LONGEVITY MEME NEWSLETTER
October 01 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.
- Healthy Life Extension is Inevitable
- Autographed Copies of Ending Aging Available
- Latest Healthy Life Extension Headlines
HEALTHY LIFE EXTENSION IS INEVITABLE
I can say with fair confidence that the development of any technology allowed under the laws of physics is inevitable. The burning question in this case is whether or not it will happen soon enough to benefit those of us reading this today:
"The choice of living a healthy, youthful life of centuries and more is inevitable - it will come to pass. That much is obvious, written in the present breadth of human civilization, knowledge of what is possible under the laws of physics, and pace of progress in biotechnology. Replacement biological organs are a decade away, and commercial efforts to develop sophisticated repairs to age-damaged cells and vital biomechanisms will be rife in the 2020s. Computational power will be so great and so cheap that tens of thousands and then millions of research programs will be accomplished in simulation for a tiny fraction of their cost today; the priesthood of bioscience will dissolve and progress will be as diverse, energetic and imaginative as it is for open source software at present. Redesigning human biochemistry and greatly augmenting our biology with nanomachinery will be hot areas for venture funding in the 2030s and 2040s."
I see development of the baseline technologies required for greatly extending the healthy human life span as a given for the next few decades. The biotechnology revolution is roaring ahead, and there's no halting the relentless advance of computational power. But just because we can doesn't mean we will - there is still the need to take that baseline technology and turn it to a desired use.
Given that there is no massive, serious life extension research and development community in existence today - and here, I'm thinking of a community to match the cancer research establishment in breadth and support - the future we'd like to see is still in doubt. If we want the awe-inspiring biotechnologies of the 2020s promptly put to use in repairing the damage of aging, right out of the starting gate, then we'd better get working on that now:
AUTOGRAPHED COPIES OF ENDING AGING AVAILABLE
The Methuselah Foundation is giving away autographed copies of Aubrey de Grey and Michael Rae's Ending Aging with donations of $100 or more:
Here's your chance - take it while it's there.
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!
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/
Telomeres, Correlation and Causation (September 28 2007)
From Ouroboros: "Is telomere length important to the mechanism of aging, in addition to being a marker of advanced chronological age? The jury is still out on that, likely frustrated by the circumstantial nature of the evidence. We know that telomere length appears to be inversely proportional to life expectancy, but of course correlation [does not imply] causation, and lifespan and telomere length could be unrelated signifiers of the same underlying phenomenon. To complicate the issue, we are reminded in a recent review that all telomere ends are not equal ... bulk telomere length might be less important than the lengths of particular telomeres, a forest hiding the most significant trees. More to the point, the telomere lengths of the various chromosomes might be regulated independently, making bulk telomere length something of a red herring." A number of different research groups and young companies are presently working on therapies based upon altering telomere length; expect to see new knowledge and clarity in the field over the next five years.
Another Path to Mouse Longevity (September 28 2007)
There are many ways to engineer mammalian metabolism for greater longevity, and more are discovered with each passing year. Any significant upgrade is likely to be a greater challenge to deploy in humans than repairing the metabolism we have, however. Here's a more impressive than average new example of engineered mice; these overexpress PEPCK-C, or Phosphoenolpyruvate carboxykinase. Note that the full PDF-format paper is freely available: "These mice were seven times more active in their cages than controls. On a mouse treadmill, PEPCK-C mice ran up to 6 km at a speed of 20 m/min while controls stopped at 0.2 km. ... The PEPCK-C mice eat 60% more than controls, but had half the body weight and 10% the body fat ... In addition, the number of mitochondria and the content of triglyceride in the skeletal muscle of PEPCK-C mice was greatly increased as compared to controls. PEPCK-C mice had an extended life span relative to control animals; mice up to an age of 2.5 years ran twice as fast as 6-12 month old control animals. We conclude that over-expression of PEPCK-C repatterns energy metabolism and leads to greater longevity."
On Preventing AGE Formation (September 27 2007)
AGEs are bad news - a component of the biomolecular damage that causes aging, an ongoing buildup of compounds your body cannot break down rapidly enough, or at all in some cases. A branch of science, not as robust as we'd all like, focuses on how to break down AGEs, but there is always another approach: suppress their formation in the first place. At Ouroboros: "report that silks from several modern corn strains are capable of inhibiting nonenzymatic glycation in vitro, with the activity strongest in varieties bred to resist specific types of fungal infection. The mechanism of inhibition is not clear or even a ready subject for idle speculation (if you will, take a moment and bend your head around how one might specifically inhibit an uncatalyzed, non-specific reaction that can occur between a broad range of molecules); nor is it not obvious whether the phenolic compounds in the silk extracts could be made bioavailable without extensive modification. Still, once the chemistry of inhibition is elucidated, the silk-derived molecules could provide inspiration for therapeutics capable of stopping AGEs before they start."
CR in Practice and CR Research (September 27 2007)
The Baltimore Sun looks at calorie restriction (CR) as it is practiced, and at a little of the latest research into CR biochemistry: "Known as calorie restriction, or CR, the Spartan diet is one of several avenues researchers are exploring in their quest to understand and delay aging. They're also interested in genes that appear to play a role in getting older, along with a variety of chemical compounds, including one found in red wine, that may possess life-extending properties. ... But assembling the clues to solve the aging puzzle is no easy feat. ... We know a lot more than when Ponce de Leon was wandering around Florida looking for the Fountain of Youth. But these things are tied together in ways that aren't completely understood. ... Even so, paragons of self-control [are] forging ahead, as are scientists intent on developing anti-aging therapies. ... Your hamburger could be turning off your longevity. But there may be ways to turn on the body's genes and to still protect you from diseases of aging."
Do What You've Always Been Talking About (September 26 2007)
I am always very pleased to see supporters of healthy life extension make the leap to activism and activity - if everyone who thought about living a longer life did but a tenth as much as Richard Schueler, we'd be much further along: "I love to talk about things I believe in. The subject that I’ve found myself telling people about the most the last few years is longevity research. If you CURE cancer and CURE heart disease, it adds 7 years to our life expectency. 100,000 people died yesterday from age. Yes, 100,000 real live people. They didn't die from starvation, they didn’t die from aids, they died from age. Why not work on something that can give us 3.5 years? 7.5 years? ... So I went a few years preaching and preaching about it, the world didn't change. ... So I made the next step. I decided to dedicate my life to the combat and elimination of age related diseases wherever possible. My fiancee [and] I bought our tickets for Cambridge, England and our tickets to the SENS3 conference, the largest conference in the world with a focus on age related disease and prevention. I met up with Aubrey de Grey a day before the show with the aim of finding where I would fit best in helping progress happen. I volunteered to take charge of the video of the event." And take charge he did; check out his website for a selection of conference video in processing. Do you want to see progress in healthy life extension in your lifetime? Then get out there and help those who are trying to make it happen.
Support for Alzheimer's as a Type of Diabetes (September 26 2007)
You might recall intriguing research from 2005 that cast Alzheimer's disease as a form of diabetes. Here's more from EurekAlert!: researchers "have discovered why brain insulin signaling -- crucial for memory formation -- would stop working in Alzheimer's disease. ... a toxic protein found in the brains of individuals with Alzheimer's removes insulin receptors from nerve cells, rendering those neurons insulin resistant. (The protein, known to attack memory-forming synapses, is called an ADDL for 'amyloid beta-derived diffusible ligand.') ... ADDLS are small, soluble aggregated proteins. The clinical data strongly support a theory in which ADDLs accumulate at the beginning of Alzheimer's disease and block memory function by a process predicted to be reversible. ... ADDLs bind very specifically at synapses, initiating deterioration of synapse function and causing changes in synapse composition and shape. ... the molecules that make memories at synapses - insulin receptors - are being removed by ADDLs from the surface membrane of nerve cells. ... We think this is a major factor in the memory deficiencies caused by ADDLs in Alzheimer's brains. ... We want to find ways to make those insulin receptors themselves resistant to the impact of ADDLs. And that might not be so difficult." Note the important word in the middle there - "reversible."
Growing Neurons To Order (September 25 2007)
(From EurekAlert!). One aspect of research into controlling cells to keep an eye on: growing neurons to order. How much support can a carefully controlled supply of new neurons provide for an aging brain? Researchers are applying their first efforts to answer this question towards the repair of named neurodegenerative conditions: "The team used gene therapy to guide the development of endogenous stem cells in the brains of mice affected by a form of Huntington's. The mice that were treated lived significantly longer, were healthier, and had many more new, viable brain cells than their counterparts that did not receive the treatment. ... While the promise of stem cells is broadly discussed for many diseases, it's actually conditions like Huntington's - where a very specific type of brain cell in a particular region of the brain is vulnerable - that are most likely to benefit from stem-cell-based therapy ... Once we worked out the molecular signals that control the development of these brain cells, the next logical step was to try to trigger their regeneration in Huntington’s disease."
SENS3 Science Report at Ouroboros (September 25 2007)
Okie of Ouroboros reports on the recent SENS3 conference: "As a scientist, it is a challenge to present my work to a mixed group of scientists and (particularly well-educated) lay people. Where translational research is concerned, however, I think that lay people do a great job keeping us researchers focused on the prize and not just on (interesting) esoteric points." Okie goes on to give a punchy overview of the science presented, ending with: "I would like to see more theoretical and statistical work on which problems of aging are the most pressing/serious ones. I think Aubrey's '7 deadly things' is a well thought out plan for tackling the problem of universal aging. What I would like to see is some data on which problem(s) are rate limiting. For example, what if solving the problem of 'too few cells' (cell death and senescence in aging) would double human lifespan all by itself while all the others put together would barely accomplish the same? The keynote talk (by Ryan Phoenix) included some modeling of how soon SENS treatments could be available, how soon we would need to solve the 7 things in order to treat people alive today, and how often treatments would need to be repeated. This all relied, however, on the assumption than all 7 deadly things were created equally. Everyone agrees that we should take steps to provide the most immediate benefits to humankind, but no one agrees on what these are."
Looking to the Future of Stem Cell Medicine (September 24 2007)
The next decade will see ever more ambitious stem cell medicine made commercially available, very much despite the regulatory and legislative atmosphere at present. From the Sunday Herald: "Stem cells are primal cells at an early stage of development. Scientists hope to use their properties to study diseases and to develop 'repair' kits for the body by enabling healthy tissue to be grown. ... researchers around the world were already considering the use of stem cells to repair corneas, bones and specific cases of spinal cord injury. ... New therapies are just the same as medicines, they have to be tested and shown to be effective and safe. So it will be a small number of cases and a small number of treatments first, which will grow over the years and the decades. If you look back to when, for example, antibiotics first came along, there was a small number of them, but progressively they became more and more effective and now we take them for granted."
Aubrey de Grey at the Boston Stem Cell Summit (September 24 2007)
As noted at the Methuselah Foundation blog, biomedical gerontologist Aubrey de Grey will be speaking at the Boston Stem Cell Summit early next month: "Following the successful conclusion of the third SENS conference in Cambridge, and the recent publication of my book, 'Ending Aging', which has received uniformly favourable reviews, I feel that we're turning the corner - the plausibility of retarding and eventually reversing aging is beginning to percolate into the public consciousness. A telling sign of increasing mainstream acceptance of our work at the Methuselah Foundation is the invitation I recently received to speak at the prestigious Stem Cell Summit to be held in Boston on October 2nd and 3rd. On 3rd October I will be attending the session on aging, followed by heading a table at the 'Conversations with Experts' luncheon." Late notice, I know, but supporters of healthy life extension research might want to attend - the conference is an interesting one, quite aside from any Methuselah Foundation presence.