Longevity Meme Newsletter, January 05 2009

January 05 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.



- The Edge Annual Question For 2009
- Debating Compression of Morbidity
- Discussion
- Latest Healthy Life Extension Headlines


This year, Edge magazine asked "What game-changing scientific ideas and developments do you expect to live to see?" Perhaps not surprisingly, engineered longevity featured in many of the answers. I picked out a few of the more interesting responses:


"I have little doubt that progress in fighting disease and patching up our genetic weaknesses will make it possible for people to routinely reach the full human lifespan of about 120. Going far beyond that will require halting or reversing the core aging process, which involves not just genetic triggers but also oxidation and simple wear-and-tear. Engineering someone to have gills is probably a much easier proposition. Still, if we can hit 200 I see no reason why the same techniques couldn't allow people to live to 1,000 or more. Odds: 60 percent."

Few of them showed an appreciation of aging as a process of damage, however, or any great depth of knowledge of the debates within the aging research community. Fair enough, but I think that shows we have work yet to do in raising awareness and channeling support in the best possible direction. The end result of scientific debates over the best way forward to influence the aging process will determine whether we see significant progress or little progress in our lifetime:



Compression of morbidity is the goal of reducing the time spent in frailty and ill health in old age. It's something of a loaded term, however, as it's much used by researchers who either don't want to talk about extending overall longevity, or genuinely think that extending overall longevity is impossible or undesirable. Can you even extend healthy life without extending overall life span, however? Whether or not compression of morbidity is possible is still the subject of healthy debate, given that much of the evidence for and against is statistical in nature:


"Theories of aging based upon accumulation of biochemical damage and incremental system failure are very convincing, and have a great deal of experimental support, but don't predict that compression of morbidity is possible to any great degree. The only way to push out healthy life span is to prevent or repair damage, and that will also push out overall life span."


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/

Revisiting Methionine Restriction and Veganism (January 02 2009)
With the evidence backing methionine restriction, researchers are examining various forms of non-calorie restricted diet to see if reduced methionine intake could plausibly produce health benefits: "Recent studies confirm that dietary methionine restriction increases both mean and maximal lifespan in rats and mice, achieving 'aging retardant' effects very similar to those of caloric restriction, including a suppression of mitochondrial superoxide generation. Although voluntary caloric restriction is never likely to gain much popularity as a pro-longevity strategy for humans, it may be more feasible to achieve moderate methionine restriction, in light of the fact that vegan diets tend to be relatively low in this amino acid. Plant proteins - especially those derived from legumes or nuts - tend to be lower in methionine than animal proteins. Furthermore, the total protein content of vegan diets, as a function of calorie content, tends to be lower than that of omnivore diets, and plant protein has somewhat lower bioavailability than animal protein. ... Furthermore, low-fat vegan diets, coupled with exercise training, can be expected to promote longevity by decreasing systemic levels of insulin and free IGF-I; the latter effect would be amplified by methionine restriction - though it is not clear whether IGF-I down-regulation is the sole basis for the impact of low-methionine diets on longevity in rodents."

Further Investigation of Parkinson's Mechanisms (January 02 2009)
Researchers are further uncovering how Parkinson's disease kills brain cells: "Neurologists have observed for decades that Lewy bodies, clumps of aggregated proteins inside cells, appear in the brains of patients with Parkinson's disease and other neurodegenerative diseases. The presence of Lewy bodies suggests underlying problems in protein recycling and waste disposal, leading to the puzzle: how does disrupting those processes kill brain cells? One possible answer: by breaking a survival circuit called MEF2D. ... MEF2D is sensitive to the main component of Lewy bodies, a protein called alpha-synuclein. In cell cultures and animal models of Parkinson's, an accumulation of alpha-synuclein interferes with the cell's recycling of MEF2D, leading to cell death. MEF2D is especially abundant in the brains of people with Parkinson's. ... MEF2D is a transcription factor, a protein that controls whether several genes are turned on or off. Previous studies have shown MEF2D is needed for proper development and survival of brain cells. To function, MEF2D must be able to bind DNA. ... most of the accumulated MEF2D [in cases of Parkinson's disease] can't bind DNA. This may indicate that the protein is improperly folded or otherwise modified."

Refuting the Rate of Living Theory Again (January 01 2009)
Being thorough: "The proposition that increased energy expenditure shortens life has a long history. The rate-of-living theory states that life span and average mass-specific metabolic rate are inversely proportional. Originally based on interspecific allometric comparisons between species of mammals, the theory was later rejected on the basis of comparisons between taxa (e.g., birds have higher metabolic rates than mammals of the same size and yet live longer). It has rarely been experimentally tested within species. Here, we investigated the effects of increased energy expenditure, induced by cold exposure, on longevity in mice. Longevity was measured in groups of 60 male mice maintained at either 22 degrees C (WW) or 10 degrees C (CC) throughout adult life. ... we observed no significant differences in median life span among the groups ... [energy expenditure] in CC mice significantly exceeded that of WW mice. This result demonstrates that increased energy expenditure does not shorten life span and adds evidence to the intraspecific refutation of the rate-of-living theory."

Progress in Organ Cryopreservation (January 01 2009)
Mainstream research into cryopreservation of tissue will likely provide benefits to the cryonics community: researchers "have developed a new approach for producing more effective medical antifreeze fluids for preserving kidneys, hearts, and other organs donated for transplantation. These next-generation antifreezes can decrease damage to organs caused by ice crystals, and thus prolong the time a donated organ will remain viable prior to transplantation. ... the scientists describe the development of 'hydration index' that can be used to more reliably predict how prospective antifreeze materials will behave. Their index provides a clearer picture of how water molecules interact with the sugar component [and] affect their chemical behavior. This is a key to understanding their ability to resist the formation of ice crystals when chilled." Cryonics researchers have already developed antifreezes in conjunction with vitrification, but a more rigorous way forward to better antifreezes certainly can't hurt.

On Compression of Morbidity (December 31 2008)
The basic idea behind compression of morbidity is to reduce the span of time spent frail in old age without extending life span. This is an incoherent goal from the point of view of any theory of aging that presents degeneration as a result of accumulated damage, and it is a pity that compression of morbidity is so firmly entrenched in the research philosophy of mainstream aging research. The only way to ensure more years of health is to repair or prevent damage, which will also lead to a longer life. This SAGE Crossroads podcast is a discussion with Aubrey de Grey on the topic: "In some statistics we see a little bit of compression in some people; in some places we see a little bit of expansion. By in large what we are seeing is exactly what you would expect from postponing aging. In other words, you postpone the onset of morbidity and you also postpone death by about the same amount. ... the compression of morbidity theory as you call is not really a theory, it's more of an aspiration. People say 'well wouldn't it be a good thing if we could compress morbidity,' but they don't really say how we would expect to be able to do it. ... [the focus of research should be on] postponing morbidity so much that there is a much higher probability that people will die of causes that have nothing to do with aging just because they've got longer to do it before they become frail and decrepit."

On Artificial Retinas (December 31 2008)
A general interest piece from PhysOrg.com: "Tests of a relatively crude artificial retina [called Argus One] began on six patients in 2002. With the aid of these devices, people who'd been totally blind were able to read foot-high letters, tell a plate from a cup, find doors and windows, and navigate around large objects ... Argus One is still in use, but it's being succeeded by Argus Two, a smaller, more sophisticated device with an array of 60 electrodes, providing a much sharper image to its users. The newer device is being tested on 17 blind people in the U.S. and Europe, and more patients are being enrolled. At a retina conference in October, patients reported improvements in orientation and mobility. They were able to find a door from 20 feet away and to follow a line on the floor for 20 feet ... Meanwhile, researchers [are] creating a third-generation artificial retina. Much smaller than its predecessors, the device will contain 200 or more electrodes on a thin, flexible film that curves to fit the shape of the retina. Human tests are scheduled to begin in 2011. ... We're aiming for a 1,000-electrode array ... Such a device would 'let a blind patient recognize objects and read large-scale newsprint.'"

Seventy-Five Percent (December 30 2008)
A reminder of the degree of control you have over your future health and longevity, even absent advances in medical science: "Seventy-five percent of the variation in lifespan can be attributed to a modification of risk factors during early old age. The modifiable behaviors that can positively affect longevity included smoking abstinence, weight management, blood pressure control and regular exercise. ... Smoking, diabetes, obesity and hypertension significantly reduced the likelihood of a 90-year life span, while regular vigorous exercise substantially improved it. Furthermore, men with a lifespan of 90 or more years also had better physical function, mental well-being and self-perceived health in later life compared with men who died at a younger age. ... Restricting caloric intake and daily exercise positively lowered most of the risk factors noted in the study. Many illnesses such as diabetes and high blood pressure can be eliminated or reduced through maintaining an active lifestyle."

Neurodegeneration and Excess Blood Sugar (December 30 2008)
While too little blood sugar appears to contribute to Alzheimer's, too much - as in diabetes - also brings on degeneration of the brain: "This research used imaging in both human volunteers and in animal models to help us better understand the basic mechanisms behind hippocampal dysfunction in the aged ... The research found that decreasing activity in the dentate gyrus only correlated with levels of blood glucose. ... Beyond the obvious conclusion that preventing late-life disease would benefit the aging hippocampus, our findings suggest that maintaining blood sugar levels, even in the absence of diabetes, could help maintain aspects of cognitive health. ... By improving glucose metabolism, physical exercise also reduces blood glucose. It is therefore possible that the cognitive enhancing effects of physical exercise are mediated, at least in part, by the beneficial effect of lower glucose on the dentate gyrus. Whether with physical exercise, diet or through the development of potential pharmacological interventions, our research suggests that improving glucose metabolism could be a clinically viable approach for improving the cognitive slide that occurs in many of us as we age."

Prospects for Repairing the Brain (December 29 2008)
From Nanowerk: "In order for neural prostheses to augment or restore damaged or lost functions of the nervous system they need to be able to perform two main functions: stimulate the nervous system and record its activity. To do that, neural engineers have to gain a full understanding of the fundamental mechanisms and subtleties of cell-to-cell signaling via synaptic transmission, and then develop the technologies to replicate these mechanisms with artificial devices and interface them to the neural system at the cellular level. A group of European researchers has now shown that carbon nanotubes may become the ideal material for repairing damaged brain tissue. ... The new carbon nanotube-based interface technology discovered together with state of the art simulations of brain-machine interfaces is the key to developing all types of neuroprosthetics - sight, sound, smell, motion, vetoing epileptic attacks, spinal bypasses, as well as repairing and even enhancing cognitive functions."

Autophagy Genes and Aging (December 29 2008)
A review: "Ageing in divergent animal phyla is influenced by several evolutionarily conserved signalling pathways, mitochondrial activity and various environmental factors such as nutrient availability and temperature. Although ageing is a multifactorial process with many mechanisms contributing to the decline, the intracellular accumulation of damaged proteins and mitochondria is a feature common to all aged cells. Autophagy (cellular self-eating) - a lysosome-mediated catabolic process of eukaryotic cells to digest their own constituents - is a major route for the bulk degradation of aberrant cytosolic macromolecules and organelles. Indeed, genetic studies show that autophagy-related genes are required for lifespan extension in various long-lived mutant nematodes and promote survival in worms and flies exposed to prolonged starvation. These data implicate autophagy in ageing control. Furthermore, results in Drosophila demonstrate that promoting basal expression of the autophagy gene Atg8 in the nervous system extends lifespan by 50%, thereby providing evidence that the autophagy pathway regulates the rate at which the tissues age."



Post a comment; thoughtful, considered opinions are valued. New comments can be edited for a few minutes following submission. Comments incorporating ad hominem attacks, advertising, and other forms of inappropriate behavior are likely to be deleted.

Note that there is a comment feed for those who like to keep up with conversations.