Longevity Meme Newsletter, June 15 2009

LONGEVITY MEME NEWSLETTER
June 15 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.

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CONTENTS

- Read the Fable of the Dragon-Tyrant
- SENS 4 Early Registration Deadline is Today
- The Benefits of Falling Costs in Biotechnology
- Discussion
- Latest Healthy Life Extension Headlines

READ THE FABLE OF THE DRAGON-TYRANT

I was reminded yesterday that a great many folk new to the pro-longevity community haven't yet read the Fable of the Dragon-Tyrant. It is a short and powerful fairy tale that points out how people both blind themselves to the great suffering caused by aging and fail to work towards medical technologies to ameliorate or reverse aging. Go and read it if you haven't done so:

http://www.nickbostrom.com/fable/dragon.html

"Once upon a time, the planet was tyrannized by a giant dragon. The dragon stood taller than the largest cathedral, and it was covered with thick black scales. Its red eyes glowed with hate, and from its terrible jaws flowed an incessant stream of evil-smelling yellowish-green slime. It demanded from humankind a blood-curdling tribute: to satisfy its enormous appetite, ten thousand men and women had to be delivered every evening at the onset of dark to the foot of the mountain where the dragon-tyrant lived. Sometimes the dragon would devour these unfortunate souls upon arrival; sometimes again it would lock them up in the mountain where they would wither away for months or years before eventually being consumed."

SENS 4 EARLY REGISTRATION DEADLINE IS TODAY

Monday June 15th is the early registration and abstract submission deadline for the 4th Strategies for Engineered Negligible Senescence (SENS) conference.

https://www.fightaging.org/archives/2009/06/sens-4-early-registration-and-abstract-submission-deadline-approaches.php

"The conference program features 45 confirmed speakers, all of them world leaders in their field. As with previous SENS conferences, the emphasis of this meeting is on 'applied gerontology' - the design and implementation of biomedical interventions that may, jointly, constitute a comprehensive panel of rejuvenation therapies, sufficient to restore middle-aged or older laboratory animals (and, in due course, humans) to the physical and mental robustness of young adults."

You'll recognize many of the names in the program and list of accepted abstracts from past discussions at Fight Aging!. You should also take a look at the materials from the last few SENS conferences - there's a great deal of video and many fascinating presentations:

http://www.sens.org/files/sens3/
http://www.sens.org/files/sens2/

THE BENEFITS OF FALLING COSTS IN BIOTECHNOLOGY

I believe that one of the major benefits produced by the falling cost of biotechnology will be to make irrelevant the US regulatory regime that presently forbids the commercial development of therapies to slow or reverse aging.

https://www.fightaging.org/archives/2009/06/the-benefits-of-falling-costs-in-biotechnology.php

"The most important benefit of this trend, to my eyes at least, is that it will lead to a robust garage biotechnology and applied research industry, skilled amateurs working to produce new technologies in medicine, collaborating and expanding in the same way as the open source movement in software. Perhaps not in the US, given the characteristic regulatory response of the FDA to anything new in medicine, but certainly in many regions in the world. Costs will fall to the point at which small groups of reasonably intelligent people can educate themselves and work to apply to humans metabolic, genetic, and other biotechnological manipulations developed in mice or primates.

"Consider myostatin knockout mutants and their muscles, for example. Or the mice with tinkered p53 and telomerase that live 50% longer. Or the mice with additional mitochondrially-targeted catalase that also live longer. Or the efforts by SENS Foundation funded researchers to move mitochondrial DNA into the nucleus and thereby remove that contribution to the aging process: that'll be done in the lab in a handful of years if all goes according to plan.

"There are many people who would - given the opportunity to proceed - carefully assess the risk / reward scenarios and use these technologies on themselves after they are proven in mice. There are others who would wait another decade for primate studies. But there exists a large pool of potential human volunteers willing to be one of the first to use potential longevity technologies or other improvements to our biology. So I believe that this will happen in many locations despite the likely outcome of regulators effectively outlawing such activities in the US and similar countries. There is no real technical obstacle to adapting these and many other strategies to human use over the next decade or so."

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

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LATEST HEALTHY LIFE EXTENSION HEADLINES

Alzheimer's as Failure of Microglial Cells (June 12 2009)
https://www.fightaging.org/archives/2009/06/alzheimers-as-failure-of-microglial-cells/
Yet another view of Alzheimer's disease, this time as a consequence of increasing numbers of senescent microglia that no longer do their job of protecting brain cells: "In view of the recent work demonstrating presence of dystrophic (senescent) microglia in aged human brain, the purpose of this study was to investigate microglial cells in situ and at high resolution in the immediate vicinity of tau-positive structures in order to determine conclusively whether degenerating neuronal structures are associated with activated or with dystrophic microglia. ... We now report histopathological findings from 19 humans covering the spectrum from none to severe AD pathology, including patients with Down's syndrome, showing that degenerating neuronal structures positive for tau (neuropil threads, neurofibrillary tangles, neuritic plaques) are invariably colocalized with severely dystrophic [microglia] rather than with activated microglial cells. ... [The findings] support the idea that progressive, aging-related microglial degeneration and loss of microglial neuroprotection [contributes] to the onset of sporadic Alzheimer's disease."

Another View of Graying Hair (June 12 2009)
https://www.fightaging.org/archives/2009/06/another-view-of-graying-hair/
From ScienceNews: "Colorful locks depend on a group of special cells in hair follicles called melanocyte stem cells. Each of these cells divides into two cells: One that replaces itself and another that differentiates into a pigment-producing daughter cell called a melanocyte, which imbues hair with its browns, reds and blacks. Earlier research has suggested that the depletion of these stem cells was to blame for grayness. But how exactly these stem cells disappeared was mysterious. With no more stem cells around to produce melanocytes, hair turns gray. ... DNA damage causes them to lose their 'stemness,' the new report shows. Once the cells have racked up enough DNA damage, they become melanocytes and lose the ability to replace themselves or to replenish melanocyte cell populations. Once the melanocytes die, the hair is left with no pigment-producing cells." This should fuel the debate over the contribution of stochastic DNA damage to aging - perhaps diminishing stem cell populations is the important mechanism there. You might also compare this view of gray hair with the evidence for buildup of hydrogen peroxide as a cause.

Myostatin Knockout as Generally Beneficial Mutation (June 11 2009)
https://www.fightaging.org/archives/2009/06/myostatin-knockout-as-generally-beneficial-mutation/
The existence of myostatin knockout mutations suggests that we should expect to find as many beneficial single gene mutations in humans are have been discovered in mice. There are at least one or two humans walking around with a naturally occurring version of this mutation. Here's more research into the benefits: "Humans and animals with a mutation in the myostatin gene are extremely muscular and have little fat, past research shows. Also, when the gene encoding myostatin is knocked out in mice, their muscle mass increases. ... The researchers took mice that were genetically altered to develop atherosclerosis and then cross-bred them with myostatin knockout mice. Ten generations later, they had mice who were genetically predisposed to both atherosclerosis and inactivation of myostatin. ... All mice received a high-fat diet for 12 weeks, to spur the development of atherosclerosis. ... the mice with deleted myostatin gene had much less body fat and 30 percent lower fasting blood sugar and 80% lower fasting insulin levels, showing a reduction in obesity and a strong resistance to developing diabetes, the authors reported. They also had 50 percent lower low-density-lipoprotein ("bad") cholesterol and 30 to 60 percent lower levels of total cholesterol and triglycerides (fats in the blood), respectively. These results indicate protection against the development of atherosclerosis."

Never Too Late to Exercise (June 11 2009)
https://www.fightaging.org/archives/2009/06/never-too-late-to-exercise/
It's never too late to gain significant health benefits from exercise - but that's no excuse to put it off, given the ongoing damage you'll do to yourself via years of a sedentary lifestyle. "It seems that the older we get, the less active we are. But why? According to the findings of a [recent study], the most powerful 'deterrent' among the over-65s is a lack of interest, and disbelief that exercise can enhance and/or lengthen life. It's what Bob Laventure [classifies] under the 'it's too bloody late for me' excuse. [But] studies show improvements in balance, strength, gait, muscular power, blood pressure, endurance and bone density as a result of regular physical activity in older age. For example, one study on 90-year-old women in a nursing home found that 12 weeks of strength training took the equivalent of 20 years off their thigh muscle age, resulting in improved walking and mobility. Another study found that six months of regular exercise increased VO2 max (a measure of aerobic fitness) by 30% in 60-70-year-olds. Exercise even helps you live longer - research from Harvard University found that men who burned 2,000 calories a week through exercise lived two-and-a-half years longer, on average, than sedentary men."

Viral Vectors Versus Lung Cancer (June 10 2009)
https://www.fightaging.org/archives/2009/06/viral-vectors-versus-lung-cancer/
An example of the sort of work presently taking place in cancer research laboratories: "A new lung cancer therapy employing a vaporized viral vector to deliver a cancer-inhibiting molecule directly to lung tissue shows early promise in mouse trials ... Aerosol delivery targets the lungs specifically and represents a noninvasive alternative for targeting genes to the lung ... [researchers] targeted the Akt signaling pathway, which has been shown to be an important regulator of cell proliferation and cancer progression. A recent report found that 90 percent of non-small cell lung carcinomas were associated with the activation of the Akt signaling pathway. They chose a lentiviral vector [known] for its ability to infect nondividing cells and effect persistent genetic changes. They transfected the lentiviral vector with a negative regulator of Akt signaling [which] would theoretically inhibit Akt signaling, thus suppressing cancer cell proliferation and tumor growth." This strategy produced material benefits in mice, albeit not quite as impressive as some other technology demonstrations of virally delivered therapies.

Hourglass X (June 10 2009)
https://www.fightaging.org/archives/2009/06/hourglass-x/
The tenth Hourglass blog carnival is up: "As we age, we all suffer from some level of neurodegeneration, though in most cases this falls below the threshold of a clinical pathology. Slow chronic change isn't the only form of age-related brain damage: let's not forget about strokes, which can wipe out otherwise healthy neurons in macroscopic regions of the brain. While the risk factors for stroke and neurodegeneration are distinct, therapies might ultimately be quite similar - since in both cases, the goal is to regrow neurons to replace those that have been lost. At Brain Stimulant, Mike tell us about a clinical trial that will use stem cells to treat stroke ... Colin Farrelly of In Search of Enlightenment has submitted two long, thoughtful articles, the first about the clinical and social importance of tackling aging, the second about the cognitive biases that affect the way we think about risk and the significance of aging as a cause of mortality ... In a rational world, aging research would be at the forefront of a global collaborative initiative to improve the health and economic prospects of today's aging populations (and all future generations). But humans are not rational. We suffer many cognitive biases."

Blaming Senescent Cells For Autoimmune Disease (June 09 2009)
https://www.fightaging.org/archives/2009/06/blaming-senescent-cells-for-autoimmune-disease/
Senescent cells accumulate with age, a way to suppress cancer risk by shutting down damaged cells, but one that leads to all sorts of other biochemical damage. Here, researchers theorize that senescent cells lead to issues with the immune system and thus the age-related increase in risk of autoimmune disease. Compare this with the theory that issues with the immune system lead to an inability to destroy senescent cells, and thus their accumulation. As you can see many very fundamental and important issues of cause and effect in the aging body are still up for debate. "If the hypothesis is correct, the control of the formation, accumulation and elimination of senescent cells can be used to prevent and/or treat autoimmune diseases. The accumulation or removal of senescent cells would modify the microenvironment and therefore the immune reaction. Many other problems caused by immunosenescence can be also partially explained by our hypothesis. Basically, the accumulation of senescent cells is a finely regulated process. Every imbalance in the accumulation of senescent cells between the immune system and the potential target organs can initiate a chronic inflammation or autoimmunity."

Growing New Organs in the Lab (June 09 2009)
https://www.fightaging.org/archives/2009/06/growing-new-organs-in-the-lab/
From Singularity Hub: "Why transplant an organ when you can grow yourself a new one? This research isn't something that might happen in the distant future. It's being used today to grow fresh organs, open up new ways to study disease and the immune system, and reduce the need for organ transplants. ... So how many different types of human organs have been grown and transplanted? The lab-grown bladders are among the only transplants of an entire organ, but a wide variety of partial organ transplants have taken place. Skin cells are regularly grown in culture and grafted onto patients' bodies. A graft was grown from a patient's trachea cells and transplanted to replace part of her airway that had degraded due to disease. Cartilage has been grown and transplanted into a patient's knee. ... Merely a decade ago, tissue engineering was still a new field that struggled to find funding and support. Today, thousands of scientists worldwide are coordinating efforts to reach new breakthroughs, and the demonstrated potential of these methods has helped bring in investors."

Theorizing on Germline Cells and Induced Longevity (June 08 2009)
https://www.fightaging.org/archives/2009/06/theorizing-on-germline-cells-and-induced-longevity/
An interesting line of thought via EurekAlert!: "In the sense that organisms existing today are connected through a chain of life - through their parents, grandparents and other ancestors - almost a billion years back to the first animals of the pre-Cambrian era, an animal's reproductive cells can be considered to be immortal. These germline cells generate their offspring's somatic cells - other cells involved in all aspects of growth, metabolism and behavior, which have a set lifespan – and new germline cells that continue on, generation after generation. [Researchers] have found that certain genetic mutations known to extend the lifespan of the C. elegans roundworm induce 'mortal' somatic cells to express some of the genes that allow the 'immortality' of reproductive germline cells. ... The idea that somatic cells can reacquire genetic pathways usually restricted to germline cells is fascinating, and since germline protection is seen across species, the activity of these genes may play a role in controlling mammalian lifespan. Understanding the mechanisms involved in this transformation could help us develop new ways to repair and even regenerate key cells and tissues."

Aging and Healthy Lifespan Conference (June 08 2009)
https://www.fightaging.org/archives/2009/06/aging-and-healthy-lifespan-conference/
Some of the better known folk in the aging research community will be speaking at a conference held at Harvard this September: "Over the next 20 years, the population of Americans over age 65 is expected to double, and health care spending is projected to increase by 25%. With an aging society, it is crucial to understand the challenges and address the opportunities to target diseases of aging, such as cancer and type 2 diabetes, to allow people to live longer, healthier lives. The Aging and Healthy Lifespan Conference will address these timely issues. Hear leading experts discuss emerging research into scientific and medical advances in aging, as well as lifestyle and demographic trends. This first-ever conference will feature two speaker tracks. One track will focus on new research and insights in the science of aging, while the second track will feature emerging social trends in lifestyles, behaviors and activities of the aging population." I believe this is associated with the Alliance for Aging Research, and therefore much in line with the longevity dividend viewpoint.

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