Longevity Meme Newsletter, January 15 2007

January 15 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.



- Two Conferences of Note For 2007
- Four Years of Longevity Meme Newsletters
- Discussion
- Latest Healthy Life Extension Headlines


Two conferences from the folk behind the Methuselah Foundation will be held this year, and are worthy of your attention. Firstly, the Edmonton Aging Symposium in March:


"This symposium is designed to bring an awareness of the rapid pace of the development of intervention-oriented therapies in age-related dysfunction to the educated layman and lab-hardened researcher alike, as well as draw the attention of policy-makers to the massive economic benefits available to those who create an environment where these technologies can be developed and implemented at all possible speed."

Secondly, the third Strategies for Engineered Negligible Senescence (SENS) conference is scheduled for September


"The purpose of the SENS conference series, like all the SENS initiatives (such as the journal Rejuvenation Research and the Methuselah Mouse Prize), is to expedite the development of truly effective therapies to postpone and treat human aging by tackling it as an engineering problem: not seeking elusive and probably illusory magic bullets, but instead enumerating the accumulating molecular and cellular changes that eventually kill us and identifying ways to repair - reverse - those changes, rather than merely to slow down their further accumulation."

Registration is presently open for both conferences; in each case, I think you'll recognize the weight and reputation of the folk listed in the program. The contingent of those within and without the scientific community willing to put their weight behind serious efforts to extend the healthy human life span is growing with each passing year. A very good thing for our future health and longevity!


This marks something of an anniversary, give or take a few days - it's been four years since the first newsletter went out to a hundred or so folk in healthy life extension community. If you care to take a look, all the newsletters remain available online:


I've learned a great deal in these years of leafing through the popular science press, and in my association with groups like the Methuselah Foundation, Immortality Institute and Calorie Restriction Society. Beyond the clutter and useless noise of the "anti-aging" marketplace, there really is an opportunity for real science and meaningful progress towards greatly extending our healthy life span. Cutting through the nonsense to find this out for myself required far too many years, back in the day - I hope that I've trampled out more of a trail for you:



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/

Mitochondrial Uncoupling and Tissue Aging (January 14 2007)
Mitochondria are the powerplants of your cells, churning away to turn food into ATP, the common currency of cellular energy. They are also a factor in aging, via the creation of damaging free radicals (such as reactive oxygen species) as a side-effect of their chemical processing. Mitochondrial uncoupling is much as it sounds; a feedback mechanism in which processing is disconnected from ATP production; energy from food goes elsewhere, as heat for example. Because this affects free radical production, it seems to be important in tissue aging: "Faster aging is predicted in more active tissues and animals because of greater reactive oxygen species generation. Yet age-related cell loss is greater in less active cell types, such as type II muscle fibers. Mitochondrial uncoupling has been proposed as a mechanism that reduces reactive oxygen species production and could account for this paradox between longevity and activity. ... These results reject respiration rate as the sole factor impacting the tempo of cellular aging. Instead, they support mild uncoupling as a mechanism protecting mitochondrial function and contributing to the paradoxical longevity of the most active muscle fibers."

Improving Control of Stem Cells (January 14 2007)
A common theme at the Longevity Meme is the scientific path towards ever greater, more precise and useful control over our cells - and stem cells in particular, given their importance to cancer, some manifestations of aging and regenerative medicine. Here, EurekAlert! looks at another step forward: "researchers genetically mapped a stem cell gene and its protein product, Laxetin ... This particular gene is important because it helps regulate the number of adult stem cells in the body, particularly in bone marrow. ... The only stem cell population that has been examined for effects of Latexin to date is in bone marrow. ... it is possible, even probable, that other stem cell populations in tissues such as the liver, skin, pancreas or brain may be similarly affected by Latexin. This could open up new therapeutic strategies such as using stem cells for the treatment of other diseases and conditions such as liver disease, diabetes and central nervous system damage as a result of trauma or stroke. ... The findings also will help scientists develop effective methods to modulate stem cell numbers and function for therapeutic uses, and also provide a better understanding of the age-related changes that occur in stem cells."

Another Nanoparticle Demonstration (January 13 2007)
As I've mentioned in the past, scientists are making great strides in applying nanoparticles to therapies requiring the carefully destruction of specific cells - such as cancers. The trick is to use the nanoparticle as a keychain to hold all the biochemical keys, homing devices, sensors, identifiers and therapies needed to get the job done. Over at Nanowerk, you'll find another example of this sort of work, complete with some nice diagrams: researchers "designed nanoparticles they dubbed Probes Encapsulated by Biologically Localized Embedding (PEBBLEs) to carry a variety of agents on their surface, each with a unique function. The particles consist of an iron oxide core that serves as an MRI contrast agent. Attached to them are copies of a cancer-targeting peptide called F3, as well as a light-absorbing compound called photofrin that kills cells when hit with red light. When [researchers] used their PEBBLEs to treat rats previously injected with cancer cells inside their brains they saw very clear results: A single IV injection of a targeted therapeutic nanoparticle dose, coupled with a single 5 min photodynamic therapy treatment, leads not only to an increase in the rat survival rate but accomplishes complete tumor remission."

Oh Woe, the Future Will Be Better (January 13 2007)
Over at cnews you'll find an article that tries valiantly to make the technologies of the future look like terrible, horrible challenges. This sort of journalistic silliness is far too common. A cure for cancer! Better, more resiliant bodies! No more disease and frailty! Oh no, how will we cope? "Schroeder describes the kind of albatross midnight's children may have to bear. During their lifespan - described as possibly indeterminate by many futurists - this generation could reach what Schroeder calls 'technological maximum' - the peak of technology when humans have exhausted all their potential." More accurately, the point at which this fellow's rather limited imagination can't keep up. The world isn't bounded by what one person can imagine. Thankfully. "We'll still get killed in a car accident, get sick and die, get shot and commit suicide. Death will not go away. What will go away is the assumption that after 70 years, you'll die of natural causes . . . that has huge impacts on society." How horrible, that tens of millions will not be forced to suffer, decay and die each year. What a curse it will be, this promised removal of pain, anguish and millions of deaths. How will we bear it?

Life Span as a Stochastic Result (January 12 2007)
From Ouroboros, a look at the way in which the relationship between your genes and their effect on your life span is both a little random and a little determined: "[I]n humans only about 25% of the variation in life span can be ascribed to genetic factors to any degree, and even in lab animals where variables can be greatly reduced, only 10-40% of the life span variation has a genetic component. ... Life is like a long dice game, and while starting with a good endowment might let you keep playing for a longer time, eventually everyone craps out, and a run of bad luck can wipe out even the richest starting position rapidly. In between these extremes of genetic predetermination and pure luck, though, a recent paper in Nature Genetics finds another possibility: factors in the organism that are not heritable, yet from an early age can be reasonably good predictors of mortality." It's all very interesting - but you shouldn't forget that the real determination of your healthy life span will be made by the efforts of you and those you band with to support the development of working anti-aging medicine.

The Third SENS Conference (January 12 2007)
Early registration is now open for the third Strategies for Engineered Negligible Senescence (SENS) conference: "The purpose of the SENS conference series, like all the SENS initiatives (such as the journal Rejuvenation Research and the Methuselah Mouse Prize), is to expedite the development of truly effective therapies to postpone and treat human aging by tackling it as an engineering problem: not seeking elusive and probably illusory magic bullets, but instead enumerating the accumulating molecular and cellular changes that eventually kill us and identifying ways to repair -- reverse -- those changes, rather than merely to slow down their further accumulation. Almost 50 illustrious speakers are already confirmed. ... SENS 3 will therefore continue and extend the superlative quality of the first and second SENS conferences, held in 2003 and 2005. The calibre of those meetings can be seen from the abstracts [IABG10, SENS2], the online audio recordings of the talks [IABG10, SENS2] and most of all from the proceedings volumes, which were published as volume 1019 of the prestigious Annals of the New York Academy of Sciences and as issues 9(1) and 9(2) of the high-impact (IF 8.571) journal Rejuvenation Research."

More on Calorie Restriction and the Immune System (January 11 2007)
ScienCentral looks at recent research into the beneficial effects of calorie restriction on the aging immune system: "when we say caloric restriction we typically mean ... taking about a third fewer calories, or about 30 percent [of] calories, compared to what you would take if you had no dietary restriction at all. And ... not only do animals live longer under this treatment, but also they're much, much healthier. They don't seem to be showing many of the diseases characteristic of old age. ... monkeys on caloric restriction had significantly stronger immune systems. They had more immune cells overall, and, most significantly, had more of a valuable type of immune cell called a naive T cell. Most naive T cells are created early in life. Once they get called into action to fight a specific pathogen, they turn into 'memory T cells' that are only capable of fighting that specific pathogen. But naive T cells are capable of attacking any pathogen, including ones the body has never encountered. ... As we use this naive T cell reserve, we're less and less really prepared to fend off new pathogens."

Update on Telomere Length and Heart Disease (January 11 2007)
Scientists have been looking into telomere length and age-related decline for a number of years now: "The researchers, who measured telomere length in leukocytes, or white blood cells, in 1,500 men aged 45-64 years old, found short telomeres indicate a higher likelihood of developing heart disease. ... Telomeres protect the ends of chromosomes from fraying. They shorten each time a cell divides and the loss is associated with ageing. As telomeres get smaller, the chromosomes can become unstable and at greater risk of mutation. Earlier research had shown that people with heart disease have shorter telomeres but it was not clear until now if telomere length could be a predictive marker for the illness. ... They have shown that it is a predictor. It doesn't say it is functionally linked to heart disease but it is certainly associated with it." The next steps involve a better understanding of how this all fits together - is more pronounced telomere shortening only a symptom of years of stressed and worn biochemistry, or is it sufficiently high in the chain of cause and effect to merit preventative therapies aimed at reducing the progression of age-related decline?

A Little Biochemistry of "Use It Or Lose It" (January 10 2007)
When exercise, mental and physical, improves your condition, this means that a great many changes are taking place in your cells. You are a machine composed of many, many machines; wear and tear in you is built of wear and tear at the level of cells and molecules. "Mice with (a) high spontaneous neurological activity, or subjected to (b) moderate exercise or (c) dietary supplemented with high doses of vitamin E from [showed] an increased survival and a retardation in the development of the neurological deficits associated to aging. During aging there was an increase in dysfunctional brain mitochondria, characterized by an increased content of oxidation products and by a diminished functional activity. ... In brain mitochondria, the activities of enzymes that are critical for mitochondrial function [decreased] progressively during aging. ... increased neurological activity, moderate exercise, and vitamin E supplementation, proved to be effective in increasing mice survival and neurological performances, along with a better mitochondrial function and a lower content of oxidation products." Use it or lose it.

Another Key To Calorie Restriction Biochemistry (January 10 2007)
Scientists continue to narrow down the biochemical components vital to healthy life extension through calorie restriction (CR). A recent paper (the full PDF is freely available) pins CR effects in yeast down to one gene in the mitochondria: "Deleting the LAT1 gene abolishes life span extension induced by CR. Over-expressing Lat1 extends life span and this life span extension is not further increased by CR. Similar to CR, life span extension by Lat1 over-expression largely requires mitochondrial respiration indicating mitochondrial metabolism plays an important role in CR. Interestingly, Lat1 over-expression does not require the Sir2 family to extend life span, suggesting Lat1 mediates a branch of the CR pathway that functions in parallel to the Sir2 family. ... Our studies suggest that Lat1 over-expression extends life span by increasing metabolic fitness of the cell. CR may therefore also extend life span and ameliorate age-associated diseases by increasing metabolic fitness through regulating central metabolic enzymes." At the present rate of research, I imagine it won't be long before the relevance of this finding to mammals is known.

On the Development of Sirtuin Activators (January 09 2007)
Chris Patil notes a number of recent papers on progress towards the commercial deployment of sirtuin activators - calorie restriction mimetics, in other words - and ostacles yet in the way: "Given the current regulatory laws in the US and elsewhere, getting drugs approved as anti-aging therapies per se is difficult to say the least, approaching the level of practical impossibility. Beyond the political and sociological challenges of defining aging as a pathology in itself are a huge number of nuts-and-bolts issues: How does one measure successful delays in aging? How does one define a Phase I (or II, or III) population, and secure subject compliance over the relevant timescales? But suppose compounds with anti-aging properties (to be more precise, I should say, 'compounds that target pathways known to modulate lifespan in experimental organisms') are approved for clinical treatment of acute or shorter-term chronic diseases, where the trial populations and standards for efficacy are easier to define. We'd then have anti-aging drugs ready for off-label use after they've been proven effective for their on-label purpose."

Machinery Will Make Us Long-Lived and Utterly Healthy (January 09 2007)
Those of us who live to see the world four decades hence will have access to a panoply of impressive medical nanomachinery and biotechnology, as Michael Anissimov points out: "Between 20 and 40 years into the future, we will become capable of building artificial antibodies that outperform their natural equivalents. ... Through their presence and continued operation, they will eliminate all susceptibility to disease in those who have them running through their veins. ... The ultimate upgrade would be [physical] immortality. Everything else pales by comparison. Today, there are already entire movements based around the idea. Realizing the possibility of immortality requires seeing a human being as a physical system - composed of working parts that cooperate to make up the whole, some of which have the tendency to get old and break down. ... Defeating aging, then, would simply require addressing these one by one." We're rubbing sticks together in biotechnology today in comparison to what is known to be possible - but today's work is absolutely necessary if we are to live long enough see the wonders yet to come.

Ever More Capable Nanoparticles (January 08 2007)
(Via EurekAlert!). Medical researchers are demonstrating the construction of ever more complex nanoparticles; as soon as you can safely chain together multiple utility molecules, the sky is the limit. Every new key to metabolism and cellular processes is another tool to add to your latest creation. This is important, because these sorts of modular nanoparticles are looking very promising indeed when it comes to curing cancer. For example, researchers have "developed nanoparticles that seek out tumors and bind to their blood vessels, and then attract more nanoparticles to the tumor target. ... the homing nanoparticle could be used to deliver a 'payload' of an imaging compound, and in the process act as a clotting agent, obstructing as much as 20% of the tumor blood vessels. ... we are now optimizing the process, hoping to obtain a more complete shut-down of blood flow into the tumor to strangle it. We are also in the process of adding a drug delivery function to the particles. These two approaches are synergistic; the more particles we bring into the tumor, the greater the obstruction of the blood flow and more of the drug is delivered into the tumor."

Geriatrics, Gerontology and Engineering (January 08 2007)
From Anne C.: "At a meeting yesterday with a group of fellow longevity advocates, one issue that turned into a point of discussion was that of whether it is worth presenting longevity treatments as means to mitigate specific diseases, or whether doing so is simply a distraction from the fundamental issue of addressing aging itself (or whether it really matters). ... Geriatricians are devoted to the alleviation of pain and maintenance of healthy functioning (at least as much as possible) in the face of age-related pathology ... On the other side of things, gerontology is interested in things like root causes and systemic differences between young and old bodies, however, the gerontological approach is more exploratory than action-oriented ... The engineering approach to addressing age-related decline and death is something of a new approach -- one that very well might be the needed 'missing link' between geriatrics and gerontology. An engineering approach is one that focuses on appropriate maintenance of bodily systems, through repair and replacement of worn-out or disease-causing physical elements."



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