Michael Fossel Michael is President of Telocyte

August 10, 2017

Progeria and Telomerase

Recently, John Cooke at the Houston Methodist Research Institute, showed that telomerase, when expressed in cells from progeric children, caused a “substantial physiologically relevant and meaningful effect on the lifespan and function of the cells.” As many of you know, progeria is a disease in which young children appear old, with baldness and osteoarthritis, and usually die of advanced cardiovascular disease, such as heart attacks, typically around age twelve. In short, they appear to have extremely rapid aging. Cooke’s results suggested that telomerase might offer a therapy. Oddly enough, both Cooke and the media described this finding as “surprising”.

While these results are promising, they are hardly surprising. In 1996, I published a book going into this prospect in detail, then wrote the first medical papers on this the medical potential in JAMA in 1997 and 1998. This was followed up with a medical textbook which explored the entire area in 2004, and another book in 2015 that described the medical potential of telomerase. What is truly surprising is not the most recent results, but that anyone finds the results at all surprising.

While not actually surprising, they present a bitter irony, in that any number of deaths, including deaths of progeric children, might have been prevented and may still be prevented if we only understand and act upon what we have known for two decades and which Cooke’s results only highlight again.

The irony – and my exquisite personal frustration – is that I proposed this approach annually in our global meetings for progeric children, starting twenty years ago. For about a decade, beginning several years before the turn of the millennium, I had been part of the annual global reunion of progeric children. Each year, we gathered with perhaps three dozen progeric children and their families from around the world, giving them a chance to meet one another, to talk with experts, and … to feel normal among other children and families who had the same problems. In 1999, among those progeric children was a young boy, whose parents were both physicians, and who were desperate to find a cure for progeria. Although I explained the potential of using telomerase as an intervention, they founded the Progeria Research Foundation and aimed it solely at genetic markers rather than epigenetic intervention. They managed to get significant funding through the NIH, fund raising, and government contacts in order to fund a set of studies that localized the genetic error responsible for progeria. As I predicted, none of the subsequent therapies based on their approach have had any effect on the disease. Worse yet, and like all the other progeric children I have known over the years, their son died of progeria. Had we gone straight to telomere-based interventions rather than taking the detour, many progeric children – not merely their son — might have been treated more effectively.

John Cooke and his colleagues have done well to show that they can reverse the problems seen in progeric cells, yet others have gone further. Maria Blasco’s group, for example, has shown that she can not merely reset aging in cells, as Cooke’s group has, but can do the same in animals. Moreover, we are collaborating with her group to take this approach in our upcoming human clinical trials next year, initially aiming at Alzheimer’s disease.

The fact that this comes as a surprise, given what we have known about the potential of telomerase for more than 20 years is a tragic example of wasted opportunities, wasted funding, and wasted lives. Telomerase was shown to reverse aging in cells 20 years ago; telomerase showed its value in animals 5 years ago; Telocyte is ready to show the benefits of telomerase in human trials next year.

November 22, 2016

Teaching Cells to Fish

Aging is the slowing down of active molecular turnover, not the passive accumulation of damage. Damage certainly accumulates, but only because turnover is no longer keeping up with that damage.

It’s much like asking why one car falls apart, when another car looks like it just came out of the showroom. It’s not so much a matter of damage (although if you live up north and the road salt eats away at your undercarriage, that’s another matter), as it is a matter of how well a car is cared for. I’ve see an 80-year-old Duesenberg that looks a lot better than my 4-year-old SUV. It’s not how well either car was made, nor how long either car has been around, but how well each car was cared for. If I don’t care for my SUV, my SUV rusts; if a car collector gives weekly (even daily) care to a Duesenberg, then that Duesenberg may well last forever.

The parallel is apt. The reason that “old cells” fall apart isn’t that they’ve been around a long time, nor even that they are continually being exposed to various insults. The reason “old cells” fall apart is that their maintenance functions slow noticeably and that maintenance fails to keep up with the quotidian damage occurring within living cells. If we look at knees, for example, the reason that our chondrocytes fail isn’t a matter of how many years you’ve been on the planet, nor even a matter of how many miles a day you spend walking around. The reason chondrocytes fail is because their maintenance functions slow down and stop keeping up with the daily damage. As it turns out, that deceleration in maintenance occurs because of changes in gene expression, which occur because telomeres shorten, which occur because cells divide. And, not at all surprisingly, the number of those cell divisions is related to how long you’ve been on the planet (how old you are) and how many miles you walk (or if you play basketball). In short, osteoarthritis is distantly related to your age and to the “mileage” you incur, but not directly so. The problem is not really the age nor is it the mileage; the problem is the failure to repair the routine damage and THAT failure is directly controlled by changes in gene expression.

So what?

The telomeres and gene expression may play a central role, but if your age and the “mileage” is distantly causing all those changes in cell division, telomere lengths, gene expression, and failing cell maintenance, then what’s the difference? Why bother with all the complexity? Why not accept that age and your “mileage” are the cause of aging diseases and stop fussing? Why not simply accept age-related disease?

Because we can change it.

The question isn’t “why does this happen?” so much as “what can we do about it?” We can’t change your age and it’s hard to avoid a certain amount of “mileage” in your daily life, but we CAN change telomeres, gene expression, and cell maintenance. In fact, we can reset the entire process and end up with cells that keep up with damage, just as your cells did when you were younger.

Until now, everyone who has tried to deal with only the damage (or the damaged cells) failed because they focused on damage rather than focusing on repair. For example, if you focus only on cell damage (as most big pharma and biotech companies do when they go after beta amyloid or tau proteins in trying to cure Alzheimer’s disease), then any clinical effect is transient and the disease continues to progress – which is why companies like Eli Lily, Biogen, TauRx, and dozens of other companies are frustrated. And small wonder. Or if you focus only on the damaged cells (and try removing them), then the clinical effect is not only transient, but will end up accelerating deterioration (as discussed in last week’s blog, see figure below) – which is why companies like Unity will be frustrated. Their approaches fail not because they don’t address the damage, but because they fail to understand the deceleration of dynamic cell maintenance that occurs with age – and fail to understand the most effective single clinical target. The key target is not damage, nor damaged cells, but the changes in gene expression that permit that damage, and those damaged cells, to lead to pathology. We can’t cure Alzheimer’s or osteoarthritis by removing senescent cells, but we can cure them by resetting those same cells.

Why you shouldn't kill senescent cells.

Why you shouldn’t kill senescent cells.

In the cases of removing senescent cells (an approach Unity advocates), wouldn’t it be better to remove the damaged cells and then reset the telomeres of those that remain? But why remove the damaged cells if you can reset them as well, with the result that they can now deal with the damage and remove it – as well as young cells do?

Why remove senescent cells at all?

While you could first remove senescent cells, then add telomerase so that the remaining cells could divide without significant degradation of function, why would you bother? You could much more easily, more simply, and more effectively treat all the cells in an aging tissue, reset their aging process and have no need to ever remove senescent cells in the first place. Instead of removing them, you simply turn them into “younger” and more functional cells. For an analogy, imagine that we have a therapy that could turn cancer cells into normal cells. If that were true, why would anyone first surgically remove a tumor? If you could really “reset” cancer cells into normal cells, there would be no need to do a surgical removal in the first place. While there is no such therapy for cancer cells, the analogy is still useful. Removing senescent cells is not only counter-productive, but (if we reset gene expression) entirely unnecessary.

Removal is unnecessary (both as to cost and pathology), risky, and medically contraindicated. You’d be performing a completely unnecessary procedure when a more cost-effective and reliable procedure was available. It would be exactly like removing your tonsils if you already had overwhelming data showing that an antibiotic was reliable, cheap, and without risk.

A cell with full telomere lengths – regardless of prior history – is already superior. The accumulated damage is not a static phenomenon, but a dynamic one. Reset cells can clean up damage. This is not merely theory, but supported well in fact, based on both human cells and whole animal studies. We shouldn’t think of damage as something that merely accumulates passively. All molecules are continually being recycled. The reason some molecular pools show increased damage isn’t because molecules denature, but because the rate of turnover slows, thereby allowing denatured molecules (damage) to increase within the pool.

Try this analogy: we have two buildings. One is run by a company that invests heavily in maintenance costs, the other is run by a company that cut its maintenance budget by 50%. The first building is clean and well-kept, the second building is dirty and poorly-kept. Would you rather raze the second building and then rebuild it or would you rather increase the maintenance budget back to a full maintenance schedule and end up with a clean building? This is precisely the case with young versus old cells: the problem is not the dirt that accumulates, the problem is that no one is paying for routine maintenance. There are cells that are “too senescent” to save, but almost all the cells in human age-related disease can be reset with good clinical outcome. There is no reason to remove senescent cells any more than (in the case of a dirty building), we need to send in the dynamite and bulldozers.

Too often, we try to approach the damage rather than looking at the longer view. Instead of addressing the process, we address the outcome. It’s like the problem that often occurs in global philanthropy, where we see famine and think we can solve the problem with food alone. While the approach is necessary – as a stopgap – many are surprised to find that simply providing free food for one year, results in bankrupt farmers and recurrent famines in the following years. Or we provide free medical care in a poor nation, then wonder why there is a dearth of medical practitioners in years to come, without realizing we have put them out of business and accidentally encouraged them to emigrate to someplace they can make a living and feed their families. We intend well, but we perpetuate the problem we are desperately trying to solve. Treating famine or medical problems, like treating the fundamental causes of age-related disease, is not simple and cannot be effectively addressed with band aids and superficial interventions, such as addressing damage alone or removing senescent cells. Effective clinical intervention – like effective interventions in famine or global healthcare – require a sophisticated understanding of the complexity of cell function, an understanding of the dynamic changes that underlie age-related pathology.

An adage (variously attributed to dozens of sources) about fish and fishing provides a useful analogy here:

Give a man a fish, and you feed him for a day.

Teach a man to fish, and you feed him for a lifetime.

If we want to intervene effectively in age-related diseases – whether Alzheimer’s, osteoarthritis, or myriad other problems of aging – we shouldn’t throw fish at medical problems.

We should teach our cells to fish.


November 8, 2016

Revolution in Medicine

Every pharmaceutical firm, every biotech company, every hospital, every clinic, and every conference makes revolutionary claims, albeit seldom with any logic or thought behind the claims. Every product is a “revolutionary” therapy, every surgery is a “revolutionary” procedure, and everyone has a “revolutionary” way of looking at clinical medicine. Reality is strikingly different. Despite claims to the contrary, almost all advances in medicine are accretionary, not revolutionary. About sixty percent of all FDA applications for “breakthrough” status are turned down for not being breakthroughs, but merely incremental advances (if that). Even granting a third of these applications is overly kind, but then breakthroughs, like revolutions, are remarkably rare. I am reminded of my years consulting for hospitals around the world, where I was entertained to find every hospital, in every town, in every country, bragging that they were ranked as “one of the best ten hospitals!” Sometimes, they bragged that they were THE best hospital. Somehow, it appears that thousands of hospitals are among the best ten hospitals and hundreds are THE best hospital. In the entire world or on that block?

It clearly depends on who’s counting and on who does the ranking.

Therapies are much the same: they are seldom “the best” (in the world?) and they are almost never revolutionary. To the contrary, almost all current therapy is based on incremental change: we find a slightly better statin, an antibiotic with slightly less resistance (at least this year), and a procedure with a slightly lower risk. We rank our interventions by statistical significance and we deal with percentage points in the adverse effect profile. Scarcely the stuff of revolution.

We can do better; much better. To do so, however, requires both an open mind and a very disciplined one. We need both creativity and intelligence to envision a path to revolutionary therapies. If we do so, we may be able to cure diseases that are thought to be “incurable”, a true revolution I both clinical thinking and clinical practice.

Many people, in a totally practical vein, think of diseases in three categories. The first includes those diseases that we have “cures” for, by means of vaccines, antibiotics, and routine surgeries (think of tetanus, cellulitis, and appendicitis). The second category includes diseases for which we have no cure yet, but for which we see a cure on the horizon (think of treating sickle cell anemia with gene therapy). This second category includes type 1 diabetes: while we use insulin to good effect, we eagerly imagine the days when we simply replace the missing cells in the pancreas and truly cure diabetes. While we have – or imagine that we may soon have – true cures for these diseases in both the first two categories, the third category brings a sense of futility. When it comes to age-related disease (think of Alzheimer’s disease, cardiovascular disease, osteoporosis, etc.), we are caught up by the assumption that while we can treat symptoms, use grafts or stents, lower the risk factors, or replace the damaged part (a total knee replacement comes to mind), we will never be able to entirely prevent or cure the underlying disease. After all, they’re simply the outcome of aging, yes? And who could possibly change the aging process?

Oddly enough, we already have.

We first showed we could reverse cell aging in 1999, followed by the reversal of tissue aging (in the laboratory) in the following few years. The question isn’t “can we reverse the aging process in human cells or tissues”, but “can we reverse the aging process in human patients”? Can we take someone with age-related disease, treat them, and reverse the disease reverse at the cellular and genetic levels? Can we prevent and cure age-related disease? Based on both theory and animal data, the answer is almost certainly to be “yes, we can”. All it requires is intelligence, a modicum of work, and a small commitment of funding.

Instead of treating Alzheimer’s as something to live with, we can treat it and have it be something we can live without. Only then we will have a true revolution.

November 1, 2016

Making Things Worse

Imagine a factory which is operating at capacity, with a thousand workers. Some of the workers are doing a great job, but some are ill and not working hard. In fact, they are actively interfering with those who are working hard. In this factory, you can’t hire anyone new, so you have two choices: you can fire the bad workers or you try to improve their health. If you simply fire the bad workers, you have increased the work load for those who remain. Not surprisingly, they begin to get tired and ill as well, so the factory ends up failing even faster and before you know it, everyone is out of a job. On the other hand, if you can improve the health (and the attitude) of the workers who are tired and ill, the factory can become a success.

The factory is human tissue; the workers are your cells.

Let’s look at an example, such as the cells in your knee. Over time, the chondrocytes divide, become gradually more senescent, and begin to fail. The result is osteoarthritis. If you have mild osteoarthritis, you might (naively) consider simply removing senescent cells. This reliefs some of the inflammation and removes the cells that aren’t doing a good job (the tired workers), but the result is that you’ve just asked all the remaining cells to take up the slack (increased the work load for the remaining factory workers). In order to replace the cells that you’ve removed, the remaining cells now have to divide, which accelerates their own senescent changes, and hastens the failure of the entire tissue. In the case of the knee joint, the osteoarthritis improves temporarily, but you’ve just accelerated osteoarthritic changes in the long run. Instead of a slow joint failure, you’ve ensured that it fails even faster.

Several people have, in a charming burst of innocence, recommended that we do just that. Instead of resetting senescent cells and restoring cell and tissue function, they want to remove senescent cells in older tissues. Their hope is understandable, but their understanding is simplistic. Studies show that you may see temporary improvement in inflammation and secretory profiles, but what about long term risks? The problem is that those who want to kill off senescent cells lack a full appreciation of the dynamic pathology and the cellular consequences. They offer a simplistic view, but biology is seldom simplistic.

Why you shouldn't kill senescent cells.

Why you shouldn’t kill senescent cells.


Consider the knee again. A common concern is that of chondrocyte senescence (leading to osteoarthritis) in professional basketball players. Because of repetitive high-impact trauma, they lose chondrocytes at an accelerated rate compared to people whose knees are not subject to traumatic cell loss. The remaining chondrocytes divide to replace the lost chondrocytes, accelerating telomere loss, and accelerating osteoarthritic changes. The clinical result is due to tissue failure at an early age.

Those who are trying to treat tissue senescence by selectively removing senescent cells (instead of resetting them to a normal pattern of gene expression) are causing a transient improvement in tissue function, coincident upon the removal of dysfunctional, senescent cells (temporarily decreasing inflammatory biomarkers, for example), but the longer-term result is to accelerate cell senescence in all remaining cells. The result is a transient hiatus in inflammation and other biomarkers of cell senescence, followed by a more rapid decline in cell and tissue function. In the case of OA, for example, the outcome is to relief symptoms temporarily, only to then ensure a more rapid failure of the joint.

Our analogy remains apt. If you have a group of workers in a factory, some of whom are suffering from fatigue and are no longer producing, you have two possible interventions. Intervention #1 might be to fire all the tired workers, but the long-term result is that you increase the workload and failure rate among the remaining workers. Intervention #2 would be to find a way to restore the energy and interest among those workers who are fatigued. The analogy is a loose one, but the outcomes are predictable. Removing the “tired” cells within a tissue will accelerate pathology. Resetting the “tired” cells within a tissue will resolve pathology.

If you want to cure age-related disease, the solution is not to kill senescent cells, but to reset their gene expression to that of young cells.


August 8, 2016

Regenerative Medicine: What Is It? Where Is It Going?

What is regenerative medicine?

To bystanders, regenerative medicine might be merely a catch-all category or simply a current medical fashion. The reality, however, is that regenerative medicine represents a conceptual, material, and historical transformation of human medical care. Even the key researchers and clinicians who are moving this field ahead are often so busy in advancing the technology that they are less aware of the extraordinary changes that they represent, changes that are about to change the face of human medicine forever.

Regenerative medicine has marked differences, both conceptual and concrete differences, when compared to previous approaches to clinical intervention. These differences not only define the field, but they point our way to future progress and, frankly, to improvements in our health and in our lives.

The conceptual key is that regenerative medicine results in long-term (rather than transient) clinical improvements. Regenerative medicine is just that: an intervention that re-generates. Effective regenerative interventions change the body itself – and not merely a set of biomarkers or symptoms. Bluntly, regenerative medicine aims to improve biological function, rather than merely attempting to normalize abnormal biomarkers or symptoms of biological dysfunction. Even admitting the often impressive utility and efficacy of our standard medical interventions to date – for certainly we have come a long way in our ability to treat human disease – such approaches act as pharmacological Band-Aids. In contrast, regenerative medicine seeks to optimize the underlying genetic, cellular, and tissues processes that go awry.

Nor is this the only conceptual difference, for the time course is equally different. Standard clinical interventions generally have transient effects, for example in modifying inflammation, cholesterol, glucose levels, etc., while regenerative interventions generally have long-term (even permanent) changes to tissue and organ function. When most standard interventions may last for hours to days, regenerative interventions may last for years to decades. Even “definitive” surgical approaches (CABG, joint replacements, etc) have no effect upon the underlying disease process and are often merely recurrent stopgaps. Why replace an artificial joint (every decade or so), if we can possibly regrow a normal joint that might last a lifetime?

At its conceptual core, regenerative medicine offers us a more accurate and enlightened view of biological function. Regenerative medicine encompasses a view of biology that is active and dynamic, a view in which we aim to alter the processes rather than the products of biology. Consider diabetes, in which a regenerative approach strives to recreate normal islet cell function, where standard approaches strive to manage glucose levels. The difference is critical to understanding the efficacy of regenerative medicine: it views pathology as a dynamic process and aims to alter the process itself, rather than focusing on the products of such processes and aiming to alter the clinical results of those processes. The same pertains to surgical interventions in which regenerative medicine aims to alter the process of joint failure, rather than the product of joint failure. Regenerative medicine would regenerate a normal joint, where standard approaches implant an artificial joint.

Essentially, regenerative medicine aims to reset biological processes to those of a normal, healthy body.

The material features of regeneration medicine are equally distinctive. Instead of employing what are current called “small molecular” approaches, regenerative medicine uses “large molecular” approaches, generally by employing genes, stem cells, and other large biological structures. We might legitimately include immunization in this category: it not only employs a large biological structure (i.e.., an active virus or a complex set of antibodies), but it also results in a long-term change to the organism (i.e., improved immunity). Contrast this approach to the more common “small molecular” approach, typified by the use of non-steroidal anti-inflammatories, statins, blood pressure medications, antibiotics, etc. While many such molecules are fairly complex and certainly not simple, nor are they large-scale biological structures such as viral vectors, plasmids, genes, or stem cells.

Regeneration medicine is typified by two common approaches: genes and cells. In either case, these interventions are large and active biological structures rather than small and passive chemical structures. Genes and cells do not merely interact with biological structures, they ARE biological structures. They not only interact with genes and cells, they ARE genes and cells.

The historical perspective on regenerative medicine is enlightening. What can the past tell us and what does the future hold? An apt historical analogy is that of infectious disease, particularly when we compare antibiotics and immunization. No one would be so naïve as to underestimate the value of antibiotics, but nor should we underestimate the limits of antibiotics. Faced with most viral infections, such as polio, tetanus, or diphtheria, antibiotics are ineffective. Those same viral infections are readily preventable, however, by immunization, using large and active biological structures (whether antigens or live virus).

Immunization is essentially a form of regenerative medicine, in that it results in a long-term change in the human body, a change that results in long-term health. The one difference is that immunizations don’t “re-generate” so much as they “generate” a healthier organism. Nonetheless, the similarity in addressing basic biological functions, in having a long-term effect, and in using large, active biological structures places immunization an historical forerunner for regenerative medicine. Consider a further analogy, that of Ebola. During the height of the Ebola epidemic, small molecular approaches (IV fluid, pressor support, etc) were useful, but far from optimal. Only an effective Ebola vaccine promises to lower the fatality rate into the single digit percent range. In viral infections (as we look backwards) and for the entirety of medicine (as we look forward) standard small molecular approaches are simply not good enough.

Such is the past, but what of the future? Our current standards of medical care cannot reasonably be considered optimal standards of care. We can do better, but only by moving to a regenerative approach. The upcoming standards of medical care will encompass two main approaches: genetic interventions and cellular interventions. In the first case, we will deliver both genes meant to replace pathologic genes and genes that are intended to reset gene expression. In the second case, we will deliver cells that are meant to replace pathologic (or absent) cells.

Genetic interventions encompass both genetic and epigenetic optimization. While the bulk of interest is currently focused on gene changes, remember that genes that regulate expression are far more important than genes that express proteins, both clinically and in terms of percentage of genes in our genome (we have 10-20 times more regulatory genes than we have protein-expressing genes). Although 20th century medicine has made dramatic inroads in our understanding of genes and disease, it remains to the 21st century to move into the far more difficult – and more important – task of understanding patterns of gene expression. In short, it is not genetics, but epigenetics that will prove to be the key to medical interventions. Viral delivery, telomere effects, cell senescence, and a host of other factors will define what we will soon be capable of. We have scarcely begun to enter this complex and confusing field.

Cellular interventions encompass a spectrum of cells, from somatic cells to pluripotent stem cells – and the entire gamut in between those extremes. It has become clear that pluripotent stem cells need not derive from fetal sources, but equally clear that our understanding of the complex path from stem cell to somatic cell is still inadequate – although increasing by the month.

Using an historical perspective to project forward, we begin to see where we can – finally – begin to address diseases that we have long ignored as being “facts of life”, such as the diseases of aging. Although public understanding (indeed, even academic understanding) lags behind the tantalizing and growing data, there is mounting evidence that we will be able to slow, stop, prevent, and even reverse diseases that we have no current treatment for. Consider, for example, osteoporosis. Until now, we have had no therapy that alters the clinical course that begins in the aging osteocyte and the bony matrix. Likewise, our treatment for osteoarthritis, joint replacement, may have value to the patient, but is an admission of failure when we realize that we have no therapy that alters the clinical course of this pathology, that begins in the aging chondrocyte and its matrix either. Arterial disease, Alzheimer’s disease, and a host of other diseases, almost all of which appear to be linked to basic cellular-related aging processes, are fast becoming viable targets for the advances of regenerative medicine.

From a purely practical perspective, how will a regenerative approach change medical care? Currently, medicine is – to a large extent – organized by organ (nephrology, neurology, cardiology, dermatology, etc.), although with an overlay based on the type of intervention (surgical versus medical). At the moment, regenerative medicine is something of a step-child, although gaining traction yearly. Although the approach is innovative, the tools themselves are adaptable within the current framework of medical specialties. There is, for instance, no reason that gene or cell therapy cannot be adopted by and adapted to most current medical specialties, a process that will come to completion within the coming two decades. Regenerative medical techniques equally become the intervention-of-choice for the pulmonologist, the gastroenterologist, or the endocrinologist. For medical specialties, regenerative medicine is an approach which is largely specialty-agnostic.

Surgical specialties, however, will fare a bit differently: where is the need for cardiovascular or orthopedic surgical approaches when we can regenerate both normal coronary arteries and normal joints? Over the next two decades, the face of surgical practice will change rapidly and will lose many of the most common procedures, as regenerative medicine makes effective inroads. Yet there will remain a place for both standard medical care (small molecular drugs) and for surgical procedures, even within a transformed medical landscape. The landscape will continue to change, requiring rapid adaptation for specialties and their practitioners as our knowledge and our capacity to intervene evolve.

Ultimately – if the word is even remotely appropriate to the future of medicine – medical care will still be left with two prongs: a medical approach that fixes the genetic, epigenetic, and cellular problems and a surgical approach that deals with acute, externally imposed disasters, such as trauma. The role of the first specialty will be to deal with non-emergent and known problems at cellular levels. The role of the second specialty will be to deal with emergent and largely unpredictable problems at the organ (rather than cellular) level. The parallel with the modern division between medicine and surgery is apt, but the tools will have evolved, as will the ability to not merely ameliorate, but actually cure disease and to optimize health.

If we are to define regenerative medicine, we might best understand its conceptual underpinnings, its materially different approach, or the historical inflection point that it now represents. In the venue of human disease, regenerative medicine thinks differently, uses different tools, and represents an historic sea-change. Looking at it practically, however, the most striking feature – and perhaps the defining feature – of regenerative medicine is that it offers all of us a more compassionate and a far more effective medical future.

This article is cross-posted at Regenera Global: http://bit.ly/2aMPKIq


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