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Longevity Meme Newsletter, April 16 2007

LONGEVITY MEME NEWSLETTER
April 16 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.

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CONTENTS

- A Minor Change of Address
- Growth at the Methuselah Foundation
- Discussion
- Latest Healthy Life Extension Headlines

GROWTH AT THE METHUSELAH FOUNDATION

There are plenty of signs of growth to be found at the Methuselah Foundation, home of the Mprize for longevity science and sponsor of SENS research, starting with ever more members of The Three Hundred:

http://blog.methuselahfoundation.org/2007/04/welcome_to_many_new_members_of_1.html

"Membership in the Methuselah Foundation's Three Hundred, dedicated folk like you and I who stand together in support of meaningful longevity research, is growing by leaps and bounds. A warm welcome to Michael Silverton, Andrew Hessel, Ryan Scott, Michael Potter, Ross Baker, Matthew W.A. Gress, Harry Huttunen and Steve Rozenblat - all of whom have stepped up within the last month to show their support for scientific research and longer, healthier lives."

Meanwhile, fundraising for longevity research in Silicon Valley continues apace. The Foundation volunteers were back this past weekend for a series of engagements, including one hosted by the Alliance for Aging Research:

https://www.fightaging.org/archives/001183.php

"As many of you have no doubt experienced in the past, keeping the wheels turning at best speed in a growing, changing organization is an interesting challenge. This is especially true in the non-profit space, where people are so much more driven by passion, and many of the key resources are volunteers. It is a testament to the intelligence and dedication of the volunteers and supporters of the Methuselah Foundation that they have surmounted each challenge to date, and that the organization continues to move forward apace to new goals in the grand plan."

I consider it a very positive sign that an organization like the Alliance for Aging Research, aligned with the Longevity Dividend folk and mainstream gerontology, is willing to hold hands with Aubrey de Grey and the "rapid progress towards practical rejuvenation" faction of modern aging science. To me, this indicates a willingness to help bring on the tide of support for engineering greater human longevity, and more importantly to do so in the spirit of floating all boats. There are heartfelt debates over the merits of various scientific approaches, but everyone is essentially playing for the same team when it comes to building a better environment for research funding:

https://www.fightaging.org/archives/001050.php

If this is a good example of the trend for the years ahead, we should all be very pleased. The largest hurdle to improving our prospects for increased healthy longevity is the search for funding by those with the big, bright ideas for the future. In other words, you have to keep your eye on the science of 20 years hence, not the science of today - because it is the science of 20 years hence that will be the real determinant of your health and longevity. Replacement organs grown from your own cells; efficient cancer vaccines; precision drugs and enzymes to clean out the buildup of damaging metabolic byproducts; viral replacement of worn and damaged mitochondrial DNA; the cure for Alzheimer's; the first mass-produced medical nanorobots; and so forth.

https://www.fightaging.org/archives/001047.php

The ideas and interest already exist within the scientific community. The most important present groundwork for that future science is the raising of funds, building a research community, and gathering public support for healthy life extension. There are so many ways for us to miss the boat - let it not be because we saw the ring but didn't organize to grasp it.

DISCUSSION

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!

Reason

Founder, Longevity Meme

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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/

On Biomarkers of Aging (April 15 2007)
http://websites.afar.org/site/PageServer?pagename=IA_spotlight_main
InfoAging interviews Richard Sprott of the Ellison Medical Foundation in connection with a conference on biomarkers of aging later this year: "The National Institute on Aging began its Biomarkers of Aging project in 1987. I headed up the program, which was looking to identify biomarkers of aging in mice with the ultimate goal of developing a panel of biomarkers that would be useful for humans. Over the course of 10 years, we invested thousands of research hours and millions of federal dollars, only to end up with some interesting possibilities but no clear winners. ... using new tools that weren't available 10 years ago, [there's] a feeling among a number of us that the time is right to have a new effort and that there's the real possibility that we can achieve what wasn't possible 10 or 15 years ago. ... a so-called 'anti-aging' medicine industry has promulgated the notion for a very long time that there are lots of biomarkers of aging out there when they're trying to sell certain kinds of products to the general public. Those biomarkers, in fact, don't exist. The biomarkers work we are doing will help provide information about what's real and what's not. So there's the sort of reality-testing aspect that's important."

Inkjets and Bone Regrowth (April 15 2007)
http://www.dailymail.co.uk/pages/live/articles/news/news.html?in_article_id=448654
The Daily Mail illustrates the use of inkjet printing technology to fabricate scaffolds for bone regrowth: "The 'paper' in our printer is a thin bed of cement-like powder. The inkjets spray the cement with an acid which reacts with it and goes hard. That deals with one layer. Then new layers of fresh powder are sprayed on top, and the layers build up to the shape we need ... It takes only ten minutes for the printer, which is the size of about three filing cabinets, to print a typical bone graft. The printed graft acts as a bridge to allow the body to replace the damaged section with new bone. Crucially, the substance created by the printing process contains the same building blocks as real human bone, allowing the graft to eventually dissolve harmlessly into the body. The sections made by the printer are so precise that spaces can be left to encourage the regrowth of tissue and blood vessels through the graft, mirroring the make-up of normal bone. ... You can design it so you encourage it in a particular direction, to get different tissue repair. It is mainly useful in areas where you need a very good sort of fit, like cosmetic surgery or reconstructive surgery, or in the spine where you don't want to be playing around to get something to fit."

A Part of the Smokescreen (April 14 2007)
http://www.nytimes.com/2007/04/15/business/yourmoney/15aging.html?pagewanted=print
Real, actual anti-aging science - aimed at repairing the damage that causes aging - is largely obscured in the public eye by the smokescreen of the "anti-aging" marketplace, complete with flares and sirens. Much of it is nonsense or cargo cult imitations of real science, but the money and volume are such that it obscures the real scientific prospects for rejuvenation of the old in the years ahead. The better end of that marketplace is constantly on the verge of being more useful than damaging to the cause of healthy life extension - as Robert Butler points out in this New York Times article: "On the good side, it encourages healthy behaviors. On the other side, it sells things like human growth hormone, which is harmful." The article is, in general, a fair profile of the folk behind that nearly-of-net-benefit better end of the marketplace, Klatz and Goldman of the American Academy of Anti-Aging Medicine. They believe in what they are doing - it's unusual to find success in business on the part of those who don't - but I see precious little merit in most of their activities.

The Long Road to Artificial Eyes (April 14 2007)
http://www.newscientist.com/article/dn11607-retinal-implant-learns-to-polish-the-picture.html
The New Scientist reports on another small step on the long road to artificial replacement eyes. These are the days of slow, incremental work - but then the same was true of the internet 30 years ago. "Software that can be taught to refine the information sent from a bionic eye to its wearer is being trialled in Germany. ... These people report seeing light and dark and maybe some limited fuzzy shapes. But they don't have any gestalt perception. Eckmiller says the secret to improving these implants is to match the signals they produce with the signals that a healthy eye sends to the brain. One team in California, US, is trying to do that by building a copy of the retina's neurons in silicon. Eckmiller, along with colleagues Oliver Baruth and Rolf Schatten, plan to use learning software instead. ... It does this through a "dialogue module" that tries different settings while a user looks at standard shapes. The user selects the three settings that most closely match the real shape and the software then presents six more settings based on these three. Over time, the system learns to produce a signal that provides a more accurate picture to the user's brain. ... Currently the biggest challenge is to make a working device that interfaces with neurons properly."

On the Hormonal Regulation of Aging (April 13 2007)
http://pmid.us/17360245
Complementing the mainstream gerontological focus on genetic influences on aging is the study of the endocrine system, as illustrated in this paper: "Multiple biological and environmental factors impact the life span of an organism. The endocrine system is a highly integrated physiological system in mammals that regulates metabolism, growth, reproduction, and response to stress, among other functions. As such, this pervasive entity has a major influence on aging and longevity. The growth hormone, insulin-like growth factor-1 and insulin pathways have been at the forefront of hormonal control of aging research in the last few years. Other hormones, including those from the thyroid and reproductive system have also been studied in terms of life span regulation. The relevance of these hormones to human longevity remains to be established, however the evidence from other species including yeast, nematodes, and flies suggest that evolutionarily well-conserved mechanisms are at play and the endocrine system is a key determinant." The path to complete understanding is the slow path; it will make future therapies better and more effective, but we are already at the point of being able to make serious inroads in the fight to defeat aging.

On the Genetic Regulation of Longevity (April 13 2007)
http://dx.doi.org/10.1371/journal.pgen.0030056
A paper at PLoS Genetics gives a good idea of the present thrust of much mainstream aging research: genes, metabolism and the possibility of altering them for the better. "The lifespan of an animal is determined by both environmental and genetic factors, and many of the mechanisms identified to increase lifespan are evolutionarily conserved across organisms. ... We identified 64 genes that can extend lifespan when inactivated postdevelopmentally. More than 90% of the genes we identified are conserved from yeast to humans. Many of the newly identified longevity genes extend lifespan as robustly as the most well-characterized longevity mutants. It is possible that the homologues of these genes may also regulate lifespan in other organisms as well. Genetic analysis places some of these genes in known pathways regulated by insulin-like signaling, although many of these gene inactivations function independently of this mechanism of lifespan extension. Surprisingly, a subset of these gene inactivations that induce potent developmental arrest also facilitate enhanced survival in the arrested state, suggesting that aging at any stage may be subject to regulatory control."

The Proteomic Approach to Aging Research (April 12 2007)
http://pmid.us/17425465
This paper is a reminder of the power of modern biotechnology to pull information from our biochemistry. Want to learn more about aging? Why not start by building a database of changes in levels, usage and alterations in every protein in the body with age? "The scope of the current paper is to review existing and potential applications of proteomic analysis to aging research. The focus will lie on the unique opportunities of high-throughput studies for uncovering specific alterations in protein expression, protein complexes or protein modifications caused by biological aging. The result of such studies will outline aging phenotypes and potentially indicate pathways involved in the pathogenesis of age-associated disfunctions. Specific attention is paid to the illustrations of successful applications of proteomic technologies and potential applications of new proteomic concepts to biogerontological studies." The rate at which scientists can build such a database is presently far in advance of the rate at which they can extract meaning from it, but that's no reason not to get started.

Longevity, Economics and Other Motivations (April 12 2007)
http://rationallongevity.blogspot.com/2007/04/longevity-disability-and-economic_11.html
Thoughts from Anne C.: "It might be necessary, at times, to invoke primarily economic arguments when dealing with people whose own main argument in opposition to healthy life extension is that "older" old people will decrease the amount of resources available for activities not related to health crisis management. Here, the economic argument is appropriate in the sense that it corrects what is more than likely factually untrue from an economic standpoint -- it is obvious that if a person doesn't get heart disease, nobody is going to need to spend any money to treat heart disease in that person, which means that money is free to be used elsewhere. But the reason we want to prevent heart disease -- at least, the primary reason -- isn't an economic one, but one that I hope stems from compassion. Heart disease left untreated will most likely kill you. Aging left unaddressed will definitely kill you, whether indirectly or directly. So of course I'm in favor of things like longevity research -- because it has tremendous potential to save many, many innocent lives. Sure, it might end up having a particular economic effect that will make some people happy, but even if there was no chance of that, I would still support such research."

Revisiting Calorie Restriction in Dogs (April 11 2007)
http://www.rsc.org/chemistryworld/News/2007/April/11040701.asp
From Chemistry World, a look at a canine calorie restriction study: "48 puppies from seven litters were raised at a research centre in the US ... Animals were fed either a restricted or normal (control) diet and subjected to regular clinical assessment. Urine samples collected from each dog during these check-ups provided a metabolic record that UK scientists have used to study the biological process of aging and metabolism. The dogs on the restricted diet lived about two years longer than those on the control diet. The last of the dogs died just over two years ago, and [researchers] have now used updated analytical techniques on the old samples to measure life-long biochemical changes. ... levels of gut microbial metabolites, like methylamines, cresols and other aromatic compounds, were different between the two groups of dogs. ... This is significant because altered gut microflora has already been linked to obesity in humans." An interesting fact to add to the list of changes wrought by calorie restriction, and a good comparison to the ongoing primate studies.

Liver Regeneration Easier Than Thought? (April 11 2007)
http://www.eurekalert.org/pub_releases/2007-04/asfb-lrm041107.php
EurekAlert! reports that some researchers are optimistic about enhancing liver regeneration: they tested "whether regenerating cells behave like embryonic ones, as is commonly assumed for other organs. New processes may explain why the liver is so uniquely capable of renewal and repair after injury, the scientists thought. ... The results were unexpected. The researchers noticed that only a few proteins were common to both processes. Proteins called transcription factors, which affect DNA in the cell's nucleus, were highly involved in the development of embryos' livers but not in adult liver regeneration. Instead, proteins that help cells proliferate were active in both the developing and regenerating livers. These findings showed that a regenerating liver does not behave as a developing embryo. Instead, regeneration could actually be only due to an increase in cells that multiply through regular cell divisions, a process called hyperplasia. ... Not only did we discover that the number of proteins involved in liver regeneration is relatively low, but they don't include transcription factors, so we may be closer to being able to stimulate liver regeneration than we thought."

Explaining ApoE4 (April 10 2007)
http://www.omrf.ouhsc.edu/OMRF/News_Releases/Releases/2007/20070410.asp
The Oklahoma Medical Research Foundation reports on new understanding of the role of ApoE4 in the development of Alzheimer's: "ApoE4 (along with other apolipoproteins) attaches itself to a particular receptor on the surface of brain cells. That receptor, in turn, adheres to a protein known as amyloid precursor protein. The brain cells then transport the entire protein mass inside. Once inside, cutting enzymes - called proteases - attack the amyloid precursor protein. These cuts create protein fragments that, when present in the brain for long periods of time, are believed to cause the cell death, memory loss and neurological dysfunction characteristic of Alzheimer's. ... this new study is the first to connect the process of protein fragment formation to ApoE4. ... ApoE4 apparently interacts better with the receptor than its cousins. This may explain why people who carry the E4 gene have a higher risk of developing Alzheimer's." Differences in susceptibility can be used to discover biochemical mechanisms in just this way - and knowing the mechanisms in this day and age is a fast road to interfering in their progression.

More On Rebooting the Immune System (April 10 2007)
http://www.newscientist.com/article/dn11571-rebuilt-immune-system-shakes-off-diabetes.html
I've pointed out work on systematically destroying and recreating an immune system, so as to remove life-threatening damage or errant behavior. Here, the New Scientist reports on a practical demonstration of the technique: "recruited 15 people aged 14 to 31 years who had recently been diagnosed with type 1 diabetes. Roughly 60% to 80% of these patients' insulin-producing cells had been destroyed [by their own immune system] by the time of their diagnosis, and all needed regular insulin shots. The researchers removed bone marrow stem cells from the patients, who were then given drugs such as cytotoxan to wipe out their immune cells. Without an immune system, the patients were vulnerable to infection and so they were given antibiotics and kept in an isolation ward. ... Two weeks later, the patients received infusions of their own stem cells into their bloodstream via the jugular vein, which re-established their immune systems. ... Of the 15 patients, 12 no longer needed insulin shots within a few days of undergoing the procedure." How beneficial could this sort of strategy be for an aged immune system, choked by a buildup of useless cells devoted to fighting non-threatening chronic infections?

Uploading 101 (April 09 2007)
http://ieet.org/index.php/IEET/more/brain20070409/
Looking more than a single step ahead at the IEET, a gentle introduction to attaining extreme longevity through copying ("uploading") the mind into the computer hardware of tomorrow. "We are going to want to store our brain in a permanent medium. That is where this whole idea of mind uploading comes from. Back up our consciousness and run it on another medium where we don't have 30 million neurons dying every year. ... There are maybe ten to twenty different commonly discussed possible ways to do this. ... The second way is neuron simulation of some sort. You have to somehow get inside the brain, probably destructively, and look at every single neuron and see how is it connected to all the other neurons around it, how are the synapses weighted, how are the synapses connected, and somehow tease that out of the structure. ... The thing that is so interesting is that all of these things are probably possible, perhaps within 40 years." The points made on the speed of progress and our unwillingness to recognize this speed are good. It may turn out to be more efficient in the end to radically change our bodies and minds than to keep repairing what we have. But uploading as commonly presented strikes me as an expensive form of procreation - your copy will live a long, long time, but you'll be stuck exactly where you are. Or destroyed in the copying process, under some schemes.

Another Candidate For Gender Longevity Differences (April 09 2007)
http://www.eurekalert.org/pub_releases/2007-04/chop-tss040407.php
The much debated difference in longevity between human genders might be due to differing levels of stem cell effectiveness. From EurekAlert!: "Female stem cells derived from muscle have a greater ability to regenerate skeletal muscle tissue than male cells ... Regardless of the sex of the host, the implantation of female stem cells led to significantly better skeletal muscle regeneration. Based on these results, future studies investigating regenerative medicine should consider the sex of the stem cells to be an important factor. Furthermore, investigations such as ours could lead to a better understanding of sex-related differences in aging and disease and could explain, at least partially, the high variability and conflicting results reported in the literature on stem cell biology. ... [researchers] injected female and male muscle-derived stem cells into dystrophic mice and [then] calculated the regeneration index (RI) ... Only one of the 10 male populations of implanted stem cells had an RI over 200. In contrast, 40 percent of the female stem cell populations had an RI higher than 200, and 60 percent of the female populations of stem cells had an RI higher than the mean RI of the male cells (95)."

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