Robert Freitas, the nanotechnologist and longevity science advocate, has an article in the current Life Extension Magazine, also available online:

Nanotechnology is the engineering of molecularly precise structures and, ultimately, molecular machines. The prefix 'nano-' refers to the scale of these constructions. A nanometer is one-billionth of a meter, the width of about five carbon atoms nestled side by side. Nanomedicine is the application of nanotechnology to medicine. The ultimate tool of nanomedicine is the medical nanorobot - a robot the size of a bacterium, composed of molecule-size parts somewhat resembling macroscale gears, bearings, and ratchets. Medical nanorobotics holds the greatest promise for curing disease and extending health span. With diligent effort, the first fruits of medical nanorobotics could begin to appear in clinical treatment as early as the 2020s.

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Right now, medical nanorobots are just theory. To actually build them, we need to create a new technology called molecular manufacturing. Molecular manufacturing is the production of complex atomically precise structures using positionally controlled fabrication and assembly of nanoparts inside a nanofactory.

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But now it’s time to put our theories to the test. After working closely for three years with Philip Moriarty, one of the leading scanning probe microscopists in the UK, our international colleague is now undertaking direct experiments to build and validate several of our proposed mechanosynthesis tooltips in his laboratory. We are also preparing a research program proposal of our own to solicit additional funding from various US public or private sources to support further mechanosynthesis-related experimental and theory work on a greatly accelerated schedule. We expect these efforts will ultimately lead to the design and manufacture of medical nanorobots for life extension, possibly during the 2020s.

But read the whole article: make machines small enough, and they could interface with our cells to repair damage, replace worn structures, or even replace the function of cells entirely. More effective oxygen-carrying blood cell machines, for example, or hyper-efficient immune cell machines. Cells are just complicated small devices, and we humans are becoming very good at making complicated small devices - it's just a matter of time until we can build better machinery than than the evolved biological devices presently powering our bodies.

Scientists are a cautious lot, and funding is available for careful studies that replace sound assumptions with even more sound established facts. Now that calorie restriction (or dietary restriction, DR) research is attracting so much funding at the development end of R&D, you'll see more studies aimed at firming up the foundations. Take this open access paper for example:

One of the promising advances towards the goal of uncovering the mechanisms by which DR extends life was the discovery that the effect is evolutionarily conserved. However, even with the use of short-lived model organisms for relatively rapid lifespan experiments, the mechanisms remain elusive. This is likely to be largely due to the complexity of physiology involved in determining length of life, but may be also in part due to technical issues in experimental design hampering a clear path of progress.

The ease with which complexity can be introduced into these studies can be illustrated by the large effects on fly lifespan caused by very small changes in nutrition. For example, substituting one source of the dietary yeast Saccharomyces cerevisiae, with another from a different supplier in an otherwise identical diet can have large effects on fly lifespan. Similarly, lifespan differences have been reported due to the use of different bacterial strains as food for Caenorhabditis elegans or by interchanging casein and soy peptone as the source of dietary protein for rodents. In fact, a recent article has proposed that DR itself may have arisen as a by-product of laboratory life as animals are unintentionally subjected to selective breeding in the presence of an artificially rich nutritional environment. Clearly, these issues need to be addressed if we are to uncover the molecular mechanisms of DR.

As might be expected from the weight of existing evidence for calorie restriction to extend healthy longevity, increasing the rigor of the experiments didn't prevent the beneficial effects:

In this study, we have examined the effect of laboratory stock maintenance, genotype differences and microbial infection on the ability of dietary restriction (DR) to extend life in the fruit fly Drosophila melanogaster. None of these factors block the DR effect.

This year's Edge annual question is:

What game-changing scientific ideas and developments do you expect to live to see?

With that lead-in, it's perhaps not surprising to see a range of thoughts on engineered longevity in amongst a range of less relevant but still interesting responses:

Gregory Benford:

Live to 150: I expect to see this happen, because I'll be living longer. Maybe even to 150, about 30 more years than any human is known to have lived. I expect this because I've worked on it, seen the consequences of genomics when applied to the complex problem of our aging.

Emanuel Derman:

The biggest game-changer looming in your future, if not mine, is Life Prolongation. It works for mice and worms, and surely one of these days it'll work for the rest of us.

David Eagleman:

While medicine will advance in the next half century, we are not on a crash-course for achieving immortality by curing all disease. Bodies simply wear down with use. We are on a crash-course, however, with technologies that let us store unthinkable amounts of data and run gargantuan simulations. Therefore, well before we understand how brains work, we will find ourselves able to digitally copy the brain's structure and able to download the conscious mind into a computer.

Bart Kosko:

Society will change when the poor and middle class have easy access to cryonic suspension of their cognitive remains - even if the future technology involved ultimately fails.

Today we almost always either bury dead brains or burn them. Both disposal techniques result in irreversible loss of personhood information because both techniques either slowly or quickly destroy all the brain tissue that houses a person's unique neural-net circuitry. The result is a neural information apocalypse and all the denial and superstition that every culture has evolved to cope with it.

Corey S. Powell:

I have little doubt that progress in fighting disease and patching up our genetic weaknesses will make it possible for people to routinely reach the full human lifespan of about 120. Going far beyond that will require halting or reversing the core aging process, which involves not just genetic triggers but also oxidation and simple wear-and-tear. Engineering someone to have gills is probably a much easier proposition. Still, if we can hit 200 I see no reason why the same techniques couldn't allow people to live to 1,000 or more. Odds: 60 percent.

I can't say as I think any of these folk are exactly on the ball, even Benford, who clearly subscribes to the mainstream view of genetic and metabolic reprogramming to slow aging rather than the damage repair view of the Strategies for Engineered Negligible Senescence. It is promising to see engineered longevity as a prominent topic, but it still looks like a lot of fumbling around in the dark is taking place. That shows that more work is needed on the part of advocates to direct interest and potential support onto the best paths forward.

The lates two podcasts at SAGE Crossroads look at either side of views on compression of morbidity:

Fries' hypothesis is that the burden of lifetime illness may be compressed into a shorter period before the time of death, if the age of onset of the first chronic infirmity can be postponed before the age of death. In order to confirm this hypothesis, the evidence must show that it is possible to delay the onset of infirmity, and that corresponding increases in longevity will be modest.

On the one side:

Longevity will continue to increase under hopeful scenarios for the human future, and morbidity will continue to decrease. The question is the relative rate of those, and I’m just telling you and anybody else who would make such an argument that in fact the data is in. The mortality rates are going down 1 percent a year. That’s a substantial decline in mortality rates. That’s been continuing for a century, that’s almost a straight line, at 1 percent a year. The morbidity rates are going down 2 percent a year. It’s the story.

And on the other side:

KYLE JENSEN: Now do you feel that the compression of morbidity theory should be the focus of biomedical gerontology?

AUBREY DE GREY: No, not really I don’t. It’s important first of all to remember that the original description of compression of morbidity by Jim Fries in 1990 did not even propose this. What he proposed was that actually it would be easier to implement changes in lifestyle that would postpone the onset of morbidity than it would be to develop medical technologies to postpone death. In other words, he felt that by changes of lifestyle we could compress the period between the two, but he never suggested that we would actually compress morbidity by intervening in the biology of aging. Indeed, he felt that intervening in the biology of aging was essentially impossible. What we are actually seeing is failure to implement those changes of lifestyle that Jim Fries suggested. We are seeing increase in lifespan and also [delay in] onset of morbidity. Not much change in the rates of those two so the interval between the two [remains the same]. There is not progress being made in compressing morbidity. There is a bit of variation. In some statistics we see a little bit of compression in some people; in some places we see a little bit of expansion. By in large what we are seeing is exactly what you would expect from postponing aging. In other words, you postpone the onset of morbidity and you also postpone death by about the same amount.

As they say, you can do all sorts of things with statistics and definitions, and I'm far from qualified to put forward any sort of firm opinion as to whether present statistics better support one side or another. Compression of morbidity is something of the declared goal of those in the mainstream of aging research who don't want to talk about extending life span, however, which makes it a little more than a matter of statistical interpretation. When a researcher talks about compression of morbity, that is something of a cipher, an identifying mark as to where he stands on the topic of engineered longevity: possibly in favor, but not willing to risk offending conservative funding organizations, possibly against. Either case has much the same result - a researcher who isn't working as freely as he might to extend human longevity.

From my reductionist viewpoint, I find it hard to reconcile an existence of compression of morbidity with the performance of reliability theory as applied to aging, amongst other things. Theories of aging based upon accumulation of biochemical damage and incremental system failure are very convincing, and have a great deal of experimental support, but don't predict that compression of morbidity is possible to any great degree. The only way to push out health life span is to prevent or repair damage, and that will also push out overall life span.

I noticed a mortality study that illustrates some of the common wisdom regarding the common diseases of aging:

The remaining lifetime risk of cancer at age 40 was 45.1% and at age 90 was 9.6%. The remaining lifetime risk of major cardiovascular disease at age 40 was 34.8% and at age 90 was 16.7%.

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The remaining lifetime risk of both diseases approached a plateau in the 10th decade. This may be due to decreased detection of disease and reporting of symptoms and increased resistance to disease in those who survive to old age.

The older a person becomes - or rather, the more capable a person is of achieving longevity - the less likely he or she is to suffer from the major diseases of aging. As the authors point out, however, it's a challenge to build reliable data:

The measurement and interpretation of the incidence of disease in advanced age is complex. Lower incidence in late life may reflect decreased screening and medical surveillance rather than decreased risk. ... This cohort of health conscious doctors has several advantages for studying the incidence of disease in men of advanced age, as it has a large proportion of participants surviving to age 90 and beyond, as well as a higher level of screening for disease and diagnosis than in a general population.

This and other collections of data on mortality risk consistantly show that incidence of cancer and cardiovascular disease is lower for those who live longer. Other research shows that living longer within the present state of medical science is a matter of making consistently sensible choices in life for most of us - not a matter of good genes to any great degree. Join the dots: all that exercise and good diet really does make a difference in the long term.

Now if you have a good few decades left before getting to the point at which you have to start worrying in earnest about your heart and runaway cells killing you from the inside, it's probably the case that the future trajectory of your life will be far more determined by progress in medical science than living well. Absent progress, your life will look much like that of your parents. With exceptional progress, the sky is the limit - aging itself might be defeated before you reach the point at which it will kill you. So while you're on the execise machine, or pondering a good diet, spare some thought for how you can support the future of medical research as well. There is where the real difference lies.

We can never know absolutely and for sure whether doing the "right things" for our health will make a significant difference to our own healthy longevity. You have to wait and see, one chance to get it right, no going back to fix things up. We do, however, have a wealth of evidence that actions long commonly regarded as the "right things" for good health will indeed be good for our future healthy longevity. This evidence is quite separate from the comparatively recent investigations of medical science into the biochemical roots of good health and longevity.

What is this evidence? That wealthier, higher IQ people tend to live longer and suffer less age-related illness. For example:

Lower scores on measures of IQ at two time points were associated with [cardiovascular disease] and, particularly, total mortality, at a level of magnitude greater than several other established risk factors.

I don't think that it's ever been a grand mystery that regular exercise, a good physician relationship, and eating sanely are going to be good for you; the common wisdom for good health long predated the scientific studies showing that it was the case. The grand mystery is why so few people keep up with those efforts in their own lives, and suffer because of that negligence. I've been inclined to interpret results like the research above to mean that more intelligent people tend to get wealthier but also tend to do more of the right things for their health - you can be as rich as you like, but if you weren't exercising all that time you were making money, you're still going be at a higher risk for suffering cardiovascular disease at the end of the day.

Smarter people have a greater tendency to keep up with common sense health practices and gain a benefit by doing so. That's my thesis. As to why that is the case - well, that gets back to what IQ actually measures, whether time preference is very different between individuals, and so forth.