Longevity Meme Newsletter, November 17 2008

November 17 2008

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.



- Conversing on Radical Life Extension
- On Genetic Redesign for Longevity
- Discussion
- Latest Healthy Life Extension Headlines


The popular link site Reddit hosted a very active discussion on radical life extension for a few days last week. The trend towards a greater proportion of positive views of engineered longevity in these large online discussions seems to be continuing - a sign of progress. You'll find a link and excerpts in the following Fight Aging! post:


"Obviously entirely new systems would come into play. We can't see what they will be now, but they will be self-evident once they evolve. To extrapolate current systems into extremely long lives, where people could keep their health and strength and work at what they want far longer than they do now, is bootless. Maybe with a greater time span of non-age-ossified brains people would have time to emotionally mature more than they do now, and make better decisions. Certainly there would be time to use the power of compounding interest to far greater advantage than is possible now. With youth and vigor extended, the expansion of life-possibilities would be immense, and would extend into spaces we can't even see."


Reworking human genetics and metabolism so that we age more slowly is possible, but very much the slow, rocky road that will lead to little benefit for those already old when therapies finally emerge:


"If you had to pick the absolute hardest, most challenging goal possible in biomedical science, I think it might be to alter the genes of adult humans so as to safely extend healthy life. Yet this is pretty much the course of the mainstream aging research community - and so I believe they are setting themselves up for maximal expense and minimal progress."

There is another, far better way forward - which is to keep the genes and metabolism we have, and learn how to repair the accumulated biochemical damage that causes aging. Scrub away the rust on the regular basis, in other words, rather than trying to invent a new type of engine that rusts less rapidly. This type of approach is outlined in the Strategies for Engineered Negligible Senescence:



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!




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/

Researchers on Aging (November 14 2008)
An article of quotes from various noted aging reseachers: "Aging is caused by the gradual, lifelong accumulation of a wide variety of molecular and cellular damage ... The free radical theory is the most widely accepted theory of aging. But the idea that aging is caused by one thing is naive. One general theory can never fit all. Clearly, it's the combination of genes that your parents dealt you and the lifestyle choices you make and the environmental toxins one is exposed to. One need only count the number of ways a car will fail to start to appreciate that aging can be caused by a large number of problems. Like any machine, it's going to wear out ... about 25 percent of how a person ages is due to inherited genes. Certain genes control a cell's ability to repair damaged DNA. If those genes are defective, they can't do their job. ... Not everybody will be susceptible to diseases like Parkinson's or cancer as they age. But each one of us will lose muscle mass and muscle strength. That's why this research is so important. Frailty affects all of us."

Enhanced Longevity Through Telomerase (November 14 2008)
From Science News: "the enzyme telomerase can extend the lifespan of mice by about 24 percent. ... Telomerase lengthens telomeres - the 'caps' on the end of chromosomes that protect DNA from damage. Like burning fuses, telomeres normally get shorter each time that most body cells divide. ... While the enzyme enables cells to keep dividing, it also takes cells one step closer to growing and proliferating out of control - that is, becoming cancerous. Lab animals with extra genes for telomerase often die young from tumors. ... [researchers] engineered mice to have not only an extra copy of the gene for telomerase, but also extra anti-tumor genes to combat the enzyme's cancer-causing potential. In the altered mice, signs of aging such as poor coordination or degraded tissue health were delayed compared to mice that had only the extra copies of anti-tumor genes." Most interesting; you might also want to look at recent research that suggests telomerase operates by protecting mitochondria, and less damaged mitochondria means better preservation of telomeres - but, more importantly for life span, less oxidative stress.

Better Synthetic Cartilage (November 13 2008)
From ScienceDaily: "Until now, creating synthetic cartilage was complex but not impossible. The problem was that it was impossible to imitate the perfection of human cartilage due to the difficulty in orienting the collagen nanofibers [in] a particular configuration: in parallel, in a circle, or crossed. The fibers that form the cartilage that protects the knee are aligned in parallel. ... [Researchers have now] achieved this using the electrospinning method. ... collagen nanofibers are obtained by exposing the collagen to electrical discharges. The collagen is extruded, in the form of a nanofiber thread, through a fine needle and is deposited on an electric collector consisting of two grounded plates. The student placed a nonconductive material between the two conducting plates. The nanofibers aligned on top of each other perfectly in parallel lines between the two conducting plates." Innovations in engineering the simpler forms of human tissue have been arriving more rapidly of late - more scientists are involved, the tools are improving, and the cost of research is falling. This is all groundwork for the next decade and tissue engineering of complex replacement organs.

Steps Towards Liver Regeneration (November 13 2008)
Discovering a stem cell population is the first step to regenerating the tissue they support: "A novel protein marker has been found that identifies rare adult liver stem cells, whose ability to regenerate injured liver tissue has the potential for cell-replacement therapy. ... In the future, this marker will allow for the isolation and expansion of these stem cells, which could then be used to help patients whose livers can no longer repair their own tissue. ... In a healthy liver, proliferation of mature liver and bile-duct lining cells is sufficient to maintain the necessary size and function of the organ. This even works when the liver is confronted with mild and acute injury, but the situation changes when injury to the liver is chronic and severe ... For chronic injury, the liver uses a back-up system that stimulates stem cells to proliferate and eventually differentiate into new liver cells. [Researchers] found that these dual-potential stem cells can be identified and potentially isolated from other liver cells."

More on Myelin Loss (November 12 2008)
You might recall that age-related thinning of the myelin that insulates nerves strongly correlates with declining brain function. Researchers investigating MS are making progress into the mechanisms by which this happens: the protein netrin-1 "is known to guide and direct nerve cell axons to their targets. ... blocking the function of netrin-1 and one of its receptors in adult neural tissue causes the disruption of myelin. ... We've known for just over 10 years that netrin is essential for normal development of the nervous system, and we also knew that netrin was present in the adult brain, but we didn't know why. ... the new findings show that netrin-1 and its receptor are needed to hold paranodal junctions in place, and thereby maintain the structure of myelin. The paranodal junction is a highly specialized region of contact where an oligodendrocyte cell attaches itself to the nerve cell's axon. This juncture acts as a molecular fence, which organizes and segregates the distribution of key proteins along the nerve cells axon and plays an imperative role in the proper conduction of electrical signals along the length of the nerve cell. When the function of netrin-1 and its receptor is disrupted, the organization of this adhesive junction comes apart, disrupting the function of nerve cells in the brain and spinal cord."

The Economist on Targeted Therapies (November 12 2008)
From the Economist: "a second generation of nanoparticles has entered clinical trials. Some are so good at hiding their contents away until they are needed that the treatments do not merely reduce side-effects; they actually allow what would otherwise be lethal poisons to be supplied to the tumour and the tumour only. Others do not depend on drugs at all. Instead, they act as beacons for the delivery of doses of energy that destroy cancer cells physically, rather than chemically. ... To get them to the cancer, you whip up a batch of, say, 80 trillion of them and inject it into the patient's bloodstream. The particles end up in the tumour, rather than in healthy tissue, because tumours have abnormal blood capillaries. The pores in these vessels are larger than those in healthy tissues. Make your nanoshells the right size, then, and they can pass through the capillary pores and lodge in a tumour, but not in a normal organ. Twelve to 36 hours later, when enough shells have accumulated, you insert an optical fibre into the tumour, and deliver an appropriate blast of infra-red. That heats the particles up and cooks the tumour."

Hourglass V (November 11 2008)
The fifth Hourglass blog carnival on the science of aging and longevity is hosted at psique: "It seems that prohibiting olfaction pharmacologically, by ablation of olfactory regions or genetic manipulation can result in an extension of life span, at least in C. elegans and Drosophila. Interestingly, [calorie restriction (CR)] and blocking olfaction appear to act in synergy, increasing life span most effectively when applied together, while exposure to food odours is capable of reducing the positive effects of CR to some extent. The obvious question is whether losing the sense of smell could also extend life span in humans. Failing the possibility of clogging up people's noses, Plunet proposes a straightforward test - one could compare the life span of anosmics, who are people that have chronically lost their ability to smell for a variety of reasons, to carefully matched controls."

Engineered Longevity and Its Detractors (November 11 2008)
Via the Daily Galaxy: biomedical gerontologist "Aubrey de Grey has famously stated, 'The first person to live to be 1,000 years old is certainly alive today ... whether they realize it or not, barring accidents and suicide, most people now 40 years or younger can expect to live for centuries.' Perhaps de Gray is way too optimistic, but plenty of others have joined the search for a virtual fountain of youth. In fact, a growing number of scientists, doctors, geneticists and nanotech experts - many with impeccable academic credentials - are insisting that there is no hard reason why ageing can't be dramatically slowed or prevented altogether. Not only is it theoretically possible, they argue, but a scientifically achievable goal that can and should be reached in time to benefit those alive today. ... But not everyone thinks ageing can or should be cured. Some say that humans weren't meant to live forever, regardless of whether or not we actually can." From there the piece leads into a rogue's gallery of quotes from pro-death advocates who want to see us all age, decay, and slowly, painfully die.

Brain Growth Receptors and Lifespan (November 10 2008)
A very readable overview of recent research from PLoS Biology: "When resources are short, growing organisms face an existential choice: should you ignore the shortage and hope for better times soon, or scale back and live within your limited means? And if you do scale back, will there be any payoff later in life? For animals, these choices are played out hormonally, with environmental fluctuations leading to internal rearrangements in endocrine signal and response throughout the growing body. In mammals, two principal hormones - growth hormone (GH) and insulin-like growth factor 1 (IGF-1) - promote growth. Remarkably, inhibiting one or both of these two not only retards growth, but also extends lifespan, not just in lab animals, but possibly also in people: mutations that reduce the function of the IGF-1 receptor have recently been discovered in centenarians (who are also short). Growth occurs throughout the body, and receptors for IGF-1 are found in every organ on virtually every cell. But [researchers have now shown] that it is the IGF-1 receptors in the brain that set the pattern for growth and lifespan."

Mainstream Press on the Singularity and Longevity (November 10 2008)
An interesting, if flawed, article on the singularity and engineered longevity via the Korean OhmyNews: "Amidst the rapid changes of society ranging from general advances in science and technology to politics and social policy, with respect to knowledge, there is an emergent issue that promises to radically change our lives and our reality. It is predicted that within less than 20 years, the human lifespan will be extended to perhaps 150 or more years. Scientists and futurists on the cutting edge of thought about science and society believe that the increase in lifespan is one step towards what will be known as the Singularity, at which time, life might be extended indefinitely depending upon environmental conditions. The Singularity is the term used for a technological integration unheard of; it is a theoretical future point of unprecedented technological progress, caused in part by the ability of machines to improve themselves using artificial intelligence. ... it was just over a hundred years ago, when the human lifespan began to double to what it is today. It is possible that most people who lived only to 35 years of age thought that to live to 72 years would be too long and that they would be too tired. Nevertheless, we have adjusted and found life to be meaningful, even in our current 'long' life of 72 years."



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