reasonattlm

Undeniably the case that it works really well, however, especially given how easy it is to arrange for the people holding the fundraiser. Broadcasting a matching fund is news, adds an extra touch to potential donors, inspires people to donate when they wouldn't otherwise have done so, and costs very little in additional administrative time.

Administrative time is always at a premium in non-profits, and optimizing for lower overhead in time and work is a reason for many things that might otherwise seem a little puzzling in their persistence.

This seems like one of those not terribly relevant statements one can make for any environmental factor that correlates with lower life expectancy. Aging is damage, age-related disease is caused by damage, and thus people with shorter life expectancies have more damage and more age-related disease.

Air pollution is quite well correlated with lower life expectancy, though it is one of those factors, like wealth, intelligence, education, and social status, that are all entwined with one another and with observed variations in life expectancy. There are direct mechanisms whereby exposure to pollutants can cause harm, but it is also true that there is evidence for the genetics of intelligence to also provide greater physical robustness. There is no really good data to sort out which of the mix of many correlations is actually driving the observed relationships between air pollution and age-related disease, given that greater wealth means evading or lowering air pollution, and the true causes of the wealth-longevity relationship are obscure. Much the same could be said for any of the individual relationships in this web.

There's also a type 4 now as well, which appears to be another distinct age-related form of immune dysfunction that impacts insulin-related functionality.

http://www.salk.edu/news/salk-news/faq-on-type-4-diabetes/

Change this to the nature article, it is much better.

http://www.nature.com/news/alzheimer-s-treatment-appears-to-...

Other references:

Publicity materials: http://www.eurekalert.org/pub_releases/2016-08/uoz-arh083016...

Paper (not open access): http://dx.doi.org/10.1038/nature19323

Alzheimer's disease research is perhaps the largest single theme in the aging research community, with the majority of National Institute on Aging funding going towards Alzheimer's programs. The most advanced of efforts in Alzheimer's research are those that seek to clear the accumulation of amyloid-β in the brain through the use of immunotherapies, enlisting the immune system to break down and remove the unwanted amyloid. To date, however, this has proven to be a road of great expense characterized by disappointment and slow progress, to the point at which it was possible to question whether amyloid was the right target. Other theories and lines of research have begun to prosper due to the lack of tangible human results for anti-amyloid immunotherapies, in particular that neurofibrillary tangles of misfolded tau protein are just as much a target for clearance as is amyloid-β, and that perhaps it is time to focus on the decline of known clearance mechanisms rather than the amyloid itself.

Still, over the past couple of years, one of the latest entries to the class of anti-amyloid immunotherapies has lived up to some of the promise first seen in animal studies of amyloid clearance. It may well be that the light at the end of the tunnel is in sight. In a human trial that has now lasted a year, this new immunotherapy cleared near all detectable amyloid-β from patients, and the patients showed improvement in the sense that their decline appeared to slow significantly. The caveat here is that a year is not long enough to declare a slowing of the condition in certainty given the number of people treated in the trial, 165 individuals. Certainty will arrive given time and more patients. Regardless, simply through the demonstrated clearance of amyloid in human patients this is a big step forward for the field. If this holds up over the next few years of larger trials it should become very clear as to the degree to which amyloid-β is or is not in fact the primary cause of pathology in Alzheimer's disease.

I have long said that the best way to answer these questions of cause and contribution is to remove the mechanism in question and see what happens. As an approach that is much, much faster - and thus more cost-effective - than trying to infer the answer by analyzing the enormously complex workings of cellular biochemistry. This principle is well demonstrated here in the matter of amyloid, I think, given the past decade of theorizing on the degree to which the harm of Alzheimer's is due to amyloid, tau, or other causes, and the lack of progress on that front from theorizing alone. As soon as a treatment can reliably and safely remove the amyloid from a sizable number of Alzheimer's patients, we will have the answer.

Reversing aging doesn't work that way. Aging is damage, and reversal of aging is damage repair. Damage repair can be rapid and sweeping, and usually is.

You might examine some of the animal studies for, say, stem cell therapy or senescent cell clearance. Benefits are rapid and very evident for things that do actually work. Even slower items like myostatin blockade to provoke muscle growth show sizable, obvious benefits over a period of a few weeks to a few months.

You probably recall the hype surrounding sirtuins in cellular metabolism, followed by the breathless marketing of compounds supposed to affect their expression such as resveratrol, all of which went to the usual destination for such things, which is to say nowhere. Some knowledge was added to the grand map of mammalian biochemistry, some people were fleeced, some people made a bunch of money on the backs of promises that never materialized, and that was that. This happens over and again. Every time a new link is uncovered in the complex chain of protein machinery relating to cellular repair mechanisms, upregulated in many of the ways to extend life in lower animals, or calorie restriction, a practice that extends life in short-lived mammals such as mice, and along the way alters near every aspect of the operation of metabolism, then the marketing begins for any supplement that can be linked, tenuously or otherwise, to that research.

If you recognize the general pattern, then you should be well placed to see how things will play out for nicotinamide riboside. This is yet another molecule that can be used as a supplement, and which influences some of the mitochondrial biochemistry associated with cellular maintenance processes. In mice it has been shown to modestly reduce some forms of age-related decline, either by spurring greater maintenance or greater stem cell activity. It is an open question as how much of this will be recapitulated in humans; short-lived species are much more readily influenced by this sort of thing. Their life spans are plastic, and so are their metabolic operations. Regardless, it is of course the case that a bunch of people got together to form a company in order to sell nicotinamide riboside as a supplement. That company is called Elysium Health.

The differences between this and past efforts of this nature are that (a) more reputable scientists from the aging research field are involved, more is the pity for their reputations, and (b) the whole affair is just a little closer to a sensible take on how to make progress in the field, rather than being an absolute money grab. In fact I agree with a fair bit of what cofounder Leonard Guarente has said in public on his motivations for doing this: that progress must be made more rapidly, that there is a space between the worthless supplement market and the highly regulated world of medicine in which good work can be done, and that it is important to put new approaches out there in the world to gather data. I just don't think that this particular approach has any merit in and of itself. My position on tinkering with metabolism via drugs and found compounds in order to gain tiny and dubious benefits is that it is a a waste of time and effort, and definitely not the road to meaningful outcomes in the treatment of aging. Further, even putting that to one side, the founders of Elysium haven't gone about this in the right way at all. They should have sold their product as an open trial of nicotinamide riboside wherein people pay for participation, doubled the price of the supplement, and used that extra money to collect data from participants. Instead they, as everyone is, are corrupted by the fiduciary duty that comes with running a company where the primary focus is selling a branded supplement - so now they are in the supplement business, not the science business. It should be an object lesson for the next group who are thinking of doing something like this.

I'm very much in favor of freedom. For my money, all of medicine should be as open as this: that anyone can invest the time and money to package and sell a product, that consumers can easily find all of the research online to read up on what the scientific community has to say, and that reviewers can take that information to provide digests for those who don't want to read the research. Freedom means the existence of marginal products as well as great products, and people doing things you personally think are a waste of time as well as people doing things you agree with, but you can always identify these as such. You just have to take a little time to read around the topic before you reach for your wallet. Freedom also means a far greater set of activity and greater experimentation and availability of new approaches than would take place if all of this was hammered flat beneath the cost of regulation, and that, I think, would be worth the price of admission. Successes will prove themselves by virtue of the fact that sellers will find it worth the cost of setting up formal trials to demonstrate effectiveness, for example.

The fascinating thing about the transition of aging research from mere investigation to the possibility of intervention is that many researchers don't even want to talk about extending life, but only a small expansion of healthspan. This lack of ambition, and refusal to engage with the large body of evidence that suggests we can do far better, is why we need organizations like the SENS Research Foundation and Methuselah Foundation, working to make the better option happen. It is possible and plausible to extend healthy life and overall lifespan indefinitely by implementing the approach of repairing the cell and tissue damage that causes aging. Yet all too much of the rhetoric and effort in the scientific community still goes towards tinkering with the operation of metabolism to slightly slow the pace at which damage accumulates - a clearly far inferior approach, that can at best produce only marginal outcomes.

All of the technologies and approaches mentioned in this article are marginal, ways to only modestly slow the damage of aging from accumulation. They are very limited in what they can achieve - adding five to ten years to life would be an enormous, unlikely success for any one of these. Calorie restriction we know doesn't add more than that to human life spans, since we have plenty of examples to look at. Metformin data is all over the map in animal studies, just as contradictory and half-refuted as sirtuins. The transfer of young plasma to old individuals doesn't extend life in animal studies; it is pretty unlikely to have the desired effect in humans - that isn't the same thing as parabiosis. Human Longevity Inc is a personalized medicine company in fancy clothing, doing nothing that will greatly extend life, but rather looking for incremental gains in ordinary medicine. And so on.

Sadly journalists typically don't distinguish between the potential value and outcome of different approaches to aging - it is all the same to them, just a flat list. So they pull five or ten items from the larger list to populate their articles, and mark them all equivalent. That's something of a problem when the differences are in fact enormously important and the expected outcomes are night and day when comparing approaches that repair damage versus approaches that do not repair damage. If there is to be significant progress towards healthy life extension in our lifetimes, the better strategies, those involving damage repair, must gain far greater support. This means the SENS list: senescent cell clearance, mitochondrial DNA damage, clearing metabolic waste like amyloid, lipofuscin, and cross-links, and so on.

The big challenge at the moment is coverage; getting enough of the cells successfully edited by the gene therapy to make a meaningful difference. There are promising signs in mice, such as the muscular dystrophy study from earlier this year [1], but in general this is still an ongoing battle, without a standard approach.

The coverage issue is why you can't go out and get any one of a hundred edits [2] and expect things to happen as a result. As soon as that is robustly solved, well, gene therapies will be out there in the medical tourism market, starting with telomerase, myostatin, and follistatin, I'd imagine. Most likely the second of those up front since its already fairly robustly proven in humans via antibody therapies. [3]

I would be extraordinarily surprised to find that there were no humans already tinkering with their myostatin balance via genes or antibodies, given the number of people with access to the technology, and the ease with which such a therapy could be assembled.

[1]: http://www.nature.com/cr/journal/v26/n5/full/cr201628a.html

[2]: https://www.fightaging.org/archives/2016/06/a-short-list-of-...

[3]: http://news.iupui.edu/releases/2015/12/myostatin-warden-musc...

Telomere dynamics are sufficiently different between mice and humans to be cautious about extracting meaning from mouse studies.

Birds have very much more different telomere dynamics.

So aside from that, average telomere length is typically measured in immune cells from a blood sample. Telomere length shortens with each cell division, and stem cells delivery new cells with long telomeres. So in immune cells you are going to get a fuzzy metric that depends on everything known to influence immune function filtered through a combination of immune cell replication and replacement rates. So stress, injury, exertion, diet, infection, age, etc, etc.

What you end up with is a statistical measure that can support any number of theories, being fairly distant from underlying processes, and influenced by many processes. There's a lot of variation in the literature, and many contradictory datasets and interpretations.

That again is entirely distinct from the evolutionary background that leads to a species having telomeres that start at a given length, and there are wide variations in that metric across species - just look at mice and humans.

If you look at previous research on exercise, inflammation, and brain volume:

http://dx.doi.org/10.1016/j.neuroscience.2014.05.005

and the mountain of evidence showing that excess visceral fat tissue produces greater levels of chronic inflammation:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3437966/

Then it seems that inflammation would be the first place to start looking for mechanisms linking weight with white matter volume.

Certainly more visceral fat is associated with higher risk of all of the common forms of dementia, and most age-related conditions are sped up in their progression by inflammation.

All the more reason to be investing more than a pittance in the development of rejuvenation biotechnologies. So very close to realization, yet widely ignored.

Actually, it seems crazy to me that the economic argument gets more play than the humanitarian argument. People, including the old, seem happy to consign the aged to suffering and death, but that aging and age-related disease impacts the economy gets a larger fraction of them up in arms.

The future of cancer is targeting, in one way or another. It has been interesting to watch immunotherapy win out as the dominant approach to targeting; there are other options, such as nanoparticle platforms in which targeting and kill mechanisms could be assembled as needed, or oncolytic viruses, and so forth. All of those are still under development, just with nowhere near as much backing as, collectively, goes to forms of immunotherapy.

Still, most immunotherapies packaged and deployed to trials are more of the same in terms of being very specific to specific types of cancer. There are hundreds of types of cancer, depending on how you want to count. It is much better to be able to build a therapy with few side-effects, given that chemotherapy has a very unpleasant effect on health and life span over the long term even when successful, but the extreme specificity is still problematic from the strategic point of view. The cancer community has shown that they can't produce new therapies for all cancers at a fast enough rate to completely control cancer any time soon. The strategy needs to shift to producing therapies that can target many types of cancer.

Once class of immunotherapy shows particular promise on this count, and that's the chimeric antigen receptor approaches that have produced such good results for leukemia. It should considerably reduce the cost of building new therapies for many types of cancer once a couple of types of cancer have been successfully treated that way and the basic platform is defined. We'll see how that goes over the next fifteen years or so. All in all, immunotherapies look to be the replacement for chemotherapy / radiotherapy as the coming generation of cancer therapies, and people will keep their hair, and will get treated as outpatients in clinics, and cancer survivorship will increase, and it is likely that they won't lose a decade of life expectancy as a result of treatment.

It is worth looking beyond that, however, as the technical basis for the generation of therapies after immunotherapy is actually being worked on today. For my money the thing that comes after immunotherapy will involve blocking telomere lengthening, as that is a - possibly the only - basis for a universal cancer therapy. All cancers need to lengthen telomeres, cannot evolve their way around that need, and building one therapy to control every type of cancer seems a much better path forward than the present strategy of seeking ever more specific biochemistry to interfere with. A fair number of people are working on the telomerase side of that equation, and not enough people are working on the alternative lengthening of telomeres (ALT) side of that equation, but this will all come to a useful conclusion somewhere in the late 2020s, I'd imagine.

There is way too much acceptance and compensation in the way people approach problems relating to old age. It just doesn't exist in other fields in the same way. So much is done atop the axiom that whatever is wrong with the old - in a biological, physical sense - is set in stone and cannot be changed, and thus, collectively, vast resources are addressed to coping or compensating rather than addressing. Problems should be solved, not papered over.

I don't run this research. It is a non-profit initiative. I have donated myself. I'm persuading other people to do so as well because I think it is a good idea, an important idea, and very necessary for the strategic reasons noted above. The benefit I'm going to get out of it is that my odds of surviving future incidence of cancer increase should it succeed. But then the same is true of everyone else.

You see the argument for this approach to cancer as being less valid because in addition to making it, I have chosen to act on it? Strange thought process.

If peak cancer years are two or more decades in your future, I'd argue that the best thing you can do today is donate to research programs that are likely to change the economic landscape of cancer research. You should also not get fat, not smoke, and all the other things that require no money, but research is much more transformative. You want the future to be no cancer, not less cancer.

Why economic transformation in cancer research? The cancer research community suffers from a high level strategy problem: the majority of treatments are only applicable to a small number of cancer types, out of the hundreds of known types, and the majority of new technology platforms under development will be just as expensive to adapt to a different type of cancer as to build in the first place. A much more efficient approach is needed, as there are only so many researchers and only so much funding in the world.

This is much on my mind because I'm helping to raise funds for one such project right now. It involves taking on the less well-supported but still necessary part of building a universal cancer treatment platform, one that can target all cancers. This could be built for about the same cost as one of today's highly specific single-cancer treatments. Obviously that is an immensely better path forward.

The approach is to block telomere lengthening: all cancers must lengthen their telomeres in order to grow, and abuse a small number of target mechanisms in order to do so. These mechanisms, telomerase and alternative lengthening of telomeres (ALT), are very fundamental to cellular biochemistry. If they are turned off, it is expected that there is no way for a cancer to evolve around that dead end. Many of today's cancer therapies, in addition to being very specific, also leave room for a cancer cells to evolve a different way of conducting business that renders them immune.

A number of research groups are working on sabotage of telomerase, but next to no-one is working on ALT. It is known that telomerase cancers can turn into ALT cancers, so it is probably the case that both doors have to be slammed shut to have a truly effective universal cancer therapy. So I'm helping a fundraiser to use an ALT assay to scan the standard drug candidate library for compounds that act to suppress ALT, something that should greatly advance that part of the field, both by identifying more lines of investigation, and by finding potential therapies for ALT cancers. Since ALT doesn't happen in normal cells, completely suppressing ALT should be a pretty safe treatment if an approach with limited side-effects can be identified. The telomerase blocking will need more work on compensating or targeting for other effects, since stem cells require it. But that is still a lot less work than producing one therapy per cancer type.

Disaster stories sell papers, but the situation is not a disaster story. Rather it is the standard plot for development of new things. People see possible scarcity and react accordingly, far in advance of the non-specialists of the press figuring it out. The scientific community is and has been responding well to the threat of running out of antibiotics. In particular, new advances in mining the bacterial world - a 100-fold enhancement in that mining - mean that we'll be flooded with many new antibiotic drug candidates in the years ahead. For example, see:

https://www.edge.org/response-detail/26701

http://www.popsci.com/ichip-new-way-find-antibiotics-and-oth...

Antibiotics Malthusianism has the same problem as all other forms of Malthusianism, which is that people work to fix the problems they see arising in the future, and resources are far from static as a result.

Studies of health and activity have started to use accelerometers over the past decade. This has shown that even very modest levels of activity - on the order of washing dishes and puttering around the garden - have a meaningful correlation with health. This is causing something of a rethinking of the lower end of the dose-response curve for exercise.

So when looking at the correlations between retirement and health, I'm inclined to think that physical activity level has a lot to do with it.

Arguably the best approach to dealing with this sort of thing is not the hair shirt use less medicine line of thinking, but rather to focus much more effort on creating therapies that work more effectively and for more people and under more circumstances. Then you won't see non-beneficial treatments in action so often.

Sadly, much of the present generation of medicine was created in an environment that prioritizes a focus on late stage disease state, discovery of proximate rather than root causes, and adjustment of disease state without addressing root causes. Making a damaged machine work better and longer is really, really hard if you don't fix the damage. Medicine is one illustration of this point.

It is quite amazing to me that someone can seriously suggest that a scientific community with the biotechnology to control aging as a chronic medical condition would somehow lack the biotechnology to defeat inherited and infectious disease.

If you actually spend any time looking at what is going on in the labs, treatments for any and all viral infections, universal cancer therapies, ways to repair some of the cell and tissue damage that causes aging, ways to repair any and all genetic defects, and more, are all on the verge and will emerge over the next decade or two.

So you fix brain plasticity as well. The point of the exercise is identify and revert changes, and loss of synaptic/neural plasticity with age is well known and well studied already.

As to population growth, even putting aside the point that Malthusian predictions have always been wrong, and that there is more than enough food production to feed everyone in the world going forward for even quite large increases in population:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3192186/

"This study explores different demographic scenarios and population projections, in order to clarify what could be the demographic consequences of a successful biomedical war on aging. A general conclusion of this study is that population changes are surprisingly slow in their response to a dramatic life extension. For example, we applied the cohort-component method of population projections to 2005 Swedish population for several scenarios of life extension and a fertility schedule observed in 2005. Even for very long 100-year projection horizon, with the most radical life extension scenario (assuming no aging at all after age 60), the total population increases by 22% only (from 9.1 to 11.0 million)."

Deming's Longevity Fund was at its founding somewhat ahead of the times, as it should given that she put in time at the SENS Research Foundation and related groups back in the day.

The rest of the venture community is beginning to wake up now - if even I, with my limited connections, am aware of a couple of groups raising new venture funds to target the biotechnologies of longevity, then I'm sure there are a bunch more I don't know about.

Expect to see a crop of companies working with the biochemistry of aging over the next few years now that deep pockets like Google, Abbvie, and the Human Longevity backers have expressed their interest with dollars. That sets up all the right signals for acquirers and other liquidity events.

Sadly I imagine that most of these companies will be garbage - either a waste of everyone's time like Elysium or a clever way of getting for-profit investors to pay for fundamental research that goes nowhere other than knowledge generation, like Sirtris.

Still, there are gems in there for those who understand the science well enough to identify high expectation value lines of research. Oisin Biotechnologies, for example, and perhaps UNITY Biotech if they choose a good therapy. Both are aiming to clear senescent cells, which has a lot of backing as an approach.

True. In fairness, that's much harder to do at lower levels of money than either of the options I suggested, despite efforts like labcures.com. You need to know a lot more about the field than you'd need to know in order to give to a non-profit in the space.

The SENS approach to cancer is pretty much to turn off its ability to grow in unlimited fashion. If you could compensate for the side-effects, it would be possible to delete telomerase and ALT genes from humans, which would produce cancer free humans - if cancers can't lengthen their telomeres, they die.

Unfortunately, it would also produce humans would be dependent on some form of periodic telomerase therapy targeted to stem cells, or stem cell replacement, or similar. This might be a net gain in a suitably high-tech environment.

A better approach would be something other than permanent removal of telomerase and ALT genes, but perhaps suppressing them globally for a while, or suppressing them in cancerous tissue only. RNAi or other methodologies are pretty reliable for this sort of thing at the present time in the general sense.

They're actually pretty terrible. It isn't a high bar to do better than the NIH when it comes to supporting new technologies. Almost all important early fundamental research, the high-risk part leading up to new knowledge and potential new technologies, is supported by philanthropy.

The NIH really only funds follow-on work for things that are already known. In order to win a grant you have to have already proven your thesis. It is somewhat ridiculous.

So if you want to delegate your vote, delegate it to a non-profit. Or invest in a startup in the field you care about. Anything other than giving to the NIH.

CAR-T is a step in the right direction for the cancer research establishment, not because it solves the problem noted by the parent comment, but because it offers the prospect of greatly reducing the cost of targeting many different types of cancer.

It is very much the luck of the draw going cancer by cancer as to whether you can pick a target that is more or less likely to be evolved around by the cancer. Leukemias were a lucky hit, but that may or may not hold up for other targets and other cancers as they are put forward.

Which is a good reason to back things like telomere lengthening interdiction. That would work on all cancers, and cancers can't evolve around that dramatic a hurdle, so far as we know. It is a very fundamental set of machinery, and all cancers have to lengthen telomeres in order to stay ahead of the limits to replication.

Some groups are working on blocking the action of telomerase, but to make a viable treatment ALT (alternative lengthening of telomeres) will have to be blocked too, since researchers have already seen telomerase-abusing cancers turn into ALT-abusing cancers.

This seems to miss a very important incentive, which is to change the world in a specific way.

For example there is a growing informal network of angels and VCs associated with the SENS Research Foundation / Methuselah Foundation community and the so-far handful of companies that are emerging from the past years of research funding into treating aging by repairing its root causes. The goal here is as much to produce specific new capabilities in medical science and get them to the clinic as it is to make money. In many cases these investors have the view that the only use for making money is to funnel it back into growing this research and development community.

There are analogous groups in other spaces.

This is an important motivation because it lets you look further than just for-profit funding. If I were launching a fund today, I'd try to set it up as 90% for-profit, 10% non-profit investment, with the latter going to nudge promising research across the line into startup viability. With the right connections in the research community, a group that is split between scientists, advocates, and funding sources can be meaningful minority owners in the creation of an entire new field by shepherding the research and seed funding the startups. Modern day early stage life science research, and proving mouse studies, are so cheap in comparison to later development for the clinic that this is a great investment model.

One reason most people don't do this is that they don't understand how to understand the spaces they invest in at the level of research and seeding new companies, and finding things that are a year or two away from viability, and could be pushed across the line with a little money and coordination, and the people who do understand that typically have little interest in investment. It is very hard to gather the necessary knowledge and will in one room.

This seems pretty silly at first glance. It is just as easy to argue for increased complexity due to stochastic mutational damage and proteopathy followed by a sudden enormous cellular diversity of individual responses to that damage, and responses to the responses by nearby cells. When you can easily pull out data points to argue both sides of an overarching vision that's usually a good sign that the wrong tree is being barked up.

My suspicion, based on limited experience, but still, is that investing in startups purely for the potential gains is the road to a bad end comprising one part disinterest and one part disconnection. Startups are a tool to achieve an end, which is to say some form of change in the world. If you have a very clear view of the change you wish to achieve, that can be useful, and indeed I'd argue it is essential if you want to avoid the aforementioned bad end.

For me, the goal is specific new capabilities in medicine, with a fairly strong opinion on which strategies are worthwhile when it comes to achieving those goals. Everything else flows from that point: I care about getting research done, answering specific questions about whether X works or Y does not work, and then moving working research closer to the clinic.

From the point of view of where the money goes, there is actually little difference between investing in an early stage biotechnology startup and making charitable donations to a late-stage laboratory group. In both cases those funds buy research: use of laboratory resources, the ever-expensive reagents needed for modern research, mice for animal studies, the efforts of scientists, and all the other essentials. There is no rule that says a particular research project has to be carried out before or after the point at which non-profit labwork transitions to for-profit labwork; where the work happens in the typical chronology of the clinical translation of science to medicine is very much a matter of circumstance and the character of those involved.

When you are putting money into research with this philosophy, where the for/non profit split isn't as important as getting the job done, you'll find yourself better placed in the for-profit side.

Investing is something that investors do moderately well - there is a method and a discipline and a body of tradition and knowledge. But it isn't the only thing that investors can do to speed the development of medical science. What the investment community should do, attempts to some degree, but remains very poor at accomplishing, is the process of nudging along pre-commercial scientific efforts, of strategically funding specific research projects in order to produce a new crop of biotech/medtech companies. This seeding of the field can be highly effective, yet for the most part even personally interested investors leave philanthropy in their field to other people. Thus funding for truly radical, high-risk, high-reward new research is next to non-existent. The other side of the coin, targeted funding for medical research projects with excellent prospects, or that are only a few years and a million dollars away from the leap to a candidate therapy and a startup, nudging them into the target zone, is also very thin on the ground.

All of this is to note that the launch of a company happens a long way after the start of the development process, and investors should become involved well before that point if they want to better achieve their goals. Building on what has been learned so far, better and more organized ways to meld philanthropy and investment might be assembled. A community with deep pockets that can build the intricate networking tools and the energetic, highly networked approach to for-profit investment that presently exists should be able to make the leap over the barrier to organize and assist the non-profit research pipeline as well.