I note a symptom of the highly restrictive FDA regulations on development of clinical therapies:

The indictment alleges the four distributed stem cells and other biological products without federal Food and Drug Administration approval, and for unapproved treatments of cancer, amyotrophic lateral sclerosis, multiple sclerosis, and Parkinson's Disease. ... Court records unsealed Wednesday show that the scheme made more than $1.5 million in sales between January 2007 and April 2010, from procedures Morales performed in Mexico on patients he met in the United States.

This is the standard situation: when regulation makes it impossible to meet demand or to try to develop and offer meaningful products, a black market will arise. That market will be less transparent, more costly, and less effective at delivering quality products than a free market would be in the absence of regulation. A black market will also tend to attract a larger contingent of sellers willing to commit fraud than would otherwise be the case, as the buyers have lower chances of success in any legal action or other means of forcing restitution.

So these fellows may be frauds, or they may be legitimate businesspeople trying to operate a medical tourism business, offering services that are perfectly legal - and even admirable - outside the US, while within the US forthright invention and competition in medicine is pretty much forbidden. Either way, other would-be legitimate businesspeople are going to look at this and think twice about trying to make the world a better place by offering better medical services.

So it goes. The FDA and its legal penumbra are monstrosities that distort all of the usual incentives involving profit and progress, and steer them towards bad ends. The FDA must go if we are to see progress in medicine that approaches the pace of progress in less regulated industries like computing.

There is a very simple solution to the problems of medicine. It's called freedom: freedom for providers to develop and compete as they see fit, and freedom for people to choose or reject their offerings with the money in their own pockets and savings accounts. For progress and efficiency to reign in an industry, people have to pay for goods with their own funds, and providers have to be free to innovate. Competition and the care with which people manage their own money keeps both sides as honest as any human culture is going to be.

Look at fashion. Shoes. Computers. DNA sequencing. Or any one of a thousand other important goods whose value has fallen over time and continues to do so. These are less regulated markets, not stifled and buried beneath chains like the provision of medicine. They are vibrant, constantly innovating and competing, and this is exactly because people pay for these products with the money they care about most.

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

Pulling together the connections in a review paper: "Obesity is a condition in which excess or abnormal fat accumulation may present with adverse effects on health and decreased life expectancy. Increased body weight and adipose tissue accumulation amplifies the risk of developing various age-related diseases, such as cardiovascular disease, Type 2 Diabetes Mellitus, musculoskeletal disorders, respiratory diseases and certain types of cancer. This imbalance in body composition and body weight is now recognized as a state of increased oxidative stress and inflammation for the organism. Increasing oxidative stress and inflammation affect telomeres. Telomeres are specialized DNA-protein structures found at the ends of eukaryotic chromosomes and serve as markers of biological aging rate. They also play a critical role in maintaining genomic integrity and are involved in age-related metabolic dysfunction. Erosion of telomeres is hazardous to healthy cells, as it is a known mechanism of premature cellular senescence and loss of longevity. The association of telomeres and oxidative stress is evident in cultured somatic cells in vitro, where oxidative stress enhances the process of erosion with each cycle of replication. Shorter telomeres have been associated with increasing body mass index, increased adiposity, and more recently with increasing waist to hip ratio and visceral excess fat accumulation. Furthermore, many of the metabolic imbalances of obesity (e.g. glycemic, lipidemic, etc.) give rise to organ dysfunction in a way that resembles the accelerated aging process."

Link: http://www.ncbi.nlm.nih.gov/pubmed/22186032

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

In aging there is a lot of correlation - many biological systems that are traditionally studied separately are declining at once, so most researchers are only looking in detail at one tiny part of aging. Part of the challenging facing researchers has always been how to figure out what is cause and what is consequence given the need for specialization to make progress in any given small area of the biology of aging. Here, researchers focus on the immune system, and you can see the biases inherent in being a specialist: "The aging process is accompanied by an impairment of the physiological systems including the immune system. This system is an excellent indicator of health. We have also observed that several functions of the immune cells are good markers of biological age and predictors of longevity. In agreement with the oxidation-inflammation theory that we have proposed, the chronic oxidative stress that appears with age affects all cells and especially those of the regulatory systems, such as the nervous, endocrine and immune systems and the communication between them. This fact prevents an adequate homeostasis and, therefore, the preservation of health. We have also proposed an involvement of the immune system in the aging process of the organism, concretely in the rate of aging, since there is a relation between the redox state and functional capacity of the immune cells and the longevity of individuals. A confirmation of the central role of the immune system in oxi-inflamm-aging is that several lifestyle strategies such as the administration of adequate amounts of antioxidants in the diet, physical exercise, physical and mental activity through environmental enrichment and hormetic interventions improve functions of immune cells, decreasing their oxidative stress, and consequently increasing the longevity of individuals."

Link: http://www.ncbi.nlm.nih.gov/pubmed/22188449

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

A commentary at the journal Aging: "In the past 15 years, genomics has penetrated all areas of the life sciences, and this dramatic change in the way science is done is often viewed as genome revolution. However, application of genomics to study senescence and aging lagged behind. Until this year, no genomes have been sequenced explicitly to understand aging. In this regard, the recent completion of the genome of the naked mole rat marks an important milestone, as this study was performed primarily to better understand the exceptional longevity of this rodent. Naked mole rats live in the subterranean niche in southeast Africa and are the longest-lived rodents (maximum lifespan of 32 years). Being the size of a mouse, naked mole rats can be conveniently studied in the laboratory setting and compared with other rodents. What have we learned from the initial analysis of the genome of this remarkable animal? First, the genome is characterized by the reduced level of polymorphism, consistent with low DNA mutation rate (although other explanations are also possible). Second, an unusual thermogenesis of naked mole rats, which may be linked to longevity through metabolic rate, is consistent with the altered sequence of a key thermoregulator, UCP1, which modified its sequences that mediate regulation by nucleotides and fatty acids. Another interesting finding is the unique sequence of a tumor suppressor p16, a protein whose mutations were linked to a variety of human diseases associated with aging. In addition, analyses of gene expression as a function of age distinguished naked mole rats from other mammals. ... The availability of the genome of the naked mole rat should be viewed as the first step in the process of understanding of the delayed aging of this mammal, and also as a useful resource for studying the aging process in general. It is clear that much of its value lies in comparison with the genomes of other mammals, both with long and short lifespans, as well as in downstream functional genomic studies that assess genetic and epigenetic regulation networks. Comparative genomics of short-lived and long-lived organisms offers great opportunities to understand evolutionary forces and molecular mechanisms that regulate lifespan."

Link: http://www.impactaging.com/papers/v3/n12/full/100417.html

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

This year saw a demonstration showing noteworthy benefits to health and longevity from the targeted destruction of senescent cells in mice - an expected result for many researchers, but one that had yet to happen up to that point. Senescent cells, cell that have removed themselves from the cycle of proliferation, are an evolutionary response to the growing threat of cancer with age, but once in a senescent state they progressively cause harm to surrounding cells and tissue. The immune system destroys many senescent cells, but becomes much worse at this task - along with all its other duties - as time progresses because it suffers from its own age-related issues. As the numbers of senescent cells grow, so does their contribution to the physical failures and declines of aging.

But this entire portion of the basis for degenerative aging could be removed with a therapy that destroyed senescent cells sufficiently well. This is why the earlier mentioned demonstration of senescent cell destruction - and corresponding health benefits - in mice was a welcome advance. Unfortunately, the method used was based on some clever genetic engineering and while effective at eliminating senescent cells without harming other cells in the engineered mouse breed, it has little direct application to the development of human clinical medicine.

Meanwhile, the cancer and immunotherapy research communities are making great strides in developing many forms of nanoscale technology that can be coupled to a sensor and sent to destroy those cells that the sensor reacts with - and without harming any other nearby cells. Researchers have used nanoparticles, antibodies, viruses, and bacteria to home in on cells with specific surface markers or other characteristics, and there deliver some form of killing blow. The trick here is not so much the killing blow, as many of the successful demonstrations of targeted cancer cell destruction did no more than deliver old-style chemotherapy drugs - just in very small doses and on a cell-by-cell basis rather than flooding the whole body. That works very well to minimize side-effects and maximize harm to the cancer.

The point of this sidebar is that these technology platforms could be quickly repurposed to attack senescent cells, but only when there emerges a robust way of distinguishing between senescent and non-senescent cells. So now we watch with interest for published research that touches on that topic, such as this recent open access paper:

Changes in the shape of the nuclear lamina are exhibited in senescent cells, as well as in cells expressing mutations in lamina genes. To identify cells with defects in the nuclear lamina we developed an imaging method that quantifies the intensity and curvature of the nuclear lamina. We show that this method accurately describes changes in the nuclear lamina. Spatial changes in nuclear lamina coincide with redistribution of lamin A proteins and local reduction in protein mobility in senescent cell. We suggest that local accumulation of lamin A in the nuclear evelope leads to bending of the structure. A quantitative distinction of the nuclear lamina shape in cell populations was found between fresh and senescent cells, and between primary myoblasts from young and old donors. Moreover, with this method mutations in lamina genes were significantly distinct from cells with wild-type genes. We suggest that this method can be applied to identify abnormal cells during aging, in in vitro propagation, and in lamina disorders.

As an aside, you might recall that mutant lamin A is the culprit in progeria, and has been postulated to be a low-level contribution to normal aging as well. Expect to see more interest in progeria and potential therapies for that condition if more evidence emerges to link it to cellular senescence and ways to reliably distinguish senescent cells.

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

Human studies may reveal a correlation between longevity and lower rates of reproduction: "A number of leading theories of aging, namely The Antagonistic Pleiotropy Theory (Williams, 1957), The Disposable Soma Theory (Kirkwood, 1977) and most recently The Reproductive-Cell Cycle Theory (Bowen and Atwood, 2004, 2010) suggest a tradeoff between longevity and reproduction. While there has been an abundance of data linking longevity with reduced fertility in lower life forms, human data have been conflicting. We assessed this tradeoff in a cohort of genetically and socially homogenous Ashkenazi Jewish centenarians (average age ~100 years). As compared with an Ashkenazi cohort without exceptional longevity, our centenarians had fewer children (2.01 vs 2.53, p<0.0001), were older at first childbirth (28.0 vs 25.6, p<0.0001), and at last childbirth (32.4 vs 30.3, p<0.0001). The smaller number of children was observed for male and female centenarians alike. The lower number of children in both genders together with the pattern of delayed reproductive maturity is suggestive of constitutional factors that might enhance human life span at the expense of reduced reproductive ability."

Link: http://www.impactaging.com/papers/v3/n12/full/100415.html

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

So what is the Methuselah Foundation up to these days? As you might know, the Foundation has administered the Mprize for longevity science since 2003: a multi-million dollar prize fund that encourages researchers to find ways to extend healthy life in mice - a good marker for technologies that may then be applicable to other mammals, such as we humans. Last year, the Foundation inaugurated a new prize, the NewOrgan prize that aims to spur greater progress in tissue engineering and the creation of functional new organs from a patient's own cells. This dovetails with the Foundation's investment strategy: helping to fund companies that focus on advanced tissue engineering, such as Organovo, and solving organ transplant issues, such as Silverstone Solutions.

The Methuselah Foundation sent out a sneak peek email yesterday with a pointer to the New Organ Mprize website and the first pledge drive with matching funds: this will be the big thing for the coming year. Here is the text:

Time for something new and personal.

In 2012, the next chapter for Methuselah and the journey for an enduring answer for millions will begin. We are excited to share this preview with our closest supporters and friends.

Introducing New Organ Mprize.

Think of a time when no one has to suffer and die waiting for an organ that never arrives. New Organ is creating the public prize that builds urgency for that future.

Sneak peek.

While we're finishing the campaign's site, we'd like to give you a preview of its homepage. We hope you like it as much as we do. Look for more pages in a few weeks.

Showing momentum.

Our goal is $200,000 by February 28th. To help achieve this and establish traction at launch, Organovo's Keith Murphy has pledged to match gifts up to $25,000.

Become a New Organ Founder.

We invite you to join us at the beginning. Let?s start New Organ with 25% of the job done. Kickstart the prize!

My yearly round of donations remain divided between the SENS Foundation and Methuselah Foundation - the two organizations to appear prominently on the Fight Aging! Take Action page. Both are worthy causes, consistently achieving a great deal more behind the scenes in networking and persuasion with the scientific and research funding communities than is apparent from the front end. A large fraction of the sea change in the aging research community in recent years can be attributed to the communities centered on these organizations.

Aiming to extend the healthy human life span has come to be a respectable goal in the scientific community over the past ten years. That wasn't always the case, and it's easy to forget just how much of a sea change has taken place since the [turn of the century].

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

Here is another of the many theories aiming to explain why women live longer than men: "One of the most significant achievements of the twentieth century is the increase in human lifespan. In any period studied, females live longer than males. We showed that mitochondrial oxidative stress is higher in males than females and that the higher levels of estrogens in females protect them against ageing, by up-regulating the expression of antioxidant, longevity-related genes. The chemical structure of estradiol confers antioxidant properties to the molecule. However, the low concentration of estrogens in females makes it unlikely that they exhibit significant antioxidant capacity in the organism. Therefore we studied the mechanisms enabling estradiol to be antioxidant at physiological levels. Our results show that physiological concentrations of estrogens activate estrogen receptors and the MAPK and NFKB pathway. Activation of NFkB by estrogens subsequently activates the expression of Mn-SOD and GPx. Moreover, we have demonstrated that genistein, the most abundant phytoestrogen in soya, reproduces the antioxidant effect of estradiol at nutritionally relevant concentrations by the same mechanism ... We conclude that estrogens and phytoestrogens up-regulate expression of antioxidant enzymes via the estrogen receptor and MAPK activation, which in turn activate the NFkB signalling pathway, resulting in the up-regulation of the expression of longevity-related genes."

Link: http://www.ncbi.nlm.nih.gov/pubmed/22188448

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

A recent paper: "Birds generally age slower and live longer than similar sized mammals. For birds this occurs despite elevated blood glucose levels that for mammals would in part define them as diabetic. However these data were acquired in respiration states that have little resemblance to conditions in healthy tissues and mitochondrial [reactive oxygen species] production is probably minimal in healthy animals. Indeed mitochondria probably act as net consumers rather than producers of [reactive oxygen species]. Here we propose that (1) if mitochondria are antioxidant systems, the greater mitochondrial mass in athletic species, such as birds, is advantageous as it should provide a substantial sink for [reactive oxygen species]. (2) The intense drive for aerobic performance and decreased body density to facilitate flight may explain the relative insensitivity of birds to insulin, as well as depressed insulin levels and apparent sensitization to glucagon. Glucagon also associates with the sirtuin protein family, most of which are associated with caloric restriction regulated pathways, mitochondrial biogenesis and life span extension. (3) We note that telomeres, which appear to be unusually long in birds, bind Sirtuins 2 and 4 and therefore may stabilize and protect nuclear DNA. Ultimately these flight driven responses may suppress somatic growth and protect DNA from oxidative damage that would otherwise lead to ageing and non-viral cancers."

Link: http://www.ncbi.nlm.nih.gov/pubmed/22198369

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

An example of the sort of immune system engineering that is presently taking place in the laboratory: "Until this research, we thought the immune system needed to attack the cancer directly in order to be effective. Now we know that isn't necessarily so. Attacking the dense tissues surrounding the cancer is another approach, similar to attacking a brick wall by dissolving the mortar in the wall. Ultimately, the immune system was able to eat away at this tissue surrounding the cancer, and the tumors fell apart as a result of that assault. These results provide fresh insight to build new immune therapies for cancer. ... pancreatic cancer patients received standard gemcitabine chemotherapy with an experimental antibody [that] binds and stimulates a cell surface receptor called CD40, which is a key regulator of T-cell activation. The team initially hypothesized that the CD40 antibodies would turn on the T cells and allow them to attack the tumor. The treatment appeared to work, with some patients' tumors shrinking substantially and the vast majority of tumors losing metabolic activity after therapy, although all of the responding patients eventually relapsed. When the researchers looked at post-treatment tumor samples, obtained via biopsy or surgical removal, there were no T cells to be seen. Instead, they saw an abundance of another white blood cell known as macrophages. ... When the investigators treated mice that developed pancreatic cancer with gemcitabine in combination with CD40 antibodies, the results looked like those of the human trial. Some mouse tumors shrank and were found to be loaded with macrophages but contained few or no T cells. Closer inspection showed that the macrophages were attacking what is known as the tumor stroma, the supporting tissue around the tumor. Pancreatic tumors secrete chemical signals that draw macrophages to the tumor site, but if left to their own devices, these macrophages would protect the tumor. However, treating the mice (or patients) with CD40 antibodies seemed to flip that system on its head. ... It is something of a Trojan horse approach. The tumor is still calling in macrophages, but now we've used the CD40 receptor to re-educate those macrophages to attack - not promote - the tumor."

Link: http://www.eurekalert.org/pub_releases/2011-03/uops-pru031611.php

Economies of scale apply to all endeavors, including the production of human tissue: "The high-tech production lines of [a] laboratory in Germany began moving this week turning out a unique product - human skin. Nicknamed 'The Flesh Factory' by the boffins who work at the Stuttgarter Fraunhofer-Institute, it aims to produce 5,000 circles of skin as big as a one-euro cent every month. Costing around 45 pounds each, when the skin circles are perfected they will be sold to hospitals and clinics around the world for life-saving operations. Project leader Professor Heike Walles, 48, has devoted her whole life to the goal of reproducing human skin on an industrial scale - to save human life and protect animals; it can be used for the kind of testing currently requiring the sacrifice of live creatures. ... Until now, methods of culturing tissue like that used for skin transplants have been very expensive. Most of the steps are carried out manually, which means that the process is not particularly efficient. ... The new production line is entirely mechanical and controlled by computers. ... The process works like this; a biopsy - a sample of human tissue - is checked for sterility. A gripper arm then transports the biopsy into an automated cutting device. The machine snips the biopsy into small pieces, isolates the different cell types, stimulates their growth, and mixes the skin cells with collagen. A three-dimensional reconstruction of the different skin layers is produced with the aid of a special gel matrix - and the skin is ready. In the final step, the machine packages the cells for shipment. Alternatively, the tissue can be cryopreserved - that is, deep-frozen and stored for later use."

Link: http://germanherald.com/news/Allan_Hall's_Germany/2011-04-13/647/The_Flesh_Factory_goes_online

Nitric oxide levels are a possible target for therapies aimed at some of the signs of aging in blood vessels: "Many disorders emerge with advancing aging, and cardiovascular diseases (CVD) are a major cause of morbidity and mortality in the elderly. The term vascular aging encompasses all the structural and functional alterations in the blood vessels with progressive aging. Both smooth muscle cells and intima layers are affected. These vascular changes lead to endothelial dysfunction, arterial stiffness in consequence of intense remodeling and calcification, impaired angiogenesis, greater susceptibility to vascular injury and atherosclerotic lesions. The mechanisms underlying vascular aging are complex and involve multiple pathways and factors ... In this complex scenario, vascular function depends on the balanced production/bioavailability of nitric oxide (NO), which is maintained by the normal activity of endothelial nitric oxide synthase (eNOS). On the other hand, excessive amount of NO produced by inducible nitric oxide synthase (iNOS) up-regulation contributes to vascular dysfunction. Evidence obtained from experimental models indicates that decreased NO bioavailability as well as increased reactive nitrogen species (RNS) production contributes to aging-associated vascular dysfunction. ... Pharmacological modulation of NO generation and expression/activity of NOS isoforms may represent a therapeutic alternative to prevent the progression of cardiovascular diseases."

Link: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3382417/

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

This study crunches the numbers to show that being socially connected has an effect on life expectancy comparable to that of exercise. Why this correlation exists is still up for debate, but it is worth considering that skill at networking and possessing a large social network enable success in other aspects of life: "These findings indicate that the influence of social relationships on the risk of death are comparable with well-established risk factors for mortality such as smoking and alcohol consumption and exceed the influence of other risk factors such as physical inactivity and obesity. Furthermore, the overall effect of social relationships on mortality reported in this meta-analysis might be an underestimate, because many of the studies used simple single-item measures of social isolation rather than a complex measurement. Although further research is needed to determine exactly how social relationships can be used to reduce mortality risk, physicians, health professionals, educators, and the media should now acknowledge that social relationships influence the health outcomes of adults and should take social relationships as seriously as other risk factors that affect mortality, the researchers conclude."

View the Article Under Discussion: http://dx.doi.org/10.1371/journal.pmed.1?000316

Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

A recent paper points to mitochondrially induced hormesis as a root cause of increased longevity with reduced calorie intake - which meshes well with the role of autophagy in this process. It confirms the importance of mitochondria in longevity, and once again shows that a little ongoing damage is actually a good thing: "Calorie restriction (CR) is the only proven regimen which confers lifespan extension benefits across the various phyla right from unicellular organisms like yeast to primates. In a bid to elucidate the mechanism of calorie-restriction-mediated life span extension, the role of mitochondria in the process was investigated. In this study, we found that the mitochondrial content in CR cells remains unaltered as compared to cells grown on nonrestricted media. However, mitochondria isolated from CR cells showed increased respiration and elevated reactive oxygen species levels without augmenting adenosine triphosphate (ATP) generation. The antioxidant defense system was amplified in CR mitochondria, and in CR cells a cross protection to hydrogen-peroxide-induced stress was also observed. Moreover, we also documented that a functional electron transport chain was vital for the life span extension benefits of calorie restriction. Altogether, our results indicate that calorie restriction elicits mitohormetic effect, which ultimately leads to longevity benefit."

View the Article Under Discussion: http://www.ncbi.nlm.nih.gov/pubmed/20640543

Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

As researchers continue to explore calorie restriction, intermittent fasting, and other forms of lowering food intake, then make discoveries like this: "Man may not live by bread alone, but cancer in animals appears less resilient, judging by a study that found chemotherapy drugs work better when combined with cycles of short, severe fasting. Even fasting on its own effectively treated a majority of cancers tested in animals, including cancers from human cells. ... For example, multiple cycles of fasting combined with chemotherapy cured 20 percent of mice with a highly aggressive type of children's cancer that had spread throughout the organism and 40 percent of mice with a more limited spread of the same cancer. No mice survived in either case if treated only with chemotherapy. Only a clinical trial lasting several years can demonstrate whether humans would benefit from the same treatment. ... As with any potential cancer treatment, fasting has its limits. The growth of large tumor masses was reduced by multiple fasting and chemotherapy cycles, but cancer-free survival could not be achieved. [Researchers] speculated that cells inside a large tumor may be protected in some way or that the variety of mutations in a large mass may make it more adaptable. ... The cell is, in fact, committing cellular suicide. What we're seeing is that the cancer cell tries to compensate for the lack of all these things missing in the blood after fasting. It may be trying to replace them, but it can't. ... A way to beat cancer cells may not be to try to find drugs that kill them specifically but to confuse them by generating extreme environments, such as fasting that only normal cells can quickly respond to."

Link: http://www.eurekalert.org/pub_releases/2012-02/uosc-fwc020212.php

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

The aging of bacteria has been a topic of interest in the years since its discovery; firstly, it overturns the long-held assumption that bacteria are essentially immortal, and secondly it provides insight into the very early evolutionary origins of aging. Here is a recent update: "Evidence for aging in symmetrically dividing bacteria such as Escherichia coli has historically been conflicting. Early work found weak or no evidence. More recent studies found convincing evidence, but negative results are still encountered. Because bacterial aging is believed to result from non-genetic (e.g. oxidative) damage, we tested the possibility that the negative outcomes resulted from the lack of an extrinsic damage agent. We found that streptomycin, which produces mistranslated proteins that are more vulnerable to oxidation, was able to induce both damage and aging in bacterial populations. A dosage effect relating the level of damage to the concentration of streptomycin was observed. Our results explain the previous inconsistencies because all studies that failed to find evidence for bacterial aging did not use a damage agent. However, all studies that succeeded in finding evidence utilized fluorescent proteins as a visual marker. We suggest that aging in those studies was induced by the harmful effects of an extrinsic factor, such as of the proteins themselves or the excitation light. Thus, all of the previous studies can be reconciled and bacterial aging is a real phenomenon. However, the study and observation of bacterial aging requires the addition of an extrinsic damage agent."

Link: http://www.ncbi.nlm.nih.gov/pubmed/22422756

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

The build up of senescent cells is one of the contributing causes of aging, and is partially due to the progressive failure of the immune system to destroy these cells as they crop up. Many of the changes that come with aging accelerate as they progress, and this piece provides one example as to why this is the case; for senescent cells, the more you have the faster they accumulate: "Cells may become senescent in an effort to protect the body such as when tumor suppressor genes shut down division to prevent cancer. However other sorts of damage may lead cells to stop dividing as well. A pivotal study last year showed elegantly using a trangenic approach that if senescent cells were regularly cleared from the body of mice, signs of aging in many tissues were dramatically reduced. The explanation for this result was that somehow senescent cells were damaging nearby cells, perhaps by excreting toxic materials. ... A newly published study [proves] or the first time that senescent cells do indeed damage nearby cells causing them to become senescent too. It also shows this occurs through direct cell to cell contact and resultant spread of reactive oxygen species. Furthermore it shows evidence this process occurs in the living organism as clusters of cells bearing senescent makers are found in mice livers. Clearly the next and important step for helping to reduce aging in humans is developing a safe and effective method presumably using a pharmacological agent in which senescent cells can be removed from the body."

Link: http://extremelongevity.net/2012/06/11/study-proves-senescent-cells-cause-nearby-cells-to-become-senescent/

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

Chemistry Tutor in Baltimore Maryland

I have a PhD in Chemistry with over 5 years experience as a chemistry tutor. I have had a lot of successes in tutoring.

For example I was hired by the mother of a high school student, who failed his final Grade 12 chemistry exams to prepare him for a retake of the exam. After meeting with the student for 2 hours he retook the exam and passed. I also tutored an undergraduate student (in general chemistry, organic chemistry, and DAT chemistry preparation), who had no background in science but was interested in going to dental school. He had a minimum of B's in his classes and he is now in dental school. My tutoring methods involves bringing chemistry to the level of the student and approaching the problems from their perspective whether middle school, high school, or college students.

Contact me

Source:
http://www.ilcusa.org/modules/mediablog/rss.php?page_id=43

You folk should take the time to look over the recently launched New Organ Mprize website. It's an attractive initiative of the Methuselah Foundation, and you'll find a fair amount of motivational content there on the subject of growing complex organs for transplant:

Imagine a future where no one has to suffer and die while waiting for an organ that never arrives. New Organ funds that future. With your help, everyone who needs an organ can have one custom made for them from their own cells.

A crowd funded prize to award the team that creates the first complex organ - heart, lung, pancreas, liver, or kidney - from a person's cells.

Banking: Preserve a complex organ for 30 days. Thousands die because the best we can do is less than a day.

Engineering: Build a complex whole organ from a person's cells, transplant it, and have it function for two years.

If you support these goals, then I note that there is currently a matching fund for donations: a pledge drive to raise the first $200,000 by the end of March. They have raised more than $45,000 in pledges this year - so do your part and help! In a world in which a Kickstarter project can pull in a million dollars for an iPhone widget, I'd like to think that it's also possible to rapidly raise a few hundred thousand dollars for a cause that actually matters.

As we walk the road of life, ever more set upon by subtle decay and damage along the way, our health and remaining life expectancy becomes ever more dependent on the state of medical technology. It would be good to wake up twenty years from now knowing that you had made a reasonable contribution in those past decades towards helping ensure your own life and health. When we get to the point in old age at which we need, as a matter of life and death, futuristic tissue engineering and regenerative medicine that can rebuild us from the inside, we'll only have ourselves to blame if it is not yet developed and deployed. The course ahead for the science of human rejuvenation and regeneration is very clear, and whether or not it happens is largely a matter of money and will - how many people are persuaded to work on it, and how greatly are they funded.

So do your part to help! It's not as though you have anything to lose.

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

Uncoupling proteins (UCPs) govern the process of mitochondrial uncoupling, which changes the operation of the mitochondria in our cells to generate more heat and less of the cellular fuel chemical ATP. It's one of the mechanisms by which mammals regulate their body temperature. As for many processes that alter the behavior of mitochondria, uncoupling has an effect on life span, with more uncoupling usually leading to longer life spans:

Mitochondria are the power plants of your cells: they toil to turn food into ATP, used as fuel by the cell. In recent years, the eye of the research community has turned towards the process of mitochondrial uncoupling, whereby the processing of food is uncoupled from the generation of ATP. The result is less ATP and more energy in the form of heat - this is a part of the temperature regulation process in mammals, for example. It also appears to be important in calorie restriction, and therefore possibly important to longevity and aging.

The mitochondria are clearly very important in any consideration of aging, given that there are so very many ways to manipulate them to either shorten or lengthen life in laboratory animals. This is one of the reasons that any serious program of rejuvenation biotechnology has to include efforts to repair accumulated, age-related mitochondrial damage: there is an enormous weight of evidence telling us that mitochondria are a lynchpin in aging.

But back to uncoupling: there are compounds that promote uncoupling in mammals, such as DNP, but you can't just load up on an uncoupler and wait for the benefits to roll in. If your mitochondria produce too much heat for too long, you will simply roll over and die from something that looks a lot like heat stroke. Metabolism is a finely balanced machine, and taking it beyond its limits is easy to do once you bring this sort of process manipulation into the picture.

There exists a sizable amount of published work on uncoupling and longevity, and this field is, I think, helped by the fact that it borders on the study of calorie restriction, which is a heated area of research these days. A group that has published previously on human uncoupling protein variations and longevity in the past recently put out an open access paper on their research, which goes into more detail as to the findings.

Further Support to the Uncoupling-to-Survive Theory: The Genetic Variation of Human UCP Genes Is Associated with Longevity:

In humans Uncoupling Proteins (UCPs) are a group of five mitochondrial inner membrane transporters with variable tissue expression, which seem to function as regulators of energy homeostasis and antioxidants. In particular, these proteins uncouple respiration from ATP production, allowing stored energy to be released as heat. Data from experimental models have previously suggested that UCPs may play an important role on aging rate and lifespan. We analyzed the genetic variability of human UCPs in cohorts of subjects ranging between 64 and 105 years of age (for a total of 598 subjects), to determine whether specific UCP variability affects human longevity. Indeed, we found that the genetic variability of UCP2, UCP3 and UCP4 do affect the individual's chances of surviving up to a very old age.

...

Substantial evidence suggests that the ability of UCPs to reduce ROS and regulate energy utilization underpins the ability of UCPs to promote lifespan in various experimental models. In the present study we found that variants in UCP2, UCP3, and UCP4 significantly affect an individual's chances of becoming ultra-nonagenarians. The different localization of the proteins we found associated with longevity allows us to predict the areas where the uncoupling process may play an important role in survival at very old age.

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