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Longevity Meme Newsletter, December 28 2009

LONGEVITY MEME NEWSLETTER
December 28 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

- Video From the Manhattan Beach Project Longevity Summit
- Longevity Changes Economic Behavior for the Better
- Trust But Verify
- Discussion
- Latest Healthy Life Extension Headlines

VIDEO FROM THE MANHATTAN BEACH PROJECT LONGEVITY SUMMIT

The recent Longevity Summit organized by Dave Kekich of the Maximum Life Foundation generated a fair number of recorded presentations and discussions. Many of these are now online at YouTube, in the Manhattan Beach Project channel. You'll find a selection of links in the following Fight Aging! post:

https://www.fightaging.org/archives/2009/12/video-from-the-manhattan-beach-project-longevity-summit.php

LONGEVITY CHANGES ECONOMIC BEHAVIOR FOR THE BETTER

We can learn a great deal from the past. Take 18th century England for example: a time and place where, for perhaps the first time in history, an established nation underwent rapid population growth alongside an equally rapid rise in standards of living. Why did this happen? The evidence points to the root cause being an increase in human longevity:

https://www.fightaging.org/archives/2009/12/longevity-tends-to-change-economic-behavior-for-the-better.php

"The paper makes a fine argument that the roots of this growth lie in a sudden increase in adult life expectancy - how many more years someone can expect to live on average once old enough to own property and make meaningful economic decisions. Those people who expect to be around longer make for better stewards of property, more diligent investors, and overall better engines of compound growth. ... When reading about transformative growth in economic activity and resulting changes in society due to enhanced longevity in the past, one has to wonder what might be in store for us in the years ahead. The proposed roots of 18th century progress are at work again today as human adult life expectancy continues to rise. None of the fundamental line items are meaningfully different between then and now: economic activity today might be more complex, but it is built upon the same truths of physics and human nature as it was hundreds of years ago. So many choices flow from our expectations of life remaining to us: what grand projects and greater wealth for all will be enabled through longer healthy lives?"

TRUST BUT VERIFY

Why should you choose to believe anything that is said about engineered longevity? Some thoughts on the matter:

https://www.fightaging.org/archives/2009/12/the-maesgarreau-tendency.php

"Ideally, we'd never take anyone's word for anything, and have the time and means to dig up supporting evidence for any position or statement that we encounter. But who has the time for that? We have to organize our busy lives around blocks of selective ignorance, portions of human knowledge and culture wherein we choose to take statements at face value, or follow the consensus viewpoint without doing the necessary groundwork to validate it.

"I put value on what Kurzweil and de Grey have to say about the potential future of increased human longevity - the future we'll have to work to bring into being - because I have performed the due diligence, the background reading, the digging into the science. I'll criticize the pieces of the message I don't like so much (the timescale and supplements in the case of Kurzweil, WILT in the case of de Grey), but generally I'm on board with their vision of the future because the science and other evidence looks solid. But few people in the world feel strongly enough about this topic to do what I have done. I certainly don't feel strongly enough about many other allegedly important topics in life to have done a tenth as much work to validate what I choose to believe in those cases. How should one best organize selective ignorance in fields one does care about, or that are generally acknowledged to be important? What if you feel - correctly, in my humble opinion - that engineered longevity is very important, but you cannot devote the time to validate the visions of Kurzweil, de Grey, or other advocates of longevity science?"

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

LONGER TELOMERES, LESS NEURODEGENERATION (December 25 2009)
https://www.fightaging.org/archives/2009/12/longer-telomeres-less-neurodegeneration/
Here is one of many studies to show some correlation between longer telomeres and slower accumulation of age-related damage. Questions remain as to where telomere length fits into aging: is it more of a cause or more of a marker of other processes? From the abstract: "Telomere shortening is a marker of cellular aging and has been associated with risk of Alzheimer's disease. Few studies have determined if telomere length is associated with cognitive decline in non-demented elders. We prospectively studied 2734 non-demented elders (mean age: 74 years). We measured cognition with the Modified Mini-Mental State Exam (3MS) and Digit Symbol Substitution Test (DSST) repeatedly over 7 years. Baseline telomere length was measured in blood leukocytes and classified by tertile as 'short', 'medium', or 'long'. At baseline, longer telomere length was associated with better DSST score (36.4, 34.9 and 34.4 points for long, medium and short) but not for change in score. However, 7-year 3MS change scores were less among those with longer telomere length. ... Findings were similar after multivariable adjustment for age, gender, race, education, assay batch, and baseline score. ... Thus, telomere length may serve as a biomarker for cognitive aging."

EXERCISE: GOOD FOR THE BRAIN (December 25 2009)
https://www.fightaging.org/archives/2009/12/exercise:-good-for-the-brain/
There exist any number of studies to demonstrate that exercise slows age-related degeneration of the brain. One obvious mechanism is a reduction in the type of damage that leads to vascular disease. Most of these are long-term investigations, but here is a comparatively short-term study demonstrating the benefits of exercise in the old: "To evaluate the effects of endurance exercise training (EET) on the cognitive status of healthy community-dwelling older adults, [a] randomized controlled trial was conducted involving community-dwelling older adults from the town of Pianoro (northern Italy). We randomized 120 healthy subjects aged 65-74 years, both genders, to treatment (N = 60) and control (N = 60) groups. The treatment consisted of 12 months of supervised EET in a community gym, 3 h a week. All participants were assessed both at baseline and after 12 months on an intention-to-treat analysis. Cognitive status was assessed by one single test (Mini Mental State Examination, MMSE). ... The control group showed a significant decrease in MMSE score, which differed significantly from the treatment group scores. The odds ratio for the treated older adults to have a stable cognitive status after 1 year, as compared to the control group, was 2.74 after adjustment for age, gender, educational level and several other possible confounders. Blood pressure, body mass index, waist circumference and serum cholesterol did not differ significantly between the two groups."

EXERCISE AND THE AGING IMMUNE SYSTEM (December 24 2009)
https://www.fightaging.org/archives/2009/12/exercise-and-the-aging-immune-system/
This review suggests that some fraction of immune system failure in later life can be laid at the feet of a sedentary lifestyle over the years - and that starting to exercise when older is not going to reverse all of that decline. "The elderly population is at an unprecedented risk of infectious diseases and [cancer] due to apparently inevitable age-related declines in immunity. The 'immune risk profile' (IRP) is an array of biomarkers that has been used to predict morbidity and mortality in older adults. As it is generally accepted that middle-aged and elderly individuals who habitually participate in moderate-intensity exercise are less likely to incur an infection than their sedentary counterparts, this review addresses current knowledge on the effects of regular exercise on aspects of adaptive immunity as they relate to the IRP. Findings from cross-sectional studies mostly show enhanced immunity in physically active compared to sedentary older adults. These include greater T-cell responsiveness to mitogens in vitro, a reduced frequency of antigen-experienced and senescent [T-cells], enhanced IL-2 production and T-lymphocyte expression of the IL-2 receptor, longer chromosome telomere lengths in blood leukocytes and in vivo immune responses to vaccines and recall antigens. In contrast, the evidence from the available longitudinal studies that have used an exercise training intervention in previously sedentary elderly to improve similar immune responses is less compelling."

AUTOPHAGY AND SIRTUIN-1 (December 24 2009)
https://www.fightaging.org/archives/2009/12/autophagy-and-sirtuin-1/
We know that autophagy is required for the health and longevity benefits of calorie restriction. Here is more on that topic: "The life span of various model organisms can be extended by caloric restriction as well as by autophagy-inducing pharmacological agents. Life span-prolonging effects have also been observed in yeast cells, nematodes and flies upon the overexpression of the deacetylase Sirtuin-1. Intrigued by these observations and by the established link between caloric restriction and Sirtuin-1 activation, we decided to investigate the putative implication of Sirtuin-1 in the response of human cancer cells and Caenorhabditis elegans to multiple triggers of autophagy. Our data indicate that the activation of Sirtuin-1 (by the pharmacological agent resveratrol and/or genetic means) per se ignites autophagy, and that Sirtuin-1 is required for the autophagic response to nutrient deprivation, in both human and nematode cells, but not for autophagy triggered by downstream signals such as the inhibition of mTOR or p53. Since the life span extending effects of Sirtuin-1 activators are lost in autophagy-deficient C. elegans, our results suggest that caloric restriction and resveratrol extend longevity, at least in experimental settings, by activating autophagy."

AN UPDATE ON TISSUE ENGINEERING OF CORNEAS (December 23 2009)
https://www.fightaging.org/archives/2009/12/an-update-on-tissue-engineering-of-corneas/
From the Telegraph: "Russell Turnbull, 38, lost most of the vision in his right eye when he had ammonia sprayed into it as he tried to break up a fight on a late night bus journey home. The attack, which badly burned and scarred his cornea, left him with permanent blurred sight and pain whenever he blinked. Now however his sight has been almost fully restored thanks to a new technique where doctors regrow the outside membrane of his cornea from stem cells taken from his healthy eye. The new operation involves cutting away a millimetre squared section of his left eye complete with stem cells and growing it to 400 times that size in the laboratory. The new outer skin of the eye is then stitched onto the badly damaged cornea in place of the damaged membrane. The technique [has] been used on eight patients and for most of them including Mr Turnbull it has almost completely restored their vision."

SEEKING FUNDING TO EXPLAIN GRANULOCYTE CANCER THERAPY (December 23 2009)
https://www.fightaging.org/archives/2009/12/seeking-funding-to-explain-granulocyte-cancer-therapy/
A press release: "In an effort to accelerate the development of a cancer treatment based on innate cancer immunity, the Direct Oncology (DO) Foundation is launching an appeal to raise $100,000 to sequence cancer resistant mice at Wake Forest University. The project is being coordinated by Livly, a Silicon Valley based non-profit corporation dedicated to the development of sustainable cures for the major diseases plaguing humankind. ... The immune systems of the mice successfully fight off different types of advanced cancer. Immune cells from these Spontaneous Regression / Complete Resistance (SR/CR) mice can be used to protect other mice from advanced cancer. Evidence suggests that there is a single place in the SR/CR mouse's genome that confers the remarkable cancer resistance. Ironically, the gene for the cancer resistance has proven inaccessible to standard mouse genetic methods, and its identity and sequence have remained elusive. The progress of clinical efforts was hampered by lack of knowledge of the genetics underlying the cancer resistance."

IMPROVING CELLULAR REPROGRAMMING (December 22 2009)
https://www.fightaging.org/archives/2009/12/improving-cellular-reprogramming/
With so many researchers working on it, potential improvements to the process of reprogramming normal cells into stem cells are arriving rapidly. Here is one example: "Scientists believe there is much promise for induced pluripotent stem cells: normal adult cells that have been manipulated to develop the stem-cell-like ability to differentiate into other types of cells, potentially to be used to repair damaged tissue and treat the ravages of disease. But making these so-called iPS cells is both time-consuming and inefficient. Now researchers [have] discovered a protein required to quickly and efficiently reprogram human skin cells to express embryonic stem cell genes. The finding could eliminate a major bottleneck in the generation of iPS and embryonic stem cells - that of removing molecular tags called methyl groups from specific regions of cellular DNA. Without this process of demethylation, the stem cell genes are silent in adult, or differentiated, cells. ... The mechanism of DNA demethylation in mammals has eluded us for decades. Now we've identified a protein involved in targeted DNA demethylation, and we've also shown that it's critically important in reprogramming adult cells to function more like their stem cell predecessors."

COAXING BLOOD VESSEL GROWTH WITH HYDROGELS (December 22 2009)
https://www.fightaging.org/archives/2009/12/coaxing-blood-vessel-growth-with-hydrogels/
From PhysOrg: "Regenerative medicine therapies often require the growth of functional, stable blood vessels at the site of an injury. Using synthetic polymers called hydrogels, researchers [have] been able to induce significant vasculature growth in areas of damaged tissue. ... Because hydrogels are very compatible with biological tissues, they are a promising therapeutic delivery vehicle to improve treatment of peripheral artery disease, ischemic heart disease, and survival of cell and tissue transplants. ... the researchers incorporated specific chemical cross-links into the gels so that they would maintain their structural integrity and only degrade in the presence of enzymes called matrix metalloproteinases that are typically expressed by invading cells. They also incorporated into the matrices a protein, vascular endothelial growth factor (VEGF), which stimulates the growth of blood vessels. ... Incorporating these cross-links controlled the release of VEGF from the matrix so that VEGF was only released as the matrix was digested by invading cells ... With the degradable implant that included growth factors, after two weeks we saw that new vessels were growing into and around the implant."

TRIIODOTHYRONINE LEVELS AND HUMAN LONGEVITY (December 21 2009)
https://www.fightaging.org/archives/2009/12/triiodothyronine-levels-and-human-longevity/
Triiodothyronine is a thyroid hormone, one of the more important central regulators of metabolic function in mammals. Longer lived mammal species, such as naked mole rats, have markedly lower levels of this hormone. As it turns out, long-lived humans seem to have slightly lower levels of triiodothyronine as well: "The hypothalamo-pituitary-thyroid axis has been widely implicated in modulating the aging process. Life extension effects associated with low thyroid hormone levels have been reported in multiple animal models. In human populations, an association was observed between low thyroid function and longevity at old age, but the beneficial effects of low thyroid hormone metabolism at middle age remain elusive. ... We have compared serum thyroid hormone function parameters in a group of middle-aged offspring of long-living nonagenarian siblings and a control group of their partners, all participants of the Leiden Longevity Study. ... When compared with their partners, the group of offspring of nonagenarian siblings showed a trend toward higher serum thyrotropin levels [in] conjunction with lower free thyroxine levels [and] lower free triiodothyronine levels ... Compared with their partners, the group of offspring of nonagenarian siblings show a lower thyroidal sensitivity to thyrotropin. These findings suggest that the favorable role of low thyroid hormone metabolism on health and longevity in model organism is applicable to humans as well."

GLUCOSE RESTRICTION IN CELL CULTURES (December 21 2009)
https://www.fightaging.org/archives/2009/12/glucose-restriction-in-cell-cultures/
One method of researching potential mechanisms of calorie restriction is to restrict glucose intake of cells in culture. Here that is shown to inhibit precancerous cells: "Cancer cells metabolize glucose at elevated rates and have a higher sensitivity to glucose reduction. However, the precise molecular mechanisms leading to different responses to glucose restriction between normal and cancer cells are not fully understood. We analyzed normal WI-38 and immortalized WI-38/S fetal lung fibroblasts and found that glucose restriction resulted in growth inhibition and apoptosis in WI-38/S cells, whereas it induced lifespan extension in WI-38 cells. Moreover, in WI-38/S cells glucose restriction decreased expression of hTERT (human telomerase reverse transcriptase) and increased expression of [cancer suppressing gene] p16(INK4a). Opposite effects were found in the gene expression of hTERT and p16 in WI-38 cells in response to glucose restriction. ... Furthermore, glucose restriction resulted in altered hTERT and p16 expression in response to epigenetic regulators in WI-38 rather than WI-38/S cells, suggesting that energy stress-induced differential epigenetic regulation may lead to different cellular fates in normal and precancerous cells. Collectively, these results provide new insights into the epigenetic mechanisms of a nutrient control strategy that may contribute to cancer therapy as well as antiaging approaches." You might recall other studies showing the practice of calorie restriction to reduce cancer risk.

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