The industry that provides antioxidant supplements to the world has tremendous inertia: enormous income and a very loud voice, and thus little incentive to react to advances in scientific knowledge that might reduce that revenue stream if acted upon. So despite the scientific consensus that ingested antioxidants are not in fact wonderful for your health, and may even be modestly harmful over the long term, the larger players in the industry continue onward as though it's still 1992 outside their offices.

On the other side of the fence, the public at large keeps buying the products as though it's still 1992, just as blithely ignoring what the scientific community has to say on the matter. Everyone wants that silver bullet to be available now rather than tomorrow, and wants it badly enough to buy lead painted up to a nice sheen if that's all there is. All in all it's a good reminder that any institutional knowledge or common wisdom is likely to be a decade or two out of date - it takes time for information to percolate, even in this age of instant electronic overcommunication. There is seemingly so much that everyone has to say, day in and day out, and yet the important data still takes years to get from point A to point B.

Here is a good open access paper on antioxidants and just how far removed from reality the common wisdom is these days. I imagine it will take a few more years of authoring similar review papers for the point to start to sink in:

Antioxidants are assumed to provide numerous benefits, including better health, a reduced rate of aging, and improved exercise performance. Specifically, antioxidants are commonly "prescribed" by the media, supplement industry, and "fitness experts" for individuals prior to training and performance, with assumed benefits of improved fatigue resistance and recovery. This has provoked expansion of the supplement industry which responded by creation of a plethora of products aimed at facilitating the needs of the active individual. However, what does the experimental evidence say about the efficacy of antioxidants on skeletal muscle function? Are antioxidants actually as beneficial as the general populous believes? Or, could they in fact lead to deleterious effects on skeletal muscle function and performance?

...

Experimental evidence does not support the "common knowledge" that antioxidant treatment greatly improves exercise performance and recovery. On the contrary, studies with antioxidant supplementations generally show no effect on muscle function during and after exercise.

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Less fat tissue is unambiguously good for you over the long term, and one side effect of calorie restriction is the loss of excess fat tissue - but that is only a side effect. More interesting stuff is going on at the level of cells and their mechanisms: "Caloric restriction (CR) slows the aging process and extends longevity, but the exact underlying mechanisms remain debatable. It has recently been suggested that the beneficial action of CR may be mediated in part by adipose tissue remodeling. Mammals have two types of adipose tissue: white adipose tissue (WAT) and brown adipose tissue (BAT). In this study, proteome analysis [was] performed on both WAT and BAT from nine month old male rats fed ad libitum or subjected to CR for six months. Our findings suggest that CR activates mitochondrial energy metabolism and fatty acid biosynthesis in WAT. It is likely that in CR animals WAT functions as an energy transducer from glucose to energy-dense lipid. In contrast, in BAT CR either had no effect on, or down-regulated, the mitochondrial electron transport chain, but enhanced fatty acid biosynthesis. This suggests that in CR animals BAT may change its function from an energy consuming system to an energy reservoir system. Based on our findings, we conclude that WAT and BAT cooperate to use energy effectively via a differential response of mitochondrial function to CR." It is worth noting that there are other signs that the biochemistry of fat tissue, and its effects on health, can be dramatically altered - see the research on fat in GHRKO mice, for example.

Link: http://www.ncbi.nlm.nih.gov/pubmed/22414572

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

One of the underlying mechanisms by which the advanced glycation endproducts (AGEs) that build up with age cause harm is through hammering on the receptor for AGEs, or RAGE. Some Alzheimer's researchers are looking into targeting RAGE in order to remove the contribution of AGEs to that condition, and it is possible that the results of their work may have more general application to AGEs in aging - though the best possible strategy would be to remove the AGEs rather than work around them: "Researchers have taken another crack at a promising approach to stopping Alzheimer's disease that encountered a major hurdle last year. ... scientists have developed a compound that targets a molecular actor known as RAGE, which plays a central role in mucking up the brain tissue of people with the disease. Scientists [synthesized] a compound that stops RAGE in mice - reversing amyloid deposits, restoring healthy blood flow in the brain, squelching inflammation, and making old, sick mice smarter. But the scientists caution that the work has a long way to go before it's considered as a possible treatment in people. ... A phase 2 study in 399 people of another compound designed to stop RAGE - which stands for Receptor for Advanced Glycation Endproducts - was halted prematurely in November when scientists had questions about the compound's safety at high doses, and after early results indicated that the compound was not helping patients with Alzheimer's disease. ... The benefits of blocking RAGE are even greater than has been realized. RAGE is central to many mechanisms that wreak havoc in the brains of people with Alzheimer's disease. It turns out that when you inhibit RAGE, you block molecules central to creating inflammation in the brain, and that is a major problem with Alzheimer's disease."

Link: http://www.urmc.rochester.edu/news/story/index.cfm?id=3440

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

A billion people will die between now and the earliest plausible date for the first package of rough and ready but working rejuvenation therapies - say twenty years from now. Another few decades will pass for the technology to work its way out to global availability at low cost, and the deaths by aging will continue in less fortunate regions while this happens. Even after aging is completely conquered, there will be an ongoing toll of death due to accidents and whatever passes for disease in the age of medical nanotechnology. Death isn't going away completely for we biological folk, no matter how well we do in the field of medicine in the foreseeable future: medicine can't wave away falling rocks.

Thus will always be a role for what we might term post-mortem critical care: technologies and services to preserve the fine structure of the brain and the mind it contains following death, and keep them preserved until such time as that patient can be restored to life. At present the only post-mortem critical care option is cryonics, with what looks like a fair few years to wait for technology to advance to the point of restoration, and thus an unknown chance of eventual success for any individual - but a significantly greater chance than is offered by the grave, of course. In contrast, in a future in which the technology to restore a preserved person exists, cryonics and other preservation technologies like plastination will occupy a more dynamic position in the medical toolkit, and patients might expect to wait in a preserved state only for transport to the nearest major population center.

At last year's SENS5 conference, Max More, CEO of cryonics company Alcor, gave this presentation on the future of his industry:

Cryonics involves the cryopreservation of humans as soon as possible after legal and clinical "death". Legal and clinical death differ importantly from biological death or true (irreversible) cessation of function. It is therefore a mistake to portray cryonics as an alternative to cremation or burial. It is true that cryopreserved people are not alive but neither are they dead. Cryonics should be seen as part of the field of life extension. Cryonics enables the transport of critically ill people through time in an unchanging state to a time when more advanced medical and repair technologies are available. Even after "longevity escape velocity" has been attained and aging has been largely tamed, cryonics will continue to be needed for people who die of accidents or diseases for which there is no cure at the time.

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Here is a study claiming a noticeable impact on mortality rates from eating red meat. Weight is considered to some degree via body mass index, but I have to wonder if this only reflects a modest association of red meat consumption with other, less healthy lifestyle choices rather than an actual red-meat-based mechanism - as an obvious candidate mechanism for that isn't also present in all meat consumption isn't springing to mind: researchers "found that red meat consumption is associated with an increased risk of total, cardiovascular, and cancer mortality. The results also showed that substituting other healthy protein sources, such as fish, poultry, nuts, and legumes, was associated with a lower risk of mortality. ... [Researchers] observed 37,698 men from the Health Professionals Follow-up Study for up to 22 years and 83,644 women in the Nurses' Health Study for up to 28 years who were free of cardiovascular disease (CVD) and cancer at baseline. Diets were assessed through questionnaires every four years. ... One daily serving of unprocessed red meat (about the size of a deck of cards) was associated with a 13% increased risk of mortality, and one daily serving of processed red meat (one hot dog or two slices of bacon) was associated with a 20% increased risk. ... These analyses took into account chronic disease risk factors such as age, body mass index, physical activity, family history of heart disease, or major cancers. ... Replacing one serving of total red meat with one serving of a healthy protein source was associated with a lower mortality risk: 7% for fish, 14% for poultry, 19% for nuts, 10% for legumes, 10% for low-fat dairy products, and 14% for whole grains. The researchers estimated that 9.3% of deaths in men and 7.6% in women could have been prevented at the end of the follow-up if all the participants had consumed less than 0.5 servings per day of red meat."

Link: http://www.sciencedaily.com/releases/2012/03/120312162746.htm

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Via ScienceDaily: researchers "have made early retina structures containing proliferating neuroretinal progenitor cells using induced pluripotent stem (iPS) cells derived from human blood. And in another advance, the retina structures showed the capacity to form layers of cells - as the retina does in normal human development - and these cells possessed the machinery that could allow them to communicate information. ... Put together, these findings suggest that it is possible to assemble human retinal cells into more complex retinal tissues, all starting from a routine patient blood sample. Many applications of laboratory-built human retinal tissues can be envisioned, including using them to test drugs and study degenerative diseases of the retina such as retinitis pigmentosa, a prominent cause of blindness in children and young adults. One day, it may also be possible replace multiple layers of the retina in order to help patients with more widespread retinal damage. ... We don't know how far this technology will take us, but the fact that we are able to grow a rudimentary retina structure from a patient's blood cells is encouraging, not only because it confirms our earlier work using human skin cells, but also because blood as a starting source is convenient to obtain."

Link: http://www.sciencedaily.com/releases/2012/03/120313185232.htm

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

This is an era of data in the sciences - endless, vast stores of data, with more pouring in constantly from new studies. In most fields the infrastructure to manage that data is still under construction; in the life sciences, for example, the rapid advance of bioinformatics and biotechnology in general has outpaced the strategies for data management. The data infrastructure is lacking, even as it is being built up rapidly. This has consequences on the efficiency of research and the speed of progress, but researchers are not blind to this present state of affairs.

Here, for example, Maria Konovalenko of the Science for Life Extension Foundation presents at last year's SENS5 conference, calling for better and more systematic management of data in longevity research initiatives - which is effectively a form of advocacy for lowering the cost of exchange of information between research groups.

Traditionally evaluation of age-related changes is performed by physiological, functional and psychological tests, by visual examination and some biochemical analyses. There is a big gap between the molecular data of aging and their implementation in practice mainly because aging data is scarce and it gets lost in the stream of bio-medical knowledge. As we know only a few databases exist that concern the molecular aspects of aging and none of them describes age-related changes and phenotype context like cell type or tissues.

We propose creation of an open web-based Integrated Information System on Aging Biomarkers. The goals of the System: 1. Systematization of data on age-related changes happening on various levels of organization in humans and model animals 2. Systematization of experimantal data on interventions in aging processes in model animals 3. Integration of clinical data on the impact of various interventions on aging processes in patients 4. Creation of a basis for modeling of aging processes, therapeutic interventions and their impact on patients' health and longevity

When development of life extending therapies begins in any earnest way (as opposed the present expensive dabbling with metabolic manipulation to slightly slow aging), it will be necessary to start keeping score and measuring well. Even before then, and as I pointed out above, there is more data than can easily be made useful at this time - that has to change in order to build a better foundation for the next generation of research projects.

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

With advancing age - and accumulating damage - the immune system moves into a state wherein it is constantly roused and on alert, exacting a toll on the integrity of tissue and cells through its signaling and activity, but also ineffective at actually tackling pathogens, senescent cells, precancerous cells, and other things that should be destroyed. So you have constant chronic inflammation and all its downsides with none of the compensatory immune activity boost that comes with short-term inflammation in the young. Researchers have given the name "inflammaging" to this progressive and increasingly harmful disarray of the immune system, and you'll find a few introductions to inflammaging as a concept back in the Fight Aging! archives.

Below is an open access paper that gives an overview of inflammaging and how it relates to some of the forms of cellular damage that cause aging. In this paper, the researchers paint a picture of inflammaging derived from root causes that involve mitochondrial damage and progressive failure of autophagy to clear out that damage, two line items that have been examined a fair number of times here in the past - under the Strategies for Engineered Negligible Senescence (SENS) viewpoint these two are amongst the fundamental, root causes of aging.

Inflammaging: disturbed interplay between autophagy and inflammasomes

In 2000, Franceschi et al. coined the term "inflammaging" in order to refer to a low-grade pro-inflammatory status appearing during the aging process. They emphasized the role of macrophages as well as cellular stress and genetic factors in the generation of the inflammaging condition. In addition, they hypothesized that this inflammatory environment could predispose the organism to the development of several age-related diseases. During recent years, this scenario has been confirmed by a plethora of experimental evidence. ... Interestingly, the aging process is simultaneously accompanied by both the features accelerating inflammaging and the counteracting, so-called anti-inflammaging characteristics. It seems that the balance between these opposite forces controls the outcome of the aging process, either leading to frailty and degenerative diseases or a healthy old age and longevity.

...

The aging process is associated with a decline in autophagic capacity which impairs cellular housekeeping, leading to protein aggregation and accumulation of dysfunctional mitochondria which provoke reactive oxygen species (ROS) production and oxidative stress.

Recent studies have clearly indicated that the ROS production induced by damaged mitochondria can stimulate intracellular danger-sensing multiprotein platforms called inflammasomes. [As a result of inflammasome activity, signaling molecules called] cytokines provoke inflammatory responses and accelerate the aging process by inhibiting autophagy.

There has been some good progress in recent years in pulling things together in the big picture - and the more that we see the mechanisms of SENS featured, the better to my eyes. That ways lies increased support for rejuvenation biotechnology that will actually work to reverse aging, rather than the present mainstream course of aiming to slow down aging just a little sometime in next few decades.

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

The immune system falls apart with age in ways that are as much a matter of configuration as wear and tear - it is a machine in which the programming runs awry, leading it to do the wrong things at the wrong time, or just do nothing when it should be doing something. This activity leads to damage, which in turn accelerates aging: "Immune aging is associated with loss of critical immune functions, such as host protection from infection and malignancy. Unexpectedly, immunosenescence also renders the host susceptible to inflammation, which may translate into tissue-damaging disease as the senescent immune system loses its ability to maximize inflammatory protection while minimizing inflammatory injury. On the other hand, chronic inflammation associated with immune-mediated disease represents a profound stress factor for the immune system, affecting cellular turn-over, replication and exhaustion. Immune cell longevity is tightly connected to the functional integrity of telomeres which are regulated by cell multiplication, exposure to oxidative stress and DNA repair mechanisms. Lymphocytes are amongst the few cell types that can actively elongate telomeres through the action of telomerase. In patients with the autoimmune disease rheumatoid arthritis (RA), telomerase deficiency is associated with prematurity of immune aging. Patients with RA have other defects in DNA repair mechanisms, including the kinase Ataxia telangiectasia mutated (ATM), critically involved in the repair of DNA double strand breaks. ATM deficiency in RA shortens lymphocyte survival. Dynamics of telomeric length and structure are beginning to be understood and have distinct patterns in different autoimmune diseases, suggesting a multitude of molecular mechanisms defining the interface between chronic immune stimulation and progressive aging of the immune system."

Link: http://www.ncbi.nlm.nih.gov/pubmed/22396899

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Via EurekAlert!: "Alzheimer's disease is characterized by abnormal deposits in the brain of the protein Amyloid-ß, which induces the loss of connections between neurons, called synapses. Now, scientists [have] discovered that specific antibodies that block the function of a related protein, called Dkk1, are able to completely suppress the toxic effect of Amyloid-ß on synapses. ... Dkk1 is elevated in the brain biopsies of people with Alzheimer's disease but the significance of these findings was previously unknown. Scientists [have] found that Amyloid-ß causes the production of Dkk1, which in turn induces the dismantling of synapses (the connections between neurons) in the hippocampus, an area of the brain implicated in learning and memory. ... scientists conducted experiments to look at the progression of synapse disintegration of the hippocampus after exposure to Amyloid-ß, using brain slices from mice. They were able to monitor how many synapses survived in the presence of a specific antibody which targets Dkk1, compared to how many synapses were viable without the antibody. The results show that the neurons that were exposed to the antibody remained healthy, with no synaptic disintegration."

Link: http://www.eurekalert.org/pub_releases/2012-03/ucl-sdt030512.php

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Via EurekAlert!: "Alzheimer's disease is characterized by abnormal deposits in the brain of the protein Amyloid-ß, which induces the loss of connections between neurons, called synapses. Now, scientists [have] discovered that specific antibodies that block the function of a related protein, called Dkk1, are able to completely suppress the toxic effect of Amyloid-ß on synapses. ... Dkk1 is elevated in the brain biopsies of people with Alzheimer's disease but the significance of these findings was previously unknown. Scientists [have] found that Amyloid-ß causes the production of Dkk1, which in turn induces the dismantling of synapses (the connections between neurons) in the hippocampus, an area of the brain implicated in learning and memory. ... scientists conducted experiments to look at the progression of synapse disintegration of the hippocampus after exposure to Amyloid-ß, using brain slices from mice. They were able to monitor how many synapses survived in the presence of a specific antibody which targets Dkk1, compared to how many synapses were viable without the antibody. The results show that the neurons that were exposed to the antibody remained healthy, with no synaptic disintegration."

Link: http://www.eurekalert.org/pub_releases/2012-03/ucl-sdt030512.php

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

If you've been reading Fight Aging! for a while, you'll recall that I've discussed organized crowdsourcing of funding of life science research - and longevity science in particular - for a few years now. This is a concept whose time has come: the Internet is providing great transparency and insight into all fields of endeavor, the cost of biotechnology has fallen rapidly to the point at which graduate students and a few tens of thousands of dollars can accomplish meaningful novel research, and crowdsourcing is achieving critical mass in other markets.

So we have ventures like Kickstarter, which is making a name for itself in art, publishing, and manufacturing projects. That is an example of a successful marketplace, where workers and funders can come together to raise sums comparable to pre-angel investments in start up companies - but on their own terms, and usually far better terms.

If you can raise money for books, art projects, and widgets, why not for discrete life science research projects with determined goals? The LongeCity (previously the Immortality Institute) crowd have been trying this for some years, with a great deal of success considering the limited audience of this community in comparison to the audience available through Kickstarter. It is sad but true that far more people are brought to a state of excitedly opening their wallets for the development of an iPhone widget than for any sort of biotechnology project, even one that will contribute to the reversal of aging.

But regardless, the groundwork is laid - this is the time for growth in crowdsourced funding. For the scientific community, the remaining piece of the puzzle at this time would seem to be a viable first marketplace, some Kickstarter-for-science that captures an audience and replicates the success of Kickstarter in this field. Once that is done a single time, then the idea will be accepted by the public and many such ventures can blossom.

Today, I see a fairly professional offering is put forward as a contender: Petridish:

Petridish lets you fund promising research projects and join first hand in new discoveries. World famous researchers post projects and expeditions that need your help to get off the ground. Each project has a minimum threshold it must hit in pledges, or it will not be funded. Backers in successful projects join the team and get insider rewards such as: Early access to news about progress and findings, souvenirs from the field, acknowledgements in journals, naming rights for new discoveries, or the ability to join an expedition in person.

Crowdsourced funding is a tremendously powerful tool for minority research fields - such as the rejuvenation biotechnology of the SENS Foundation. This is true for exactly the same reasons that make it a powerful tool for indie publishers and other entities largely removed from the traditional funding sources in their industry. In fact, the history of the SENS Foundation and Methuselah Foundation has been one long crowdsourced funding effort, launched by the early interest of the transhumanist community and carried onward by a broader community of people who value longer lives enough to do something about it.

What an organization like Petridish can bring to the table, if successful, is a larger audience and a formalism of the crowdsourced funding process that enables it to proceed much more smoothly - and more successfully. There are economies of scale that emerge quite quickly if you want to break down your fundraising into ten small programs rather than one big one, but it takes something like a Petridish or a Kickstarter to make this work well.

I believe that the SENS Foundation folk should contact the Petridish folk and set something up: there is no shortage of discrete, interesting projects that the Foundation would like to undertake, and I think this would be an excellent test of the waters. This is the future of small to mid-sized project funding, both in the sciences and elsewhere: if you want enthusiastic, knowledgeable supporters, then you have to get them more involved in the nuts and bolts of your work - in the small victories and accomplishments that are the foundation of the bigger picture. This is the best way to do that.

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

You'll find some thoughts on incentives, politicians, and longevity science over at h+ Magazine. I don't agree with all of them, but then my views on the state as a millstone hung upon the neck of medical progress are known: "After finding out I was an economist, [Aubrey de Grey] effectively challenged me to work out what we should want politicians to do ... With over 150,000 people dying every day, I hope governments would respond to the animal experiments by accelerating our journey to [actuarial] escape velocity through massively increasing funding for longevity medical research, because the cost of dying this year goes way up if it causes you to just miss out on the chance to live long enough to live forever. But since a rational world would already make abolishing death a top priority, we can't count on politicians automatically doing this. Still (as I will explain at the end of this article) people will likely be made aware of any inevitable approach to escape velocity which should cause at least some voters to reward politicians who increase taxpayer support for medical research. ... Once we actually reach escape velocity, U.S. politicians would face enormous political pressure to make the necessary medical treatments available to all Americans, regardless of income. The U.S. government might well do this by limiting how much companies could charge for the needed medicines. Predicting this, pharmaceutical companies would have fewer incentives to develop the cures in the first place."

Link: http://hplusmagazine.com/2012/02/28/the-politics-of-medical-immortality/

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Via EurekAlert!: "This paper reports the discovery of one of the first targeted drugs specifically developed to reverse fibrosis and regenerate the kidney. We're optimistic about the benefits, but the real proof will come from clinical testing. ... In the kidneys and other organs, fibrosis develops from normal repair mechanisms that do not stop. Scar tissue slowly builds up and replaces the working cells of the organ. In 2003, [researchers] reported that the destructive fibrosis in mice can be countered by the human protein BMP-7, originally named for its ability to spur bone growth. ... However, the large protein needs to be injected or surgically implanted and, therefore, is not useful for long-term treatment protocols. Probing deeper into the biology of the kidney, they identified the protein Alk3 [and] based on the details about the molecular interaction between the BMP protein and the ALK receptor, [scientists] developed a class of small functional peptides, including THR-123, which then underwent further testing. ... This receptor must be present for the new molecule to function ... Working through the receptor, the molecule suppressed inflammation, cell death and fibrosis formation, as well as reversing established fibrosis and allowing kidneys to regenerate functional cells ... Further experiments showed that the test drug worked even better in the mice when given in combination with ACE inhibitors, the anti-hypertensive drugs now considered a standard therapy for chronic kidney disease which work by targeting another molecular process. ... Targeting the receptor not only stops fibrosis, it removes established fibrosis, and it works in combination with an existing drug used in patients. The next step is to test this molecule in the clinic."

Link: http://www.eurekalert.org/pub_releases/2012-03/bidm-stk030712.php

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

The near future of organ transplants will become very varied, as a range of different viable types of technology are presently undergoing active development. A short list looks much like this:

• Incremental progress in old-style organ transplants, such as improving the donation system, allowing organs to be stored outside the body for longer periods of time, and so forth.
• Decellularization, in which a donor organ is stripped of cells, leaving only the scaffold of the extracellular matrix. The scaffold is repopulated from the patient's cells, removing the possibility of immune rejection and need for immunosuppressant drugs.
• Electromechanical and bioartificial organs, including hearts, lungs, and kidneys, continue to improve at a good pace. New types of small artificial organ are becoming possible thanks to advances in materials science.
• Creating organ tissue and scaffolds from scratch through a variety of methods, such as the 3-D printing pioneered by a number of groups.
• Xenotransplantation, the use of animal organs for human patients, is also becoming more viable as a near-term prospect.
• Lastly, there are the researchers who aim to rebuild damaged organs in situ through manipulation of stem cells and signaling processes in normal regeneration.

There will be a great deal of innovation and healthy competition over the next two decades before this larger cycle of technological progress in medicine settles down to a few mature and tried and tested ways of fixing broken and age-damaged organs in the body.

To add to the list of strategies, I noticed an article today on a possible middle path between old-style donor transplants (immunosuppressant drugs and all) and the near future of organs that are populated by the patient's own stem cells. It may be possible to use the knowledge acquired by stem cell researchers to date in order to minimize or completely remove the risk of immune rejection of a donor organ:

In a standard kidney transplant, the donor agrees to donate their kidney. In the approach being studied, the individual is asked to donate part of their immune system as well. The process begins about one month before the kidney transplant, when bone marrow stem cells are collected from the blood of the kidney donor using a process called apheresis. The donor cells are then sent to the University of Louisville to be processed, where researchers enrich for "facilitating cells" believed to help transplants succeed. During the same time period, the recipient undergoes pre-transplant "conditioning," which includes radiation and chemotherapy to suppress the bone marrow so the donor's stem cells have more space to grow in the recipient's body.

Once the facilitating cell-enriched stem cell product has been prepared, it is transported back to Northwestern, where the recipient undergoes a kidney transplant. The donor stem cells are then transplanted one day later and prompt stem cells to form in the marrow from which other specialized blood cells, like immune cells, develop. The goal is to create an environment where two bone marrow systems exist and function in one person. Following transplantation, the recipient takes anti-rejection drugs which are decreased over time with the goal to stop a year after the transplant.

...

Less than two years after her successful kidney transplant, 47-year-old mother and actress Lindsay Porter of Chicago, is living a life that most transplant recipients dream of - she is currently free of anti-rejection medications and says at times, she has to remind herself that she had a kidney transplant. ... Doctors are hopeful that Porter will not need immunosuppressive drugs long-term, given her progress thus far.

You might look on this as creating a form of engineered chimerism. We know that some animals and humans exist with, for example, multiple blood types and genetically distinct systems in their body as a result of the fusion of two zygotes in the womb. These individuals don't seem to suffer any great harm from being chimeric, which might be taken as a promising sign for the long-term prospects of this form of stem cell medicine.

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Most known cancer suppression genes and mutations shorten life in laboratory mice, as they suppress the mechanisms of cell replication needed to maintain tissues. There are exceptions that have emerged as researchers find more sophisticated methods of genetic engineering to work around these limitations, but this life-extending example of gene engineering seems to be more straightforward than most: "Mice with an extra dose of a known anti-cancer gene lose weight even as their appetites grow. Not only that, but [the] animals also live longer, and that isn't just because they aren't getting cancer, either. ... One of the animals' youthful secrets is hyperactive brown fat, which burns energy instead of storing it. The findings add to evidence that tumor suppressors aren't designed only to protect us against cancer, the researchers say. They also point to new treatment strategies aimed to boost brown fat and fight aging. ... Tumor suppressors are actually genes that have been used by evolution to protect us from all kinds of abnormalities. ... In this case, the researchers studied a tumor suppressor commonly lost in human cancers. Mice with an extra copy of the gene known as Pten didn't get cancer, but that's not the half of it. Those mice were also leaner, even as they ate more than controls ... That suggested that the animals were experiencing some sort of metabolic imbalance - and a beneficial one at that. Cancer protection aside, the animals lived longer than usual. They were also less prone to insulin resistance and had less fat in their livers. Those benefits seem to trace back to the fact that those Pten mice were burning more calories thanks to overactive brown fat."

Link: http://www.sciencedaily.com/releases/2012/03/120306131252.htm

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm