This is an old story for regular readers, but I’ll restate it anyway: people are dying of aging at a rate of something more than a hundred thousand lives a day. It is a mark of our inventive ongoing engagement with ways and means of death that despite this vast toll, aging still only manages to kill two thirds of us – and that in this era of comparatively advanced medicine, comparative peace, and comparative risk aversion.

Biotechnology is today’s revolutionary industry in the making. Costs are falling, capabilities increasing just as dramatically as happened for computers two decades ago. We could be well on the way to removing aging as a cause of death at this point. A detailed plan is in hand, the way forward to achieve the goal of rejuvenation biotechnology is as clear as life science research ever gets, and the cost of an initial demonstration of rejuvenation in mice is ten years and a sum of money that’s a rounding error in comparison what is spent on developing new and better ways to kill people.

Here’s the thing, though, the point that’s enough to make bitter old folk of us all: we’re not actually well on the way to removing aging as a cause of death. We could be, but we’re not – we’re only just getting started at a time when we could be far further ahead, and we’re moving slowly when we could be moving far faster. The hard-won funding and solid research programs for SENS and related initiatives are a trickle where a river is needed. You have to start at the start, of course, and every flood of effort started with a few drops back at the beginning. Nonetheless the flood does not yet exist, despite every reason for it to do so: a hundred thousand lives a day, the suffering of hundreds of millions more, and yet it’s hard to get anyone to care enough to even think much about the topic, let alone do anything to help stop it from happening.

Where is rationality in all this? It’s that the world is an asylum, run by the inmates, that makes people bitter before their time. To a first approximation those with resources build wars and circuses, and sometimes throw a crust to to the few who work on making the human condition better than it was yesterday. Those without resources heartily support this strategy, even while they owe pretty much every affordable comfort to work accomplished by a few centuries of researchers and developers – the tiny crust-fed minorities of their time.

Over at Edge, you’ll find a commentary from Aubrey de Grey on the topic of human rationality and the high cost of its absence in matters relating to support of medical research aimed at human rejuvenation:

Visionary topics are of necessity long-term, hence high risk, and of almost equal necessity high gain. In the area of medical research, for example, the question must be raised: are we benefiting the most people, to the greatest extent, with the highest probability, by the current distribution of research funding? In all such areas that I can think of, the fundamental bias apparent in public opinion and public policy is in favour of approaches that might, arguably (often very arguably), deliver modest short-term benefits but which offer pretty much no prospect of leading to more effective, second-generation approaches down the road. The routes to those second-generation approaches that show the best chance of success are, by contrast, marginalised as a result of their lack of “intermediate results”.

We should be very, very worried about this. I would go so far as to say that it is already costing masses – masses – of lives, by slowing down life-saving research. And how hard is it to address, really? How hard is Bayes’ Theorem, really? I would assert that the single most significant thing that those who understand the issue I have highlighted here can do to benefit humanity is to agitate for better understanding of probabilistic reasoning among policy-makers, opinion-formers and thence the public.

Source:
http://www.fightaging.org/archives/2013/01/people-are-not-good-at-being-rational-and-that-costs-a-great-many-lives.php

Source:
http://www.longevitymedicine.tv/people-are-not-good-at-being-rational-and-that-costs-a-great-many-lives/

As might be expected, older people with a greater loss of muscle mass and strength – the condition known as sarcopenia – also tend to exhibit a higher risk of death:

Sarcopenia has been indicated as a reliable marker of frailty and poor prognosis among the oldest individuals. We evaluated the impact of sarcopenia on the risk of all-cause death in a population of frail older persons living in community. We analysed data from the Aging and Longevity Study, a prospective cohort study that collected data on all subjects aged 80 years and older residing in the Sirente geographic area (n = 364). The present analysis was conducted among those subjects who were between 80 and 85 years of age at the time of the baseline assessment (n = 197). The main outcome measure was all-cause mortality over 7-year follow-up.

According to the European Working Group on Sarcopenia in Older People (EWGSOP) criteria, the diagnosis of sarcopenia required the documentation of low muscle mass and the documentation of either low muscle strength or low physical performance. [Using] the EWGSOP-suggested criteria, 43 subjects with sarcopenia (21.8%) were identified. During the 7-year follow-up, 29 (67.4%) participants died among subjects with sarcopenia compared with 63 subjects (41.2%) without sarcopenia. After adjusting for potential confounders including age, gender, education, activities of daily living (ADL) impairment, body mass index, hypertension, congestive heart failure, chronic obstructive pulmonary disease, number of diseases, TNF-?, participants with sarcopenia had a higher risk of death for all causes compared with non-sarcopenic subjects.

Link: http://www.ncbi.nlm.nih.gov/pubmed/23321202

Source:
http://www.fightaging.org/archives/2013/01/sarcopenia-correlates-with-increased-mortality.php

Source:
http://www.longevitymedicine.tv/sarcopenia-correlates-with-increased-mortality/

Here is news of a research tool for those developing ways to target and destroy senescent cells. A successful method should minimize the contribution of cellular senescence to degenerative aging and thus extend healthy life – this is one of the necessary biotechnologies for human rejuvenation that is closest to actual implementation:

Researchers have long known that the gene, p16INK4a (p16), plays a role in aging and cancer suppression by activating an important tumor defense mechanism called ‘cellular senescence’. The [team] has developed a strain of mice that turns on a gene from fireflies when the normal p16 gene is activated. In cells undergoing senescence, the p16 gene is switched on, activating the firefly gene and causing the affected tissue to glow.

Throughout the entire lifespan of these mice, the researchers followed p16 activation by simply tracking the brightness of each animal. They found that old mice are brighter than young mice, and that sites of cancer formation become extremely bright, allowing for the early identification of developing cancers. “With these mice, we can visualize in real-time the activation of cellular senescence, which prevents cancer but causes aging. We can literally see the earliest molecular stages of cancer and aging in living mice.”

The researchers used these mice to make several unexpected discoveries. First, the group was able to track the accumulation of senescent cells in aging mice by assessing how brightly each mouse glowed. Surprisingly, the brightest animals were no more likely to die from spontaneous cancer than dimmer animals of the same age. That is, the number of senescent cells in the mouse did not predict its risk of dying.

Another surprise came from the disparities in p16 levels among the mice. The authors studied a large group of genetically identical animals that were all housed in the same way and fed the same diet. However, despite identical genetic and environmental conditions, the brightness of individual mice at any given age was highly variable, suggesting that factors beyond genetics and diet influence aging.

Link: http://www.eurekalert.org/pub_releases/2013-01/uonc-uru011713.php

Source:
http://www.fightaging.org/archives/2013/01/luminescent-marking-of-cellular-senescence.php

Source:
http://www.longevitymedicine.tv/luminescent-marking-of-cellular-senescence/

Since we’re on the subject of cryonics today, I thought I’d point you to a review of the Alcor-40 conference published in Alcor’s house magazine. The conference was held a few months back; you might compare this review with another conference report that was published in October.

This is a fairly long piece, so look through at your own pace:

Alcor-40 Conference Review

In honor of its 40th anniversary, Alcor held its first conference in 5 years on October 19-21, 2012, in Scottsdale, Arizona. The program featured a wide variety of topics for presentation, with themes regarding how to improve the odds of a successful cryopreservation and theories of aging and their implications for stopping or reversing aging (as argued by their primary scientific proponents).

…

The Chief Scientific Officer of 21st Century Medicine, Inc. (21CM), Greg Fahy, kicked off the event with an overview of the work being carried out at 21CM in his talk “Progress Toward Reversible Cryopreservation of Complex Systems.” Because cryonics is reliant upon technologies that do not yet exist, it is sometimes likened to religion. “Unlike religion, cryonics must be based on evidence,” Fahy began, emphasizing that reversibility is the key component of successful suspended animation.

Fahy rounded things out with an update on 21CM’s “20 year plan.” Begun in 2010, their work in whole body vitrification has marched forward with the ultimate goal of reversibility by 2030. Precision perfusion control systems have allowed for unprecedented data collection during whole body vitrification experiments. Currently, the company is focusing on studies of cryoprotectant toxicity to make the next advance toward reversible cryoprotection of the most complex system of all, the whole organism.

The cryonics movement is perhaps the oldest continuous portion of the modern community of advocates and supporters interested in radical life extension and the defeat of aging. This is a community distinguished from all those that came before it by the fact that is members are in a position to actually do something about the issues of death and aging. Technology is far enough along for people to work on preserving the minds of those who die too early, and we now have a shot at building working rejuvenation therapies over the next twenty to thirty years. All it needs is money. Present efforts are foundation work or crude first attempts in comparison to what lies ahead, but they exist, which is more than could be said just a few decades ago.

Source:
http://www.fightaging.org/archives/2013/01/a-review-of-the-alcor-40-conference.php

Source:
http://www.longevitymedicine.tv/a-review-of-the-alcor-40-conference/

Plastination seems to have the potential to become a viable alternative to cryonics as a long-term storage method for the brains of those who die before the advent of rejuvenation biotechnology. If the fine structure that encodes the data of the mind is preserved, then these individuals can wait indefinitely for the arrival of molecular nanotechnology needed to restore them to life. Cryonics has been around for decades, and has had its challenges, while plastination remains a comparatively new idea – and thus we should expect there to be hurdles to overcome.

One of my concerns with room temperature storage of plastinated individuals is the potential for bacteria and bugs than might like to consume the fixative compounds, something that isn’t a concern in low-temperature storage. Here is another:

I have always been interested in chemical fixation as a (low cost) alternative for cryonics. In fact, years before all the talk about the “connectome” and “plastination” I spent considerable time exchanging messages with Michael Perry at Alcor about the technical and practical feasibility of chemical brain preservation. But no matter how open minded I tried to be about this approach, I kept running into the same challenges over and over again.

The challenge that has concerned me the most is whether a delayed start of chemical brain fixation will produce incomplete distribution of the chemical fixative in the brain because of ischemia-induced perfusion impairment. Thinking about the technical problem of “no-reflow” is not the first thing on the mind of someone who first hears about the idea of using chemical fixatives to preserve the brain. In my case, this concern was not just “theoretical.” In my lab I have spent many years looking at the effects of cerebral ischemia on cryopreservation and chemical fixation. Last year we decided to broaden our investigations to delayed chemical fixation and we have not been pleased at what we have observed so far. After 1.5 years of room temperature storage the delayed aldehyde fixed brains are falling apart and continue to decompose. In small animals one might imagine that such perfusion impairment could be overcome by immersing the brains in the fixative instead but human brains are simply too large. By the time that the fixative would have reached the core of the brain, extensive autolysis will have occurred.

Link: http://www.evidencebasedcryonics.org/2013/01/14/in-praise-of-cold/

Source:
http://www.fightaging.org/archives/2013/01/plastination-will-have-its-challenges-just-like-cryonics.php

Source:
http://www.longevitymedicine.tv/plastination-will-have-its-challenges-just-like-cryonics/