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Longevity Meme Newsletter, January 19 2009

LONGEVITY MEME NEWSLETTER
January 19 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

- The LifeStar Project
- Another Glenn Foundation Lab Funded
- Six Years of Newsletters
- Discussion
- Latest Healthy Life Extension Headlines

THE LIFESTAR PROJECT

Allow me to draw your attention to the LifeStar Project, the brand under which the Millard Foundation will be pushing for the development of methods to repair and reverse the effects of aging:

https://www.fightaging.org/archives/001656.php
http://www.lifestarproject.org

"The Millard Foundation principals, and by extension the LifeStar Project, differ from other large Foundations interested in aging and longevity - such as the Glenn Foundation and the Ellison Foundation - by virtue of their strong support for the "repair the damage" viewpoint that informs the Strategies for Engineered Negligible Senescence. Aging is exactly the results of an accumulation of biochemical damage acquired over time: we should be trying to directly repair that damage, not just slow down its accumulation by tinkering with genes and metabolism."

The mission of the Foundation:

"To do or cause to be done whatever is necessary to develop and make available to all human beings repeatable clinical protocols which repair, reverse, and reduce the accumulations of damage and changes which interfere with the human body's innate ability to defend itself from disease and loss of functionality, as soon as humanly possible."

ANOTHER GLENN FOUNDATION LAB FUNDED

The Glenn Foundation is moving ahead steadily on the path of funding the expansion of existing centers of research into metabolism, genetics, and aging:

https://www.fightaging.org/archives/001655.php

"Breaking news was announced at the very start of the [Processes of Aging Conference at the Salk Institute] by Marc Collins that The Paul Glenn Foundation will fund the Salk Institute for aging studies at the rate of $1 million per year for the next five years, along with the prior MIT and Harvard Glenn Centers."

This is work aimed at slowing aging by manipulating metabolism and gene expression to reduce the rate at which biochemical damage occurs, usually through the standard path of drug development. As I've long said, this is a road ahead that will result in therapies that are of no use to those of grown old waiting for them - and the first generation of drugs look to be no more effective than plain old exercise and calorie restriction.

Repairing the damage of aging is most likely no harder than slowing it down, based upon the evidence to date for the types of damage that cause aging, and will produce a better class of therapy - one that can be used over and over again to reset the clock. The standard reference for this school of thought is, as ever, the Strategies for Engineered Negligible Senescence:

http://www.mfoundation.org/index.php?pagename=mj_sens_sens

SIX YEARS OF NEWSLETTERS

Time flies - it certainly doesn't seem like six years have gone by since the first Longevity Meme newsletter. That's a lot of newsletters when you look at it all in one place:

http://www.longevitymeme.org/newsletter/newsletter_list.cfm

Browsing back through the archives - an exercise recommended only for people with a lot of time to waste - gives an interesting perspective on the rate at which research and pro-longevity activism are moving forward.

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

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/

Centenarians, Cancer, and p53 (January 16 2009)
http://pmid.us/19139887
A proposed theory: "Centenarians are exceptionally long living individuals who escaped the most common age-related diseases. In particular they appear to be effectively protected from cancers. The mechanisms that underlie this protection are quite complex and still largely unclear. ... Centenarians appear to be characterised by low IGF-1-mediated responses and high levels of anti-inflammatory cytokines such as IL-10 and TGF-beta, a condition that results in protection from cancer. Both inflammation and IGF-1 pathway converge on the tumour suppressor p53. Accordingly, some studies indicate that genetic variants of p53 are associated with human longevity by providing protection from cancer mortality. ... The available data let us to hypothesise that among other possible mechanisms, well-preserved p53-mediated responses are likely a key factor contributing to protection from cancer in centenarians." You might recall research from 2007 demonstrating that suitable tinkering with p53 expression both protects from cancer and extends life in mice.

Uncoupling Protein and Longevity (January 16 2009)
http://pmid.us/19141680
Studies show that a range of strategies to reduce the level of reactive oxygen species produced by mitochondria extend life in lesser mammals - pointing to the operation of mitochondria as an important determinant of aging. One of these strategies is to increase uncoupling protein 2 (UCP2) expression, which causes mitochondria to generate more heat rather than packaged chemical energy for use in the cell. "The long-term effects of uncoupled mitochondrial respiration by uncoupling protein 2 (UCP2) in mammalian physiology remains controversial. Here we show that increased mitochondrial uncoupling activity of different tissues predicts longer lifespan of rats compared to mice. UCP2 reduces reactive oxygen species (ROS) production and oxidative stress throughout the aging process in different tissues in mice. The absence of UCP2 shortens life span in wild type mice ... Thus, UCP2 has a beneficial influence on cell and tissue function leading to increased lifespan."

Yet More On SkQ1 (January 15 2009)
http://dx.doi.org/10.1016/j.bbabio.2008.12.008
Here's a paper published last month that contains more information on the research behind mitochondrial antioxidant SkQ1: "Antioxidants specifically addressed to mitochondria have been studied to determine if they can decelerate senescence of organisms. For this purpose, a project has been established with participation of several research groups from Russia and some other countries. This paper summarizes the first results of the project. A new type of compounds (SkQs) [has] been synthesized. ... In the fungus Podospora anserina, the crustacean Ceriodaphnia affinis, drosophila, and mice, SkQ1 prolonged lifespan, being especially effective at early and middle stages of aging. In mammals, the effect of SkQs on aging was accompanied by inhibition of development of such age-related diseases and traits as cataract, retinopathy, glaucoma, balding, [graying hair], osteoporosis, involution of the thymus, hypothermia, torpor, peroxidation of lipids and proteins, etc. SkQ1 manifested a strong therapeutic action on some already pronounced retinopathies, in particular, congenital retinal dysplasia. With drops containing [SkQ1], vision was restored to 67 of 89 animals (dogs, cats, and horses) that became blind because of a retinopathy. Instillation of SkQ1-containing drops prevented the loss of sight in rabbits with experimental uveitis and restored vision to animals that had already become blind. A favorable effect of the same drops was also achieved in experimental glaucoma in rabbits. ... Thus, SkQs look promising as potential tools for treatment of senescence and age-related diseases."

How Aging Hurts Bone Healing (January 15 2009)
http://www.eurekalert.org/pub_releases/2009-01/uorm-rdh011509.php
Via EurekAlert!: "Researchers have unraveled crucial details of how aging causes broken bones to heal slowly, or not at all, [and] also successfully conducted preclinical tests on a potential new class of treatments designed to 'rescue' healing capability lost to aging. ... COX-2 levels drop dramatically with age, and that the drop most explains why stem cells no longer turn into cartilage as efficiently, an early step in the chain reaction of healing. While a role for COX-2 in bone repair had been detailed prior to the current study, the cell populations responsible for the supply of COX-2 to the fracture callus, the layer of pre-cartilage cells (cartilage progenitors) that form first around a fracture to guide bone building, had not. The team also confirmed for the first time that healing ability lost with age can be rescued by manipulating the COX-2 pathway with existing, experimental drugs. The study was in mice, but is especially relevant to human medicine because of the similarity between human and mouse COX-2 gene."

Hourglass VII Carnival: Call For Submissions (January 14 2009)
http://ouroboros.wordpress.com/2009/01/13/hourglass-vii-call-for-submissions/
Time is creeping up on the year's first Hourglass blog carnival. Get your submissions ready: "Topics of posts should have something to do with the biology of aging, broadly speaking - including fundamental research in biogerontology, age-related disease, ideas about life extension technologies, your personal experience with calorie restriction, maybe even something about the sociological implications of increased longevity. Opinions expressed are not necessarily those of the management, so feel free to subvert the dominant paradigm. If in doubt, submit anyway. Submissions should be emailed to [hourglass.host][at][gmail][dot][com]. ... By the way, if you’d like to volunteer to host, please email me directly - basically all of 2009 is wide open. If you've already hosted before, don't let that hold you back; while the carnival is young, some repeat hosting is going to be par for the course."

The LifeStar Project (January 14 2009)
http://www.lifestarproject.org
The LifeStar Project is a new initiative from the Millard Foundation, folk who are very interested in longevity science and the Strategies for Engineered Negligible Senescence view of research in particular: potential longevity therapies "are rapidly being developed, in labs all over the world, which, in combination, will be able to actually prevent age-related diseases and loss of functionality. The governments of the world are unprepared to answer this challenge, but potentially could be. What is needed - and does not yet exist - is a concerted, focused, competent, and fully-funded effort to catalyze the coalescing of this work into the complete set of therapies and protocols that will prevent the occurence of these diseases. The LifeStar World Health Initiative has been created to respond to this need. With the right approach, we believe this result can be produced within the next 10-15 years." The mission statement: "To do or cause to be done whatever is necessary to develop and make available to all human beings repeatable clinical protocols which repair, reverse, and reduce the accumulations of damage and changes which interfere with the human body's innate ability to defend itself from disease and loss of functionality as soon as humanly possible."

The Kronos Longitudinal Aging Study (January 13 2009)
http://www.acceleratingfuture.com/people-blog/?p=2769
Future Current provides a transcript for an interesting presentation from a few years back: "To be practically useful, the measurement of aging rate (by monitoring the decline of a global index of functional capacity, expressed as a rate function) must be relatively easy and inexpensive. Measured aging rate should enable empirical testing of purported anti-aging interventions in relatively short-term human clinical trials. ... The reason people don't make it to a hundred is because we don't age in our own bodies uniformly. You have different processes that are declining at different paces. In this case, this gentleman's cardiovascular system declined prematurely (this happens quite often) and hit the threshold for the viability of his cardiovascular system with a heart attack and died at age 65. He might have had perfectly good bones and perfectly good muscle, but he is just as dead at 65 and was cheated out of an extra thirty years of lifespan because his weakest link bumped him off early. Traditional medicine identifies those problems late in the game and intervenes in targeted ways to address the symptoms of the disease. If they are successful they can buy a few additional years. What we suggest as a better approach is to identify those degenerative processes as early as possible and use targeted interventions as early as possible to head it off at the pass, offering the individual many more years of healthy life expectancy."

A Mechanism For Cartilage Loss (January 13 2009)
http://esciencenews.com/articles/2009/01/12/scripps.research.scientists.find.cause.cartilage.degeneration.osteoarthritis
Via e! Science News: "loss of the protein HMGB2, found in the surface layer of joint cartilage, leads to the progressive deterioration of the cartilage that is the hallmark of osteoarthritis. ... the protein HMGB2 is uniquely expressed on the surface layer of cartilage in joints, where it supports the survival of chondrocytes, the cells that produce and maintain cartilage. Aging is associated with the loss of HMGB2 and an accompanying reduction or total elimination of chondrocytes in the superficial zone. The scientists provided further links between HMGB2 and osteoarthritis by breeding mice to be genetically deficient in HMGB2; these mice had an earlier and more severe onset of osteoarthritis. ... If small molecules can be found to prevent or stop the loss of HMGB2, or conversely, to stimulate the production of this protein, then it is possible that osteoarthritis may one day either be prevented or reversed ... Because cartilage is unable to heal itself, scientists have been searching for ways to use stem cells to grow replacement cartilage in the lab that could be used to surgically replace damaged or non-existent cartilage. With the discovery of the link between HMGB2 and surface layer protein, scientists now have a clue about how they might be able to engineer the surface layer cartilage."

The Useless Side of Aging Research (January 12 2009)
http://www.theglobeandmail.com/servlet/story/RTGAM.20090109.wtelomeres-DONOTPOST/BNStory/specialScienceandHealth/home
A long piece from the Globe and Mail looks at the folk behind supplement makers Juvenon and TA Sciences. Supplements are not the way forward, are utterly unimportant in the grand scheme of what is possible through scientific research, but somehow attract all the attention: "Once considered a fringe field littered with charlatans and quacks, anti-aging research has entered its prime. Respected scientists are pursuing regenerative medicine through stem cells, searching for clues to longevity in the genes of fruit flies, flat worms and really old men and women. Dozens of legitimate companies are developing anti-aging drugs. ... We have all the tools - we understand genes, metabolism, and these things are much easier [now] to measure and manipulate. I think we can push back all the degenerative diseases of aging. I think we can add a few years to everyone's life." No supplement or drug being sold now can do as much for a healthy person - or has anywhere near the weight of science backing it - as exercise and calorie restriction.

Influencing the Immune System (January 12 2009)
http://www.newscientist.com/article/dn16391-implant-raises-cellular-army-to-attack-cancer.html
One strategy for future immune therapies is to control existing immune cells in the body and direct them to take specific actions. For example: "Implants that sit in the body and reprogram a person's immune cells could be used to treat a range of infectious diseases and even cancer. In a trial on mice with an aggressive melanoma that usually kills within 25 days, the new treatment saved 90% of the group. Because cancer cells originate within the body, the immune system usually leaves them alone. Therapies exist that involve removing immune cells from the body before priming them to attack malignant tissue and injecting them back into a patient. Results are not encouraging, though - more than 90% of re-injected cells die before they can have any effect ... [researchers] have now developed a technique that directs the immune system from within the body - a method that is more efficient and potentially cheaper too. ... The team thinks modified versions of [their work] could be effective against a range of cancers and infectious diseases. These might also help reprogram the immune system to combat autoimmune diseases such as type 1 diabetes, caused by immune cells destroying insulin-producing cells in the pancreas."

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