Longevity Meme Newsletter, January 29 2007

January 29 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.



- "Do You Want To Live Forever?" Documentary
- A Blind Book Recommendation
- Discussion
- Latest Healthy Life Extension Headlines


Allow me to draw your attention to a Christopher Sykes documentary on biomedical gerontologist Aubrey de Grey - and the Strategies for Engineered Negligible Senescence (SENS) - that will be shown on February 3rd in the UK, and should be viewable online at the same time. You'll find links and more information by following the link below:


Aging is damage, and damage can in principle be repaired. SENS is a first coherently proposed path towards rapidly developing the medical technology to achieve this end - the more attention it receives, the better, to my mind.



It seems a little odd to be making a recommendation prior to reading the book in question, but look on this as a recommendation to at least pay attention to the discussion surrounding "How to Live Forever or Die Trying: On The New Immortality." If nothing else, it reinforces the view that we need to spend much more time and effort hammering on the basics of educating people about healthy life extension, the science, and the possibilities for the years ahead. A brace of commentary can be found via the links below:


"Immortality" here is shorthand for "greatly extending the healthy human life span" or "defeating aging" - a meaning that has crept in over the years, but continues to cause confusion. It would have been nice if a different, less loaded word had come into use, but the use of loaded words is the way of journalism. In this case, I think it helps heighten and better illustrate a certain class of response to the science of healthy life extension: the greater the proposed improvement over the present dire state of suffering and decrepitude of the old, the greater the knee-jerk resistance to any consideration of the merits of the science. As this insightful fellow notes:


"Oh yes, very funny. Let's all have a good laugh at these nutters. That's how many of us will want to feel. As you read this book, your willingness to laugh will tell you something, namely that you are rather more attached to death than you thought you might be. One becomes defensive when death is challenged. That's interesting, isn't it?"


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



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/

Alzheimer's Vaccine Delivered Via Skin (January 28 2007)
Medgadget notes work on delivering vaccines for Alzheimer's via the skin: "The Alzheimer's vaccine works by triggering the immune system to recognize Ab -- a protein that abnormally builds up in the brains of Alzheimer's patients -- as a foreign invader and attack it. Previous research on an injectable Alzheimer's vaccine proven safe and effective in an animal model was suspended indefinitely when the initial clinical trial caused brain inflammation and death in a small percentage of patients. These serious side effects were secondary to an autoimmune reaction, which occurred when immune cells aggressively attacked the body's own proteins produced by the vaccine. ... transdermal immunization with Ab does not appear to trigger specific toxicities associated with past immunization strategies. Specialized immune cells prevalent in the skin, called Langerhans, may direct the body's reaction to the vaccine toward a response that is beneficial instead of overly aggressive and ultimately harmful."

The Past and Future of Longevity Science and Advocacy (January 28 2007)
Here, Anne C. comments on an issue I have brought up at times in the past: the healthy life extension advocates of 30 years ago were absolutely wrong in their focus and predictions. They existed in the old school world of producing desired changes in aging through the brute force application of simple chemicals, with meaningful success promised in the 1990s - an impossible dream, given the science of the time. Yet today advocates say essentially the same things, and with similar timescales for predictions of progress and success. Why are we right while the past generation was so wrong? The answer to this question is clear: it is the capabilities and speed of advance of modern biotechnology, the same reason that cancer will be successfully treated and managed in the late 2010s rather than the late 1980s. We must be wary, however, of falling into the same trap as those past advocates - of seeking an answer, any answer that promises success soon, at the expense of the most plausibly correct answer. We're not here to promise rescue from aging - leave that to the "anti-aging" charlatans. We're here to make meaningful, rapid progress towards the technology that will one day rescue us from aging. We need to be realistic about whether that is possible within our lifetimes - but the goal is worthy whether or not that is the case.

Science Backing Up Common Sense (January 27 2007)
At Newswise, you'll find more science backing up common sense practices for long term health: calorie restriction and exercise. "Dieting alone is equally effective at reducing weight and fat as a combination of diet and exercise - as long as the calories consumed and burned equal out. The research also indicates that the addition of exercise to a weight-loss regimen does not change body composition and abdominal fat distribution, debunking the idea that specific exercises can reduce fat in targeted areas ... It's all about the calories. So long as the energy deficit is the same, body weight, fat weight, and abdominal fat will all decrease in the same way." But exercise and calorie restriction do not have the same results on long-term health, even through they both reduce the excess fat that is a risk for many age-related conditions. "Exercise improved aerobic fitness, which has other important cardiovascular and metabolic implications." And calorie restriction has benefits in terms of resisting age-related disease that exercise does not. "For overall health, an appropriate program of diet and exercise is still the best." You're going to have wait out the arrival of real, working rejuvenation medicine - so why shorten your healthy life through neglect of the basics?

Oligonucleotides and You (January 27 2007)
You should pay attention to the basic building blocks of biotechnology - you'll be far better placed to determine hype from important breakthrough. With that in mind, have a look at this NYAS overview: "novel drugs made from short nucleic acid segments, or oligonucleotides, can target DNA and RNA to inactivate genes involved in causing disease. ... Some of these oligonucleotides have the ability to stimulate the immune system [and] could be employed against cancer, viral diseases, or as immune system boosters for vaccines or chemotherapeutics. Perhaps the most important discovery to affect the development of oligonucleotide therapeutics has been that of RNA interference (RNAi), a mechanism by which RNA inhibits gene expression. ... small 21- to 23-nucleotide double-stranded RNAs called short interfering RNAs (siRNA) [are] capable of knocking down specific gene expression to a few percent of its original level. ... Therapeutics based on siRNA are also being developed as treatments for age-related macular degeneration, respiratory syncytial virus infection, hepatitis C, and HIV infections." Perhaps most interestingly, given the prominent role of HCMV in the age-related decay of our immune systems, "RNAs known as ribozymes can inactivate viruses such as human cytomegalovirus (HCMV)."

More Investment in Stem Cell Banking (January 26 2007)
Via Fox News, an article illustrative of present levels of investment in the stem cell banking industry: "Sir Richard Branson will launch his most controversial business to date as he moves into stem-cell storage and the biotech sector ... The Virgin-branded company will be launched next Thursday and is expected to offer parents the chance to put the umbilical blood of their newborn children into cold storage. Scientists believe that future advances in medical technology will use stem cells to cure diseases such as Alzheimer's and cancer. ... Public cord storage is becoming more common, particularly in the U.S., but there is also a growing private industry taking advantage of the promise of these cures." It's a form of insurance in an uncertain world; as I've pointed out previously, it's an open question as to how rapidly the advance of biotechnology will render stored cells moot. But if the cost becomes low enough, why not bank the cells anyway? The sure way to lower cost and better service is more investment and competition between service providers.

Another "Live Forever or Die Trying" Review (January 26 2007)
Here, via the Guardian is another commentary on "How to Live Forever or Die Trying" to accompany the reviews noted in past days at Fight Aging! "Will immortality even devalue love, and work, and other things we find meaningful in this earthly life? If there is a limitation to Appleyard's field of reference, it is that he doesn't acknowledge the fact that such questions have been worried at, and dramatised, for a long time now by science-fiction writers. The colourful, scholarly, serially monogamous existences of very long-lived humans in the novels of Iain M Banks or Peter F Hamilton - the writers of 'space operas' who combine cosmological speculation with dense social imagination - certainly don't seem bored to death. And if such existences can be imagined, they may not turn out to be quite so alien to us as the pessimists suppose. Appleyard rightly notes that the initial advent of medical immortality will have huge and perhaps dangerous social consequences, but disruptive technologies always do: the question is whether the benefit - freedom from death, which is the condition of all other possible freedoms - can really be passed up."

Don't Speak For Those Who Can Speak For Themselves (January 25 2007)
Sad to say, but there exist any number of people willing to stand up and tell us how wonderful and necessary suffering and death by aging are to the world. They're all full of it, terrified of change or living - and how dare they stand up and speak for those who are aged now. Read this blog entry by a 93-year old, and consider what the Kasses and Fukuyamas of the world would like to do to all of us - condemn us all to age, suffer and die to their schedule, rather than the years we strive to make for ourselves. "At this age, I must say that I do delight in people's amazement when I tell them how old I am. But under all this is the knowledge that I am the oldest male on either side of my family, maternal or paternal, and I know I must go fairly soon. I just don't like the idea. ... There are many reasons. For too long I have behaved as if I could postpone going indefinitely, and thus have so many things that I must do first. I don't want my successors to find out how much I could have done that isn't done, not by a long shot. There are numerous notes and letters I must write. There are places I've wanted to travel, but never had the chance. Actually, each of you can, if you think yourself into my age, fill out the list. At least you can try to understand why I say that I hate to go." We strive for a world in which no-one has to experience this - in which there is no daily toll, no 100,000 deaths by each new sunset.

Linking Inflammation and Cancer (January 25 2007)
Chronic inflammation appears to raise risk across the board for the diseases of aging - it is a source of damage to the cellular machinery that is you. Here, ScienceDaily looks at an advance in understanding why inflammation leads to a greater risk of cancer: "Cellular defense is a rapid process compared to cellular development [but] safeguarding against threats and building structures have certain steps in common and require similar types of workers, or molecules. ... the parallel sets of steps in cellular defense and development [are] not distinct from one another because they are linked by a protein called p100. ... inflammation leads to an increase in p100, but that p100 is also used in certain steps in development. ... Studies with animals have shown that a little inflammation is necessary for the normal development of the immune system and other organ systems. We discovered that the protein p100 provides the cell with a way in which inflammation can influence development. But there can be too much of a good thing. In the case of chronic inflammation, the presence of too much p100 may overactivate the developmental pathway, resulting in cancer."

Turning p53 Knowledge Into p53 Therapies (January 24 2007)
EurekAlert! notes progress towards developing cancer therapies from past years of investigating the p53 gene: "p53 has long been known to play a critical role in the development of many tumors - it is mutated in more than 50 percent of human cancers. Researchers have identified a few compounds that restore p53 function, but until now, it has not been known whether such activity would actually reverse tumor growth in primary tumors. ... In normal cells, p53 controls the cell cycle. ... When p53 is turned off by mutation or deletion, cells are much more likely to become cancerous, because they will divide uncontrollably even when DNA is damaged. ... researchers used engineered mice that had the gene for p53 turned off. But, they also included a genetic 'switch' that allowed the researchers to turn p53 back on after tumors developed. Once the switch was activated, p53 appeared in the tumor cells and the majority of the tumors shrank between 40 and 100 percent. ... The study also revealed that turning on p53 has no damaging effects in normal cells. ... This means you can design drugs that restore p53 and you don't have to worry too much about toxic side effects."

Premature Aging and Calorie Restriction (January 24 2007)
An interesting and speculative post from Ouroboros: "small body size due to genetic dwarfism and calorie restriction (CR) are both known to extend lifespan in many organisms ... One would therefore expect that animals with DNA repair-related progeroid syndromes would be dissimilar in every regard from dwarf and CR animals - but [results] from a multi-lab collaboration suggest that certain kinds of (life-shortening) DNA repair deficiencies trigger the same alterations in metabolism that are activated during (life-prolonging) CR. ... Short-lived repair mutants seem to divert resources away from growth and into maintenance and repair - because they need more repair. Long-lived dwarf mutants and CR animals divert resources away from growth and into maintenance and repair - because they don't necessarily have (or don't believe they have) enough food to rapidly mature to adulthood. In both cases, we can understand the change in priorities as an attempt to wait out temporarily adverse conditions, waiting for things to change for the better so that the process of maturing to adulthood and sexual maturity can begin again. The DNA repair mutants, sadly, don't know that there's nothing temporary about their adversity."

More on Learning and Alzheimer's (January 23 2007)
EurekAlert! brings us more on the search for biochemical mechanisms linking learning with a slower progression of Alzheimer's disease: "This study with genetically modified mice is the first to show that short but repeated learning sessions can slow a process known for causing the protein beta amyloid to clump in the brain and form plaques, which disrupt communication between cells and lead to symptoms of Alzheimer's disease. Learning also was found to slow the buildup of hyperphosphorylated-tau, a protein in the brain that can lead to the development of tangles, the other signature lesion of the disease. Scientists say these findings have large implications for the understanding and treatment of Alzheimer's disease, as it is already known that highly educated individuals are less likely to develop the disease than people with less education." Use it or lose it again. What is the machinery of a more active brain doing differently? Insight at the biochemical level may inform the search for more brute-force therapies and preventions.

Attitude: Hacking Life Span (January 23 2007)
A truth about the engineering mindset from Wired: "Engineers accept that anyone who understands a system also has the power to change it. A real engineer refuses to accept bugs in any code, whether his own, his tools, his operating system or his own body." Biology is information: a mesh of operating systems and programming languages built out of molecules and evolved into a state of complexity. With understanding and tools, control will follow. This is all true. Unfortunately, the author of this article falls into the same old trap of failing to see the difference between the dead end path of pharmacology and basic good health - that will leave us aging and dying in the same way as we are now - and the open path of supporting and encouraging serious research aimed at repairing the damage of aging. It is the latter path of rejuvenation engineering that will lead to radical life extension - healthy, youthful lives of centuries and more. But we won't get there if all that people see is the next drug, the next metabolic tweak to slightly slow the rate of damage. There is a better way forward. Scratch that - there is only one way forward that will not lead all of you reading this now to death by aging, and that is full steam ahead to repair the damage of aging with biotechnology, not slow the rate of damage with metabolic drugs.

Gene Therapy To Knock Out the Tools of Cancer (January 22 2007)
A growing tumor is successful in its fight to kill the aging body that hosts it by evolving its way into the set of mutations that best help its growth - but what if we could remove the best and most obvious tools from the cancer growth toolkit? Progress in that direction can be found at the Independent: "Doctors often describe cancer as a genetic disease because of the role played by genes in causing the uncontrolled proliferation of a cancerous cell into a tumour. The radical approach is to use molecules of RNA - a substance similar to a gene's DNA - to 'silence' or switch off certain key genes known to be involved in the growth of tumours. One team [has] shown in a laboratory study that it is possible to use large molecules of RNA to switch off a gene responsible for an enzyme called dihydrofolate reductase (DHFR), which is essential for the rapid proliferation of tumour cells. Another team [has] used smaller molecules of RNA in an animal study to switch off a separate gene known to be involved in the rapid growth of brain tumours."

Screening For Longevity Interventions (January 22 2007)
CCNews notes that researchers at the Buck Institute for Age Research are embarking upon a large screening exercise, searching for new ways to manipulate metabolism to extend longevity: scientists "will screen as many as 120,000 chemical compounds over the next four years to discover which ones impact lifespan in four research models - yeast, nematode worms, fruit flies and mice. ... at the very least we hope to identify 100 chemically distinct compounds that slow aging, opening up new avenues to treat, prevent or postpone age-related conditions ... The largest number of compounds will be screened, in many cases via the use of robotics and other high-tech devices, in the simplest organisms - budding yeast and nematode worms. Chemicals that extend lifespan in those species will go on to be tested in the fruit fly. Chemicals that cause all three species to live longer will be looked at in mice, to see if there is a reversal of the molecular characteristics of aging. The evolutionary distance between yeast and worms predicts that compounds active in both these species are likely to be relevant to mice and humans."



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