Longevity Meme Newsletter, March 02 2009
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March 02 2009

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.



- Science Against Aging, in Russia
- Aubrey de Grey in Russia
- Discussion
- Latest Healthy Life Extension Headlines


The Science for Life Extension organization is a Moscow-based pro-longevity advocacy group with strong ties to the Russian research community. The spirit of the endeavor is very similar to the Methuselah Foundation and the Strategies for Engineered Negligible Senescence, but their take on the science needed to intervene in the aging process is different. There are two detailed PDF documents available in English linked from this Fight Aging! post:


"The value of a long and healthy life is obvious to every reasonable person. Therefore, aging is a serious and until now unsolved problem. Slowly but inexorably, aging decreases the quality of life, makes people weak and powerless, prevents the realization of people's aspirations. Sooner or later, it leads to death.

"Today, the growing desire for a long, high-quality and healthy life becomes increasingly obvious in developed countries. This is confirmed by the strong demand for fitness, anti-aging services, etc. The share of people who openly express this desire for life extension is growing. According to a public opinion poll conducted in Russia in 2008, 78% of Russians do not ever want to age."

The documents go on to outline a strategy for research and supporting science: the present understanding of aging, and signs that we can extend healthy life through medical research. A lot of work has gone into this, and it is a welcome sign to see sophisticated independent efforts emerging to this same important end.


The Science for Life Extension group is hosting a visit to Moscow State University by Aubrey de Grey of the Methuselah Foundation. There are links to automated translations of a Russian media interview at this Fight Aging! post:


"Until recently, there was no hope that the aging process can be stopped. Everyone knew that must die, and therefore it cannot be helped. And people have learned not to think about it. To protect themselves, they think of the arguments in favor of the fact that aging is necessary that it has its advantages. And now we, the Methuselah Foundation, spend a lot of effort to explain than do. Yes, our goal - to make a life long, but it is equally important to ensure that this life was healthy.

"In Russia, [there is] a very strong School of Gerontology. But more importantly, there are scientists-biologists who study how the aging process, and finding the means to combat them. It is my great pleasure to discuss with them various aspects of the problem, even if we do not all agree with each other. In addition, I am going to discuss strategies to combat [aging with Russian groups], including the Foundation "Science for Life Extension" who organized my visit to Russia. But the main thing [is] to communicate with young scientists, students and the public. I am going to speak to the public lectures."


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/

The Longevity of Bats (February 27 2009)
Here's a paper on the biochemistry of comparatively long-lived bats and their resistance to oxidative damage. "Altered structure, and hence function, of cellular macromolecules caused by oxidation can contribute to loss of physiological function with age. Here, we tested whether the lifespan of bats, which generally live far longer than predicted by their size, could be explained by reduced protein damage relative to short-lived mice. We show significantly lower protein oxidation [in] Mexican free-tailed bats [relative] to mice, and a trend for lower oxidation in samples from cave myotis bats ... Both species of bat show in vivo and in vitro resistance to protein oxidation under conditions of acute oxidative stress. These bat species also show low levels of protein ubiquitination in total protein lysates along with reduced proteasome activity, suggesting diminished protein damage and removal [of damaged proteins] in bats. ... Together, these data suggest that long lifespan in some bat species might be regulated by very efficient maintenance of protein homeostasis." This sounds similar to current thinking on the naked mole rat - lots of oxidative stress, but little resulting protein damage, perhaps due to a different, more resistant structure of cell membranes.

Ouroboros on Leaky Cellular Pores (February 27 2009)
Some small but important collections of cells in our body are as old as we are - they are never replaced. So for those cells, we should be interested in what happens to them as they grow old with us. Here, Ouroboros looks at a recently uncovered phenomenon: "How do cells get rid of their garbage? ... slowly dividing or postmitotic cells must activate degradative pathways [e.g. autophagy] in order to prevent accumulation of potentially toxic damaged macromolecules and dysfunctional organelles. ... As an example, let’s consider the nuclear pore complex (NPC): it's [huge, complex, and topologically challenging] (the pore crosses the nuclear envelope and creates a hole in the process). Many NPC components aren't in dynamic equilibrium with cytosolic pools, so if we want to turn over any of these proteins we would have to somehow take out the entire NPC, repair the ensuing damage to the membrane, and then either re-insert the NPC (which I don't believe actually happens) or synthesize a new NPC to restore the lost import/export capacity. Unfortunately, new nuclear pores are probably only created during [mitosis as a part of cell division] .... So how do postmitotic cells turn over and degrade NPCs? The answer [is] that they probably don't. Instead, NPCs get old, and accumulate damage, and eventually stop doing their job."

Stem Cells Versus Kidney Damage (February 26 2009)
This press release shows the potential for stem cell transplants to spur regeneration of the kidney: "Cytori Therapeutics, Inc. finds adipose tissue-derived stem and regenerative cells (ADRCs) significantly reduce mortality and improve renal function in an acute kidney injury model ... Acute kidney injury is a tremendous medical and financial burden to the healthcare system due to high mortality rates and the lack of effective therapies beyond supportive treatments. ... acute kidney injury was induced in 29 preclinical research subjects by occluding blood flow into and out of both kidneys for 38 minutes. Twenty minutes after reperfusion of the kidneys, ADRCs or saline only were injected intra-arterially. All subjects were assessed daily for 7 days for markers of kidney function (serum creatinine and blood urea nitrogen) and survival. After seven days, 100% of ADRC-treated preclinical subjects survived compared to only 57% in the control group. The ADRC-treated subjects also showed statistically significant improvements in kidney function ... In addition, substantial improvement in the histologic structure within the kidney was observed ... This study suggests that ADRCs significantly accelerate renal repair and preserve renal function, offering a potential therapeutic approach in renal reparative medicine."

Spring Edition of h+ Magazine (February 26 2009)
The latest h+ magazine is a flash / PDF offering that contains a couple of short pieces that might be of interest for pro-longevity readers. Take a look at "Is Anti-Aging Medicine Coming to the Mainstream" and "Nanorobots in the Bloodstream," for example. The rest is of more general futurist interest this time around. "A microscopic-sized vessel injected into the bloodstream to destroy a lung tumor? [Researchers] have created such a vessel using live, swimming bacteria coupled to polymer beads. [They] have successfully steered these nanobots through the carotid artery of a living pig at 10 centimeters per second using magnetic resonance imaging (MRI). Their latest research shows they can do this with human blood vessels as well. The bacteria bots contain magnetic particles and swim using tiny corkscrew-like tails, or flagella. ... [researchers are] confident that a stealth seak-and-destroy mission could be completed against a tumor before the body's immune system wipes out the bacteria."

Revisiting Gray Hair (February 25 2009)
Researchers are digging deeper into the mechanisms that lead to gray hair: "Going gray is caused by a massive build up of hydrogen peroxide due to wear and tear of our hair follicles. The peroxide winds up blocking the normal synthesis of melanin, our hair's natural pigment. ... All of our hair cells make a tiny bit of hydrogen peroxide, but as we get older, this little bit becomes a lot. We bleach our hair pigment from within, and our hair turns gray and then white. ... the build up of hydrogen peroxide was caused by a reduction of an enzyme that breaks up hydrogen peroxide into water and oxygen (catalase). ... hair follicles could not repair the damage caused by the hydrogen peroxide because of low levels of enzymes that normally serve this function (MSR A and B). Further complicating matters, the high levels of hydrogen peroxide and low levels of MSR A and B, disrupt the formation of an enzyme (tyrosinase) that leads to the production of melanin in hair follicles. ... The researchers speculate that a similar breakdown in the skin could be the root cause of vitiligo."

Neurons From iPS Cells (February 25 2009)
From ScienceDaily: "researchers were able to generate functionally mature motor neurons from induced pluripotent stem (iPS) cells, which are engineered from adult somatic cells and can differentiate into most other cell types. A potential new source of motor neurons that does not require human eggs or embryos could be an enormous boon to research into conditions such as amyotrophic lateral sclerosis (ALS) and spinal cord injury and could open the door to eventual treatments. ... To our knowledge, our results present the first demonstration of the electrical activity of iPS-derived neurons and further suggest the feasibility of using these cells to explore how changes in motor neuron activity contributes to the degeneration of these cells underlying these disorders. ... [the team] used skin fibroblasts and reprogrammed them back into an embryonic state, with the ability to differentiate into any cell type in the human body. They then took those cells and differentiated them into motor neurons."

The Perils of Excess Fat Tissue (February 24 2009)
Letting yourself become very overweight and staying that way - something that is definitely a choice for most of us - is not good for your health and longevity, not to mention your wallet once those medical expenses start to roll in: "We prospectively assessed the association between an increase in body mass index (BMI) category since age 20 years and risk of all-cause, cardiovascular disease (CVD) and cancer mortality. Self-reported information pertaining to BMI was collected from 38,080 Japanese men and women aged 40-79 years at study entry in 1994 ... We observed an increased risk of all-cause mortality both among participants who had been persistently obese since early adulthood and participants who showed an increase in BMI category from normal to obese ... In contrast, we did not observe an increased risk of all-cause mortality for normal weight at age 20 years and overweight at study entry, and stable overweight. For CVD and cancer mortality, these results were consistently observed."

A Mainstream Article on Cancer and Aging (February 24 2009)
From U.S. News: "Cancer is characterized by cells dividing wildly, with no brakes; if a cell can't divide, it can't become cancerous. One solution that evolved: a whole class of naturally occurring tumor suppressor molecules that can disable cells in danger of going haywire. They do it either by telling the cell to kill itself, through a process called apoptosis, or by simply turning off the potentially dangerous cell's ability to divide, a process called senescence. ... But there's a tradeoff. The problem is that those senescent cells, while they have lost their ability to divide out of control, may trigger inflammation in nearby cells and tissues, and inflammation is linked with a host of age-related disease, including late-life cancers. Experiments in mice show that goosing one important tumor suppressor gene, p53, so it's a little bit activated all the time, does certainly hold off cancer ... but the mice age prematurely. It has been possible to regulate the action of p53 in a kind of Goldilocks mode - not too much, not too little - and that produces mice that are both tumor-free and don't age prematurely ... that's easy to do in mice, but difficult to do in people ... Some other possible tactics include figuring out why the senescent cells are secreting molecules that promote the dangerous inflammation and whether suppressing that secretion would help. Or [maybe] there's a way to get rid of the senescent cells entirely."

MRL Mice and Inflammation (February 23 2009)
MRL mice, as you might recall, are a laboratory breed that demonstrates extraordinary powers of regeneration for a mammal. Here, EurekAlert! notes large differences in their inflammatory response as well: " A strain of laboratory mice that has 'superhealing' powers has been found to resist inflammation after a knee injury, and also to avoid developing arthritis at the injury site in the long term ... Their findings illuminate the mechanisms of post-traumatic arthritis and could point to therapies for this condition ... The superhealer can almost regenerate tissue. We thought, 'if they can regenerate cartilage in the ear, what about cartilage in the knee?' This happened in our pilot study, and we now have taken these results further and learned what happens in terms of inflammation. If you can figure out why the animal is a superhealer and apply that to people, then you may help prevent the development of arthritis ... control mice showed a greater than 700-fold increase in the expression of one cytokine, [interleukin], in the first four hours after a fracture and 37-fold difference in that cytokine level at 7 days after the fracture. ... Interleukin generally promotes inflammation and an increase in temperature. The superhealer mice showed a similar trend, but in much lower amounts: a 70-fold peak in expression at day 0 down to a 3.5-fold increase by day 7."

Freedom of Research (February 23 2009)
Here is the concept document for this year's meeting of the World Congress for Freedom of Scientific Research. As for the last meeting in 2006, I can't help but feel that they're missing the forest for the trees. The problem is simply and only government and regulation - the structure of "representative" democracry produces a accelerating creep of lost freedom over time. From the document: "Does a constitutional protection of freedom of scientific research exist in some, or all, liberal democracies? Does this protection - where it actually exists – find some implementation in juridical criteria which guarantee the objectivity of facts, faced to political and personal interests in manipulating the scientific truth? Does the chance to elaborate a quantitative pointer-indicator of freedom of scientific research in different countries exist, adding it to other pointers-indicators of political and economic freedom? In which way bioethics has contributed to the promotion of, or otherwise has contrasted the freedom of scientific research? How can the prohibitionist flow of many bioethical committees be faced? How can the political agenda manage the 'precautionary principle', which is often formulated as internally irrational, and applied in order to paralyze scientific research and technological innovation?"


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