Fight Aging!

LONGEVITY MEME NEWSLETTER
December 11 2006

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.

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CONTENTS

- There's a Power In Understanding Your Biochemistry
- Discussion
- Latest Healthy Life Extension Headlines

THERE'S A POWER IN UNDERSTANDING YOUR BIOCHEMISTRY

There is a large difference between driving a car, and driving a car as an amateur mechanic and tinkerer. The same goes for the human body - the more you know, the more empowered you are. Aging is fearsome and inevitable only when it is mysterious and unknown, just like that rattling from the transmission you know you're going to hear some day. But if you know how the engine runs, you know what to look for from the mechanics of this world - even if that means knowing that some things are, in fact, still unknown, or that the mechanics have a lot work to do in order to be able to fix the issues that concern you.

In that vein, here is a brief trip past a portion of your aging biochemistry:

https://www.fightaging.org/archives/001057.php

"Evolution is a harsh but efficient mistress; you can consider yourself surprisingly well optimised as a piece of machinery, but your warranty only goes so far as the number of years in which your recent ancestors contributed to the success of their offspring. After that, you're on your own - biochemical processes unwind and break down free from any past selective pressure to do better. Take the immune system, for example, one of many absolutely vital components in the very complex system that supports your life. It is remarkably well optimized for reliable and effective use of resources in early and mid-life, but the rules that govern that optimization lead to a system that breaks down badly after extended usage."

https://www.fightaging.org/archives/001058.php

"A chain of dominos exists in your cellular biochemistry. It starts with the accumulation of damaged mitochondrial DNA and ends with a good 1% of your cells turned into bloated generators of damaging chemicals. These chemicals spread throughout your body, degrading important systems, causing pain, illness and suffering - until eventually something fails explosively enough to kill you. So it is probably of interest to most of us just how and when mitochondrial DNA might be repaired. As it turns out, there has been some debate in past years as to whether or not the body does perform these repairs, or is capable of doing so, and what sort of repairs are possible."

Knowledge is power. If you are unfamiliar with the details of the engine, you won't know that you can benefit from helping mechanics develop the necessary skills to repair it. So it is with aging and the human body. We know enough to set the path ahead, to determine what must be repaired, to visualize the toolkit we would like to have available - but much more help and support is needed.

http://www.longevitymeme.org/projects/

DISCUSSION

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!

Reason

Founder, Longevity Meme

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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/

The Growing Role of Ink-Jets (December 10 2006)
http://www.eurekalert.org/pub_releases/2006-12/cmu-pte120506.php
Ink-jet printing is well on the way to becoming a foundation stone for the next generation of tissue engineering technology. From EurekAlert!: "The custom-built ink-jet printer [can] deposit and immobilize growth factors in virtually any design, pattern or concentration, laying down patterns on native extracellular matrix-coated slides (such as fibrin). These slides are then placed in culture dishes and topped with muscle-derived stem cells (MDSCs). Based on pattern, dose or factor printed by the ink-jet, the MDSCs can be directed to differentiate down various cell-fate differentiation pathways ... Because the ink-jet system employs such precision, it could be used one day to co-culture multiple MDSC lineages - including bone, muscle and other cell types - in complex, patterned configurations that could be incorporated directly into specific areas of the body in need of repair of multiple tissue types ... such as joints where bone, tendon, cartilage and muscle interface."

More On IGF-1 and Calorie Restriction (December 10 2006)
http://mednews.wustl.edu/news/page/normal/8388.html
Calorie restriction (or rather protein restriction in this case - there is a difference) is linked with reduced levels of insulin-like growth factor-1 (IGF-1): "people on a low-protein, low-calorie diet had considerably lower levels of a particular plasma growth factor called IGF-1 than equally lean endurance runners ... That suggests to us that a diet lower in protein may have a greater protective effect against cancer than endurance exercise, independently of body fat mass. ... Past research has linked pre-menopausal breast cancer, prostate cancer and certain types of colon cancer to high levels of IGF-1, a powerful growth factor that promotes cell proliferation. Data from animal studies also suggest that lower IGF-1 levels are associated with maximal lifespan." Some commenters feel that the study didn't control enough of the other variables to make any strong suggestion, but the evidence is piling up.

Cholesterol and Alzheimer's (December 09 2006)
http://www.nyas.org/ebriefreps/main.asp?intEBriefID=579
The New York Academy of Sciences on cholesterol and Alzheimer's disease (AD): "Over the past decade, as cell biologists and biochemists have investigated the complex pathogenesis of AD with new tools in neurochemistry, the metabolic pathways of cholesterol in the brain have generated fruitful and promising research, produced new ideas, and helped to advance old hypotheses. Epidemiologic observations support a relationship between lipid metabolism in the brain and AD, but much work remains to elucidate it and harvest any clinical yield. ... Importantly, the AD-cholesterol link is consonant with the amyloid cascade hypothesis. Although not the only proposed explanation, it is by far the best supported and has generated a preponderance of research. It proposes that AD arises through a chronic and deleterious imbalance between ß-amyloid (Aß) formation and clearance, leading to the accumulation of insoluble plaques and tangles."

An Interview With John Schloendorn (December 09 2006)
http://pimm.wordpress.com/2006/12/08/john-schloendorn-the-lysosens-connection-chat-on-life-extension/
Over at Pimm, you'll find an interview on healthy life extension with LysoSENS researcher John Schloendorn: "LysoSENS by itself is meant to address only parts of the age-related damage we accumulate. Magically achieving all LysoSENS goals would not extend life greatly, because other exponentially rising causes of death should rapidly take over, most importantly cancer. Thus, LysoSENS by itself would presumably count as moderate life extension. However, the major part of the reason I am doing LysoSENS is to support the Methuselah Foundation and all of its efforts. The goal of the Methuselah Foundation is to 'declare the arrival of the real war on aging and use our new tools to attack aging at its root, the fundamental biological processes which drive it.' A proof of concept for LysoSENS would presumably greatly increase the resource influx for the Methuselah Foundation, and so all things considered this would probably make me committed to 'maximum' life extension."

Tackling Osteoporosis (December 08 2006)
http://www.eurekalert.org/pub_releases/2006-12/uops-ob120806.php
One potential approach to halt osteoporosis is to reprogram the underlying processes of bone growth and destruction. From EurekAlert!: "Bone health is maintained by the balanced activities of osteoblasts and osteoclasts. The study shows that the inactivation of gene Atp6v0d2 in mice results in dramatically increased bone mass due to defective osteoclasts as well as enhanced bone formation. These findings may provide some clarity into the regulation of bone metabolism and show that targeting the function of a single gene could possibly inhibit bone decay while stimulating bone formation. ... Now that we have demonstrated a new approach that is theoretically attainable, one that combines the best of both worlds, we can go to work on the genes up and down stream from our target gene. If we can find a way to get to our target gene with a drug we may be able to help the millions of seniors with osteoporosis."

Stepping Towards Replacement Hearts (December 08 2006)
http://www.eurekalert.org/pub_releases/2006-12/uomh-ana120706.php
(From EurekAlert!). Scientists are rapidly working their way up the tissue engineering ladder, from small and simple to large and complex. Replacement organs for the old or damaged are in our future, and a good thing too. "It looks, contracts and responds almost like natural heart muscle - even though it was grown in the lab. And it brings scientists another step closer to the goal of creating replacement parts for damaged human hearts, or eventually growing an entirely new heart from just a spoonful of loose heart cells. ... researchers are reporting significant progress in growing bioengineered heart muscle, or BEHM, with organized cells, capable of generating pulsating forces and reacting to stimulation more like real muscle than ever before. The three-dimensional tissue was grown using an innovative technique that is faster than others that have been tried in recent years, but still yields tissue with significantly better properties."

Attacking Cancer Stem Cells (December 07 2006)
http://www.eurekalert.org/pub_releases/2006-12/jhmi-nps120706.php
Now that scientists are getting a handle on cancer stem cells, it comes time to develop the means to precisely attack these cells, and thereby strike at the root of cancer. EurekAlert! outlines one of many early attempts: "The most common type of brain cancer - glioblastoma - is marked by the presence of these stem-cell-like brain cells, which, instead of triggering the replacement of damaged cells, form cancer tissue. Stem cells, unlike all other cells in the body, are capable of forming almost any kind of cell when the right 'signals' trigger their development. For their treatment experiment, the researchers relied on a class of proteins, bone morphogenic proteins, that cause neural stem-cell-like clusters to lose their stem cell properties, which in turn stops their ability to divide." The first step to working the machine is understanding what the levers do; our understanding at this level is still very crude, but even this is sometimes enough to get the job done.

Stem Cell Transplants For Parkinson's (December 07 2006)
http://www.sciencedaily.com/releases/2006/12/061204123212.htm
A number of research groups are working on different approaches to regenerating the neurons that fail and die in Parkinson's disease. From ScienceDaily: "a human neural stem cell transplant essentially enables an animal model for Parkinson's to continue functioning normally ... researchers compared animals that received placebo treatment with those that received only protective neurotrophic factors secreted by stem cells and those that had a transplant. Animals that received transplants essentially regained control of their movement, placebo-treated animals did not recover and those that received neurotrophic factors, called stem cell factors, recovered partially. ...transplanted neural cells had formed synapses to communicate with each other and ultimately the striatum, the portion of the brain dopaminergic cells act on to control movement."

And What About the Whales? (December 06 2006)
http://www.rochester.edu/news/show.php?id=2698
The expression of telomerase, and therefore risk of cancer, has apparently been tailored by evolution to scale by body mass (meaning total number of cells): "Until now, scientists believed that our relatively long lifespans controlled the expression of telomerase - an enzyme that can lengthen the lives of cells, but can also increase the rate of cancer. ... Mice express telomerase in all their cells, which helps them heal dramatically fast ... but the flip side of it is runaway cell reproduction - cancer ... evolution has found that the length of time an organism is alive has little effect on how likely some of its cells might mutate into cancer. Instead, simply having more cells in your body does raise the specter of cancer - and does so enough that the benefits of telomerase expression, such as fast healing, weren't worth the cancer risk. ... What, then, does this mean for animals that are far larger than humans? If a 160-pound human must give up telomerase to thwart cancer, then what does a 250,000-pound whale have to do to keep its risk of cancer at bay? ... It may be that whales have a cancer suppressant that we've never considered."

Australians End Research Ban (December 06 2006)
http://www.washingtonpost.com/wp-dyn/content/article/2006/12/06/AR2006120600215.html
The Washington Post notes that Australian politicians have ended their ban on therapeutic cloning - a vital technology for the advance of stem cell medicine. Australia is a representative democracy of an authoritarian bent; this sort of thing should be a clear warning for those who call for more power in the hands of government. When that happens, it will be people who don't know you and don't care what happens to you who will control your access to medicine and longevity technologies, both directly and by suppressing research. Is that really what you want? "The law passed Wednesday allows therapeutic cloning, the splicing of skin cells with eggs to produce stem cells, also known as master cells, which are capable of forming all the tissues of the human body. Scientists hope stem cell research will eventually lead to treatments for conditions including Parkinson's and Alzheimer's, as well as spinal cord injuries, diabetes and arthritis."

Sinclair on Metabolism and Aging (December 05 2006)
http://www.msnbc.msn.com/id/15994157/site/newsweek/
Scientist David Sinclair holds forth on metabolism, aging, calorie restriction and his research at Newsweek: "About 70 years ago, scientists discovered that when animals are forced to live on 30 to 40 percent fewer calories than they would normally eat, something unusual happens: they become resistant to most age-related diseases - cancer, heart disease, diabetes, Alzheimer's - and live 30 to 50 percent longer. Restricting calories slows aging. But how? What are the underlying genes that preserve vitality and stave off disease? ... Many scientists are encouraging Congress to increase funding for aging research, to launch the equivalent of the Apollo program. Only a few humans made it to the moon. In the future, millions may live a century or more, and remain vital and productive during those added years." But there are better ways forward than tinkering with metabolism (or than involving government in anything, for that matter).

CR Slows Immune System Aging (December 05 2006)
http://www.the-scientist.com/news/home/37246/
More good news for calorie restriction (CR) practitioners via The Scientist: "The link between caloric restriction and longevity may be mediated by reduced susceptibility to disease ... scientists found that calorie-restricted older adult rhesus monkeys have at least 30% more naive T cells than controls. ... Some people said there's something special about short-lived animals and that this wouldn't work in humans. This is one of the very best pieces of evidence that show those doubters may be wrong. If it works in something as long-lived as a rhesus monkey, then there's reason to hope that caloric restriction principles can work in people as well." Recall that you need naive T cells to mount a response to new invasions, and that the number of these cells declines with age - a significant part of age-related frailty is the inability to deal with infections and other microscopic threats.

All About Identification (December 04 2006)
http://www.newswise.com/articles/view/525619/
(From Newswise). This is an interesting juncture in the advance of biotechnology: scientists can accomplish a great deal with the latest tools, but learning to identify specific cells is still somewhat harder than taking action with the cells in hand. We should therefore be following the advance of identification strategies with some interest: "A sugar molecule present on embryonic stem cells also has been found on the surface of a type of adult stem cell, a discovery that may help researchers isolate and purify adult stem cells for use in therapies aimed at bone healing, tendon repair and cartilage regeneration ... With a purer cell population, you should have a more effective therapy ... Is the expression of this marker elevated in a tumor? If so, perhaps it might be useful to identify cancer stem cells."

Regenerating Intervertebral Discs (December 04 2006)
http://www.medicalnewstoday.com/medicalnews.php?newsid=57953
Another nice application of early regenerative medicine via Medical News Today: "Lower back pain (LBP) affects a large proportion of the adult population at some point in their lives and in many of these cases it is persistent, eventually leading to debilitating pain. The majority of the cases of LBP are due to degeneration of the intervertebral disc (IVD), the soft tissue which separates the vertebrae in the spine and protects them from damage ... The treatment Dr Richardson is developing uses a cell-based tissue engineering approach to regenerate the IVD at the affected level. This is achieved through the combination of the patients' own mesenchymal stem cells (MSCs) and a naturally occurring collagen gel that can be implanted through a minimally-invasive surgical technique." So far as timing goes, the researcher is "hoping to enter pre-clinical trials next year."

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