LONGEVITY MEME NEWSLETTER
September 29 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.
- Google's 10^100 Initiative
- Blogging the Cold Spring Harbor Labs Conference
- Latest Healthy Life Extension Headlines
GOOGLE'S 10^100 INITIATIVE
That's 10 to the 100th power. Google has launched a philanthropic initiative that looks very similar to the Amex Members Project that we gave the old college try some weeks ago:
"People are invited to submit ideas for charitable projects that will benefit humanity; Google employees winnow down the (no doubt thousands of) entries to the 100 they like the most; the public at large vote on the 100; and an advisory board picks five to split $10 million in funding."
The project submission phase started last week, and we have nothing to lose at this stage by entering many sensible projects for consideration. This is a competition of merit in this early phase: if you think your plan has merit, then submit it. It doesn't matter if someone else has submitted a similar plan, and in fact I suspect that volume of similar (not the same, but similar) project submissions is a metric all of its own by which Google staff will judge merits. The more varied project submissions there are relating to engineered longevity, the more likely it is that Google employees sympathetic to the cause will see them and move one or more of ahead into the top 100.
So have at it! My first submission is reproduced in the following Fight Aging! post, as an example of the sort of scope appropriate to the level of funding that could be gained:
"I propose that the most promising of nascent mitochondrial repair technologies be funded from their present early-stage standing to readiness for Phase I clinical trials in humans. As a condition of funding, methodologies will be published free of restriction for any group to further develop and bring to market. This will be accomplished with the aid of a non-profit research organization like the Methuselah Foundation, with a history of raising matching funds for large donations, so as to maximize the impact of the funding program."
BLOGGING THE COLD SPRING HARBOR LABS CONFERENCE
Chris Patil of Ouroboros has been blogging the Cold Spring Habor Labs conference on the molecular genetics of aging. If you'd like to learn more about the areas of focus for the mainstream of aging and (potential) longevity research - largely seeking to manipulate metabolism to slow down damage rather than repairing that damage - this is a good place to start. Links are collected in this Fight Aging! post:
"This first session focused on the smaller model organisms that led the first wave of modern biogerontology: yeast, worm, and fly. The talks covered a wide range of systems and techniques, but they held together nicely because they (mostly) converged on common themes: control of calorie-restriction-mediated lifespan extension, and the genetics of the insulin-like growth factor pathway that governs lifespan in many organisms.
"Stephen Spindler (current Mprize record holder for mouse rejuvenation) started off with the refreshing title 'Searching for longevity therapeutics.' He discussed a variety of strategies to identifying lifespan extension drugs, as well as some of their shortcomings, and then proceeded to describe aging-intervention studies currently ongoing in his lab."
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!
LATEST HEALTHY LIFE EXTENSION HEADLINES
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/
Revisiting the Boredom Objection (September 26 2008)
A common objection to engineered longevity is that long lives will mean boredom. People leap directly in their minds from "longer life" to "immortality" and postulate all sorts of unrealistic outcomes. From Depressed Metabolism: "The argument that immortality leads to boredom can take two forms; empirical and logical. In the first case we would observe immortal people and conclude they will become (increasingly) bored. Clearly, this approach is not possible. A milder form of this approach would be to observe very old people and to extrapolate from this to immortality. But this does not seem to be very promising. Many old people are still very curious and involved with the world, even when struggling with aging-induced medical complications. Perhaps there is a tipping point after which old people will get bored. Perhaps not. ... The assumption in [logical] arguments is that an immortal person will exhaust all there is to live for. There are at least two problems with such a line of reasoning. The first problem is whether such a state of affairs (a fixed person with finite possibilities and experiences) logically follows from immortality. Why not assume there will be infinite possibilities and experiences (even if the person stays 'the same') instead? The other problem is that such a line of reasoning reflects an impoverished view of life, emphasizing just quantity and progress."
Writing Off Telomolecular (September 26 2008)
I was on the way to writing off research company Telomolecular earlier this year. It looks like that was the right sentiment; I am disappointed, as the science they were claiming looked very promising. From the Sacramento Bee: Telomolecular "was accused of bilking investors nationwide out of $6.5 million by lying about the progress it was making in finding cures for cancer. ... Telomolecular's lawyer, Gerald Nieser, said the company has already cleaned up its act. 'The company has got all new management. Virtually no one is there now who was involved in the activities that the charges are based on.' ... the Securities and Exchange Commission said Telomolecular Corp. boasted to potential investors that was 'on the verge of success as a biotechnology firm.' That claim was untrue, the SEC said. The company instead was selling a cosmetic skin cream over the Internet and had done less than $100,000 in business in two years." There's no telling what's actually going on under the covers here, but any future science emerging from this direction should meet with skepticism.
Update on Calorie Restriction and Bone Loss (September 25 2008)
The pendulum of evidence is swinging back to suggest that the practice of calorie restriction doesn't lead to bone loss. Via ScienceDaily: "Calorie restriction is the only intervention known to decrease the rate of biological aging and increase longevity ... Young adults who follow a diet that is low in calories but nutritionally sound for six months appear to lose weight and fat without significant bone loss ... After six months, average body weight was reduced by 1 percent in the control group, 10.4 percent in the calorie restriction group, 10 percent in the calorie restriction plus exercise group and 13.9 percent in the low-calorie diet group ... Bone mineral density and blood markers of bone resorption and formation (processes by which bone is broken down and regenerated on a regular basis) were measured at the beginning of the study and again after six months. ... Compared with the control group, none of the groups showed any change in bone mineral density for total body or hip."
Calorie Restriction: Animals Versus People (September 25 2008)
The present scientific consensus on calorie restriction in humans is that it will do wonderful things for your health and resistance to age-related disease, but won't extend the maximum human life span to the same degree that is seen in lower animals: "In the majority of the animal models of longevity, extended lifespan involves pathways related to a growth factor called IGF-1 (insulin-like growth factor-1) ... In calorie-restricted animals, levels of circulating IGF-1 decline between 30 percent and 40 percent. ... We looked at IGF-1 in humans doing calorie restriction [and] found no difference in IGF-1 levels between people on calorie restriction and those who are not. ... we know there are two major influences on IGF-1 levels: calorie intake and protein intake. So we decided to look at the influence of protein ... six [human testers] agreed to lower their protein intake and after three weeks their circulating IGF-1 declined dramatically ... It's much easier to restrict protein than to restrict calories. If our research is on the right track, maybe humans don't need to be so calorie restricted. Limiting protein intake to .7 or .8 grams per kilogram per day might be more effective. That's just a hypothesis. We have to confirm it in future studies."
Nitric Oxide and Aging Blood Vessels (September 24 2008)
Nitric oxide is important in the operation of the endothelium - the lining of blood vessels - but diminishes with age: "The normal endothelium exerts a major vascular protecting role by secreting substances, above all nitric oxide (NO). In disease conditions (such as the presence of cardiovascular risk factors) the activation of endothelial cells can lead to the production and release of contracting factors, which counteract the beneficial effects of NO, and reactive oxygen species (ROS), which in turn cause NO breakdown. ... ageing has been demonstrated to be associated to a progressive impairment in endothelial function both in conduit arteries and resistance vessels, mainly because of an increased production of ROS. Therefore, it is conceivable that endothelial dysfunction plays a major role in favoring age-related increased cardiovascular risk in the elderly." This is an example of the way in which age-damaged cells cause problems in the normal operation of surrounding tissue: cells taken over by damaged mitochondria are exporting reactive oxygen species that breakdown NO, and senescent cells are pushing out their own cocktail of unhelpful chemical instructions as well.
Rust in Your Mitochondria (September 24 2008)
From ScienceDaily: "A restricted-calorie diet, when started in early adulthood, seems to stymie a mitochondrial mishap that may contribute to muscle loss in aging adults ... scientists found pockets of excess iron in muscle cell mitochondria, the tiny power plants found in every cell. The excess iron affects the chemistry inside the mitochondria, sparking the formation of harmful free radicals that can lead a mitochondrion straight to the emergency exit ... Researchers don't know exactly what causes iron to accumulate in mitochondria in aging animals, but a breakdown in how iron is transported through cells could be one reason why. ... If the mitochondria become unhappy or are ready to kick the bucket, they have proteins in the inner and outer membranes that they can open up and commit suicide. ... suicidal mitochondria can damage the rest of the muscle cell, leading to cell death and perhaps to muscle wasting."
Out of Context, Many Old Cells Work Just Fine (September 23 2008)
It is a recurring theme in stem cell and immune system research that cells removed from the context of the aging cellular environment can do their jobs just as well as cells in a young environment: "Understanding how aging impacts the function of memory CD4 T cells is critical for designing effective vaccines. Our studies show that immunological memory generated during youth functions well into old age, whereas that generated later in life functions poorly. This is the result of declines in the function of naive CD4 T cells from aged individuals and contributes to reduced efficacy of vaccines in the elderly. To begin to identify the cause of this defect, we examined the function of memory T cells generated from bone marrow precursor cells (BMPC) from young or aged mice in young hosts. In two different models, memory cells derived from young and aged BMPC exhibit good ex vivo and in vivo function. Importantly, memory CD4 T cells generated from aged BMPC exhibit potent cognate helper function for humoral responses, which are critical for effective immunization. These results indicate that there are no apparent age-related intrinsic defects in BMPC with regards to generation of functional memory T cells." As for many aspects of aging, the problem is one of failing systems and signal controls, not failing components.
A Recellurization Update (September 23 2008)
Via Popular Science: "Some people say they can grow a heart from scratch in 10 years, which is ridiculous. But Dr. Taylor's approach is more realistic because it's so simple and elegant. By using an existing heart, she's taken away all of the structural issues. ... Taylor's system involves flushing animal hearts of cells using a cleanser, at which point only the extracellular matrix remains and 'the hearts look almost clear' ... The next step is to infuse the hearts with a mix of mature and progenitor cardiac cells, which can come from a patient's own body to ensure compatibility. Incredibly, for reasons the team still doesn't understand, the cells seem to know how to divide and proliferate into cardiac tissue inside the empty-shell hearts. This year, Taylor has continued to forge ahead toward her goal of creating transplantable, made-to-order human organs. Soon after she published her rat-heart results, she started working on making recellularized pig hearts - closer in size and shape to the human equivalent - that could pump blood and generate electrical impulses. ... Our hope is that someday we'll be able to take a cadaver or pig organ, decellularize it, and transplant your own cells into the matrix to make an organ that matches your body."
A Potential Downside to Exercise Mimetics (September 22 2008)
From Ouroboros: "AMP-activated kinase (AMPK) agonists mimic the effects of exercise, raising the possibility of a 'workout pill' that could simulate the effects of vigorous activity. The applications to human health are, to mildly understate the case, significant; it sounds almost too good to be true, and it leaves one looking for the catch. ... it turns out that AMPK is activated by certain types of genotoxic stress, and contributes to UV-induced apoptosis in the skin ... activation of AMPK could exacerbate the pro-aging effects that UV light exerts on the skin. Judging from the peroxide results, this also applies to endogenously generated reactive oxygen species (ROS) - which one can't avoid by simply staying out of the sun. Before we panic and throw the exercise mimetic baby out with its carcinogenic bathwater, I'd want to see whether AMPK agonists like AICAR do in fact synergize with stresses like UV and peroxide to increase apoptotic cell death in the skin. If they do ... well, I think we found that catch."
More Multipotent Stem Cells Discovered (September 22 2008)
From EurekAlert!: "The scientists [identified] cells known as pericytes that are multipotent, meaning they have broad developmental potential. Pericytes are found on the walls of small blood vessels such as capillaries and microvessels throughout the body and have the potential to be extracted and grown into many types of tissues ... We believe pericytes represent one of the most promising sources of multipotent stem cells that scientists have been searching for in the quest to make regenerative medicine possible. ... These cells can be extracted easily and painlessly from convenient sources such as fat tissue, dental pulp, umbilical cord and placental tissue, then grown in culture to large numbers and, possibly, re-injected into the patient to heal a broken bone, a failing joint or an injured muscle. ... researchers were able to identify pericytes in all human tissues they analyzed, including muscle, fat, pancreas, placenta and many other samples. Through purification in the lab, these pericytes could then be coaxed into becoming whatever type of tissue the scientists desired. For instance, the researchers took pericytes from the pancreas and then reinjected them into an injured muscle. The cells immediately began regenerating muscle tissue."