LONGEVITY MEME NEWSLETTER
August 18 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.
- Vote for "Undergrads Against Age Related Disease"
- Some Thoughts on Halting Aging in the Liver
- Podcasts on Biomarkers of Aging
- Latest Healthy Life Extension Headlines
VOTE FOR "UNDERGRADS AGAINST AGE RELATED DISEASE"
I don't know if you're familiar with the American Express Members Project: it is an open vote to determine how that company will set up a philanthropic program. One of the suggested projects was put forward by a Methuselah Foundation volunteer, and we're looking for enough votes to move it into the next round of consideration:
"You can help by voting: it's free and won't take more than a few minutes. We just need you to go to the Members Projects website and nominate the "Undergrads Against Age Related Disease" project. You don't need to be an Amex card holder, but you do need to be a US resident."
You'll find the project description at the following link:
"A program that utilizes college undergraduates to perform research in a variety of scientific venues surrounding fighting age related diseases such as Alzheimer's, Parkinson's, Heart Disease, [Cancer, and] overall extension of healthy human life. Hiring researchers is exceedingly expensive. By outsourcing projects to undergraduate students, laboratory use and labor costs are negligible, and the students receive college credit for their work"
SOME THOUGHTS ON HALTING AGING IN THE LIVER
You'll recall the recent news of a demonstrated halting of age-related decline of liver function. The lysosomes - the garbage recyclers of the cell - were less efficient in older mice, allowing damaging chemicals to build up and choke the cells. That loss of efficiency apparently has a single root cause, and that cause was removed through genetic manipulation. The evidence suggests that this problem accounts for all or most of liver function decline in old mice. I offer some thoughts and caveats here:
"Dr. Cuervo found that the chaperone surveillance system, in particular, becomes less efficient as cells become older, resulting in a buildup of undigested proteins within the cells. She also detected the primary cause for this age-related decline: a fall-off in the number of lysosomal receptors capable of binding chaperones and their damaged proteins.
"The researchers demonstrated old mouse livers functioning as well as young mouse livers. On the one hand, this is solid support for a range of scientific initiatives aimed at lysosomal issues and buildup of damaging material in cells. For example, the work of the Methuselah Foundation under the LysoSENS program. On the other hand, this result suggests that - in the liver at least - the problem simply goes away if you deal with the missing receptors. This is interesting, as I was under the impression that a large portion of the issue in old humans stemmed from material that would never be broken down - the human lysosome just doesn't have the tools for the job.
"This work on liver function was performed in mice; will this same sort of result hold in longer-lived mammals? We humans have tens of mouse life spans in which to build up even more impressive collections of gunk in our cells. Work on AGE-breaker drugs has demonstrated that old rodents and old humans don't necessarily have a lot in common when it comes to what sorts of biochemical gunk predominantly cause degeneration."
This is an interesting enough result to attract other research teams, so I expect that we shall see how it all turns out over the next five years or so.
PODCASTS ON BIOMARKERS OF AGING
The latest podcasts from SAGE Crossroads focus on the search for biomarkers of aging. If you don't have good measures for biological age, how do you determine whether your potential new rejuvenation therapy is working? You'll find links and excerpts in this Fight Aging! post:
"[The search for biomarkers has] gone through various times when it was a high priority and then given a lack of success in identifying biomarkers, it lost some its priority, but I see a resurgence now given [that] we are at an important state in gerontological research where there are specific interventions that can be evaluated."
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!
LATEST HEALTHY LIFE EXTENSION HEADLINES
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/
Towards Tissue Engineered Corneas (August 15 2008)
From the Hindustan Times: "Half a dozen eye hospitals in India are collaborating with a research centre in Chennai to create the inner layer of the cornea, the vital window of the human eye. ... Nichi-In Centre for Regenerative Medicine (NCRM) hopes to make corneal endothelium (inside cell layer) available on a commercial scale ... About 100,000 people are in need of eye transplant every year, yet only about 10,000 are able to get donated eyes. The wait for a donor can be endless for the other 90,000. Imagine what a boon it will be if an eye stem cell bank could provide these lab generated endothelial layer of the cornea ... The eye has three main parts. The first is the cornea, which is a transparent film like structure that transmits light into the eye. The other two are the lens and retina. During eye transplant, only the cornea is taken from the donor, not the whole eye. ... Nichi-In is now growing the animal and human corneal inner layer cells on a nano-scaffolding. The research centre is hoping to begin phase I clinical trials on humans in six months."
Ouroboros On Open Science (August 15 2008)
Open science, analogous to open source software development, is the way of the future. It greatly increases diversity and speed of work by lowering the cost of information, and thereby allowing many more people to participate in research. In a world in which information transmission is easy, it makes no sense to lock up scientific data. Publish early, publish often should be the mantra. From Ouroboros: "The world implied by these concepts is one of radical sharing, in which credit still goes where credit is due but by dramatically different mechanisms. Open science isn’t so much 'pay it forward' (though there is a bit of that) as an effort to create a (scientific) world in which no one is paying at all, a world in which there's no incentive to withhold or protect ownership of data. The science fiction writer Iain M. Banks once wrote that 'money implies poverty' - indeed, many of the current models of data ownership and publication, and their accompanying 'currencies' of proprietorship, prestige and closed-access publication, imply a world in which data is scarce and must be hoarded. But data is not scarce anymore."
Cryonics Versus Rejuvenation Medicine (August 14 2008)
Via Depressed Metabolism, arguments for a present focus on the development of cryonics over the development of rejuvenation medicine: "In his article 'Why Cryonics Will Probably Help You More Than Antiaging' (2004), cryonics activist Thomas Donaldson contrasts cryonics with antiaging as a means to life extension and argues that a major advantage of cryonics is that cryobiology research can move at a much faster pace than anti-aging research, especially as it pertains to humans ... Not only that, but its progress almost totally lacks the problems of proving that an advance has happened. The state of a brain, or even a section of brain, after vitrification and rewarming to normal temperature, shows directly whether or not the method used improved on previous methods. ... cryonic suspension able at least to preserve our brains in a reversible form, allowing restoration of vital functions, looks likely to come much sooner [than rejuvenation medicine]." Which is all true - but problems left to other people to solve have a way of remaining unsolved. We should work on both cryonics and rejuvenation medicine, not leave the latter for future generations.
Vote For "Undergrads Against Age Related Disease" (August 14 2008)
The Methuselah Foundation is asking supporters to vote for aging science in the Amex Members Project program: "we are supporting a project named 'Undergrads Against Age Related Disease,' submitted as part of the Amex Members Project initiative. In order to move forward, this project must obtain more than 2000 votes in the next 2 weeks - by September 1st, 2008. You can help by voting: it's free and won't take more than a few minutes. We just need you to go to the Members Projects website and nominate the "Undergrads Against Age Related Disease" project. You don't need to be an Amex card holder, but you do need to be a US resident." From the project description: "a program that utilizes college undergraduates to perform research in a variety of scientific venues surrounding fighting age related diseases such as Alzheimer's, Parkinson's, Heart Disease, [Cancer, and] overall extension of healthy human life. Hiring researchers is exceedingly expensive. By outsourcing projects to undergraduate students, laboratory use and labor costs are negligible, and the students receive college credit for their work."
Removing the Worst Aspect of Chronic Infection (August 13 2008)
An important aspect of immune system aging is the lack of naive T cells resulting from long periods of chronic infection by viruses like cytomegalovirus. What if we could reconfigure the immune system to behave more rationally when presented with recurring threats, and thus not exhaust its resources? That might be a possibility: "preventing white blood cells' circulation by trapping them in the lymph nodes can help mice get rid of a chronic viral infection ... laboratory mice can fight off infection by the Armstrong strain of lymphocytic choriomeningitis virus (LCMV), but are vulnerable to chronic infection by a variant called clone 13. ... infecting mice with the Armstrong strain sequesters white blood cells in the lymph nodes, while clone 13 does so less stringently. ... Our hypothesis was that if we could artificially induce conditions like those produced by the Armstrong strain, it would help the immune system clear an infection by clone 13 ... an experimental drug called FTY720 [prevents] white blood cells from leaving lymph nodes ... Even if mice have a stable chronic LCMV clone 13 infection, treatment with FTY720 can still improve their immune response against LCMV enough to have them rid it from their systems ... FTY720 appears to prevent 'exhaustion' in the group of white blood cells called CD8+ T cells."
Hourglass II: A Carnival of Biogerontology (August 13 2008)
From Ouroboros: "Welcome to the second installation of Hourglass, a blog carnival devoted to the biology of aging. The entries are representatives of the excellent (and growing) community of bloggers who are writing about biogerontology, lifespan extension technologies, and aging in general. ... Anne C. shares a parable about taking care of her friend Nigel the Fish and what that led her to realize about longevity: specifically, that environment is critical, and that the combination of extrinsic factors that one might collectively term 'nurture' can make all the difference between a short unhappy life and a long fulfilled one. ... Old and damaged cells enter a permanent growth arrest known as senescence, which is both good (because they can’t initiate tumors) and bad (because persistent senescent cells behave in a ridiculously antisocial manner, secreting growth factors and proteases that both encourage nearby tumors to metastasize and degrade tissue function). ... At his new site Anti-Ageing Research, Dominick Burton discusses ways in which specifically targeted cancer therapies might be adapted to attack senescent cells instead."
Building Better Tendons (August 12 2008)
Laboratory tissue engineering continues to improve in sophistication, as noted by the New Scientist: "only now have researchers managed to make different tissues blend into one another, as they do naturally in the body. Such gradients are necessary for some structures and organs to function properly ... In the body, gradients like this strengthen the ends of tendons that attach to bones. Currently, lab-grown tendons put into the body often fail at the attachment end because they lack this property ... [the] new technique should lead to more lifelike artificially-grown tendons, and better treatments for injuries like ruptured Achilles tendons. The technique could also be applicable to other tissues, such as blood vessels .. At the heart of the new technique is a gene that triggers the fibroblast cells that make up tendons to start forming bone. The team used viruses carrying that gene to transform a tendon made from normal fibroblasts into one with a gradient of bony properties ... So far, the researchers have shown that tendons made this way are stable when implanted under the skin of rats. The next step is to graft a tendon to connect bone and muscle in a rat and see if it really does perform better."
Demonstrating the Value of Exercise (August 12 2008)
Via Medical News Today, another reminder of the value of exercise: "US scientists comparing middle aged and older regular runners with healthy equivalents for more than 20 years found that vigorous regular exercise was linked to longer life and less disability in old age. ... Fries and his team had 538 members of a nationwide running club and 423 healthy controls from northern California fill in questionnaires every year for as long as they could, from 1984 to 2005 ... The mean disability score was higher for the controls than the runners at all stages of the study and went up with age in both groups, but on average, for runners the onset of disability started later. ... Runners' initial disability was 16 years later than nonrunners ... Runners had a significantly lower risk of having a disability score of 0.5. ... 19 years into the study, 15 per cent of the runners and 34 per cent of the controls had died, and after adjusting for possible confounders, runners showed a greater chance of living longer. ... The differences in disability and longevity between the runner group and the control group continued to diverge at the end of the study, as the participants approached their 80th birthday."
Full Paper on Visceral Fat and Longevity (August 11 2008)
You may recall a solid demonstration that visceral fat tissue negatively affects longevity from earlier this year. The full paper is now open access and available at PubMed Central: "Visceral fat (VF) accretion occurs in obesity and with aging, and a reduction in VF is a common phenotypic change in calorie-restricted [CR] mammals. VF has been shown to be the single most important determinant of metabolic syndrome, and its removal in rats results in improved insulin action and delays the onset of diabetes. Given the hazards associated with abdominal obesity, it seems plausible that the beneficial effects of CR on longevity may be due at least in part to an attenuation of VF. ... Our data clearly demonstrate that in mammals, VF removal and CR are associated with an increase in mean and maximum lifespan. ... The mean and maximum lifespan of CR rats was greater than that seen in VF-removed animals, suggesting that the life-prolonging benefit of CR is mediated in part by pathways other than those modulated by an attenuation of VF. By comparing median lifespans, we estimate that the contribution of CR to longevity in this model was 47 weeks, whereas VF removal was 9.5 weeks, as compared to [ad libitum]-fed rats, suggesting that VF reduction offered approximately 20% of the effect of CR on longevity."
Repairing Age-Related Damage in the Liver (August 11 2008)
ScienceDaily reports on a promising demonstration: "The cells of all organisms have several surveillance systems designed to find, digest and recycle damaged proteins. ... One of these surveillance systems - responsible for handling 30 percent or more of damaged cellular protein - uses molecules known as chaperones to seek out damaged proteins. After finding such a protein, the chaperone ferries it towards one of the cell's many lysosomes ... Dr. Cuervo found that the chaperone surveillance system, in particular, becomes less efficient as cells become older, resulting in a buildup of undigested proteins within the cells. She also detected the primary cause for this age-related decline: a fall-off in the number of lysosomal receptors capable of binding chaperones and their damaged proteins. Could replenishing lost receptors in older animals maintain the efficiency of this protein-removal system throughout an animal's lifespan and, perhaps, maintain the function of the animal's cells and organs as well?" As it turned out, this strategy does indeed work to maintain liver function at young levels in older animals.