Longevity Meme Newsletter, July 07 2008

July 07 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.



- Unofficial Aging 2008 Video
- The AnAge Database
- Longevity Science Podcasts
- The Latest Rejuvenation Research
- Discussion
- Latest Healthy Life Extension Headlines


While we're waiting on the Methuselah Foundation volunteers to process raw video from the Aging 2008 conference, here's a link to an unofficial recording of Aubrey de Grey's presentation:


"This is how my Macbook saw Aubrey de Grey's talk exactly 1 week ago on the [preconference] at UCLA."

The conference was a great success, the opening symposium hall was full, and congratulations are due to the many volunteers who worked hard to make it all happen.


What are the life spans of the longest lived species, as best researchers can determine? You might be surprised. The AnAge database is a creation of researcher Joao Pedro de Magalhaes, hosted at his ever-expanding senescence.info website:


"Among mammals alone there is at least a 40-fold variation in maximum longevity. We still do not know why different species of similar body plan, biochemistry, and physiology can age at such different rates, but these differences must be seated in the genome."


SAGE Crossroads focuses on the policy implications of aging and longevity research; not my cup of tea, but I know that many folk like this sort of thing. The most recent four podcasts focus on economic issues. Links and comments can be found in this Fight Aging! post:


"Don't be afraid of [the economics of longevity science]; it's actually the leading industry. The demands of healthcare are going to pull all other industries forward. Of course they require new technologies in steel and heavy industry and as well as delivery systems. I think they should be looked at positively. Again I say if this were a privatized system, we would all say 'gee it's wonderful. All these people want more health care, this industry is thriving'. Let me put one other analogy. Suppose we made cars a government entitlement. Instead of cheering when auto production went up, we'd say, 'Oh my God, we can't afford this!'. How you finance it may greatly affect the psychology and actually the freedom of the economy to take advantage of these new opportunities."


The latest issue of Rejuvenation Research is out, including some interesting thoughts on methionine restriction. There's a fairly good argument for the beneficial effects of calorie restriction to largely result from restriction of methionine, one of the essential amino acids in the diet. If so, one might ask, why is that?


The paper proposes that since methionine is required for protein synthesis, lower levels of dietary methionine slows down the rate of protein synthesis, which also slows down the rate of errors in protein synthesis. Errors have the effect of building up malformed proteins in a cell, which degrade its operation - so fewer bad proteins means that the machinery of your body is running more effectively, and degenerating more slowly.

It's an interesting view, but I think more evidence is required to show that this effect is important versus the way that calorie restriction lowers the overall rate of mitochondrial free radical generation (and thus damage to your cells), probably via increased autophagy. You can read about that by following the two links below.



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!




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/

Surprise, Surprise (July 04 2008)
From the PHG Foundation: "a new publication in the journal Cell Stem Cell has claimed that countries with less restrictive regulatory regimes account for a disproportionately high level of scientific publications, supporting concerns cited by many prominent US researchers that without easing of current legislation such as current restrictions on the use of federal funding for stem cell research [the] country will lag behind in this area of medicine. Countries dubbed 'overperforming' in stem cell publications were Singapore, the UK, Israel, China and Australia, whilst 'underperformers' included the US, Japan, France and Switzerland ... The author concludes that the most highly performing countries had generally permissive policy environments for [embryonic stem cell] research, whilst those lagging behind were characterised by 'protracted policy debates and ongoing uncertainty, regardless of their current policy environment'." No great shock there. The more you make it hard to move forward, the less moving forward there will be. This has little to do with degrees of public funding, and everything to do with levels of regulation.

The Bionic Human Checklist (July 04 2008)
We're a fair way from being able to produce a complete replacement for the functions of human body - a very sane goal if you'd like to live a lot longer - but the checklist of what can be replaced is getting longer by the month. From the New Scientist: "More and more of the body is becoming, if not obsolete, then certainly replaceable. But which of our body parts can be engineered today, and which will we have to make do with? ... Implants that copy the simple structural job of skeletal tissue are the easiest to build ... by culturing normal or stem cells it is now possible to grow pretty much any type of tissue. Some complete organs have already been grown from scratch. ... Other parts of the body's plumbing network, such as the lymphatic system, are becoming replaceable too. Last year, mice were implanted with an artificial lymph node made from collagen and cells taken from a gland in newborn mice. ... Implants can also help the blind see, by stimulating the retina, optic nerve or the brain's visual cortex. ... Other research seeks to replace entire limbs with robotic replacements."

Ouroboros on Michael Rose's SENSE (July 03 2008)
Over at Ouroboros, comments on SENSE, Michael Rose's consideration of his research as it impacts the "repair damage to cure aging" viewpoint of the Strategies for Engineered Negligible Senescence (SENS): "Rose concludes that life-extension therapeutics must address the issue of age-specific adaptation in order to be effective ... In the evolutionary view, increasing risk of mortality is the consequence of a failure to adapt to the selection-pressure landscape specific to a particular age; because post-reproductive lifespan is largely (but not always) masked from selection, it is easy to see how such age-specific failures of adaptation might occur. The 'mortality plateaus' to which the author refers are life-history periods of constant, rather than increasing, mortality risk. Rose argues that the existence of these plateaus in the survival curves of many species imply that accumulation of irreparable damage is - at the very least - not the whole cause of aging. Therefore, the argument goes, reversing this damage cannot be sufficient to prevent or reverse aging as such."

Resveratrol in Normal Mice (July 03 2008)
From EurekAlert!: "Scientists have found that the compound resveratrol slows age-related deterioration and functional decline of mice on a standard diet, but does not increase longevity when started at middle age. ... Dietary restriction has well-documented health benefits in mammals, and the study of possible mimetics of it, such as resveratrol, are of great interest. ... Resveratrol did not have a significant effect on lifespan in animals fed standard chow, suggesting that the intervention did not affect all aspects of the basic aging process. Mice on a high-calorie diet without resveratrol lived the shortest length of time and mice on an every-other-day regimen lived the longest, regardless of resveratrol treatment. However, for mice on a high-calorie diet, mean and maximum lifespan increased for mice on resveratrol when compared with the control mice. Researchers found that resveratrol's effects on longevity could be completely uncoupled from changes in body weight, meaning that mice on a high-calorie diet with resveratrol did not necessarily lose weight but did experience a longer (and healthier) life than mice on the same high-calorie diet not taking resveratrol. They speculate that improved cardiovascular health and reduced fatty changes in the liver may have contributed to the increased lifespan of resveratrol-treated mice."

The Longevity of the Echidna (July 02 2008)
When it comes to the source of longevity in mammals, the finger is pointing to the mitochondria. Either the mitochondria are more efficient, or as is shown to the be the case in the mole-rat and now the echidna, the surrounding biochemistry is more resistant to damage. The echidna "is exceptionally long-living. Its documented maximum lifespan of 50 years is 3.7 times that predicted from its body mass. Other exceptionally long-living mammals (naked mole-rats and humans) are known to have peroxidation-resistant membrane composition .... The peroxidation index (=peroxidation susceptibility) calculated from this membrane composition was lower-than-expected for their body size, indicating that the cellular membranes of echidnas would be peroxidation-resistant. Additionally when the calculated peroxidation index was plotted against maximum lifespan, the echidna values conformed to the relationship for mammals in general. These findings support the membrane pacemaker theory of aging and emphasise the potential importance of membrane fatty acid composition in aging and in the determination of maximum longevity." Mitochondrial damage is the first domino in a long and spreading line of follow-on processes of damage. Ongoing research into mitochondrial repair, replacement and damage resistance deserves far more funding, given the potential payoff for human healthy longevity.

The Hourglass Aging Science Blog Carnival (July 02 2008)
Chris Patil of Ouroboros is organizing a blog carnival for aging science and longevity research topics: "There's enough good science blogging about the biology of aging that the community deserves its own monthly carnival (along the lines of the general-biology carnival Tangled Bank, or the neuroscience carnival Encephalon, both of which we've hosted here before). So let's start one. I thought long and hard about names and settled on 'Hourglass,' which is topical enough to be appropriate, but general to be inclusive. ... 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. About the only sorts of things I'm going to turn away are quackery or promotions of a commercial product."

Turning Off Half of All Cancers (July 01 2008)
EukekAlert! reports on a mechanism that may reverse half of all cancers - assuming that the cancer cells don't promptly evolve their way around it, that is. "Researchers identified a precise threshold level of the signaling molecule Myc that determined the fate of tumor cells in a cancer of the immune system in mice. Above the threshold, high levels of Myc drove immune cells to grow too large and multiply uncontrollably. When the researchers lowered Myc levels below the threshold, the same cells shrank to normal size, stopped multiplying and began dying normally. ... But Myc is essential, at lower levels, for normal cell function. So, switching Myc all the way off is not an option for treating cancer. ... In the past, scientists have shown that cancer signals such as Myc are 'like light switches' [and the] idea that this is a threshold is really not the way we were all thinking ... We were able to experimentally prove that we can turn Myc off a little bit, or for a little time, and that's enough to have a profound effect on cancer."

Inflammation and Cancer Risk (July 01 2008)
Chronic inflammation raises the risk of pretty much everything you don't want to happen to your body and mind as you age. In effect, it is a source of damage to your biochemistry - and damage has consequences. Here, The Future of Things looks at what inflammation does to your risk of cancer: "It is well known that inflammation produces cytokines (immune response chemicals that encourage cell proliferation and suppress cell death), which could lead to cancer if proper cell monitoring mechanisms are not activated. In addition, another process that is evoked during inflammation has been suspected as a possible cancer inducer. During the inflammatory response to infection, immune cells, such as macrophages and neutrophils, release reactive elements, such as oxygen and nitrogen, often damaging the DNA. When DNA repair mechanisms function properly, the damage caused by inflammation is repaired before it can develop into cancer. However, the MIT team showed that once the mechanisms are not intact, the damage to the DNA can develop into mutations, possibly leading to cancer." Don't forget that packing on the visceral fat is in essence agreeing to suffer a lifetime of enhanced chronic inflammation.

Controlling Neural Stem Cells (June 30 2008)
Via ScienceDaily, continued progress in instructing our cells to do the right thing: "In recent years, stem cell researchers have become very adept at manipulating the fate of adult stem cells cultured in the lab. Now, [researchers] achieved the same feat with adult neural stem cells still in place in the brain. They successfully coaxed mouse brain stem cells bound to join the neuronal network to differentiate into support cells instead. ... It was quite surprising that stem cells in the adult brain maintain their fate plasticity and that a single gene was enough to reprogram these cells. We can now potentially tailor the fate of stem cells to treat certain conditions such as multiple sclerosis. ... The discovery [not] only attests to the versatility of neural stem cells but also opens up new directions for the treatment of neurological diseases, such as multiple sclerosis, stroke and epilepsy that not only affect neuronal cells but also disrupt the functioning of glial support cells."

Granulocytes Heading For Trials (June 30 2008)
EurekAlert! reports on a very promising cancer therapy that's been featured at SENS conferences in the past: "The treatment will involve transfusing specific white blood cells, called granulocytes, from select donors, into patients with advanced forms of cancer. A similar treatment using white blood cells from cancer-resistant mice has previously been highly successful, curing 100 percent of lab mice afflicted with advanced malignancies. ... In mice, we've been able to eradicate even highly aggressive forms of malignancy with extremely large tumors. Hopefully, we will see the same results in humans. Our laboratory studies indicate that this cancer-fighting ability is even stronger in healthy humans ... The team has tested human cancer-fighting cells from healthy donors against human cervical, prostate and breast cancer cells in the laboratory - with surprisingly good results. ... In a small study of human volunteers, the scientists found that cancer-killing activity in the granulocytes was highest in people under age 50. They also found that this activity can be lowered by factors such as winter or emotional stress. They said the key to the success for the new therapy is to transfuse sufficient granulocytes from healthy donors while their cancer-killing activities are at their peak level."



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