LONGEVITY MEME NEWSLETTER
February 08 2010
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.
- Looking Ahead to Mitochondrial DNA Therapies
- So Very Many Pressing Distractions
- Six Years of Fight Aging!
- Latest Healthy Life Extension Headlines
LOOKING AHEAD TO MITOCHONDRIAL DNA THERAPIES
The number of researchers interested in repairing damaged mitochondrial DNA is slowly growing:
"Mitochondria are the cell's power plants, important in the operation of metabolism, central to the mechanisms by which metabolism determines life span, and implicated as the culprit in many age-related diseases. As described in the mitochondrial free radical theory of aging, a small number of mitochondrial genes are known to be crucial to its operation as the cell's power plant. Damage to those genes is unfortunately a natural consequence of the operation of a mitochondrion, and leads to a Rube Goldberg sequence of events in which is a healthy cell is turned into a damaged cell that spews forth damaging biochemicals into your body. As these errant cells accumulate, their actions collectively give rise to many of the unwelcome forms of change and damage that come with age: systems failing, organs shutting down, and important biochemical processes running awry because their component molecules are corrupted."
But if you could replace damaged mitochondrial DNA - or even just the few crucial genes governing the core of the mitochondrial power plant - throughout the body every few decades, none of this would be a problem. Indeed, replacing damaged mitochondrial DNA in the elderly would be a limited form of rejuvenation, restoring one bodily system to its youthful state. This goal has already been achieved in the laboratory in a couple of different ways over the past five years. This is a field of research in which the only obstacles to bringing mitochondrial DNA replacement to the clinic are (a) lack of funds, and (b) lack of public understanding and support.
SO VERY MANY PRESSING DISTRACTIONS
But of course there are shiny objects and bright lights to distract us from the matter of our own aging and what might be done about it:
"I suspect many theorists think my interest in aging is odd, if not frivolous. When there are so many pressing problems in the world today the idea of fixating on aging has little, if any, intuitive appeal. A few years ago I use to think this same way. But after pondering these questions, learning some biology and following the pace of scientific discovery in the field of aging research, I have come to now hold the view that the stakes at risk in these debates are very important indeed. I would go so far as to suggest that tackling global aging is one of this century's most important challenges. And because very few people see aging as a problem the challenge of tackling aging is an even bigger problem than it would otherwise be if we all saw it for the problem it really is.
"We live in a world in which most people don't give much thought to degenerative aging until it happens to them, and once in that unfortunate position, they don't give much thought to what might be done to stop this from happening to everyone. Consider how easy it is for a state-level politician in the US to raise a million dollars from the public at large (done in under a week in some cases that spring to mind) versus how hard it is for even a noted researcher in the field of aging research to do the same. Yet that politician doesn't matter in the grand scheme of things; he cannot create new technology, he will be fat on bribes and gone in a few years, and all his actions will be unimportant in comparison to the daily toll of death and suffering caused by aging:"
SIX YEARS OF FIGHT AGING!
The Fight Aging! blog marks its sixth anniversary:
"If the earlier posts contained more advocacy than science, the last couple of years have been fairly evenly divided between those two topics. But the archives have grown large indeed - somewhere in the vicinity of 1800 posts - and almost every topic related to engineered longevity that I consider useful or interesting has been touched on in some way. Indeed, six years of writing has generated more than enough material to surprise me on a regular basis by what turns up in the Fight Aging! archives. Memory is the first thing to go, or so they say."
This newsletter has been running for seven years, and the Longevity Meme is more or less nine. Like the Fight Aging! archives, the newsletter archives have grown large:
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
NANOPARTICLES, LASERS, AND CANCER (February 05 2010)
Researchers have been killing cancer cells in the lab through a combination of targeted nanoparticles and laser heating for a couple of years now, but here is an interesting advance on that method: scientists "have discovered a new technique for singling out individual diseased cells and destroying them with tiny explosions. The scientists used lasers to make 'nanobubbles' by zapping gold nanoparticles inside cells. In tests on cancer cells, they found they could tune the lasers to create either small, bright bubbles that were visible but harmless or large bubbles that burst the cells. ... Single-cell targeting is one of the most touted advantages of nanomedicine, and our approach delivers on that promise with a localized effect inside an individual cell. The idea is to spot and treat unhealthy cells early, before a disease progresses to the point of making people extremely ill. ... In laboratory studies published last year [researchers also] applied nanobubbles to arterial plaque. They found that they could blast right through the deposits that block arteries. ...The bubbles work like a jackhammer. ... nanobubble technology could be used for 'theranostics,' a single process that combines diagnosis and therapy. In addition, because the cell-bursting nanobubbles also show up on microscopes in real time, [the] technique can be use for post-therapeutic assessment, or what physicians often refer to as 'guidance.'"
TO CURE AGING: HOW MUCH AND HOW LONG? (February 05 2010)
From the Maximum Life Foundation blog, a video from the Manhattan Beach Project meeting on the projected cost and time taken to develop various aging-slowdown or actual rejuvenation therapies: "How much will it cost and how long will it take to develop an effective caloric restriction mimetic - one that will add many years if not decades to the human lifespan? What will it take to come up with a drug that turns on telomerase and thus lengthens telomeres? How about immune system restoration, tissue/organ storage, mitochondrial medicine, and other medical technologies?" For another perspective on time and cost, you might look at the SENS Foundation information on pushing to completion therapies for the seven contributing aspects of aging. We could expect working rejuvenation in mice with ten years of work and a billion dollars, for example - the challenge has always been convincing people that this is in fact the case, and raising those funds. Predicting how long it will take to move from mice to people is much harder, as this depends far more on regulation and politics than anything else. Two decades doesn't seem unreasonable in the present environment.
WORKING ON LUNG REGENERATION (February 04 2010)
Via ScienceDaily: "Stem cell researchers exploring a new approach for the care of respiratory diseases report that an experimental treatment involving transplantable lung cells was associated with improved outcomes in tests on mice with acute lung injury. ... Respiratory diseases are a major cause of mortality and morbidity worldwide. Current treatments offer no prospect of cure or disease reversal. Transplantation of pulmonary progenitor cells derived from human embryonic stem cells may provide a novel approach to regenerate endogenous lung cells destroyed by injury and disease. ... [Researchers] used a genetic selection procedure they created to generate a type of lung cell known as alveolar epithelial type II, which secretes surfactant, a substance that keeps the lung inflated, and can turn into another important lung cell that regulates the transfer of oxygen into the blood and the removal of carbon dioxide. ... the experimental stem cell treatment [not only] prevented or reversed visual hallmarks of pulmonary injury, but also restored near normal lung function to mice. ... additional tests in other animal models and eventually humans will be needed before these cell transplants can be used to treat respiratory diseases."
AN ARTICLE ON CALORIE RESTRICTION (February 04 2010)
From the Huffington Post, an article on the science and practice of calorie restriction that focuses on extended longevity, and so manages to omit mention of the demonstrated health benefits in human studies: "The science of aging is among the most dynamic and provocative in modern biology. Over the past two decades we have seen a virtual explosion in research investigating the molecular and behavioral systems that control the aging process. But the more researchers uncover about the science of aging, the more questions emerge. Dietary restriction has long been considered the most potent regulator of aging. Restricting food intake by any means induces a series of metabolic changes in organisms from yeast to primates that serve to extend life. Studies are currently underway to investigate the ability of dietary restriction to extend life in humans. ... The genes linking diet and aging are highly conserved through evolution, indicating that there is a great chance human aging is sensitive to diet. Indeed, insulin-related genes have been found to be important in long-lived human populations. This suggests that the pathways discovered in worms and other organisms have similar functions in humans. What is not clear is how much influence diet has on lifespan and to what extent we are able to manipulate it."
RAPAMYCIN REVIEWED AT OUROBOROS (February 03 2010)
From Ouroboros: "One of [the] most significant breakthroughs [in biogerontology] last year was the announcement that the macrolide drug rapamycin can extend longevity in mice. More specifically, rapamycin can accomplish this when administered to adult, wildtype mice. In other words, no genetic modification or early-life intervention is necessary, making rapamycin one of the first compounds that meets the criteria for an anti-aging drug that could be used for people who are already alive and well down the road toward aging themselves. The lifespan extension achieved is modest (~10%), but this is more impressive in light of the fact that the mice were quite old at the time treatment began, and the study used only a single dose rate. Future studies will undoubtedly seek to optimize the dose and regimen with the goal of achieving greater enhancement of lifespan. How does it work? As the saying goes, further study is required, and at multiple levels. ... There's a good deal left to discover about the rapamycin’s effects on aging in general - and regarding the specific mechanistic relationship between translational control, senescence, and organismal aging - but I have it on good authority that there's a great deal of effort being exerted in that direction. Watch this space for future developments."
THE DEATHIST VIEWPOINT (February 03 2010)
From EconLog: "Ron Bailey's Liberation Biology quoted Frank Fukuyama: 'Life extension seems to me a perfect example of something that is a negative externality, meaning that it is individually rational and desirable for any given individual, but it has costs for society that can be negative.' I couldn't believe my eyes. Did Frank Fukuyama actually mean that when a person has another year of healthy life, the net effect on other people is negative? If so, why do people cry at funerals, instead of celebrating? Fukuyama's statement was so hateful and twisted that I wondered if he was being quoted out of context. So I dug up the full paragraph ... The extra words definitely make Fukuyama's position more confusing, but they take away none of the horror. The extra words definitely make Fukuyama's position more confusing, but they take away none of the horror. You'd think that a 'perfect example' of a negative externality would be easy to explain and hard to dispute - like air pollution. But to make his case, Fukuyama has to appeal to the controversial notion of group selection: Human beings evolved to die because it's adaptive for society. His specific mechanism - death stops elders from impeding progress - would be controversial even for believers in group selection. After all, during our evolutionary history, there was almost no progress to impede! ... On purely pragmatic grounds, then, Fukuyama's argument is about as feeble as 'Life extension is bad for morticians.'"
PREMIERE SCREENING OF TO AGE OR NOT TO AGE (February 02 2010)
A new film on aging and longevity science, "To Age or Not to Age," will be premiered in New York on February 11th, with a discussion panel of biogerontologists to follow: "The New York City screening will be followed by a live panel discussion. The panel discussion will be simulcast to venues screening the film nationwide and will stream live online. Panelists include: Dr. Robert Butler, Gerontologist, Psychiatrist & Pulitzer-Prize Winner; President and CEO of the International Longevity Center. ... Dr. Aubrey de Grey, Biomedical Gerontologist; Chief Science Officer, SENS Foundation. ... Dr. Leonard P. Guarente, Novartis Professor of Biology, MIT; Director, Paul F. Glenn Lab for Science of Aging. ... Dr. Gordon Lithgow, Biomolecular Geneticist; Head of the Lithgow Lab, Buck Institute on Aging. Moderated by Robert Kane Pappas, director of To Age or Not to Age. The scientists featured in To Age or Not to Age have found the means to postpone and possibly mitigate diseases tied to aging, such as cancer, cardiovascular disease, neurodegenerative diseases, and diabetes."
IMPROVING THE HUMAN IMMUNE SYSTEM (February 02 2010)
From h+ Magazine: "For now, the best way to supplement the body's own defenses is through vaccines, but vaccines are far from a panacea. Each vaccine must be prepared in advance, few vaccines provide full protection to everybody, and despite popular misconception, even fewer last a lifetime. For example, smallpox vaccinations were lifelong, but tetanus vaccines generally last 5-10 years. There is still no vaccine for HIV infection. And when it comes to bacteria like tuberculosis, current vaccines are almost entirely ineffective. What's more, the whole process is achingly indirect. Vaccines work by first stimulating B cells and T cells in order to induce production of antibodies. They don't directly produce the needed antibodies. Rather, they try (not always successfully) to get the body to generate its own antibodies. In turn, stimulation of T cells requires yet another set of cells - called dendritic cells - and the presence of a diverse set of molecules called the major histocompatibility complex, creating still further complexity in generating an immune response. Our best hope may be to cut out the middleman. Rather than merely hoping that the vaccine will indirectly lead to the antibody an individual needs, imagine if we could genetically engineer these antibodies and make them available as needed. Call it immunity-on-demand. At first blush, the idea might seem farfetched. But there's a good chance this system, or something like it, will actually be in place within decades."
VETTING STEM CELL THERAPIES (February 01 2010)
First generation stem cell therapies are offered in many locations around the world, and medical tourism is booming, but what sort of due diligence should you perform before trying to take advantage of a particular therapy? Here are some good suggestions: "The International Cellular Medicine Society (ICMS) has promulgated laboratory, practice standards and maintains a non-profit stem cell treatment registry. The easiest way to determine if the cell therapy is credible is to see if the clinic is ICMS certified. ... The development of treatment protocols for stem cells is difficult and disease as well as tissue specific. This means that valid treatment isn't as easy as sprinkling magic stem cells on the patient. For example, the treatment protocol for knee osteoarthritis has a completely different approach than cardiac disease. Some stem cell clinics are operating at a high level focus on a small collection of diseases and perfect their protocols for those diseases. This may take years for each application. So if the clinic advertises that it treats everything from ALS to Parkinson's to knee arthritis, this usually indicates that it's not operating at a high level of credibility.... Where are the stem cells obtained? Are they from the same patient (autologous) or from an allogeneic source? Many experts agree that autologous cells are more likely to have a much more robust safety profile than cells obtained from a donor. In particular, genes of the donor remain active in the host (which could have either a potentially positive or negative impact)."
KILLING CELLS TO STOP RHEUMATOID ARTHRITIS (February 01 2010)
Promising news for sufferers of autoimmune conditions: "A researcher [has] invented a novel way to halt and even reverse rheumatoid arthritis. He developed an imitation of a suicide molecule that floats undetected into overactive immune cells responsible for the disease. ... This new therapy stopped the disease cold in 75 percent of the mice. The best part was we didn't see any toxicity. ... Healthy immune cells are supposed to die after they attack an invading virus or bacteria. But in rheumatoid arthritis, the immune cells called macrophages live and go rogue. They proliferate in the blood, build up in the joints and invade cartilage and bone. Currently, there is no effective, nontoxic way to stop them. ... immune cells in rheumatoid arthritis are low in a critical molecule called Bim, whose job is to order the cells to self-destruct. To correct that shortage, [researchers] developed an imitation of the molecule, called BH3 mimetic. When [injected into] mice with rheumatoid arthritis, it floated ghostlike into their macrophages and bam!, the misbehaving immune cells self destructed. ... the molecule could prevent the development of rheumatoid arthritis as well as trigger a remission of existing disease. ... the next step is to develop nanotechnology for a more precise method of delivering the drug."