Cryonics industry figure Ben Best attended the fifth SENS conference that was held some weeks back in England, and his report can be read at Depressed Metabolism:

People who attend SENS conferences are the demographic that is the most receptive to cryonics of any identifiable group I have yet found. They are mostly scientists interested in intervening in the aging process.

...

great progress has been made in starting research programs on each of the SENS strategies, and by 2012 research on all the strategies is expected to be in progress.

...

In addition to my oral presentation on cryonics I also had a poster. Scientific conferences usually have poster sessions where scientists present research, reviews, or ideas in the form of a poster. Poster presenters stand by their posters at scheduled times to discuss their work on a one-to-one basis with individuals rather than to an audience. My poster dealt with challenging the concept of biological age and denying the possibility of a biomarker of aging that could determine biological age. I contended that biological age and biomarkers of aging assume a singular underlying aging process, which I denied on the grounds that aging is multiple forms of damage.

His view on biomarkers is an interesting one; you might look back in the Fight Aging! archives for a background on the search for biomarkers of aging - there are a good number of posts on the topic, and it's an area of research that has some importance to the future pace of progress. Absent good biomarkers, it's going to be hard to rapidly tell the difference between a working rejuvenation therapy and a non-working rejuvenation therapy - and time is in short supply.

I did want to draw you attention to a point from Best that I disagree with. He says:

I consider gene therapy to be an essential tool for the ultimate implementation of SENS, and a deficiency of SENS that there is so little attention paid to this technology. I don't see how SENS can be implemented by any means other than genetic re-programming. LysoSENS, for example, would require new genes to create new, more effective enzymes for the lysosomes. MitoSENS would require all mitochondrial proteins be made in the nucleus and imported into the mitochondria.

For mitochondrial repair, agreed, all of the most plausible paths look like gene therapy. The problem that MitoSENS seeks to solve is the accumulation of damage to mitochondrial DNA, and so that DNA either needs to be protected, repaired, or replaced. Fair enough. But I think there will be a wide range of other practical mechanisms for the delivery of necessary enzymes to lysosomes as a part of the LysoSENS program. Recent years have made it clear that biotechnologies other than gene therapy can target small molecules to specific cells and even specific portions of a cell, such as by hijacking normal protein targeting mechanisms or through carefully designed nanocarrier structures. I would agree that an ultimate implementation would be one that is always on - an unambigiously beneficial genetic change to allow lysosomes to digest what is presently indigestible and which will be passed on to future generations. But it seems far more likely that initial implementations will be periodic clinical treatments - injections and infusions - designed to flush the body's lysosomes with enzymes for a short period of time, and thereby clean them out. This would seem to be sufficient, given that we humans manage three decades of life at the outset without the obvious degenerations of aging starting to show up.

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

A review paper on one of the trailing areas of tissue engineering - lungs present a harder and more complex challenge than many other organs: "End-stage lung disease is a major health care challenge. Lung transplantation remains the definitive treatment, yet rejection and donor organ shortage limit its broader clinical impact. Engineering bioartificial lung grafts from patient-derived cells could theoretically lead to alternative treatment strategies. Although many challenges on the way to clinical application remain, important early milestones toward translation have been met. Key endodermal progenitors can be derived from patients and expanded in vitro. Advanced culture conditions facilitate the formation of three-dimensional functional tissues from lineage-committed cells. Bioartificial grafts that provide gas exchange have been generated and transplanted into animal models. Looking ahead, current challenges in bioartificial lung engineering include creation of ideal scaffold materials, differentiation and expansion of lung-specific cell populations and full maturation of engineered constructs to provide graft longevity after implantation?in vivo. A multidisciplinary collaborative effort will not only bring us closer to the ultimate goal of engineering patient-derived lung grafts, but also generate a series of clinically valuable translational milestones such as airway grafts and disease models."

Link: http://www.ncbi.nlm.nih.gov/pubmed/22026560

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

The aging of bacteria grants us insight into the very earliest evolutionary origins of aging: "When a bacterial cell divides into two daughter cells and those two cells divide into four more daughters, then 8, then 16 and so on, the result, biologists have long assumed, is an eternally youthful population of bacteria. Bacteria, in other words, don't age - at least not in the same way all other organisms do. ... [But] not only do bacteria age, but [their] ability to age allows bacteria to improve the evolutionary fitness of their population by diversifying their reproductive investment between older and more youthful daughters. ... Aging in organisms is often caused by the accumulation of non-genetic damage, such as proteins that become oxidized over time. So for a single celled organism that has acquired damage that cannot be repaired, which of the two alternatives is better - to split the cellular damage in equal amounts between the two daughters or to give one daughter all of the damage and the other none? ... bacteria appear to give more of the cellular damage to one daughter, the one that has 'aged,' and less to the other, which the biologists term 'rejuvenation' ... In a bacterial population, aging and rejuvenation goes on simultaneously, so depending on how you measure it, you can be misled to believe that there is no aging. ... We ran computer models and found that giving one daughter more the damage and the other less always wins from an evolutionary perspective. It's analogous to diversifying your portfolio."

Link: http://www.sciencedaily.com/releases/2011/10/111027150207.htm

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

So how are things coming along with the Open Cures project? (If this is new to you, please do follow that link to see what this is all about).

I should preface this post by noting that my work on any given project tends to take place in waves, and the past couple of months have been a trough of comparatively low activity for Open Cures. The earlier part of this year was a crest in which planning was accomplished, discussions held, an email group and web site site up, posts and articles written, and a few thousand dollars expended to test the waters for paid writing of protocol documents, largely through contractors with life science backgrounds met via the oDesk marketplace. A start, in other words, for something that I anticipate will run at a more modest rate for a number of years.

You never get as far as you'd like in any given period of time, of course, and the rest of the world rarely cooperates by conforming to initial expectations. Since the last update posted here, work on finding reliable authors and writing has proceeded at a slow but steady pace. I'm comfortable with my ability to source these folk now - there are a surprisingly large number of life science graduates and researchers offering their services on the global market for distance work. So the focus has been on establishing high quality baseline documents as examples, templates to help future writers toe the line, and similar issues. One of the slowdowns here has been a matter of dealing with the questions that bedevil the setup for any process: what exactly do we want the results to look like, what is the best way to obtain them, how does it all fall into place in detail.

From an operations perspective, I've shifted most of the ongoing publishing into the Open Cures Wiki: if I'd decided to do that at the outset it would have saved some time in setting up the website, but such is life. I'm presently within striking distance of finishing up the LysoSENS bacterial discovery protocol: a final and rewritten draft is in hand, just not yet posted, and the author will be fixing up the outline to conform with it. A protocol outline for the synthesis of SkQ1, the targeted mitochondrial antioxidant, was completed and posted last month and is awaiting expansion into a full document. There's a nice backlog of other items to be reworked into the final template, and a nice list of research results that I'd like to produce protocols to describe.

I had hoped that the LysoSENS bacterial discovery would prove to be a useful overture to the DIYbio community - it's an interesting project with bacteria and various chemical synthesis activities, well suited as a hobbyist project but one which can assist real, significant research. Watching and interacting with the DIYbio community has led me to think that I'm too early, however, and that they are not going to be particularly receptive any time soon for a range of reasons. Firstly, the movers and shakers are focused on growth and technology over specific projects; they are a small community still, and the most important things for them right now involve producing low-cost and open versions of common technologies (such as OpenPCR), and building shared laboratory spaces to help grow and solidify local groups (such as BioCurious).

Secondly, most of these folk are either disinterested or hostile towards engineered longevity and human rejuvenation as long-term goals. I would guess that this stems in part from the fact that this describes the population in general, and there's no particular reason that a selection of entrepreneurial life science folk should be any different, and in part from the plant biotech / third world farming assistance / environmentalist roots of a fair-sized fraction of the community. They have a tendency to look down on things that they can argue do not primarily help the poor and disadvantaged first; environmentalist hostility towards human longevity is well known and widespread.

Thirdly, the DIYbio community is somewhere between scared and terrified of the possibility of hostile government regulation arriving before they have a large enough community and mindshare to effectively resist it - so there is considerable self-censorship, caution, and opposition to any proposed work with animals, animal cells, or indeed anything that might touch on the heavy regulation that attends professional life science research on the medical side. Similarly, you won't win many friends by having the declared goal of working around the FDA as is the case for Open Cures - and for much the same reasons.

So, in short, I'm thinking that it's too early to expect useful allies there. That community needs to become larger, have listened to what the longevity advocacy community has to say for longer, and Open Cures needs more than just an idea and a website to demonstrate its solidity and useful nature. A nice library of protocols would be a good start, and that's underway at a modest, side-project sort of pace.

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

PCG-1 is known to be connected to the benefits of calorie restriction in a range of species, and here researchers are working with flies: "One of the few reliable ways to extend an organism's lifespan, be it a fruit fly or a mouse, is to restrict calorie intake. Now, a new study in fruit flies is helping to explain why such minimal diets are linked to longevity and offering clues to the effects of aging on stem cell behavior. Scientists [found] that tweaking a gene known as PGC-1, which is also found in human DNA, in the intestinal stem cells of fruit flies delayed the aging of their intestine and extended their lifespan by as much as 50 percent. ... While little is known about the biological mechanisms underlying this phenomenon, studies have shown that the cells of calorie-restricted animals have greater numbers of energy-generating structures known as mitochondria. In mammals and flies, the PGC-1 gene regulates the number of these cellular power plants, which convert sugars and fats from food into the energy for cellular functions. ... The researchers found that boosting the activity of dPGC-1, the fruit fly version of the gene, resulted in greater numbers of mitochondria and more energy-production in flies - the same phenomenon seen in organisms on calorie restricted diets. When the activity of the gene was accelerated in stem and progenitor cells of the intestine, which serve to replenish intestinal tissues, these cellular changes correspond with better health and longer lifespan."

Link: http://www.newswise.com/articles/fruit-fly-intestine-may-hold-secret-to-the-fountain-of-youth

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

Via EurekAlert!: "Research into differentiation has led to a variety of breakthroughs as stem cell researchers harvest cells from one part of the body and genetically adapt them to fulfill a specialized role. However, if the implanted cells are too much like the cells of the targeted area they may not have the plasticity to engraft and repair the injured tissue. ... Stem cell differentiation and transplantation has been shown to improve function in conditions including degenerative diseases and blood supply disorders. However, the survival rate of transplanted cells in patients limits their overall effectiveness, which is a barrier to clinical use. ... To overcome this issue [researchers] explored de-differentiation, a process that reverts specialized, differentiated cells back to a more primitive cell. The team focused their research on multipotent stem cells, (MSCs) which can be altered into a variety of cell types through differentiation. Bone marrow MSCs have the potential to differentiate into each of the three basic types of lineage cells which form bone (osteocytes), cartilage (chondrocytes) and fat tissue (adipocytes). The team first differentiated bone marrow MSCs towards a neuronal lineage, but then removed the differentiation conditions, allowing the cell to revert back to a form with more basic cellular characteristics. Following this process the team recorded increased cell survival rates following transplants. In an animal model de-differentiated cells were found to be more effective in improving cognitive functions and in aiding recovery from strokes, compared to un-manipulated stem cells both in living specimens and in laboratory experiments."

Link: http://www.eurekalert.org/pub_releases/2011-11/w-rsc110111.php

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

At any given time a whole bunch of cells in your body need to be destroyed before they cause harm - cells that are past the productive stage of their life cycle and have become senescent, cells that are damaged and malfunctioning, and so forth. The majority of these cells are indeed destroyed, either by the immune system or through self-destruction mechanisms that evolved to trigger when vital cellular processes begin to run ragged. But this protective culling fails with age, and the accumulation of cells that should have been destroyed but were not is one of the driving forces of degenerative aging.

This fact is reflected in the proposed apoptoSENS research program, one of the seven branches of the Strategies for Engineered Negligible Senescence. Where the body isn't keeping up with cells that should be destroyed, appropriate forms of biotechnology can could be developed to perform this necessary work - and thereby remove and reverse this contribution to aging. The first array of therapies will probably look much like the targeted cell killing strategies under development in the cancer research community: using bacteria, viruses, nanoparticles, or the patient's own immune system to selectively seek out and destroy cells based on their surface markers.

I see that recent research adds weight to proposals for therapies that will eliminate senescent cells:

Scientists at the Mayo Clinic, in the US, devised a way to kill all senescent cells in [mice genetically engineered to age more rapidly than normal, and therefore accumulate senescent cells more rapidly than normal]. ... when they were given a drug, the senescent cells would die. The researchers looked at three symptoms of old age: formation of cataracts in the eye; the wasting away of muscle tissue; and the loss of fat deposits under the skin, which keep it smooth. Researchers said the onset of these symptoms was "dramatically delayed" when the animals were treated with the drug. When it was given after the mice had been allowed to age, there was an improvement in muscle function.

[The study] suggests if you get rid of senescent cells you can improve [physical traits] associated with ageing and improve quality of life in aged humans.

The caveat here is that these are not normal mice. Animals that suffer accelerated aging are used for the standard cost effectiveness reasons: the researchers were already working with the breed, effects will be easier to find, and can be found in a shorter period of time. Now that the researchers have an effect and a mechanism by which they can reliably destroy senescent cells, the next step is to repeat the study in ordinary mice and see what happens - which will of course take a few years if they want to evaluate the effects on life span as well as health, risk of age-related disease, and so forth.

Here's a link to the research paper and a little detail on how the authors are clearing out senescent cells:

Senescent cells accumulate in various tissues and organs with ageing and have been hypothesized to disrupt tissue structure and function because of the components they secrete. However, whether senescent cells are causally implicated in age-related dysfunction and whether their removal is beneficial has remained unknown. To address these fundamental questions, we made use of a biomarker for senescence, p16Ink4a, to design a novel transgene, INK-ATTAC, for inducible elimination of p16Ink4a-positive senescent cells upon administration of a drug.

The mice used were BubR1 mutants, and you can find an interesting article on that topic at the laboratory website.

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

An interesting open access review paper - the full thing is in PDF format only: "The development of materials and technologies for the assembly of cells and/or vesicles is a key for the next generation of tissue engineering. Since the introduction of the tissue engineering concept in 1993, various types of scaffolds have been developed for the regeneration of connective tissues in vitro and in vivo. Cartilage, bone and skin have been successfully regenerated in vitro, and these regenerated tissues have been applied clinically. However, organs such as the liver and pancreas constitute numerous cell types, contain small amounts of extracellular matrix, and are highly vascularized. Therefore, organ engineering will require the assembly of cells and/or vesicles. In particular, adhesion between cells/vesicles will be required for regeneration of organs in vitro. ... adhesive materials and technologies will work as 'glues' for assembling various kinds of cells. The adhesive materials should be degraded when cells themselves biosynthesize cell adhesion molecules ... Although integration of newly developed materials and technologies will be required for the regeneration of organs in vitro, this will ultimately lead to the creation of three-dimensionally engineered organs with functions similar to those of natural organs."

Link: http://dx.doi.org/10.1088/1468-6996/12/6/064703

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

Making therapies that can work in older patients despite their frailty and damage is an important part of progress in stem cell medicine of all sorts: "Age alone no longer should be considered a defining factor when determining whether an older patient with blood cancer is a candidate for stem cell transplantation. That's the conclusion of the first study summarizing long-term outcomes from a series of prospective clinical trials of patients age 60 and over ... the five-year rates of overall and disease-progression-free survival among mini-transplant patients were 35 percent and 32 percent, respectively. Patients in three age groups - 60 to 64, 65 to 69 and 70 to 75 - had comparable survival rates, which suggested that age played a limited role in how patients tolerate the mini-transplant. ... Conventional transplants, which are generally not perfomed on people over age 60 or others who are medically unfit, use high doses of total-body irradiation and potent chemotherapy to eliminate leukemic cells. The intense treatment destroys the blood and immune system and is fatal unless the patient is rescued by infusion of donor bone marrow or stem cells isolated from peripheral blood. The mini-transplant, in contrast, relies on the ability of donor immune cells to target and destroy the cancer - without the need for high-dose chemotherapy and radiation. Instead, low-dose radiation and chemotherapy is used to suppress the immune system rather than destroy it. This helps the body accept the donor stem cells, which then go to work to attack cancer cells - called the graft-vs.-leukemia effect - and rebuild the immune system."

Link: http://www.eurekalert.org/pub_releases/2011-11/fhcr-anl102611.php

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

In response to a news item posted yesterday, a commenter asks:

The fact that rejuvenation in mice seems to have been ten years away for around eight years now does not fill me with confidence. I understand of course that those estimates were for a scenario in which SENS had been adequately funded, and that it hasn't come remotely close. ... I want to know how far we are from actually achieving our goals given that funding is likely to continue to be inadequate. Fifteen years? Twenty? Fifty?

Which is a fair question. For reference, the fully funded SENS scenario called for a budget of $100 million per year over ten years the last time I checked, those funds spread between work on the seven categories of repair biotechnology required to prevent and reverse the degenerations of aging. That scenario is proposed to give a fifty-fifty shot at mouse rejuvenation by the end of the ten year period. As the clock keeps ticking without funding at that level materializing, one would expect the cost estimates to fall somewhat over time even if no-one is working on SENS: the cost of research and development in biotechnology is falling across the board, and in addition researchers benefit from a steady rate of progress throughout the fundamental life sciences. Some things that were obscure will become clear and some things that were hard will become easier because of progress in related areas of the broader field.

If SENS work stopped tomorrow and someone were to return to the drawing board ten years from now and run the numbers again, would rejuvenation in mice still be ten years and $100 million? Quite possibly yes on the ten years, and no on the $100 million - I think the cost would be significantly lower. But that doesn't mean it would take less time: as I've argued in the past there is a certain lower limit in the time taken for human endeavors. Organization of large projects, large-scale fundraising, and sequential tasks that depend upon one another can't be brought down below a certain minimum length of time for so long as there are humans in the decision loop. From this perspective, spending tens of millions of dollars on research in a few years is just as large and complex an undertaking as raising venture capital and starting a company - you can't expect to get much of anywhere without it taking a few years, no matter how good your tools and ideas are.

So watching estimated future costs ticking down is one form of progress - but not the one we want to see. The trouble with the question in the comment that I quoted above is that research funded at very low levels is inherently unpredictable:

I would say that the principal cause of uncertainty for the timeline leading to rejuvenation biotechnology - ways to repair and reverse the cellular and molecular damage that causes aging - is the fact that we lack a large, well-funded, well-supported research community at this time. Only comparatively small initiatives exist now, such as the SENS Foundation, and the actions, choices, and happenstance of individuals have large effects on the future timeline leading to the desired solid research community. That future community will be large enough that individual choices don't tend to have much of an effect on its progress one way or another, but here and now the element of chance is significant.

If funding of $100 million per year results in a big enough research group to allow for an averaging of the risks and reasonable predictions for a decade of work, then $1 million a year (the 2010 budget of the SENS Foundation) is far removed from predictability. If that continues for ten or twenty years, who can say what will result - certainly not fully implemented SENS, but my point is that no prediction of the actual resulting science and technology can be reasonable at these levels of funding.

The lesson to take away here is that we should view the SENS research program as a growth endeavor, and success in the long term goal of building a toolkit for human rejuvenation can only come through tremendous growth. These are still the early, formative years in a curve spanning decades. Present small scale work is accomplished to build the case beyond mere advocacy, to prove that the SENS vision leads to positive and useful results at every stage, and to attract greater levels of funding and support and greater numbers of researchers. Early outputs from SENS research will likely be technologies of use in producing therapies for end-stage age-related diseases, for example, or new science that contributes to these ends.

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

Here's a question for you: why does the triumvirate of astrophysics, astronomy, and cosmology get such good press and widespread public approval in comparison to, say, the fundamental life sciences? I have to think it has something to do with the succession of scientists who evolved into successful media figures, educators, and advocates for their field, such as Carl Sagan, the present day Neil deGrass Tyson, or Patrick Moore - and I'm probably dating myself here by knowing of the existence of the latter. If asked to name noted scientists who went on to become media figures, off the cuff, I think I'd be hard pressed to quickly come up with more than one or two who didn't come from an astrophysical or similar background (right now my brain is delivering Attenborough, Dawkins, and blank). So clearly there's been a lot of groundwork accomplished over the past decades: bringing the broad field of physics and cosmology to the masses, and along the way gaining public support for the ongoing and often thankless work of understanding the universe and its myriad components.

A cynic might think that that having a massive government agency like NASA floating around for a good number of decades and spending lavishly on flashy programs intended in part to assure its own popularity might have something to do with it. I'd be that cynic, but it seems to me that most of the comparatively less popular and less beloved fields of scientific research are also ridden by large government agencies in the US - big budgets and just as much need for popular support. So I do think that there's something interesting going on here in that small sliver of the media spectrum that scientists have colonized. Something we can learn from.

To be a media figure of this sort is a career path option that's certainly open to researchers who garner either sufficient fame or media experience across the years, but for best effect it requires you to remove yourself from the business of science. The scientific community tends to behave like an aggravated immune system when confronted with someone who is both a media figure and actively publishing scientific research. Throughout history a great many people have subverted the scientific method for personal gain, using influence, fame, money, and other forms of corruption - and the modern media is all that rolled up into one neat package. Taking your work to the press before taking it to your peers is thus a grand heresy in modern science, one which leads to harsh judgement and excommunication. Consider what happened to the reputations of Pons and Fleischmann, for example. From that, all things associated with the mass media come to be eyed with suspicion by the rank and file scientists: publicizing a field is very welcome, but even the slightest hint of use of position to influence matters of publication is going to stir up wrathful mutterings at the very least.

So the scientist turned media figure must feel strongly enough about his field to want to be an advocate and educator, but must also essentially give up his work in favor of talking about what he used to do. Not, I think, the easiest of paths for someone who truly enjoys the scientific life.

Regardless, the future of longevity science - or the foundations of rejuvenation biotechnology, or SENS-like research, or whatever you want to call it - must come to include scientist-educators in the media. A Carl Sagan for this presently minor field must eventually arise: to my mind that will be one of the signs of growth and progress, meaning that it will happen as a matter of course along with (a) the expansion of the community of researchers actively working on ways to repair the damage of aging, and (b) increasing public awareness. But sooner is always better than later.

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

The opening up of information, communication, and organization brought by the internet is changing business as normal in every field, making it far easier for ideas on the edge to gain support and activity. This is important for the development of rejuvenation biotechnology, as the changing nature of scientific work can speed the move to the mainstream, and allow for far more useful progress to be achieved while the flow of funding is still comparatively small: "our entire model of education and what it means to be a 'trained professional' is shifting. There's a hell of a lot of resistance from the status quo - which makes it difficult and inconvenient for rapid progress - but it isn't enough to stop it from happening. ... When the university system and the current PhD paradigm was invented, it was a different time. ... If you wanted to study advanced topics, or apprentice under someone famous to learn from their expertise, you needed to go to a university. But things are different now. Technology allows us access to some of the leading minds of our age [making] proximity to a university campus nearly irrelevant in order to meet other students and benefit from valuable peer-to-peer discussions. With the world's information available on the web, and with all of these advances in technology allowing for rapid data sharing and collaboration, how much value is there in the Ivory Tower? We are becoming a society of autodidacts, with information at our fingertips 24/7. Citizen Science is a natural consequence of that. Have an interesting scientific inquiry? Get on the web and investigate it. Learn from the millions of sources out there. Crowdsource some ideas, generate some hypotheses. Have discussions with others. Make a plan. Get your equipment. The scientific method is in-progress. Science is free for all to explore. Why waste time jumping through bureaucratic hoops when you can begin investigating what you want, when you want? Need to fund your research? Crowdsourced methods of funding, such as Kickstarter, are becoming more popular for these types of endeavors. Instead of 100 scientists chasing the same grant, why not go to the public and let them fund what they think is valuable? I think we'll be seeing a lot more of this in the future."

Link: http://ieet.org/index.php/IEET/more/4935

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

Another review of Sonia Arrison's 100+: "I have to congratulate Sonia Arrison on putting together a book that is both highly accessible to newbies with no prior background in transhumanist thinking or longevity research, and also richly interesting to those of us who have playing in these regions of conceptual space for a long time. The main concepts in the book are indeed things I've been familiar with for a long time: (a) There is a host of rapidly accelerating technologies with the apparent capability of dramatically extending human healthspan, (b) Most likely, human psychology and society will adapt to dramatically increased human healthspan as it occurs, so that it will be experienced primarily as a Good Thing rather than as something traumatic or troublesome However, the book is packed with a sufficient number of interesting informational tidbits, that I found it well worth reading in spite of my general familiarity with the biology, psychology and sociology of radical longevity. ... Arrison reviews the key technological streams leading us toward radically increased healthspan - including gene therapy, stem cell therapy, Aubrey de Grey's SENS concept, artificial organs, tissue regeneration, the potential application of advanced AI to longevity research, and so forth. Both current research and envisioned future advances are considered. Then, in what is probably the greatest strength of the book, she considers the potential psychological and social impact of progressively increasing healthspan: the effects, as the book's subtitle indicates, on personal life, family relationships, marriage, careers and the economy etc. Combining common sense with appropriate invocations of rigorous research and statistics, Arrison provides the most systematic refutations I've seen of the standard anti-longevity arguments - 'death gives life meaning', 'overpopulation will starve or bankrupt us all', and so forth. Step by step, and in an invariably good-natured and friendly way, she demolishes these arguments, making a solid case that increased healthspan is likely improve rather than degrade our emotional health and family lives and enhance our careers and economies."

Link: http://hplusmagazine.com/2011/10/26/sonia-arrisons-100-plus-book-review/

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