Fight Aging! Newsletter, May 16th 2011

May 16th 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!



- SENS Foundation 2010 Year-End Report
- Open Biotech: the Lunch-Eating Helping Hand
- More on Body Temperature and Calorie Restriction
- Discussion
- Latest Headlines from Fight Aging!


I strongly encourage you to read the entirety of the SENS Foundation year-end report for 2010. Progress is being made on the science; you'll find information on recent advances that you might not have heard about from other sources. Further, the Foundation has found its feet in the broader scientific community, and is now supported by many of the major figures in aging research. This bodes well for the next ten years of work on the biotechnologies of human longevity:

"In 2009 we launched SENS Foundation. We did it to drive biomedical research towards a functional and cost-effective approach to extending individual health. We did it to raise awareness for an alternative to an increasingly complex and problematic pathology chase in medicine; to redefine regenerative medicine as applied to aging; to enable doctors to think about fixing patients before they were sick.

"We did it to transform the way you think about medicine. We knew it was a big agenda when we set out, and we were fully conscious of how small a public charity we were. We recognized that our first successful steps would depend upon our demonstration of fundamental credibility to the medical science community.

"That is why I am especially pleased to present this 2010 end of year report. As you will read, we have created a mature organization and delivered the networks and collaborations needed to build the rejuvenation biotechnology field. We've expanded our own research programs and have used that expansion to develop collaborations with leading universities and research institutions in regenerative medicine, around the nation and the world. We have, in short, found our voice with a substantial and mainstream scientific community. Rejuvenation biotechnology, as a research field, is emerging, and SENS Foundation has led that charge."

The work of the SENS Foundation is supported by the philanthropy of donors and patrons. If you like what you're reading, then you know what to do:


Open biotechnology will reshape and accelerate the life science industry - including the development of working rejuvenation biotechnology - in the same way that open source software has shaped the the computing industry:

"What are the effects of a large and energetic open development community on an industry? What happens when tens of thousands of people start making their products available for free, sharing data, designs, and improvements openly, and making money for services and expertise rather than through selling protected secrets? Fortunately we don't have speculate on this topic: we know. Look at the software industry, which is presently more vibrant and accomplished than it has ever been, whilst a large proportion of the most important software used around the world is open, freely shared, and constructed by a mix of professional and amateur contributors. Open source software is big business and that community gets things done.

"Why is this relevant? It is relevant because what happens in software today will happen in biotechnology tomorrow. The tools and techniques of biotechnology continue to fall in price, and the knowledge of how to use them is already spread widely beyond the ivory towers in which it originated. I'll note two interesting effects of a future large and bustling open development community in biotechnology: if you're managing a company that's in the business of biotech, then the open community will (a) constantly threaten to eat your lunch, and (b) help you and your employees be far more productive."

You should read the rest: the threat of lunch-eating is also a benefit, believe it or not.


Some interesting comments on calorie restriction research and the biochemistry of natural longevity can be found in the following Fight Aging! post:

"Individuals who significantly reduce their calorie intake have lower core body temperatures compared to those who eat more. The new finding matches research in animals. ... What we don't know is whether there is a cause/effect relationship or whether this is just an association. ... For now, animal models suggest that simply lowering body temperature isn't enough to increase lifespan. In mice and rats that regularly swam in cold water, core body temperature dropped due to exposure to the cold water. But those animals didn't live any longer than normal rodents. Fontana says it appears that how lower temperatures are achieved is important. 'I don't think it ever will be possible to be overweight and smoking and drinking and then take a pill, or several pills, to lower body temperature and lengthen lifespan,' he says. 'What may be possible, however, is to do mild calorie restriction, to eat a very good diet, get mild exercise and then take a drug of some kind that could provide benefits similar to those seen in severe calorie restriction.'"


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, May 13, 2011
Another part of the biochemical mechanisms of calorie restriction is uncovered in nematode worms: "The study [was] conducted on Caenorhabditis elegans (nematodes or roundworms), which are a widely accepted model for human aging research. ... Not only have we been able to identify some of these molecules for the first time in the worm, but we have also been able to show they act as a signal of nutrient availability and ultimately influence the worm's lifespan. What makes this important is that the same molecules are present in both humans and C. elegans, so these molecules may play similar roles in both organisms. ... The molecules identified in the new study are N-acylethanolamines (NAEs), a group of signaling molecules derived from lipids that help indicate nutrient availability in the environment and maintain an animal's internal energy balance. [Researchers showed that] NAE abundance in the worm is reduced during periods of dietary restriction, and that NAE deficiency in the presence of abundant food is sufficient to extend the animal's lifespan. ... It is well known that if you put C. elegans on a restricted diet, you can extend its lifespan by 40 to 50 percent. However, we were amazed to see that if you add back just one of these NAE molecules, eicosapentaenoyl ethanolamide, it completely abrogates the lifespan extension. ... Importantly, this particular NAE is similar to endocannabinoids in mammals, which regulate many different physiological processes including nutrient intake and energy balance, as well as inflammation and neuronal function."

Friday, May 13, 2011
For a variety of reasons lung tissue engineering has lagged behind foundational work on other organs - but there are signs that it is catching up: researchers "have identified a human lung stem cell that is self-renewing and capable of forming and integrating multiple biological structures of the lung including bronchioles, alveoli and pulmonary vessels. ... This research describes, for the first time, a true human lung stem cell. The discovery of this stem cell has the potential to offer those who suffer from chronic lung diseases a totally novel treatment option by regenerating or repairing damaged areas of the lung ... Using lung tissue from surgical samples, researchers identified and isolated the human lung stem cell and tested the functionality of the stem cell both in vitro and in vivo. Once the stem cell was isolated, researchers demonstrated in vitro that the cell was capable of dividing both into new stem cells and also into cells that would grow into various types of lung tissue. Next, researchers injected the stem cell into mice with damaged lungs. The injected stem cells differentiated into new bronchioles, alveoli and pulmonary vessel cells which not only formed new lung tissue, but also integrated structurally to the existing lung tissue in the mice."

Thursday, May 12, 2011
More signs of progress in regenerative medicine: "researchers have demonstrated that human liver cells derived from adult cells coaxed into an embryonic state can engraft and begin regenerating liver tissue in mice with chronic liver damage. ... liver cells derived from so-called "induced-pluripotent stem cells (iPSCs)" could one day be used as an alternative to liver transplant in patients with serious liver diseases, bypassing long waiting lists for organs and concerns about immune system rejection of donated tissue. ... iPSC-derived liver cells not only can be generated in large amounts, but also can be tailored to each patient, preventing immune-rejection problems associated with liver transplants from unmatched donors or embryonic stem cells. ... Although the liver can regenerate in the body, end-stage liver failure caused by diseases like cirrhosis and cancers eventually destroy the liver's regenerative ability ... Currently, the only option for those patients is to receive a liver organ or liver cell transplant, a supply problem given the severe shortage of donor liver tissue for transplantation. In addition, mature liver cells and adult liver stem cells are difficult to isolate or grow in the laboratory."

Thursday, May 12, 2011
Accumulating damage to mitochondrial DNA is one of the causes of aging, and here researchers investigate its role in the aging of stem cells: "Somatic stem cells mediate tissue maintenance for the lifetime of an organism. Despite the well-established longevity that is a prerequisite for such function, accumulating data argue for compromised stem cell function with age. Identifying the mechanisms underlying age-dependent stem cell dysfunction is therefore key to understanding the aging process. Here, using a model [that suffered a greater rate of mitochondrial DNA damage], we demonstrate hematopoietic defects reminiscent of premature [stem cell] aging, including anemia, lymphopenia, and myeloid lineage skewing. However, in contrast to physiological stem cell aging, rapidly accumulating mitochondrial DNA mutations had little functional effect on the hematopoietic stem cell pool, and instead caused distinct differentiation blocks and/or disappearance of downstream progenitors. These results show that intact mitochondrial function is required for appropriate multilineage stem cell differentiation, but argue against mitochondrial DNA mutations per se being a primary driver of somatic stem cell aging."

Wednesday, May 11, 2011
News of another potential way to manipulate mitochondrial function to slow aging: "Mitochondria are the body's energy producers, the power stations inside our cells. Researchers [have] now identified a group of mitochondrial proteins, the absence of which allows other protein groups to stabilise the genome. This could delay the onset of age-related diseases and increase lifespan. ... When a certain MTC protein is lacking in the cell, e.g. because of a mutation in the corresponding gene, the other MTC proteins appear to adopt a new function. They then gain increased significance for the stabilisation of the genome and for combating protein damage, which leads to increased lifespan. These studies also show that this MTC-dependent regulation of the rate of aging uses the same signalling pathways that are activated in calorie restriction - something that extends the lifespan of many different organisms, including yeasts, mice and primates. Some of the MTC proteins identified in this study can also be found in the human cell, raising the obvious question of whether they play a similar role in the regulation of our own aging processes. It is possible that modulating the activity of the MTC proteins could enable us to improve the capacity of the cell to delay the onset of age-related diseases. These include diseases related to instability of the genome, such as cancer, as well as those related to harmful proteins, such as Alzheimer's disease and Parkinson's disease. At the moment this is only speculation, and the precise mechanism underlying the role of the MTC proteins in the aging process is a fascinating question that remains to be answered."

Wednesday, May 11, 2011
From the Washington Post: "The machine looks like the offspring of an Erector Set and an inkjet printer. The 'ink' feels like applesauce and looks like icing. As nozzles expel the pearly material, layer by layer, you imagine the elaborate designs this device could make on gingerbread cookies. But the goo is made of living cells, and the machine is 'printing' a new body part. These machines - they're called three-dimensional printers - work very much like ordinary desktop printers. But instead of just putting down ink on paper, they stack up layers of living material to make 3-D shapes. The technology has been around for almost two decades, providing a shortcut for dentists, jewelers, machinists and even chocolatiers who want to make custom pieces without having to create molds. In the early 2000s, scientists and doctors saw the potential to use this technology to construct living tissue, maybe even human organs. They called it 3-D bioprinting, and it is a red-hot branch of the burgeoning field of tissue engineering. ... The possibilities for this kind of technology are limitless. Everyone has a mother or brother or uncle, aunt, grandmother who needs a meniscus or a kidney or whatever, and they want it tomorrow. ... The promise is exciting. The goal is not to squash that excitement, but to temper it with the reality of what the process is. ... The reality for now is that making such things as vertebral disks and knee cartilage, which largely just cushion bones, is far easier than constructing a complicated organ that filters waste, pumps blood or otherwise keeps a body alive. Scientists say the biggest technical challenge is not making the organ itself, but replicating its intricate internal network of blood vessels, which nourishes it and provides it with oxygen. Many tissue engineers believe the best bet for now may be printing only an organ's largest connector vessels and giving those vessels' cells time, space and the ideal environment in which to build the rest themselves; after that, the organ could be implanted."

Tuesday, May 10, 2011
An op-ed from writer Ben Bova: "'The first immortal human beings are probably living among us today.' That is the opening line of my 1998 nonfiction book, 'Immortality.' Today, more than a dozen years later, a growing number of research scientists and philosophers are beginning to sing much the same tune. They are speaking and writing about our post-human future, a coming era where human beings will be able to live youthful, vigorous, healthy lives for centuries or even longer. There might well be people alive today who may live for centuries, not as crumbling, aging wrecks, but as strong, youthful and active men and women. There is even evidence that aging itself might be not merely slowed or delayed, but actually reversed. One researcher, biogerentologist Aubrey de Grey, flatly states, 'I think the first person to live to a thousand might be 60 already.' Such views are certainly not mainstream. De Grey's detractors have called his ideas 'science fiction.' Yeah. Like space travel, nuclear power, lasers and pocket-sized computers." Bova's view of the medical technologies that will get us there is not complete - he focuses on a third of the overall picture as described in the Strategies for Engineered Negligible Senescence - but his vision of the future is right in the larger sense. The coming age will deliver rejuvenation biotechnology, and it is up to us to work to make that happen soon enough to matter.

Tuesday, May 10, 2011
Thoughts from In Search of Enlightenment: "for the past 5 years or so, I have devoted the bulk of my time and energy contemplating the following question - why hasn't humanity undertaken an ambitious effort to advance the science that could help us redress the single leading cause of disease and death in the world today - namely, biological aging? What I have found most surprising, and alarming, in my teaching and research on this topic is the extent to which people will go to justify their intuition that we should not aspire to modify the current rate of the molecular and cellular decline of humans. These reasons typically range from sentiments like 'aging is natural' and 'doing so will exacerbate inequality', to 'it will cause overpopulation' and 'it will cause ecological disaster'. And yet no one raises these same objections when the discussion is about supporting the science which could help redress just one specific disease of aging - like cancer, heart disease or stroke. No one objects to medical research on stroke by claiming 'a disturbance in blood flow to the brain is natural' or 'preventing or curing strokes will exacerbate inequality' or 'all those people who would be saved from strokes will cause overpopulation or ecological disaster, so it is better they suffer a stroke'. Why not? Why is it that different moral sensibilities tend to be activated when the topic turns to modifying aging?"

Monday, May 9, 2011
This article on the future of being old talks about a failure of the imagination, the broad assumption by many people that their lives will look like the lives of their parents and grandparents in scope and length. Yet the article is itself a failure of the imagination - doing nothing more than projecting present slow trends, without looking at what is taking place in the laboratories. "It used to be that we knew what old age looked like. ... This was back when people over 65 accounted for a relatively small proportion of the US population - under 10 percent in 1960, according to the census from that year - and the average age at the time of death hovered under 70. Since then, advances in medicine and increasingly widespread health-consciousness have caused these numbers to rise precipitously. Demographers predict that by 2030, average life expectancy will have climbed past 80 and people over 65 will account for more than 20 percent of the country's population. ... Plenty has been said about how old age is changing now. But what will it be like for those of us who won't be hitting our 50th reunions for several more decades? Amid all the demographic projections, and all the worries about resources, we tend to assume that the actual texture of life as an old person in the future will be more or less what it is today - that even as old age lasts longer and becomes more prevalent in society, the concept itself, and the kind of life one associates with it, will remain intact. But this is a failure of imagination: In fact, old age in the future - particularly if you're looking at 2050 and later - promises to bear little resemblance to old age as it is experienced in 2011."

Monday, May 9, 2011
Via ScienceDaily: researchers "have established a new method to patch a damaged heart using a tissue-engineering platform that enables heart tissue to repair itself. ... They were able, for the first time, to combine the use of human repair cells that were conditioned during in-vitro culture to maximize their ability to revascularize and improve blood flow to the infarcted tissue with a fully biological composite scaffold designed to deliver these cells to the damaged heart. With this platform, they could both keep the cells within the infarct bed (in contrast to the massive cell loss associated with infusion of cells alone) and enhance cell survival and function in the infarct bed, where most of the cells would have died because of the obstruction of their blood supply. ... [Researchers] removed the cells of a human heart muscle - the myocardium - leaving a protein scaffold with intact architecture and mechanical properties. They filled the scaffold with human mesenchymal progenitors (stem cells that can differentiate into many cell types) and then applied the patches to damaged heart tissue. The patches promoted the growth of new blood vessels and released proteins that stimulated the native tissue to repair itself."



Post a comment; thoughtful, considered opinions are valued. Comments incorporating ad hominem attacks, advertising, and other forms of inappropriate behavior are likely to be deleted.

Note that there is a comment feed for those who like to keep up with conversations.