Longevity Meme Newsletter, October 08 2007

October 08 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.



- Gigabytes of SENS3 Conference Video
- Reports From the Alcor 2007 Conference
- The Cost of Aging Illustrated
- Discussion
- Latest Healthy Life Extension Headlines


You'll find links to presentation video from the third conference on Strategies for Engineered Negligible Senescence (SENS3) in the following Fight Aging! post:


We should all thank the Methuselah Foundation volunteers who worked hard to make this happen - these presentations will make their way to video sharing networks, and will be bringing new support to longevity research for years to come.


This year's Alcor conference was held over this past weekend: the conference is an interesting event at the intersection of the cryonics, biotechnology, healthy life extension, nanotechnology and transhumanist communities:


The Alcor blog provides good coverage:


You'll find further conference reporting at the Frontier Channel:


For an introduction to cryonics and its role in the broad scientific path to greater human longevity, take a look at the topic page at the Longevity Meme:


However - and however soon - the development of effective longevity medicine comes to fruition, there will always be people who do not live long enough to benefit. Cryonics, if developed to its full potential as a technology and industry, offers a way to save those people. There should be no argument that cryonics is important and should be supported to the hilt alongside work to repair the damage of aging.


The Milken Institute has provided another window into the staggering cost of aging with their latest work, focused on the economic cost of chronic disease:


"Take a look a look at the major categories of chronic disease examined in the report website - almost all are age-related conditions. The greatest correlation for suffering chronic disease and associated costs is with age, with the toll of cellular and biochemical damage established across a lifetime of metabolic activity. But aging is always the elephant in the room when you're looking at the work of those close to the regulators. Obvious, behind all the facts and figures, and absolutely unmentioned. That has to change if progress is to be made."

If you read around, you'll see that the Milken Institute is pitching to government and the public in a similar manner to the folk behind the Longevity Dividend initiative, but without any overt discussion of aging. This is better than sitting around doing nothing, but it's not the way to make meaningful progress.


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/

Not Sure What To Make of This One (October 05 2007)
I am unable to tell whether this Huffington Post op-ed on biomedical gerontologist Aubrey de Grey and the Strategies for Engineered Negligible Senescence (SENS) is pure snark or not. The author clearly grasps the idea and the scientific backing of SENS, yet omits any mention of de Grey's role in editing a high impact factor scientific journal, organizing a respected conference series attended by the best and brightest of biotechnology and medical research, and pushing forward ongoing research into developing the nuts and bolts of SENS technology. I can't help but feel that if the topic to hand was anything other than the plausible case for a path to radical life extension through biotechnology, this would not be the case - none so blind, and all that. See what you think, and I will content myself with noting that there truly is no such thing as bad publicity for facts, truths and success in the making. As SENS is brought to the attention of more people, more people will decide that it's the better way forward for longevity science.

Biomechanisms of Type 2 Diabetes (October 05 2007)
ABC News reports on an advance in understanding of type 2, age-related diabetes: "The team has identified an enzyme in diabetics as the active agent that blocks the production of insulin, which is a hormone that helps the pancreas convert blood-sugar into energy. Current treatments try to control insulin levels but do not address the reasons why insulin production is failing. ... the next step will be to work with pharmaceutical companies to develop a drug to block the enzyme, known as PKCepsilon, allowing cells in the pancreas to function normally. ... What we've identified is a target that we can now latch onto to get therapy, but the journey from target to tablet of course is a long one ... It's probably going to take another 10 years at least to get something that's effective in humans. ... In their study, the researchers used genetically modified mice to observe the link between an oversupply of fat and type 2 diabetes. They found mice without the enzyme did not develop diabetes, despite gaining weight on a high-fat diet." It's worth remembering that diabetes is a lifestyle condition and very avoidable for most of us. It's just not smart to expect or rely on future medical science to rescue us from the consequences of health negligence - the cavalry only arrives on time in the movies, while the world helps those who help themselves.

More Telomere Complexity (October 04 2007)
As a companion to recent posts on telomere science, here's an example of yet more complexity in the engines inside our cells: "At the end of [chromosomes] are telomeres, zones of repeated chains of DNA that are often compared to the plastic tips on shoelaces because they prevent chromosomes from fraying, and thus genetic information from getting scrambled when cells divide. The telomere is like a cellular clock, because every time a cell divides, the telomere shortens. After a cell has grown and divided a few dozen times, the telomeres turn on an alarm system that prevents further division. If this clock doesn't function right, cells either end up with damaged chromosomes or they become 'immortal' and continue dividing endlessly - either way it's bad news and leads to cancer or disease. Understanding how telomeres function, and how this function can potentially be manipulated, is thus extremely important. ... It was thought that telomeres were 'silent' - that their DNA was not transcribed into strands of RNA. The researchers have turned this theory on its head by discovering telomeric RNA and showing that this RNA is transcribed from DNA on the telomere." All new understanding of how to manipulate telomere length will be eagerly applied by those groups working on telomere-based therapies for age-related conditions.

The Longevity of Naked Mole Rats (October 04 2007)
Here's a good popular science piece on research into the longevity of naked mole rats: "Some of the 'hottest' research on naked mole rats today concerns senescence, or aging. Naked mole rats in the lab have reached up to 28 years of age. And it's not just the controlled environments of their captivity that are doing this. Braude has observed mole rats in the wild that are 17 years and older. ... For a rodent of this size, they are ridiculously long-lived ... A key component in the aging of any species is oxidative damage, where the cells accrue damage from poisons, environmental toxins and other effects throughout life. In such a long-lived rodent, it was thought that naked mole rats had a very efficient way of repairing oxidative damage. This wasn't the case, however, and current theory points to the strange metabolism of this hairless wonder. Naked mole rats appear to deal with oxidative stress in pulses, largely due to their ability to essentially shut down their metabolism when there are hardships, such as lack of food. In this way, mole rats may be able to rid their body of harmful reducing agents and poisons more easily during these metabolic pulses. ... Another way to think of it is, their gross life span might be 28 years, but their metabolism is going in these short bursts so maybe the net damage is only 3 or 4 years of net use. They're living their life in pulses."

Continual Discovery of Stem Cell Populations (October 03 2007)
A few years ago, uncovering another multipotent stem cell population would have been big news. That this one will pass by without much notice is a sign of progress. From ScienceDaily: scientists have "succeeded in finding and manipulating a population of cells that strongly resemble stem cells in the stomachs of mice. They have been able to show that these cells, which they call 'gastric progenitor cells,' can give rise to all the different types (or lineages) of specialized cells needed to form the functional stomach glands that line the lower portion of the stomach. ... The epithelial cells that make up the millions of glands of the stomach are constantly turning over. Most of the mature functioning cells live only 20 to 60 days before being replaced by progeny of dividing resident stem cells. These stem cells are not only a constant source of new cells, but they represent an important reservoir for repair of damage to the stomach caused by injury or inflammation. In addition, since the stem cells are the longest-lived of the gastric cells, it is thought that these are the only cells that live long enough to accumulate the multiple mutations that can cause cancers. For these reasons, the ability to identify and manipulate stomach progenitor cells has been an important goal for decades."

More Progress in Engineered Blood Vessels (October 03 2007)
WebMD reports on a trial of tissue engineered blood vessels: researchers "gathered cells from the skins and blood vessels of 10 adults with end-stage renal (kidney) disease. Next, the scientists put those cells in test tubes (keeping each patient's cells separate from the other patients' cells) and coaxed those cells to grow into blood vessels. After making sure that the lab-made blood vessels wouldn't burst under expected conditions, the researchers implanted the tailor-made blood vessels into the patients. So far, results are available for the first six patients, who got their tissue-engineered blood vessels more than a year ago. One of those patients died of unrelated causes. The lab-made blood vessel failed in another patient. A third patient used the lab-made blood vessel for more than 13 months until receiving a kidney transplant. The three other patients haven't had any problems with their engineered blood vessels. Those early results show that 'this new approach may be feasible,' write the scientists." The age of reliable, low-cost, on-demand replacements for age-damaged organs comes ever closer.

ScienceNOW on Stem Cell Heart Therapies (October 02 2007)
ScienceNOW takes a conservative look at issues in the development of regenerative medicine for heart damage. It is good to take stock of the challenges in any field alongside the breakthroughs: "It's been more than 6 years since the first person was injected with stem cells to rescue a failing heart. Hundreds of patients have since followed the lead of that 46-year-old German man. But experts are still divided on how well the strategy works. ... Clinical trials and animal studies are supplying a wealth of information; so far, the treatment seems safe. But it is not at all clear which stem cells should be given, or by what method - or, most importantly, whether patients who get them are likelier to survive. Cardiologists seized on cell therapy as a way to prevent decay of heart muscle immediately after a heart attack and restore muscle long after it had died. But three of the four largest clinical trials have failed to accomplish what they set out to do - improve a particular measure of heart function, measured as an increase the amount of blood pumped, the so-called ejection fraction. By other measures of health, however, such as regeneration of heart muscle or preventing heart attacks, the trials may have been a success, argued some of those who conducted them. ... It's sad, but it's life. should we be discouraged? Certainly not."

Another Engineered Calorie Restriction Method (October 02 2007)
It's been worms all the way down the past few days, and more worm engineering here via ScienceDaily: "worms live to an older age when they are unable to process the simple sugar glucose ... The findings may also cast some doubt on the prevailing treatments for type 2 diabetes, all of which are aimed at lowering blood levels of glucose by increasing the amount of sugar taken up by body tissues ... researchers exposed the nematode Caenorhabditis elegans to a chemical that blocked the worms' ability to process glucose, producing a metabolic state the researchers said resembles that of dietary glucose restriction. That treatment extended the worms' life span up to 20 percent ... Unable to depend on glucose for energy, the long-lived worms ramped up the activity of cellular powerhouses known as mitochondria to fuel their bodies ... That mitochondrial activity led to the increased production of reactive oxygen species, sometimes referred to as free radicals. In turn, the worms' defenses against 'oxidative stress' increased."

SIRT1 Benefits Demonstrated in Mice (October 01 2007)
There has been some discussion and back and forth in recent years as to whether manipulation of SIRT1 is really going to trigger calorie-restriction-like benefits in mammals. Researchers have now amply demonstrated that it can in mice: "We generated mice that overexpress the sirtuin, SIRT1. Transgenic mice have been generated by knocking in SIRT1 cDNA into the beta-actin locus. Mice that are hemizygous for this transgene express normal levels of beta-actin and higher levels of SIRT1 protein in several tissues. Transgenic mice display some phenotypes similar to mice on a calorie-restricted diet: they are leaner than littermate controls; are more metabolically active; display reductions in blood cholesterol, adipokines, insulin and fasted glucose; and are more glucose tolerant. Furthermore, transgenic mice perform better on a rotarod challenge and also show a delay in reproduction. Our findings suggest that increased expression of SIRT1 in mice elicits beneficial phenotypes that may be relevant to human health and longevity."

Joining the Dots in CR Biochemistry (October 01 2007)
While researchers continue to blaze ahead to find new dots in the calorie restriction (CR) puzzle, there's much to be said for the steady work of joining the existing dots and establishing chains of cause and effect. "Dietary restriction (DR) is the most effective environmental intervention to extend lifespan in a wide range of species. However, the molecular mechanisms underlying the benefits of DR on longevity are still poorly characterized. AMP-activated protein kinase (AMPK) is activated by a decrease in energy levels, raising the possibility that AMPK might mediate lifespan extension by DR. ... we find that AMPK is required for this DR method to extend lifespan and delay age-dependent decline. We find that AMPK exerts its effects in part via the FOXO transcription factor DAF-16. FOXO/DAF-16 is necessary for the beneficial effects of this DR method on lifespan. Expression of an active version of AMPK in worms increases stress resistance and extends longevity in a FOXO/DAF-16-dependent manner. Lastly, we find that AMPK activates FOXO/DAF-16-dependent transcription and phosphorylates FOXO/DAF-16 at previously unidentified sites, suggesting a possible direct mechanism of regulation of FOXO/DAF-16 by AMPK."



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