Longevity Meme Newsletter, February 15 2010

February 15 2010

The Longevity Meme Newsletter is a weekly email containing news, opinions, and happenings for people interested in aging science and engineered longevity: making use of diet, lifestyle choices, technology, and proven medical advances to live healthy, longer lives. This newsletter is published under the Creative Commons Attribution 3.0 license. In short, this means that you are encouraged to republish and rewrite it in any way you see fit, the only requirements being that you provide attribution and a link to the Longevity Meme.



- Malthusianism Revisited
- Time Magazine on Aging and Longevity
- Transparency in Life Science Research
- Discussion
- Latest Healthy Life Extension Headlines


Until such time as erroneous Malthusian thinking on resources and population fades from the mainstream of our culture, it will be necessary to regularly speak out against it. Modern Malthusians are the most vocal and numerous opponents of efforts to extend the healthy human life span:


"Despite the occurrence of localized pits of suffering and poverty that last for decades or lifetimes, our broader human culture has benefited from centuries of sustained, accelerating economic and technological growth. This growth is thanks to the incentives put upon people to profit, compete, build better devices, and access new resources. As early as the 18th century, increased longevity went hand in hand with increased population and increased standards of living. Despite this big picture, each new generation spawns devotees of Malthus, each crying out that the sky is falling, that resources will soon run out, that there are too many people. All past Malthusians were wrong, and the present generation is just as wrong; these are people who do not understand how the world works, how development and growth happens, or how people respond to foreseen shortages. In short, economic development and competition ensures that people work to create new resources and makes old ones far more productive in response to demand."


On the one hand it is good to see the mainstream media devoting significant energy to discussing extended healthy longevity, but on the other hand they continue to focus exclusively on things that won't make much difference to you or I:


"As is usual in the most popular of the popular press, the authors are oblivious to the important distinction between slowing and reversing aging. That state of affairs is something that we advocates need to work on, as the only research strategies likely to produce rejuvenation medicine that will meaningfully help us when we are old are those based on reversing aging ... It is likely to be easier and less costly to produce rejuvenation therapies than to produce a reliable and significant slowing of aging. A rejuvenation therapy doesn't require a whole new metabolism to be engineered, tested, and understood - it requires that we revert clearly identified changes to return to a metabolic model that we know works, as it's used by a few billion young people already. Those rejuvenation therapies will be far more effective than slowing aging in terms of additional years gained, since you can keep coming back to use them again and again. They will also help the aged, who are not helped at all by a therapy that merely slows aging.

"But so far as most people are concerned, longevity science presently means studying old people, finding genes associated with small differences in human life expectancy, or working on drugs that modestly slow down aging - no more than calorie restriction or exercise can already achieve. This work will probably lead to some new knowledge that will help efforts to reverse aging, but I very much doubt it will lead to significant extension of human life spans within the lifetime of people who are middle aged now."


The times are changing, and researchers must change with them if we are to see the rapid progress in medical technology that is possible:


"Transparency in fundraising and early stage research is the wave of the future. Young biotechnologists - and especially those in the open source biology movement - should be out there blogging their ongoing work, itemizing their costs, and engaging in microscale fundraising. ... At some point, the culture of the scientific establishment that sets a wall between the public and fundraising activities has to change. As ever more areas of biotechnology become so cheap that anyone with a will and a goal can pitch in, the priesthood of science must adapt or wither away. Researchers who fail to issue regular updates on what they are doing will be out-evolved by a new breed of folk who keep their funding circle close, engaged, and up to date."


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!




From the Telegraph: The Gene Therapy Advisory Committee (GTAC) - the ethics body for stem cell clinical trials - has given the research the green light following months of delay. Following the approval, ReNeuron will start the world's first trial of injecting stem cells into patients' brains in the hope they will repair areas damaged by stroke and improve both mental and physical function. ... ReNeuron was first granted permission to conduct the trial by the Medicines and Healthcare Regulatory Agency last January, but needed a recommendation from the GTAC before it could start the Phase 1 clinical trial. A year later, the company has been given the go-ahead and the first of twelve stroke patients is expected to receive treatment in Scotland later this year. Michael Hunt, ReNeuron chief executive, said the approval represented 'the culmination of many months of work'." This is an apt illustration of why it requires so much time and money to bring new medical technology to the clinic - it's the regulators who cause the loss of a year here and a few years there, not the challenges of research and development.

Via Nanowerk: researchers have "developed a fast and cost-efficient method for producing sufficient amounts of bone and cartilage tissue using the body's own cells ... Damage to larger joints such as knees, feet, hips and shoulders is often the beginning of a painful process during which mobility continues to decrease. Because cartilage cannot regenerate after the body has stopped growing, defects caused by injuries and 'wear and tear' cannot be absorbed by producing new cartilage. Genetic engineering and molecular biology have now made it possible to remove healthy cartilage cells and grow these outside the body in special solutions. This cartilage tissue is then applied to the defective cartilage where it attaches and grows. Repairing cartilage and bone damage using the body's own cells is still a difficult process. Cultivating the body's own tissue is still time-consuming and expensive, and much time is needed until the implant has reached its desired functionality. [Researchers now] present a strategy for the 'de novo engineering' of cartilage and bone tissue which requires only three weeks."

I think that this news is illustrative of a slow shift that is taking place in the culture of aging research. It now acceptable - and more importantly fundable - for researchers to talk openly about slowing or reversing aspects of aging: "Leading neuroscientists gathered in Dallas last week to discuss recent major findings about the aging brain and to celebrate the launch of the UT Dallas Center for Vital Longevity ... The Center for Vital Longevity is a research center focused on understanding and expanding the capacity of the aging mind. Center researchers use cutting edge brain imaging technologies and advances in cognitive science to understand (a) how the brain changes from young to old adulthood; (b) the consequences of neural aging for everyday function; and (c) what interventions show promise for slowing cognitive aging. ... Denise Park, Ph.D. focuses her research program on understanding how the mind changes and adapts as we age. She is interested not only in the function of the mind and brain, but in determining whether stimulation can maintain the health of the aging brain." The mainstream will slowly catch up to where advocates of the Strategies for Engineered Negligible Senescence have been for a decade: that working to defeat aging is plausible, possible, and what we should be doing.

Researchers continue to offer their thoughts and predictions on how greatly they expect the practice of calorie restriction to extend life in humans. The consensus seems to be "not as much as in mice," but a range of arguments are used to arrive at that position. Here is one of them: "Although it has been known since 1917 that calorie restriction (CR) decelerates aging, the topic remains highly controversial. What might be the reason? Here I discuss that the anti-aging effect of CR rules out accumulation of DNA damage and failure of maintenance as a cause of aging. Instead, it suggests that aging is driven in part by the nutrient-sensing TOR (target of rapamycin) network. CR deactivates the TOR pathway, thus slowing aging and delaying diseases of aging. Humans are not an exception and CR must increase both maximal and healthy lifespan in humans to the same degree as it does in other mammals. Unlike mice, however, humans benefit from medical care, which prolongs lifespan despite accelerated aging in non-restricted individuals. Therefore in humans the effect of CR may be somewhat blunted. Still how much does CR extend human lifespan? And could this extension be surpassed by gerosuppressants such as rapamycin?"

THE DEEP ROOTS OF AGING (February 10 2010)
The evolution of aging might be traced all the way back to how dividing cells split up their load of damage and unwanted byproducts. From Ouroboros: "One approach is to distribute everything equally amongst your two offspring. ... A second approach is to give all the crap to one of the two new cells and keep the other one pristine. Lets call these two cells the crap cell and the pristine cell. ... The crap cell (I love this nomenclature) will become inviable sooner under this strategy, but the alternative would be a symmetric division strategy in which all descendants accumulate garbage, ultimately causing the extinction of the entire lineage. ... Both single-celled yeast and mammalian stem cells employ this asymmetric strategy in order to preserve the viability of an indefinitely dividing lineage. ... One of our initial premises was that aggregates are biochemically hard to handle, which is why they accumulate rather than being degraded. But now we know that cells can bundle aggregates onto actin cables and move them around - why not sort the aggregates into vesicles or membrane blebs and dispose of them? Granted, in order to export an aggregate out of the cell, it would have to cross a membrane, but this would be no more difficult topologically than mitophagy. The obvious (and trivial) answer to this question is 'because it didn't evolve that way,' but I'm curious to know whether there's some compelling reason why it couldn't have evolved that way."

Published at PLoS Genetics, an unexpected longevity gene: "Expansion of a stretch of glutamines near the amino-terminus of huntingtin (htt), the protein product of the IT15 gene, is a deleterious mutation that causes Huntington's disease (HD). Here we show, in contrast, that deletion of htt's normal polyglutamine stretch (deltaQ-htt) is a potentially beneficial mutation that can ameliorate HD mouse model phenotypes when deltaQ-htt is expressed together with a version of htt with the HD mutation. In addition, deltaQ-htt expression can enhance longevity when expressed in either an HD mouse model or in non–HD mice. deltaQ-htt's effects on both lifespan and HD model phenotypes are likely due to an increase in autophagy, a major recycling pathway in cells that is involved in the turnover of cellular components, and aggregated protein. Based on our results, we suggest that development of therapeutic agents that can stimulate autophagy may help both in treating neurodegenerative disorders like HD and also in increasing longevity."

An unexpected potential use for embryonic stem (ES) cells: "One of the most auspicious, yet challenging, avenues for combating malignancies is to enlist the immune system to come to the defense of the patient. However, myriad components of the immune system interact in extraordinarily complex ways with active or dormant neoplastic cells, an interaction matrix that is incompletely understood at best. ... [Researchers] reason that exposure of the immune system to novel tumor-associated antigens might boost an otherwise inadequate immune response into an effective antitumor action. What distinguishes the study is the source of these tumor-associated antigens: human ES and iPS cells. Specifically, the study investigated whether vaccination of mice with human ES or iPS cell lines would trigger an enhanced immunological response against shared antigens expressed by the primitive normal cells and the colon carcinoma cell line CT26 ... vaccination of mice with the human ES cell line H9 induced both strong cellular and humoral immune responses against CT26 colon carcinoma. ... There is a certain irony in the fact that human ES cells, which themselves possess many features of neoplastic cells - including sustained telomerase activity, formation of tumors after injection into mice, and infinite growth - would be exploited against cancer. By analogy, it is like fighting fire with fire."

OUROBOROS ON CRYONICS (February 09 2010)
Chris Patil of Ouroboros is a cryonics skeptic: "I'm a cryonics skeptic of the 'extraordinary claims require extraordinary evidence' flavor. As I've said before, I suspect that long-term preservation of the potential for life by freezing or other means is physically possible, but at present I don't think we’re making any significant progress in that direction. Part of the problem is that there's very little serious initiative within the mainstream of academia or industry to build the many, many necessary precursor technologies. Another part is that the problem is really, really hard - harder than the comparatively simple but still unsolved problem of maintaining cellular viability within tissues at low temperatures." From reading what he's written, I think he's either out of the loop on the technology of vitrification, or not convinced that present day vitrification methods as used by Alcor are actually going to preserve fine structure in brain cells (i.e. preserve the data that is the mind). I disagree with him on that last point, if that is his view - the evidence clearly points to the viability of vitrification on that count.

A novel approach to the treatment of age-related bone loss is demonstrated: "An investigational drug that inhibits serotonin synthesis in the gut, administered orally once daily, effectively cured osteoporosis in mice and rats ... Serotonin in the gut has been shown in recent research to stall bone formation. The finding could lead to new therapies that build new bone; most current drugs for osteoporosis can only prevent the breakdown of old bone. ... Prior to this discovery, serotonin was primarily known as a neurotransmitter acting in the brain. Yet, 95 percent of the body's serotonin is found in the gut, where its major function is to inhibit bone formation (the remaining five percent is in the brain, where it regulates mood, among other critical functions). By turning off the intestine's release of serotonin, the team was able, in this new study, to cure osteoporosis in mice that had undergone menopause. ... [Researchers] administered the compound orally, once daily, at a small dose, for up to six weeks to rodents experiencing post-menopausal osteoporosis. Results demonstrated that osteoporosis was prevented from developing, or when already present, could be fully cured. Of critical importance, levels of serotonin were normal in the brain, which indicated that the compound did not enter the general circulation and was unable to cross the blood-brain barrier, thereby avoiding many potential side effects."

The title of this EurekAlert! release is misleading - this isn't the first identified genetic variant associated with human longevity. But is is nonetheless interesting: scientists "have identified for the first time definitive variants associated with biological ageing in humans. The team analyzed more than 500,000 genetic variations across the entire human genome to identify the variants which are located near a gene called TERC. ... two forms of ageing - chronological ageing i.e. how old you are in years and biological ageing whereby the cells of some individuals are older (or younger) than suggested by their actual age. ... There is accumulating evidence that the risk of age-associated diseases including heart disease and some types of cancers are more closely related to biological rather than chronological age. What we studied are structures called telomeres which are parts of one's chromosomes. Individuals are born with telomeres of certain length and in many cells telomeres shorten as the cells divide and age. Telomere length is therefore considered a marker of biological ageing. In this study what we found was that those individuals carrying a particular genetic variant had shorter telomeres i.e. looked biologically older. ... The effect was quite considerable in those with the variant, equivalent to between 3-4 years of 'biological aging' as measured by telomere length loss."



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