When will the future arrive? When does the nifty new science you read about in the popular press turn up in the clinic? When will the new medical technology be reliable and widespread in availability? I've found the best way to think about these sorts of things is to play a speculative game of counting development cycles.

It takes a certain amount of time to move from proof of concept to fundraising to development to commercialization of an actual product in fields dependent on scientific research. Much of this time has to do with human organization, communication and collaboration, rather than the actual work of progress. Even in the least regulated of such fields, a five year turn around is not unreasonable. Only after five years will the first widespread feedback, adaptation and planning begin for the next iteration of the broad, competitive development cycle.

It's important to realize that large differences in timing exist between what is theoretically possible, the expected dates on which a funded scientific community can deliver technology demonstrations, and availability of a commercial product. This is especially true when government regulation is involved in the process.

But on to the estimations. My view of the biotech and medical research field suggests that the development cycle for new products medians out at around a decade - a far cry from the rate of advance possible in less regulated industries, such as the development of computing devices. Calorie restriction mimetics look to come in under that median, while gene therapy is lagging far behind. Applications of autologous stem cell therapies look to fall somewhere in between. There are plenty of other examples if you care to go digging.

The conservative late adopter waits for the second business cycle for any product he can afford to wait for. The second round is always better than the first, more effective, cheaper and more widely available.

So to pick an example: I believe the estimates of the late 2010s for the first commercial organ generation via tissue engineering. That seems plausible, given progress to date; the first technology demonstrations are still a couple of years away, pending solution of the blood vessel problem. That suggests that the late 2020s would the time of routine, widely available organ replacement - a procedure analogous to preventative surgery today - at the completion of the second development cycle.

Another example: replacement of all damaged mitochondrial DNA through one or other of the vectors presently demonstrated. Should one of these research groups obtain sufficient funding, they will enter the ten year track - but it might take years more to arrive at that point. It can't hurt to assume that any promising, generally unfunded science is at least five years away from building critical mass. For that reason, I think the early 2020s are the earliest we are likely to see commercially developed mitochondrial DNA replacement technologies.

Following the two cycle rule again, that means the early 2030s will be age of routine mitochondrial DNA replacement starting in late middle age, an outpatient procedure that your physician will badger you into doing every couple of years. It'll be a pain to schedule, like the biopsies and exams, but skipping it will be like not checking for cancer - just dumb.

Posted by Reason at 9:11 PM
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As Chris Patil notes, things have moved fast in the field of sirtuin research:

The work represents the culmination of a huge amount of progress in a relatively short time: in less than 15 years, the sirtuin story has evolved from basic biology in the simplest model organisms, through exhaustive (though essential) testing in larger animals, into a source of potential therapies for a major human disease.

Furthermore, for the first time we have a clearly defined path toward the regulatory approval and widespread use of a compound that could be used as a frank anti-aging drug.

It's a good model for modern biotechnology research - an example of the speed with which mechanisms can be traced and understood, once a starting point is made. The process is ongoing, for many other proteins and genes related to beneficial metabolic response to calorie restriction. Sirtuins are just the start.

I would not, however, agree that it is a good model for the application of such research. One can applaud the success of researchers in obtaining funding and carving out a viable, competitive, well-funded field from the first studies of genes and calorie restriction. But the path to applied longevity science is not to call triumph at finally pushing something (anything!) past the impossible hoops blocking applied aging research - it should be to destroy the regulatory nonsense rules preventing progress.

Why, despite the great range of potential applicable biotechnology, do we not see hundreds of millions of dollars invested in startups attempting to address the aging process? The answer is buried in this New York Times article on Sirtris: "Dr. Westphal and Mr. Sinclair stress that they are not working to 'cure' aging, a condition that, so far at least, is common to all humanity and that most physicians do not consider a disease. 'Curing aging is not an endpoint the federal drug agency would recognize,' Dr. Westphal says dryly. Instead, both men say, they are working to ameliorate the diseases of aging." For so long as unelected government employees can declare, with no accountability and full force of law, what medicine is permitted and what is not, there will be no direct venture funded efforts to cure aging - or even to take the first steps by aiming to repair specific, identified age-related damage in order to intervene in the aging process. There is no lack of companies, research groups and billions of dollars ready to be directed to that end, as any brief survey of the biotechnology marketplace will show you - but the ignorant few who write policy continue to bury all that potential. The work that could have gone to advance the cause of healthy longevity is instead confined towards the backwaters of patching specific age-related conditions.

The press is running another round of articles on Sirtris Pharmaceuticals at the present time, focusing on the next line of drugs that improve greatly upon the basic model of resveratrol - at least in terms of their effectiveness in stimulating sirtuin activity.

The potent new pills mimic resveratrol in mice by activating the SIRT-1 gene, which appears to trigger a process called caloric restriction. In many organisms, that process acts to slow down aging and ramp up cellular defenses in the face of a reduced diet during times of scarce food supplies. Sirtris's new compounds, however, act without the little critters having to reduce their diet.

As most of you probably know, I'm not convinced that this is all any more than a sideshow. For one, it is in no way an attempt to directly repair the damage of aging, and for two, for so long as the present regulatory structure forbids the development and commercialization of real, working anti-aging medicine, there is no financial incentive to develop real, working anti-aging medicine. Even if you have a promising start, of any sort, every venture-funded, competitive effort to turn science into medical technology will go towards turning that start into a patch, an after-the-fact and comparatively ineffective treatment for some age-related condition, rather than a treatment for aging itself.

Here is a simple rule for life: you won't accomplish task A by working on task B. That task A is cut off by regulatory fiat is the real problem here.

Posted by Reason at 9:28 PM
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Researcher S. Jay Olshansky will be the guest at the next Sunday chat hosted by the Immortality Institute:

I am happy to announce SJ Olshansky will be joining Imminst for the Sunday Night Chat this Sunday December 2nd at 6:30pm CST U.S. If you are not familiar with Professor Olshanksy...you should be. He was researching methods to slow aging while most Imminst members were still in diapers. He has seen all the hype, the successes, and failures. His latest endeavor is the The Longevity Dividend, which proposes to set aside 3 billion (that's billion with a B) dollars a year of NIH funding for the study of aging.

Chat Room: http://www.imminst.org/chat

Sun December 2nd
- 4:30 Pacific
- 5:30 Mountain
- 6:30 Central
- 7:30 Eastern

You can look back in the archives here for much more on the Longevity Dividend:

• Pitching Healthy Life Extension as the "Longevity Dividend"
• Criticizing the Longevity Dividend
• The Longevity Dividend: A Call for Endorsements
• From the Longevity Dividend Symposium
• Update on the Longevity Dividend

As far as I can see, Olshansky is in the camp of "metabolic re-engineering and slow but solid progress in slowing aging is the way ahead, but it'd be wonderful if things that worked far better were demonstrated to be plausible." Which is hopefully a transitionary stage on the way to "I always thought that the Strategies for Engineered Negligible Senescence was a great idea." We'll see.

Posted by Reason at 9:05 PM
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One of the constants of our present age of change and progress is that biology is always more complex than first thought. It's a given. Evolution is under no constraint to produce designs that fall within the bounds of complexity we feel comfortable taking in at one sitting.

The scientific community will still master our biology - reverse-engineer it, replicate it, and ultimately greatly improve on it - but we shouldn't be surprised when hoped-for simplicities in biological mechanisms fail to materialize. That's all the more reason for greater support and funding for efficient, goal-driven medical research.

MIT: Stem-cell therapies for brain more complicated than thought:

MIT scientists report that adult stem cells produced in the brain are pre-programmed to make only certain kinds of connections - making it impossible for a neural stem cell originating in the brain to be transplanted to the spinal cord, for instance, to take over functions for damaged cells.

...

"A stem cell that produces neurons that could be useful to replace neurons in the cerebral cortex (the type of neurons lost in Alzheimer's disease) will be most likely useless to replace neurons lost in the spinal cord. [Moreover], because there are many different types of neurons in the cerebral cortex, it is likely that we will have to figure out how to program stem cells to become many different types of neurons, each of them with a different set of pre-specified connections."

"In the stem cell field, it is generally thought that the main limitation to achieve brain repair is simply for the new neurons to reach a given brain region and to ensure their survival. Once there, it has been assumed that stem cells will ‘know what to do’ and will become the type of neuron that is missing. It seems that is not the case at all. Our experiments indicate that things are much more complicated."

Posted by Reason at 7:22 PM
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The Immortality Institute volunteers are upgrading; always a painful process with a large forum and a content management system extensively customized over the years. If you haven't stopped by the Institute forum in a while, you should do so. Where else are likely to be able to participate in a discussion on the first recorded practitioner of calorie restriction - and noted author of the Renaissance - with researcher S. Jay Olshansky and other noteworthies?

A noble idea is a noble idea, and we shouldn't be surprised to find people from the past with constructive contributions to make on the topic of healthy longevity - taking into account the state of scientific knowledge in their time:

Sixteenth century Venetian Ambassador and Renaissance Christian Luigi Cornaro was celebrated in his time for his stance on dietary self-restraint, moderate living, and living to the age of 103. For these hundred of years his classic book has survived as a renowned text on longevity and an inspiring treatise on the path of temperance that the author believed could lead anyone out of a state of illness and into a healthy long life. The Art of Living Long contains Cornaros four discourses, respectively concerned with demonstrating his ideas through his own example, exploring the necessity of temperate habits, assuring a happy old age, and exhorting mankind to follow his rule. With introductions by Dr. Gerald Gruman and Joseph Addison, and additional essays by Lord Bacon and Sir William Temple.

To take a contrary point of view, however, is this really any different - important names of centuries past aside - from the standard mainstream media coverage of centenarians today? The form requires the journalist to ask for the centernarian's thoughts on longevity, but living for a long time doesn't make you an expert on how to live for a long time. Everyone has an opinion on how it is they've lived so long, but opinion isn't science.

When you're wandering through the vast libraries of writing on the topics of aging and longevity, remember that the scientific method is how progress is made. Opinions can be good, can be well-thought, can even be right as it later turns out, but opinions alone are not the foundation for a path forward.

Posted by Reason at 6:24 PM
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This caught my eye while I was meandering my way through PubMed; a nice turn of phrase in this way of looking at the mechanisms of aging and the future of aging in a world shaped by human action.

Senescence Viewed through the Lens of Comparative Biology:

Although mortality and longevity are inherently biological phenomena, their study has historically been the purview of demography and the actuarial sciences. An infusion of biological thinking into these disciplines transforms demography into biodemography and provides expectations and coherency to observations on age-determined mortality that would not be explainable otherwise.

Comparative biology teaches us that reproduction is life's solution to the inevitability of death in the hostile environments of Earth. That solution, however, places a higher priority on investing physiological resources into reproduction that could otherwise have been used to maintain the soma (body) longer. As such, aging is an inescapable but inadvertent byproduct of imperfect maintenance and its attendant surveillance and repair. Biology also reveals that while bodies are not designed to fail, neither are they designed for extended operation. In other words, bodies are subject to biological warranty periods for normal operation. For sexually reproducing species, that warranty period includes the time from conception to sexual maturity, the production and nurturing of offspring, and a period of grand-parenting in some species.

Humans are the only species capable of exploiting the loophole in the biological contract of life (bodies that are not designed to fail). Human ingenuity (science, medicine, public health) has produced interventions that manufacture survival time by delaying death, and in so doing, has created a phenomenon never before seen in the history of life - population aging (and all the societal and health consequences that go with it).

Aging and individual death might well be the inevitable consequence of evolutionary pressure on cellular life, but it's far more noteworthy that we have the capacity to do something about it. Intelligence and technology are a loophole big enough to created physical immortality - given enough resources and time. The big question is whether the first stages on the road to the repair of aging and greatly increased healthy life spans happen rapidly enough to benefit you and I, or whether cryosuspension will be our only opportunity.

The choice is ours; how much do we want healthy longevity and how much are we prepared to work towards that goal?

Posted by Reason at 7:40 PM
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Mice lacking the gene to create the protein adenylyl cyclase 5 (AC5) live longer. This was accidentally discovered during research into potential heart therapies, and published earlier this year:

The new discovery, that knocking out a single cardiac gene could lengthen lifespan, was an unexpected byproduct of heart research. ... mutant mice lacking [the gene for protein] AC5 were more resistant to heart failure caused by pressure within the heart. But in the process, the research team also realised that the mutant mice lived longer than their normal counterparts. [Now] they report that the treated mice lived 30% longer and did not develop the heart stress and bone deterioration that often accompanies ageing.

Like many longevity mutations of this magnitude, this is thought to invoke the beneficial mechanisms of calorie restriction in some way. Researchers are still working on clarifying the action of the AC5 mutation, as illustrated by the latest paper on the topic:

Adenylyl Cyclase 5: A New Clue in the Search for the "Fountain of Youth"?

It is proposed that these beneficial effects may be the result of the increased activity of second messenger signaling proteins such as mitogen-activated or extracellular signal-regulated protein kinase kinase (MAPKK, also known as MEK) and extracellular signal-regulated kinase (ERK), or of enzymes such as manganese superoxide dismutase (MnSOD) that promote cell survival through protection against oxidative stress and apoptosis. These intriguing findings should stimulate additional research aimed at dissecting the complex cellular mechanisms regulated by AC isoforms and may lead to novel genetic and pharmacological approaches to delay aging-related conditions and to extend life span.

A fair number of bases covered there. "We don't really know yet, but have some places to start looking" would have been fine. Metabolism is complex; there's no end to the resouces we can productively sink into understanding the space of potential beneficial alterations to mammalian metabolic processes. Those same resouces, I feel, would be better directed to understanding how to repair the metabolism we have. After all, if you can repair age-related metabolic damage once, you can come back in ten years time and do it again - and again and again, for so long as you care to continue. If developing that possibility is on the table for the same sort of cost as developing a one-time manipulation that slows the accumulation of damage by 30%, I know which route I'd choose.

This is exactly the choice facing us today, and for some strange reason the mainstream of medical science is headed down the inferior, more costly, less effective path of metabolic manipulation. Comparatively little attention is given to the more effective strategies of repair. Changing this reality is one very good reason to support the work of the Methuselah Foundation.

Posted by Reason at 8:15 PM
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You might recall research from last year suggesting age-related decline in the choroid plexus contributes to the buildup of amyloid characteristic to Alzheimer's disease.

the choroid plexus acts as a sort of 'fishnet' that captures the protein, called beta-amyloid, and prevents it from building up in the cerebrospinal fluid, which surrounds and bathes the brain and spinal cord. Moreover, tissue in the organ is able to soak up large amounts of the protein and may contain enzymes capable of digesting beta-amyloid.

I noticed a paper today that focuses on a quite different aspect of decline in the choroid plexus, but one that still leaves the brain the worse for it.

Aging reduces the neuroprotective capacity, VEGF secretion, and metabolic activity of rat choroid plexus epithelial cells:

Delivery of neurotrophic molecules to the brain has potential for preventing neuronal loss in neurodegenerative disorders. Choroid plexus (CP) epithelial cells secrete numerous neurotrophic factors, and encapsulated CP transplants are neuroprotective in models of stroke and Huntington's disease (HD).

...

In vitro, young CP epithelial cells secreted more VEGF and were metabolically more active than aged CP epithelial cells.

...

Implants of young CP were potently neuroprotective as rats receiving CP transplants were not significantly impaired when tested for motor function. In contrast, implants of CP from aged rats were only modestly effective and were much less potent than young CP transplants.

If (still a big if) Alzheimer's turns out to look a lot like Parkinson's at root, in that it stems from the failure of an important population of cells or narrow range of processes in the brain, the door is wide open for the next decade of regenerative therapies. There is so much we could do with the ability to grow fresh, healthy tissue to order - even in the brain.

Posted by Reason at 9:16 PM
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I feel compelled to come back to a comment by Richard Sprott, director of the Ellison Medical Foundation, quoted in a recent article on investment in longevity research:

"We're all going to croak," says Richard Sprott, the Ellison Medical Foundation's director, who expects that humans may eventually live as much as 30 years longer, but only in the distant future.

The archives at SAGE Crossroads boast a debate between Sprott and Aubrey de Grey, each exemplifying a polar opposite of approach to aging research and its goals. From where I stand, Sprott is firmly in the full employment act for gerontologists camp, while de Grey is all goal all the time.

There are more people who think like de Grey out there, but I don't think they're talking loudly enough. There are certainly far too many scientists who coast, with no inspiring goals to their work. What is the purpose of research if not to get the damn job done? What is work without purpose? In the case of aging research it's not about making life easy for career scientists, it's about stopping a worldwide, horrendous, terrible, ongoing avalanche of death and suffering.

Even the most widely recognized greatest disasters in human history pale in comparison to natural death. For example, the typhoon that struck Bangladesh in 1970 washed away a million lives. In 1232 AD, Genghis Khan burned the Persian city of Herat to the ground. It took his Mongol horde an entire week to slaughter the 1.6 million inhabitants. The Plague took 15 million per year, World War II, 9 million per year, for half a decade each. The worldwide influenza pandemic of 1918 exterminated less than 22 million people – not even half the annual casualties from natural death. But natural death took 52 million lives last year. We can only conclude that natural death is measurably the greatest catastrophe humankind has ever faced.

It's about building a world in which we can create more of the most valuable commodity there is - time spent alive, healthy and ready to act.

So back to the quoted view of Richard Sprott above. How on earth does one manage to reconcile the belief that it's going to take an age to extend healthy human life by a mere 30 years with even a passing understanding of the present state of science, human knowledge and capabilities? Has he failed to notice the scorching pace of progress in understanding and controlling cells? That biotechnology is now firmly harnessed to exponential progress in computational capacity - and all the benefits that brings? That the laws of physics firmly allow nanoscale machinery capable of replacing and surpassing in every respect all organs and functions of the human body? That the tissue engineers predict a decade or two until we can grow and replace any damaged tissue aside from the brain? That the system biologists think tacking ten years onto healthy life over the next ten years is feasible? That even the tired, slow-moving, government cancer establishment is shooting for victory in a decade?

I want to point out just how outlandish it is to stand in the midst of outright revolution, of wild, foaming progress in bioscience, and say that things aren't going to change all that much. You're out there on your own, Sprott, with few others beside Hayflick for company. The position you hold is extreme and strange to me.

Posted by Reason at 9:55 PM
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Sometimes there's just too much interesting research out there to link to one by one: inroads against age-related disease; uncovering new and important mechanisms of metabolism; progress in promising classes of future therapy. The list is endless. So sometimes, I throw together these roundups of diverse topics. Let's start with some promising gene therapy work for Parkinson's disease, and move on to Alzheimer's and cancer:

PET scans show gene therapy normalizes brain function in Parkinson's patients:

Brain scans used to track changes in a dozen patients who received an experimental gene therapy show that the treatment normalizes brain function - and the effects are still present a year later.

...

The patients only received the viral vector-carrying genes to the side of the brain that controls movement on the side of their body most affected by the disease. ... The gene makes an inhibitory chemical called GABA that turns down the activity in a key node of the Parkinson’s motor network. The investigators were not expecting to see changes in cognition, and the scans confirmed that this did not occur.

Position emission tomography (PET) scans were performed before the surgery and repeated six months later and then again one year after the surgery. The motor network on the untreated side of the body got worse, and the treated side got better. The level of improvements in the motor network correlated with increased clinical ratings of patient disability, added Dr. Feigin.

A novel way found to prevent protein plaques implicated in Alzheimer's:

Both studies used mice that were genetically engineered to produce human cystatin C as well as abundant amounts of amyloid beta plaques in their brains. The cystatin C bound to the soluble, non-pathological form of amyloid beta in these mice and inhibited the aggregation and deposition of amyloid beta plaques in the brain.

The research shows that cystatin C binds soluble amyloid beta also in the human brain, and suggests that this binding inhibits its aggregation into insoluble plaques in humans, says Dr. Levy. Cystatin C production and body fluid levels vary among healthy individuals and can be influenced by certain hormones, aging, and certain pathological conditions, she says. Furthermore, it was recently demonstrated that a genetic variation in the cystatin C gene in human populations is linked to a greater risk of developing Alzheimer’s disease during aging.

These findings suggest, says Dr .Levy, that even subtle modifications of cystatin C protein levels could affect amyloid beta accumulation and deposition in the brain, thereby modifying disease progression.

I seem to recall research indicating that the rate of turnover of amyloid is very fast, on the order of days. Alzheimer's is not a slow buildup of a compound that can just be removed, but rather a slow increase in the difference between generation and clearance rates. The best answer would be to determine where the fault lies and fix it; some work is aimed in that direction, but the majority aims to introduce new ways to clear amyloid without doing anything to repair the underlying issue. This is, alas, the dominant path in present day medical research.

But on to cancer:

Immune system can drive cancers into dormant state:

Like the older theory, cancer immunoediting suggests that conflict between cancers and the immune system naturally takes place but proposes that three very different outcomes can result. The immune system can eliminate cancer, destroying it; the immune system can establish equilibrium with cancer, checking its growth but not eradicating it; or the cancer can escape from the immune system, likely becoming more malignant in the process.

Until this latest study, evidence for the second outcome was lacking.

...

"We don't think the immune system has evolved to handle cancers," Schreiber notes. "Cancer is typically a disease of the elderly, who have moved beyond their reproductive years, so there probably was no evolutionary pressure for the immune system to find a way to fight cancer."

Schreiber, Smyth and Old speculate that from the immune system's point-of-view, a cancerous cell may look like a cell infected by an invading microorganism. To overcome the safeguards that prevent the immune system from attacking the body's own tissues, the tumor has to have a high level of immunogenicity, or ability to provoke an immune reaction. Cancer cells can reduce their immunogenicity by changing the materials they present to the immune system to more closely resemble those presented by normal tissue. This enables the third outcome of the immunoediting theory: escape.

Equilibrium sometimes may be a more common outcome of tumor-immune encounters than elimination. According to the researchers' theory, some of us may harbor dormant tumors that either developed spontaneously or from exposure to carcinogens. They propose that these quiescent tumors are unleashed only as we age or are exposed to environmental, infectious or physical stresses that cause a breakdown of the immune system.

Greater understanding of the tools already present in our body will be a real boost to fighting cancer, coming in the midst of a revolution in our capacity to alter and make use of those biochemical tools. Improving, retraining and redirecting the mechanisms of the immune system to attack specific cells is a very promising field of research. A good thing too, as we need effective, reliable cures for cancer if we're going to benefit from other strands of healthy life extension research.

Posted by Reason at 8:46 PM
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I, and no doubt you folk as well, noted the press on the first verified success for therapeutic cloning (also known as somatic cell nuclear transfer, or SCNT) in primates. The research group produced totipotent embryonic stem cells from a starting point of the skin cells of rhesus macaques.

Monkey embryo cloned in major breakthrough

Reproductive biologist Shoukhrat Mitalipov, of the Oregon Health & Science University, and his colleagues reported in the online version of the journal Nature that they have cloned rhesus macaque embryos using DNA from skin cells taken from the ear of a 9-year-old male. The resulting stem cells grew into viable heart and nerve cells, among others.

"This is a giant step toward showing that human therapeutic cloning is possible," said Dr. Robert Lanza, who is trying to produce human embryonic stem cells at Advanced Cell Technology in Worcester, Mass., and was not involved in the research. "It proves once and for all that primate cloning is not impossible ... as many people had thought."

Work has begun to use the new technique to clone human embryos, although the process remains very inefficient. Even so, Mitalipov said, "I am quite sure that it will work in humans."

What is the signficance of this? Well, one has to look at what a source of your own totipotent stem cells can be used for:

Over the past 25 years, mouse embryonic stem cells have been used to create models for scores of human diseases, including cancer, heart disease, obesity, and Alzheimer's. Research discoveries based on these models has led to new drug development and therefore touched countless lives. ... I believe it is only a matter of time before human embryonic stem cells are used in drug development research and become the basis for important new cell therapies.

Producing tissue in specific states to analyze and learn from is just the start. Totipotent cells on tap form an important resource for complex tissue engineering: totipotent stem cells generated from your own cells will be used to produce replacement parts for age-damaged organs and systems in your body in the next few decades.

The bottom line is that increasing control over our cells is a broad highway to increasing control over our healthy life spans. All progress is very welcome.

Posted by Reason at 10:28 PM
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For some people, nothing should exist outside a state of complete regulation, every choice you could potentially make hemmed in by rules made and enforced by faceless others. It is somewhat strange that people are comforted by regulatory control: even when they obviously have no say in the results of that control, even when the consequences of that control are obviously terrible; even when such control is obviously more along the lines of suppression and destruction. That latter results when habitual and empowered controllers, unable to conceive of any other response to the new, are faced with something they do not understand.

Or perhaps this is all not so strange; many people would - and do - choose suffering over change, the familiar over the new, no matter how terrible the familiar might be at the moment. Human nature is, at heart, terribly flawed in many ways.

Community attitudes to the regulation of life extension:

Technologies purported to extend human life are already being marketed widely, and are being used by community members, despite a lack of evidence on their efficacy or safety: in fact, the use of some putative anti-aging technologies (e.g., human growth hormone) is illegal. Existing regulation is proving to be ineffective, especially in the face of Internet sales.

Further advances in the field of life extension are a distinct possibility, exacerbating the need for a policy response. This paper presents the preliminary results of a study of community attitudes to life extension, with a focus on attitudes to the control and availability of strong life-extending technologies.

Can't be having those advances, now, can we? I'm always deeply suspicious of people waving terms like "society" and "community." Invariably, those in fact mean something along the lines of "we who would like to think of ourselves as elites, but who prefer not to say so quite so openly."

It's rather sad that we live in an era of the downward spiral, right at the time at which there is so much progress in technology and human capabilities to be seized. Ever greater control and abrogation of personal responsibility leads to an irresponsible, demanding, passive-aggressive population, which leads to ever greater centralized control and destruction of freedom. We're overdue a revolution, a sea change in attitudes, or an unpleasant dip once more into comparative poverty of choice, vision and opportunity.

Posted by Reason at 10:10 PM
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