hurdles standing in the way of widespread support to develop rejuvenation biotechnology.

Do you want yourself and your children to live longer than your parents and grandparents? That's an enhancement, and talking heads would like to see laws written to prevent such technologies from ever seeing the light of day.

The bureaucrats of the FDA do not recognize aging as a disease, so they will not approve treatments for it. In a culture that is hostile to human enhancement, winning support for reversing aging will be that much harder. This is one of many ways in which freedom matters greatly in medical research. Under the systems of regulation in place in the largest markets of the world, researchers and commercial developers are far from free to turn proven science into commercial products, and far from free to convince their fellow countrymen to try something new.

We humans are the species that improves ourselves and creates value from our surroundings. That is our defining characteristic - and yet, paradoxically, so much time and effort in this day and age is devoted to sabotaging the engines of progress.

Why else hasn't humanity undertaken an ambitious effort to advance the science that could help us address the single leading cause of disease and death in the world today - namely, biological aging? People go to extremes to justify their intuition that we should not aspire to modify the current rate of the molecular and cellular decline of humans.

These reasons typically range from sentiments like 'aging is natural' and 'doing so will exacerbate inequality' to 'it will cause overpopulation' and 'it will cause ecological disaster.’ But no one raises these same objections when the discussion is about supporting the science which could help address just one specific disease of aging - like cancer, heart disease or stroke.

No one objects to medical research on stroke by claiming 'a disturbance in blood flow to the brain is natural' or 'preventing or curing strokes will exacerbate inequality' or 'all those people who would be saved from strokes will cause overpopulation or ecological disaster, so it is better they suffer a stroke.’

Why not? Why is it that different moral sensibilities tend to be activated when the topic turns to modifying aging?"
 
Long Life,
David Kekich
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LATEST HEADLINES FROM FIGHT AGING!

LUNG STEM CELLS DISCOVERED Friday, May 13, 2011 http://www.fightaging.org/archives/2011/05/lung-stem-cells-discovered.php
For a variety of reasons lung tissue engineering has lagged behind foundational work on other organs - but there are signs that it is catching up: researchers "have identified a human lung stem cell that is self-renewing and capable of forming and integrating multiple biological structures of the lung including bronchioles, alveoli and pulmonary vessels. This research describes, for the first time, a true human lung stem cell. The discovery of this stem cell has the potential to offer those who suffer from chronic lung diseases a totally novel treatment option by regenerating or repairing damaged areas of the lung. Using lung tissue from surgical samples, researchers identified and isolated the human lung stem cell and tested the functionality of the stem cell both in vitro and in vivo.

Once the stem cell was isolated, researchers demonstrated in vitro that the cell was capable of dividing both into new stem cells and also into cells that would grow into various types of lung tissue. Next, researchers injected the stem cell into mice with damaged lungs. The injected stem cells differentiated into new bronchioles, alveoli and pulmonary vessel cells which not only formed new lung tissue, but also integrated structurally to the existing lung tissue in the mice."

INDUCED PLURIPOTENT STEM CELLS VERSUS LIVER DAMAGE Thursday, May 12, 2011 http://www.fightaging.org/archives/2011/05/induced-pluripotent-stem-cells-versus-liver-damage.php
More signs of progress in regenerative medicine: "researchers have demonstrated that human liver cells derived from adult cells coaxed into an embryonic state can engraft and begin regenerating liver tissue in mice with chronic liver damage. Liver cells derived from so-called "induced-pluripotent stem cells (iPSCs)" could one day be used as an alternative to liver transplant in patients with serious liver diseases, bypassing long waiting lists for organs and concerns about immune system rejection of donated tissue.

iPSC-derived liver cells not only can be generated in large amounts, but also can be tailored to each patient, preventing immune-rejection problems associated with liver transplants from unmatched donors or embryonic stem cells. Although the liver can regenerate in the body, end-stage liver failure caused by diseases like cirrhosis and cancers eventually destroy the liver's regenerative ability. Currently, the only option for those patients is to receive a liver organ or liver cell transplant, a supply problem given the severe shortage of donor liver tissue for transplantation. In addition, mature liver cells and adult liver stem cells are difficult to isolate or grow in the laboratory."

MITOCHONDRIAL DNA DAMAGE AND AGING STEM CELLS Thursday, May 12, 2011 http://www.fightaging.org/archives/2011/05/mitochondrial-dna-damage-and-aging-stem-cells.php
Accumulating damage to mitochondrial DNA is one of the causes of aging, and here researchers investigate its role in the aging of stem cells: "Somatic stem cells mediate tissue maintenance for the lifetime of an organism. Despite the well-established longevity that is a prerequisite for such function, accumulating data argue for compromised stem cell function with age. Identifying the mechanisms underlying age-dependent stem cell dysfunction is therefore key to understanding the aging process. Here, using a model [that suffered a greater rate of mitochondrial DNA damage], we demonstrate hematopoietic defects reminiscent of premature [stem cell] aging, including anemia, lymphopenia, and myeloid lineage skewing. However, in contrast to physiological stem cell aging, rapidly accumulating mitochondrial DNA mutations had little functional effect on the hematopoietic stem cell pool, and instead caused distinct differentiation blocks and/or disappearance of downstream progenitors. These results show that intact mitochondrial function is required for appropriate multilineage stem cell differentiation, but argue against mitochondrial DNA mutations per se being a primary driver of somatic stem cell aging."

MTC PROTEINS, MITOCHONDRIA, AND AGING
Wednesday, May 11, 2011
http://www.fightaging.org/archives/2011/05/mtc-proteins-mitochondria-and-aging.php
News of another potential way to manipulate mitochondrial function to slow aging: "Mitochondria are the body's energy producers, the power stations inside our cells. Researchers [have] now identified a group of mitochondrial proteins, the absence of which allows other protein groups to stabilize the genome. This could delay the onset of age-related diseases and increase lifespan. When a certain MTC protein is lacking in the cell, e.g. because of a mutation in the corresponding gene, the other MTC proteins appear to adopt a new function. They then gain increased significance for the stabilization of the genome and for combating protein damage, which leads to increased lifespan.

These studies also show that this MTC-dependent regulation of the rate of aging uses the same signaling pathways that are activated in calorie restriction - something that extends the lifespan of many different organisms, including yeasts, mice and primates. Some of the MTC proteins identified in this study can also be found in the human cell, raising the obvious question of whether they play a similar role in the regulation of our own aging processes. It is possible that modulating the activity of the MTC proteins could enable us to improve the capacity of the cell to delay the onset of age-related diseases. These include diseases related to instability of the genome, such as cancer, as well as those related to harmful proteins, such as Alzheimer's disease and Parkinson's disease. At the moment this is only speculation, and the precise mechanism underlying the role of the MTC proteins in the aging process is a fascinating question that remains to be answered."

A POPULAR SCIENCE ARTICLE ON ORGAN PRINTING TECHNOLOGY Wednesday, May 11, 2011 http://www.fightaging.org/archives/2011/05/a-popular-science-article-on-organ-printing-technology.php
From the Washington Post: "The machine looks like the offspring of an Erector Set and an inkjet printer. The 'ink' feels like applesauce and looks like icing. As nozzles expel the pearly material, layer by layer, you imagine the elaborate designs this device could make on gingerbread cookies. But the goo is made of living cells, and the machine is 'printing' a new body part. These machines - they're called three-dimensional printers - work very much like ordinary desktop printers. But instead of just putting down ink on paper, they stack up layers of living material to make 3-D shapes. The technology has been around for almost two decades, providing a shortcut for dentists, jewelers, machinists and even chocolatiers who want to make custom pieces without having to create molds.

In the early 2000s, scientists and doctors saw the potential to use this technology to construct living tissue, maybe even human organs. They called it 3-D bioprinting, and it is a red-hot branch of the burgeoning field of tissue engineering. The possibilities for this kind of technology are limitless. Everyone has a mother or brother or uncle, aunt, grandmother who needs a meniscus or a kidney or whatever, and they want it tomorrow. The promise is exciting. The goal is not to squash that excitement, but to temper it with the reality of what the process is. The reality for now is that making such things as vertebral disks and knee cartilage, which largely just cushion bones, is far easier than constructing a complicated organ that filters waste, pumps blood or otherwise keeps a body alive. Scientists say the biggest technical challenge is not making the organ itself, but replicating its intricate internal network of blood vessels, which nourishes it and provides it with oxygen. Many tissue engineers believe the best bet for now may be printing only an organ's largest connector vessels and giving those vessels' cells time, space and the ideal environment in which to build the rest themselves; after that, the organ could be implanted."

BEN BOVA ON AGELESSNESS THROUGH FUTURE BIOTECHNOLOGY Tuesday, May 10, 2011 http://www.fightaging.org/archives/2011/05/ben-bova-on-agelessness-through-future-biotechnology.php
An op-ed from writer Ben Bova: "'The first immortal human beings are probably living among us today.' That is the opening line of my 1998 nonfiction book, 'Immortality.' Today, more than a dozen years later, a growing number of research scientists and philosophers are beginning to sing much the same tune. They are speaking and writing about our post-human future, a coming era where human beings will be able to live youthful, vigorous, healthy lives for centuries or even longer.
There might well be people alive today who may live for centuries, not as crumbling, aging wrecks, but as strong, youthful and active men and women.

There is even evidence that aging itself might be not merely slowed or delayed, but actually reversed. One researcher, biogerentologist Aubrey de Grey, flatly states, 'I think the first person to live to a thousand might be 60 already.' Such views are certainly not mainstream. De Grey's detractors have called his ideas 'science fiction.' Yeah. Like space travel, nuclear power, lasers and pocket-sized computers." Bova's view of the medical technologies that will get us there is not complete - he focuses on a third of the overall picture as described in the Strategies for Engineered Negligible Senescence - but his vision of the future is right in the larger sense. The coming age will deliver rejuvenation biotechnology, and it is up to us to work to make that happen soon enough to matter.

OLD AGE IN THE FUTURE, AND A FAILURE OF THE IMAGINATION Monday, May  9, 2011 http://www.fightaging.org/archives/2011/05/old-age-in-the-future-and-a-failure-of-the-imagination.php
This article on the future of being old talks about a failure of the imagination, the broad assumption by many people that their lives will look like the lives of their parents and grandparents in scope and length. Yet the article is itself a failure of the imagination - doing nothing more than projecting present slow trends, without looking at what is taking place in the laboratories. "It used to be that we knew what old age looked like. This was back when people over 65 accounted for a relatively small proportion of the US population - under 10 percent in 1960, according to the census from that year - and the average age at the time of death hovered under 70. Since then, advances in medicine and increasingly widespread health-consciousness have caused these numbers to rise precipitously.

Demographers predict that by 2030, average life expectancy will have climbed past 80 and people over 65 will account for more than 20 percent of the country's population. Plenty has been said about how old age is changing now. But what will it be like for those of us who won't be hitting our 50th reunions for several more decades? Amid all the demographic projections, and all the worries about resources, we tend to assume that the actual texture of life as an old person in the future will be more or less what it is today - that even as old age lasts longer and becomes more prevalent in society, the concept itself, and the kind of life one associates with it, will remain intact. But this is a failure of imagination: In fact, old age in the future - particularly if you're looking at 2050 and later - promises to bear little resemblance to old age as it is experienced in 2011."

PATCHING A DAMAGED HEART Monday, May  9, 2011 http://www.fightaging.org/archives/2011/05/patching-a-damaged-heart.php
Via ScienceDaily: researchers "have established a new method to patch a damaged heart using a tissue-engineering platform that enables heart tissue to repair itself. They were able, for the first time, to combine the use of human repair cells that were conditioned during in-vitro culture to maximize their ability to revascularize and improve blood flow to the infarcted tissue with a fully biological composite scaffold designed to deliver these cells to the damaged heart. With this platform, they could both keep the cells within the infarct bed (in contrast to the massive cell loss associated with infusion of cells alone) and enhance cell survival and function in the infarct bed, where most of the cells would have died because of the obstruction of their blood supply.

[Researchers] removed the cells of a human heart muscle - the myocardium - leaving a protein scaffold with intact architecture and mechanical properties. They filled the scaffold with human mesenchymal progenitors (stem cells that can differentiate into many cell types) and then applied the patches to damaged heart tissue. The patches promoted the growth of new blood vessels and released proteins that stimulated the native tissue to repair itself."

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