Longevity Meme Newsletter, September 11 2006

September 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.



- What To Learn From Nanotechnology Advocacy
- Gene of the Week: p16INK4a
- Discussion
- Latest Healthy Life Extension Headlines


Matters always become interesting when large sums of money enter a young field - everything speeds up and conflicts come to the fore. This has happened in nanotechnology research, development and advocacy over the past few years. In this sense, advocacy for advanced nanotechnology research is years in advance of advocacy for healthy life extension research: greater funding has entered their field; public awareness and support is more widespread.

We advocates for healthy life extension science can learn from the struggles, successes and setbacks in the nanotechnology arena. In particular, we'd like to avoid any sort of internal warfare wherein the supporters of short-term, modest goals attack and denigrate those who advocate long-term planning or ambitious - but still plausible and scientific - goals. Exactly this has happened in the nanotechnology field, for reasons I believe have a lot to do with name and brand confusion:


"When I talk about nanotechnology or nanomedicine, I have to clarify what I mean. 'Nanotechnology' has become such a broad term that it is meaningless to invoke it without qualifiers (early, advanced, existing, future, etc). Are you talking about nanoscale engineered such as that under development for new cancer therapies to guide drugs with pinpoint accuracy? Or are you talking about molecular manufacturing and the future production of goods, atom by atom? There are many other shades and meanings.

"Once you have a collision of namespaces, conflict is inevitable. We can see this in the healthy life extension community for the term 'anti-aging.'


"The actual details of conflict, personalities involved and so forth are somewhat irrelevant - it all stems from the brand collision and resulting issues with conservative funding sources, public perception, support and so forth. I think we can trace back all the real acrimony over the nanotechnology namespace to the point at which initiatives to gain large-scale public funding started to obtain results. Some folk felt that molecular manufacturing advocates were reducing their chances of obtaining funding, and so went on the attack. Human nature at its worst, as usual."

I believe we can avoid the worst of this sort of situation while still moving towards what we believe to be the fastest, best possible path forward to the development of working longevity medicine. It all comes down to not stepping on other people's namespaces and brands; carving out your own space and making your position very clear.


There has been a deal of discussion this week on research demonstrating the importance of the gene p16INK4a in aging, cancer and stem cell activity. The scientists are still chewing it over, but expect to hear much more about this one.


"I think if you asked before these studies whether you could delete a single gene and rescue stem cell function in multiple tissues, and neurogenesis in an old brain, many people would have said that aging is such a complex phenomenon that you would not get a significant effect."

Like many such mechanisms discovered in recent years, it aptly demonstrates the evolutionary trade-off between reduced function (aging) and cancer. Future, very advanced biotechnology might be able to give you a biochemistry that does neither of these two things - but waiting for that day isn't the fastest path to a longer life span. From where I sit on the sidelines, it seems that tinkering with the structure of the engine - building better, longer-lasting components for hot-swapping on the go - is not as utilitarian a way forward as developing the means to repair accumulated age-related damage to the present engine. Building longer-lasting components is a matter of slowing aging; repairing damage is a matter of preventing and reversing aging.

Look at it this way: you might gain as much in the first decade of full-on commercialization from the results of either of these two different philosophies of development, but replacing a component of your biochemistry in order to slow aging is a one-time deal per component. You change your biochemistry, and there you go, running on the same old timer with a few extra ticks of the second hand. With a working repair technology, you can keep coming back again and again until something else becomes the limiting factor to your health and life span.


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!


Founder, Longevity Meme



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/

ACT As Funding Barometer (September 10 2006)
The health of Advanced Cell Technology (ACT) is still, I think, a fair barometer of support and funding for embryonic stem cell research. The latest from UPI: "Advanced Cell Technology said Friday it has closed two financings generating approximately $13 million in cash. ... ACT said it would also use the proceeds toward three therapeutic programs that the company said it hopes to bring to clinical trials, including therapies to treat degenerative eye disease, heart and vascular disease, and technology to regenerate skin damaged by wounds, burns and in surgical procedures." It seems that private investors have decided there is now little risk of US politicians criminalizing therapeutic cloning or otherwise directly suppressing freedom of research in ways that would impact companies like ACT.

To Defeat Frailty (September 10 2006)
Viewpoints on aging - on therapies, what aging is, and how much can be done to stop it - continue to change for the better. From the San Franciso Chronicle: "Researchers are finding that frailty may not be the inevitable result of aging but rather is a preventable and perhaps treatable condition. The muscle weakness, exhaustion, and weight loss typical of frailty were until recently considered just byproducts of diseases and the general loss of vitality during one's advanced years. Now scientists are studying the condition in its own right." The article looks at very early first steps, both in opinions of aging and medical science. In the years ahead, we will be able to do far more to prevent aspects of age-related degeneration and thus extend healthy life span - but only if a foundation of widespread support and understanding for scientific longevity research is set down now.

He Did Nothing, But Neither Did You (September 09 2006)
A light and fluffy article from the Guardian can be taken quite seriously at its heart: "He was the first yuppy president. But he did nothing to stop a process even more urgent than global warming: ageing. ... Clinton was our first yuppy president, and yuppies thought that we owned youth. Nobody else has ever been as young as us, and nobody else ever will be." We are entering an era in which every one of us can make a contribution to the fight against aging. Not on a personal level, because there's precious little you can do there at this time, but to support the science and research that will actually stop age-related degeneration in its tracks. You can contribute to the MPrize or the research supported by the Methuselah Foundation. You can get out there and encourage others to do the same. You can help show people just how close medical science is to successfully tackling the underlying causes of aging. If you don't do this, you'll only have yourself to blame if we fail to make meaningful progress in our lifetimes.

Biotechnology From the Labs (September 09 2006)
A new mini-feature from the MIT Technology Review: short digests to explain the significance of selected research. Scientists "found that a drug similar to ones used to treat Parkinson's disease can spur growth of new neurons in the substantia nigra, the brain area damaged in the disease. ... Current treatments for Parkinson's disease replace or mimic dopamine, an important signaling molecule in the brain. But those treatments lose their effectiveness over time; boosting the brain's ability to make more of the dopamine-­producing cells could provide a more effective strategy. ... Ultimately, they hope to find compounds that will help replace cells lost in a range of neurodegenerative diseases, such as Alzheimer's and Huntington's."

Longevity Dividend, September 12th (September 08 2006)
A reminder from the newswires: the Longevity Dividend symposium in Washington DC is coming up on the 12th. "The Alliance for Aging Research, along with prominent scientists, will call for governments and health care organizations to invest in the extension of healthy life in order to produce a 'longevity dividend.' Scientists will urge U.S. policymakers to invest in scientific discovery to slow aging in humans. As lifespan dramatically increases, so does national health care spending on a wave of chronic diseases and disabilities such as Alzheimer's, congestive heart failure, cancer, stroke, diabetes and vision loss. Speakers will address such topics as: when science will be able to slow aging and the cost; can older populations make nations both healthier and wealthier; and international perspectives." The list of endorsements of the Longevity Dividend position statement is growing rapidly, by the look of it.

Stem Cells for Enhancement? (September 08 2006)
If the introduction of more stem cells helps when you're aged and injured, could it also help you push off age-related degeneration, or otherwise improve the duration of some youthful capacities? The profit motive in professional sports seems the most likely way to answer that open question, given that enhancement (and even prevention, all too often) isn't on the regulatory agenda for mainstream medical research funding. "There's a spin-off technology from stem cells that could produce super-athletes ... injecting stem cells into healthy muscles might increase their size and even restore them to their youthful capacity. ... You could potentially find a 40-year-old man with 20-year-old legs." Sadly, there's all to much to aging that you can't fight with forms of regenerative medicine or enhancement via boosting stem cell activity - if such proves plausible. That shouldn't stop us from trying for those gains that can be had.

Attacking Neurofibrillary Tangles (September 07 2006)
Most Alzheimer's research is focused on understanding and eliminating amyloid plaque, although there's some evidence of late that the plaque itself may not be the best point of aim for potential therapies. Another line of investigation revolves around neurofibrillary tangles. From Forbes, news of progress on this front: "In tests with mice and fruit flies, an enzyme appeared to both eliminate the tangles and reduce the brain's decline. ... It's not clear if tangles hurt brain cells or are just a symptom of a dementia problem. ... The point is that they're totally correlated with neurodegeneration in Alzheimer's disease, and in a number of other dementias. ... In some forms of dementia, tangles are 'the whole story' because amyloid plaques aren't present. ... it will likely take years for a drug for humans to be developed ... research into tangles has lagged behind research into ways to combat amyloid plaques."

Cause of Angiogenesis in AMD (September 07 2006)
EurekAlert! notes another step towards preventing age-related macular degeneration (AMD): "Uncontrolled blood vessel growth (angiogenesis) is a major contributor to the development of age-related macular degeneration (AMD) ... [researchers] found that the molecule, Carboxyethylpyrroles (CEPs), attaches to proteins found in the eye, triggering the uncontrolled growth of blood cells. ... The researchers did in vivo animal studies with membranes from chicken eggs and rat eyes and found that CEPs attached to proteins induce angiogenesis. They also found that the protein part of CEP-protein adducts is not important for producing the growth of the blood vessels. Rather, the actual CEP is the cause of angiogenesis. In an attempt to block CEP from triggering the angiogenesis process [we] are now trying to find the receptors - the keyholes - in the retina cells that are activated by CEPs. We are also designing drugs that can mop up the CEPs or prevent their formation."

Smad7, Aging Skin and Cancer (September 07 2006)
(From the Medford News). "In humans, scientists and medical doctors documented the aging skin phenotype a long time ago, and the [gene] Smad7 over-expression in aged skin was reported a few years ago, but nobody knew whether these two events had any link ... They found that Smad7 over-expression shifts the epidermal stem cell differentiation program from forming hair follicles to sebaceous glands, causing the mice to exhibit balding and oily skin. ... independent of its normal role in blocking signaling from a group of genes called Smad, Smad7 shuts down signaling of another group of genes called Wnt ... Wnt signaling is critical for organ development, but if Wnt signaling is too active, it also causes cancer." Once again, aging or cancer is the choice in an aspect of our present biochemistry; many of the changes seen in aging turn out to have something to do with cancer suppression.

A Mechanism of Cellular Aging (September 06 2006)
Via EurekAlert!, a biomechanism of cellular aging: "Three separate studies confirm a gene that suppresses tumor cell growth also plays a key role in aging. The researchers found increasing concentration, or expression, of the gene p16INK4a in older cells; these aging cells worked poorly compared to young cells and remembered their 'age' even when transferred from old mice to young mice. ... The studies indicate that certain stem cells lose their ability to divide and replace themselves with age as the expression of p16INK4a increases ... even though old mice lacking p16INK4a show enhanced stem cell function, they do not live longer. This is because p16INK4a is an important cancer-suppressor gene, and mice lacking p16INK4a develop more cancers than old, normal mice ... p16INK4a loss was associated with an improvement in some but not all of the consequences of aging." The age-old story: cancer or aging, pick one. Setting forth to repair the accumulation of damage seems like a better plan than tweaking the mechanism for greater performance at this point.

The State of Glycosylation Engineering (September 06 2006)
An interesting article on the state of glycosylation biochemical engineering can be found at Chemical & Engineering News. A great deal of expertise and practice in the use of biochemistry to perform and reverse glycation reactions exists, by the look of it. "Carbohydrate chemists and biochemists tend to be controlling personalities. They aren't satisfied with the way sugar groups are attached naturally to glycosylated proteins and natural products. These scientific drill sergeants think they can do better. So they're busy most days devising new ways to whip fractious glycosylated biomolecules into shape. And these control freaks are actually making remarkable progress at achieving their desired results." All this expertise could be turned towards developing the means of dealing with advanced glycation endproducts (AGEs) and their role in age-related conditions.

Rheumatoid Arthritis and p38 (September 05 2006)
The New Scientist reports on a recent PLoS Medicine paper: "People with rheumatoid arthritis tend to die about five to 10 years earlier than others, so this is not just feeling stiff in the morning ... Nerves in bodily extremities, such as hands and feet, can produce compounds that increase inflammation. The new results suggest that p38 [an enzyme involved in joint inflammation] is an early part of the pathway that sends signals from the central nervous system to these distant nerves ... Clinical trials are currently underway to test if blocking p38 throughout the body can stop the progression of arthritis in humans." Chronic inflammation is no joke when it comes to consequences for your health and life span; it seems to be a potent source of age-related damage.

Stem Cells In the Heart (September 05 2006)
From News-Medical.net, a look at further discoveries in adult stem cell populations: "We have first demonstrated in humans that, as in the animal model, failing hearts still possess cells that show all the features of stem cells in vitro. Cardiac stem cells (CSC) are indeed able to proliferate giving rise to other stem cells (property named self-renewal); they can differentiate into all the cells composing the cardiac tissue, for example myocytes and endothelial cells, (property named multipotency)." The authors show that the stem cell populations in damaged hearts differ from their counterparts in healthy hearts. That doesn't tell us what is cause and what is effect, however. It does raise the possibility of existing stem cells being mobilized in some way rather than the use of transplanted stem cells (autologous or otherwise) for therapy.

Korean Funding For Longevity Research (September 04 2006)
Via the International Herald Tribune: "The [South Korean] Science and Technology Ministry will provide [US$20.9 million] to scientists over the next nine years for research to develop technologies to help people avoid the effects of aging. The main areas for the work will be how to improve cardiovascular fitness, prevent diabetes and other aging-related diseases and prevent oxidation-reduction reaction in cells, the main cause of aging ... This project is aimed at helping people live long, healthy lives. We gave this project a higher priority when selecting new projects, considering the problem of aging society." Allowing for mangling of the science after multiple layers of translation, this sounds like a trial run of funding for something similar to the Longevity Dividend research proposal. The open acknowledgement of the goal of healthy life extension is very positive. If you can talk about that goal in grant proposals and still get funded - by no means the case in most funding infrastructures - better and more effective longevity science is only a step away.

Progress Towards Artifical Eyes (September 04 2006)
I'm going to go out on a limb and predict, from progress in the past few years, that regenerative medicine for age-related blindness will be practical and effective before artificial eyes arrive on the scene. Which is not to say that the present state of bionic vision is bad: extremely limited vision is far, far better than no vision, and this technology will only get better with time. From COSMOS Magazine: "Early tests of a 'bionic eye' developed by Australian researchers have successfully stimulated limited visual sensation in people suffering a rare form of genetic blindness. ... the prototype bionic eye was a low-risk device for patients because it sat on the eye's surface and did not require invasive surgery. He said it was an exciting development for people suffering conditions such as retinitis pigmentosa, an irreversible genetic condition where the retina's cells gradually die but the optic nerve survives."



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