Fight Aging! Newsletter, October 17th 2011

October 17th 2011

The Fight Aging! 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 Fight Aging!



- Character Traits and Longevity
- A Comprehensive Summary of Calorie Restriction
- The Skeptics and the Peripherally Interested
- The Prospects for a Near Term Funding Desert
- Discussion
- Latest Headlines from Fight Aging!


We know that psychological stress and measures of health are linked by physical mechanisms, so we might hypothesize that other states of mind subtly affect long term health in more direct ways than lifestyle choice:

"The difficulty of establishing measures of mental states makes this an unpopular topic for discussion in some reaches of the scientific community, and I'd be the first to say that a great deal of what passes for soft science these days is a waste of time and money. But there are physiological links between metabolism, aging, and the physical structure that forms the mind, so in the long run there should be some way to measure, assess, and correlate these links. ... The authors [of a recent open access paper] pull in data gathered from hundreds of study participants across the better part of a decade to support their hypothesis for [links between character traits and life expectancy] - including levels of distrust and the degree to which individuals see an open and expansive future ahead of them. The authors see definitive correlations between these comparatively narrow traits and mortality rates, and we might make guesses as to the mechanisms by which these correlations are established. Mechanisms similar to those linking stress with our biology, or more to do with the practice of good health over the years? The paper makes for interesting reading no matter your thoughts on whether this sort of research has any real merit."


What is presently known about calorie restriction, intermittent fasting, and their effects on human health and longevity?

"Lowering calorie intake while still obtaining optimal levels of micronutrients is a practice that, much like regular exercise, has long term beneficial effects on health and longevity in healthy animals and people. These benefits are very reliable and exceed those that can be provided by any presently available medical technology - they also exceed the results of many of the interesting ways to extend healthy life in laboratory animals. This state of affairs won't last, given the pace of progress in biotechnology, but based on the present landscape for medical development we should expect calorie restriction and exercise to remain the best available tools for most of us for a good twenty years yet. I noticed a good open access review paper today [that] covers all of what has been learned of calorie restriction (CR) in the past decade or two. That includes the results of a fair number of human studies, what is now known of the underlying biochemistry and mechanisms, differences between intermittent fasting versus constant dietary restriction (DR), and more."


People who are not moved by your ideas tend not to talk about your ideas - this is one of the challenges inherent in advocacy and activism. How do you find out why you're not reaching as many people as you'd like to reach? Given that, it's helpful to read the works of skeptics who take the time to explain why they're not interested:

"I see that Aubrey de Grey of the SENS Foundation recently gave a talk in Baltimore on SENS and the path to rejuvenation biotechnology. One of those attending was Kavan Peterson, a writer from ChangingAging, which is something of a pro-aging organization - both in the sense of empowerment and opposition to ageism, which are noble causes, but also in the less desirable sense of apologism for aging. There are already far too many talking heads trying to persuade the world that progressively accumulating pain, suffering, and loss of function are just fine and dandy. In any case Peterson, unlike most skeptics, took the time to write. So we should take the time to learn from that."


It looks to me as though we're set to enter a longer downturn in the economy, and thus reduction in the ability of researchers to raise funds:


"From where I stand, it looks much like the equities market has given the sign of doom over the past couple of months. .... what does the sign of doom in the markets mean for the next few years of research funding, and especially speculative research funding for efforts such as SENS? In my experience it means much the same as it does for raising funds to launch startup companies. This is to say that when the economy is in the doldrums, raising funds is very challenging - especially when the equity markets have just started on their way down in earnest and fear is rife. Funding agencies and investors pull back, either because they've suffered losses or because they have the luxury of waiting for a few years for better times.

"To my eyes that makes the next few years the time to double down on raising funds from high net worth philanthropists. These are people who will be slowing their normal flow of deals and investment, but who have most likely not suddenly lost wealth in any meaningful way. There is an argument to be made that investments in early stage research made in the shadow of a falling market and economic destruction will be more effective on a dollar for dollar basis: there may be greater access to researchers and resources at lower prices due to a downturn in the normal state of their employment, for example."


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!



Friday, October 14, 2011
This is an open access report in book format that delves into the factors that cause regional variations in life expectancy and rates of age-related disease - and thus longevity - in the first world. Given its origins, don't expect to see much on the stifling regulation that raises prices and reduces quality and innovation in medicine, but most of the other important contributing factors are addressed: "Over the past 25 years, life expectancy has been rising in the United States at a slower pace than has been achieved in many other high-income countries. Consequently, the United States has been falling steadily in the world rankings for level of life expectancy, and the gap between the United States and countries with the highest achieved life expectancies has been widening. International comparisons of various measures of self-reported health and biological markers of disease reveal similar patterns of U.S. disadvantage. The relatively poor performance of the United States with respect to achieved life expectancy over the recent past is surprising given that it spends far more on health care than any other nation in the world, both absolutely and as a percentage of gross national product. Motivated by these concerns, the National Institute on Aging requested that the National Research Council convene a panel of leading experts to clarify patterns in the levels and trends in life expectancy across nations, to examine the evidence on competing explanations for the divergent trends, and to identify strategic opportunities for health-related interventions to narrow this gap."

Friday, October 14, 2011
From Next Big Future: "The [SENS5] conference itself was high quality - many of the scientists that I describe in my book, 100+, were there. Hearing about the tangible progress that these researchers are continually making was very exciting. I noticed that there were many companies that attended this conference, which is an indication that extending health span is a prospect which is starting to garner serious consideration. ... There are a large and growing number of corporations which, although not explicitly focused on anti-aging, are developing treatments and drugs related to longevity. Gene therapy and personalized medicine are the future, and these companies know that. ... The field of regenerative medicine is getting substantial resources. That includes tissue engineering, which is essentially growing organs. The recent successes with growing and implanting human tracheas are exciting. ... The most common concern is that increased life spans will lead to overpopulation. This fear rests on the false Malthusian idea that population grows faster than our ability to provide for ourselves. We haven't run out of resources as population has grown because humans are a resource themselves, providing problem-solving ideas. Also, fertility and world population growth rates are on the decline. ... Perceptions [of longevity science] have changed. The term health extension is actually less controversial than life extension, since everyone wants robust health. There is little resistance to treatments designed to keep people healthy."

Thursday, October 13, 2011
Via EurekAlert!: "As a person ages, the ability of their beta cells to divide and make new beta cells declines. By the time children reach the age of 10 to 12 years, the ability of their insulin-producing cells to replicate greatly diminishes. If these cells, called beta cells, are destroyed - as they are in type 1 diabetes - treatment with the hormone insulin becomes essential to regulate blood glucose levels and get energy from food. Now, [researchers] have identified a pathway responsible for this age-related decline, and have shown that they can tweak it to get older beta cells to act young again - and start dividing. ... a protein called PDGF, or platelet derived growth factor, and its receptor send beta cells signals to start dividing via an intricate pathway that controls the levels of two proteins in the beta cell nucleus, where cell division occurs. Working with young mice, [researchers] found that PDGF binds to its receptor on the beta cell's surface and controls the level of these regulating proteins allowing cells to divide. However, in older mice, they discovered that beta cells lose PDGF receptors, and that this age-related change prevents beta cells from dividing. [Researchers] further found that by artificially increasing the number of PDGF receptors, they can restore the ability of the beta cell to divide and generate new cells. ... By understanding what genes are turned on and off in a young beta cell, we can try to recreate that genetic environment in older beta cells such that they divide in a desirable, controlled manner."

Thursday, October 13, 2011
Sequencing of the genome of the long-lived naked mole rat was announced earlier this year, but here's more: "Scientists have sequenced the complete genome of the naked mole rat, a pivotal step to understanding the animal's extraordinarily long life and good health. A colony of more than 2,000 naked mole rats at The University of Texas Health Science Center at San Antonio contributed to the findings ... If we understand which genes are different or are expressed differently in naked mole rats - compared to short-lived mice that clearly have poor defenses against aging and cancer - we might find clues as to why the naked mole rat is able to extend both health span and longevity, as well as fight cancer, and this information could be directly relevant and translatable to humans. ... The mouse-sized naked mole rat is the longest-lived rodent known, surviving up to 31 years in captivity. This is much longer than its laboratory rodent relatives, and the naked mole rat maintains good health and reproductive potential well into its third decade. Naked mole rats live underground in large family groups, like termites and bees, with only a single breeding female. These social rodents are extremely tolerant of life in low oxygen and high levels of carbon dioxide."

Wednesday, October 12, 2011
Following on from an earlier consideration of state of the mind and how that may interact with the operation of metabolism over the long term to affect aging, here is a very readable open access paper that tries to draw lines between longevity, psychological factors, and mitochondrial biochemistry: "A central question concerning longevity remains: Why do some people live long whereas others die early? Another equally critical question concerns morbidity: Why is aging associated with a greater incidence of almost every categorized disease - including degenerative, metabolic, and malignant disorders? Since disease incidence, mortality, and longevity are all associated terms in the same aging equation, a more general question may be posed: What are the pathways that impact individuals' rate of aging? ... Compelling evidence suggests that both biological and psychosocial factors impact the process of aging. However, our understanding of the dynamic interplay among biological and psychosocial factors across the life course is still fragmentary. For example, it needs to be established how the interaction of individual factors (e.g., genetic and epigenetic endowment and personality), behavioral factors (e.g., physical activity, diet, and stress management), and psychosocial experiences (e.g., social support, well-being, socioeconomic status, and marriage) in perinatal, childhood, and adulthood influence health across the aging continuum. This paper aims to outline potential intersection points serving as an interface between biological and psychosocial factors, with an emphasis on the mitochondrion."

Wednesday, October 12, 2011
An accumulation of advanced glycation endproducts (AGEs) is one of the changes thought to be a root cause of aging. The research quoted below is only a correlation, but there is plenty more where this came from to back up the viewpoint of AGEs as a contributing cause of aging: "Several studies report that diabetes increases risk of cognitive impairment; some have hypothesized that advanced glycation end products (AGEs) underlie this association. AGEs are cross-linked products that result from reactions between glucose and proteins. Little is known about the association between peripheral AGE concentration and cognitive aging. ... We prospectively studied 920 elders without dementia, 495 with diabetes and 425 with normal glucose (mean age 74.0 years). Using mixed models, we examined baseline AGE concentration, measured with urine pentosidine and analyzed as tertile, and performance on the Modified Mini-Mental State Examination (3MS) and Digit Symbol Substitution Test (DSST) at baseline and repeatedly over 9 years. ... Older adults with high pentosidine level had worse baseline DSST score but not different 3MS score. On both tests, there was a more pronounced 9-year decline in those with high and mid pentosidine level compared to those in the lowest tertile ... [Thus] high peripheral AGE level is associated with greater cognitive decline in older adults with and without diabetes."

Tuesday, October 11, 2011
An open access paper: "Age-related changes in innate immune function and glial-neuronal communication are early and critical events in brain aging and neurodegenerative disease, and lead to a chronic increase in oxidative stress and inflammation, which initiates neuronal dysfunction and reduced synaptic plasticity, and ultimately disruption in learning and memory in the aged brain. Several lines of evidence suggest a correlation between adult neurogenesis and learning. It has been proposed that a decline in hippocampal neurogenesis contributes to a physiologic decline in brain function. Recently, new and important insights relating to the production of new neurons affecting hippocampal-dependent memory ability have been provided. A multitude of factors have been shown to regulate the production of new neurons in the adult hippocampus, many of which change as a result of aging. Yet, the potential importance of neurogenesis in some affective and cognitive behaviors, as well as endogenous tissue repair mechanisms, makes further investigation of neurogenic regulators warranted. We have recent evidence that key regulators of communication between neurons and microglia are disrupted in the aged brain and may be one of the factors that precedes and initiates the observed increase in chronic inflammatory state. In this review the role of dysfunction in these neuronal-glial communication regulators underlying age-related impairments in cognition and hippocampal neurogenesis will be discussed. An understanding of these mechanisms will lead to the development of preventive or protective therapies."

Tuesday, October 11, 2011
From the New Scientist: "Beta cells in the pancreas produce insulin, which regulates glucose levels. People with diabetes either have type 1, in which native beta cells are destroyed by the immune system, or type 2, in which beta cells cannot produce enough insulin. To replace lost or malfunctioning beta cells, [researchers] turned to neural stem cells in the brain. First, they extracted a tiny amount of tissue from the rats' olfactory bulb, the part of the brain which deals with smell, or from the hippocampus, involved in memory. Each area is accessible through the nose, both in rats and humans. Next, the team extracted neural stem cells from the tissue and exposed them to Wnt3a - a human protein that switches on insulin production - and to an antibody that blocks a natural inhibitor of insulin production. After multiplying the stem cells for two weeks, they placed them on thin sheets of collagen which act as a removable scaffold. This allowed the team to lay the sheets incorporating the cells on top of the rats' pancreas without harming the organ itself. Within a week, concentrations of insulin in the blood of both type 1 and type 2 rats that had received treatment matched those in non-diabetic rats. Elevated blood glucose concentrations also returned to normal."

Monday, October 10, 2011
An open access review paper that covers some of the ground leading into the need for mitochondrial repair therapies to be a part of any comprehensive biotechnology toolkit capable of reversing aging: "Aging is an intricate phenomenon characterized by progressive decline in physiological functions and increase in mortality that is often accompanied by many pathological diseases. Although aging is almost universally conserved among all organisms, the underlying molecular mechanisms of aging remain largely elusive. Many theories of aging have been proposed, including the free-radical and mitochondrial theories of aging. Both theories speculate that cumulative damage to mitochondria and mitochondrial DNA (mtDNA) caused by reactive oxygen species (ROS) is one of the causes of aging. Oxidative damage affects replication and transcription of mtDNA and results in a decline in mitochondrial function which in turn leads to enhanced ROS production and further damage to mtDNA. In this paper, we will present the current understanding of the interplay between ROS and mitochondria and will discuss their potential impact on aging and age-related diseases."

Monday, October 10, 2011
The largest, most vocal and organized opposition to engineered longevity emerges from the environmentalist movement and their misguided view of resources and overpopulation. Here is a modest answer to those viewpoints: "Increased health and life spans may be a dream come true, but many worry that it could turn nightmarish owing to problems like overcrowding, resource depletion, and greater pollution. Living a long time might be wonderful on an individual basis, but if many people can do it, would the world still be a place in which we would want to reside? ... Consider the idea that more people automatically means less food for everyone. In reality, as population grew, so did our ability to produce food. Today, many around the world are struggling with obesity, or the consumption of too much food, all while the world's population has been growing. Since 1800, the price of wheat has been steadily declining and the daily intake of calories per capita in both the developed and developing countries has been on the rise. Though it may seem counterintuitive, greater numbers of humans do not necessarily translate to fewer available resources. A key reason for this is that the more people there are, the more ideas there are, and more ideas lead to new and better ways of producing the things that we need. Fiber optic cables, which turned out to be superior to copper as a conduit for data communications, were invented in response to prohibitively high copper prices. Analogous innovations have been engineered in the food industry, such as high-yield dwarf wheat that has saved countless lives in India and Pakistan, and crops that can flourish in areas with less pure or plentiful water. As the innovations driving the longevity revolution improve the length and quality of our lives, concurrent improvements in the environment can be expected. Numerous studies have shown that the less people have to focus their energy on survival and meeting their basic needs, the more they care about making their environment cleaner. This pattern has occurred, and continues to occur, in developed countries like the United States and is now beginning in developing countries."



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