LONGEVITY MEME NEWSLETTER
May 24 2010
The Longevity Meme Newsletter is a weekly email containing news, opinions, and happenings for people interested in aging science and engineered longevity: making use of diet, lifestyle choices, technology, and proven medical advances to live healthy, longer lives. This newsletter is published under the Creative Commons Attribution 3.0 license. In short, this means that you are encouraged to republish and rewrite it in any way you see fit, the only requirements being that you provide attribution and a link to the Longevity Meme.
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CONTENTS
- Is Aging a Disease?
- Applying Reliability Theory to Aging
- Sarcopenia Caused by Blood Vessel Aging?
- Discussion
- Latest Healthy Life Extension Headlines
IS AGING A DISEASE?
This is an often debated question amongst researchers and advocates, but it isn’t really about words and definitions – this has far more to do with research fundraising and the consequences of regulation:
http://www.fightaging.org/archives/2010/05/talking-point-is-aging-a-disease.php
“At the moment, drug companies and scientists keen to develop their research on aging into tangible results are hampered by regulators in the United States and Europe who will license medicines only for specific diseases, not for something as general as aging. … Because aging is not viewed as a disease, the whole process of bringing drugs to market can’t be applied to drugs that treat aging. This creates a disincentive to pharmaceutical companies to develop drugs to treat it. … Unelected officials of organizations like the FDA in the United States cause untold harm to progress in medical science by (a) placing huge and unnecessary burdens upon research and development, and (b) forbidding outright commercial application for any purpose or disease that is not in their list. It can take a decade – and millions of dollars in the formalized bribery known as lobbying – for a new discovery, new classification, or new form of therapy to be recognized by regulators. Or even longer, as is the case for aging.”
Thus many promising lines of technology are developed very slowly, or not at all. Those that do gain traction are sidelined into commercial development as treatments for specific late-stage diseases of aging – typically far from their most optimal usage. As is true of everything touched by bureaucrats, this situation is a debacle and a vast waste.
APPLYING RELIABILITY THEORY TO AGING
Reliability theory is a way of making predictions on failure modes and mean time to failure for complex systems consisting of many redundant parts. It has seen extensive use in the electronics industry, for example, though its roots are far older than that. There is a growing interest in applying reliability theory to considering aging and longevity:
http://www.fightaging.org/archives/2010/05/applying-reliability-theory-to-aging.php
“Biological organisms can be considered as reliability-engineered, robust systems and applying reliability theory to their basic non-aging components, proteins, could provide insight into the aging mechanism. Reliability theory suggests that aging is an obligatory trade-off in a fault-tolerant system such as the cell which is constructed based on redundancy design. Aging is the inevitable redundancy loss of functional system components, that is proteins, over time. In our study we investigated mouse brain development, adulthood and aging from embryonic day 10 to 100 weeks. We determined redundancy loss of different protein categories with age using reliability theory. We observed a near-linear decrease of protein redundancy during aging.”
If you visit the SENS Foundation science pages, you’ll see that many of the root causes of aging involve accumulating damage to the protein building blocks used by our cells and by the machinery within our cells:
http://www.sens.org/sens-research/research-themes
SARCOPENIA CAUSED BY BLOOD VESSEL AGING?
Sarcopenia is the characteristic loss of muscle mass and strength with advancing age, and there is a healthy debate in the gerontology community over its root causes. Here, researchers put forward a fairly convincing demonstration in support of their theory that sarcopenia results from age-related declines in blood vessel function:
http://www.fightaging.org/archives/2010/05/sarcopenia-as-a-consequence-of-failing-blood-vessel-function.php
“Normally, [the tiny blood vessels in muscle] are closed, but when a young person eats a meal and insulin is released into the bloodstream, they open wide to allow nutrients to reach muscle cells. In elderly people, however, insulin has no such ‘vasodilating’ effect. … We found that by blocking vasodilation, we reproduced in young people the entire response that we see in older persons – a blunting of muscle protein response and a lack of net muscle growth. In other words, from a muscle standpoint, we made young people look 50 years older.”
Blood vessels are an important form of biological infrastructure in our bodies: not just tubes, but in fact complex reactive machinery. They become progressively more damaged by age, unable to adjust as they should, and this causes harm to many of our bodily systems.
DISCUSSION
The highlights and headlines from the past week follow below. If you have comments for us, please do send e-mail to newsletter@longevitymeme.org
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Reason
reason@longevitymeme.org
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LATEST HEALTHY LIFE EXTENSION HEADLINES
AFFIBODIES AND AGGREGATES (May 21 2010)
http://www.longevitymeme.org/news/vnl.cfm?id=4735
From the SENS Foundation: “Aggregates of beta-amyloid (Abeta) and other malformed proteins accumulate in brain aging and neurodegenerative disease, leading progressively to neuronal dysfunction and/or loss. The regenerative engineering solution to these insults is therapeutic clearance of aggregates, extracellular (such as Abeta plaques) and intracellular (such as soluble, oligomeric Abeta). Immunotherapeutic Abeta clearance from the brain is a very active field of Alzheimer’s research, with at least seven passive, and several second-generation active, Abeta vaccines currently in human clinical trials … One challenge to optimal vaccine design is matching the specificity of antibodies the range of Abeta aggregates that form in vivo … agents that sequester one Abeta species may leave other species intact, and in some cases a shift in assembly dynamics can actually promote the formation of one species while clearing or reducing the formation of others … Although in very early in vivo testing, a new approach has emerged that may offer that promise. This is the use of an Abeta-targeting affibody, i.e., a novel non-immunoglobulin binding protein generated through combinatorial protein engineering.”
ANOTHER STUDY LINKING FAT AND DEMENTIA RISK (May 21 2010)
http://www.longevitymeme.org/news/vnl.cfm?id=4734
Via EurekAlert!: “excess abdominal fat places otherwise healthy, middle-aged people at risk for dementia later in life. … [The study] included 733 community participants who had a mean age of 60 years with roughly 70% of the study group comprised of women. Researchers examined the association between Body Mass Index (BMI), waist circumference, waist to hip ratio, CT-based measures of abdominal fat, with MRI measures of total brain volume (TCBV), temporal horn volume (THV), white matter hyperintensity volume (WMHV) and brain infarcts in the middle-aged participants. … Our results confirm the inverse association of increasing BMI with lower brain volumes in older adults and with younger, middle-aged adults and extends the findings to a much larger study sample. … Prior studies were conducted in cohorts with less than 300 participants and the current study includes over 700 individuals. … More importantly our data suggests a stronger connection between central obesity, particularly the visceral fat component of abdominal obesity, and risk of dementia and Alzheimer’s disease … the association between VAT and TCBV was most robust and was also independent of BMI and insulin resistance. Researchers did not observe a statistically significant correlation between CT-based abdominal fat measures and THV, WMHV or BI.”
THE COST OF EXCESS FAT TISSUE (May 20 2010)
http://www.longevitymeme.org/news/vnl.cfm?id=4733
Another paper looks at some of the consequences of becoming obese. In a more fair and productive world, medical costs would be an individual responsibility rather than being socialized as they are at present: “The prevalence of adult obesity has increased in recent decades. It is important to predict the long-term effect of body weight, and changes in body weight, in middle age on longevity and Medicare costs in older ages. … We predicted longevity and lifetime Medicare costs via simulation for 45-year-old persons by body weight in 1973 and changes in body weight between 1973 and 1983. … Obese 45-year-olds had a smaller chance of surviving to age 65 and, if they did, incurred significantly higher average lifetime Medicare costs than normal-weight 45-year-olds ($163,000 compared with $117,000). Those who remained obese between ages 45 and 55 in 1973 to 1983 incurred significantly higher lifetime Medicare costs than those who maintained normal weight. … Chronic obesity in middle age increases lifetime Medicare costs relative to those who remained normal weight. As the survival of obese persons improves, it is possible that Medicare costs may rise substantially in the future to meet the health care needs of today’s obese middle-aged population.”
TRANSFORMING BRAIN CELLS (May 20 2010)
http://www.longevitymeme.org/news/vnl.cfm?id=4732
From the Technology Review: “Support cells in the brain called astroglia can be turned into functioning neurons. … Researchers found that they could transform the cells into two different classes of neurons, and that the neurons could form connections with one another in a dish. Although the research is at an early stage, the finding suggests that scientists could someday recruit existing cells in the brain to repair the brain and spinal cord after a stroke, injury, or neurodegenerative disease. … The addition of one specific gene generated excitatory neurons, which promote activity in other cells. By adding a different gene, they generated inhibitory neurons, which dampen cell activity. In principle, [you] could generate other types of neurons if you choose the appropriate factors … The study adds to growing evidence that certain cell types can be transformed directly into other cell types without first being converted into stem cells. … one of the next challenges is to determine whether these reprogrammed neurons can survive and function in a living brain. Fortunately, the brain seems to have a ready source of astroglia. When the brain is injured, these cells proliferate, similar to the way the skin repairs itself after a wound. The researchers found they could also derive neurons from injury-induced astroglia taken from the brains of adult mice.”
H+ MAGAZINE ON SWITCHING MEMORY BACK ON (May 19 2010)
http://www.longevitymeme.org/news/vnl.cfm?id=4731
From h+ Magazine: “A new study [sheds] some light on how ‘memory disturbances’ in an aging mouse brain are associated with altered ‘hippocampal chromatin plasticity’ – the combination of DNA, histones, and other proteins that make up the chromosomes associated with the hippocampus. Specifically, the study describes an acetyl genetic switch that produces memory impairment in aging 16-month-old mice. Because the acetyl wasn’t present in young 3-month-old mice, the study concludes that it acts as a switch for a cluster of learning and memory genes. … when young mice are learning, an acetyl group binds to a particular point on the histone protein. The cluster of learning and memory genes on the surrounding DNA ends up close to the acetyl group. This acetyl group was missing in the older mice that had been given the same tasks. By injecting an enzyme known to encourage acetyl groups to bind to any kind of histone molecule, [researchers] flipped the acetyl genetic switch to the ‘on’ position in the older mice and their learning and memory performance became similar to that of 3-month-old mice. … [Researchers hope] that the study of hippocampal chromatin plasticity and gene regulation in mice will help them to identify therapeutic strategies to encourage neuroplasticity (the formation of new neural networks in the brain), to improve learning behavior, and to recover seemingly lost long-term memories in human patients.”
MEMORY AND LONGEVITY TREATMENTS (May 19 2010)
http://www.longevitymeme.org/news/vnl.cfm?id=4730
Via EurekAlert!: “Two methods of extending life span have very different effects on memory performance and decline with age. … While the nematode C. elegans is already well known for its utility in longevity research, previously it was not known how the memory of C. elegans compares with that of other animals, or whether longevity treatments could improve learning and memory. To answer these questions, [researchers] designed new tests of learning and memory in C. elegans, then used these tests to identify the necessary components of learning, short-term memory, and long-term memory. They found that the molecules required for learning and memory appear to be conserved from C. elegans to mammals, suggesting that the basic mechanisms underlying learning and memory are ancient. The authors also determined how each of the behaviors declines with age, and tested the effects of two known regulators of longevity – dietary restriction and reduced Insulin/IGF-1 signaling – on these declines. Surprisingly, very different effects on memory were achieved with the two longevity treatments: dietary restriction impaired memory in early adulthood but maintained memory with age, while reduced Insulin/IGF-1 signaling improved early adult memory performance but failed to preserve it with age. These results suggest not only that longevity treatments could help preserve cognitive function with age, but also that different longevity treatments might have very different effects on such declines.”
STEM CELL INDUCED REGENERATION IN THE LUNG (May 18 2010)
http://www.longevitymeme.org/news/vnl.cfm?id=4729
Researchers here demonstrate that comparatively simple stem cell transplants may be effective in regenerating lung injuries: “Human stem cells administered intravenously can restore alveolar epithelial tissue to a normal function in a novel ex vivo perfused human lung after E. coli endotoxin-induced acute lung injury (ALI) … ALI is a common cause of respiratory failure in the intensive care units, often leading to death. It can be caused by both direct injury such as aspiration and pneumonia, and indirect injury such as sepsis and from trauma. … Yearly, ALI affects approximately 200,000 patients in the US and has a 40 percent mortality rate despite extensive investigations into its causes and pathophysiology. Innovative therapies are desperately needed. … we found that intravenous infusion of [stem cells] preferentially homed to the injured areas of the lung, which means that the cells find their way from the bloodstream to the sites in the lung of injury. … In addition to having restored function of alveolar epithelial cells, lungs treated with [stem cells] showed a reduction in inflammatory [cytokine] levels suggesting a favorable shift away from a proinflammatory environment in the injured alveolus.”
AN INTERVIEW WITH A TISSUE ENGINEER (May 18 2010)
http://www.longevitymeme.org/news/vnl.cfm?id=4728
From the Guardian: “The human body has tremendous capacity to repair itself after disease or injury. Skin will grow over wounds, while cells in our blood supply are constantly being manufactured in our bone marrow. But there is a limit to the body’s ability to replace lost tissue. Cartilage cells are notoriously poor at regrowing after injury, for example. As a result, accidents and illnesses – including cancers – often leave individuals with disfiguring wounds or life-threatening damage to tissue. The aim of Molly Stevens, a nanoscience researcher at Imperial College, London, and founder of the biotech firm Reprogen, is a simple but ambitious one. Working with a team of chemists, cell biologists, surgeons, material scientists and engineers, she is developing techniques that will help the body repair itself when it suffers damage. This is the science of regenerative medicine. … One approach that we have had considerable success with involves taking quite straightforward materials including simple polymers and using them to boost bone growth in a person. We made them into gels that we could inject into bones. The key to this technique lies with the fact that our bones are covered in a layer of stem cells. We inject our material under that layer and that wakes up those stem cells. They start to multiply and produce lots of new bone.”
ANOTHER STEP FORWARD FOR TOOTH REGENERATION (May 17 2010)
http://www.longevitymeme.org/news/vnl.cfm?id=4727
Researchers have regrown teeth in rats by manipulating existing stem cells: “a new technique [can] orchestrate the body’s stem cells to migrate to three-dimensional scaffold that is infused with growth factor. This can yield an anatomically correct tooth in as soon as nine weeks once implanted in the mouth. … These findings represent the first report of regeneration of anatomically shaped tooth-like structures in vivo, and by cell homing without cell delivery. … By homing stem cells to a scaffold made of natural materials and integrated in surrounding tissue, there is no need to use harvested stem cell lines, or create a an environment outside of the body (e.g., a Petri dish) where the tooth is grown and then implanted once it has matured. The tooth instead can be grown ‘orthotopically,’ or in the socket where the tooth will integrate with surrounding tissue in ways that are impossible with hard metals or other materials. … A key consideration in tooth regeneration is finding a cost-effective approach that can translate into therapies for patients who cannot afford or who aren’t good candidates for dental implants. Cell-homing-based tooth regeneration may provide a tangible pathway toward clinical translation.”
MORE DATA TO PONDER ON GENDER LONGEVITY DIFFERENCES (May 17 2010)
http://www.longevitymeme.org/news/vnl.cfm?id=4726
From the Max Planck Institute: “Marriage is more beneficial for men than for women – at least for those who want a long life. Previous studies have shown that men with younger wives live longer. While it had long been assumed that women with younger husbands also live longer, [a new study] has shown that this is not the case. Instead, the greater the age difference from the husband, the lower the wife’s life expectancy. This is the case irrespective of whether the woman is younger or older than her spouse. … The mortality risk of a husband who is seven to nine years older than his wife is reduced by eleven percent compared to couples where both partners are the same age. Conversely, a man dies earlier when he is younger than his spouse. For years, researchers have thought that this data holds true for both sexes. They assumed an effect called ‘health selection’ was in play; those who select younger partners are able to do so because they are healthier and thus already have a higher life expectancy. … These theories now have to be reconsidered. It appears that the reasons for mortality differences due to the age gap of the spouses remain unclear.”
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