Fight Aging Newsletter, February 14th 2011
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February 14th 2011

The Fight Aging! Newsletter is a weekly email containing news, opinions, and happenings for people interested in aging science and engineered longevity: making use of diet, lifestyle choices, technology, and proven medical advances to live healthy, longer lives. This newsletter is published under the Creative Commons Attribution 3.0 license. In short, this means that you are encouraged to republish and rewrite it in any way you see fit, the only requirements being that you provide attribution and a link to Fight Aging!



- Welcome to the Fight Aging! Newsletter
- Three Clades
- A Mixed Batch of Regenerative Medicine News
- The Sirtuin Faction
- Linking Mitochondrial Dysfunction and Telomere Erosion


The merge of Longevity Meme content into Fight Aging! is complete, the old Longevity Meme website is shut down, and the Longevity Meme Newsletter is now the Fight Aging! Newsletter. Hopefully this will be a seamless change for you all. Please note that the newsletter email address is now different, so if you were whitelisting the address in your email software to prevent spam filters from triggering, you will need to add it again.


Many different types of people talk seriously about aging and human longevity. Not all of them have useful viewpoints, and separating the wheat from the chaff is one of the challenges for any newcomer to the community. In the post linked below I paint - with overly-broad strokes - a division between optimists, pessimists, and fools:

"The optimists understand the promise of rejuvenation biotechnology - that we stand on the verge of being able to greatly extend the healthy human life span - while remaining aware of the challenges that lie ahead. It will require decades to get to where we're going, but the goal of human agelessness can be attained if we put our shoulders to the wheel.

"A pessimist is dismissive of technological progress, either deliberately or through simply being one of those people who don't spend a lot of time in the consideration of change. Their thoughts on aging are locked to the here and now, caught in the moment. While rigorous in their examination of what is, their projections of what will be are unreliable - their view of aging tomorrow is that it looks much the same as aging today.

"The optimistic fool believes some or all of the nonsense propagated by the 'anti-aging' marketplace, or has deluded himself into thinking that a silver bullet lies just around the corner, some combination of lifestyle and ingested substance if it could just be found. In reality he is only spinning his wheels, just like all who came before him."

Nothing is ever clear cut, of course, and many folk in the community embody aspects of all three clades above, depending on the particular topic at hand. The outright fools are very vocal in this age of ours, however, and dominate many of the largest media channels.


There is always some new news from the large and active regenerative medicine scientific community. In the post linked below, you'll find pointers to research in a number of important themes: tissue engineering of new organs, examining the ability of lower animals to regenerate limbs, the use of stem cells to build tissue that can be used to test new therapies, and the advanced state of progress in veterinary stem cell science:

"This is the sort of research community we want to see for every field that might impact human aging and longevity: large, thriving, dynamic, and attracting plenty of attention and funding. The practical result is that we live in exciting times - organ regrowth is right around the corner, as is the prospect of meaningful repair or replacement of many types of aged tissue. Regenerative medicine is not a one-stop solution for all of aging, but it is one of the necessary pillars of the true rejuvenation biotechnology that will be developed in the decades to come."


Sirtuin research is here for the long term, but I predict that it will be only a small part of that long term:

"By virtue of the fact that very large sums of venture capital, big pharma investment, and public funding have been sunk into the examination of sirtuins in connection with longevity in mammals, I think we'll see a strong sirtuin research contingent in the scientific community for some years to come - and this regardless of the ultimate merits of this work. While there are promising signs that sirtuins may do something useful in terms of enhancing cellular housekeeping, after some years of research we have yet to see any of the promise of slowed aging that looked possible at the outset.

"Research and development always takes longer than expected, but at this point I look at research into sirtuins as an early step forward on a much longer road - a part of the foundations of some later work, and producing little of direct use in and of itself. The newer technologies and newer companies who work on the same strategy of slowing aging via identification of ways to manipulate metabolism will leap over the work of the last five years, producing a hundred-fold more genetic and biochemical data in the process. Biotechnology is advancing so rapidly that each generation of development is made obsolete before it even hits its stride."


Mitochondrial damage and shortening telomeres are two biochemical characteristics of aging implicated in numerous forms of disease and degeneration. Mitochondria are the cell's powerplants, which can become sources of damaging reactive molecules when they start to fail, while telomeres are the caps that protect the ends of your DNA. These may be independent mechanisms, which have to be dealt with by separate future rejuvenation therapies, but in recent years evidence has surfaced to suggest that one may be secondary to the other. You can read some of the details in the following post:

"From an economic perspective, we should all be hoping that some of our present candidates for the primary causes of aging turn out to be secondary effects - because then we don't have to devote any time towards developing repair biotechnologies to fix them."

As of the moment, there are viable theories for either short telomeres or damaged mitochondria to be the primary mechanism, and the other the secondary - or perhaps they both influence the other in a form of feedback loop. Biology is very complex, which is why - in the midst of research towards as as yet unreached conclusion - you can point to an array of data that are supportive of both A causing B and B causing A.


The highlights and headlines from the past week follow below. Remember - if you like this newsletter, the chances are that your friends will find it useful too. Forward it on, or post a copy to your favorite online communities. Encourage the people you know to pitch in and make a difference to the future of health and longevity!



Friday, February 11, 2011
I'm always pleased to see more good writing on the topic of longevity science: "To extend our longevity, we'll have to advance in stages. ... With a healthy lifestyle and some luck (absence of accidents and natural disasters) we not only can increase our lifespan, we can increase the health in that lifespan and postpone debilitating illness to the very end of our life ... To go beyond this achievable life extension, we need more advances in the basic sciences. Considering aging as a disease is new concept. It will take time before we accept this not just as wishful thinking but as a real possibility in our lifetime. The end of aging does not mean that we will never die; we will still die of other diseases, accidents, or natural disasters but no longer of aging itself. ... Aging is not yet recognized as a disease. Some among us would like the Food and Drug Administration (FDA) to recognize it as a disease so that we could get funding for basic, translational, and clinical research on aging. ... These changes will be implemented incrementally. The unprecedented biological and technological evolution we face today will be the driving force for social, economic, and even political changes. Working conditions will change significantly: retirement will be changed, people will no longer retire after a certain age, they will take time off from work every few years and then return to it afterwards. Our goal is not to reach immortality but to postpone and eventually prevent aging. For now and the immediate future we can change our lifestyle toward healthier living. This will buy us time so that we can survive long enough for the advances in basic sciences, which will be made in the next 15 to 20 years, helping us move to the next stage where aging will no longer be the biggest killer of our species."

Friday, February 11, 2011
There is no shortage of people trying to convince us that degenerating into frailty, suffering, and death is a wonderful thing: "Mr Agronin is an optimist. He does not deny - how could he? - the sufferings and indignities of old age. Scanning slices of old brain, 'stained and prepped for the microscope', his eye is unsparing: 'the aged folds' like 'the withered meat of a walnut', the blood vessels like 'hardened tendrils', the 'small plaques of toxic amyloid protein surrounded by a debris field of dead neurons'. But alongside the science, he sees something else: the people themselves. Old age, he says, has become our blind spot, neglected by the medical profession, lumped together with dementia and disease, something to be endured, dreaded, mercifully pre-empted, or even - as one researcher in the field, Aubrey de Grey, argues - reversed. Mr Agronin, by contrast, embraces it. He sees it as intrinsic to life, with its own 'ways and meanings', its particular wisdom. Even at its most tenuous and hollowed out, he finds some shape, a sense of cyclic pattern. In an almost mystical passage, inspired by his professor, Erik Erikson, a psychologist, Mr Agronin likens life to a stream which eventually seeps down unseen into the bedrock, and opens 'like a flower into the aquifer below'." From where I stand, there needs to be more of a healthy dread of aging - perhaps that would motivate more people to help develop the rejuvenation biotechnologies that can do something about it. To try to pretend that aging to death, suffering terribly along the way, is just peachy keen has an air of desperate madness to it.

Thursday, February 10, 2011
Time here looks at Ray Kurzweil's timeline for the development of biotechnologies that can defeat aging: repair the old, remove biological damage, and eliminate frailty and age-related death. "The Singularity isn't just an idea. it attracts people, and those people feel a bond with one another. Together they form a movement, a subculture; Kurzweil calls it a community. Once you decide to take the Singularity seriously, you will find that you have become part of a small but intense and globally distributed hive of like-minded thinkers known as Singularitarians. ... At the 2010 summit, which took place in August in San Francisco, there were not just computer scientists but also psychologists, neuroscientists, nanotechnologists, molecular biologists, a specialist in wearable computers, a professor of emergency medicine, an expert on cognition in gray parrots and the professional magician and debunker James 'the Amazing' Randi. ... After artificial intelligence, the most talked-about topic at the 2010 summit was life extension. Biological boundaries that most people think of as permanent and inevitable Singularitarians see as merely intractable but solvable problems. Death is one of them. Old age is an illness like any other, and what do you do with illnesses? You cure them. Like a lot of Singularitarian ideas, it sounds funny at first, but the closer you get to it, the less funny it seems. It's not just wishful thinking; there's actual science going on here. ... People have begun to realize that the view of aging being something immutable - rather like the heat death of the universe - is simply ridiculous. It's just childish. The human body is a machine that has a bunch of functions, and it accumulates various types of damage as a side effect of the normal function of the machine. Therefore in principal that damage can be repaired periodically. This is why we have vintage cars. It's really just a matter of paying attention. The whole of medicine consists of messing about with what looks pretty inevitable until you figure out how to make it not inevitable." I don't see it as plausible that we'll have everything in hand by 2045, but if we make a good start now, then we could have enough to put us into actuarial escape velocity - gaining life expectancy faster than we age, and thus able to wait for far better technologies that arrive later.

Thursday, February 10, 2011
The early posts at Chronosphere are well done and worth reading. The theme is a detailed and picture-strewn look at the history of cryonics, mixed in with considerations of our presently imperfect society and where it might be going next: "Chronosphere is your gateway to a fundamentally new way of living - in pursuit of physical immortality in a world of our own making - free from the tyranny of time, and the burden of injustice. Chronosphere will explore and create interfaces with the scientific, technological, social and moral resources needed to achieve these ends. Because we are all at risk of dying, cryonics will be a central focus of Chronosphere for the foreseeable future, but will be by no means be the only technology explored here. Interventive gerontology, with a strong emphasis on immediate, or very near term interventions to slow cognitive aging, will also be explored in detail. Join us on our quest to transcend the limits of time!"

Wednesday, February 9, 2011
You might recall that the olm (Proteus anguinus) is a type of small salamander that lives as long as we do. Here researchers point out that olm life span is inconvenient for some theories of aging: "Recent work on a small European cave salamander (Proteus anguinus) has revealed that it has exceptional longevity, yet it appears to have unexceptional defences against oxidative damage. This paper comes at the end of a string of other studies that are calling into question the free-radical damage theory of ageing. This theory rose to prominence in the 1990s as the dominant theory for why we age and die. Despite substantial correlative evidence to support it, studies in the last five years have raised doubts over its importance. In particular, these include studies of mice with the major antioxidant genes knocked out (both singly and in combination), which show the expected elevation in oxidative damage but no impact on lifespan. Combined, these findings raise fundamental questions over whether the free-radical damage theory remains useful for understanding the ageing process, and variation in lifespan and life histories." Yet there are still the studies demonstrating extended life span through targeting antioxidants to mitochondria, which imply that at least so far as those cellular structures are concerned, oxidative damage is very important. It may be that the olm, like naked mole rats, has mitochondria that are highly resistant to damage in comparison to other species.

Wednesday, February 9, 2011
A fair chunk of degenerative aging is caused by the accumulation of various kinds of damaging biochemicals, and here dry macular degeneration is added to that list: "A team of researchers, led by University of Kentucky ophthalmologist Dr. Jayakrishna Ambati, has discovered a molecular mechanism implicated in geographic atrophy, the major cause of untreatable blindness in the industrialized world. ... Concurrent with this discovery, Ambati's laboratory developed two promising therapies for the prevention of the condition. ... Geographic atrophy, a condition causing the death of cells in the retina, occurs in the later stages of the 'dry type' of macular degeneration, a disease affecting some 10 million older Americans and causing blindness in over 1 million. There is currently no effective treatment for geographic atrophy, as its cause is unknown. Ambati's team discovered that an accumulation of a toxic type of RNA, called Alu RNA, causes retinal cells to die in patients with geographic atrophy. In a healthy eye, a 'Dicer' enzyme degrades the Alu RNA particles. ... We discovered that in patients with geographic atrophy, there is a dramatic reduction of the Dicer enzyme in the retina. When the levels of Dicer decline, the control system is short-circuited and too much Alu RNA accumulates. This leads to death of the retina. ... Alu elements make up a surprisingly large portion - about 11 percent by weight - of the human genome, comprising more than 1 million sequences. However, their function has been unknown, so they have been called 'junk' DNA or part of the 'dark' genome. The discovery of Alu's toxicity and its control by Dicer should prove of great interest to other researchers in the biological sciences ... Ambati's team developed two potential therapies aimed at preventing geographic atrophy and demonstrated the efficacy of both approaches using laboratory models. The first involves increasing Dicer levels in the retina by 'over-expressing' the enzyme. The second involves blocking Alu RNA using an 'anti-sense' drug that binds and degrades this toxic substance. ... Ambati's group is preparing to start clinical trials by the end of this year."

Tuesday, February 8, 2011
From Fast Company: "The mice in the video flickering on his colleague's computer screen were moving their legs. Their back feet trailed behind them from time to time, but the fact that they were walking at all was astounding. Only a few weeks earlier, they'd been paralyzed from the waist down. Then Stupp's team at Northwestern University injected them with made-to-order molecules. Now the mice were trying to run around their cage. ... Those mice were the first living glimpse of the future that Stupp is hoping to accelerate in his role as the director of the Institute for BioNanotechnology in Medicine at Northwestern. It's a future in which molecular self-assembly - where researchers direct molecules to spontaneously combine into ordered structures - will help the body heal itself. ... It wasn't until 1995 that one of his nanotechnology experiments steered him onto an entirely new scientific course. He was trying to make molecules called rodcoils line up side by side to create a large polymer sheet with one side shiny and the other sticky, properties that might make the sheet useful for industrial applications. But something unexpected happened. Instead of forming a single thin membrane, the rodcoils coalesced into trillions of tiny individual structures that looked like mushrooms. Stupp initially wrote off the result as a failure, but he quickly realized that the mushroom-shaped nanoparticles might have a host of advantages. ... What if he could inject the nanomolecules into the bloodstream so they could serve as microscopic vehicles to deliver therapeutic compounds? Even better, what if he could modify the nanomolecules so that they would attract the body's own healing compounds to an injured area, kick-starting the repair process without introducing any foreign cells at all? The 'mushroom' paper Stupp published in 1997 attracted lots of attention, and Northwestern lured the rising star to its materials-science program in 1999. The very next year, Stupp founded IBNAM, the lab he hoped would bring his interdisciplinary ideas to fruition."

Tuesday, February 8, 2011
Another confirmation that your natural longevity is more a matter of your choices than the luck of the draw: "It is often assumed that people with parents who lived to be very old are more likely to live to a grand old age themselves. 'But that's just not true - our study shows that hereditary factors don't play a major role and that lifestyle has the biggest impact,' says professor emeritus Lars Wilhelmsen, referring to the 1913 Men study that formed the basis of the current research. Those who did not smoke, consumed moderate amounts of coffee and had a good socio-economic status at the age of 50 (measured in terms of housing costs), as well as good physical working capacity at the age of 54 and low cholesterol at 50 had the greatest chance of celebrating their 90th birthday. ... We're breaking new ground here. Many of these factors have previously been identified as playing a role in cardiovascular disease, but here we are showing for the first time that they are important for survival in general. The study clearly shows that we can influence several of the factors that decide how old we get. ... The 1913 Men epidemiological study started up in 1963. A third of all male 50-year-olds in Gothenburg were called for a check-up that focused on cardiovascular health. Every ten years since, a new group of 50-year-olds has been called in and those who were already taking part in the study have been given another check-up. This has enabled researchers to follow the development of illnesses in a specific age group, and to compare the health of 50-year-olds in 2003 with that of 50-year-olds in 1963, for example." The choices you make become even more important when we consider the prospects for future medical technology: are you helping to bring about the rejuvenation biotechnology that will extend all healthy human lives, or are you merely sitting on the sidelines and hoping?

Monday, February 7, 2011
Here is an example of the way in which advances in delivery methodology can greatly improve an existing therapy: "Doctors have invented a revolutionary skin spray-gun that heals severe burns within days. The spray-gun which fires stem cells on to the damaged skin has already been used successfully on a dozen patients. Rather than sheets of skin being laboriously grown over a period of a month and applied to the patient, stem cells are harvested from a small patch of healthy skin, put into a solution and sprayed back on to the affected area. The process takes only 90 minutes [and] burns can heal in as little as four days. It eliminates a major flaw of existing burns treatment, the time taken to grow new layers of skin in the lab, during which time patients can die from infection. ... the process involved isolating stem cells from a healthy patch of the patient's skin, putting those cells in a water solution, and then spraying the mixture back on. After being sprayed, the patient's wound is covered with a special dressing that provides glucose, sugar, amino acids, antibiotics and electroytes to the treated area, to provide nutrition and clean the wound until the stem cells get established. ... For Matthew Uram, a police officer from Pennsylvania, the radical technical has already saved his skin. Last July he received severe burns to his face, neck, shoulder, arm and hand after someone threw a cup of petrol on to a bonfire at a party. His hand looked like a 'charred piece of meat', he said. Quickly taken to hospital, he was offered the chance to be one of the first patients to benefit from the skin gun. ... They did it on a Friday, and my follow up was that Monday and the burns unit said it was completely healed."

Monday, February 7, 2011
A look at what might be accomplished in the years ahead: "In work that could jumpstart the promising field of cell therapy, in which cells are transplanted into the body to treat a variety of diseases and tissue defects, researchers [have] engineered cells that could solve one of the key challenges associated with the procedure: control of the cells and their microenvironment following transplantation. ... the team reports creating tiny internal depots within human mesenchymal adult stem cells, which among other functions are key to the generation of several tissues. These depots can slowly release a variety of agents to influence the behavior of not only the cells containing the depots, but also those close to them and even much farther away. The team demonstrated this by prompting mesenchymal stem cells to differentiate into the cells that make bone. ... This work could allow programmable cell therapies where the cell or the agent is the therapeutic. For example, depots containing specific agents could enhance cell survival or expression of a particular growth factor. Cells could also be used as a delivery vehicle to shuttle drugs to target tissues that may be useful to accelerate tissue regeneration, or to deliver chemotherapeutics to tumors while minimizing systemic side effects. ... Ten to fifteen years from now, people will visit cell infusion centers to receive routine therapy for multiple diseases and tissue defects. ... For example, a person who has had a heart attack could be infused with cells that could help stimulate regeneration of new heart cells to replace those that have died and prevent eventual heart failure."


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