FIGHT AGING! NEWSLETTER
January 30th 2012
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!
- An Online Chat With Aubrey de Grey and S. Jay Olshansky
- A Culture of Controlling, Malicious Timidity
- SENS5 Video: Trachea Tissue Engineering
- 2012 Buck Symposium in March
- Testing Autophagy as a Mechanism for Longevity through Exercise
- Latest Headlines from Fight Aging!
AN ONLINE CHAT WITH AUBREY DE GREY AND S. JAY OLSHANSKY
Science recently held a live online chat with researchers Aubrey de Grey and S. Jay Olshansky, who more or less represent the two camps to either side of the most important division in longevity science today - not whether or not to work on extending healthy human life span, but rather how to go about it, and how much progress is plausible. The archives are well worth reading:
"S. Jay Olshansky: [Think] about this for a moment. In 1900 life expectancy at birth was about 45. Now it's about 80 for women and 76 for men. We gained 30 years of life - most healthy. Wasn't that worth it? It's hard to imagine the goal of extending healthy life as being harmful in any way - it would enable people to remain working longer if they want, or retire healthier for a longer time period. Health also begets wealth for individuals and populations."
A CULTURE OF CONTROLLING, MALICIOUS TIMIDITY
Sad to say, but progress in medicine is shackled to the desires of the malicious, the timid, and the controlling:
"The course of our future lives, our health and longevity, is swayed by a population of timid mice - but malicious mice, ever ready to use state force to punish and hold back anyone they see as being insufficiently timid. These are people who support the ball and chain of centralized regulation of medical research, people who fear all change, people who fear everything they don't understand, and people who rush to prevent anyone else from enjoying the freedom to undertake personal risk in the course of advancing progress. This describes the vocal mainstream of Western culture: risk-averse, ignorant, and enamored of control for its own sake: a dangerous combination for those who pull upon the strings of law and regulation.
"As I have often remarked in the past, freedom is absolutely essential to progress in medicine: the freedom for researchers to attempt goals as they see fit; the freedom for anyone to fund the research and clinical development they desire; the freedom for people to take personal risks in the use of medical technology; the freedom for groups to create an unhampered marketplace in medicine, in which technologies are rapidly sifted for those with the greatest benefit. These are all simply parts of economic and personal liberty, something that is in extremely short supply in the medical industry.
"So the mice stamp their little feet, and the impersonal engines of government - the unaccountable employees of bureaucratic bodies such as the FDA - move to prevent us all from undertaking rapid development in medicine, on penalty of jail. For our own good, supposedly."
SENS5 VIDEO: TRACHEA TISSUE ENGINEERING
One of the many presentations at SENS5 last year was given by Paolo Macchiarini, who leads the group that works on the tissue engineered trachea transplants that have been in the news of late:
"The ramifications of stem cell research and therapy are enormous. We provided evidence that stem cells can be successfully applied to laryngo-tracheal and windpipe transplants for adults and children but why not imagine to use stem cell therapy in patients with otherwise untreatable end stage diseases of the respiratory system?"
2012 BUCK SYMPOSIUM IN MARCH
The Buck Institute for Research on Aging, based in the Bay Area, California, will be hosting this year's symposium in March:
"At the Buck Institute, world-class scientists work in a uniquely collaborative environment to understand how normal aging contributes to the development of conditions specifically associated with getting older such as Alzheimer's and Parkinson's disease, cancer, stroke, heart disease, diabetes, macular degeneration and glaucoma. Our interdisciplinary approach brings scientists from disparate fields together to develop diagnostic tests and treatments to prevent or delay these maladies. ... At the Buck Institute, world-class scientists work in a uniquely collaborative environment to understand how normal aging contributes to the development of conditions specifically associated with getting older such as Alzheimer's and Parkinson's disease, cancer, stroke, heart disease, diabetes, macular degeneration and glaucoma. Our interdisciplinary approach brings scientists from disparate fields together to develop diagnostic tests and treatments to prevent or delay these maladies."
TESTING AUTOPHAGY AS A MECHANISM FOR LONGEVITY THROUGH EXERCISE
Autophagy shows up in many processes shown to influence longevity in laboratory animals, and so naturally there are research groups trying to pin down exactly how important it is for the workings of exercise:
"Exercise extends healthy life in laboratory animals, but not maximum life span as is the case for calorie restriction. ... There is a school of thought that places the processes of autophagy front and center when it comes to natural methods of adjusting metabolism for length of health and life. Autophagy is the process by which cells break down damaged components, the first step in recycling and replacement: fewer damaged components at any given time is a good thing, and so more autophagy should also be a good thing. You might recall a demonstration that autophagy is essential to the life span and health benefits of calorie restriction, 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!
LATEST HEADLINES FROM FIGHT AGING!
FALLING HEART DISEASE RATES
Friday, January 27, 2012
From the Independent: "It is one of medicine's mysteries: what has caused Britain's plummeting rate of heart disease over the last decade? Deaths from heart attacks have halved since 2002 and no one is quite sure why. Similar changes have occurred in countries around the world but the death rate in England, especially, has fallen further and faster than almost anywhere. ... The researchers looked at 840,000 men and women in England who had suffered a total of 861,000 heart attacks between 2002 and 2010. Overall, the death rates fell by 50 per cent in men and 53 per cent in women. ... For the last 70 years we have been in the grip of a heart disease epidemic that began in the 1940s, rose to a peak in the 1970s and then began to fall. All Western countries were affected and all followed broadly the same pattern. ... researchers conclude that just under half the decline in heart attack death rates in England over the last decade is due to better hospital treatment; the rest is due to changes in lifestyle and the widespread use of pills to lower cholesterol and blood pressure." One might theorize that - at the high level - increased heart disease across the last seven decades is a consequence of the fat and sedentary lifestyles that tend to accompany increases in wealth across the board, while reductions are largely due to improvements in medical technology.
ON GROWTH HORMONE AND "SMALLER IS BETTER"
Friday, January 27, 2012
Here is an open access PDF format mini-review on what is known of growth hormone and aging - that less of it is generally better: "A recent report of virtually complete protection from diabetes and cancer in a population of people with hereditary dwarfism revived interest in elucidating the relationships between growth, adult body size, age-related disease and longevity. In many species, smaller individuals outlive those that are larger and a similar relationship was shown in studies of various human populations. Adult body size is strongly dependent on the actions of growth hormone (GH) and the absence of GH or GH receptor in mice leads to a remarkable extension of longevity. Many mechanisms that may account for, or contribute to, this association have been identified. It is suggested that modest modifications of the diet at different ages may extend human healthspan and lifespan by reducing levels of hormones that stimulate growth."
CREATING SMOOTH MUSCLE CELLS FROM SKIN CELLS
Thursday, January 26, 2012
Here is another example of work on creating patient-specific cells to order, one of the necessary building block technologies needed for an industry that constructs organs and other larger masses of tissue in the body: researchers have "discovered a method of generating different types of vascular smooth muscle cells (SMCs) - the cells which make up the walls of blood vessels - using cells from patients' skin. ... Cardiovascular disease is the leading cause of death in the world. These deaths are mainly caused by the hardening and subsequent blockage of blood vessels due to the accumulation of fatty materials, a condition called atherosclerosis. As not all patients are suitable for conventional stenting or bypass treatment, an option in the future may be to grow new blood vessels to bypass their own blocked vessels. The [team] worked with embryonic stem cells and reprogrammed skin cells, collectively known as human pluripotent stem cells (hPSCs), which have the potential to form any cell type in the body. They discovered a method of creating all the major vascular smooth muscle cells in high purity using hPSCs which can also be easily scaled up for production of clinical-grade SMCs. This is the first time that such a system has been developed and will open the door for comparative studies on different subtypes of SMCs to be carried out, which are otherwise extremely difficult to obtain from patients."
CREATING ALZHEIMER'S NEURONS FROM STEM CELLS
Thursday, January 26, 2012
The principle use of stem cells in the near future is actually research, not therapy - generating diseased cells to order will lower the cost of better understanding the mechanisms of disease and age-related conditions. For example: "scientists have, for the first time, created stem cell-derived, in vitro models of sporadic and hereditary Alzheimer's disease (AD), using induced pluripotent stem cells from patients with the much-dreaded neurodegenerative disorder. ... It's a first step. These aren't perfect models. They're proof of concept. But now we know how to make them. It requires extraordinary care and diligence, really rigorous quality controls to induce consistent behavior, but we can do it. ... We're dealing with the human brain. You can't just do a biopsy on living patients. Instead, researchers have had to work around, mimicking some aspects of the disease in non-neuronal human cells or using limited animal models. Neither approach is really satisfactory. ... With the in vitro Alzheimer's neurons, scientists can more deeply investigate how AD begins and chart the biochemical processes that eventually destroy brain cells associated with elemental cognitive functions like memory. Currently, AD research depends heavily upon studies of post-mortem tissues, long after the damage has been done. ... The differences between a healthy neuron and an Alzheimer's neuron are subtle. It basically comes down to low-level mischief accumulating over a very long time, with catastrophic results. ... The researchers have already produced some surprising findings. ... In this work, we show that one of the early changes in Alzheimer's neurons thought to be an initiating event in the course of the disease turns out not to be that significant."
EARLY TRIALS OF EMBRYONIC STEM CELLS TO TREAT DEGENERATIVE BLINDNESS
Wednesday, January 25, 2012
From the New York Times: "A treatment for eye diseases that is derived from human embryonic stem cells might have improved the vision of two patients. The report, published online in the medical journal The Lancet, is the first to describe the effect on patients of a therapy involving human embryonic stem cells. ... The results [come] from the second clinical trial involving the stem cells, using a therapy developed by Advanced Cell Technology to treat macular degeneration, a leading cause of blindness. ... Both patients, who were legally blind, said in interviews that they had gains in eyesight that were meaningful for them. One said she could see colors better and was able to thread a needle and sew on a button for the first time in years. The other said she was able to navigate a shopping mall by herself. ... esearchers at Advanced Cell Technology turned embryonic stem cells into retinal pigment epithelial cells. Deterioration of these retinal cells can lead to damage to the macula, the central part of the retina, and to loss of the straight-ahead vision necessary to recognize faces, watch television or read. Some 50,000 of the cells were implanted last July under the retinas in one eye of each woman in operations that took about 30 minutes. ... Before the treatment, the woman with Stargardt's was able to see the motion of a hand being waved in front of her but could not read any letters on an eye chart. Twelve weeks after the treatment, she was able to read five of the biggest letters on the eye chart with the treated eye, corresponding to 20/800 vision, according to the paper."
ON STEM CELLS AND THEIR AGING AND POTENTIAL REJUVENATION
Wednesday, January 25, 2012
An interview with a researcher: "Advances in the study of stem cells have fueled hopes that someday, via regenerative medicine, doctors could restore aging people's hearts, livers, brains and other organs and tissues to a more youthful state. A key to reaching this goal - to be able to provide stem cells that will differentiate into other types of cells a patient needs - appears to lie in understanding 'epigenetics,' which involves chemical marks stapled onto DNA and its surrounding protein husk by specialized enzyme complexes inside a cell's nucleus. These markings produce long-lasting changes in genes' activity levels within the cell - locking genes into an 'on' or 'off' position. Epigenetic processes enable cells to remain true to type (a neuron, for instance, never suddenly morphs into a fat cell) even though all our cells, regardless of type, share the same genetic code. But epigenetic processes also appear to play a critical role in reducing cells' vitality as they age. ... Aging seems to involve a gradual deterioration of function as cells and tissues are exposed to stresses either from outside the body, such as chemicals we ingest or irradiation from the sun, or from inside the body, such as free radicals, produced every moment when cells are making energy. These myriad insults can, among other things, alter a cell's epigenetic settings, resulting in changed patterns of gene activity that diminish the cell's overall ability to function. ... Although some aspects of cellular aging - DNA mutations, for instance - would be difficult to 'reset,' we and others have done experiments suggesting that many of the characteristics of old cells and tissues can indeed be reversed, restoring them to a more youthful state. Much of our work has focused on stem cells, and in particular on the changes that occur with age and that reduce stem cells' ability to maintain or repair tissues. Our findings fit nicely with the idea that some of the causes of aging are epigenetic in character, as opposed to actual damage to genes. Most importantly, our data suggest that cells and tissues can be rejuvenated without losing their specific characteristics - old muscle stem cells, when rejuvenated, remain muscle stem cells rather than become some more generic, undifferentiated cell."
AN INTERVIEW WITH PAOLO MACCHIARINI
Tuesday, January 24, 2012
NPR interviews Paolo Macchiarini, who leads the group working on transplanted tissue engineered tracheas: "How was the scaffold for the synthetic trachea built? Well, basically, by the same fibers that everybody of us has, nanofibers; very, very small fibers that are composed and native to the human trachea. So when we wanted to transplant this organ, we thought what is best. And the best would be to just replicate what human nature has done. And this is the reason why we use these very thin fibers. ... So I imagine you could try to do this with other organs in the body, other things. ... Well, we are starting to learn what happens with this still experimental therapy. So I'm not so pessimistic to try to do the same with other tissues or organs. And since I'm a thoracic surgeon, I deal with organs of the chest. So I would think of the esophagus at the chest wall, at the liver - at the lung, and eventually at the heart. Yes. ... depending on the degree of difficulty of the three dimensional aspect of the tissue, you can produce a trachea, for instance, just the tube, in two days. And a bifurcated trachea in 10 days. So now - then you need two days for getting the cells, reseeding the grafts, or in two weeks you have an entire trachea. ... And perhaps you might extend your work further, because you deal in this and possibly into the lungs. ... Well, ideally, yes. But to me my dream would be another one. It would be rather than replacing the lung or replacing the heart, you use cell therapy to treat these organs before they ultimately do not work anymore. so rather than doing a transplantation, just when we have the first signs of insufficiency, whether to treat these organs with the patient's stem cells, probably targeting the defect that they have, so prolonging and extending their life." This last point is the likely future of tissue engineering - not to build outside the body and require major surgery, but rather regenerate in situ by issuing commands to existing stem cell populations, or repair those stem cells where they are deficient.
BETTER CHOICES LEAD TO GREATER LONGEVITY
Tuesday, January 24, 2012
The ape inside is troubled when it learns that someone else has more than you do - which is something that you should strive to ignore if you like living in a peaceful society. The lesson to take away from this article and research is that the generally better choices made by the wealthy when it comes to health are equally available to near everyone - the effects of diet and exercise outweigh most other factors in the wealthier nations, assuming that you didn't suffer rare bad luck in your genetic legacy. "Wealthy people possess more than just spending power. They also have more time to live than poor people do, a new study has found. The wealthiest people in the United Kingdom live longer than the poor, according to a new study from the U.K.-based Longevity Science Advisory Panel. Male higher managers and professionals in the U.K. have a life expectancy of 83.8 years, and female higher managers and professionals can expect to live 86.7 years, in contrast to workers with routine tasks who die about three years earlier. The study found that the longevity gap has widened between the rich and poor over time. While male lower management and higher management had virtually the same life expectancy in the early 1980s, now their longevity gap has widened to almost a year, according to the study. Similarly, while male workers with routine tasks died two years earlier than male higher managers in the early 1980s, now male workers with routine tasks die 3.5 years earlier than male higher managers on average, according to the study. The study said that poorer people die earlier because they tended to lead less healthy lifestyles. The study pointed to less access to health services, alcohol consumption, smoking, and obesity as leading to lower life expectancy."
A CHART ON TELOMERES AND AGING
Monday, January 23, 2012
The Science for Life Extension Foundation produces very attractive materials to both explain the science of aging and advocate for larger research programs aimed at the extending healthy human life span. Most of these documents and posters start out in Russian, but a fair number are translated over time. Here, Maria Konovalenko shows off an English-language poster describing what is known of the relationships between telomeres, telomerase, and aging. Telomeres are caps of repeated DNA sequences attached to the ends of chromosomes, shortening with cell divisions, and lengthened by the actions of telomerase. They are a central part of evolved feedback loops involving cell aging and replication, and are influenced by health, stress, and many other factors not yet fully understood. Telomeres generally become shorter on average with increased age and ill health, but the roots of that process are complicated: it is unclear as to whether changes in telomere length maintenance are a contributing cause or a resulting consequence of age-related degeneration and accumulated cell-level damage."
ETHANOL AND NEMATODE LIFE SPAN
Monday, January 23, 2012
An interesting result, albeit with no immediate application - it is perhaps surprising that this wasn't discovered long ago, given the common uses of ethanol in the laboratory: "Minuscule amounts of ethanol, the type of alcohol found in alcoholic beverages, can more than double the life span of a tiny worm known as Caenorhabditis elegans, which is used frequently as a model in aging studies. ... The worms normally live for about 15 days and can survive with nothing to eat for roughly 10 to 12 days. ... Our finding is that tiny amounts of ethanol can make them survive 20 to 40 days. ... Initially, [researchers] intended to test the effect of cholesterol on the worms ... The scientists fed the worms cholesterol, and the worms lived longer, apparently due to the cholesterol. They had dissolved the cholesterol in ethanol, often used as a solvent, which they diluted 1,000-fold. ... It's just a solvent, but it turns out the solvent was having the longevity effect. The cholesterol did nothing. We found that not only does ethanol work at a 1-to-1,000 dilution, it works at a 1-to-20,000 dilution. That tiny bit shouldn't have made any difference, but it turns out it can be so beneficial. ... It's possible there is a trivial explanation, but I don't think that's the case. We know that if we increase the ethanol concentration, they do not live longer. This extremely low level is the maximum that is beneficial for them. ... What is even more interesting is the fact that the worms are in a stressed developmental stage. At high magnifications under the microscope, it was amazing to see how the worms given a little ethanol looked significantly more robust than worms not given ethanol."