Why Seek to Classify Aging as a Disease?
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There is a growing determination in some portions of the aging research community to obtain a formal classification of aging as a disease. This means different things to different people, and there are numerous independent regulatory or classification bodies involved in defining and declaring disease. It is a highly politicized process in wealthier regions of the world, tending to involve lining the pockets of politicians and, indirectly, their appointees and allies in regulatory agencies. It takes years to make any sort of progress - just look at ongoing efforts to have the age-related muscle loss known as sarcopenia defined as a disease rather than normal aging in the US regulatory system. That has been underway for nearly as long as I've been an advocate for this cause, with no end in sight, and at a cost of untold millions and wasted years that could have been spent on getting a treatment working and out there in the clinics.

The incentive is there for scientists and research institutions to have aging declared a disease because that opens doors to funding sources, and permits treatments aimed at controlling aging to run through the regulatory process at all. The FDA does not consider aging to be a medical condition at this time, and this position must change in order to allow any sort of meaningful development pipeline to form: everything that happens in cutting edge aging research today happens despite the fact that no-one is permitted to go out there and directly commercialize a treatment. As you might imagine that has a considerable damping effect on funding. I'd prefer change to involve tearing down the FDA and all similar bodies, but most people just want to see a little adjustment: to petition the powers that be until they grudging allow you just that little extra degree of freedom within the straitjacket.

Whether or not aging is a disease from the point of medical philosophy or dictionary definition is somewhat beside the point in comparison to issues of money and issues of freedom to act within the regulatory system. Not that this stops people from pouring on the philosophy, and any other argument to hand, in service of trying to change present regulation:

It is time to classify biological aging as a disease

Is aging a disease? Traditionally, aging has been viewed as a natural process and consequently not a disease. This division may have, in part, originated as a way of establishing aging as an independent discipline of research. Some authors go as far as to create a division between intrinsic aging processes (termed primary aging) and diseases of old age (termed secondary aging). For example, photoaging, the accelerated deterioration of skin as a result of UV rays during one's lifetime, is considered by dermatologists as a condition leading to pathology. In contrast, chronological skin aging is accepted as the norm. As well as being seen as separate from disease, aging is looked at as a risk factor for developing disease. Interestingly, the so-called "accelerated aging diseases" such as Hutchinson-Gilford Progeria Syndrome, Werner syndrome and Dyskeratosis Congenita are considered diseases. Progeria is considered a disease but yet when the same changes happen to an individual 80 years older they are considered normal and unworthy of medical attention.

Additionally, normal in a medical context is generally defined as no deviation outside of the normal reference range for that age and sex, whilst diseases are seen as deviation from this normal condition for that age and sex. Thus someone with a blood pressure of below 120/80 is seen as normal while a blood pressure above 140/90 or below 85/55 is abnormal and a sign of disease. The stratification of reference ranges for age is needed to distinguish fully developed adults from still developing children. Aging as the passage of time and the accumulation of wisdom is not undesirable; the physiological decline that accompanies the process, however, most certainly is.

Whilst aging is a nearly universal occurrence, it should be noted that other medical problems such as muscle wastage leading to sarcopenia, reduction in bone mass and density leading to osteoporosis, increased arterial hardening resulting in hypertension, atherosclerosis, and brain tissue atrophy resulting in dementia, all of which are nearly universal in humans, are classified as diseases in need of medical interventions. Also, autopsy studies indicate that amyloidosis may be almost universal in elderly people and, in autopsies performed by the Supercentenarian Research Foundation (SRF), amyloidosis has been identified as the cause of death in about 70% of people over 110 years of age. Should we remove amyloidosis from medical textbooks as an age-related disease just because it happens to occur in almost every elderly subject?

While most still seem to consider aging not to be a disease others have started to question this position. Some have argued that aging should be considered a disease, a syndrome or a 'disease complex'. Whilst many aging researchers have openly declared that the universality of the aging process means it is not a disease, aging fits the given medical definition of a disease. There is no disputing the fact that aging is a 'harmful abnormality of bodily structure and function'. What is becoming increasingly clear is that aging also has specific causes, each of which can be reduced to a cellular and molecular level, and recognisable signs and symptoms.

Researchers write: "In short, not only does aging lend itself to be characterised as a disease, but the advantage of doing so is that, by rejecting the seeming fatalism of the label 'natural', it better legitimises medical efforts to either eliminate it or get rid of those undesirable conditions associated with it". The goal of biomedical research is to allow people to be "as healthy as possible for as long as possible". Having aging recognized as a disease would stimulate grant-awarding bodies to increase funding for aging research and develop biomedical procedures to slow the aging process. Indeed, others have stated that calling something a disease involves the commitment to medical intervention. Furthermore, having a condition recognized as a disease is important to have treatment refunded by health insurance providers.

We believe that aging should be seen as a disease, albeit as a disease that is a universal and multisystemic process. Our current healthcare system doesn't recognize the aging process as the underlying cause for the chronic diseases affecting the elderly. As such, the system is setup to be reactionary and therefore about 32% of total Medicare spending in the Unites States goes to the last two years of life of patients with chronic illnesses, without any significant improvement to their quality of life. Our current healthcare system is untenable both from a financial and health and well-being prospective. Even minimal attenuation of the aging process by accelerating research on aging, and development of geroprotective drugs and regenerative medicines, can greatly improve the health and wellbeing of older individuals, and rescue our failing healthcare system.

A Collection of Recent Mitochondrial Research
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Mitochondria are the power plants of the cell, a herd of cell components evolved from symbiotic bacteria that are responsible for generating energy supplies to power cellular processes, among other tasks. Mitochondria are important in aging, and their dysfunction is involved in many age-related conditions; that much is the consensus in the scientific community. After that, however, there is much ongoing debate and a rapid generation of new papers when it comes to the details of what exactly it is that matters, which aspect of age-related mitochondrial changes are most important, and what the various chains of cause and consequence look like.

There are numerous different research perspectives to muddy the waters, of course. Not every wise man is looking at the same part of the elephant. For example, scientists primarily interested in slowing aging via some form of drug-based therapy tend to look at mitochondria and aging through the lens of cellular housekeeping and mitohormesis. In some genetic or other interventions shown to extend healthy life spans in laboratory species, mitochondria emit more reactive molecules in the course of supplying the cell with stored chemical energy, which causes cells to react with greater housekeeping efforts - and the result is a net gain in reduction of damage. There are other perspectives, however, leading on from variants of the mitochondrial free radical theory of aging in which mitochondrial DNA damage is seen as the start of a chain of consequences that leads to malfunctioning cells. Mitochondria need the right protein building blocks in order to function, and if the genes encoding those proteins are broken, then failures begin to occur. Some of the SENS rejuvenation research programs follow on from that theory, and so attempt to ensure that even with DNA damage, the proteins will be available. There are other potential approaches to repair and workaround as well.

These are not the only viewpoints. Many researchers have very narrow interests in mitochondrial function with respect to one specific age-related condition, and are focused down on that one thin slice of biochemical complexity. Then there are those scientists who work to catalog natural variations in longevity and their genetic causes, engaged in identifying a contribution caused by different mitochondrial haplogroups through surveys of population data. Were scientists more minded towards intervention this could be the starting point on the road to developing a better set of mitochondrial DNA, an improved, optimized version that could be provided via gene therapy. Not as important as learning how to fix the set of mitochondrial DNA we have, of course: it doesn't much matter that your engine is more fuel-efficient if you still cannot repair it.

But you get the picture. Mitochondria research is a very active field, with a lot of different goals, interests, and back and forth at the cutting edge. New data arrives on a weekly basis, and always something in there to disagree with. Here is a small collection of some recent papers, which should give you an insight into how things go in this slice of aging research.

Reconsidering the Role of Mitochondria in Aging

Mitochondrial dysfunction has long been considered a major contributor to aging and age-related diseases.The Mitochondrial Free Radical Theory of Aging postulated that somatic mitochondrial DNA mutations that accumulate over the life span cause excessive production of reactive oxygen species that damage macromolecules and impair cell and tissue function. Indeed, studies have shown that maximal oxidative capacity declines with age while reactive oxygen species production increases. The hypothesis has been seriously challenged by recent studies showing that reactive oxygen species evoke metabolic health and longevity, perhaps through hormetic mechanisms that include autophagy.

The importance of mitochondrial biology as a trait d'union between the basic biology of aging and the pathogenesis of age-related diseases is stronger than ever, although the emphasis has moved from reactive oxygen species production to other aspects of mitochondrial physiology, including mitochondrial biogenesis and turnover, energy sensing, apoptosis, senescence, and calcium dynamics. Mitochondria could play a key role in the pathophysiology of aging or in the earlier stages of some events that lead to the aging phenotype. Therefore, mitochondria will increasingly be targeted to prevent and treat chronic diseases and to promote healthy aging.

Mechanisms linking Mitochondrial DNA damage and aging

In the last century, considerable efforts were made to understand the role of mitochondrial DNA (mtDNA) mutations and of oxidative stress in aging. The classic mitochondrial free radical theory of aging, in which mtDNA mutations cause genotoxic oxidative stress, which in turn creates more mutations, has been a central hypothesis in the field for decades. In the last few years, however, new elements have discredited this original theory. The major source of mitochondrial DNA mutations seems to come from replication errors and failure of the repair mechanisms, and the accumulation of these mutations as observed in aged organisms appears to occur by clonal expansion and are not caused by a reactive oxygen species-dependent vicious cycle.

New hypotheses of how age-associated mitochondrial dysfunction may lead to aging are based on the role of reactive oxygen species as signaling molecules and on their role in mediating stress responses to age-dependent damage. Here, we review the changes that mtDNA undergoes during aging, and the past and most recent hypotheses linking these changes to the tissue failure observed in aging.

Dietary restriction, mitochondrial function and aging: from yeast to humans

Dietary restriction (DR) attenuates many detrimental effects of aging and consequently promotes health and increases longevity across organisms. While over the last 15 years extensive research has been devoted towards understanding the biology of aging, the precise mechanistic aspects of DR are yet to be settled. Abundant experimental evidence indicates that the DR effect on stimulating health impinges several metabolic and stress-resistance pathways. Downstream effects of these pathways include a reduction in cellular damage induced by oxidative stress, enhanced efficiency of mitochondrial functions and maintenance of mitochondrial dynamics and quality control, thereby attenuating age-related declines in mitochondrial function. However, the literature also accumulates conflicting evidence regarding how DR ameliorates mitochondrial performance and whether that is enough to slow age-dependent cellular and organismal deterioration. Here, we will summarize the current knowledge about how and to which extent the influence of different DR regimes on mitochondrial biogenesis and function contribute to postpone the detrimental effects of aging on healthspan and lifespan.

A Mitochondrial Haplogroup is Associated with Decreased Longevity in a Historic New World Population

Interest in mitochondrial influences on extended longevity has been mounting, as demonstrated by a growing literature. Such work has demonstrated that some haplogroups are associated with increased longevity and that such associations are population-specific. Most previous work however, suffers from the methodological shortcoming that long-lived individuals are compared with "controls" who are born decades after the aged individuals were. The only true controls of the elderly are people who were born on the same time period, but who did not have extended longevity. Here we present results of a study in which we are able to test if longevity is independent of haplogroup type, controlling for time period, by using mitochondrial DNA genealogies. Since mtDNA does not recombine, we know the mtDNA haplogroup of the maternal ancestors of our living participants. Therefore, we compare the haplogroup of people with and without extended longevity, who were born during the same time period.

Our sample is an admixed New World population which has haplogroups of Amerindian, European and African origin. We show that women who belong to Amerindian, European and African haplogroups do not differ in their mean longevity. Therefore, to the extent that ethnicity was tied in this population to mtDNA make up, such ethnicity did not impact longevity. In support of previous suggestions that the link between mtDNA haplogroups and longevity is specific to the population being studied, we found an association between haplogroup C and decreased longevity. Interestingly, the lifetime reproductive success and the number of grandchildren produced via a daughter of women with haplogroup C are not reduced. Our diachronic approach to the mtDNA and longevity link allowed us to determine that the same haplogroup is associated with decreased longevity during different time periods, and allowed us to compare the haplogroup of short and long-lived individuals born during the same time period. By controlling for time period, we minimize the effect of different cultural and ecological environments on differential longevity. With our diachronic approach, we investigate the mtDNA and longevity link with a biocultural perspective.

How the Wnt signaling pathway protects from neurodegeneration: the mitochondrial scenario

Alzheimer's disease (AD) is the most common neurodegenerative disorder and is characterized by progressive memory loss and cognitive decline. One of the hallmarks of AD is the overproduction of amyloid-beta aggregates that range from the toxic soluble oligomer (Aβo) form to extracellular accumulations in the brain. Growing evidence indicates that mitochondrial dysfunction is a common feature of neurodegenerative diseases and is observed at an early stage in the pathogenesis of AD. Reports indicate that mitochondrial structure and function are affected by Aβo and can trigger neuronal cell death.

On the other hand, the activation of the Wnt signaling pathway has an essential role in synaptic maintenance and neuronal functions, and its deregulation has also been implicated in AD. We have demonstrated that canonical Wnt signaling prevents the permeabilization of mitochondrial membranes through the inhibition of the mitochondrial permeability transition pore (mPTP), induced by Aβo. In addition, we showed that non-canonical Wnt signaling protects mitochondria from fission-fusion alterations in AD. These results suggest new approaches by which different Wnt signaling pathways protect neurons in AD, and support the idea that mitochondria have become potential therapeutic targets for the treatment of neurodegenerative disorders.

Mitochondrial pharmaceutics: A new therapeutic strategy to ameliorate oxidative stress in Alzheimer's disease

Association between amyloid-β (Aβ) toxicity, mitochondrial dysfunction, oxidative stress and neuronal damage has been demonstrated in the pathophysiology of Alzheimer's disease (AD). In the early stages of the disease, the defect in energy metabolism was found to be severe. This may probably due to the Aβ and ROS-induced declined activity of complexes in electron transport chain (ETC) as well as damages to mitochondrial DNA. Though clinically inconclusive, supplementation with antioxidants are reported to be beneficial especially in the early stages of the disease. A mild to moderate improvement in dementia is possible with therapy using antioxidants.

Since mitochondrial dysfunction has been observed, a new therapeutic strategy called 'Mitochondrial Medicine' which is aimed to maintain the energy production as well as to ameliorate the enhanced apoptosis of nerve cells has been developed. Mitochondrial CoQ10, Szeto-Schiller peptide-31 and superoxide dismutase/catalase mimetic, EUK-207 were the mitochondrial targeted agents demonstrated in experimental studies. This article discusses the mitochondrial impairment and the possible mitochondria targeted therapeutic intervention in AD.

That last one is interesting for related reasons: it seems that efforts to selectively target antioxidants to mitochondria continue to spread on the basis of promising early results from some lines of development published over the past decade or so. There's a post back in the Fight Aging! archives on Szeto-Schiller peptide-31, and many of you probably know about the development of plastiquinones such as SkQ1.

A Few New Fight Aging! Fundraising Posters
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We are nearing the first phase of this year's Fight Aging! fundraiser in support of the rejuvenation research programs carried out at the SENS Research Foundation. We are on the cusp of important progress in medical science, balanced close to a shift from the less effective research strategies of the past to SENS-like repair biotechnologies of the future. The frailty and disease that presently accompanies aging will be defeated by addressing its root causes, through means that are already clearly envisaged: it is only hard work and funding that separates the state of medicine today from a near future in which aging is brought under medical control. The road ahead for research and development is just about as clear and direct as these things ever get. I'll be asking people to step forward and contribute, just as last year, but there are a few things left to organize first. Don't let that stop you from sending me email if you have the ability to help.

Among the items left to be done before the later stages of the fundraiser roll around is the creation of a new brace of fundraising posters. I'd like to put together something more general and diverse this year, at least in comparison to last year's two posters. Primary colors, large text, flat backgrounds; the sort of thing that makes it easier for other advocates to retool the wording for their own usage. Not coincidentally, it also makes it easier for me to try out a more ideas prior to pulling in a professional. If some of them turn out to be terrible ideas, well, no great loss. There are always the others. Not all of us are Photoshop wizards, but simple poster designs go a long way towards letting everyone play.

This latest attempt is intended for placards and other printed displays, where the color catches the eye but is nowhere near as lurid as it appears upon your screen just about now. For those who want to tinker, the font used here is Tex Gyre Heros bold condensed, at 500px and 200px for the two sizes:

Choose Life: Scientists Work to End Frailty Poster: 4200 x 2800px

Choose Life: No More Frailty Poster: 4200 x 2800px

Discussing Science and Aging: Aubrey de Grey and Cynthia Kenyon at NPR
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NPR recently ran a show interviewing a number of people who have given TED talks relating to aging, among them Aubrey de Grey, cofounder of the SENS Research Foundation and coordinator of rejuvenation research programs, and Cynthia Kenyon, whose work on single gene manipulations that extend nematode longevity back in the 1990s arguably kicked off the modern wave of interest in slowing aging. It makes for interesting listening; you should certainly take a little time and at least look at the transcripts.

In these short interviews you can see illustrated the most important division in the modern work aimed at intervention into the aging process: on the one hand the mainstream approach of altering the operation of metabolism so as to slow down aging, based on traditional drug discovery methodologies, and on the other hand the radical, disruptive approach of repairing the damage caused by the normal operation of metabolism, requiring the development of new biotechnologies. The strategy here is to avoid changing the operation of metabolism, because that is very hard and far too little is known of the important details, but rather periodically clean up the consequences of normal metabolic activity in order to prevent that damage from overwhelming and altering biological systems so as to cause degenerative aging.

As I'm sure all of you know by now, I'm greatly in favor of the latter approach because all the signs suggest it should be far more efficient and effective at extending healthy life spans, not to mention producing actual rejuvenation in the old. You can't greatly help the old by slowing down aging: better technologies are needed. Rejuvenation is needed. You can't bring aging under medical control by working on metabolic alteration to slow aging. Repair is needed, not merely dialing down the pace of new damage.

How Do You Make An Elderly Worm Feel Young Again?

Have you ever wanted to stay young a little longer and put off aging? This is a dream of the ages, but scientists have for a long time thought this was just never going to be possible. They thought, you know, you just wear out - there's nothing you can do about it, kind of like an old shoe. But if you look at nature, you see that different kinds of animals can have really different life spans. Now, these animals are different from one another because they have different genes. So that suggests that somewhere in these genes, somewhere in the DNA, are genes for aging, genes that allow them to have different life spans. So if there are genes like that then you can imagine that if you could change one of the genes in an experiment, an aging gene, maybe you could slow down aging and extend life span. And if you could do that then you could find the genes for aging, and if they exist, and you can find them then maybe one could eventually do something about it.

You would think to extend the life span of an animal for such a long time, you know, you'd have to kind of go around in a way and fix things or shore them up. You'd have to do something for the skin and something for the intestine, something for the nervous system. You'd have to - it would be really hard because old tissues all look old, but they all have their own separate problems. But what's the big surprise is that there are these systemic or system-wide control circuits that you can tap into. And what happens is that there are circulating factors, factors in the blood that can move through the animal and tell all the tissues to slow down their aging. Not to slow down their movement, but to slow down their aging. The great secret of all this is that, you know, all animals are much more similar to one another than they are different. Worms have muscles, they have nerve cells, they have serotonin, they have acetylcholine, they have all the neurotransmitters we have, the very same ones. So what that means is, you can easily interrogate the genome by making mutations to find genes that control things, things that you didn't even know were controlled, like aging. And there are actually hints that gene changes in humans that mimic the effects of these changes in animals may contribute to exceptional longevity to becoming a centenarian, in a human.

Can Aging Be Cured?

RAZ: And we just heard from Dan Buettner. He's an explorer and a researcher who studies Blue Zones. These are the areas of the world where people live much longer than anywhere in the...

AUBREY DE GREY: Well, let me stop you right there. How much? How much? It's very important to look at the numbers here.

RAZ: Aubrey de Grey would argue the handful of extra years you can get from, say, a Blue-Zone lifestyle is really pretty minor.

DE GREY: People often laugh at the U.S.A. on this kind of thing because the U.S.A. spends far more money per capita on healthcare than any other country in the world.

RAZ: Right.

DE GREY: And yet, if you look at the league table of life expectancy, it comes down in the 40s somewhere - like, 45 or whatever. But then if you look at the actual absolute numbers, the difference in lifespan between the U.S.A. and the number-one country, Japan, guess what it is? Just guess. Go on.

RAZ: I don't know - four years, five years.

DE GREY: Indeed, only four years. So you know - and these Blue Zones, you know, they might get another couple of years, but you know, the numbers are so small that we've got to do something that nobody has today.

RAZ: Aubrey is an Evangelist, probably one of the loudest voices for what might be described as the anti-aging movement. He's one of the leaders of a group called the SENS Research Foundation. It funds research into what he calls rejuvenation biotechnologies.

DE GREY: Which means new medicines that don't yet exist that will be able to repair the various types of molecular and cellular damage that the body does to itself throughout life and that eventually contribute to the ill health of old age.

RAZ: Aubrey basically looks at the human body in the same way he sees any other machine. You keep it oiled. You replace parts. You do preventative maintenance, and the machine can keep going a lot longer than it was ever meant to. So instead of just focusing on, say, a cure for cancer, he wants researchers to channel their energy into finding ways to prevent cancer and other diseases from ever developing in the human body in the first place. And he thinks if we could do that...

DE GREY: Basically, the types of things you could die of at the age of a hundred or 200 would be exactly the same as the types of things that you might die of at the age of 20 or 30.

RAZ: An accident, for example.

DE GREY: Exactly.

RAZ: Alzheimer's, dementia, cancer - these diseases occur because as you age, your body gets damaged. Molecules get damaged. Cells mutate. Junk accumulates in your body. All of this is natural. It happens to everyone. And Aubrey believes that that damage can be grouped into seven different categories, all of which could be prevented or at least slowed down.

DE GREY: So for illustration, let me just talk about one category.

RAZ: Sure.

DE GREY: Cell loss - what is cell loss? It's simply cells in a particular organ or tissue dying and not being automatically replaced by the division of other cells. Now, it turns out that that is actually an important contributor to certain aspects of aging - Parkinson's disease, for example. Now, the thing is, we know what the fix for that one is. We know that the right way to repair that kind of damage is stem cell therapy. Now, progress in that area has been patchy over the past 20 years that people have been thinking about this. But now, it's going really well. There are a couple of clinical trials going on. And I'm really optimistic. I think most people are very optimistic. I would say that we've got a very good chance of actually totally curing Parkinson's disease with stem cells in the next 10 years, even.

RAZ: But you're arguing that the right investment in certain scientific research couldn't just get us to a hundred or 110, but it could get us to 110, playing tennis.

DE GREY: That's exactly right - in fact, keeping up with your granddaughter on the dance floor.

RAZ: Is that going to happen?

DE GREY: Well, I've just told you it would. You sound as though you don't quite believe me.

RAZ: I do, but you can understand why it still, today, in 2015, sounds like science fiction, right?

DE GREY: Things that are only - have only a 50 percent chance of happening in 20 years from now are supposed to sound like science fiction.

On Social Media and Advocacy for Radical Life Extension
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Changing the world is an activity built atop a foundation of persuasion and relationships, whether is a matter of creating entirely new technology or ensuring the widespread use of existing technologies. It always moves more slowly than advocates would like, even when things are progressing well, such as at the present time with regard to the public view of research into the effective treatment of aging. The past couple of years have seen a real transition in public perception and media treatment of aging research, the result of more than a decade of hard work and investment behind the scenes, all largely unnoticed. There are never any breakthroughs or sudden sweeping reversals in life: it is all a matter of the pieces finally falling into place, of the finale to a play that you just weren't paying all that much attention to while it was taking place.

The great revolution of our era is the plummeting cost and increasing capacity of computation. That has enabled all of the other transformative revolutions presently underway, such as in the cost, capabilities, and availability of communications technology and biotechnology. In communication especially, the cost of near instantly delivering old-style text from one person to another has fallen so far as to be essential zero, minuscule in comparison to the opportunity cost of time taken in composition of the message. Similarly, the cost of publishing to an audience has fallen to be essentially zero in comparison to the cost of finding that audience.

It is no coincidence that advocacy for longevity research, just like every goal originally held by a tiny fraction of the populace, has taken off in parallel with the growth of the internet. Beforehand, how were the one in a hundred or one in a thousand interested enough to talk and do something ever going to find one another? Now a special interest group of just a few hundred or few thousand people can span the globe and yet still be organized and effective, and for next to no cost beyond the time taken to participate. This is ideally suited to non-profit and advocacy organizations, and the last few decades of initiatives relating to extending the healthy human life span have seen many such organizations assemble via connections made online.

In this sense social media, a term I detest, means nothing more than communication. Everyone today has a near-zero-cost printing press and mail room. When everyone can act as their own newspaper, most people will do just that. Most of the resulting output is trivial, of course, because most conversations are trivial. But of those who have something to say that is worth listening to, more of that message will find a willing audience rather than being lost to the void. Of course there is always a power law of attention, there are always the professionals sitting on top of the pyramid, but ultimately we are expanded and improved by our new capabilities, each of us our own media outlet.

There are always those who mistake the shell for the snail, however. You can't force a conversation, or indeed any sort of meaningful outcome, by turning a crank and sending links here and there aimlessly, by counting posts and metrics. If there is no conversation, all of those mechanical actions, "social media activity", are just hollow. In all of my experiments in that, and all of the other experiments I've had the dubious pleasure of watching in the course of gainful employment as a technologist, I've become convinced that the only thing to do is have conversations. Talk to people. Publish what you want, and let people talk about it at the pace they want to talk about it. You can't force growth in advocacy, and it's really hard to measure where exactly you are in that process with the tools that social media companies force upon you. Advocacy for a cause doesn't have conversions and funnels that can be measured on a website or in an email, no matter what those selling you metrics engines might say. You end up with a lot of numbers and no real way to connect those numbers to anything that actually matters as a bottom line. So why try? There are share buttons here at Fight Aging!, hidden, not loaded at all until you request the tool, because people kept asking for them, not because I'm hot on creating larger numbers in a report.

So: we live in an age of ever more pervasive communication. That is important, very important, to all endeavors, and in ways that we haven't yet figured out. A lot of the more active members of the longevity science advocacy community are engaged in trying out new modes of organization and communication, building the community, present in ever new form of social media. But this is all, ever and always, at heart a conversation. It goes at its natural pace. We shouldn't forget that just because the tools of the trade are shiny and in everyone's hands these days.

Longevity online: can social media take life extension ideas from the radical to the mainstream?

To confront death is to face our biggest fear, and unfortunately for advocates of life extension, this is something which the majority of people are not presently inclined to do. Like any industry, the level of investment in life extension technologies and the resultant supply of treatments are directly related to demand. Therefore, for governments, scientific institutions, and venture capitalists to invest within the field, the demand from consumers simply has to be there. Recent big budget ventures spearheaded by some of Silicon Valley's most high profile companies and individuals go a long way to speeding up the rate of research and development as well as raising awareness of the cause, but for those looking to really accelerate the rate of progress, the question is how to get enough of the population onboard to significantly impact upon the rate of change.

In the 21st Century, social media has emerged as by far the most efficient and accessible platform for engagement between like-minded individuals, promoting shared ideas, and ultimately mobilising the general population into action. In fact, in our increasingly globalised world, such is the centrality of social media and its capacity to facilitate instant worldwide communication, one can argue that without it any movement or form of promotion is likely doomed to fail.

As a characteristically tech-minded community, it is therefore no surprise that the power of networks such as Facebook, Twitter, Google+, Linkedin, and Reddit as tools for furthering the cause of life extension has not been lost upon its most engaged advocates. One only has to peruse the most popular channels Facebook and Twitter to find literally hundreds of groups and profiles dedicated to life extension and longevity, with thousands of members based all over the world. Such high-levels of activity, one would assume, can only be a good thing for the life extension movement, but in terms of really taking life extension ideas from the radical to the mainstream, how far does social media currently go?