It is good to see that cryonics is now sufficiently widely known that business magazines are willing to write articles on the financial engineering and legal explorations associated with establishing a successful cryopreservation: "Financial planning, like most disciplines, generally relies on the assumption that the dead will remain that way. Some people, however, are not as willing to accept this premise. Cryonicists believe science will eventually give us the ability to reanimate the dead. In preparation for this possibility, they elect to have their bodies, or sometimes merely their heads, stored in extreme low temperatures so that, when the time comes, they can be restored to life. Some anticipate a future in which their bodies will be thawed and cured of their ailments, while others see the process as akin to data storage, preserving the organic record of their thoughts and memories until these can be downloaded onto some new medium. ... the legal and financial questions surrounding cryonics require serious believers to make plans in the present, before they start their hiatus. Since cryonics remains well outside the mainstream, most end-of-life matters have yet to be thought through as temporary-suspension-of-life concerns. Ordinarily, at death, social security numbers are cancelled and made public, and citizenship privileges such as voting are revoked (at least in most jurisdictions). What would the temporarily dead need to do to put their legal status on ice along with their bodies?" If you want a serious consideration of the details, you might look at some of Rudi Hoffman's articles on cryonics and financial planning.

Link: http://www.businessinsider.com/financial-planning-for-the-formerly-deceased-2011-5

You have at least two ages: your chronological age, how long you have lived, and what we might call your biological age - which is a measure of how damaged you are. Aging, meaning the process of physical degeneration, is really just a matter of damage at the level of cells and molecular machinery. The more damage, the greater your biological age. If you are 56, you might have the damage load of the average 50 year old or the average 60 year old. Or worse, or better - and in either case that will reflect in your current health and remaining life span.

In actual fact, biological age is probably far more complex than this. There is every reason to expect different systems in your body to suffer different rates of damage accumultion. Consider the immune system in AIDS patients for example, which is prematurely aged into exhaustion and frailty. That is an extreme example of differential rates of damage: you would expect to find smaller differences in levels of accumulated damage in the biological components of a healthy person. But the differences are there.

Recognize that a lot of what I have said above is theory. Anyone who claims to be able to measure your biological age is largely blowing smoke: there's no standard for such a thing, and not much in the way of biomarkers of aging. Biomarkers are measurable aspects of our biology that can be scaled against age or remaining life expectancy - and so might be used to determine a subject's chronological age, or how much longer they might expect to live. The absence of good biomarkers poses a strategic challenge for the ongoing development of longevity science, because in order to efficiently evaluate a potential therapy to slow or reverse aging, researchers need to rapidly understand its actual effects on healthy life span. Sitting around and waiting is the only presently foolproof strategy, and that is one of the reasons that even mouse studies of longevity therapies are very expensive. No-one wants to run an experiment for going on four years if there is a way to call a halt after a few months and some biomarker measurements.

That difference in experimental run time represents a large sum of money in every sizable study, not to mention the opportunity cost in research that might otherwise move ahead, but must wait for years for results to arrive. Further, when you stop to consider human studies, you'll see that that the present state of affairs rules out a wide range of possible trials - "wait and see" isn't viable when the time frame is decades. This is why we should all be interested in progress towards the establishment of biomarkers for aging, and today I'll point you to recent work on DNA methylation, undertaken with that aim in mind. You might recall that DNA methylation correlates with age and age-related frailty, and here researchers greatly improve upon the precision of that correlation.

UCLA scientists accurately predict age with saliva sample:

Using saliva samples contributed by 34 pairs of identical male twins ages 21 to 55, UCLA researchers scoured the men's genomes and identified 88 sites on the DNA that strongly correlated methylation to age. They replicated their findings in a general population of 31 men and 29 women aged 18 to 70. ... Vilain and his team envision the test becoming a forensic tool in crime-scene investigations. By analyzing the traces of saliva left in a tooth bite or on a coffee cup, lab experts could narrow the age of a criminal suspect to a five-year range.

Epigenetic Predictor of Age:

From the moment of conception, we begin to age. A decay of cellular structures, gene regulation, and DNA sequence ages cells and organisms. DNA methylation patterns change with increasing age and contribute to age related disease. Here we identify 88 sites in or near 80 genes for which the degree of cytosine methylation is significantly correlated with age in saliva of 34 male identical twin pairs between 21 and 55 years of age. Furthermore, we validated sites in the promoters of three genes and replicated our results in a general population sample of 31 males and 29 females between 18 and 70 years of age. The methylation of three sites - in the promoters of the EDARADD, TOM1L1, and NPTX2 genes - is linear with age over a range of five decades. Using just two cytosines from these loci, we built a regression model that explained 73% of the variance in age, and is able to predict the age of an individual with an average accuracy of 5.2 years.

There are some subtleties here. DNA methylation occurs in different regions of DNA at different rates (and probably at different rates in the same region of DNA in cells in different locations in the body). The researchers here have found a statistical model based on methylation of a few specific genes in one portion of the body that is a biomarker of chronological age. For our purposes that is the less useful biomarker: we want one that measures remaining life expectancy, or in other words a biomarker that is effectively a measure of present levels of biological damage.

We know that methylation patterns correlate with age-related frailty. There is every reason to expect that researchers will soon be able to build a range of statistical measures based on DNA methylation that will predict remaining life expectancy across most common states of health and ages. The research described above gives further weight to that expectation.

At Forbes, a profile of one of the Thiel Fellowship recipients who focuses on longevity science: "Deming started working in a research lab when she was 12, enrolled at MIT at age 14 and last month, the now 17 year-old was awarded one of 24 $100,000 Thiel Foundation Fellowships for her work in the realm of anti-aging, specifically efforts to identify the genes that control aging and to use discoveries about age-defying therapies effective in worms to unlock the key to extending the human lifespan ... I had a fantastic childhood. Growing up, I had complete freedom to investigate whatever I was interested in, so I puzzled around with math and science, and got hooked on biology. When I was 12, Cynthia Kenyon, one of the coolest people I know, let me come to her lab. She works with a wonderful little worm called C. elegans, so I got to spend the next few years peering down a microscope at the fascinating critters. Then I went to MIT. I'm leaving as a physics major after a whirlwind couple of years spent exploring the magical properties of the quantum realm. ... 'I'd been mulling over what to do after college. The optimal scenario I came up with was exactly what the 20 Under 20 program offers; an opportunity to spend two years working to extend the human healthspan.' She will take up her award in the fall and will initially focus on identifying promising anti-aging research projects that are close to commercialization."

Link: http://blogs.forbes.com/jmaureenhenderson/2011/06/20/meet-the-teen-who-got-paid-100-000-to-drop-out-of-school/

Modern advocacy for engineered longevity and methods of preventing permanent death (such as cryonics) began in earnest in the 1970s, give or take, and has thus been around for long enough to establish a distinct and fascinating cultural past that most younger people are unaware of. The last decades of the last century are being buried rapidly indeed. The more thoughtful older folk who lived through that past there are sponsoring a growing range of initiatives to help ensure the continuation and growth of this present community of advocates, supporters, writers, and researchers. It is in everyone's interest for there to be more people working on human life extension, talking about it, and advocating for longer, healthier lives.

In this sense, the future is something that is constructed, not something that just unfolds without any effort on anyone's part - and that includes the future of communities. If there is growth it is because people planned carefully and worked hard to create that growth. Following this theme, in recent posts over at Depressed Metabolism you'll find both a little of the past and a little of the present work to build the future of the cryonics community:

Gerald Feinberg on physics and life extension

Gerald Feinberg, a Columbia university physicist who, among other things, hypothesized the existence of the muon neutrino, had a strong interest in the future of science and life extension. In 1966 he published the article "Physics and Life Prolongation" in Physics Today in which he reviews cryobiology research ... Feinberg recognized that it might be possible for people dying today to benefit from future advances in science in the absence of perfected techniques.

Teens & Twenties 2011 Gathering

On the evening of Thursday, May 19 and on Friday, May 20, I attended the 2011 (2nd annual) Teens & Twenties young cryonicists gathering which preceded the Suspended Animation, Inc. conference in Fort Lauderdale, Florida.

...

Many members of this group were impressively highly educated, mostly in computer technologies, and secondarily in biotechnologies. There were six Russians: five from KrioRus, and one from CryoFreedom. KrioRus is located near Moscow, whereas CryoFreedom is further south in Russia, closer to Ukraine. Dr. Yuri Pichugin (formerly the Cryonics Institute's cryobiologist), is associated with CryoFreedom. CryoFreedom advertises neuropreservation for $7,500. Although it currently has no human patients, two pets are in liquid nitrogen. I also learned that there is a man named Eugen Shumilov who is working to start a new cryonics company in St. Petersburg, Russia, but there was no representation of Shumilov's organization at this event.

There are two overlapping goals of the Teens & Twenties event. One is the opportunity for members of the Asset Presevation Group to meet the young cryonicists. The other is the opportunity for the widely dispersed young cryonicists to become acquainted with each other, and to build lasting networks (community building).

A little more on efforts to help build the next generation of cryonics supporters, advocates, and engineers can be found back in the Fight Aging! archives:

• The 2nd Annual Young Cryonicists Gathering
• Reports From a Youthful Cryonics Meeting

Some numbers to consider, since everyone and their dog seems to be talking about the disposition of inordinately large sums of money - and little else - at the moment:

• Between 1970 and 2000, increasing life expectancy added $3.2 trillion per year in effective wealth.
• The yearly cost of natural death: more than 50 million lives and $100 trillion in wealth.
• The estimated cost of developing robust rejuvenation in mice via SENS, the Strategies for Engineered Negligible Senescence: $100 million per year over ten years.
• The 2010 budget for the US National Institute on Aging: $1 billion.
• The 2010 budget for the US National Institutes of Health: in the vicinity of $35 billion.
• The NIH comprises perhaps a third of medical research funding in the US.
• The cost of acquiring sirtuin research company Sirtris: $720 million.

• The 2010 research budget at the SENS Foundation: a little over $650,000.

We all have our ideas as to how to spend money in ways better than the choices made by its current owner. It can be frustrating when the course ahead is so very clear indeed, yet not taken ... but that is what advocacy is for. When you have a vision, share it, persuade others, and make it happen. When you don't like the numbers you see in front of you, work to change them.

From Cryonics Magazine: "As a neuroscientist whose day job is to map neural circuits, I know exactly what type of evidence is needed to convince the scientific community that cryonics preserves the neural circuits encoding our unique memories and personality. What is required is a systematic whole-brain survey with an electron microscope. Recently I, along with my colleagues John Smart and Jacob DiMare, formed the Brain Preservation Foundation (BPF) to promote new scientific research in the field of whole brain preservation for long-term static storage. The BPF has announced the Brain Preservation Technology Prize (purse currently at $106,000) for the first team to demonstrate that an entire large mammalian brain can be preserved for long-term storage such that the connectivity between neurons remains intact and traceable using today's electron microscopic imaging techniques. A complete set of rules for the prize can be found on our BPF website. ... This prize is being presented as a challenge to cryonics providers like Alcor and their research partners: 'Demonstrate the quality of your product in a rigorous, independent, and open way to the scientific community and to your customers.' The BPF is hard at work raising funds to promote this prize and to help perform the electron microscopic evaluation required, and we are recruiting a board of scientific advisors and judges that will give the prize credibility."

Link: http://www.alcor.org/magazine/2011/06/07/the-brain-preservation-technology-prize/

Allow me to point you to an attractively blunt assessment of the human condition from the Russian end of the rejuvenation research advocacy community, tidied up a little after the automated translation made a hash of it:

Needless to say, a catastrophe - something unpleasant. Global catastrophe - unpleasant globally. And what is the most global of global catastrophes? Probably the one that leads to widespread death. And here we must note that if nothing is done, then all living people will die with 100% probability. Of aging. Therefore, it is aging that is the global catastrophe that is unfolding silently throughout the course of human history.

"Unfolding silently" because nearly everyone in the world studiously refuses to characterize the consequences of aging for what they in fact are. Everyone will die of aging - everyone! - and that is somehow removed from the normal fervor and unified efforts that greet any other form of mass death. Take the tsunamis of recent years, for example, one of which managed to kill about as many people as die of aging in any given day. There was a global outpouring of funds, support, and activity following that tsunami. Yet every day, without cease, that many people again are killed by the effects of aging - and next to no-one cares enough to do something in response to this horrible ongoing loss of life.

This is an age of biotechnology, in which we have a good grasp on the causes of degenerative aging and how to approach treating them. The goal of producing medical technologies that can rejuvenate the old and grant additional decades of life might be accomplished within a few decades, given billions of dollars in funding and and tens of thousands of researchers and supporting workers. But that support doesn't exist today. The peoples of the world think about aging little differently than they did a thousand years ago - they haven't yet woken up to see what could be accomplished through medical science within their lifetimes. As a consequence of this lack of support, many, many more people will age, suffer, and die than might have been the case - ourselves included, unless we get our act together.

There is no shortage of people trying to convince us that degenerating into frailty, suffering, and death is a wonderful thing: "Mr Agronin is an optimist. He does not deny - how could he? - the sufferings and indignities of old age. Scanning slices of old brain, 'stained and prepped for the microscope', his eye is unsparing: 'the aged folds' like 'the withered meat of a walnut', the blood vessels like 'hardened tendrils', the 'small plaques of toxic amyloid protein surrounded by a debris field of dead neurons'. But alongside the science, he sees something else: the people themselves. Old age, he says, has become our blind spot, neglected by the medical profession, lumped together with dementia and disease, something to be endured, dreaded, mercifully pre-empted, or even - as one researcher in the field, Aubrey de Grey, argues - reversed. Mr Agronin, by contrast, embraces it. He sees it as intrinsic to life, with its own 'ways and meanings', its particular wisdom. Even at its most tenuous and hollowed out, he finds some shape, a sense of cyclic pattern. In an almost mystical passage, inspired by his professor, Erik Erikson, a psychologist, Mr Agronin likens life to a stream which eventually seeps down unseen into the bedrock, and opens 'like a flower into the aquifer below'." From where I stand, there needs to be more of a healthy dread of aging - perhaps that would motivate more people to help develop the rejuvenation biotechnologies that can do something about it. To try to pretend that aging to death, suffering terribly along the way, is just peachy keen has an air of desperate madness to it.

Link: http://www.economist.com/node/18111554

It is known that the hypoxic response at a cellular level is involved in the longevity induced by calorie restriction, and works like most forms of hormesis - by stimulating cells to greater housekeeping efforts. Here is an open access paper on the subject: "A mild reduction in mitochondrial respiration extends the life span of many species, including C. elegans. We recently showed that hypoxia-inducible factor 1 (HIF-1) is required for the acquisition of a long life span by mutants with reduced respiration in C. elegans. We suggested that increased levels of reactive oxygen species (ROS) produced in the respiration mutants increase HIF-1 activity and lead to this longevity. In this research perspective, we discuss our findings and recent advances regarding the roles of ROS and HIF-1 in aging, focusing on the longevity caused by reduced respiration. ... Many interesting questions remain unanswered. Which tissues and functional target genes are important in the regulation of aging by HIF-1? How can both up-regulation and down-regulation of HIF-1 promote longevity? What is the molecular mechanism by which mitochondrial ROS stimulates HIF-1 activity? ... Since many aging-regulatory processes are conserved between C. elegans and mammals, these studies may also provide insights into the regulatory mechanisms of aging in mammals, including humans. Moreover, in addition to aging, HIF-1 and mitochondrial impairment have been implicated in various human diseases such as cancer, diabetes, and neurodegenerative diseases. Thus, we believe that these future studies will help us better understand the pathophysiology of these diseases."

Link: http://www.impactaging.com/papers/v3/n3/full/100292.html

Researchers continue to investigate how to replicate the limb regeneration found in lower animals: "Move over, newts and salamanders. The mouse may join you as the only animal that can re-grow their own severed limbs. Researchers are reporting that a simple chemical cocktail can coax mouse muscle fibers to become the kinds of cells found in the first stages of a regenerating limb. Their study, the first demonstration that mammal muscle can be turned into the biological raw material for a new limb ... their 'relatively simple, gentle, and reversible' methods for creating the early stages of limb regeneration in mouse cells 'have implications for both regenerative medicine and stem cell biology.' In the future, they suggest, the chemicals they use could speed wound healing by providing new cells at the injured site before the wound closes or becomes infected. Their methods might also shed light on new ways to switch adult cells into the all-purpose, so-called 'pluripotent' stem cells with the potential for growing into any type of tissue in the body. The scientists describe the chemical cocktail that they developed and used to turn mouse muscle fibers into muscle cells. [They] then converted the muscle cells turned into fat and bone cells. Those transformations were remarkably similar to the initial processes that occur in the tissue of newts and salamanders that is starting to regrow severed limbs."

Link: http://www.eurekalert.org/pub_releases/2011-04/acs-scc040611.php

Here is a dense scientific post from the SENS Foundation that might be better read back to front, starting with the research partnership announcement at the end. Some fraction of degenerative aging is caused by an accumulation of various forms of amyloids between cells, probably the best known of which is that involved in Alzheimer's disease. One goal for the Strategies for Engineered Negligible Senescence (SENS) approach to aging is to establish a general technology platform that can be used to remove any form of amyloid: "In late 2008, we reviewed then-unpublished work by Dr. Mark Pepys, who was working on an ambitious project anticipated to allow for the disaggregation of nearly all disease-associated amyloids. ... I am therefore delighted to have the privilege to be given permission [to] make the first public announcement that the Supercentenarian Research Foundation has recently helped to facilitate a collaboration between researchers already working in amyloid diseases, to develop antibodies to cleave aggregated wild-type and mutant transthyretin - the form responsible for senile cardiac amyloidosis (a prevalent, but not exclusive, cardiac amyloidosis in supercentenarians)."

View the Article Under Discussion: http://www.sens.org/node/831

Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

An opinion paper by researchers who feel that too much emphasis is placed on the discovery of longevity mutations: "The biological reasons for ageing are now well known, so it is no longer an unsolved problem in biology. Furthermore, there is only one science of ageing, which is continually advancing. The significance and importance of the mutations that lengthen the lifespan of invertebrates can be assessed only in relationship to previous well-established studies of ageing. The mutant strains of model organisms that increase longevity have altered nutrient signalling pathways similar to the effects of dietary restriction, and so it is likely that there is a shift in the trade-off between reproduction and maintenance ... To believe that the isolation and characterisation of a few invertebrate mutations (as well as those in yeast) will 'galvanise' the field and provide new insights into human ageing is an extreme point of view which does not recognize the huge progress in ageing research that has been made in the last 50 years or so." I believe that the focus on longevity mutations is not the most effective use of resources, but for different reasons: it's a part of the metabolic manipulation school of slowing aging, which is a slow path to a poor end result in comparison to repair strategies.

View the Article Under Discussion: http://www.ncbi.nlm.nih.gov/pubmed/20549352

Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

This year's BIL unconference will be held on March 3rd, on the Queen Mary in Long Beach, California.

BIL is an ad-hoc conference for people changing the world in big ways. It's a place for passionate people to come together to energize, brainstorm, and take action. ... Most of you have heard of TED or watched the talks online, but do you know about BIL, the quirky, populist, unconference taking place nearby? Open to the public and fully participant powered, BIL features a wild mix of technologists, scientists, artists, hackers, and those with a passion for community awareness.

Amongst those scheduling themselves to speak are Aubrey de Grey of the SENS Foundation and Max More of Alcor:

De Grey's research focuses on whether regenerative medicine can thwart the aging process. He works on the development of what he calls "Strategies for Engineered Negligible Senescence" (SENS), a tissue-repair strategy intended to rejuvenate the human body and allow an indefinite lifespan. To this end, he has identified seven types of molecular and cellular damage caused by essential metabolic processes. SENS is a proposed panel of therapies designed to repair this damage.

...

Max More is an internationally acclaimed strategic philosopher widely recognized for his thinking on the philosophical and cultural implications of emerging technologies. ... At the start of 2011, he became President and CEO of the Alcor Life Extension Foundation, the world's leading cryonics organization. ... Max will give a fresh perspective on cryonics as a bridge to an indefinitely extended life.

You'll find some other familiar faces in the list of participants, some of whom are also quite active in the longevity science advocacy community.

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

From the Methuselah Foundation blog: "A thin layer of human skeletal muscle is being printed by Chirag Khatiwala in a small, sterile room of San Diego-based startup Organovo. Each muscle cell from the company's signature 3-D printer is uniformly deposited in closely spaced lines on a petri dish. This allows the cells to grow and interconnect until they form working muscle tissue nearly indistinguishable from a human muscle biopsy. Unlike other experimental approaches that utilize ink-jet printers to deposit cells, Organovo's technology enables cells to interact with each other the way they do in the body. How? They are packed tightly together, sandwiched, if you will, and incubated. This prompts them to cleave to each other and interchange chemical signals. When printed, the cells are grouped together in a paste that helps them grow, migrate, and align themselves properly. In the case of muscle cells, the way they orient themselves in the same direction allow for contractions of the tissue. ... Methuselah Foundation honors the efforts of Organovo through early funding and support as well as through its new, highly anticipated New Organ Mprize. The true prize is elevated health and quality of life for those that have had to or will suffer the blows of a failing organ. Every $10 helps us work in tandem with today's stunningly advanced technology so that at some tomorrow, no one will have to suffer or die because of a diseased organ."

Link: http://blog.mfoundation.org/2012/02/_fantastical_scenes_from_the.html

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Damaged mitochondria cause problems because their electron transport chains, the core mechanism by which they generate power for the cell, stop working the right way. That leads to a situation in which sub-par mitochondria in a cell are not recycled despite being damaged, and since they replicate like bacteria the bad mitochondria take over the cell. It goes downhill from there, and this whole process is one of the fundamental causes of aging. Ways of addressing this situation include repairing the mitochondria directly or working around their damage by creating replacements for the damaged parts of mitochondrial protein machinery elsewhere in the cell. Here is another line of research that looks at trying to minimize the consequences of that damaged machinery by providing substitute components, but with a different focus: "Mitochondrial dysfunction (primary or secondary) is detrimental to intermediary metabolism. Therapeutic strategies to treat/prevent mitochondrial dysfunction could be valuable for managing metabolic and age-related disorders. Here, we review strategies proposed to treat mitochondrial impairment. We then concentrate on redox-active agents, with mild-redox potential, who shuttle electrons among specific cytosolic or mitochondrial redox-centers. We propose that specific redox agents with mild redox potential improve mitochondrial function because they can readily donate or accept electrons in biological systems, thus they enhance metabolic activity and prevent reactive oxygen species (ROS) production. These agents are likely to lack toxic effects because they lack the risk of inhibiting electron transfer in redox centers. ... This view has been demonstrated by testing the effect of several redox active agents on cellular senescence. Methylene blue (MB) appears to readily cycle between the oxidized and reduced forms using specific mitochondrial and cytosolic redox centers. MB is most effective in delaying cell senescence and enhancing mitochondrial function in vivo and in vitro. Mild-redox agents can alter the biochemical activity of specific mitochondrial components, which then in response alters the expression of nuclear and mitochondrial genes. We present the concept of mitochondrial electron-carrier bypass as a potential result of mild-redox agents, a method to prevent ROS production, improve mitochondrial function, and delay cellular aging. Thus, mild-redox agents may prevent/delay mitochondria-driven disorders."

Link: http://www.ncbi.nlm.nih.gov/pubmed/22419586

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

There should be no such thing as "I don't know what to do with my life." Scratch that statement away and erase it, as it should be "I will aid the development of life extension technology until I do know."

It should be no surprise to anyone that many, or perhaps even a majority of people at any given time have no real idea as to what they want to do with their lives. No vision, no grand dream that captures them, no burning desire to achieve a specific great work. That isn't because they are incapable - far from it, it is because they haven't found their own personal blue touch paper yet. The space of ideas and ideals is vast, and even the most aggressively autodidactic internet-addicted polymath cannot embrace more than a fraction of the sphere of human knowledge. Yet you cannot know your grand vision, the one that resonates with everything your life has led to up until that point, if you never encounter its roots.

Which is where we come back to time. We tell the younger folk that it doesn't matter if they don't know what they want to do with their lives, as that knowledge will come with time. The rituals and mythology that spring from the passage from childhood to adulthood, repeated billions of times over the course of history, are as much about expanding horizons as they are about anything else. In our comparatively wealthy modern society, that process of expansion doesn't have to stop when you stop growing in body - except for the fact that we are all limited by the realities of the human condition, and aging in particular.

Our lives have a timer, and we are all well aware of it, for all that many of us prefer not to think about it at all. The whole structure of life and society revolves around the existence of that timer, as it ticks away the freedom we have remaining in which to find and work on something worthwhile. The rush to find meaning in life? There because we don't have enough time. The need to save for retirement and medical costs? The timer again, ticking away our health and ability to fend for ourselves.

When you cannot see even the first shape of what will be your life's work, and time is ticking away, the best thing you can do is to offer a helping hand to those who work on making more time - scientists, advocates, and others who support research and development of rejuvenation biotechnologies. You can do that at the same time as you search for the cause or idea that truly speaks to you, and it beats slumping back into the grey doldrums that seem to afflict so much of our society: people who never found that fire inside, and who have no time left in which to do so.

You have an option that the older folk of previous generations did not: you can help make more time for everyone, more health, more years, and time enough to find meaning in what you do.

It is worth watching the prevalence of longevity insurance offerings, as this is a measure of the degree to which the actuarial community and insurance industry believes that increases in human life span will happen in the near future, but that they will not be large. For the insurer, longevity insurance is a bet on earlier than anticipated death: "Most people buy life insurance to protect against the risks of dying too soon. Now, there are new products offering the same protection if you live too long. It's known as longevity insurance, and there's clearly a huge market for it: Life expectancies are on the rise, cushy pensions are on the decline, and most people don't have enough savings to carry them through two decades or more of retirement. This is not lost on insurance companies, which would like you to think about the product as a pension of sorts - albeit one that you have to buy with your own money. ... But what happens if Merck invents the magic pill and we all live until 105? ... Continued improvements in medicine that allow people to live longer could create losses on our individual annuity business. but these would be more than offset by higher gains on the life insurance. ... Still [if] something like that were to happen, 'at some point, capacity might be limited.'" Companies that bet against large increases in longevity are likely to suffer greatly in decades to come - which is unfortunate for the rest of us, because these concerns are large enough to run to the nearest government for a bailout, and thus we all end up paying for collective bad bets.

Link: http://bucks.blogs.nytimes.com/2011/06/28/longevity-insurance-buying-down-the-risks-of-living-too-long/

An open access paper: "One of the most important and complex diseases of modern society is metabolic syndrome. This syndrome has not been completely understood, and therefore an effective treatment is not available yet. We propose a possible stem cell mechanism involved in the development of metabolic syndrome. This way of thinking lets us consider also other significant pathologies that could have similar [or shared biological pathways], like lipodystrophic syndromes, progeria, and aging. All these clinical situations could be the consequence of a progressive and persistent stem cell exhaustion syndrome (SCES). The main outcome of this SCES would be an irreversible loss of the effective regenerative mesenchymal stem cells (MSCs) pools. In this way, the normal repairing capacities of the organism could become inefficient. ... Stem cell restoration has already demonstrated therapeutic activities in certain systems. For example, it is known that after a stroke, endogenous stem cells are mobilized from the bone marrow in an attempt to heal the damaged neural tissue. Most interestingly, a recent study demonstrated that stroke patients who exhibit a high level of stem cell mobilization have better functional outcomes as opposed to patients with a lower mobilization. ... If [MSCs exhaustion syndrome] is true, then a stem cell therapy approach could be feasible. For instance, ex vivo expansion and reinfusion of MSCs from the patient's own or from allogeneic donors, as evidence shows that MSCs are not immunogenic at all, have been already tested in many clinical trials .... In the best case scenario, MSCs therapy could retard the onset of irreversible lesions associated with metabolic syndrome or at least partially improve those already present."

Link: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3118295/

Artificial cells are one possible line of future biotechnology; devices built to resemble the body's building blocks, essentially nanomachines constructed of proteins. Here researchers take a modest step in that direction, by developing "a novel method of disguising nanoparticles as red blood cells, which will enable them to evade the body's immune system and deliver cancer-fighting drugs straight to a tumor. ... The method involves collecting the membrane from a red blood cell and wrapping it like a powerful camouflaging cloak around a biodegradable polymer nanoparticle stuffed with a cocktail of small molecule drugs. Nanoparticles are less than 100 nanometers in size, about the same size as a virus. ... This is the first work that combines the natural cell membrane with a synthetic nanoparticle for drug delivery applications. This nanoparticle platform will have little risk of immune response. ... Stealth nanoparticles are already used successfully in clinical cancer treatment to deliver chemotherapy drugs. They are coated in a synthetic material such as polyethylene glycol that creates a protection layer to suppress the immune system so that the nanoparticle has time to deliver its payload. ... today's stealth nanoparticle drug delivery vehicles can circulate in the body for hours compared to the minutes a nanoparticle might survive without this special coating. But in [this latest] study, nanoparticles coated in the membranes of red blood cells circulated in the bodies of lab mice for nearly two days. ... one of the next steps is to develop an approach for large-scale manufacturing of these biomimetic nanoparticles for clinical use. ... Researchers will also add a targeting molecule to the membrane that will enable the particle to seek and bind to cancer cells, and integrate the team's technology for loading drugs into the nanoparticle core so that multiple drugs can be delivered at the same time."

Link: http://www.sciencedaily.com/releases/2011/06/110620161300.htm

From the Technology Review: "The drug rapamycin has been found to reverse the effects of Hutchinson-Gilford progeria syndrome, a fatal genetic disease that resembles rapid aging, in cells taken from patients with the disease. Rapamycin, an immunosuppressant drug used to prevent rejection of transplanted organs, has already been shown to extend life span in healthy mice. Researchers hope the findings will provide new insight into treating progeria as well as other age-related diseases. Skin cells from patients with progeria show a slew of defects: deformities in their membranes, decreased growth, and early death. [Researchers] found that rapamycin could reverse these defects by enhancing the cells' ability to degrade the protein progerin, which accumulates in abnormal amounts in progeria patients. It's not yet clear whether the drug will have similar effects on animals or patients. But progeria researchers are planning a clinical trial of rapamycin. ... Researchers say the findings could be relevant beyond this rare genetic disease. Although accumulation of progerin is associated with progeria, the protein also accumulates in small amounts in normal cells, and may be partially responsible for the aging process."

Link: http://www.technologyreview.com/biomedicine/37916/