Longevity Meme Newsletter, March 23 2009

March 23 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.



- Aubrey de Grey's BIL Presentation
- Russian Media on Aubrey de Grey and SENS
- The Life Lost to Fat
- Discussion
- Latest Healthy Life Extension Headlines


A transcript of Aubrey de Grey's presentation at the BIL unconference is available at Future Current, in which he discusses some of the longevity research presently funded by Methuselah Foundation donors:


"A fantastic, originally Serbian immunologist called Janko Nikolich-Zubich, who is a prominent gerontologist and works in Tucson at the University of Arizona, has become very interested in the possibility of being more ambitious about repairing and rejuvenating the immune system than anyone has previously been. ... He is basically applying a combination therapy to mice whose immune systems are going downhill because of aging and seeing whether the immune systems can be really rejuvenated so that the mice are better at resisting infection, getting back to where they were in early adulthood. It is a reasonably long project, as is more or less any project involving the aging of mice, but it is already underway. It is being funded by the Methuselah Foundation and we are extremely happy about it."

This work has to do with cytomegalovirus (CMV), amongst other things, and long-time readers of Fight Aging! may recall how it is that CMV is thought to cause a large portion of the immune system degeneration that occurs over a lifetime. A summary is given in the following post from the archives:



The Russian Science for Life Extension foundation staff were kind enough to assemble a list of Russian language media coverage of Aubrey de Grey's recent Moscow presentation on the Strategies for Engineered Negligible Senescence (SENS). I've assembled links to machine translated versions, and audio of the presentation itself, in the following Fight Aging! post:


It is encouraging to see the interest with which news of the prospects for engineered longevity is received in that part of the world.


Yes, we're revisiting this topic again: quantifying the damage done to health and longevity by excess fat held over years.


"Peto and colleagues found that people who were moderately fat, with a BMI from 30 to 35, lost about three years of life. People who were morbidly fat - those with a BMI above 40 - lost about 10 years off their expected lifespan, similar to the effect of lifelong smoking. Moderately obese people were 50 percent more likely to die prematurely than normal-weight people ... obese people were also two thirds more likely to die of a heart attack or stroke, and up to four times more likely to die of diabetes, kidney or liver problems. They were one sixth more likely to die of cancer."

Levels of fat are a choice for almost all of us. A choice that requires commitment and work over time if we're not where we'd like to be - but who wants to suffer unduly and then die young? If you let yourself go, however, then you are setting up exactly that fate for yourself.


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!




On Terror Management Theory (March 20 2009)
Thoughts from Ouroboros: "if an arbitrary belief serves to protect an individual from their fear of death, reminding them of their mortality will cause them to cling to and elaborate this belief. (The underlying edifice, terror management theory, deals with the way in which human minds navigate the double-bind of being simultaneously aware of our desire to preserve our lives and the technical impossibility of doing so.) The classical example of such a belief would be a religion promising an afterlife ... It also works just fine with a belief in which the individual, by dint of some combination of industry, sagacity and/or having been born in the right century, has a chance of not dying at all. A prediction: life extension advocates might tend to increase their estimation of the feasibility of significant longevity enhancement after being confronted by reminders of their own finite lifespans. (I know I feel a twinge even writing those words, so I suspect this prediction has some real teeth.)"

Living Scaffolds For Nerve Regeneration (March 20 2009)
Via ScienceDaily: researchers "have engineered transplantable living nerve tissue that encourages and guides regeneration in an animal model. ... We have designed a cylinder that looks similar to the longitudinal arrangement of the nerve axon bundles before it was damaged. The long bundles of axons span two populations of neurons, and these neurons can have axons growing in two directions - toward each other and into the host tissue at each side. ... The constructs were transplanted to bridge an excised segment of the sciatic nerve in rats. Up to 16 weeks post-transplantation, the constructs still had their pre-transplant shape, with surviving transplanted neurons at the extremities of the constructs spanned by tracts of axons. Remarkably, the host axons appeared to use the transplanted axons as a living scaffold to regenerate across the injury. ... the constructs survived and integrated without the use of immunosuppressive drugs, challenging the conventional wisdom regarding immune tolerance in the peripheral nervous system."

Aubrey de Grey at TEDMED2009 (March 19 2009)
Biomedical gerontologist Aubrey de Grey will be presenting at TEDMED2009 in October. Registration is now open: "His research interests encompass the causes of all the accumulating and eventually pathogenic molecular and cellular side-effects of metabolism ('damage') that constitute mammalian aging and the design of interventions to repair and/or obviate that damage. He has developed a possibly comprehensive plan for such repair, termed Strategies for Engineered Negligible Senescence (SENS), which breaks the aging problem down into seven major classes of damage and identifies detailed approaches to addressing each one. A key aspect of SENS is that it can potentially extend healthy lifespan without limit, even though these repair processes will probably never be perfect, as the repair only needs to approach perfection rapidly enough to keep the overall level of damage below pathogenic levels. Dr. de Grey has termed this required rate of improvement of repair therapies 'longevity escape velocity.'" From the other side of the pro-longevity research community, David Sinclair of Sirtris is also presenting.

Towards a Cytomegalovirus Vaccine (March 19 2009)
Cytomegalovirus (CMV) causes much of the decay of our immune system over the years by cluttering it up with uselessly specialized anti-CMV cells. Via EurekAlert!: "results of a trial involving 441 CMV-negative women give rise to optimism that a vaccine to prevent congenital CMV may be closer. Women who received the trial vaccine were 50 percent less likely to later become infected with CMV ... Aspects of CMV biology have caused skeptics to question whether it is possible to prevent infection through vaccination, explains ... The virus is well adapted to persist in an infected person and is readily passed from person to person through direct contact with numerous bodily fluids ... Healthy people typically experience no symptoms after being infected with CMV. There is a strong immune response to the initial infection, but this immunity cannot always prevent subsequent infections if a person re-encounters the virus. Finally, natural infection does not elicit a response sufficient to completely eliminate the virus. On the contrary, once a person is infected, the virus persists for life." A vaccine is a start, but it doesn't help those of us already damaged by exposure: some methodology must be developed to remove specialized immune cells and restore function rather than just prevent loss.

Validating Animal Studies of Aging (March 18 2009)
Most work on aging and longevity research involves the study of comparatively short-lived animals. It is important that scientists demonstrate this research to be relevant to human aging, however: "Studies of longevity in model organisms such as baker's yeast, roundworm, and fruit fly have clearly demonstrated that a diverse array of genetic mutations can result in increased life span. In fact, large-scale genetic screens have identified hundreds of genes that when mutated, knocked down, or deleted will significantly enhance longevity in these organisms. Despite great progress in understanding genetic and genomic determinants of life span in model organisms, the general relevance of invertebrate longevity genes to human aging and longevity has yet to be fully established. In this study, we show that human homologs of invertebrate longevity genes change in their expression levels during aging in human tissue. We also show that human genes encoding proteins that interact with human longevity homolog proteins are also changed in expression during human aging. These observations taken together indicate that the broad patterns underlying genetic control of life span in invertebrates is highly relevant to human aging and longevity."

Alzheimer's as Diabetes of the Brain (March 18 2009)
The lifestyle risk factors for Alzheimer's disease look a lot like those for diabetes - in other words get fat and don't exercise and your brain will suffer. Some researchers propose that Alzheimer's is a form of diabetes: "Insulin is the hormone that allows cells, including some brain cells, to take up energy in the form of glucose. Proper insulin function in the brain appears necessary to the formation and maintenance of memories. And, crucially, a lack of insulin or insulin resistance is connected both to amyloid protein regulation and to the modification of tau proteins, which can cause tangles. In other words, insulin seems to hold up a conceptual umbrella under which the amyloid and the tangle camps might finally meet. ... Type 2 diabetes is also a risk factor for Alzheimer's and cognitive decline. In 2005, researchers at Brown showed that by knocking out insulin production and causing brain insulin resistance in rats, they could create a model of Alzheimer's, complete with plaques and abnormal accumulations of tau. ... Scientists have also described links between abnormal insulin and other hallmarks of Alzheimer's, such as oxidative damage and inflammation."

A Mainstream Media Piece on Calorie Restriction (March 17 2009)
The quality of these sorts of articles is slowly improving, though there are still the normal errors and biases lurking in the background. From the National Post: "As early as the 1930s, it was shown that calorie reduction could double the lifespan of rats. What's more, a 1988 study noted that mice on a calorie-restricted diet had a more youthful appearance, a higher activity level and a delay in age-related diseases, compared with those on an unrestricted feeding schedule. The first studies on the effects of caloric reduction on humans were done in the 1940s, when it was observed that Scandinavians, living on a diet in which their calories were restricted by 20% because of the hardships of the Second World War, showed a decrease in cardiovascular disease. More recently, investigations have shown that a reduction in body weight decreases the risk of Type 2 diabetes, hypertension, cardiovascular disease, dementia, and cancers of the breast, prostate and colon. Other researchers examined a group who had been on a calorie-restricted diet for six years and found they had improved blood fat profiles, lower fasting glucose and insulin levels, lower body fat and a reduced level of C-reactive protein, a measure of inflammation. Further work has shown a neurological benefit for a calorie-restricted diet. One study involving mice demonstrated that intermittent fasting helped to decrease the effects of degenerative brain disease."

Telomere Length and the Sister Study (March 17 2009)
Some more evidence that shortened telomere length correlates with conditions and risk factors that are known to be bad for your long term health: "One of the studies published this week found that women who were obese for a long time had reduced telomere length. The researchers looked at the relationship between various measures of current and past body size and telomere length in 647 women enrolled in the Sister Study. They found that women who had an overweight or obese body mass index (BMI) before or during their 30s, and maintained that status since those years, had shorter telomeres than those who became overweight or obese after their 30s. ... This suggests that duration of obesity may be more important than weight change per se, although other measures of overweight and obesity were also important. Our results support the hypothesis that obesity accelerates the aging process. ... women who reported above-average stress had somewhat shorter telomeres, but the difference in telomere length was most striking when we looked at the relationship between perceived stress and telomere length among women with the highest levels of stress hormones. Among women with both higher perceived stress and elevated levels of the stress hormone epinephrine, the difference in telomere length was equivalent to or greater than the effects of being obese, smoking or 10 years of aging."

Austad's Expectations (March 16 2009)
Via the Tyler Morning Telegraph: "At least one person alive right now may live to be at least 150 years old. That's according to Dr. Steven Austad ... It seems a little far out but within a little more than 100 years in the United States, through medical research and the advances that have taken place, we have doubled life expectancy in the United States. If it doubles again we will hit that 150 year-old mark ... Your ancestry only accounts for a small amount. It turns out if you look into it, the length of time that you live is only about 25 percent affected by your genetics. How you live your life can have an enormous impact ... reasons some opposed the notion of developing drugs to delay aging are: fear that it will only preserve maladies but won't improve the quality of life; the naturalistic argument, in which people are lead by beliefs that we are not meant to tamper with the stages of life; the drug would only be available to select people; and shortages in resources including jobs and food due to a larger, older population. ... We've already made a decision as a society that things that benefit some people as long as it does not harm other people are OK. We're not going to stop all medical advances until we can make those advances to everyone. I think the history of medicine shows that new advances do tend to spread out and it may take a while ... or most of human history, humans' lifespan has increased. ... So why stop now?"

An Interview With Aubrey de Grey (March 16 2009)
An interview with biomedical gerontologist Aubrey de Grey at (Ciencia) x (Libre): "I meet Aubrey de Grey after his lecture at the CosmoCaixa Barcelona Museum. He’s had an intense day: several press, radio and television interviews in the morning, followed by a two hours lecture in front of a demanding public. ... de Grey is quite clear: aging is not inscribed in our genes, is the result of the accumulation of damage not repaired and that just ends up being fatal. Evolutionary biology says he is right: our genes allow us to live long enough to reproduce successfully, and after that [we] matter little at the 'eyes' of the selfish gene. If we repaired these damages in time [could] we not live a thousand years? ... most biogerontologists don't study ageing in order to figure out how to fix it: they study it as a phenomenon to be understood, rather in the same way that seismologist study earthquakes. You know [they] understand that earthquakes are sometimes quite bad for you, but they don't aspire to actually stopping them from happening. And most biogerontologists are the same, so that's why I call myself a biomedical gerontologist. I am not trying to use therapies that already exist, but I'm trying to develop new therapies that will actually do something about ageing."



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