Fight Aging! Newsletter, June 20th 2011

June 20th 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!



- Should We Treat Aging?
- The Global Catastrophe that Most People Ignore
- An Interview With David Gobel, Methuselah Foundation CEO
- Responding to a Critique of SENS
- Discussion
- Latest Headlines from Fight Aging!


Should we treat aging? Unfortunately this isn't a rhetorical question for a great many people - they ask it expecting to hear good reasons as to why it is a bad idea, and thus why regulators should continue to prevent researchers from turning possible treatments for aging into clinical applications.

"This is one of the uphill struggles taking place in the patient advocacy community for aging research, that most people don't consider themselves patients exhibiting the symptoms of degenerative aging, have little inclination to do anything about it, and are in fact initially hostile to the whole idea. ... For them, life extension is indeed a bad thing. Various strains of environmentalism are one of the main culprits here: so many minds are poisoned by the false ideas that spread from environmentalist and related Malthusian ideologies: that there are too many people, that people are intrinsically bad, that wealth and longevity are intrinsically bad, that economics is a zero-sum game, and so forth.

"There's nothing wrong with liking trees and wild places enough to spend your hard-earned resources on helping to maintain them. But environmentalism has a way of veering off into the worship of death and destruction, a sort of modern penitent movement focused on the mortification of society as a whole. It's so widespread and embedded in our cultures now that even mild-mannered, everyday folk declare their support for shorter and fewer human lives, for abandonment of technologies that improve the quality of human life, and for relinquishment of technological development that will greatly improve life in the future."


Here is an attractively direct viewpoint on the human condition from the Russian end of the longevity science community, mangled a little by the automatic translation, but you'll get the point:

"Needless to say, a catastrophe - something unpleasant. Global catastrophe - unpleasant globally. And what is the most global of global catastrophes? Probably the one that leads to widespread death. And here we must note that if nothing is done, then all living people will die with 100% probability. Of aging. Therefore, it is aging that is the global catastrophe that is unfolding silently throughout the course of human history.

"'Unfolding silently' because nearly everyone in the world studiously refuses to characterize the consequences of aging for what they in fact are. Everyone will die of aging - everyone! - and that is somehow removed from the normal fervor and unified efforts that greet any other form of mass death. Take the tsunamis of recent years, for example, one of which managed to kill about as many people as die of aging in any given day. There was a global outpouring of funds, support, and activity following that tsunami. Yet every day, without cease, that many people again are killed by the effects of aging - and next to no-one cares enough to do something in response to this horrible ongoing loss of life."


A recent interview with the Methuselah Foundation CEO covers a fair amount of ground, and offers some insight into why the various leading charitable organizations in the longevity science space have such different strategies:


A recent issue of Cryonics magazine contained a critique of SENS, the Strategies for Engineered Negligible Senescence under development at the SENS Foundation. In the latest issue, Aubrey de Grey of the Foundation responds, and it's worth reading both pieces.

"SENS, the Strategies for Engineered Negligible Senescence, is detailed plan for development of the biotechnologies needed to reverse the effects of aging - to repair the biological damage that causes age-related degeneration and disease, and thereby eliminate the frailty and increasing risk of death that comes with it. Strangely, SENS has gone from valid but fringe idea rejected by the mainstream of aging research to an accepted and supported, albeit small, research program over a handful of years without much in the way of widely published and debated critiques. There was the SENS challenge, a couple of scientific op-ed exchanges in the journals (some of which were quite entertaining), and that was pretty much that. In the early days, no-one would take the time to engage, and the switch from outsider concept to insider concept with a well-connected non-profit foundation backing it happened fairly rapidly as such things go. Not that I'm complaining: there are worse outcomes. But publicity is important when it comes to expanding the support available for any field of research, and well constructed critiques - and the debates that follow - are a good basis for that publicity."


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, June 17, 2011
From Cryonics Magazine: "As a neuroscientist whose day job is to map neural circuits, I know exactly what type of evidence is needed to convince the scientific community that cryonics preserves the neural circuits encoding our unique memories and personality. What is required is a systematic whole-brain survey with an electron microscope. Recently I, along with my colleagues John Smart and Jacob DiMare, formed the Brain Preservation Foundation (BPF) to promote new scientific research in the field of whole brain preservation for long-term static storage. The BPF has announced the Brain Preservation Technology Prize (purse currently at $106,000) for the first team to demonstrate that an entire large mammalian brain can be preserved for long-term storage such that the connectivity between neurons remains intact and traceable using today's electron microscopic imaging techniques. A complete set of rules for the prize can be found on our BPF website. ... This prize is being presented as a challenge to cryonics providers like Alcor and their research partners: 'Demonstrate the quality of your product in a rigorous, independent, and open way to the scientific community and to your customers.' The BPF is hard at work raising funds to promote this prize and to help perform the electron microscopic evaluation required, and we are recruiting a board of scientific advisors and judges that will give the prize credibility."

Friday, June 17, 2011
Researchers are making the first inroads into implanted machinery that can adjust the workings of memory, potentially leading in the years ahead to ways to restore memory function in the old: "Scientists have developed a way to turn memories on and off - literally with the flip of a switch. Using an electronic system that duplicates the neural signals associated with memory, they managed to replicate the brain function in rats associated with long-term learned behavior, even when the rats had been drugged to forget. ... Using embedded electrical probes, [scientists] recorded changes in the rat's brain activity between the two major internal divisions of the hippocampus, known as subregions CA3 and CA1. During the learning process, [CA3 and CA1] interact to create long-term memory ... experimenters blocked the normal neural interactions between the two areas using pharmacological agents. The previously trained rats then no longer displayed the long-term learned behavior. ... the teams then went further and developed an artificial hippocampal system that could duplicate the pattern of interaction between CA3-CA1 interactions. Long-term memory capability returned to the pharmacologically blocked rats when the team activated the electronic device programmed to duplicate the memory-encoding function. In addition, the researchers went on to show that if a prosthetic device and its associated electrodes were implanted in animals with a normal, functioning hippocampus, the device could actually strengthen the memory being generated internally in the brain and enhance the memory capability of normal rats."

Thursday, June 16, 2011
Researchers are very interested in establishing biomarkers of aging and longevity, as at present the only truly reliable way to distinguish between long-lived and not so long-lived individuals is to wait and see what happens - which isn't an efficient way to run studies of potential therapies for aging. Here's an example of one line of investigation: "Wound healing (WH) is a fundamental biological process. Is it associated with a longevity or aging phenotype? In an attempt to answer this question, we compared the established mouse models with genetically modified life span and also an altered rate of WH in the skin. Our analysis showed that the rate of skin WH in advanced ages (but not in the young animals) may be used as a marker for biological age, i.e., to be indicative of the longevity or aging phenotype. The ability to preserve the rate of skin WH up to an old age appears to be associated with a longevity phenotype, whereas a decline in WH with an aging phenotype. In the young, this relationship is more complex and might even be inversed. While the aging process is likely to cause wounds to heal slowly, an altered WH rate in younger animals could indicate a different cellular proliferation and/or migration capacity, which is likely to affect other major processes such as the onset and progression of cancer. As a point for future studies on WH and longevity, using only young animals might yield confusing or misleading results, and therefore including older animals in the analysis is encouraged."

Thursday, June 16, 2011
An interview from the Scientist: "Cartilage is a firm, yet elastic, connective tissue that cushions joints and minimizes friction between bones. It is made up mostly of a matrix of collagen and proteoglycans and lacks nerve cells or blood vessels. In fact, cartilage contains only one cell type, the chondrocyte. A joint injury is often followed by progressive degeneration of cartilage, but there is hope that stem cells injected into damaged cartilage can help repair it. University Hospital Basel tissue engineer Ivan Martin discusses a recent study that sheds light on the mysterious process of cartilage regeneration by tracking labeled, implanted cells using a conventional MRI scanner ... [For treating cartilage injury] there is a very promising, relatively new technique - the use of autologous cartilage cells, or chondrocytes, which are expanded ex vivo and injected into the defective area. Even more recently, people have considered using mesenchymal stem cells, which are the progenitors of chondrocytes. ... We cannot just continue injecting cells and looking two years down the road to see if there is a change or not in the clinical results. We need to have control over the treatment we apply in order to understand the mechanisms of action and to be able to predict with better reproducibility the clinical outcome. This [MRI-based] technique would possibly contribute or provide the technical means to address this important scientific question."

Wednesday, June 15, 2011
The interesting question regarding the removal of the human heartbeat is the impact it will have on other bodily systems. Will it extend life by reducing stress on, for example, vulnerable blood vessels in the brain, or will it shorten life by also eliminating the beneficial response to that stress? Researchers are making progress in artificial hearts, so this question will likely be answered at some point over the next few decades: "The search for the perfect artificial heart seems never-ending. After decades of trial and error, surgeons remain stymied in their quest for a machine that does not wear out, break down or cause clots and infections. But Dr. Billy Cohn and Dr. Bud Frazier at the Texas Heart Institute say they have developed a machine that could avoid all that with simple whirling rotors - which means people may soon get a heart that has no beat. Inside the institute's animal research laboratory is an 8-month-old calf with a soft brown coat named Abigail. Cohn and Frazier removed Abigail's heart and replaced it with two centrifugal pumps. ... If you listened to her chest with a stethoscope, you wouldn't hear a heartbeat. If you examined her arteries, there's no pulse. If you hooked her up to an EKG, she'd be flat-lined. ... The pumps spin Abigail's blood and move it through her body. ... The doctors say the continuous-flow pump should last longer than other artificial hearts and cause fewer problems. That's because each side has just one moving part: the constantly whirling rotor. But Cohn says they will still have to convince the world that you don't need a pulse to live. ... We look at all the animals, insects, fish, reptiles and certainly all mammals, and see a pulsatile circulation. And so all the early research and all the early efforts were directed at making pulsatile pumps. ... However, the only reason blood must be pumped rhythmically instead of continuously is the heart tissue itself. ... The pulsatility of the flow is essential for the heart, because it can only get nourishment in between heartbeats. If you remove that from the system, none of the other organs seem to care much."

Wednesday, June 15, 2011
If the level of interest the public has in their gray hair could only be transferred to an interest in practical work to repair aging, how much better off we'd be. Here is more research into the biological causes of loss of hair pigmentation with aging: "Wnt signaling, already known to control many biological processes, between hair follicles and melanocyte stem cells can dictate hair pigmentation. ... We have known for decades that hair follicle stem cells and pigment-producing melanocycte cells collaborate to produce colored hair, but the underlying reasons were unknown. We discovered Wnt signaling is essential for coordinated actions of these two stem cell lineages and critical for hair pigmentation. ... The study suggests the manipulation of Wnt signaling may be a novel strategy for targeting pigmentation such as graying hair. The research study also illustrates a model for tissue regeneration. ... Using genetic mouse models, researchers were able to examine how Wnt signaling pathways enabled both hair follicle stem cells and melanocyte stem cells to work together to generate hair growth and produce hair color. Research also showed the depletion (or inhibition or abnormal) Wnt signaling in hair follicle stem cells not only inhibits hair re-growth but also prevents melanocytes stem cell activation required for producing hair color. The lack of Wnt activation in melanocyte stem cells leads to depigmented or gray hair."

Tuesday, June 14, 2011
Researchers are making progress in changing cells directly from one type to another: "A research breakthrough has proven that it is possible to reprogram mature cells from human skin directly into brain cells, without passing through the stem cell stage. The unexpectedly simple technique involves activating three genes in the skin cells; genes which are already known to be active in the formation of brain cells at the fetal stage. ... By reprogramming connective tissue cells, called fibroblasts, directly into nerve cells, a new field has been opened up with the potential to take research on cell transplants to the next level. ... We didn't really believe this would work, to begin with it was mostly just an interesting experiment to try. However, we soon saw that the cells were surprisingly receptive to instructions. ... In experiments where a further two genes were activated, the researchers have been able to produce dopamine brain cells, the type of cell which dies in Parkinson's disease. The research findings are therefore an important step towards the goal of producing nerve cells for transplant which originate from the patients themselves. The cells could also be used as disease models in research on various neurodegenerative diseases. Unlike older reprogramming methods, where skin cells are turned into pluripotent stem cells, known as IPS cells, direct reprogramming means that the skin cells do not pass through the stem cell stage when they are converted into nerve cells. Skipping the stem cell stage probably eliminates the risk of tumours forming when the cells are transplanted."

Tuesday, June 14, 2011
Progerin is the mutant form of lamin-A implicated in the accelerated aging condition progeria. It also shows up in normal aging, to a much lesser degree, and here researchers make progress towards understanding why: "Telomeres wear away during cell division. When they degrade sufficiently, the cell stops dividing and dies. The researchers have found that short or dysfunctional telomeres activate production of progerin, which is associated with age-related cell damage. As the telomeres shorten, the cell produces more progerin. ... This study highlights that valuable biological insights are gained by studying rare genetic disorders such as progeria. Our sense from the start was that progeria had a lot to teach us about the normal aging process and clues about more general biochemical and molecular mechanisms. ... the mutation that causes progeria strongly activates the splicing of lamin A [or LMNA] to produce the toxic progerin protein, leading to all of the features of premature aging suffered by children with this disease. But modifications in the splicing of LMNA are also at play in the presence of the normal gene. The research suggests that the shortening of telomeres during normal cell division in individuals with normal LMNA genes somehow alters the way a normal cell processes genetic information when turning it into a protein, a process called RNA splicing. To build proteins, RNA is transcribed from genetic instructions embedded in DNA. RNA does not carry all of the linear information embedded in the ribbon of DNA; rather, the cell splices together segments of genetic information called exons that contain the code for building proteins, and removes the intervening letters of unused genetic information called introns. This mechanism appears to be altered by telomere shortening, and affects protein production for multiple proteins that are important for cytoskeleton integrity. Most importantly, this alteration in RNA splicing affects the processing of the LMNA messenger RNA, leading to an accumulation of the toxic progerin protein."

Monday, June 13, 2011
More reasons to be exercising - many aspects of the biology of an exercising older mammal are improved over one that is sedentary, and the bugbear of inflammation is one of them: "We tested the hypothesis that regular aerobic exercise reverses arterial inflammation with aging. Compared with young controls, old male B6D2F1 cage-restricted mice demonstrated increased arterial activation of the pro-inflammatory transcription factor, nuclear factor κB (NFκB) ... Similarly, aortic expression of the pro-inflammatory cytokines [were] greater in the old mice. Macrophage and T lymphocyte abundance was unchanged with age in the aortic intima and media, but was markedly increased in the adventitia and perivascular fat tissue of old mice. This pro-inflammatory arterial phenotype with aging was associated with vascular endothelial dysfunction, as reflected by impaired nitric oxide-mediated endothelium-dependent dilation (EDD). Voluntary wheel running (10-14 weeks) in old mice normalized [all of these age-altered features]. Short-term voluntary wheel running started late in life reverses arterial inflammation with aging in mice possibly via 'outside-in' actions. These anti-inflammatory effects may play an important role in the amelioration of age-associated vascular dysfunction by regular aerobic exercise."

Monday, June 13, 2011
An op-ed on perpetual trusts aimed at preserving wealth for cryopreserved individuals can be found at h+ Magazine: "Rudi Hoffman is an insurance salesman specializing in cryonics-related insurance policies. He's also a deep thinker about cryonics and life extension, and an incredibly funny guy. So, we thought it would be interesting to have Rudi tell our readership about cryonics trusts - the notion of setting up a trust to fund your own revival and post-resuscitation life. He put together a few words on some of the misconceptions he encounters when talking to people about the concept of cryonics trusts. ... Cryonics trusts and planning for wealth upon revival is not a new idea. Questions about cryonics estate and trust planning were being asked and explored by pioneers as early as the 1980s. These questions were also asked to me, as well as by me as early as early 1994 when I signed up with Alcor. The history of cryonics back to early days is an series of lessons in real world finance, in many cases hard lessons like the Chatsworth cryonics tragedy, a function of unrealistic funding structure for maintenence of cryonics patients. Out of these funding tragedies, real world experience has emerged. The cool thing about this is that you and I can benefit from the work that has gone before us. The underbrush has been cleared and a smoother path is now available for us to travel regarding cryonics trusts. ... While there are significant challenges in setting up a viable and effective cryonics trust, the 'Rules against perpetuities' are pretty much a non-issue. These laws have been abolished by statute in states including Alaska, Idaho, New Jersey, and South Dakota. ... Most cryonics model or prototype trusts available utilize a "dynasty trust" format. This basically sidesteps the question of whether someone pronounced dead and currently in biostasis is well and truly, permanently 'dead.' This format, used by wealthy folks seeking to control their assets even after traditional death, has been used for many decades. Basically, you direct a trustee to act in your behalf to carry out the terms of the trust. This does not require new law be made determining whether you are 'dead enough' or even 'too dead to have rights.'"



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