Regardless of level of knowledge, everyone will have an opinion, of course. We humans are good at holding opinions - possibly a little too good, but that's evolution for you. Around "the norm" of decided ignorance, holding an opinion has as much to do with learning the prevailing opinion as with actually forming one yourself based on (limited) knowledge. Which again, makes sense from the viewpoint of the economics of time, attention, and knowledge.

This is the hurdle faced by advocates for change in paradigm: it's hard to change opinions when the supporting information for a new viewpoint requires even a moderate amount of effort to obtain and analyze. So it is with aging research and engineered longevity - and most other paradigm changes based on advancing science. You can watch the spread of the ideas of engineered longevity into new discussion communities online; the tech crowd is further ahead than the politics crowd in terms of exposure, for example. But the earliest reactions are still "aging and death are good and needed, and you are most likely crazy for thinking about longevity science." This shows that in terms of advocacy for longer healthy lives, it is still very necessary to keep plugging away at the most basic concepts with the wider audience.

Here is an example of a comparatively well educated online community that is less exposed to thoughts on longevity science - read the comments, and then take a look at this commentary at the IEET:

There were lots and lots and lots of comments that critiqued transhumanism’s rejection of aging and death as natural, necessary, and good. When all the comments are distilled, we get the following arguments:

1) Death and aging is why we value children. Think of the children!
2) Death sweeps away the old, allowing the new
3) We already have too many people! Hello! Malthus!
4) Life extension would result in a nursing home society
5) Can’t do it, aging is too complicated

These are the pillars of "the norm" of opinions on engineering greater human longevity. They are all easily answered, and have been in the post above, here at Fight Aging! and by many other authors, but would that such answers were enough in and of themselves! The realm of public opinion is a long, grinding battle of atttrition that often has little to do with fact, evidence, or anything other than how widespread a particular viewpoint happens to be. Generating much greater public support for longevity science will be a long haul, and no doubt frustrating, but it is absolutely necessary to ensure significant future progress in research and development.

So-called 'senescent' cells are those that have lost the ability to reproduce themselves. They appear to accumulate in quite large numbers in just one tissue (the cartilage in our joints), but even in these small numbers they appear to pose a disproportionate threat to the surrounding, healthy tissues, because of their abnormal metabolic state. Senescent cells secrete abnormally large amounts of some proteins that are harmful to their neighbours, stimulating excessive growth and degrading normal tissue architecture.

In theory our immune system should be scouring the body to destroy senescent cells before they become an issue, but this process slowly fails - along with the other capacities of the immune system - with increasing age. But on to the posts I wanted to point out:

Cellular Senescence in Anti-Ageing Research:

Since senescent cells are potentially detrimental to the tissues in which they reside, anti-ageing research has three main aims for dealing with this problem: (1) Prevention: prevent cells from becoming senescent. (2) Removal: remove senescent cells as they appear. (3) Replacement: replacement of cells which have naturally or artificially been removed.

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Like all anti-ageing research, [prevention of senescence], senescent cell removal and cell replacement are at their infancy. Only with time, money, a deeper understanding of the ageing process and a motivation to succeed, will we begin to see the inevitable benefits of anti-ageing research.

The removal of senescent cells using therapeutic agents:

At present, no drug-based system exists which can specifically identify senescent cells and remove them. However, there is currently great interest in the development of drugs which specifically target and remove cancer cells. The problem with current cancer treatments (such as drugs used in chemotherapy) is that they are non-specific and as such can cause damage and undesirable changes to non-cancerous cells, causing side-effects. The development of cell-specific drug targeting is greatly needed and such research could be adapted to target senescent cells.

Beyond cancer and damage-causing senescent cells, there are a great many other potential applications for technologies that can kill very specific cell populations. Partially rejuvenating the immune system, for example, by removing the clutter of memory cells uselessly specialized for cytomegalovirus. Or healing autoimmune diseases by wiping out malfunctioning or errantly programmed immune cells. Such technologies even provide the foundation upon which future researchers will build entirely artificial immune systems far more effective and efficient than that provided by our biological heritage.

It's a bright future, and the longer we live, the brighter it will be for us. All the more reason to take care of your health today, so as to maximize your chances of living into the age of repair and rejuvenation.

Stresses like dietary restriction or various toxins increase lifespan in taxa as diverse as yeast, Caenorhabditis elegans, Drosophila and rats, by triggering physiological responses that also tend to delay reproduction. Food odors can reverse the effects of dietary restriction, showing that key mechanisms respond to information, not just resources. Such environmental cues can predict population trends, not just individual prospects for survival and reproduction. When population size is increasing, each offspring produced earlier makes a larger proportional contribution to the gene pool, but the reverse is true when population size is declining.

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We conclude that the beneficial effects of stress on longevity (hormesis) in diverse taxa are a side-effect of delaying reproduction in response to environmental cues that population size is likely to decrease. The reversal by food odors of the effects of dietary restriction can be explained as a response to information that population size is less likely to decrease, reducing the chance that delaying reproduction will increase fitness.

The bulk of the paper consists of the mathematical model used to argue this point: evolutionary changes that allow animals to delay reproduction at opportune times will be more successful, as will any adaptation that makes metabolism more likely to identify when those opportune times occur. This seems like a solid theory, given the evidence to hand. Population size and its relationship to the availability of food are very fundamental properties, in play for even the earliest and most primitive species, and similar for many diverse species. Thus we should expect to see what we do see in nature: that the calorie restriction response is a very old aspect of animal metabolism, present in almost all species tested, and governed by very similar genetic mechanisms in species ranging from flies to humans.

In the years ahead, researchers will work out how to permanently and safely turn on the calorie restriction response in humans. This seems like a fairly safe prediction absent a specific timeline, given that the research community for this field is well established and companies continue to raise venture funding to develop methods of metabolic manipulation. They will most likely improve on the natural version to some degree once it is fully understood. The flow of newly discovered longevity mutations in lesser species strongly suggests that all species are far from optimized for longevity, and we should expect to find longevity mutations in humans as well.

That said, a likely 20 year timeline to produce tools that do no more than slow aging will be a grand disappointment for those in middle age today. A 2030 in which we cannot repair aging and reverse its effects to any significant degree would be a death sentence - and a well deserved one, given that we had two decades in which to develop more effective medical technologies than metabolic manipulations to mimic the effects of a natural process.

Ratcliff, W., Hawthorne, P., Travisano, M., & Denison, R. (2009). When Stress Predicts a Shrinking Gene Pool, Trading Early Reproduction for Longevity Can Increase Fitness, Even with Lower Fecundity PLoS ONE, 4 (6) DOI: 10.1371/journal.pone.0006055

Growing a bladder or a body part such as a blood vessel takes about six weeks. To create an artery, say, Atala plucks some of the immature cells that make up arterial lining and muscle from a sample of the patient's blood and incubates them by the billions in liquid nutrient. The cell-rich soup is then painted on a tube-shaped scaffold made from flexible collagen, like the tissue that forms the nose. (The collagen will gradually disintegrate once the vessel is in place.) The cells mature, multiply further, and form an artery. A small machine exercises the vessel, conditioning it to function normally after it is implanted.

Building organs such as bladders and blood vessels, which have only a few different types of cells, has become almost routine for Atala's lab. A heart or pancreas is far more complex and challenging.

This is the heroic story template in which the field of vision is narrowed (one might say dumbed) down to a single face, emblematic of thousands who are performing important work in the field. That's the way the popular press works, but remember that when journalists point out one groundbreaking fellow, there are dozens of others left unmentioned in the backdrop, folk with their own labs, important projects, and promising results. Tissue engineering is a large and very active field now, constrained far more by regulatory costs and barriers than by any technical hurdles.

Given the present pace of development, I don't think it's unreasonable to expect a couple of different methods of producing organic replacements for all the major human organs (except for the brain of course) to be ready for use by 2020 - though whether they will be legally available in the US given the state of the FDA is another question entirely. The state of medical regulation is so far removed from sensible considerations of risk and readiness that countless potential therapies languish unused, undeveloped, and unrefined, along with whatever new information researchers might have learned from more widespread usage.

Genescient has a proprietary screen for substances that can extend human lifespan and healthspan. Using genetically selected long lived Drosophila and the latest genetic tools, Genescient has identified over 100 gene networks that are altered in long lived strains of Drosophila melanogaster and that are also linked to longevity and age-related diseases in humans.

In essence, you might envision Genescient as what you get when you add very rapid progress in biotechnology (and falling cost in biotech tools) to the basic aims of Sirtris. Find longevity genes and manipulate their expression for benefit and profit in other words, but where Sirtris's initial development back before 2004 focused on just a few genetic networks, Genescient is aiming for "all of them." Even in five years, costs have fallen and tools improved significantly - think about the computer you were using in 2003, for example, and compare it to the machine you're using today.

Like Sirtris, Genescient is firmly an outgrowth of the "work to slow down aging via metabolic and genetic manipulation" faction of aging research. They are not aiming to identify and repair biochemical damage, but rather shift the operation of human biochemistry into a more beneficial state for long-term operation. I'd insert the obligatory comment on how this approach is not the Strategies for Engineered Negligible Senesence, and even if wildly successful in decades to come will do little for those already old, but you're all probably all tired of hearing it by now.

Reading between the lines ("nutrigenomic supplements?"), it looks like the Genescient founders might choose to monetize the results of their work in the supplement marketplace rather than take the Sirtris path of big pharma and the FDA. If that's the case, I couldn't say I blame them: you'd have to be extraordinarily dedicated - or foolish - to want to deal with the state of medical regulation in the US if there was a viable alternative option to make your investors happy. This is one of the reasons why the US research industry is basically doomed absent a revolution. That all said, the supplement industry is what it is; if you want to relegate yourself to irrelevance in the ongoing quest to cure aging, history suggests that entering the supplement market will achieve that end. Scylla on the one hand, Charybdis on the other - and going overseas to less oppressive regulatory regions in order to develop research into applications is looking ever more like the best option.

Regardless, I think the most useful output for the long term arising from the work taking place at Genescient will likely be a wealth of data on how gene expression changes occurring with aging relate to forms of biochemical damage that are thought to cause aging. Are gene expression changes responses to damage, or are they genetic programs that themselves cause damage? Or both, or neither? How important is each particular change? These are vital questions if your goal is to revert gene expression changes in search of beneficial effects, but this data will also help those who seek to directly repair the damage itself. There's no such thing as useless information in biotechnology.