Fight Aging! Newsletter, March 7th 2011

March 7th 2011

The Fight Aging! 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 Fight Aging!



- Is Prevention of Aging Within Our Grasp?
- A Review of "The Future of Aging"
- To Die in Order to Live: Cryonics and Legal Hurdles
- Lipids and Longevity
- Discussion
- Latest Headlines from Fight Aging!


Yes and no: there are no silver bullets available for purchase at the present time, but there is a clear path of research and development that will enable us to engineer the prevention of aging in the future - and perhaps soon enough to matter, if we get our act together.

"Yes, prevention of aging is within our grasp - in the sense that a package of foreseeable medical technologies could enable repair of the low-level biochemical damage that causes aging, and those technologies might take only twenty years or so to develop. Unfortunately, that timeline is dependent on a large amount of funding and a dedicated research community, neither of which presently exists for many of the essential parts of this research program. While the regenerative medicine and cancer research communities are populous, well funded, and achieving progress, very few researchers are presently working on other goals necessary to halt the aging process - such as repair of mitochondrial DNA.

"So when I say 'within our grasp,' I mean 'if we all get up and do our part to make it happen.' It takes a wave of public interest and advocacy to steer the scientific community and large funding institutions - and they presently need steering towards repair-based strategies to deal with aging, otherwise the first working rejuvenation therapies will arrive too late for those in middle age today."


The Future of Aging is a fine book and you should read it; I wanted to draw attention to this review for a different reason, however. It delves into a line of thinking that is important and that every supporter of longevity science should be aware of:

"Everyone alive today who ultimately has the chance to benefit from future rejuvenation medicine or methods to significantly slow aging will be using what is at first essentially unproven technology. It will be developed with the best knowledge and insight of the time, but proof is a very high bar when reaching the gold standard involves waiting for decades after the introduction of new therapies. We have a very good grasp of what should extend life and reverse the damage of aging in humans, and it is simply not an option to hold off to see if the first generation of therapies based on this knowledge do in fact extend life in humans. Just as is the case for the practice of calorie restriction today, we will adopt - and are best served by adopting - the use of those technologies that early on in their development can demonstrate (a) extended life in mice, (b) impressive short term changes in the biochemistry of humans, and (c) an acceptable level of observed side-effects and safety.

"This all very reasonable given the circumstances: we lack the luxury of time. Facing the choice between calculated risk and the certain suffering that leads to death, sane people will choose risk. Unfortunately, fighting for the right to be able to take that risk - both in medical development and in the use of the resulting biotechnologies - is very necessary, given the present regulatory environment."


Cryonics, the low-temperature preservation of the recently deceased, is the only chance at a future life for those people born too early to benefit from future rejuvenation biotechnologies. We are the data stored in the fine structure of our brains, and if that data is preserved, then future technologies may one day restore a that person to life. A person is only irrevocably consigned to oblivion when that data is destroyed. Unfortunately, present day legal systems make the process of cryopreservation far harder than it should be:

"The present legalities of death and personal autonomy are not what they might be, and the cryonics industry is consequently very interested in the right to self-determination. The employees of most first world legal systems will do all they can to ensure that you cannot decide the time of your own death; it therefore becomes far, far harder to perform a good cryopreservation. The process cannot be organized to a timetable, and becomes far more costly and uncertain. Just how free are you when your government claims it controls you to such a degree that you cannot even die on your own terms?

So to the point of the post: my attention was recently directed to an open paper on law and cryopreservation. It was written by a student of law, so while recognizing the issue at hand, the solution proposed is made up of what are effectively more legal undertakings, just at a legislative level - which I fear rather misses the true source of the problem. Beyond that, the article provides a good review of the past and legal present of the cryonics industry, and is very educational in that respect."


Many lines of research indicate that our mitochondria - the swarming bacteria-like power plants of our cells - are very important in aging. This is why I regularly bemoan the lack of rapid progress in any of the potential repair technologies for accumulated mitochondrial damage that appears in the old. A recent post at Fight Aging! looks at research into the comparative composition of mitochondria between species, and how that relates to life span:

"Peroxidation of lipids in the body is effectively a form of damage: it is the reaction between a lipid and a free radical [such as those constantly generated by mitochondria], changing the molecular structure of the lipid and rendering it unable to perform its assigned task in the cellular machinery of which it is a part. More resistant lipids mean more damage-resistant mitochondria - and damage-resistant mitochondria should translate fairly directly into enhanced life span. So far the evidence supports this way of looking at matters.

That there is such a strong correlation between the building blocks of mitochondrial membranes and species life span is another strong sign that mitochondrial damage is very important in aging - and thus we should prioritize present efforts to support the development of biotechnologies that can repair or replace mitochondria throughout the body. These therapies are tantalizingly close to realization, but progress is slow and will remain slow until such time as funding and public interest are much larger than they are today."


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!



Friday, March 4, 2011
One strand of stem cell research is learning how to construct exactly the type of cell needed: "researchers for the first time have transformed a human embryonic stem cell into a critical type of neuron that dies early in Alzheimer's disease and is a major cause of memory loss. This new ability to reprogram stem cells and grow a limitless supply of the human neurons will enable a rapid wave of drug testing for Alzheimer's disease, allow researchers to study why the neurons die and could potentially lead to transplanting the new neurons into people with Alzheimer's. ... These critical neurons, called basal forebrain cholinergic neurons, help the hippocampus retrieve memories in the brain. In early Alzheimer's, the ability to retrieve memories is lost, not the memories themselves. There is a relatively small population of these neurons in the brain, and their loss has a swift and devastating effect on the ability to remember. ... Now that we have learned how to make these cells, we can study them in a tissue culture dish and figure out what we can do to prevent them from dying. ... This technique to produce the neurons allows for an almost infinite number of these cells to be grown in labs, allowing other scientists the ability to study why this one population of cells selectively dies in Alzheimer's disease. ... The ability to make the cells also means researchers can quickly test thousands of different drugs to see which ones may keep the cells alive when they are in a challenging environment. ... [Researchers] demonstrated the newly produced neurons work just like the originals. They transplanted the new neurons into the hippocampus of mice and showed the neurons functioned normally. The neurons produced axons, or connecting fibers, to the hippocampus and pumped out acetylcholine, a chemical needed by the hippocampus to retrieve memories from other parts of the brain."

Friday, March 4, 2011
Interesting research reported via ScienceDaily: "Unexpected results from a [recent study] could completely alter scientists' ideas about Alzheimer's disease - pointing to the liver instead of the brain as the source of the 'amyloid' that deposits as brain plaques associated with this devastating condition. The findings could offer a relatively simple approach for Alzheimer's prevention and treatment. ... The product of [the mouse gene corresponding to a gene known to predispose humans carrying particular variations of it to develop early-onset Alzheimer's disease], called Presenilin2, is [involved] in the generation of pathogenic beta amyloid. Unexpectedly, heritable expression of Presenilin2 was found in the liver but not in the brain. Higher expression of Presenilin2 in the liver correlated with greater accumulation of beta amyloid in the brain and development of Alzheimer's-like pathology. ... This finding suggested that significant concentrations of beta amyloid might originate in the liver, circulate in the blood, and enter the brain. If true, blocking production of beta amyloid in the liver should protect the brain. ... mice were administered imatinib [which] has poor penetration of the blood-brain barrier in both mice and humans. ... Because it doesn't penetrate the blood-brain barrier, we were able to focus on the production of amyloid outside of the brain and how that production might contribute to amyloid that accumulates in the brain, where it is associated with disease. ... the drug dramatically reduced beta amyloid not only in the blood, but also in the brain where the drug cannot penetrate. Thus, an appreciable portion of brain amyloid must originate outside of the brain, and imatinib represents a candidate for preventing and treating Alzheimer's."

Thursday, March 3, 2011
You might recall that studies of centenarians turned up an association between reaching that age and levels of HDL, high density lipoprotein, a form of cholesterol transport mechanism. Here is another study demonstrating the same correlation for younger old people: "No previous researchers have sought to determine whether high-density lipoprotein (HDL) cholesterol levels are associated with survival to 85 years of age in a prospective cohort of aging men. We selected 652 men (mean age 65 years) enrolled in the VA Normative Aging Study who had [at least one] HDL cholesterol level documented during the study and who were old enough on the date of HDL cholesterol measurement to reach 85 years of age by [2008]. ... We used proportional hazards to determine hazard ratios (HRs) for mortality before age 85 years for each category of initial HDL cholesterol compared to the reference adjusting for co-morbidities, calculated low-density lipoprotein cholesterol, medications, smoking, body mass index, and alcohol consumption. Treating HDL cholesterol as a continuous predictor, we also determined the HR for each 10-mg/dl increment in HDL cholesterol. ... Each 10-mg/dl increment in HDL cholesterol was associated with a 14% [decrease] in risk of mortality before 85 years of age. In conclusion, after adjusting for other factors associated with longevity, higher HDL cholesterol levels were significantly associated with survival to 85 years of age." Which leads to the thought that if HDL is so good, why not test to see if artificially creating more of it in the body is beneficial?

Thursday, March 3, 2011
One group of researchers believe that every tissue in the body is supported by a left-over population of fully pluripotent stem cells that might be easily accessible for use in therapies: "From the point of view of regenerative potential, the most important cells are pluripotent stem cells (PSCs). Such cells must fulfill certain in vitro as well as in vivo criteria that have been established by work with PSCs isolated from embryos, which are known as embryonic stem cells (ESCs). According to these criteria, pluripotent stem cells should: (i) give rise to cells from all three germ layers, (ii) complete blastocyst development, and (iii) form teratomas after inoculation into experimental animals. Unfortunately, in contrast to immortalized embryonic ESC lines or induced PSCs (iPSCs), these last two criteria have thus far not been obtained in a reproducible manner for any potential PSC candidates isolated from adult tissues. There are two possible explanations for this failure. The first is that PSCs isolated from adult tissues are not fully pluripotent; the second is that there are some physiological mechanisms involved in keeping these cells quiescent in adult tissues that preclude their 'unleashed proliferation', thereby avoiding the risk of teratoma formation. In this review we present an evidence that adult tissues contain remnants from development; a population of PSCs that is deposited in various organs as a backup for primitive stem cells, plays a role in rejuvenation of the pool of more differentiated tissue-committed stem cells (TCSCs), and is involved in organ regeneration. These cells share several markers with epiblast/germ line cells and have been named very small embryonic-like stem cells (VSELs). We suggest that, on one hand, VSELs maintain mammalian life span but, on the other hand, they may give rise to several malignancies if they mutate. We provide an evidence that the quiescent state of these cells in adult tissues, which prevents teratoma formation, is the result of epigenetic changes in some of the imprinted genes."

Wednesday, March 2, 2011
Stress appears to affect long-term health and biochemistry in some fundamental ways, some of which are connected to the aging process - such as telomere length, chronic inflammation, and immune system function. So what happens when a person is the opposite of stressed? There is reason to believe that being happy over the long term has just as much of a beneficial effect as stress does a negative effect: "A review of more than 160 studies of human and animal subjects has found 'clear and compelling evidence' that - all else being equal - happy people tend to live longer and experience better health than their unhappy peers. ... Its lead author [analyzed] long-term studies of human subjects, experimental human and animal trials, and studies that evaluate the health status of people stressed by natural events. ... We reviewed eight different types of studies, and the general conclusion from each type of study is that your subjective well-being - that is, feeling positive about your life, not stressed out, not depressed - contributes to both longevity and better health among healthy populations. ... A study that followed nearly 5,000 university students for more than 40 years, for example, found that those who were most pessimistic as students tended to die younger than their peers. An even longer-term study that followed 180 Catholic nuns from early adulthood to old age found that those who wrote positive autobiographies in their early 20s tended to outlive those who wrote more negative accounts of their young lives. There were a few exceptions, but most of the long-term studies the researchers reviewed found that anxiety, depression, a lack of enjoyment of daily activities and pessimism all are associated with higher rates of disease and a shorter lifespan."

Wednesday, March 2, 2011
Some species do not age in any easily detected way - lobsters, for example. Others are just far more resilient to the passage of years than we humans, living longer or losing little of their vitality over the course of their lives. What can be learned from a study of their biochemistry? "The first photo is from 1973, when a dark-haired and spry Nisbet was banding chicks of the small sea bird off the rocky Cape Cod coast. The second photo was taken 33 years later and shows a grizzled, silver-haired Nisbet holding a 29 year old tern, one of the oldest on record. Nisbet's body shows common signs of wear and tear - gray hair, wrinkles, achy joints. The tern, however, shows none of these outward signs, despite being the equivalent of a human centenarian. ... Terns don't even demonstrate diminished physical abilities as they age. They aren't the only animals that have combined a long lifespan with minimal signs of aging; other seabirds, alligators, crocodiles, and some tortoises also seem to sip from the Fountain of Youth. Although medical advances have extended the human lifespan, these same advances haven't been able to prevent the inimical onslaught of old age. Scientists hope that by studying the secrets of ageless critters, humans will one day be able to pause the hands of time. ... The main difference between humans and organisms like common terns is how growing older affects the risk of dying. ... In some animals, like freshwater hydras, risk of death remains pretty constant during life. For other animals, like the tern, the risk of death actually decreases with age. It seems almost counter-intuitive: an older tern is less likely to die than a younger one. 'My 29-year-old tern was still breeding,' Nisbet said. The oldest terns produced the healthiest offspring and were actually more likely to survive the year than younger terns."

Tuesday, March 1, 2011
This is another project of the Science for Life Extension Foundation, here translated by Google's automated tools: "All of us [are] waiting in front of old age. And along with it - illness, sickness and loneliness. [We all] fear old age. But do not do anything to delay its onset. Meanwhile, there is hope for the extension of active life and [slowing of] aging. Hope this gives the results of research being conducted in many countries around the world. In Russia the problem of aging [is that no-one cares to do anything about it] - neither society nor the researchers nor the state. The purpose of this letter [is] to get people to think about the need for scientific methods to combat aging. By signing it, you'll make a small step to solving this global problem. ... Aging [is] the main issue in the lives of everyone. Aging reduces the protective functions of the organism and its ability to resist disease, inevitably leading to death. The main causes of mortality of Russians - cardiovascular diseases and cancer - are age-related diseases. In our country the death rate exceeds the birth rate of 250,000 people annually. And for a state extension of active life should be problem number 1. To solve this problem [funding] should be prioritized in favor of scientific research of the mechanisms of aging and the search for effective methods of radical life extension."

Tuesday, March 1, 2011
From h+ Magazine: "A [trend] towards nanotechnology is evident in the miniaturization of surgical tools. Experimental microrobots are already available, and being tested in live tissues ... It seems likely that in one or two decades, microrobots will be in common use in surgery, before their eventual replacement by nanorobots. Microrobots will resemble minute machines from the macroscale. But what will nanorobots look like? They won't be akin to artistic representations of miniature submarines placed beside erythrocytes. Most likely, they will bear some resemblance to the body's existing nanomachines, such as mitochondria. ... Nanorobots will be scavengers for atherosclerotic plaque, just like artistic representations you may find online, but not with exactly the same mechanics. We will witness a gradual transition from surgical repair, to prevention. Atherosclerosis, which is in fact the gradual stenosis of the arteries due to plaque formation, will be solved at the genomic and proteomic level, and this will lead to a great enhancement of the human life span. Minimally invasive microrobots will be used instead of stents inside arteries, for repairs that are currently being performed laparoscopically. ... Last but not least, one of the greatest achievements of nanotechnology in surgery will be what we call the 'ideal graft'; that is, biocompatible and durable 'repairs' of parts of the body like arteries, joints or even organs. At first, these repairs will be used for healing, but soon afterwards, they will be used for transcendence: to enhance current human abilities."

Monday, February 28, 2011
A long post from earlier this month at Chronosphere examines technological inevitability - or rather what seems to be its absence if you look back at history. The post is in the context of science and development in cryonics, but the general theme applies just as much to the technologies of enhanced human longevity: just because we are entering an age in which it is possible doesn't mean that it will happen. "One of the most fundamental insights I've ever had came when I was in Rome, and also reading a very good biography of Leonardo da Vinci, in preparation for a visit to Florence. Da Vinci spent most of his career designing war machines, and trying to reroute the Arno River for military advantage. As I looked at the remains of the awesome Ancient Roman engineering around me, and thought of da Vinci, it occurred to me that one of the most powerful and off putting military advantages that could have been deployed, in either Ancient, or Renaissance times, would have been hot air balloons. ... Lighter than air craft are very easy to build, and both the Ancient Romans and the Renaissance Italians had the materials, the wealth, and the technology. The Colosseum was covered with canvas awnings, the Velarium, that were operated by a complex series of ropes and pulleys, and the Romans were superb canvas makers and produced the material in copious amounts to use for ships' sails. Why didn't they develop lighter than air flight - and why didn't Leonardo?" It is not inevitable that we will develop true rejuvenation biotechnology soon enough to save us from aging to death: the only way this will happen is if we make it happen, through activism, education, fundraising, and the other traditional methods of changing the path taken by our society. Sitting back, doing nothing, and assuming we're going to be rescued is the road to suffering and death.

Monday, February 28, 2011
Obtaining 501(c)(3) tax exempt status in the US is an ordeal, and one that the SENS Foundation has now completed: "SENS Foundation is pleased to announce that it has been granted tax-exempt status as a 501(c)(3) public charity, with an effective date of March 9, 2009. Donations to the Foundation are fully deductible as a charitable contribution." If you've been putting off donating to support the SENS Foundation's work on the development of rejuvenation biotechnology, now is an excellent time to jump on in. Research costs money, but in the grand scheme of things the cost of building the first generation of technologies that will enable us to live for decades longer - and thus gain the time to wait for the second generation that will be even more impressive - is small. It will take only a few tens of millions of dollars a year for each of the strands of the Strategies for Engineered Negligible Senescence. That is a rounding error when compared against either the total medical funding in the US, or total charitable donations in the US. So make a donation, and persuade a few other people to look into the work of the SENS Foundation.



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