Longevity Meme Newsletter, October 13 2008

October 13 2008

The Longevity Meme Newsletter is a weekly e-mail containing news, opinions and happenings for people interested in healthy life extension: making use of diet, lifestyle choices, technology and proven medical advances to live healthy, longer lives.



- The Way People Think About Aging
- Q3 Folding@Home Prizes Waiting To Be Won
- Longevity and the Composition of Mitochondria
- Discussion
- Latest Healthy Life Extension Headlines


Once upon a time, we all thought of aging as an immutable fact of life - we were brought up that way, and it is human nature to take the world as we are taught it to be and assume it will go forward in that way forever. Some thoughts from an academic:


"Those who have read some of my academic work, or past entries on this blog, will know I am an advocate of longevity science. I am very interested in hearing the arguments and reactions people have to the aspiration to slow human aging, for I myself shared some of these reservations when I first began thinking about these issues. But over time I realized that many of my initial reactions or concerns to longevity science where either misinformed or focused on concerns that are, in the big picture of things, minor when compared to the enormous benefits of extending healthy life."

The realization that, yes, aging is just a medical condition, and yes, we can work to cure it must happen for millions of people if we are to see the establishment of a large and vigorous longevity science research community. On a timescale of decades, significant progress happens only when a great many people wish it to happen. This is a something that we can all help with, by talking about ongoing longevity research, and the prospects for the future:



The Immortality Institute's Folding@Home competition is now in its 3rd quarter - more prizes for those who contribute to this distributed computing project:


"The 3rd quarter competition is now in swing (all competitors scores were reset to zero October 1st) and even more prize money is up for grabs due to generous support from the Life Extension Foundation."

"The process of protein folding, while critical and fundamental to virtually all of biology, in many ways remains a mystery. Moreover, when proteins do not fold correctly (i.e. 'misfold'), there can be serious consequences, including many well known diseases, such as Alzheimer's, Mad Cow (BSE), CJD, ALS, Huntington's, Parkinson's disease, and many Cancers and cancer-related syndromes. ... Folding@home is a distributed computing project - people from throughout the world download and run software to band together to make one of the largest supercomputers in the world. Every computer takes the project closer to our goals."


Comparisons of mitochondrial biochemistry between species of differing innate longevity is one several branches of research to demonstrate the importance of our mitochondria to aging:


"Mitochondria, the power plants of your cells, generate damaging reactive oxygen species (ROS) in the course of their operation: ROS will race off to damage the first thing they can find by reacting with it, such as a cell membrane. Mitochondria themselves have membranes, and are first in line to be damaged by the ROS they generate. Eventually damage accumulates and cascades to change the surrounding cellular environment very much for the worse. This process is an important root cause of degenerative aging."

This process is why those species more resistant to the damaging effects of reactive oxygen species live longer than their peers. "Resistance" here means that the membranes of mitochondria and other cellular components are built of tougher stuff: proteins less likely to be succumb to ROS attack. Even in primates, mitochondrial composition differences are significant between species and highly correlated with longevity. This all reinforces just how central our mitochondria are to aging, and how vital it is to speed research into repairing damaged mitochondria in humans:



The highlights and headlines from the past week follow below.

Remember - if you like this newsletter, the chances are that your friends will find it useful too. Forward it on, or post a copy to your favorite online communities. Encourage the people you know to pitch in and make a difference to the future of health and longevity!




To view commentary on the latest news headlines complete with links and references, please visit the daily news section of the Longevity Meme: http://www.longevitymeme.org/news/

Update on Viruses Versus Cancer (October 10 2008)
A number of groups are presently working on ways to use viruses to precisely target and kill cancer cells. Here's an update on one of them from ScienceDaily: "The Senecavirus [is] harmless to normal human cells, but could infect certain solid tumors, such as small cell lung cancer, the most common form of lung cancer. ... Scientists at Neotropix say that, in laboratory and animal studies, the virus demonstrates cancer-killing specificity that is 10,000 times higher than that seen in traditional chemotherapeutics, with no overt toxicity. The company has developed the 'oncolytic' virus as an anti-cancer agent and is already conducting early phase clinical trials in patients with lung cancer. ... researchers went on to identify several areas on the viral protein coat that they think might hook onto receptors on cancer cells in the process of infecting them. ... It will be critically important to find out what region of its structure the virus is using to bind to tumor cells, and what those cancer cell receptors are. Then we can, hopefully, improve Senecavirus enough to become a potent agent that can be used with many different cancers."

Cuervo On Autophagy (October 10 2008)
A piece from earlier this year at InfoAging: "Aging is characterized primarily by the decline of function in various cellular and molecular systems in the body. These changes are influenced by three factors: genetics, metabolism, and the environment. The focus in Dr. Cuervo's lab is the metabolic changes and resulting damage from these changes that are experienced with age, specifically damage to proteins. Every person experiences this damage to some degree, regardless of their age, but when it comes to repairing or removing the damage, the difference between young and old is clear. In younger people, the damaged or misfolded proteins can be repaired by what are known as chaperone proteins. Yet, like an old car, proteins that have undergone too much repair are not worth maintaining and so they are transported by the chaperone to the lysosome as 'trash' where they bind to a receptor and undergo autophagy (literally, self-eating) inside the organelle. Dr. Cuervo's research focuses on this pathway and how a major decline in its functionality is seen in older organisms." The piece goes on to describe how researchers restored this functionality to youthful levels in aged mice.

A Good Example of a Cell Signaling Application (October 09 2008)
An important field resulting from stem cell research is the discovery and application of biochemical signals to direct existing stem cells in the body - they can be made to repair damage where they would ordinarily remain inactive. Only where stem cells themselves are damaged would new cells be needed: in most situations, greater control over the cells you have is good enough. Via Xconomy: "Provasculon is tackling one of the bigger ideas in regenerative medicine - how to stimulate growth of new blood vessels after they've been damaged by a heart attack. ... in rat studies that a novel protein was able to stimulate a certain type of stem cells (better known to scientists as endothelial progenitor cells) to migrate to damaged heart tissue, promote growth of new blood vessels, and ultimately help the heart pump better after a heart attack. The trick here is that Provasculon is trying to make a genetically engineered form of the key protein, SDF-1, that is able to avoid certain enzymes in the body that would like to chop the protein up and render it useless."

The Hardwired Certainty of Immortality (October 09 2008)
Scientific American takes a look at one of the reasons it's hard to convince people to give an appropriate level of support to longevity research: "the only real mystery is why we're so convinced that when it comes to where we're going 'when the whole thing’s done,' we're dealing with a mystery at all. After all, the brain is like any other organ: a part of our physical body. And the mind is what the brain does - it's more a verb than it is a noun. Why do we wonder where our mind goes when the body is dead? Shouldn’t it be obvious that the mind is dead, too? And yet people in every culture believe in an afterlife of some kind or, at the very least, are unsure about what happens to the mind at death. My psychological research has led me to believe that these irrational beliefs, rather than resulting from religion or serving to protect us from the terror of inexistence, are an inevitable by-product of self-consciousness. Because we have never experienced a lack of consciousness, we cannot imagine what it will feel like to be dead. In fact, it won't feel like anything - and therein lies the problem. ... our ancestors suffered the unshakable illusion that their minds were immortal, and it's this hiccup of gross irrationality that we have unmistakably inherited from them. Individual human beings, by virtue of their evolved cognitive architecture, had trouble conceptualizing their own psychological inexistence from the start."

All Problems Are a Matter of Atoms (October 08 2008)
The ultimate goal of medicine is to be able to reliably and precisely manipulate any the molecules in our bodies: all disease, all aging, is a matter of the wrong molecules being in the wrong place at the wrong time. From Accelerating Future: "It's important to realize the obvious: that every human problem, every malady, every concern, every evil, is at root simply a suboptimal arrangement of atoms and molecules. If this sounds quasi-spiritual, it's because it is - for millennia, pre-scientific humans have attributed all ills to various agents - the gods, magicians, and other humans. This is because these ills demand an explanation, and we didn't have a plausible one, so we made it up. Now, at least in the abstract, we have a concrete, very likely correct answer: suboptimal atomic arrangements. This realization is neither trivial nor too broad to be useless. If your problems are caused by the gods (that some people sadly still believe in...), then to solve them, you either need to give up, on engage in rituals [that] have an empirical impact of precisely zero." There is a simple criteria by which to judge whether new technologies will enable better medicine: do they give us the ability to more precisely and easily move atoms around? Modern biotechnology and the molecular manufacturing that will follow are both good examples.

Pondering Aging Stem Cells in the Gut (October 08 2008)
From Science News: "Old age can hit animals in the gut. That's where elderly fruit flies experience a signaling imbalance that disrupts renewal of the gut wall, new research shows. The discovery could help scientists understand why the body's organs malfunction in old age, and why intestinal cancer is so common among older people. ... Normally, 'adult' stem cells in the intestinal wall churn out a steady stream of new cells to replenish the lining [but] in older animals, this balance seems to be breaking down ... The imbalance appears to be triggered by stress - not psychological stress, but the chemical stresses put on cells by free radicals or by chronic inflammation, both of which get worse as an animal ages. Cells in the gut lining respond to this stress by activating a protective gene [which] is part of a signaling pathway that spurs intestinal stem cells to grow and divide. In response, another signaling pathway - called the Delta/Notch pathway - ramps up to try to keep that growth in check. But too much Delta/Notch can also derail the natural conversion of these stem cells into mature gut cells, causing an abnormal accumulation of halfway converted cells. ... [This] malfunctioning of adult stem cells in old age [is] very similar to what happens in certain human stem cell populations."

Death Versus Destruction (October 07 2008)
From Depressed Metabolism: "the author argues that 'the continuing fact of death renders all talk of liberty ultimately futile.' The author further argues that our concern for the future will diminish as we approach death. But instead of facing the enemy, we devise all kinds of defensive strategies. Life extensionists often speak disparagingly of such coping mechanisms. But [one] can hardly blame people for trying to live in peace with the inevitable. Raging at the prospect of death, if no rational means can be imagined to overcome or delay it during our lifetime is foolish and unproductive. But as Herbert Marcuse said, there is a difference between accepting death and elevating it to something that gives meaning to life. ... Historically, the delay between the technical ability to place a person in low subzero temperatures to avoid decomposition and its actual implementation was not excessive at all. Perhaps the biggest technical obstacle to broader acceptance of cryonics is that most people still believe that the inability of the human body to sustain itself as an integrated organism must necessarily mean the end of the person as well." Which isn't the case, even now. Death is not destruction - at least not until the fine structures of the brain decay. That is why cryonics has a good chance of success: there is all the time in the world to wait in low temperature storage for medical science to become capable of restoring a damaged but intact person to life.

Attacking Macrophages in Fat (October 07 2008)
You might recall that the reason excess fat tissue is so damaging seems to be due to roaming macrophages that release inflammatory biochemicals. Via EurekAlert!, a demonstration that reinforces this point: "Over the past decade, it has become quite clear that obesity gives rise to a state of chronic, low-grade inflammation that contributes to insulin resistance and type 2 diabetes ... [researchers] recently found that a specific subset of macrophages invades obese fat and muscle tissue. Although little was known about them, those macrophages are defined by a CD11c marker expressed on their surfaces. They also produce high levels of proinflammatory chemicals that are linked to the development of obesity-associated insulin resistance. ... We used a genetic 'trick' that allowed us to rapidly kill these macrophages. The treatment killed these cells within hours, and insulin resistance simply reversed itself. It argues strongly that macrophages are causative for the inflammation that leads to diabetes [in those who are obese]. ... The most interesting thing is that this reversal occurs very rapidly. Twenty-four hours later the animals' insulin response had completely normalized. They were still obese, but no longer insulin resistant."

Behind the Scenes of Aging Research (October 06 2008)
This article looks at an aging research lab typical of the community presently working to better understand aging and metabolism: "Aging is not just a simple fact of life. Scientists see life span as a complex process in which genetics and environmental stresses interact involving the whole animal. Regulating the genes - switching them on or off - that control aging may increase healthy, active life spans dramatically. Why is it, ask scientists, that animals have dramatic differences in life spans? Size does not explain the difference. A canary lives only a few years while a bat can live as many as 50 years, yet both are similar in size. And even animals vastly different in size have similar factors and pathways that control life span. ... Dong and his colleagues focused on the master factor DAF-16, which some scientists call the 'Fountain of Youth' gene. They identified a co-factor that, when deactivated, can prolong C. elegan's life span by 40 percent and improve the worm's resistance to damage to its DNA and proteins. So far, researchers have identified several hundred genes in C. elegans that may affect life span. ... Dong's laboratory is collecting the research results, identifying individual genes and grouping them by their link to environmental stresses."

The Mixed Op-Eds Are Becoming More Positive (October 06 2008)
Across the years, I've seen many mixed op-ed columns holding forth on the subject of engineered longevity. There's a particular style to this sort of thing, usually involving disclaimers of any personal interest in living a longer, healthier life - because that is the Done Thing - but I think that on the whole they are trending towards a more positive outlook: "The (at present very remote) prospect of having your conscious mind uploaded on to a computer may not be so enticing, but who wouldn't choose to extend flesh and blood life by the fruits of biomedical science? We do so already, of course, taking the life-sustaining gifts of modern medicine for granted. Given the chance of a little more life, and yet a little more, most of us would take it, eking out our lives indefinitely. We'd keep on keeping on. And radically increased longevity is no longer a fantasy. Quite likely, as the present century unfolds, advances in genetic engineering, nanotechnology and regenerative medicine will deliver on their life-extending promise. ... Life is infinitely rich. The possibilities for new knowledge and experience are endless. So I don't buy the boredom argument. As the philosopher John Harris put it, only the terminally boring are in danger of becoming terminally bored."



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