I had been meaning to point out video of Cynthia Kenyon's TEDGlobal presentation recorded earlier this year and posted online last month:

Kenyon, as you might know, leads the Kenyon Lab at UCSF, and was one of the first to demonstrate meaningful life extension in lower animals through single gene mutations back in the 1990s. We've come a long way since then, even if progress towards longevity-enhancing biotechnology and growth in public acceptance of that goal seems painfully slow while you're living through it a day at a time. As Maria Konovalenko of the Science for Life Extension Foundation points out, it is sometimes encouraging to read the public comments on a presentation like this one and see a great many generally positive opinions expressed:

The more TED Talks about ways to intervene in aging processes we have, the faster people all around the world would understand the feasibility of life extension therapies. By the way, I was glad to see that there are quite a lot of folks, advocating for longevity in the comments discussion about the video. I think this is another sign of TED audience becoming more and more educated and open-minded in regard to the idea of radical life extension. I would like to address the TED events organizers and ask them to do more talks on the topic of aging.

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

A viewpoint from Vladimir Skulachev, whose research group works on mitochondrially targeted antioxidant compounds: "'It is recognized that in exceptional circumstances the possibility exists for selection to favor limiting survival. In acknowledging that at least in theory, aging might occasionally be adaptive, however, the high barriers to validating actual instances of adaptive ageing are made clear' ... A few years ago it was hardly possible to find the latter statement in an article written by the most famous proponents of non-programmed aging. Certainly, this conclusion is accompanied by some reservations. Nevertheless, the balance between concepts of programmed and non-programmed aging seems to be really shifted to the programmed one. ... The idea that programmed death was invented by biological evolution was introduced in the end of nineteenth century by August Weismann, who suggested that such a death is useful for evolution as a mechanism which (i) purifies the population from weak individuals and (ii) promotes succession of generations. For sure, both these roles may be inherent in aging. However, they failed to explain why aging represents slow and concerted decline of many physiological functions (slow phenoptosis) rather than simple fast switching off of a single function of vital importance (acute phenoptosis). ... There is, it must be acknowledged, an instinctive attraction to the idea that aging is programmed. Aging is widespread across species and applies universally to all individuals within a species in which it is observed. There is also reproducibility about changes that occur with aging .... I may only add that, if aging is programmed, it can be retarded, prevented, and perhaps even reversed by treatments interrupting execution of this program, just as we already can interrupt programs of cell death. In other words, programmed aging can be cured like a disease. As for the concept of non-programmed aging, assuming occasional accumulation of stochastic injuries as its reason, it is quite pessimistic for finding any way of successful treatment. Here we simply observe and describe such a process without the possibility of improving the situation." This last viewpoint is exactly the wrong way around - repair of damage is likely to be far easier through SENS and similar programs than safely altering the exceedingly complex systems of metabolism to change the way in which aging happens. We should hope that genetic programs are of limited and narrow influence as a driver of aging - that they are merely reactions to underlying accumulations of damage where they exist at all. Because otherwise we're in for a long, slow road when it comes to extending healthy life.

Link: http://impactaging.com/papers/v3/n11/full/100403.html

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

A commentary on recent research into the effects of rapamycin on longevity: "Aging is a complex process associated with accumulation of damage, loss of function and increased vulnerability to disease, leading ultimately to death. Despite the complicated etiology of aging, an important discovery of recent years has been that simple genetic alterations can cause a substantial increase in healthy lifespan in laboratory model organisms. Many of these longevity-extending mutations down-regulate the activity of the mTOR/S6K pathway suggesting that reduced Tor/S6K signaling promotes entry into alternative phases normally entered during periods of starvation. In fact, dietary restriction (DR), a reduction in food intake without malnutrition, lowers Tor/S6K signaling and extends the average and maximum life span of a variety of organisms including yeast, flies, worms, fish, and rodents. ... Recently, it has been demonstrated that supplementation with rapamycin (an inhibitor of mTOR) started both at 9 and 20 months of life determines a small but significant extension of average and maximal life span in genetically heterogeneous male and female mice ... More studies are needed to understand benefits and side-effects of rapamycin supplementation in different strains of mice and in monkeys as a candidate cancer-preventive and life-extension pharmacological agent. However, the efficacy of intermittent rapamycin treatment in cancer prevention and life span extension [is] very promising since it is likely to reduce the side effects associated with chronic treatment."

Link: http://impactaging.com/papers/v3/n11/full/100401.html

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

In addition to funding and coordinating research into rejuvenation biotechnology, the SENS Foundation runs an Academic Initiative program that aims to pull more people into the field at an early stage in their life science careers. We must all bear in mind that turning the vision of ways to repair the biological damage of aging into the reality of suitable therapies will be the work of several decades in the best of circumstances. We have a very clear vision of the path ahead and what needs to be done in detail to repair an old human or prevent a young human from becoming old - but it will still require decades to achieve the end goal. The fastest plausible path to this future starts with a crash program that burns $1 billion in ten years to achieve rejuvenation in mice, but the research community is far from being able to deploy even a fraction of that level of resources and determination. Work proceeds slowly and there is a lot of work to do.

Given that we are looking at 20 to 30 years passing between now and widespread first generation methods of limited age-reversal, it is important to put effort towards ensuring that there will be a growing, enthusiastic research community in the years ahead. Hence the Academic Initiative: building connections, guiding younger life scientists, and encouraging the best to work on the defeat of degenerative aging. In this vein, I see that the SENS Foundation is making a small number of grants for 2012 as a part of the Academic Initiative. Young and interested life scientists in the audience might want to take note:

The SENS Foundation Academic Initiative is pleased to announce that it will be awarding up to $30,000 in materials grants in 2012. These grants are available to undergraduate, graduate, and medical students, and may be used to cover the cost of laboratory materials for aging- and rejuvenation-related research projects. A typical grant will range from $500-$2000, but grants of up to $5000 may be awarded for group projects. These grants are meant to provide students with valuable experience in research and leadership, and to help set recipients on the course to a career in SENS-related research. As such, simple and straightforward "introductory-level" projects will receive full consideration.

The grant application can be found here. You can apply at any time. There may be a high level of competition, so students are encouraged to apply soon.

As the SENS Foundation grows in budget, so too will these long term payoff activities. The primary hurdles within the scientific community that stand in the way of progress towards enhanced human longevity and the reversal of aging are (a) lack of funding, and (b) lack of researchers who are interesting and enthused. Both of these points need fixing, and in both cases that's the long bootstrapped road of incremental progress.

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

In the next few years were going to see a lot of technology demonstrations in which one very narrow biochemical aspect of aging is reversed in laboratory animals - these are the first few pebbles in what will become an avalanche of rejuvenation biotechnology. You might recall the reversal of lysosomal functional decline in the livers of mice in 2008 as an example of the type. Here is one for the brain: "Drugs that affect the levels of an important brain protein involved in learning and memory reverse cellular changes in the brain seen during aging, according to an animal study. ... [Aging] affects brain cells' ability to alter the strength and structure of their connections for information storage, a process known as synaptic plasticity, which is a cellular signature of memory. ... compared with younger rats, hippocampi from older rats have less brain-derived neurotrophic factor (BDNF) - a protein that promotes synaptic plasticity - and less histone acetylation of the Bdnf gene. By treating the hippocampal tissue from older animals with a drug that increased histone acetylation, they were able to restore BDNF production and synaptic plasticity to levels found in younger animals. ... The researchers also found that treating the hippocampal tissue from older animals with a different drug that activates a BDNF receptor also reversed the synaptic plasticity deficit in the older rats."

Link: http://www.eurekalert.org/pub_releases/2011-12/sfn-dra120711.php

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Via MedicalXPress: "researchers [put] forward a theory for the first time based on research evidence that new air sacs, called alveoli, are constantly being formed. This contradicts information in most medical textbooks that explain that the tiny air sacs begin to develop before birth (around the 6th month of pregnancy) and continue to increase in number until the age of about 3 years. ... It was believed that there was no further increase in the number of alveoli beyond that age, and that the existing alveoli just expanded as the lungs grew bigger until final adult size was reached. Our study has challenged this by suggesting that new alveoli continue to be formed as the lungs grow. ... The researchers studied over 100 healthy volunteers aged between 7 and 21 years. Each volunteer [breathed] in hyperpolarised helium and held their breaths. ... The helium [behaves] like a magnetised gas. Within the scanner, we can measure how the magnetism decays, and this in turn depends on the size of the air sacs - alveoli - which contain the helium. ... We studied small children, whose lungs contain approximately one litre of air, and full-grown adults with lung volumes of around four litres. We found very little difference in the size of the alveoli across everyone we studied. If the size of the alveoli are hardly changing, this can only mean one thing - as our lungs increase in size, we must be growing new alveoli. ... This research has important implications. If we can continue to develop new alveoli beyond early childhood, going on through adolescence, there is the potential for lung repair following injury that was never realised before."

Link: http://medicalxpress.com/news/2011-12-fundamentally-lung-growth.html

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

You may recall the very promising form of cancer immune therapy pioneered by Zheng Cui that involves transplanting granulocytes from suitable donors - it performed very well indeed in mice, superbly in fact, but only the one anemic human trial is underway in the US. You might look back in the Fight Aging! archives for a report last year on where things were with this line of research:

You might recall that people were enthused a few years back over the work of researcher Zheng Cui, who showed that (a) one breed of lab mice shug off cancer because their immune cells are different in ways that enable them to kill cancer dead, (b) transplanting those immune cells into more vulnerable mice also kills cancer dead, and (c) this same state of affairs exists in humans. Somewhere, someone has an immune system that can kill your cancer. If you could find them and undergo a transplant of leukocyte or granulocyte immune cells, the evidence to date suggests that this would be a very effective therapy.

Unfortunately, one anemic trial and a little additional research is where things still stand, more or less. This is a funding and culture of medical development issue: it's not yet completely understood how the therapy works at the biochemical level, and the prevalent incentives are for research groups to strive to fully understand a mechanism so that they can apply for patents, develop drugs that manipulate those mechanisms, and so forth and so on. Fortunately, if work is well publicized and the scientific papers openly published, clinics and medical developers worldwide can get into the game - and not all of them have the same incentives as US-based scientists and other cancer research concerns.

So I see that there is a clinic in Mexico called NCIM that is now offering granulocyte infusion treatment, for example:

Earlier this year we at NCIM approached biomedical theoretician Dr. Anthony G. Payne and asked him for any ideas or suggestions he might have for bettering the lot of a middle-aged male end stage prostate cancer patient. As he had exhausted whatever conventional approaches were available for his particular malignancy this was time for heroic measures. With Dr. Cui's pioneering work in mind Dr. Payne then set to work to develop an experimental protocol that would combine the use of mismatched donor granulocytes from healthy young people with HLA mismatched umbilical cord stem cells from healthy newborns.

Caveat emptor and all that - this looks a great deal more ad-hoc than the Florida clinical trial setup, for example - but this sort of spread in the application of a well-publicized and openly published technique is exactly what I'd like to see happen for the range of nascent biotechnologies in longevity science. When I talk about Open Cures as a long term project for speeding up medical development and implementation, I am talking about helping to make the very early stage biotechnologies for repairing or slowing age-related biotechnology accessible and renowned, just as Zheng Cui's work and its scientific foundations have become. This accessibility helps to spur entrepreneurs, development groups, and clinicians to do what NCIM has done here - pick up where US-based organizations are slacking due to obstructive regulation or a culture of development that rejects implementation of working-but-not-yet-fully-understood therapies. It doesn't matter that the first wave of implementations are likely to include incomplete or incorrect projects - once things get underway in earnest these will be weeded out or improved.

The clinics that service the medical tourism industry are the natural starting point for this sort of spread of practice, but from their experience technologies will spread out into the region's medical and research establishment. This is ever a painfully slow process, but it is much, much faster than the alternative in which it never happens because too few people know of or understand the prospective biotechnology in question. People are only trying to implement granulocyte therapies because there have been years of advocacy and discussion - absent that, I'd wager this would another largely vanished line of research for now.

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

To what degree can you swing the odds of suffering cancer in your favor? A fair amount, if this article is to be taken at face value, as much or more as other common age-related conditions: "Nearly half of cancers diagnosed in the UK each year - over 130,000 in total - are caused by avoidable life choices including smoking, drinking and eating the wrong things, a review reveals. Tobacco is the biggest culprit, causing 23% of cases in men and 15.6% in women, says the Cancer Research UK report. Next comes a lack of fresh fruit and vegetables in men's diets, while for women it is being overweight. ... Many people believe cancer is down to fate or 'in the genes' and that it is the luck of the draw whether they get it. Looking at all the evidence, it's clear that around 40% of all cancers are caused by things we mostly have the power to change. ... We didn't expect to find that eating fruit and vegetables would prove to be so important in protecting men against cancer. And among women we didn't expect being overweight to be more of a risk factor than alcohol. ... About 100,000 (34%) of the cancers are linked to smoking, diet, alcohol and excess weight. ... The researchers base their calculations on predicted numbers of cases for 18 different types of cancer in 2010, using UK incidence figures for the 15-year period from 1993 to 2007." As usual, excess fat and smoking show up as undesirables - they are there as prominent risk factors for most of the unpleasant things that aging inflicts upon us.

Link: http://www.bbc.co.uk/news/health-16031149

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Via EurekAlert!: "Reproductive and somatic aging use different molecular mechanisms that show little overlap between the types of genes required to keep oocytes healthy and the genes that generally extend life span. ... The different genetic pathways help explain why a woman's fertility begins to decline after she is 35 years old, while her other cells do not show significant signs of aging until decades later ... To compare the molecular mechanisms that are switched on or off with the aging of oocytes and somatic cells, Murphy's lab turned to the model organism, Caenorhabditis elegans (C. elegans), the worm-like nematode that set off the whole field of longevity research with the discovery in the 1990s that gene mutations affecting insulin regulation doubled the worm's life span.Using DNA microarrays to measure the expression levels of genes, Dr. Murphy and her colleagues noted a distinctive DNA signature for aging oocytes. They also found that the oocytes of aging insulin and transforming growth factor-beta (TGF-beta) mutant mice had the same DNA profile that characterized young females. The researchers then compared the oocyte gene expression patterns with microarray transcription data on worms carrying the famous long-life mutations. Murphy and her colleagues found that even though somatic and reproductive aging in C. elegans both involve the insulin regulation pathway, the molecular mechanisms to maintain youthful oocyte function and to combat body aging are very different. ... It seems that maintaining protein and cell quality is the most important component of somatic longevity in worms, while chromosomal/DNA integrity and cell cycle control are the most critical factors for oocyte health."

Link: http://www.eurekalert.org/pub_releases/2011-12/asfc-ahb112211.php

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

There is a great deal of denial floating around when it comes to the excess weight carried by a majority of the people fortunate enough to live in wealthier parts of the world - even more denial than there is for lack of exercise, and there's plenty of that. Wealth is ever a double-edge sword, and brings the opportunity to become overweight and sedentary along with its many benefits - we mammals have evolved to find it hard to turn down large amounts of food that is both cheap and good, and we've succeeded ourselves into a challenging position on that front. Unfortunately indulgence has meaningful costs: a deterioration in health and life expectancy, and the more we overeat the worse that cost becomes. This has always been the folk wisdom of past decades and centuries, but in recent years the life science and medical research communities have brought more rigorous measurement and greater understanding to the costs of excess fat tissue and lack of exercise. Denial is becoming harder - which is a good thing, as the cost of food will continue to head towards zero as technology advances.

Here's an article written by someone who would love to remain upon the boat of denial by the sound of some of the later paragraphs, but it's hard to argue against facts established through good science:

When it comes to lowering our overall risk of death and dying from heart disease, fitness may be just as important, if not more so, than weight. That's what researchers concluded after studying fitness, weight and mortality among 14,345 middle-aged men in an 11-year study. Most studies that have previously linked weight gain, overweight and obesity to higher mortality risk have focused only on BMI, or body mass index, a ratio of height and weight. That's because weight can indirectly affect a number of different metabolic processes that contribute to mortality, such as how we burn calories or process sugars, and how high our blood pressure is. But weight may also be masking the effect of another factor that could protect or propel us to an early death: how efficiently our hearts and lungs are working, or, in other words, how fit we are.

Regular readers here will already know that both exercise and level of body fat go a fair way towards determining the future trajectory of health and life expectancy. Certainly there is no medicine or therapy that a healthy person can obtain at this time that comes even close to the benefits gained by (a) regular exercise, and (b) maintaining an optimal level of body fat. A handful of posts from the archives, for example:

• Exercise, Longevity, and Long Term Medical Costs
• On Aging and Exercise
• Exercise Slows Many of the Consequences of Aging
• There Are Old People and Fat People, But Few Old Fat People
• Don't Get Fat, and Don't Stay Fat
• More Evidence for the Costs of Visceral Fat

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