Gerontocracy:

Government by a council of elders. Government by old people.

There are many knee-jerk reactions to the prospect of greatly increased healthy human life spans, most based on mistaken beliefs regarding the technologies needed, or mistaken beliefs regarding the way the world actually works - economics, human action, incentives. Some people believe that longer lives will result in stagnation, which is actually one of the more ridiculous and improbably outcomes once you start to pick it apart in any detail. Human society is restless and changeable on timescales far shorter than current lifespans, and the reasons why are rooted in day to day human nature. Our ambitions operate on a horizon of a few years, and that wouldn't change all that much were we to live for centuries. We are driven to influence the world today, now, regardless of the years that lie ahead of us. So the fashions of this year are gone by the next. The idols of popular culture rise and fall with rapidity. The political and business leaders of this decade are gone in the next, displaced by peers. Even corruption and revolution on a grand scale are usually only a matter of a few decades, not lifetimes.

Nonetheless, rationality rarely prevails in knee-jerk reactions - so folk think of stagnation, even in the midst of this boundlessly energetic society we live in, packed wall to wall with constant, ongoing change. A subset of these beliefs on human longevity and stagnation involve the nebulous fear of a future gerontocracy, the rise of a self-perpetuating ruling elite of ageless individuals. Funnily, this is often voiced by people who are, unlike myself, perfectly comfortable with today's Western governments. I say funnily because I have to ask: are not our present societies already gerontocracies? Isn't any civilized society a gerontocracy? Who has had the most time to gather connections, a network, and make good use of them? The old. Who has had the most time to gather resources and invest them? The old. Who has had to most time to become truly talented and sought after? The old. Who has had the most time to work their way through a social hierarchy to challenge its existing leaders? The old. Where then will the elite and the leaders tend to arise? From the old.

Take a look at who just runs and influences companies, governments, knitting circles, successful non-profit initiatives, extended families, and so on and so forth for every human endeavor. Young leaders exist, but they are a minority among the ranks of the old. This is the natural state of affairs for any society that possesses enough technology to make thought and craft more important than strength and vigor.

All that is terrible in our present societies lies in the growing centralization of power, not the chronological age of those eagerly engaged in furthering the road to serfdom and empire. Even as power is centralized, there is still a year by year turnover of figures - even in the most defensible and corruptly secure positions of power and influence. They are largely kicked out by some combination of their peers and the mob in the sort of political anarchy that exists at the top, above the laws made for the little people. It is the rare individual who can stick it out long enough to be removed by the infirmities of age, even now, in this age of human lives that are all too brief in comparison to what is to come.

But back to the point. We live in a gerontocracy, and so did most of our ancestors. Yet change still happens just as rapidly as in past centuries when fewer people lived into later life in the sort of good shape they can manage today. Fear of some sort of comic-book gerontocracy emerging in the future seems, frankly, somewhat silly. But here is an article on the topic that treats such fears with a little more respect than I'm inclined to deploy.

http://io9.com/will-old-people-take-over-the-world-458358266

The human lifespan is set to get increasingly longer and longer. And it's more than just extending life - it's about extending healthy life. If we assume that the aging process can be dramatically slowed down, or even halted, it's more than likely that the older generations will continue to serve as vibrant and active members of our society. And given that seniors tend to hold positions of power and influence in our society, it's conceivable that they'll refuse to be forced into retirement on the grounds that such an imposition would violate their human rights (and they'd be correct in that assessment).

In turn, seniors will continue to lead their corporations as CEOs and CFOs. They'll hold onto their wealth and political seats, kept in power by highly sympathetic and demographically significant elderly populations. And they'll occupy positions of influence at universities and other institutions.

So I asked James Hughes how society could be hurt if an undying generation refuses to relinquish their hold on power and capital. "Again, the question should be, how is society hurt when small unaccountable elites control the vast majority of wealth?," he responded. The age of super-wealthy is pretty immaterial, he says, especially when most of the people in their age bracket will be as poor and powerless as younger cohorts.

Hughes also doesn't buy into the argument that radical life extension will result in the stagnation of society. If anything, he thinks these claims, such as risk-aversion and inflexibility, smack of ageism and simple-minded futurism. "Seniors' brains continue to make stem cells," says Hughes, "and when we are able to boost neural stem cell generation in order to forestall the neurodegeneration of aging, older people will become as cognitively flexible as younger people."

As noted in my comments above, the historical record shows that people at the top are not all that good at staying at the top for extended periods of time. There are always outliers, but they are rare in comparison to the vast majority of leaders and the famous who are just part of the churn, coming and going, displaced and quickly forgotten once their few years are done. The top of a pyramid is a challenging place to stand.

Source:
http://www.fightaging.org/archives/2013/03/we-already-live-in-a-gerontocracy.php

This paper examines some aspects of aging in the liver, giving a general review in the course of getting to a discussion on immune system changes that occur in aging and their influence on the liver. Note the importance of a buildup of unwanted protein byproducts inside liver cells, something that occurs due to the progressive failure of cellular housekeeping components known as lysosomes. You might recall that researchers reversed aspects of liver aging in mice a few years back by boosting lysosomal activity, so as to counteract some of the usual decline.

Although the human liver is not unscathed by the process of aging, the changes it undergoes are minor compared with other organ systems. It has been ascertained that there are no liver diseases specific to advanced age. However, the clinical course and management of liver diseases in the elderly may differ in several aspects from those of younger adults.

Human and experimental studies suggest that, in comparison with other organs, the liver ages fairly well. Aging is however associated with a variety of morphological changes in the liver, but their underlying mechanisms are still unclear. The liver progressively shrinks by 20-40% during the course of a human life, and there is a concomitant age-related decrease in liver volume. The classic gross appearance of the liver in the elderly is known as "brown atrophy", and the brown is due to an accumulation of highly oxidized insoluble proteins, known as lipofuscin, stored into hepatocytes. These accumulations of highly cross-linked protein are thought to relate to chronic oxidative stress and a failure to degrade damaged and denatured proteins. Increasing evidence suggests that lipofuscin interferes with complex cellular pathways.

One of the most important age-related changes in liver function observed in animal models is a significant decrease in regenerative capacity of the liver, but not in the capacity to restore the organ to its original volume. [It] has also been shown that aging is associated with multiple changes in. Elderly humans secrete less bile acid, have increased biliary cholesterol levels, and show an increased oxidative stress that is mainly attributable to a reduced capacity to eliminate metabolically generated superoxide radicals as efficiently as before. The reduction in hepatic blood flow during aging reduces the metabolism of rapidly cleared drugs. Aging of the liver is also associated with impaired metabolism of drugs, adverse drug interactions, and susceptibility to toxins.

Link: http://dx.doi.org/10.1186/1742-4933-10-9

Source:
http://www.fightaging.org/archives/2013/03/a-look-at-the-aging-liver.php

Commentary on various recently published research relevant to the SENS view of biotechnology to repair and reverse aging appears as an occasional feature at the journal Rejuvenation Research. The latest is open access, so take a look at the PDF format paper, containing commentaries such as this one on a method of wrapping enzymes in polymer nanocapsules to ensure their delivery to specific locations within cells or the body:

The accumulation of recalcitrant waste substances in cells' lysosomes is implicated in a wide spectrum of aging-related diseases, including atherosclerosis, age-related macular degeneration (AMD), and many others. Being one of the clearest examples of the build-up of "junk" in aging bodies, it is expected that means to degrade lysosomal waste will be among the first rejuvenation biotechnologies to reach clinical application.

Indeed, the required development time before an effective therapy can be deployed is expected to be so brief that SENS Research Foundation devotes a substantial portion of its budget to identifying and refining enzymes for just this purpose. However, this tight schedule poses a specific problem; it is quite probable that hydrolases effective, for example, against 7-ketocholesterol (the dominant "junk" molecule in atherosclerotic plaque) or A2E18 (predominant in AMD) will be ready for clinical use before safe and effective somatic gene therapy becomes available.

It will therefore be necessary to introduce these garbage-clearing enzymes into patients directly, rather than by genetically engineering the recipient's cells to produce them - an approach termed enzyme replacement therapy, currently in widespread clinical use to treat congenital lysosomal disorders. Of course, enzymes introduced into the body by such methods cannot be replaced once degraded (a particularly rapid fate in the harsh conditions of the lysosome), necessitating regular infusions to maintain their function. The polymer-coating method described in this study enhances the hardiness of the enzymes thus treated, and might be reasonably expected to thus appreciably reduce the required frequency of reintroduction, and/or minimise the dosages required (and hence any side-effects).

Link: http://online.liebertpub.com/doi/pdf/10.1089/rej.2013.1426

Source:
http://www.fightaging.org/archives/2013/03/comments-on-recent-research-relevant-to-combating-aging.php

What is aging? This deceptively simple question will garner you lengthy answers from the scientific community - many different lengthy answers, as it happens, some of which are even long enough to take the form of entire, complete books. There is a lot to be said on aging, and vast repositories of data, and yet there remain numerous different camps with different detailed definitions of aging - it's cause, its progression, and how best to build therapies that might slow or reverse aging.

So you have the definition put forward by Michael Rose and colleagues, or the hyperfunction theories that seem to be gaining ground among researchers of the small programmed aging camp, or the collection of mainstream views - many different interpretations and variants - that paint aging as a matter of accumulated damage.

And that is just on the matter of causes and mechanisms. The territory becomes much more of a jungle once you start down the path of asking whether aging is a disease, or whether it is a bad thing, or whether should be treated and ameliorated through medical science. Believe it or not there remain numerous researchers in the field who believe that aging should be studied but not treated, slowed, or reversed, despite the suffering and death it causes. Here is an open access opinion piece on this topic from Aubrey de Grey, via the Rejuvenation Research journal.

The desperate need for a biomedically useful definition of "aging" (PDF)

Surely everyone who studies the biology of aging fundamentally agrees on what it is they are studying, even if they may prefer somewhat different terminology to define it? I'm afraid you'd be wrong. Disagreement within the field about what aging really is and is not is very far from purely semantic, and the substance of those disagreements leads to profound differences of opinions concerning both what research gerontologists should prioritise and how they should communicate their work to others.

First: is aging a disease? Some gerontologists will just tell you "No, it is separate from age-related diseases". Some will say "No, but it is a risk factor for age-related diseases". Some will say "No, it is the set of precursors of the age-related diseases". Some will say "Yes, it is the set of precursors of the age-related diseases"! Self-evidently, whether X is a Y depends not only on the definition of X but also on the definition of Y, so one might excuse this chaos on the basis of a failure to agree on what is and is not a disease - and there is indeed no such agreement. But it gets worse.

Is aging a thing that is amenable, in principle, to medical intervention? Not if you believe the protestations of such eminent gerontologists as Bruce Carnes and Jay Olshansky, who in a recent paper critiquing (I employ classic British understatement in my choice of words here) various colleagues' work made, in spite of reviewers' efforts to educate them, the assertion that "What Wilmoth fails to acknowledge is that in order to reduce death rates at advanced ages to zero or close to it, our biology would need to be modified" (my emphasis). This sort of language, without stating explicitly that medicine can never maintain the body in a state of health so youthful that death rates will be vastly lower than today, unequivocally seeks to convey that view. So, do other gerontologists agree? Indeed they do not: if any evidence were needed, I may merely cite the fact that almost every mainstream conference on the biology of aging these days has a subtitle referring to delaying or even reversing aging.

Finally, is aging even a bad thing? At least here we find broad consensus among biogerontologists - those who study the biology of aging (though there are a few exceptions). But the same does not apply to all gerontologists: those whose field is more on the clinical, or the sociological, side tend to be among the most viciously and vocally opposed to any talk (let alone action) concerning actually doing anything about aging. As an example, a very senior (and, I am afraid to say, highly influential) clinical gerontologist from Canada recently wrote to me as follows: "I do not wish in any way shape or form to have my name associated with anti-aging medicine, regenerative or restorative medicine or some such". No kidding. I will be interested to discover, at some point, whether she is willing to defend that view publicly.

It should by now be apparent that there is a bit of a problem. Let me emphasise, however, just how much of a problem. At present, translational biogerontology (alternatively, biomedical gerontology) commands an absolutely minuscule proportion of the medical research budget of any industrialised nation. Why? Simply because the idea that postponing aging is a feasible and valuable goal, both socially and economically, has failed - despite the best efforts of many biogerontologists over many decades - to gain any significant traction among funding bodies.

I contend that gerontologists' muddled thinking outlined above concerning what aging really is is actually the number one reason for this failure.

Source:
http://www.fightaging.org/archives/2013/03/in-search-of-a-useful-scientific-definition-for-aging.php

What is aging? This deceptively simple question will garner you lengthy answers from the scientific community - many different lengthy answers, as it happens, some of which are even long enough to take the form of entire, complete books. There is a lot to be said on aging, and vast repositories of data, and yet there remain numerous different camps with different detailed definitions of aging - it's cause, its progression, and how best to build therapies that might slow or reverse aging.

So you have the definition put forward by Michael Rose and colleagues, or the hyperfunction theories that seem to be gaining ground among researchers of the small programmed aging camp, or the collection of mainstream views - many different interpretations and variants - that paint aging as a matter of accumulated damage.

And that is just on the matter of causes and mechanisms. The territory becomes much more of a jungle once you start down the path of asking whether aging is a disease, or whether it is a bad thing, or whether should be treated and ameliorated through medical science. Believe it or not there remain numerous researchers in the field who believe that aging should be studied but not treated, slowed, or reversed, despite the suffering and death it causes. Here is an open access opinion piece on this topic from Aubrey de Grey, via the Rejuvenation Research journal.

The desperate need for a biomedically useful definition of "aging" (PDF)

Surely everyone who studies the biology of aging fundamentally agrees on what it is they are studying, even if they may prefer somewhat different terminology to define it? I'm afraid you'd be wrong. Disagreement within the field about what aging really is and is not is very far from purely semantic, and the substance of those disagreements leads to profound differences of opinions concerning both what research gerontologists should prioritise and how they should communicate their work to others.

First: is aging a disease? Some gerontologists will just tell you "No, it is separate from age-related diseases". Some will say "No, but it is a risk factor for age-related diseases". Some will say "No, it is the set of precursors of the age-related diseases". Some will say "Yes, it is the set of precursors of the age-related diseases"! Self-evidently, whether X is a Y depends not only on the definition of X but also on the definition of Y, so one might excuse this chaos on the basis of a failure to agree on what is and is not a disease - and there is indeed no such agreement. But it gets worse.

Is aging a thing that is amenable, in principle, to medical intervention? Not if you believe the protestations of such eminent gerontologists as Bruce Carnes and Jay Olshansky, who in a recent paper critiquing (I employ classic British understatement in my choice of words here) various colleagues' work made, in spite of reviewers' efforts to educate them, the assertion that "What Wilmoth fails to acknowledge is that in order to reduce death rates at advanced ages to zero or close to it, our biology would need to be modified" (my emphasis). This sort of language, without stating explicitly that medicine can never maintain the body in a state of health so youthful that death rates will be vastly lower than today, unequivocally seeks to convey that view. So, do other gerontologists agree? Indeed they do not: if any evidence were needed, I may merely cite the fact that almost every mainstream conference on the biology of aging these days has a subtitle referring to delaying or even reversing aging.

Finally, is aging even a bad thing? At least here we find broad consensus among biogerontologists - those who study the biology of aging (though there are a few exceptions). But the same does not apply to all gerontologists: those whose field is more on the clinical, or the sociological, side tend to be among the most viciously and vocally opposed to any talk (let alone action) concerning actually doing anything about aging. As an example, a very senior (and, I am afraid to say, highly influential) clinical gerontologist from Canada recently wrote to me as follows: "I do not wish in any way shape or form to have my name associated with anti-aging medicine, regenerative or restorative medicine or some such". No kidding. I will be interested to discover, at some point, whether she is willing to defend that view publicly.

It should by now be apparent that there is a bit of a problem. Let me emphasise, however, just how much of a problem. At present, translational biogerontology (alternatively, biomedical gerontology) commands an absolutely minuscule proportion of the medical research budget of any industrialised nation. Why? Simply because the idea that postponing aging is a feasible and valuable goal, both socially and economically, has failed - despite the best efforts of many biogerontologists over many decades - to gain any significant traction among funding bodies.

I contend that gerontologists' muddled thinking outlined above concerning what aging really is is actually the number one reason for this failure.

Source:
http://www.fightaging.org/archives/2013/03/in-search-of-a-useful-scientific-definition-for-aging.php