LONGEVITY MEME NEWSLETTER
August 23 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.
- Help Fund a Mitochondrial Uncoupling Project
- 2nd Meeting for the SENS Foundation LA Chapter
- A Selection of Singularity Summit Coverage
- Anoxia Tolerance and Species Longevity
- Latest Healthy Life Extension Headlines
HELP FUND A MITOCHONDRIAL UNCOUPLING PROJECT
The Immortality Institute has selected the winning research project proposal for this year's fundraising drive: an investigation into mitochondrial uncoupling and longevity to be carried out in a laboratory in Singapore.
"The [Institute] community isn't rich, so we pick our priorities quite carefully. The mitochondrial uncoupling project ticks all the important boxes: (1) it investigates a crucial mechanism of how and why we age, (2) it may show the path towards practical interventions in the aging process, (3) it is small enough that your donation, every cent of which will be matched by [the Institute], *will* make a real difference, (4) it is led by a reputable scientist who will respond to community questions and update us periodically on the progress of the research.
"Any donation, of any amount is appreciated. We need at least $6000 to get going, with the matched funding in place that means at least $3000 from donors like you. Any surplus would go into the next scientific research initiative that is already in the pipeline."
I think this is a worthwhile effort, and encourage you to donate. We absolutely want to see many, many more grassroots organizations adopt this sort of fundraising operation: pick good projects that get the most out of modest donations, and make the most of new technology and established facilities. As is always the case, I'm not asking you to do anything I haven't done myself: I donated $1000 to the project on Friday, and consider it money well spent.
2ND MEETING FOR THE SENS FOUNDATION LA CHAPTER
If you're in the Los Angeles area on the 27th, you should drop in on the upcoming SENS Foundation meeting for volunteers and supporters:
"In this second meeting we will be joined by the fabulous Dr. Sarah Marr (SENS Foundation Vice President) ... Sarah is going to take this opportunity to tell you a little more about SENS Foundation's Mission, and the ways in which it is working to communicate that mission. Our hope is that we'll be able to empower all the members of the chapter to work with us in promoting the Foundation effectively. We will also talk about generalized outreach, the Foundation's structure, volunteering, fund raising and more, giving you the chance to connect more closely to us. Also, we'll discuss our plans for future chapter meetings - making them relate to both the Foundation and the wider research environment in which it works - and our ideas for bringing in outside speakers."
You can find out more about the Foundation's work on longevity science at their website:
A SELECTION OF SINGULARITY SUMMIT COVERAGE
The recent Singularity Summit generated a fair amount of press and blog coverage. You'll find a selection of links and quotes in this Fight Aging! post:
"The event was largely focused on artificial intelligence and other topics not directly related to engineering greater human longevity, but there were nevertheless one or two interesting presentations that touched on related science. ... Now if we could just arrange matters such that the engineered longevity conferences generate this much discussion, light, and noise. This is not a trivial task, of course. Behind the chatter lies a great deal of careful arrangement, networking, and years of groundwork by the Summit organizers - making a splash doesn't just happen. This is something that the longevity science community isn't good at yet, sad to say: it must be added to the list of critical areas to work on."
ANOXIA TOLERANCE AND SPECIES LONGEVITY
Researchers have recently made the case that resistance to low-oxygen environments may be a trait linked to exceptional longevity in some species, and therefore worthy of greater investigation:
"While mammals cannot survive oxygen deprivation for more than a few minutes without sustaining severe organ damage, some animals have mastered anaerobic life. Freshwater turtles [are] the champion facultative anaerobes of the vertebrate world, often surviving without oxygen for many weeks at a time. The physiological and biochemical mechanisms that underlie anoxia tolerance in turtles include profound metabolic rate depression, post-translational modification of proteins, strong antioxidant defenses, activation of specific stress-responsive transcription factors, and enhanced expression of cytoprotective proteins. Turtles are also known for their incredible longevity and display characteristics of 'negligible senescence'. We propose that the robust stress-tolerance mechanisms that permit long term anaerobiosis by turtles may also support the longevity of these animals.
"When reading this my first thought was of another unusually long-lived species that has a high tolerance for low-oxygen life: the naked mole-rat. ... brain tissue from naked mole-rats, rodents that live in a chronically low-oxygen environment, is remarkably resistant to hypoxia: naked mole-rat neurons maintain synaptic transmission much longer than mouse neurons and can recover from periods of anoxia exceeding 30 min."
Some whales are also unusually long-lived, and are noted for the length of their feeding dives - an activity that also regularly exposes them to anoxia. All in all it is an intriguing theory, and I look forward to hearing more as researchers dig in.
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!
LATEST HEALTHY LIFE EXTENSION HEADLINES
NEURAL STEM CELLS REPAIR SPINAL INJURY (August 20 2010)
This is one of several techniques shown to restore function in spinal injury using transplanted stem cells: "A UC Irvine study is the first to demonstrate that human neural stem cells can restore mobility in cases of chronic spinal cord injury, suggesting the prospect of treating a much broader population of patients. Previous breakthrough stem cell studies have focused on the acute, or early, phase of spinal cord injury, a period of up to a few weeks after the initial trauma when drug treatments can lead to some functional recovery. The UCI study [is] significant because the therapy can restore mobility during the later chronic phase, the period after spinal cord injury in which inflammation has stabilized and recovery has reached a plateau. There are no drug treatments to help restore function in such cases. ... The [team] transplanted human neural stem cells into mice 30 days after a spinal cord injury caused hind-limb paralysis. The cells then differentiated into neural tissue cells, such as oligodendrocytes and early neurons, and migrated to spinal cord injury sites. Three months after initial treatment, the mice demonstrated significant and persistent recovery of walking ability in two separate tests of motor function when compared to control groups."
ANOTHER CALORIE RESTRICTION GENE IDENTIFIED (August 20 2010)
Via PhysOrg.com: "A team of University of Michigan scientists has found that suppressing a newly discovered gene lengthens the lifespan of roundworms. Scientists who study aging have long known that significantly restricting food intake makes animals live longer. But the goal is to find less drastic ways to achieve the same effect in humans someday. ... scientists found that a gene, drr-2, is an important component in a key cellular pathway, the TOR nutrient-sensing pathway, where many scientists are looking for potential drug targets. The U-M scientists then found that when they caused the drr-2 gene to be under- or over-expressed, they could lengthen or shorten lifespan in C. elegans, a worm widely used in research. Manipulating the drr-2 gene's action produced the same effects as reducing or increasing caloric intake. ... The study also found that drr-2 appears analogous to a human gene, eIF4H, that controls similar cell functions. ... Many genes identified in C. elegans to control the speed of aging turned out to be evolutionarily conserved, meaning that you can find them in other animals, too. And many are very similar to those found in humans. ... When calories or certain nutrients are restricted, scientists detect less oxidative damage in animal cells and a slower decline in DNA repair, a decline that normally occurs with age. It's thought that limiting oxidative damage and slowing the decline in DNA repair could help postpone or avoid many age-related diseases."
BULLISH ON LONGEVITY (August 19 2010)
An author returns to an old topic: "About seven years ago, I reported regularly on the science of longevity, and the prospect of human life extension, for a site called Sage Crossroads. And then I stopped - pretty much dropping the topic for a while and going on to other things. So when I attended the Techonomy session yesterday entitled 'The Longevity Dividend,' it was a perfect chance to hear just how far scientists think their field has come since I last reported on it closely. And I have to say, I was struck by the difference in tone. Seven years ago, scientists who study aging - so-called biogerontologists - already thought it was possible or even likely that at some point in the future, we would find a way to retard its rate in humans. After all, there were already numerous studies showing that genetic interventions could lengthen the lifespan of other species, particularly mice and roundworms. ... So there were reasons to think that human life extension was coming - and more specifically, that a means of slowing the rate of human aging would be possible. But most mainstream scientists weren't so bullish then. So optimistic. In particular, they were very worried about giving false hope, and encouraging anti-aging quackery. I detected a different tone yesterday. S. Jay Olshansky, an aging expert at the University of Chicago, put it plainly. He thinks we can get an average 7 year extension of the human life span by finding a pill that tweaks the right gene pathway - perhaps mimicking the special genetics of those among us who are (or are fated to become) centenarians. 'I'm suggesting, and we are suggesting, that the time has arrived for us to go after the biggest prize of all,' said Olshansky. 'Let's alter our own biology. Let’s alter humanity.'"
A DEMONSTRATION OF STEM CELL VERSATILITY (August 19 2010)
Via EurekAlert!: "Scientists have reprogrammed stem cells from a key organ in the immune system in a development that could have implications for tissue regeneration. Their research shows that it is possible to convert one stem type to another without the need for genetic modification. Researchers, who used rat models, grew stem cells from the thymus - an organ important for our immune systems - in the laboratory using conditions for growing hair follicle skin stem cells. When the cells were transplanted into developing skin, they were able to maintain skin and hair for more than a year. The transplanted follicles outperformed naturally-produced hair follicle stem cells, which are only able to heal and repair skin for three weeks. Once they were transplanted, the genetic markers of the cells changed to be more similar to those of hair follicle stem cells. When an animal develops, embryos form three cellular or germ layers - ectoderm, endoderm and mesoderm – which then go on to form the body's organs and tissues. Ectoderm becomes skin and nerves, endoderm becomes the gut and organs such as the liver, pancreas and thymus, and mesoderm becomes muscle, bones and blood. Until now it was believed that germ layer boundaries could not be crossed - that cells originating in one germ layer could not develop into cells associated with one of the others."
STEPS TOWARDS REENGINEERING CELLS FOR TRANSPLANT (August 18 2010)
One of the challenges in developing autologous stem cell therapies for age-related conditions is that old people have damaged stem cells and damaged stem cell niches. This research demonstrates a technology platform that might eventually encompass all sorts of repair and support for cells to ensure that the age of the donor and recipient can be made irrelevant: "Therapeutic cells, such as those implanted in the body to battle cancer or replenish devastated populations of stem cells, may someday be able to carry their own life-support packets. New research [shows] how transplanted cells can be loaded with minuscule particles, or nanoparticles, which contain substances that help the therapeutic cells survive and flourish. These tiny packets of drugs may provide more effective support for the therapeutic cells, and cause less harm overall, because doctors might be able to achieve therapeutic effects with smaller doses of medicine. ... [During one immune therapy test] researchers found they could load about 100 nanoparticles on each T cell without interfering with the cells' division, or with their ability to migrate through tissue, find targets in the bloodstream, and kill tumor cells. ... Both the T cells and stem cells could keep the nanoparticles sitting on their surface - with dividing cells actually splitting up the cargo - an intriguing finding."
HORMESIS VARIES BETWEEN INDIVIDUALS (August 18 2010)
Hormetic effects, in which a little damage improves health by activating defense and repair systems, are important in the relationship between exercise, calorie restriction, and longevity. Here, researchers suggest that therapies based on manipulating hormetic mechanisms will have to be tailored to the individual: "Hormesis, the beneficial effect of a mild stress, has been proposed as a means to prolong the period of healthy ageing as it can increase the average lifespan of a cohort. However, if we want to use hormesis therapeutically it is important that the treatment is beneficial on the individual level and not just on average at the population level. Long lived lines have been shown not to benefit from [hormesis, while] in many experiments hormesis has been reported to occur in one sex only, usually males but not in females. Here we investigated the interaction between the hormetic response and genetic background, sex and duration of a mild heat stress in D. melanogaster, using three replicate lines that have been selected for increased longevity and their respective control lines. We found that genetic background influences the position of the hormetic zone. The implication of this result could be that in a genetically diverse populations a treatment that is life prolonging in one individual could be life shortening in other individuals. However, we did find a hormetic response in all combinations of line and sex in at least one of the experiments which suggests that if it is possible to identify the optimal hormetic dose individually hormesis might become a therapeutic treatment."
REVISITING THE FREE RADICAL THEORY OF AGING (August 17 2010)
Thoughts on the impact of better technology on free radical theory: "The role of oxidative stress in aging proposed by the free radical theory has been the focus of investigations for more than fifty years. The results of a large number of these investigations provide support for this theory. However, numerous recent findings point to the existence of unexpected complexity in the relationships between oxidative stress and aging. This complexity is highlighted by the discovery [that] a key element of oxidative stress defenses in the model organism budding yeast, shortens lifespan in concert with enhanced resistance to oxidative stress. In addition to the implications of this finding for understanding aging, identification of this mutation by massively parallel sequencing of whole genomes emphasizes the enormous utility of next-generation sequencing technologies as investigative tools that will likely revolutionize genetics. ... In some cases, the apparent disconnect between experimental results and predictions of the free radical theory regarding connections between oxidative stress and lifespan is related to hormesis effects that elevate oxidative and other stress defenses in response to low levels of oxidative stress. ... The more transparently clear lesson here is that not all forms of oxidative stress are equivalent in their effects on aging. This isn't surprising in the context of the multitude of pathways that respond to different forms of oxidative stress and the numerous mechanisms by which oxidants can modify different macromolecular targets. Whatever the explanation, [research findings] emphasize the enormous complexity of relationships between oxidative stress and aging."
EARLY DEVELOPMENT, MOOSE, AND LATER ARTHRITIS (August 17 2010)
From the New York Times: "In the 100 years since the first moose swam into Lake Superior and set up shop on an island, they have mostly minded their moosely business, munching balsam fir and trying to evade hungry gray wolves. But now the moose of Isle Royale have something to say - well, their bones do. Many of the moose, it turns out, have arthritis. And scientists believe their condition's origin can help explain human osteoarthritis - by far the most common type of arthritis, affecting one of every seven adults 25 and older and becoming increasingly prevalent. The arthritic Bullwinkles got that way because of poor nutrition early in life, an extraordinary 50-year research project has discovered. That could mean, scientists say, that some people's arthritis can be linked in part to nutritional deficits, in the womb and possibly throughout childhood. The moose conclusion bolsters a small but growing body of research connecting early development to chronic conditions like osteoarthritis. ... Nutrients, experts say, might influence composition or shape of bones, joints or cartilage. Nutrition might also affect hormones, the likelihood of later inflammation or oxidative stress, even how a genetic predisposition for arthritis is expressed or suppressed."
INVESTIGATING THE AGING OF STEM CELLS (August 16 2010)
From the Korea Times: "Stem cells, or early-stage cells that retain the potential to turn into other specialized types of cells, are intriguing for their immense potential in treating a wide range of difficult diseases and conditions. And holding an important key to such innovations would be adult stem cells, which are taken from mature tissue, as they could theoretically be taken from patients, grown in culture and transplanted back into the patient without the fear of provoking an immune response. ... The downside of adult stem cells, however, is that they age much faster than embryonic cells, which has limited their usefulness in transplants. ... It has been presumed that the decreasing regenerative capacity of adult stem cells, which is linked to their aging, is a result of inborn genetic variations. But [researchers suggest] that the process isn't dictated by heritable events, such as DNA damage, but rather determined by an 'epigenetic' regulation of gene expression. ... There weren't many studies on finding micro-RNAs related to the aging of cells and learn how they affect stem cells, but this area could be important in developing a way to have adult stem cells retain their normal ability for a longer time."
WHAT WE KNOW ABOUT FAT TISSUE AND LONGEVITY (August 16 2010)
In a nutshell: "Adipose tissue accounts for approximately 20% (lean) to [more than] 50% (in extreme obesity) of body mass and is biologically active through its secretion of numerous peptides and release and storage of nutrients such as free fatty acids. Studies in rodents and humans have revealed that body fat distribution, including visceral fat (VF), subcutaneous (SC) fat and ectopic fat are critical for determining the risk posed by obesity. Specific depletion or expansion of the VF depot using genetic or surgical strategies in animal models has proven to have direct effects on metabolic characteristics and disease risk. In humans, there is compelling evidence that abdominal obesity most strongly predicts mortality risk, while in rats, surgical removal of VF improves mean and maximum life span. There is also growing evidence that fat deposition in ectopic depots such as skeletal muscle and liver can cause lipotoxicity and impair insulin action. Conversely, expansion of SC adipose tissue may confer protection from metabolic derangements by serving as a 'metabolic sink' to limit both systemic lipids and the accrual of visceral and ectopic fat. Treatments targeting the prevention of fat accrual in these harmful depots should be considered as a primary target for improving human health span and longevity."