Fight Aging!

LONGEVITY MEME NEWSLETTER
June 23 2008

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

- On Aging
- Lobsters and Sea Urchins
- Calorie Restriction Protects Against Sarcopenia
- Discussion
- Latest Healthy Life Extension Headlines

ON AGING

Some thoughts on aging and where we find ourselves:

https://www.fightaging.org/archives/001503.php

"There's nothing wrong with becoming old, but everything wrong with aging. Old means experienced, invested, wealthier, time-tested and just all-round better for having been around the block. Aging, on the other hand, is the direct result of biochemical damage you picked up along the way - ongoing deterioration that is a side-effect of being alive. The passage of years brings a constant flow of opportunities for growth and self-improvement, until aging takes away your ability to compete, your ability to take care of yourself, and eventually your life. Someone should look into that.

"The short story is that aging is damage and change, rust and wear for our biology that is caused by the normal operation of human biochemistry. You can't run machinery without causing wear, and you can't run factories full of machinery without creating waste by-products. Machinery with a lot of rust and wear breaks down in any number of ways, and biological machinery is no exception - just a few classes of wear, rust and buildup of waste lead to a vast array of different malfunctions."

LOBSTERS AND SEA URCHINS

Both lobsters and sea urchins demonstrate that it's perfectly possible for an organism to age far, far more slowly than humans presently do - and possibly not age at all. Beyond our first efforts to repair aging in the biology we have today, taking place over the next few decades, is the prospect of building a better human biology that doesn't need repair:

https://www.fightaging.org/archives/001504.php

"To date, there is no proven method to determine the exact age of a lobster. ... as best scientists can tell, lobsters age so gracefully they show no measurable signs of aging: no loss of appetite, no change in metabolism, no loss of reproductive urge or ability, no decline in strength or health. ... The red sea urchin [shows] no change in annual survival probability across the 6 [largest] size classes ... In addition to no change in survival probability there is no reduction in reproductive capacity with size."

These species show it is possible. Given the long history of human borrowing from nature, I think it likely that some beneficial biotechnology of longevity will eventually result from the study of long-lived and possibly ageless creatures.

CALORIE RESTRICTION PROTECTS AGAINST SARCOPENIA

Sarcopenia is the name given to age-related loss of muscle mass, a process whose cause at the biochemical level is still up for debate. Researchers have now demonstrated that the practice of calorie restriction slows this degeneration in primates, much as it slows almost all other tested aspects of degenerative aging:

https://www.fightaging.org/archives/001507.php

"We tested the hypothesis that [calorie restriction] will reduce age-related sarcopenia in a nonhuman primate. Thirty adult male rhesus monkeys, half fed a normal calorie intake and half reduced by 30% in caloric intake, were examined over 17 years for changes in [muscle mass]. Body weight-adjusted skeletal muscle mass declined somewhat in both groups but was far more rapid in the control group."

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/

Mitochondrial Uncouplers as CR Mimetics (June 20 2008)
http://pmid.us/18505478
If you somehow prevent your mitochondria from generating as much power as they were going to, making them less efficient, you lower the rate at which damaging reactive oxygen species are produced as a byproduct. This is important: "Calorie restriction is the most effective non-genetic intervention to enhance life span known to date. A major research interest has been the development of therapeutic strategies capable of promoting the beneficial results of this dietary regimen. In this sense, we propose that compounds that decrease the efficiency of energy conversion, such as mitochondrial uncouplers, can be caloric restriction mimetics. Treatment of mice with low doses of the protonophore 2,4-dinitrophenol promotes enhanced tissue respiratory rates, improved serological glucose, triglyceride and insulin levels, decrease of reactive oxygen species levels and tissue DNA and protein oxidation, as well as reduced body weight. Importantly, dinitrophenol-treated animals also presented enhanced longevity. Our results demonstrate that mild mitochondrial uncoupling is a highly effective in vivo antioxidant strategy." Antioxidant because it prevents the oxidants from being created in the first place. A good proof of concept.

Chris Patil on Aging Research and the Media (June 20 2008)
http://ageing-research.blogspot.com/2008/06/chris-patil-ageing-research-and-media.html
Researcher Chris Patil comments on aging research and the media over at Ageing Research, which you can contrast to Aubrey de Grey's position on the same issue: "For academic biogerontologists, there are two related aims of aging research. The explicit, near-term goal is improving our understanding of the aging process at multiple levels - at the cellular and molecular levels ... The (occasionally) implicit, longer-term goal is to use this understanding to create interventions that will improve the health and happiness of human beings - and here the ambitions range from the treatment of single aging-related diseases to therapies that will delay or even reverse the aging process itself. ... I think [media representations are] largely positive. Even when individual articles get their 'zing' from focusing on what I consider to be quite long-term goals, I think they still do a tremendous amount of good by raising consciousness about the biology of aging. We're entering a period of history when people will become more and more willing to appreciate the benefit of long-term thinking, especially as related to technology - we're already seeing that with the environment, and I think aging research and anti-aging medicine will be another example."

Revisiting Double-Strand Breaks and Aging (June 19 2008)
http://ouroboros.wordpress.com/2008/06/19/dna-double-strand-breaks-and-aging/
From Ouroboros: "Do DNA double-strand breaks (DSBs) have anything to do with aging? We have some reason to believe that they do. ... Paul Hasty has written two recent reviews, critically evaluating the role of DNA DSBs in the aging process. In the first (written with colleagues Han Li and James Mitchell), the authors argue from genetic evidence that DSB repair pathways are intimately connected with aging, but that the relationship is distinct from the well-documented connection between aging and repair of UV-type damage. ... In the second review, Hasty [argues] that non-homologous end-joining (NHEJ), a major pathway of DSB repair, evolved primarily as a means to slow aging - rather than to prevent cancer, as is likely the case for other DNA repair pathways." You'll find a two part discussion on the subject back a way in the Fight Aging! archives. The role of DNA damage in aging is more hotly debated and uncertain than, say, the role of mitochondrial damage or stem cell decline in aging.

Cancer Immunotherapy Progresses (June 19 2008)
http://www.telegraph.co.uk/earth/main.jhtml?xml=/earth/2008/06/18/scicanc118.xml
The Telegraph brings news of progress in cancer immunotherapy. Interestingly, this was a comparatively "simple" immune therapy - no genetic or other manipulation of immune cells, but rather generating a very large number of them, far more than the body would generate on its own. This is a similar approach to the first autologous stem cell therapies: "A cancer patient has made a full recovery after being injected with billions of his own immune cells ... The 52-year-old, who was suffering from advanced skin cancer, was free from tumours within eight weeks of undergoing the procedure. After two years he is still free from the disease which had spread to his lymph nodes and one of his lungs ... Doctors took cells from the man's own defence system that were found to attack the cancer cells best, cloned them and injected back into his body. ... The patient was one of nine with metastatic melanoma, that is skin cancer that has spread, who were being treated in a recently completed clinical trial to test bigger and bigger doses of their own white blood cells. Larger, more elaborate, trials are now under way."

Cellular Alchemy (June 18 2008)
http://www.telegraph.co.uk/earth/main.jhtml?xml=/earth/2008/06/18/scistem118.xml
In theory, given that every cell contains all our DNA and the necessary mechanisms for replication, it should be possible to generate any type of cell from any other type of cell using little more than the biotechnology of today. We just don't yet know how. Here, the Telegraph looks at small steps forward in manipulating cell state: "a new front has opened up in regenerative medicine: the direct conversion of one cell type, say a skin cell, into another, say a brain cell. ... pioneering work [showed] it is possible, turning white blood cells into red cells, but now a new [study] 'is a timely reminder' that this method is worth more study to find out the best way to create new cells and tissues for repair. ... [researchers] took specialist 'pancreatic exocrine cells' that secrete digestive enzymes, which make up to 95 per cent of the pancreas, and converted them directly into another cell type, called beta cells, which make the hormone insulin to control blood sugar levels. ... it adds to the existing evidence that a cell's destiny is no longer fixed." If you can generate all the cells you need from any cells you have to hand, that will go a long way to speeding advances in tissue engineering and regenerative medicine.

Aiming to Regenerate Cartilage (June 18 2008)
http://www.sciam.com/article.cfm?id=nanotech-cartilage
Scientific American looks a some recent initiatives aimed at regrowing lost or damaged cartilage: "Scientists envision implanting nanotubes through small incisions (in, say, a knee) that a patient's own cartilage cells would colonize. The benefit [is] that the cartilage would grow more quickly and be stronger than if it was not supported by nanotubes - similar to the way that steel rebar is used to reinforce cement or concrete." This sort of technology platform has broader application once developed: "Nanoscale materials are increasing growth in all of these tissue types. The key is getting the nanomaterials to mimic the roughness of the natural tissue, which creates more surface energy and allows for the absorption of proteins important for the tissue to function ... Webster has come a long way since his original experiments with in vitro bone tissue growth. Over the past decade, he added bladder, cartilage, central nervous system, and vascular tissue growth to his repertoire. The principle is the same in each: Growing cells are more likely to adhere to and thrive on a rough nanotube surface than on smooth bone or fraying cartilage."

The Non-Negotiable Goodness of Saving Lives (June 17 2008)
http://www.existenceiswonderful.com/2008/06/non-negotiable-goodness-of-saving-lives.html
From Anne C.: "why is it that whenever a group characterized at least in some part by its members' vulnerability stands to benefit from some emerging development, it is assumed that the impetus falls on the vulnerable group to 'prove' its worth? More to the point, why is it not assumed instead that individual lives are of primary value, and that the socioeconomic complications which may arise from saving more lives are just things we're going to have to suck up and deal with? ... You don't (unless your name happens to be Ebenezer Scrooge) sit there playing numbers games, trying to determine whether saving this old person will mean that maybe 10 younger people don't get a big tax break that year, or whether a healthier elderly population might 'hurt the job market' for young people. ... Put another way, the acknowledgment of the goodness of saving lives when possible should be non-negotiable. In this framework, no project claiming the goal of 'improving' conditions in the world can hinge upon the necessity of people dying by a particular age."

Massachusetts Funds Embryonic Stem Cell Research (June 17 2008)
http://news.yahoo.com/s/nm/20080616/tc_nm/usa_stemcells_massachusetts_dc_3
State funding programs for embryonic stem cell research continue to be established: "Massachusetts Gov. Deval Patrick signed a bill on Monday that will direct $1 billion of state funds toward biotechnology over 10 years ... Patrick said the money would support research grants and strengthen facilities used by both public and private scientists. ... Patrick's plan includes $250 million in tax incentives to encourage companies to expand, $250 million in grants for research, fellowships or workforce training, and $500 million for infrastructure, including a stem cell bank at the University of Massachusetts Medical School. ... Polls have shown a majority of the U.S. public back stem cell research, which scientists believe could one day be used to provide individually tailored tissue and organ transplants, or repair spinal cord injuries." This has been in the works for a while, and may be followed by others in still more states; it's a popular cause that involves giving out large sums of money. That always catches the eye of politicians, for all the obvious reasons.

More Early Damage, More Later Malfunctions (June 16 2008)
http://www.eurekalert.org/pub_releases/2008-06/elar-eli061308.php
The reliability theory of aging is a framework for thinking about how biochemical damage leads to later dysfunction. When we damage ourselves, we pay the price later in an increased risk of disease and a shorter life expectancy. The body is a complex machine, and like all complex machines it runs less reliably as the wear and tear mounts. This research illustrates the point well: "Infections during the first year of life are a marker of increased risk of developing specific types of arthritis later in life ... infants who were hospitalised for infection before their first birthday had an increased likelihood of developing either juvenile idiopathic arthritis (JIA) or adult rheumatoid arthritis (RA) in later life." Some damage we can't help, but the majority is self-inflicted through poor choices in lifestyle: excess fat, lack of exercise, and so forth. Why lower your chances of living to benefit from the longevity medicine of the future?

Invigorating Old Stem Cells (June 16 2008)
http://www.eurekalert.org/pub_releases/2008-06/uoc--scr061108.php
Researchers are working their way around the signalling mechanisms that damp down stem cell activity with age. From EurekAlert!: "As we age, our stem cells are prevented, through chemical signals, from doing their jobs ... the stem cells in old tissue are still ready and able to perform their regenerative function if they receive the appropriate chemical signals. Studies have shown that when old tissue is placed in an environment of young blood, the stem cells behave as if they are young again ... Aging and the inevitable march towards death are, in part, due to the progressive decline of Notch and the increased levels of TGF-beta, producing a one-two punch to the stem cell's capacity to effectively rebuild the body ... But what would happen if researchers blocked the adult stem cells in old tissues from reacting to those TGF-beta signals? ... muscles in the old mice whose stem cell 'aging pathway' had been dampened showed levels of cellular regeneration that were comparable to their much younger peers, and that were 3 to 4 times greater than those of the group of 'untreated' old mice." The decline in function exists to protect against cancer - but if researchers solve that problem too, it seems we can get much more from our stem cells.

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