exratione

Imposing large scale engineering projects of this nature will probably have to wait until after production and point control of self-replicating nanorobots, organic or otherwise, is fairly mature. At that point the cost reduces down to design and raw materials and looks feasible when compared to simply going to other worlds in search of additional space, or building arcologies, or other methods.

Sadly much vision has been lost somewhere in the last century. People are much more conservative about preserving the present state of whatever exists, and have lost the sense of wonder and ambition that characterized the opening of the modern age of machinery.

So back when I was running numerical simulations of pop III stellar evolution (which is rather a long time ago now), the interesting thing is that, in comparison to pop II and I, the extreme metal paucity means that you can have (a) stable and extremely long-lived very dim, very small stars, verging on being warmed up gas giants, and (b) very large and extremely short-lived stars, which will supernova or otherwise give way to instability on the order of a few million years after core ignition.

You can then work back to speculative mass functions (distribution of mass in the population) by asking (a) how many large, short-lived stars you need to generate the observed metallicity of pop II, and (b) how many extremely small dim objects you'd need to fill out the missing mass without having so many that someone would have seen them by now. The latter is an interesting line of thinking; what is the upper density bound on (for example) 0.1M objects to make both the solar system's continued existence and an inability to see these things plausible.

You can also look at the paucity of candidates for ~1M extremely low metallicity stars (there are just a couple out there known that could be pop III candidates) as another constraint on the pop III mass function. Any pop III ~1M stars would have a lifetime longer than that of the universe to date, or at least such was the case in my models.

Research on missing mass and pop III has moved on considerably from those days of course.

You are overly dismissive of de Grey's approach, and if you're going to Wikipedia for the details of SENS then you are in the wrong place. It is documented in far more detail elsewhere.

The standard response to your viewpoint is to point to the SENS Research Foundation advisory board, which includes George Church, Anthony Atala, Judith Campisi, Maria Blasco, and so on and so forth for a list of luminaries in subfields of medical research relevant to aging:

http://www.sens.org/about/leadership/research-advisory-board

It is also worth looking at the ongoing research collaborations, which involve noted labs at institutions such as Wake Forest, the Buck Institute, Albert Einstein College of Medicine, Cambridge University, and so on and so forth.

http://www.sens.org/research/extramural

I'm not sure why you think this research work is not panning out when it has barely even started. This is early stage work, creating the building blocks and foundations. The most advanced of the necessary lines of research is ablation of senescent cells, which has been shown to work in accelerated aging mice and is current in studies in normal mice. That is a few years away from technical possibility in humans, further once you add in the regulatory issues, and everything else is further into the future.

Newsflash for you: in the fields I know (medical research), nearly every important early stage research project is funded by philanthropy. Government research dollars are only available to groups that have already done that early stage research and proven that the next step is incremental and low-risk.

If medical research relied on government dollars, nothing much would happen except for wheel spinning at vast cost. It would be even more of a full employment program for connected research institutes than is already the case.

That is not even to start on the fact that the existence of big government funding comes with the existence of the FDA, an entity that enormously increases the cost of research and development, outright blocks many lines of work, makes others so unprofitable as to scare away for-profit funding at all levels, and so on.

The same old blind spot in place with respect to aging I see. The cause of two thirds of all deaths worldwide, more than 90% of all deaths in the first world, and the largest share of suffering and medical expensive, all of which falls most heavily on the poor of course.

But actually do something about it in this age of biotechnology and rapid progress in medicine? No, never.

The organizers point to age-related dementia as one of the potential items, but strangely not to attempt or incentivize any work to fix the problem at all through medical research. They treat dementia as a result of aging as a given, something set in stone, a thing to be made marginally better with palliative treatments and accommodations, not fought with medical science in search of cures.

Craziness.

The world drowns and dies in this blind spot related to aging and age-related conditions.

There's the SENS approach, which is radical and based on present knowledge will absolutely prevent all cancer by striking at the one mechanism that all cancer needs. That comes with a hefty side-order of required advances in stem cell medicine in order to keep things going without said mechanism, however:

http://sens.org/research/introduction-to-sens-research/nucle...

The SENS Research Foundation is entirely supported by charitable donations.

If you want something a little less radical then helping any group working on targeted cell killing technologies is more useful than what you were probably going to do with that money otherwise - though of course finding a place to donate that will funnel your funds to this particular research is a challenge. The typical cancer charity is about five levels removed from picking research projects, but one can hope that this will change with the spread of crowdfunding techniques into the sciences. Immune therapies are the front runner technology there, but many other approaches exist (nanoparticles, viruses, bacteria, etc). Some of these approaches seem likely to effectively treat many different types of cancer, such as work on CD47:

http://news.sciencemag.org/health/2012/03/one-drug-shrink-al...

One also has to look at the surrounding studies for context and plausibility, not just this one in isolation. For example, I think you are overcautious in your comments on nutrition data in humans for calorie restriction and fasting - there is in fact quite a large amount of support for both benefits and safety in humans, both in the context of augmenting chemotherapy and as a general health practice. There is further an enormous weight of evidence in various mammal species for the benefits of calorie restriction and fasting.

In the case of this particular item, referring specifically to alterations to the white blood cell counts and lineages, the human data only goes so far as chemotherapy patients, and not very many of them. Talking about age-altered immune systems is premature. It would not be a surprising result if validated by other researchers, as calorie restriction and fasting are already known to beneficially influence immune function over the long term, but the details here should be taken as merely interesting until someone else runs larger studies to obtain more data.

The paper, which is open access and worth reading (skip to the discussion at the end if a layperson).

http://dx.doi.org/10.1016/j.stem.2014.04.014

The more interesting part of this to my eyes was the material difference between 24 hour and 72 hour fasting in human chemotherapy patients, in that the former didn't do anything to the measure of immune cell populations and the latter did. Intermittent fasting is nowhere near as well studied as calorie restriction at this point in time, so it is interesting to see these mechanisms emerge.

Now this is chemotherapy immune suppression, not aging immune dysregulation. I'll be mildly surprised to see the exact same result in people with age-damaged immune systems, as the character of the damage is very different. The animal results for aging rather than chemotherapy here are intriguing but that's all. There's still a lot of work to be done to arrive at the level of comfort with this effect that exists for other aspects of calorie restriction or intermittent fasting.

But given that (a) obtaining human data on fasting and immune cell population in old people is a comparatively low cost study to put together, and (b) the group involved here seems to have a good flow of funding to study intermittent fasting in a broader context, I'd expect to see that data emerge at some point in the next few years.

This quote is the part you should take away with you, I think. It's great advice. The rest of the article consists of largely the standard anecdotes on how long it takes the scientific community to really do a decent job of evaluating complex proposals in complex systems, and how that timing interacts poorly with the entirely admirable urge to get something done by deploying applications of scientific findings that might do some good in the world:

"So how should we respond the next time we’re asked to believe that an association implies a cause and effect, that some medication or some facet of our diet or lifestyle is either killing us or making us healthier? We can fall back on several guiding principles, these skeptical epidemiologists say. One is to assume that the first report of an association is incorrect or meaningless, no matter how big that association might be. After all, it’s the first claim in any scientific endeavor that is most likely to be wrong. Only after that report is made public will the authors have the opportunity to be informed by their peers of all the many ways that they might have simply misinterpreted what they saw. The regrettable reality, of course, is that it’s this first report that is most newsworthy. So be skeptical.

"If the association appears consistently in study after study, population after population, but is small — in the range of tens of percent — then doubt it. For the individual, such small associations, even if real, will have only minor effects or no effect on overall health or risk of disease. They can have enormous public-health implications, but they’re also small enough to be treated with suspicion until a clinical trial demonstrates their validity."

------------------

From something I wrote a while back:

"The scientific method is the greatest of inventions: when used to organize and analyze the flawed output of we flawed humans, it leads to truth and discovery. It is how we sift the gems of progress from the rubble of short-sighted human nature, magical thinking, willful ignorance, and other self-sabotaging but entirely natural behaviors.

"The scientific community doesn't produce an output of nice, neat tablets of truth, pronouncements come down from the mountain, however. It produces theories that are then backed by varying weights of evidence: a theory with a lot of support stands until deposed by new results. But it's not that neat in practice either. The array of theories presently in the making is a vastly complex and shifting edifice of debate, contradictory research results, and opinion. You might compare the output of the scientific community in this sense with the output of a financial market: a staggeringly varied torrent of data that is confusing and overwhelming to the layperson, but which - when considered in aggregate - more clearly shows the way to someone who has learned to read the ticker tape.

"So how do you read the output of the research community for a particular topic of interest? Firstly you have to recognize that the output of any single researcher is meaningless when considered in isolation. At least a good half of the results produced by scientists are in some way flawed. That is par for the course when working at the cutting edge of new knowledge, and no slur upon the hard work of those involved - they know the odds. The high failure rate of risky ventures like scientific research is why we need the scientific method to weed out those failed results as time progresses and new results emerge. So when you read up on a topic of current research, you need to read around the subject: dig in to various sources, find the work of multiple scientific groups, and assess the support for different theories and interpretations."

------------------

In terms of evidence for greater health nothing comes close to the twin mountains of data in support of calorie restriction and regular moderate exercise. If you are doing other things in the hopes of health without covering those two line items, then you really have to accept that you're not taking the best, most proven path.

Well, actually that's a complete lie. There is one thing that exceeds both of those items, and that is progress in medical science towards better treatments. The faster that goes the better off you are - so you should also put in time and energy to helping that happen. As you get older the calorie restriction and exercise fade as determinants of health in comparison to the present state of medical technology, and thus it becomes ever more important that you helped back in the day, giving your contribution a chance to snowball in effect.

There is a good book whose title and author are eluding me for the moment that examines the necessity of a frontier for freedom. Freedom requires the ability to up and move into an area that is a challenge for the nearest power to control, regulate, and abuse. That is the only meaningful check on the power of the sedentary bandits that become a region's elite.

Historically, this has all been geography. But going forward, there is the opportunity to do something new with technology and section off slices of economic activity into reaches that while existing in the same geographic location as a centralized state are prohibitively expensive to control for its bureaucrats and enforcers.

The malaise of the modern world is, I think, in large part due to the shrinking of frontiers. There is little of the world left that is easily colonized but also hard for the major players to reach into, and so the states become ever more grasping. There is no safety valve by which people can up and peacefully revolt with their feet in large numbers, and that won't return until the cost of getting into orbit falls dramatically.

Meanwhile, there is cryptography.

No:

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjourna...

"Understanding why we age is a long-lived open problem in evolutionary biology. Aging is prejudicial to the individual, and evolutionary forces should prevent it, but many species show signs of senescence as individuals age. Here, I will propose a model for aging based on assumptions that are compatible with evolutionary theory: i) competition is between individuals; ii) there is some degree of locality, so quite often competition will be between parents and their progeny; iii) optimal conditions are not stationary, and mutation helps each species to keep competitive. When conditions change, a senescent species can drive immortal competitors to extinction. This counter-intuitive result arises from the pruning caused by the death of elder individuals. When there is change and mutation, each generation is slightly better adapted to the new conditions, but some older individuals survive by chance. Senescence can eliminate those from the genetic pool. Even though individual selection forces can sometimes win over group selection ones, it is not exactly the individual that is selected but its lineage. While senescence damages the individuals and has an evolutionary cost, it has a benefit of its own. It allows each lineage to adapt faster to changing conditions. We age because the world changes."

Everyone wants to be told that it isn't their fault that bad things have happened. Its a pernicious, harmful urge most often on display in courtrooms and discussions on weight and diet. Unfortunately reality is what it is: if you eat without consideration and control in this modern world of low-cost calories, then you will get fat. Accepting and acknowledging that you are 100% accountable as to what and how much you eat is a necessary first step to avoiding that end state.

This was written by people who are much closer to your viewpoints on economic freedom than mine. They are very mild and conservative in their estimations of cost in lives. I suggest you read it:

http://fdareview.org/harm.shtml

The delay and large reduction in the total number of new drugs has had terrible consequences. It is difficult to estimate how many lives the post-1962 FDA controls have cost, but the number is likely to be substantial; Gieringer (1985) estimates the loss of life from delay alone to be in the hundreds of thousands (not to mention millions of patients who endured unnecessary morbidity). When we look back to the pre-1962 period, do we find anything like this tragedy? The historical record—decades of a relatively free market up to 1962—shows that voluntary institutions, the tort system, and the pre-1962 FDA succeeded in keeping unsafe drugs to a low level. The Elixir Sulfanilamide tragedy, in which 107 people died, was the worst of those decades. Every life lost is important, but the grisly comparison is necessary. The number of victims of Elixir Sulfanilamide tragedy and of all other drug tragedies prior to 1962 is very small compared to the death toll of the post-1962 FDA.

The FDA has probably caused more deaths in the past half century than all of the rest of the American state put together, wars and all, by slowing progress in medicine, making all sorts of avenues for research and development unprofitable, and making medicine that does exist far more expensive.

Regulators at the FDA are capricious and malign, and there are countless stories of petty revenge via increased demands for data and enormous imposed costs in time and money. This is the way things always go in the late stages of centralized, powerful bureaucracy with a side order of regulatory capture.

The only good thing I can find to say about the bureaucrats at the FDA is that they respond to regional regulatory arbitrage - to medical tourism - by loosening their grip and letting things through. Or at least they do when said treatments are so widely available elsewhere in the world that the risk of looking bad by continuing to block them in the US is worse than the risk of looking bad because one of the outcomes of a normal, low error rate in medicine gets picked up by the press. Look at simple stem cell transplants, now available in the US these last couple of years, for a good example of this in practice.

A terrible byline: "Human fat cells can be used to regenerate damaged hearts and ageing joints. So should we start piling on the pounds?"

Piling on the fat is about as effective as smoking if you want a reliably slow way to shorten your lifespan by a decade or more [1] while at the same time considerably increasing your lifetime medical expenditures [2].

That visceral fat around your organs works a number on your biochemistry, increasing chronic inflammation [3] with all its detrimental consequences. That is bad enough but other unfortunate and more poorly understood changes take place in metabolism when you eat a very high calorie diet consistently, of the sort needed to sustain a lot of fat tissue, pushing nutrient sensing mechanisms into overload. [4]

There is magical thinking everywhere when laypeople talk about medical technologies. But this fat-related example is particularly egregious.

[1]: http://www.eurekalert.org/pub_releases/2010-07/iaft-sfl07121...

[2]: http://www.eurekalert.org/pub_releases/2013-12/dumc-hcc12161...

[3]: http://www.houstonmethodist.org/body.cfm?id=495&action=detai...

[4]: http://dx.doi.org/10.1007/s10863-009-9229-3

Menopause is an oddity and a puzzle. It isn't easily used to support any of the various points of view in aging research, partially because it is a human peculiarity that doesn't seem to be present in anything like a similar form in other primates or mammals. Theorizing has it linked with the grandmother hypothesis viewpoint on why humans are so much longer lived than other primates, and the evolutionary track by which we got here. You might look at these papers:

http://www.impactaging.com/papers/v6/n2/full/100640.html

http://www.pnas.org/content/110/33/13440

Current thinking I've been privy to is that the factors in question are short-lived.

In any case, this will never turn into cross-generation blood transplants on a regular basis. The present system of medical regulation is heavily biased towards demonstrating mechanisms. If you can't explain your mechanism you are not getting approved by the FDA, or at least not until such time as everyone else in the world is already doing it and the bureaucrats are made to look bad - see the last decade of stem cell transplants for the way in which that happens.

So the attempts at therapies that result from this will likely be delivery of proteins or interference with proteins to put a thumb on the scales of metabolic machinery. At which point it lasts for the period of time in which you are getting regular injections.

The parent shouldn't be downvoted, as it is exactly true. Hypocritical even in its two sentences, but true. It is fashionable to look away, and necessary for our own health and progress in medicine to do these things, but that doesn't make it anything other than what it is.

However, what happens within the scientific community is a drop in the ocean of what happens on farms and in the wild.

If you feel strongly about animal suffering, then the following are logical things to advocate and aid:

1) Veganism, now that we are at a point in our mastery of agriculture at which this is a viable choice if everyone made it.

2) Tissue engineered meat and other animal products, made without any form of suffering.

3) Simulational approaches to animal research. Ultimately animals will be sacrificed only for calibration, at rates far lower than is presently the case.

4) The removal of all natural wildlife, to be replaced by managed systems in which there is no death or violence, only the simulation of it.

Obviously these, especially (4), are long term projects. They are not impossible, but will require progressively greater levels of technology in the order in which they are presented. If you think they are valuable, you should help these causes.

The Hedonistic Imperative is an interesting set of ideas to look into with regards to (4). [1]

[1]: http://hedweb.org/

You have to be very careful when you say "reverses aging." That is a very different thing from "reverses a couple of measurable aspects associated with aging." In the former case you are making an assertion that will immediately lead you to having to define the cause and mechanisms of aging and defend your point that it is, as a process, reversed - and the definition of aging is a contentious topic at the present time. But the press is lazy and in search of clicks, etc, etc.

The mainstream of the aging research community theorizes on the basis of mountainous evidence that aging is accumulated damage. What that damage consists of is pretty much settled, but there is a lot of argumentation over how it all hooks together, what is important, what is primary versus secondary, and how in detail it connects to visible pathologies of aging.

Outside that mainstream, the present day accepted heresy, in the sense that the minority population of heretics are engaged with rather than cast out of the cathedral, is that aging is an evolved genetic program. It is a selected adaptation and where there is damage that damage is a consequence of epigenetic changes, not the cause of them. There are factions within this heresy too, and a lot of argumentation. If you want to learn more, look for the hyperfunction theory of aging and related thoughts as representative of the field. [1]

The damage view of epigenetic and signaling changes in tissues that occur with aging is that these changes are reactions to damage. Altering them may lead to short term benefits and be worthy of use as treatments but that doesn't do anything about the underlying damage - which will grow and kill you. In the case of stem cell decline with aging, this process is thought to be a cancer suppression mechanism, and thus forcing all the dormant stem cells back to work is going to mean cancer everywhere. Equally it may turn out that evolution has produced an overcompensation and some of the benefits of doing this might be effectively free. The fastest way to find out is to conduct animal studies in something other than mice (which are little cancer factories and have telomere dynamics that are very dissimilar to that of humans).

In contrast the programmed aging view is that reversing signaling and epigenetic changes is exactly reversal of aging, and is thus a great thing to be doing and we should be making full steam ahead on this front. I think they are wrong, and that the balance of evidence clearly points in the other direction, but as I said this is a heresy with enough advocates that they are not just ignored.

(Bizarrely, most of that portion of the mainstream who work towards enhancing longevity and slowing aging actually spend their time on potential treatments that make much more sense as goals for programmed aging enthusiasts. Look at sirtuin or calorie restriction mimetic work - all about altering protein levels and signals. All too few researchers take the sensible approach of looking for means of damage repair. But that's a whole different topic. I blame regulation of medicine as a force steering research into marginal channels).

Anyway, on to the heterochronic parabiosis, which is what you call the linking of circulatory systems in two individuals, one old, one young. This has been used for some years as a way of studying what might be going on in old tissues, especially in connection with the decline in stem cell tissue maintenance activity that leads to organ dysfunction and death. The end goal is to figure out the differences and use that knowledge to produce the part of the complete map of the molecular biology of the progression of aging that covers tissue signaling - most researchers in the field have no declared interest in doing anything other than looking at what is going on.

Along the way, however, someone will produce prospective treatments based on identifying signals to stem cells involved in the choice between activity and quiescence. No-one is going to be shifting blood around as a basis for treatments between young and old when you can instead figure out what exactly it is in the blood that is causing changes - this is a change likely to occur in the stem cell transplant field also, in which much of the benefits seem to depend on the alteration of signals caused by the transplanted cells rather than any cell maintenance they are doing directly. Why sling cells around if you can just manufacture proteins that have the same beneficial effects?

One of the signals is apparently GDF11, which has been explored for a couple of years now. [2] It is interesting to see that it is more general than simply localized to heart tissue. Given the large number of quite different stem cell populations in the body it would be unexpected to find much in the way of commonality between the signaling systems that they use. Apparently there is some commonality after all. Though I wouldn't hold out for much more. In general I'm expecting the exploration of cell signaling to be every bit as complicated as the hunt-and-peck approach taken to finding ways to interfere with cancer: a lot of proteins, different in most tissues.

[1]: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3455862/

[2]: http://dx.doi.org/10.1016/j.cell.2013.04.015

There is a lot of experimentation going on now that cells can be manipulated readily and cheaply. It's still the very early days, but much can be done.

The sort of work described in the article overlaps with that of efforts to enhance cells with additional machinery, such as additional organelles [1] or programmable surface chemistry [2], and the equally interesting approach of creating entirely artificial cell-like entities, designed machinery [3] wrapped in a membrane. [4]

We will have microrobotics in our medicine before nanorobotics, I think, and those microrobots will look a lot like cells. There will eventually be a blurring at the boundary between engineered cells - such as those used in trials of some immune therapies and stem cell treatments - and things that are not natural cells but look very much like them.

The discovery and development of the moving parts is very similar to that of raw nanomedicine and rudimentary medical nanorobotics, but riding on the back of all the existing cellular machinery enables more to be done sooner and with less.

[1]: http://www.unibas.ch/index.cfm?uuid=E11708E2A1B6CA17E9F30BEA...

[2]: http://www.mccormick.northwestern.edu/news/articles/2014/04/...

[3]: http://www.sciencedaily.com/releases/2011/06/110620161300.ht...

[4]: http://www.sciencedaily.com/releases/2013/04/130404142457.ht...

This seems like the same sort of pointless hand-wringing that attends every technology at its peak. There are any number of works in progress that could replace antibiotics. None of them have yet because they are not economically competitive. As that changes - because they either realize their potential to be much, much more effective, or because the cost of working antibiotics rises - then antibiotics will fade in favor of the next technology in line.

This is what happens to every technology. Yet people seem to forget, despite the evidence all around them, that they live in a world that changes rapidly due to the fact that many, many individuals are working on new and better ways to do everything. Periods of seeming stasis to the outside observer - such as the long use of antibiotics, which is really actually a continual hectic development of new types of the single class of item - only occur because economic conditions favor them. As soon as economic conditions favor another technology, it is developed and deployed from its prototypes pretty rapidly.

Donate to research groups that are working on ways of controlling bacterial and viral infections that are a step beyond the present status quo. Things like DRACO [1] spring to mind. Present day fundamental (as opposed to translational) biomedical research is very cheap in comparison to the state of things even a decade or two ago. Small fundraising groups can make a big impact now.

[1]: https://en.wikipedia.org/wiki/DRACO_(antiviral)

My thinking on this is that by the time your banked cells might in theory be useful, the research community will have figured out how to make any old cell do everything that they want it to.

You might look at progress in induced pluripotency and very small embryonic like stem cells to see how rapidly things are moving there for the creation of useful cells.

Also worth noting: the preliminary signs are so far weighing on the side of concluding that cells from old people are not significantly less useful than cells from a young person for the purposes of therapy. The bigger differences are inside the body, in the cellular environment.

And again, all the incentives in the very well funded stem cell research community lie in the direction of fixing or working around everything that will prevent them from applying treatments to old people. The overwhelming majority of people (i.e. potential customers) with conditions that would benefit from stem cell treatments are old people, and thus large sections of the research community are working on understanding and manipulating the activities of stem cells in old tissues to try to (a) figure out exactly why they are not working as well as they used to, and (b) restore them to action.

There are some interesting experiments in heterochronic parabiosis that are worth looking into, but also many other lines of work in which researchers are identifying specific signal proteins that direct stem cells into ever greater quiescence. This is most likely an evolved program to lower the risk of death by cancer, reacting to rising levels of cellular damage, at the cost of greater dysfunction and eventual death by tissue failure.

There is something about the prospect of treating aging that makes people take leave of all economic common sense.

Move your argument to 1940 and make it about the prospect for future treatments for heart disease to see how ridiculous it is to suggest that only the wealthy would have access to these medical technologies.

One of the interesting things about our age is that medicine is largely flat. Rich people can buy more time from more expensive physicians, and pay people to do their legwork and phone calls for them, and lie in pain in better-looking ward rooms, but there are very, very few forms of medical technology available to them that is unavailable to someone with a few tens of thousands of dollars and the time to make the phone calls and do the legwork.

Given that the treatments for human rejuvenation will be infusions (made up in a lab-factory in bulk, or a specialist clinical plant to order, and requiring very little attention from trained staff to administer) rather than surgeries (requiring a great deal of time from specialist staff to carry out), I think that the odds of their remaining expensive for long are minimal. Economies of scale emerge rapidly for such things.

(Infusions because these treatments will be things like delivery of engineered bacterial enzymes, gene therapies for mitochondrial DNA, drugs to break down cross-linked proteins, stem cell transplants, and so forth).

Look at stem cell transplants as the model of how the price of such therapies rapidly moves downward due to inter-regional competitive pressure for treatments of this nature.

For my money the nuclear DNA damage angle is actually the more interesting part of this. The research community has for some years been debating whether or not stochastic nuclear DNA damage is important in aging outside of the issue of cancer. The consensus educated assumption has long been to think of course, nuclear DNA damage should lead to loss of protein homeostasis, and is therefore a meaningful contributing cause of aging, not just of raised risk of cancer. However there is nowadays plenty of evidence to support the opposite view, that the levels of stochastic nuclear mutations seen in human tissues really don't matter over the present human life span. Other than cancer.

This would be good if it continues to hold up. The less we have to fix in order to produce a first generation of treatments that effectively treat aging - i.e. produce rejuvenation - the better. Fixing nuclear DNA damage is going to be plausible via global DNA editing technologies like CRISPR, but we're a long way from doing it for all genes to restore to a template and erase damage. Cancer therapies on the other hand are going to improve enormously in the near future as forms of narrowly targeted cell destruction take over from the present standards of chemotherapy and radiotherapy, coupled with greatly improved early detection. If you're 20-40 years away from peak cancer age in a wealthy region of the world, then I don't think your odds of dying from cancer are very large at all.

The SENS Research Foundation has a network of supporters among portions of the VC crowd in the Bay Area. Some of the halo of attached or associated young researchers there should explore putting one of their lines of research more likely to get somewhere interesting soon into YC, see what happens.

A completely baked form of allotopic expression or toolkits for glucosepane breakdown in tissues could both produce viable and highly useful technology platforms prior to being far enough along to be applied to the reversal of aspects of aging. Neither of those seems too far away to be non-viable for this sort of timescale, and meaningful biotech projects are very cheap these days if you have access to a provisioned lab.

I expect the informatics stone age in aging research will start to dissipate more rapidly in the years ahead, given that Calico and Human Longevity look to be focused in that direction.

I would love to see more of the people who dismiss SENS criticize it on the published details of ongoing or proposed research rather than just hand-waving. Sadly all too few seem to be willing to do so. Clearly it isn't nonsense, since there are SENS labs and allied research programs in a number of universities now, including Cambridge, Wake Forest, etc, and a range of important figures in aging research and other life science fields relevant to regenerative medicine support SENS.

The life expectancy gain of 2.5 years every decade is for life expectancy at birth.

Remaining life expectancy in old age is growing by about 1 year per decade.

An interesting, albeit a little too populist take on the options for the future of medicine and longevity:

http://inthetank.newamerica.net/blog/2013/09/drooling-your-s...

As I mentioned elsewhere, the current trends are all due to entirely incidental effects on the processes underlying aging. We should expect to see a great discontinuous leap upwards in life expectancy in the next few decades if the present disruption in the field of aging research takes hold and wins control of the mainstream, such that there is a sea change in the community to focus on actually treating aging itself rather than focusing on patching over its late-stage consequences. This hasn't been done yet to any meaningful degree, and so we should expect interesting results once it is a going concern.

Not really. Actuarial escape velocity is a concept that emerges from the SENS proposals [0]. Next to nothing you do with your life has truly significant expected impact on your future longevity other than providing support and funding for SENS and SENS-like research aimed at repairing the root causes of all the big killer age-related conditions.

(Less significant here means a ten year swing in life expectancy. Exercise, not smoking, calorie restriction - these are things that can make 5-10 year expected differences. Everything else is pretty marginal if you exclude the obvious exogenous line items like risk of accident. But an improving implementation of SENS provides indefinite extension of healthy life out to the expected limits due to accident rates, which is somewhere in the 1000-5000 year range for present data).

The mainstream medical research community is largely focused on patching late stage manifestations of aging. Most work and funding goes towards either manipulating proximate causes rather than root causes, or trying to find ways to alter the operation of metabolism to make the disease process less terrible - but again without addressing causes. Until such time as the research community is overtaken by the "address root causes" disruption currently taking place, of which SENS is an exemplar, but by no means the only movement, then progress towards extended life and defeat of age-related disease will continue to be painfully expensive, slow, and marginal.

The trends in life extension achieved through medicine to date are all largely incidental, unintentional. Where aging itself as a collection of processes [1] has been slowed it wasn't because that was the deliberate intent. Again, because until very recently no-one has been trying to address aging itself rather than focusing on the nature of its outcomes. It is the same difference as that between working to reverse or prevent rust in metal structures versus working on repairing structural failures that occur due to that rust.

[0]: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC423155/

[1]: http://sens.org/research/introduction-to-sens-research

Allow me to put forward a historical analogy: standing in 2014 and arguing a case for gentle future changes in [pick your field here] over the next few decades, based on the past few decades, is something like standing in 1885 or so and arguing that speed and convenience of passenger travel will steadily and gently increase in the decades ahead. The gentleman prognosticator of the mid-1880s could look back at steady progress in the operating speed of railways and similar improvement in steamships throughout the 19th century. He would be aware of the prototyping of various forms of engine that promised to allow carriages to reliably proceed at the pace of trains, and the first frail airships that could manage a fair pace in flight - though by no means the equal of speed by rail.

Like our present era, however, the end of the 19th century was a time of very rapid progress and invention in comparison to the past. In such ages trends are broken and exceeded. Thus within twenty years of the first crudely powered and fragile airships, heavier than air flight launched in earnest: a revolutionary change in travel brought on by the blossoming of a completely new branch of applied technology. By the late 1920s, the aircraft of the first airlines consistently flew four to five times as fast as the operating speed of trains in 1880, and new lines of travel could be set up for a fraction of the cost of a railway. Little in the way of incrementalism there: instead a great and sweeping improvement accomplished across a few decades and through the introduction of a completely new approach to the problem.