LONGEVITY MEME NEWSLETTER
July 23 2007
The Longevity Meme Newsletter is a weekly e-mail containing news, opinions and happenings for people interested in healthy life extension: making use of diet, lifestyle choices, technology and proven medical advances to live healthy, longer lives.
- Design a Logo for the Methuselah Foundation
- A Deliberately Provocative Question
- Latest Healthy Life Extension Headlines
DESIGN A LOGO FOR THE METHUSELAH FOUNDATION
Do you have a good designer's eye? Then why not enter the contest to design a new logo for the Methuselah Foundation:
"Can you design a logo for the Methuselah Foundation? Would you like to see your work leading the charge in the fight to defeat age-related degeneration? We are upgrading our websites and outreach material, and as a part of this effort need a distinctive new logo that encapsulates and conveys the meaning of our mission and the essence of the Foundation. The Methuselah Foundation has been built by the dedication of volunteers and donors of all stripes, and so we reach out to the same community in search of a new logo."
Aubrey de Grey will be judging, and the winner and two runners up will receive autographed copies of "Ending Aging: The Rejuvenation Biotechnologies That Could Reverse Human Aging in Our Lifetime." The contest ends on August 15th, so the clock is ticking.
A DELIBERATELY PROVOCATIVE QUESTION
So you want to live a much longer, healthier life. When should you help to achieve that goal by donating 90% of your net worth in support of research?
"If you care more about posterity than your own survival, would you wait as late as possible? Or does this critical time for the present nascent longevity research community mean that 1% of that same 'late as possible' investment in research and support would better serve the future if donated now? If you care deeply about your own survival, where do the curves and trends cross for greatest effect in your opinion?
"There is no right answer in consideration of personal economic choices, but these are all questions we should ask ourselves. Wealth at any level is worthless to the dead, and being alive and healthy allows you to generate more wealth: logically we should all be willing to devote most of our net worth to longevity research at the most effective time. If we can buy time with money - and we can begin to now in earnest, for the first time in history, by supporting the research that will lead to the first healthy life extension medicine - then we should all be in that market."
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!
Founder, Longevity Meme
LATEST HEALTHY LIFE EXTENSION HEADLINES
To view commentary on the latest news headlines complete with links and references, please visit the daily news section of the Longevity Meme: http://www.longevitymeme.org/news/
Skin Cells and Cellular Aging (July 20 2007)
There's no shortage of interesting data and conclusions out there; here's a good example from researchers focused on stem cell biology: "The epidermal stem cells reside in the proliferative basal cell layer and are believed to persist for the lifetime of an individual. Acting through intermediaries known as transit amplifying cells, epidermal stem cells ensure that the enormous numbers of keratinocytes required for epidermal homeostasis to be maintained are generated. This continual demand for new cell production must be met over the entire lifetime of an individual. ... This leads us to question whether or not epidermal stem cells represent a unique population of cells which, by necessity, might be resistant to cellular aging. We hypothesized that the full physiologic functional capacity of epidermal stem cells is maintained over an entire lifetime. Using murine skin epidermis as our model system, we compared several properties of young and old adult epidermal stem cells. We found that, over an average mouse's lifetime, there was no measurable loss in the physiologic functional capacity of epidermal stem cells, leading us to conclude that murine epidermal stem cells resist cellular aging." Always a good starting point for "how," "why" and "what does this teach us?"
"A Powerful Pathologic Process" (July 20 2007)
Many specific age-related degenerations have no name and remain uncategorized, poorly understood, even undiscovered. All likely stem from a small range of types of accumulated damage, but nonetheless it should serve as something of a wakeup call that scientists continue to uncover these sorts of things: "Multiple reports have documented an age-related loss, estimated at about 10% per decade, of the pigmented neurons in the substantia nigra. This is associated with motor dysfunction, including bradykinesia, stooped posture and gait disturbance. As microglia are activated by cell death and neuromelanin pigment, we hypothesized that there should be a significant microglial reaction in normal aging human substantia nigra. ... older subjects, the percentage of substantia nigra area occupied by microglial bodies and processes was significantly greater than for younger subjects ... The marked microglial reaction in normal aging human substantia nigra, together with the previously reported 35-80% pigmented neuron loss, indicates the presence of a powerful pathologic process that may be additive with specific age-related neurodegenerative diseases, including Parkinson's disease."
An Interesting View Of Insulin Signaling (July 19 2007)
From ScienceDaily, research that provides an interesting view of the insulin signaling mechanism, metabolism and its impact on life span: "The traditional prescriptions for a healthy life - sensible diet, exercise and weight control - extend life by reducing signaling through a specific pathway in the brain [activated] when insulin and insulin-like growth factor-1 switch on proteins inside the cell called insulin receptor substrates ... Diet, exercise and lower weight keep your peripheral tissues sensitive to insulin. That reduces the amount and duration of insulin secretion needed to keep your glucose under control when you eat. Therefore, the brain is exposed to less insulin. Since insulin turns on [an insulin receptor substrate] in the brain, that means lower [insulin receptor substrate] activity, which we've linked to longer lifespan in the mouse ... We are beginning to appreciate that obesity, insulin resistance, and high blood insulin levels are connected to Alzheimer's disease, Huntington's disease, and dementias in general. It might be that, in people who are genetically predisposed to these diseases, too much insulin overactivates [insulin receptor substrates] in the brain and accelerates disease progression. Thus, insulin resistance and higher insulin levels might be the environmental influences that promote these diseases."
Telomeres and Heritability of Life Span (July 19 2007)
Chris Patil notes a point I missed on recent research into human telomere lengths: "The paper's key finding (from my perspective, at least) didn't make it into the title: Telomere length is positively correlated with lifespan. While I'm aware of studies linking telomerase activity in animal species to lifespan, the growing consensus seems to be that this is a corollary of the relationship between telomerase and body mass, which in turn is correlated with lifespan; furthermore, the relationship is the opposite of the one here (larger, longer-lived animals tend to have lower telomerase activity than smaller, shorter-lived animals with a similar body plan; see our earlier article Telomerase correlates negatively with body mass). This is the first study I'm aware of in which human-to-human variation in telomere length (which occupies a concept space somewhere between the strictly genetic and the strictly epigenetic) has been shown to correlate with lifespan. The key issue now, of course: Where are the causal links, if any, between the telomeres a person inherits and their life expectancy?" This will no doubt boost the fundraising ability of companies presently building ways to manipulate telomere length.
Alcor Conference Early Registration Deadline (July 18 2007)
The early registration deadline for the 7th Alcor Conference is the end of this month. A range of interesting presentations are lined up for this year: "Cryobiology is a small field, and cryonics is even smaller still. Finding answers to technical questions can be difficult. Common questions are: What can and cannot be cryopreserved today? How is freezing damage prevented? What lessons from cold tolerance in nature can be applied to cryopreservation? What is the difference between cryonics and suspended animation? When considering scientific fields that bring life processes to a complete stop, perhaps the most pervasive question of all is: What is the difference between life and death? This question and many others will be answered. ... For those interested in personal life extension, the news is complex. We all have busy lives and wish that effective life extension could be as easy as taking a vitamin pill, "One A Day for Longevity." Unfortunately, a quick fix is not an option today, but there is good news. Learn what you can do today to add healthy years to your life. This talk will review some of the more popular life extension approaches, beyond cryonics, because every year gained offers the benefit of yet another year of advances in longevity research."
A New Look At p53, Cancer and Aging (July 18 2007)
Susceptibility to aging and susceptibility to cancer are viewed as a balance, centered around the disposition of multipurpose biochemical machinery like the p53 gene. You can tilt the mechanism one way or another - less cancer or slower aging - but not both at once. This Nature publication throws that out of the window - it seems it is possible to tinker p53 into providing slower aging and less cancer. "The conclusion seems to stand in direct contradiction to previous work, which showed that a boost in p53 kept mice cancer free but also caused them to age more quickly. But there's a key difference between these studies, the researchers say: in the new work, the normal regulatory mechanisms remain in place, so p53 is churned out only when needed. This seems to turn an ageing protein into a youth-preserving one. It's a very impressive effect. It's very hopeful because it says under some circumstances you can get the best of both worlds. ... These mice produce more p53 protein when prompted to by cellular stress, such as DNA damage or lack of oxygen. As expected, mice with the extra copy of p53 had fewer tumours than regular mice, and their cells were less likely to turn cancerous when grown in a Petri dish. On average, the transgenic mice lived 16% longer than normal mice."
On Engineering Stem Cells (July 17 2007)
(From the Times Online). Our cells are just complex protein machinery, which means there is no obstacle to one day building all the cells we need for any given medical usage from scratch, to order. For the near term, however, researchers are focusing on manipulating cells into desired states through signaling and growth: "It is hard to predict how the science will develop, but I think we could produce a basic prototype-induced stem cell made from a human adult cell within six months to a year. Within two to three years we may be able to create a stem cell that is indistinguishable from one taken from an embryo. What we cannot do, though, is to let the optimism over my science hold us back from conducting research on embryonic stem cells while we are waiting for the alternative ... The concept of artificially inducing adult cells to return to a stem-cell state raises [attractive] possibilities for organ transplantation. If, for example, a patient's skin cell could be reverted to stem-cell form and thence converted back into any other form of tissue - such as nerve, heart or other organs - it could then be transplanted without risk of rejection by the patient." Any advance that lowers the cost of regenerative research, such as by lowering the cost of creating suitable totipotent stem cells, will speed progress.
CR and Gene Expression in Fat Cells (July 17 2007)
Here's something new to add to the list of interesting things calorie restriction (CR) does to your metabolism on the way to granting health and longevity benefits. Via Ouroboros: "Adipocytes (fat cells) are the site of much metabolic and endocrine activity; their physiology affects our energy balance, insulin sensitivity and a host of other processes throughout the body. And of course, as some of us know all too well, their behavior is dynamic not only from hour to hour but from year to year, over the course of aging. It's natural to ask questions about the impact of life-extending regimens like calorie restriction (CR) on the biology of adipocytes. A study of rat adipocytes reveals that CR influences the expression of a wide range of signaling molecules, and reverses or mitigates some of the age-related changes in gene expression observed in previous research." Wherever scientists look, the signs of CR affecting the biochemical symptoms of aging are there to be found - or so it seems, some days.
Manipulating Cell Signaling For Regeneration (July 16 2007)
As reported by Forbes, researchers continue to make progress in manipulating cell signaling to spur regeneration - a path that can be distinct from stem cell or gene therapy. This is a comparatively simple example of the type, and at an early stage in development, but still progress: "Normally, adult human hearts do not regenerate because the heart doesn't make more cardiomyocytes (heart muscle cells) after injury. It would be desirable to induce the heart to make new cardiomyocytes after injury. ... To that end, Kuhn's team created a patch that contains a compound called periostin, which helps cardiomyocytes divide and multiply ... Periostin is a natural component of tissue surrounding cells. It comes from the skin lying around bone and helps stimulate cells to divide. ... They placed the patches on the damaged heart muscle of rats in which they had induced a heart attack. After 12 weeks, the rats treated with the periostin patch experienced a 16 percent improvement in their heart's cardiac pumping ability. They also had less scarring of heart tissue, a reduction in the size of the damaged area of the heart, and more blood vessels feeding the area."
Priorities and Practicalities (July 16 2007)
Anne C. on the practicalities and priorities of working towards healthy life extension technologies: "While the idea of saving lives in general is neither new nor remarkable, the idea of saving the lives of people 100, 110, 120, and even older is often considered to be radical at best. And while there are indeed various technical and practical challenges to achieving effective health care for people who are nearing (or in) the triple-digits, the existence of political challenges is somewhat confounding. What makes someone's impending death less of an emergency when they are ninety than when they are nine? If you were told that someone was dying and you didn't know how old they were, would it even occur to you to ask, with the intent of using their age to decide whether they were worth trying to save or not? Most likely, it wouldn't. If you can understand that age should not matter as a variable in terms of whether someone's life ought to be saved, you have grasped the philosophical underpinnings of life extension." Quite so.