Fight Aging! Newsletter, May 9th 2011

May 9th 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!



- Eating and Lazing Your Way to a Shorter Life
- A Look at 55 Theses
- The Relentless Focus on Supplements is Not Helpful
- Merits of the Gung-Ho Argument for Immortality
- Discussion
- Latest Headlines from Fight Aging!


Basic health practices aren't rocket science, and do make a respectable difference to the expected future of your health and longevity:

"A great many people eat too many calories and exercise too little. It's not as though the right amounts of either for generally good health are a state secret, but that doesn't seem to make a great deal of difference. Given the inch of luxury, most people will take the mile - and their health, life expectancy, and bank account all suffer for it. We did not evolve for optimal long-term functioning in a high calorie, sedentary environment, and it shows.

"This is an age upon the verge of developing biotechnologies of rejuvenation and general repair kits for all forms of damage to human tissue and bodily systems. Maybe you're young enough for the progressive advance of science to rescue you from the consequences of being an overfed, lazy lump ... but why risk it? A ten year difference in your life span or health span could mean missing the boat, dying prior to the advent of new medical technologies capable of repairing the damage that you yourself brought about. We're all on that same downward slope; why run faster towards the failure of your body and its component systems?"


55 Theses is a site that outlines, in a methodical, step by step way, the implications of an evolutionary view of human health, based on the work of researcher Michael Rose:

"I think it is a pity that most researchers don't in fact write a book or two outlining their view of science, the world, and progress at some point in their career. Scientific papers are a narrow and entirely insufficient window into a larger worldview, and many scientists have very broad and ambitious visions for the future of their field and the resulting technology. Michael Rose is one such scientist, and has written a few books along the way, of which I recommend the Long Tomorrow for an introduction to his view of aging and necessary strategic directions in the development of longevity science. My attention was recently drawn to a site called 55 Theses that goes a step further and assembles Rose's ideas in an online series of posts, videos, and small essays - and then asks
'knowing this, what can we do to make a difference in our own health and longevity?'"

I see this as an attempt to craft a movement much like the calorie restriction community: people focused on using scientific knowledge to slow aging as much as is possible through measured, considered diet and lifestyle choices.


If even a few percentage points of the vast supplement market's value went instead to real longevity science, we'd be much further along:

"Dietary supplements elbow their way into discussions of human longevity in a very unhelpful way. The loudest voice in the room when it comes to aging is not the research community, but rather the collective megaphone wielded by the salespeople of the 'anti-aging' marketplace - a well-funded army ever ready to puff up thin evidence, misrepresent research, propagate outright lies, and sell you whatever happens to be sitting in their warehouses right this instant. They're just as good at deceiving themselves as anyone else; the best salespeople are the true believers.

"This focus on supplements is, I think, some kind of oral fixation aspect of magical thinking. It's a mythic inheritance from the days of consuming a beast's heart to gain its courage. Researchers learn something about our biochemistry, spread the word, and that then manifests in our broader culture as an urge to consume some aspect of that knowledge - and so the pill sellers and potion manufacturers prosper in every age, regardless of the actual merits of what they sell."


Why not stand up and argue for things that are far beyond the bounds of the present debate? Someone has to be out there pushing out the goal posts and extending the scope of public discussion:

"Public discourse is an arena of the timid, people who build their own cage of narrow visions and incremental goals. Without loud visionaries coming along to rattle the bars and point to the mountains in the distance, nothing would ever get done. Live to 150? Peanuts. If we enacted the goals of SENS, producing a rejuvenation biotechnology toolkit to repair the biochemical damage of aging, we'd all live for thousands of years if the present rate of fatal accidents continued as-is."

Someone has to point these things out, otherwise the entirety of the public debate over longevity science becomes "should we try to give people an extra couple of years, or should we just not bother at all."


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 6, 2011
This article looks at a research group who are working on a way to make cells more resilient to wear and tear - which may or may not have application to a range of conditions: "Their early research looked at skeletal muscle and how calcium plays a role in atrophy and aging. Then in 2006, they published a study showing cells in older mice were essentially leaking calcium - causing a natural aging process and inefficient muscle function. [Researchers] identified and isolated a naturally occurring protein that suggested [this aspect of the] aging process could possibly be reversed through future drugs. They subsequently gained worldwide attention after they identified the protein MG53 as a key initiator of membrane repair in damaged tissue, in the first study to specifically pinpoint a protein responsible for promoting cell repair. The protein is one that all humans, mice and other mammals have. It's a molecule at the forefront of repairing any and all injuries - from normal wear and tear of individual cells to widespread catastrophic trauma. The lab work shows the protein's importance under the microscope: A single needle prick completely deflates and kills a cell without the protein. But a cell bolstered with MG53 quickly recovers, repairing its torn outer layer at an accelerated rate. ... The research is now at the heart of a new drug company that is performing the first trials of an MG53 therapy on mice. ... the university granted TRIMedicine - headquartered in North Brunswick - a license to work on an application of the drug."

Friday, May 6, 2011
The latest grants made by the California Institute for Regenerative Medicine (CIRM): "The Governing Board of the California Institute for Regenerative Medicine, the State Stem Cell Agency, approved a $25 million award to support the first FDA-approved clinical trial based on cells derived from human embryonic stem cells. The award to Menlo Park-based Geron, Corp, will support the company's on-going early phase trial for people with spinal cord injury. This is the first time the agency, which was created by the passage of proposition 71 in 2004, has funded a human clinical trial testing a stem cell-derived therapy. ... The initial phase of the trial will include just a small number of people with recent spinal cord injuries who will receive injections of oligodendrocyte progenitor cells derived from embryonic stem cells into the site of the injury. In animal models, those cells mature into oligodendrocytes, which produce the insulating layer surrounding neurons. The initial phase of the three-year project is designed to test whether the cells are safe. Later phases will include different levels of spinal cord injury and will test increasing doses of the cells. ... At the same meeting, the Governing Board approved 27 Basic Biology III Awards worth $37.7 million. The awards to nine institutions will support research that leads to new insights in stem cell biology and disease origins. This work feeds the pipeline of new discoveries and also informs the work of research groups working on new disease therapies."

Thursday, May 5, 2011
A survey of calorie restriction in many mouse breeds finds that it doesn't work to extend healthy life in all, and that difference appears to be related to the degree to which calorie restriction results in fat loss. This presents an interesting complication, given that it has been clearly demonstrated that surgically removing visceral fat extends life in mice, and the human studies of calorie restriction show unambiguously positive results on health: "Since the 1930s scientists have proposed food restriction as a way to extend life in mice. Though feeding a reduced-calorie diet has indeed lengthened the life spans of mice, rats and many other species, new studies with dozens of different mouse strains indicate that food restriction does not work in all cases. ... [Researchers] studied the effect of food restriction on fat and weight loss in 41 genetically different strains of mice. The scientists then correlated the amount of fat reduction to life span. The answer: Mice that maintained their fat actually lived longer. Those that lost fat died earlier. ... Indeed, the greater the fat loss, the greater the likelihood the mice would have a negative response to dietary restriction, i.e., shortened life. This is contrary to the widely held view that loss of fat is important for the life-extending effect of dietary restriction. It turns the tables a bit."

Thursday, May 5, 2011
The ability to make the immune system act in certain ways is the foundation for a range of powerful therapies: "scientists have discovered a way to wake up the immune system to fight cancer by delivering an immune system-stimulating protein in a nanoscale container called a vault directly into lung cancer tumors, harnessing the body's natural defenses to fight disease growth. The vaults, barrel-shaped nanoscale capsules found in the cytoplasm of all mammalian cells, were engineered to slowly release a protein, the chemokine CCL21, into the tumor. Pre-clinical studies in mice with lung cancer showed that the protein stimulated the immune system to recognize and attack the cancer cells, potently inhibiting cancer growth ... The vault nanoparticles containing the CCL21 have been engineered to slowly release the protein into the tumor over time, producing an enduring immune response. Although the vaults protect the packed CCL21, they act like a time-release capsule. ... [Researchers] plan to test the vault delivery method in human studies within the next three years and hope the promising results found in the pre-clinical animal tumor models will be replicated. ... The vault nanoparticle would require only a single injection into the tumor because of the slow-release design, and it eventually could be designed to be patient specific by adding the individual's tumor antigens into the vault ... The vaults may also be targeted by adding antibodies to their surface that recognize receptors on the tumor. The injection could then be delivered into the blood stream and the vault would navigate to the tumor, a less invasive process that would be easier on the patients. The vault could also seek out and target tumors and metastases too small to be detected with imaging."

Wednesday, May 4, 2011
Researchers continue to put induced pluripotent stem cells (iPSCs) through their paces: "iPSCs, discovered in 2006, are derived by reprogramming adult cells into a primitive stem cell state. They are similar to [embryonic stem cells (ESCs)] in terms of their ability to differentiate into different types of cells in vivo, including endoderm cells that give rise to liver and lung tissue. ... induced pluripotent stem cells (iPSCs) can differentiate into definitive endoderm cells, in vitro, with similar functional potential when compared to embryonic stem cells (ESCs), despite minor molecular differences between the two cell types. These findings are particularly important given growing controversy in the scientific literature about whether subtle differences between iPSCs and ESCs should dampen enthusiasm for iPSCs to serve as an alternative source of differentiated precursor cells for various tissues, such as the liver, lung or blood. The new work provides compelling evidence that iPSCs have potential in regenerative medicine as an investigational tool for the development of treatments against diseases that affect endodermal-derived organs, such as cirrhosis, diabetes, cystic fibrosis and emphysema."

Wednesday, May 4, 2011
Long-lived naked mole-rats exhibit fairly large systematic differences in longevity within the species, and understanding the mechanisms may point the way to a class of therapies for aging: "African mole-rats (Bathyergidae, Rodentia) contain several social, cooperatively breeding species with low extrinsic mortality and unusually high longevity. All social bathyergids live in multigenerational families where reproduction is skewed towards a few breeding individuals. Most of their offspring remain as reproductively inactive 'helpers' in their natal families, often for several years. This 'reproductive subdivision' of mole-rat societies might be of interest for ageing research, as in at least one social bathyergid (Ansell's mole-rats Fukomys anselli), breeders have been shown to age significantly slower than non-breeders. These animals thus provide excellent conditions for studying the epigenetics of senescence by comparing divergent longevities within the same genotypes without the inescapable short-comings of inter-species comparisons. It has been claimed that many if not all social mole-rat species may have evolved similar ageing patterns, too. However, this remains unclear on account of the scarcity of reliable datasets on the subject. We therefore analyzed a 20-year breeding record of Giant mole-rats Fukomys mechowii, another social bathyergid species. We found that breeders indeed lived significantly longer than helpers (ca. 1.5 - 2.2fold depending on the sex), irrespective of social rank or other potentially confounding factors."

Tuesday, May 3, 2011
One of the more widespread present uses of stem cells in the clinic involves cells derived from a patient's own fat tissue. Here an Indian publication surveys the landscape: "Stem cells offer exciting medical promise for repairing or replacing organs that are diseased, damaged or worn out. This promise of repair and regeneration was taken a step further with the advent of Adipose (Fat) Derived Stem Cells (ADSC) which are derived from our own excess body fat. Much like recycling waste, our excess fat can be processed to give us a better quality of life. Currently used for breast augmentation and reconstruction as well as plastic surgery, ADSC are being researched for most debilitating diseases like Myocardial Infarction (MI), diabetes mellitus and neurodegenerative diseases also. ... Clinically, ADSCs have the advantage over their bone marrow-derived counterparts, because of their abundance in numbers - eliminating the need for culturing over days to obtain a therapeutically viable number - and the ease of the harvest procedure itself - being less painful than the harvest of bone marrow. This, in theory, means that an autologous transplant of ADSC will not only work in much the same way as the successes shown using marrow-derived mesenchymal stem cell transplant, but also be of minimal risk to the patient. ... I was a part of adipose tissue derived stem cell trial in spinal cord injury and critical limb ischemia. We could not have a large number of subjects because of cost considerations, but the results were encouraging in spinal cord injury. However in critical limb ischemia results were poor as compared to good results of other studies with bone marrow derived stem cells ... Apart from these cases, Mumbai based Kasiak Research is using ADSC for idiopathic pulmonary fibrosis. ... Apart from this, there are a number of trials investigating applications in ischemic heart disease around the world."

Tuesday, May 3, 2011
A paper that captures the present mainstream view on calorie restriction in humans: "There is increasing evidence that restricting caloric intake may have considerable health benefits in humans. Significant evidence in non-primate animals demonstrates that caloric restriction increases average and maximal life span. However, historically, caloric intake reduction in humans has been involuntary and accompanied by poverty, malnutrition, poor sanitation, and a lack of modern health care. As a result, caloric restriction in people typically has been accompanied by a reduction of both average and maximal life span. Conversely, improvements in standards of living usually are accompanied by an increased food supply and resultant improved health and longevity. The majority of the world is now in a new era where an abundance of caloric intake and its associated obesity are causing widespread chronic illness and premature death. What would happen if one were to institute caloric restriction with high-quality nutrition within an environment of modern sanitation and health care? This review argues that improved health and improved average life span would quite likely result. A lengthening of maximal human life span with this combination is perhaps possible but by no means certain."

Monday, May 2, 2011
Immune therapies are slowly making their way into clinical trials: in recent work, researchers "harvested immune cells from nine patients. They souped up the cells in their lab - in effect giving them the ability to remember cancer cells - multiplied them in number, and infused them back into the patients from whom they been taken. This technique, called adoptive t-cell therapy, primes the immune system to seek out and destroy cancer cells throughout the body. Ten weeks after starting the therapy, seven of the nine patients had more of the specially trained cells than they had started with. The disease in four of the patients had become stable - neither advancing nor retreating. In one patient, the cancer disappeared completely; two years later, it has still not returned. ... The work is not yet ready for commercialization. Laboratory methods for boosting immune cells need to be perfected and made more efficient, and more early clinical trials are needed. ... Five of the [patients] went on to take ipilimumab, a human monoclonal antibody ... With the addition of ipilimumab, [tumors] shrank in three of the five patients and stopped growing in the other two, a response far better than that shown in previous trials of the drug. [This suggests] immunotherapy may help drugs work better."

Monday, May 2, 2011
From EurekAlert!: "A gene therapy approach using a protein called CD59, or protectin, shows promise in slowing the signs of age-related macular degeneration (AMD), according to a new in vivo study ... CD59 delivered by a gene therapy approach significantly reduced the uncontrolled blood vessel growth and cell death typical of AMD, the most common cause of blindness in the elderly. ... Activation of the complement system, a part of the immune system, is responsible for slowly killing cells in the back of the eye, leading to AMD. Activation of this system leads to the generation of pores or holes known as 'membrane attack complex' or MAC in cell membranes. CD59 is known to block the formation of MAC. ... CD59 is unstable and hence previous studies using CD59 have had limited success. The gene therapy approach that we developed continuously produces CD59 in the eye and overcomes these barriers, giving us renewed hope that it can be used to fight the progression of AMD and potentially other diseases. ... [Researchers] delivered CD59 to the eye using a deactivated virus similar to one previously shown to be safe in humans. Using an established mouse model of age-related macular degeneration, they found that eyes treated with CD59 had 62 percent less uncontrolled blood vessel growth and 52 percent less MAC than controls. ... Treatment was effective when administered at a very specific location beneath the retina, but importantly, also when it was administered to the center of the eye. This finding is especially encouraging because it would allow for a safer and more convenient route of administration of treatment."



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