Longevity Meme Newsletter, March 19 2007

March 19 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.



- If the Purpose of Medicine is to Save Lives...
- Thoughts on Our Role in Producing the Future
- Discussion
- Latest Healthy Life Extension Headlines


You will find an interesting discussion underway in the comments to this Fight Aging! post:


"If you look for the greatest source of suffering and death in this world, you will find aging ... There is no greater single target for medicine - and yet we advocates for healthy life extension are forced to fight an uphill battle to effectively direct research to this end. There may be a cancer research establishment, an Alzheimer's establishment, even an aging research establishment, and so forth, but there is no longevity research establishment."

That is the starting point. Is aging the greatest cause of suffering? What resource allocations make sense to you when it comes to research and development? Who chooses? What are the plausible near future results of any attempt to enact change in these areas? How should these inform our support and actions?


The links below lead to a few other opinions from Fight Aging! in the past week that may prove to be worth a few moments of thought. All come back to our role in progress, in building the future - that is what we're busily engaged in each and every day, no matter what our actions, but how much of our work actually goes towards the future we'd like to see?


"Transhumanism, make no mistake, is just a fancy name for common sense. Change for the better is good, right? Common sense. It's what we humans do in our scattered finer moments - we work to change things for the better. It's common sense to fetch in the harvest on wheels rather than on foot, and it's common sense to repair the biomolecular damage of Alzheimer's before the mind begins to rot. It's common sense to build perfect immune systems from nanomedical robots, and it's common sense to develop the technologies of regenerative medicine to their logical end. It takes work, but what is work compared to a world of suffering? Choosing not to attain these goals makes about as much sense as standing out in the rain to spite yourself."


"Look around you the next time you're out and about; the tapping cane of a bent old man who can no longer walk unaided; the nagging cough of the elderly woman possessed of an age-damaged immune system; the pained hesitance of an arthritic senior citizen organizing materials to write a check. Folk all around you struggle and suffer over matters to which you give little thought; worse, the ones you recognize will vanish, day by day and one by one. Aging keeps death busy. Barring sufficiently rapid and radical progress in medical technology, the pain and frailty of the old form a mirror for your future regrets. Two decades hence, three decades, five, will you regret your inaction, your failure to materially support the advance of medicine at a time when your contributions would have made a great difference?"


"For all we know, yes, the projected rise of technology will lead to immensely powerful individuals and societies, as well as a complete understanding of the universe to the point at which every past event can be recreated. It's an idea that has been explored with serious intent by cosmologist Frank J. Tipler as well as in the fiction of other authors, such as Greg Bear. But I don't think it's wise to live one's life under the assumption that any of this is plausible - letting what-if speculation in physics be the guide to your life is just as much a leap of faith as temples, the supernatural and the grave."


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/

More CIRM Grants Disbursed (March 18 2007)
For those following developments at the California Institute for Regenerative Medicine (CIRM), the San Francisco Chronicle reports on the latest set of grants: "Twelve institutions, all nonprofits or part of the UC system, shared 29 large 'comprehensive' grants worth $74.6 million. Two other smaller grants, totaling $1.1 million, were added to a previous list announced last month. Scientists at UCSF and its affiliated J. David Gladstone Institutes, followed closely by Stanford University researchers, topped the comprehensive grant totals, receiving seven grants worth about $18 million. Dr. Deepak Srivastava at the Gladstone Institute received the biggest single grant, $3.1 million, for a project to unravel how molecules known as microRNAs help guide the development of stem cells into heart muscle cells. Stanford got seven grants, for $17.7 million, including a $2.4 million grant to a UCSF researcher, Renee Reijo Pera, who recently announced a move to Stanford to pursue a cloning technique known as somatic cell nuclear transfer." The full list of grants and research programs can be found in the PDF release at the CIRM website.

Another Way To Target Cancer (March 18 2007)
Researchers and medical engineers are taking the building blocks provided by modern biotechnology and assembling impressive technology demonstrations of effective cancer therapies. VOA News reports on one of the latest: "We put radio-labeled antibodies that we know bind to breast cancer on the nanoparticles' surface, and then injected them into mice in which we had implanted a very aggressive human breast cancer. ... The antibody-nanoparticle combinations attached themselves to the breast cancer tumor cells. Then the researchers applied an external 'alternating magnetic field' (AMF) to the area around the tumors [causing] the iron nanoparticles to become very hot. The heat then kills the breast cancer cells without harming the healthy tissue around the tumor. ... If we give, in 20 minutes, a certain dose of the alternating magnetic field into the tumor area, we know the dose of heat we should have created on the tumor. .. The tumors basically responded, some of them going away, some of them slowing in their growth rate, and that correlated closely with the calculated heat dose."

Longevity and Evolution (March 17 2007)
It is interesting that scientists are finding so many comparatively minor mutations that extend the healthy life spans of lower animals; why didn't evolution lead to those mutations in the first place? From Ouroboros: "Why, then, are these artificially created mutant alleles not the wildtype? In other words, if lacking a particular gene makes an animal longer-lived and more vigorous, why do all wildtype members of the species have the gene in the first place? ... longer-lived mutants are significantly less fit, in an evolutionary sense, than the wildtype. ... the fitness decrease isn't caused by the overall decrease in lifetime fertility, but rather the delay in early-life reproduction. This makes sense, in the relentless logic of exponential growth: The earlier one reproduces, the earlier one's progeny are available to do reproduction of their own. ... It's pretty clear that eventually the short-lived early-reproducer would out-compete the long-lived late-reproducer, even though [the] total lifetime fertility of the longer-lived variant is actually higher. ... Traits that shorten the overall lifespan can be positively selected for if they increase the reproductive success (fitness) of the organism." Which is a tragedy of biology inflicted upon our ancestors - but we are now in a position to start to do something about it.

Thoughts on Degeneration and Repair (March 17 2007)
FuturePundit contemplates degeneration and repair as they pertain to our eyes: "Some people are content to grow old and even try to justify the changes which happen to our bodies as the various pieces break down. But this all seems like loss to me and with no compensating upside. The tiny muscles in your irises become less able to adjust pupil sizes and so your pupils can't dilate as far and as quickly to let in more or less light as needed. As far as I'm concerned this is yet another argument for treating the development of rejuvenation therapies as an urgent matter deserving a massive research push. ... Some labs are working on designs of artificial replacement lenses. Also, other labs are working on ways to grow natural replacement lenses using cells and tissue engineering. One way or another we'll some day be able to replace aged lenses with lenses as young as those of a baby. But we need much more in order to do eye rejuvenation. ... Further on down the road we'll eventually witness the development of tissue engineering technologies so advanced that they can grow whole organ replacement parts. Replacement eyeballs will then provide much more thorough and comprehensive solutions to the problems of aging eyes."

Growing Replacement Cornea Tissue (March 16 2007)
One small piece at a time, scientists are developing the means to replace damaged portions of your body. Here, via the Daily Yomiuri, is another part of the eye, to go along with progress in regenerating retinal cells: "A team of researchers at Tokyo University Hospital has succeeded in using a cornea cell to grow cornea epithelial tissue, which is essential for treating deteriorating eyesight caused by damage to the surface of a cornea caused by the side effects of medicine or drugs. ... [the researchers] harvested limbal cornea from the peripheries of the pupils. The team then used an enzyme to turn the limbal cornea into pieces to cultivate it. The pieces grew into clumps with a diameter of 0.3 millimeters in about one week. Three weeks later, they became cornea epithelial tissue in sheets with a diameter of about two centimeters. The three-dimensional tissue is similar to ordinary cornea epithelial tissue. Yamagami said he planned to make a clinical application for it in several years."

Towards New, Engineered Immune Systems (March 16 2007)
The New Scientist reports on another step forward for medical engineering: "a 'bioscaffold' made of collagen impregnated with stromal and dendritic cells extracted from the thymus of newborn mice [was] then implanted into mice with healthy immune systems that had been vaccinated against a harmless antigen (something that triggers an immune response). ... After the artificial node had filled with antigen-specific T and B cells, Watanabe transplanted it into a mouse with no functioning immune system. The lymphocytes quickly spread out from the artificial node into the animals' own lymph nodes ... After a month, these cells' 'memory' was still maintained, and they were able to fight off challenges from the antigen. ... The next step is to use human cells in humanised mice. Then, maybe in four or five years, we might be able to make the first prototypes of a human model ... By implanting artificial nodes plump with healthy T and B cells in AIDS patients, he believes he might be able to revitalise their damaged immune systems. For cancer, he hopes to adopt a similar approach in which the transplanted nodes will contain T cells trained to hunt down the antigens produced by tumour cells and kill them off."

The Slow Creep of Ideas, Part 2 (March 15 2007)
Here is another characteristically mixed article from the Herald; There is progress in awareness of present scientific backing for healthy life extension, but the default position still seems to be to "reach for the off switch," as Aubrey de Grey puts it. "Pupils will gather in Edinburgh tomorrow for the Scottish finals of the Institute of Ideas' Debating Matters competition. The motion? 'Attempts to extend radically the human lifespan should be welcomed, not feared.' Naturally, as a judge I'll be assessing how well they argue their case and stand up to cross-questioning, but I know which side I'd prefer to be on. It may be easier to support the motion. Expanding lifespans are a fact, after all. In 1899 there were probably about 10 centenarians in Scotland and we know nothing of their frailty or mental capacity. When I set out to track down Scotland's "super-old" in 1999, there were more than 1000. ... The point was that we are not just getting older but staying fitter for longer too. Today about 35% of our over-75s do some volunteering work. Seen in this light, what we emotively call 'the demographic timebomb' looks like a blessing in disguise. But hang on. Just because some people's longevity defies our expectations, just because we CAN stretch lifespans, doesn't mean we should."

Continued Progress in Tissue Engineering (March 15 2007)
Scientists are making progress in growing more lifelike and larger masses of tissue: researchers "have created new heart muscle with its own blood supply through the use of human embryonic stem cells. ... Despite progress over the past two decades in treating cardiac disease, there are few good ways to fix damaged heart muscle. One possibility would be to rebuild a broken heart with a transplant of healthy heart tissue. However, scientists have been stymied in these efforts by a lack of human heart tissue to work with and the failure of transplanted tissue to thrive in its new home. ... heart tissue grown by the [researchers] is threaded throughout with a network of tiny blood vessels that would improve the tissue's survival after being transplanted in a human heart ... researchers engineered the heart muscle by seeding a sponge-like, three-dimensional plastic scaffold with heart muscle cells and blood vessel cells produced by human embryonic stem cells, along with cells called embryonic fibroblasts. ... Four to six days after being seeded on the scaffold, patches of the new muscle cells began to contract together, a movement that spread until the entire tissue scaffold was beating like normal heart muscle."

The Slow Creep of Ideas (March 14 2007)
For all the progress that has been made in healthy life extension advocacy, it's still taking a good long time to move ideas, knowledge and expectations into the mainstream. Take this half doom-and-gloom piece, for example, from the LA Times: "And it's not just an extension of working years that individuals will have to accept. We can also expect health problems to multiply, at least temporarily, as people live longer in bodies that didn't have the benefit of the latest in nutritional knowledge, new treatments or better working conditions. The good news is that science is going to be offering better cures faster than most expect. ... Pharmaceutical companies are developing drugs to fight the crisis of obesity, which leads to diabetes, heart disease and premature death. British bio-gerontologist Aubrey de Grey and others are pursuing a goal of 'engineered negligible senescence' - which would in theory eliminate most of the physical damage of aging and lead to indefinite life spans." The most basic of basics regarding modern longevity science - that extended healthy lives are possible, plausible, and closer than you think, provided the work is funded - are still to be communicated to the majority of people. Only when the man in the street responds to aging in the same way as cancer will we be fully underway on the road to defeat aging.

More On Telomerase and Body Mass (March 14 2007)
Ouroboros follows up on recent work on telomerase levels by size of species: "An outstanding question in the evolution of aging is whether telomerase activity (which preserves the ends of linear chromosomes and lengthens the replicative lifespan of cells) is related to lifespan per se. On on hand, it seems likely that it would be related positively: The longer one lives, the longer one's cells need to continue regenerating. On the other hand, the longer one lives, the more likely one is to accumulate [damaged, cancer-prone cells]. Since telomere maintenance is essential for tumor cell viability, one might not want these damaged cells to have ready access to telomerase expression ... and this logic might lead us to the opposite conclusion. ... Seluanov et al. show that among rodents, telomerase activity has co-evolved with body mass, but not lifespan. Furthermore, the correlation is negative: telomerase activity is more restricted in larger animals, perhaps as a defense against the increased cancer risk that comes from having more cells."

Following Up On Catalase and Longevity (March 13 2007)
I'm sure you recall the experiments demonstrating life extension in mice through boosting the level of catalase in the mitochondria. Here, The Scientist follows up with a few interesting notes in their Hot Paper series: "Replicating the findings has proven difficult. Rabinovitch says that changes in veterinary care have led to euthanasia of mice that develop dermatitis and other ailments at early ages. This practice has confounded the replication of past longevity observations. ... Richard Miller at the University of Michigan, Ann Arbor, offers his opinion: 'If [catalase-boosting mutations] do increase lifespan in mice, the effect may depend in complicated ways on a specific and not well-characterized set of background genes and environmental factors.' ... Rabinovitch says he's about two-thirds of the way through aging studies with two different mouse strains. New data, he says, clarify the protection against age-related cardiac changes and nonhematologic cancers, and they are working on new transgenic models." Stay tuned.

Revisiting Fat and Inflammation (March 13 2007)
Becoming overweight sounds like ever more of a bad idea with each passing year. From EurekAlert!: "the research team decided to analyze the blood that ran through it to determine whether visceral fat was involved in inflammation or whether, like subcutaneous fat, it was merely a marker of potential problems. ... the research team says visceral fat likely contributes to increases in systemic inflammation and insulin resistance. They sampled blood from the portal vein in obese patients undergoing gastric bypass surgery and found that visceral fat in the abdomen was secreting high levels of an important inflammatory molecule called interleukin-6 (IL-6) into portal vein blood. ... Increased IL-6 levels in the portal vein correlated with concentrations of an inflammatory substance called C-reactive protein (CRP) in the body. High CRP levels are related to inflammation, and chronic inflammation is associated with insulin resistance, hypertension, type 2 diabetes and atherosclerosis, among other things. ... These data support the notion that visceral fat produces inflammatory cytokines that contribute to insulin resistance and cardiovascular disease."

The Key To Muscle Regeneration? (March 12 2007)
ScienceDaily reports on a new discovery in the biochemical regulation of stem cells: "After injury, even adult muscles can heal very well because they have a reserve supply of muscle stem cells, called satellite cells, which they can utilize for repair. Until now, it was unclear how this supply of satellite and muscle progenitor cells, out of which both muscle cells as well as satellite cells develop, keeps itself 'fresh'. ... a molecular switch, abbreviated RBP-J, regulates this 'fountain of youth'. If the switch is absent, the satellite cells generate muscle cells in an uncontrolled way, resulting in the depletion of the satellite cell reserves." It doesn't look like the researchers have yet conclusively proven that this switch controls the age-related decline in the satellite cell population (and resulting loss of healing capacity), however. The root cause of this decline is likely an evolutionary adaptation to avoid cancer resulting from age-damaged stem cells - so even if manipulation of RBP-J can induce elderly muscles to vigor, you'd better have a good cancer therapy to hand.

On Metabolic Rate and Longevity (March 12 2007)
Joao Pedro de Magalhaes, who maintains the rather excellent senescence.info and associated resources for scientists, has been keeping himself busy with an examination of metabolic rate and life span: "One of the oldest and most popular explanations is the idea that short-lived animals like mice and shrews have high metabolic rates and thus accumulate molecular damage faster than animals with lower metabolic rates, such as elephants. ... The new study, however, disproves this simple, even intuitive explanation by finding no correlation between metabolic rate and longevity using data for several hundred species, the largest dataset ever employed in such an analysis. ... Not only the study disproves the "rate of living" theory, but it also raises doubts regarding another popular theory of aging: the free radical theory of aging, which argues that damage caused by toxic by-products of oxygen metabolism called reactive oxygen species accumulates with time resulting in aging. Because metabolic rates were estimated from oxygen consumption at rest, the study also raises questions of whether damage caused by reactive oxygen species plays a role in differences in longevity between species. ... However, we know that not all things are equal. For example, there could be differences in antioxidant levels that we did not take into consideration."



Post a comment; thoughtful, considered opinions are valued. New comments can be edited for a few minutes following submission. Comments incorporating ad hominem attacks, advertising, and other forms of inappropriate behavior are likely to be deleted.

Note that there is a comment feed for those who like to keep up with conversations.