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A leading cause of death, illness, and disability in the U.S., an estimated 10 million American adults were diagnosed with Chronic Obstructive Pulmonary Disease (COPD) in 2000, though data from a national health survey suggests that as much as 24 million were actually affected. In 2000 alone, 119,000 deaths and over 726,000 hospitalizations were caused by COPD. 2003 brought in 124,816 deaths.

Fortunately, results from a study presented at the ATS 2011 International Conference in Denver, Colorado reveal that vitamin D supplements may help patients with COPD benefit more from pulmonary rehabilitation programs.

Miek Hornikx, a Belgian physiotherapist and doctoral student in the department of pneumology at the Katholieke Universiteit Leuven in Leuven, Belgium says

"Our study shows that high doses of vitamin D supplementation on top of a standard rehabilitation program improve the outcome in terms of exercise capacity and respiratory muscle strength."

Photo Credit: Jamie Chung


50 COPD patients with a history of exacerbations and referrals for rehabilitation were randomly assigned to receive either a monthly dose of vitamin D or a placebo over the course of three months. At the beginning of the period and again after the completion of the rehabilitation programs, peripheral and respiratory muscle strength, exercise capacity and vitamin D levels were measured. Patients were also asked to complete a quality of life survey before and after.

The vitamin D group were administered 100,000 IUs (internation units) of vitamin D in their monthly dose - the recommended U.S. daily allowance of vitamin D is 600 IUs daily for adults up to age 70 and 800 IUs daily for those over 70. Vitamin D deficiency is common among COPD patients and is often linked with diet and lack of sunlight exposure. Often, sufferers are limited in physical activity as a result of difficulty breathing associated with the disease, perhaps resulting in less exposure to sunlight. It's a bit of a tricky situation that way.

"COPD can be considered as a respiratory disease with important non-respiratory consequences, such as osteoporosis, cardiovascular disease and muscle weakness," she said. "These consequences eventually will be negatively influenced by physical inactivity which, along with exercise intolerance, is a common feature among patients with COPD and is proven to be related to mortality. Low levels of vitamin D in the blood have been related with muscle weakness, a major target for respiratory rehabilitation and increased risk of falls."

She adds, "Since vitamin D is often depleted in patients with COPD, we wanted to see if vitamin D supplementation would have a beneficial effect on rehabilitation among these patients, perhaps by increasing muscle strength."

The results were heartening: At the end of the study, researchers found that patients treated with vitamin D had a significant improvement in exercise capacity and respiratory muscle strength compared to the placebo group.

"These results support the idea that correcting vitamin D deficiency by adding vitamin D supplements to training programs allows COPD patients to achieve better results from rehabilitation, including improvements in muscle strength and exercise capacity," Ms. Hornikx said.


Reference:
Schoenstadt, MD, Arthur. "COPD Statistics: An Overview." EMedTV. Clinaero, Inc. Web. 20 May 2011.
http://copd.emedtv.c...statistics.html.

"Vitamin D Improves Exercise Outcomes in Patients With COPD." Science Daily. Science Daily LLC, 15 May 2011. Web. 20 May 2011. http://www.scienceda...10515201306.htm.



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Methuselites get a $50 discount! Use code: Methuselah

WHAT: FORESIGHT@ GOOGLE
25th Anniversary Conference Celebration & Reunion Weekend

WHERE: Google HQ in Mountain View, CA

WHEN:June 25-26, 2011

CLICK: http://www.foresight.org/reunion



Topics are emerging tech with special emphasis on transformative nanotech.



A rockstar lineup of speakers include:

• BARNEY PELL, PhD - Cofounder/CTO of Moon Express making robotic lunar landers
• WILLIAM ANDREGG - Founder/CEO of Halcyon Molecular
• PAUL SAFFO, PhD - Renowned tech forecaster and strategist
• LUKE NOSEK - CoFounder of Paypal, Partner at the Founders Fund
• SIR FRASER STODDART, PhD - Knighted creator of molecular "switches"
• THOMAS THEIS, PhD - IBM's Director of Physical Sciences
• Keynote JIM VON EHR - Founder/President of Zyvex, the world's first successful molecular nanotech company

Comments on previous meetings in this series: http://www.foresight...Assoc/Comments/




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The brain, largely known as "The Final Frontier of Science", and how it ages is still a wildly exciting subject of study for the neuro-Lewis and Clarkes of our generation. Remarkable new experiments are being performed by researchers at John Hopkins University and the Center for the Neurobiology of Learning and Memory at the University of California, Irvine. Young and old volunteers come in and watch pictures flash before a screen as the scientists literally watch their brains.

Neuroscientists have already established with the use of brain scans that a substantial bit of the electrical activity and blood flow that is associated with memory processing happens in the dentate gyrus, an area within the hippocampus, known to be involved with learning and thinking.


Photo Credit: F. Netter, M.D


Published in Proceedings of the National Academy of Sciences, their study involves use of advanced magnetic resonance imaging (MRI) machines to scan the dentate gyrus and various areas within the brains of the volunteers at the very moment of their attempting to form and store certain new memories.

This is how it was done: A series of pictures of everyday objects such as fruit, pianos, computers, and telephones were shown to the volunteers who wore head sensors. Each were asked to press a button to indicate whether each picture was typically found indoors or outside. They were not told to remember these images. Later, after being shown another set of images, the volunteers were asked if they remembered seeing the specific before, or if seemed similar to one they saw before, of if the picture was completely new to them while the research team kept track of neural activity throughout both tasks.

The results aren't surprising. The young adults were adept at differentiating the images as to whether they were brand-new, already seen or similar but not the same as an earlier image--one example being that a baby grand piano is not the same as a full grand.
"There would be a lot of activity when young people saw either new or similar objects," said Michael A. Yassa, an assistant professor of psychological and brain sciences at Johns Hopkins and lead author of the study.

The activity indicates that the young people's brains were acquiring and filing the information of the new images as 'New Images', even when they were quite similar to images that they had seen from the first set. As for the older volunteers aged 60-80, they were less successful at pattern separation- the ability to differentiate between things that are quite similar. Their dentate gyri showed far less activity when they were shown a similar, not identical images. Apparently, their brains didn't create a completely new memory to correspond to the similar images, so that the photo of the baby grand piano seemed no different than the photo of the full grand. This way, the baby grand piano would be described as an "old" image, when in fact, it was a new one. Make sense?

Dr. Yassa's work suggests that aging blunts our ability to separate today's parking spot from yesterday's, from today's breakfast from last week's. There are many different ways to process memories but one of the more important for everyday functioning is pattern separation. "Otherwise [memories] can override one another and confuse things." Part of the problem, Yassa believes, is structural.

A separate section of his experiments involved newly developed MRI scanning technology. With this he found that the dentate gyrus in the majority of the older volunteers were not linked as robustly to the rest of the brain as in young people, meaning that messages did not flow as efficiently from elsewhere in the brain to the dentate gyrus memory center and vice versa.

However, there's hope. "Exercise is one of the things that might directly change this process," says Dr. Yassa. From other experiments, exercise was found to jump-start neurogenesis, the creation of new brain cells, especially in the dentate gyrus, potentially improving that area's health and functioning. This definitely was the case in rodents. The National Institute on Aging conducted an encouraging study in 2010 where mice that voluntarily ran on exercise wheels displayed an 'enhanced' ability to separate closely spaced squares on a display screen (the animal equivalent of pattern recognition), compared with sedentary mice. The active rodents also had far more new neurons in their dentate gyri than those that didn't run.

Dr. Yassa is including measures of physical fitness and exercise history as part of his ongoing research and the results look promising, he says. "What I'd say for now is that you can't go wrong by exercising," he said. "We don't know if it can reverse any damage if you already have memory slips. But there are indications that might slow or possibly prevent memory deterioration, if you begin exercising early enough."


References:

Reynolds, Gretchen. "A Memory Tonic for the Aging Brain." The New York Times. The New York Times Company, 25 May 2011. Web. 26 May 2011. http://well.blogs.ny...ain/?ref=health.

Yassa, Michael A., Aaron T. Mattfeld, Shauna M. Stark, and Craig E. L. Stark. "Age-related Memory Deficits Linked to Circuit-specific Disruptions in the Hippocampus." Proceedings of the National Academy of Sciences. The National Academy of Sciences, 9 May 2011. Web. 26 May 2011. http://www.pnas.org/...5/05/1101567108.



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When you think about vitamins and minerals deficiency, you may think about undeveloped or third world countries where food might be scarce. You may think about those who suffer from eating disorders such as anorexia nervosa or bulimia. But did you think that a modest deficiency could ever threaten your longevity?

Modest deficiency in vitamins and minerals is all too common in developed nations. In countries such as the U.S. that are known for its availability of food and soaring obesity statistics, this fact is much overlooked and largely ignored.

But as a new study published in the Federation of the American Societies for Experimental Biology (FASEB) Journal reveals, moderate selenium and vitamin K deficiency over time may lead to age-related diseases including cancer, heart disease, and loss of immune or brain function.

Sounds a little serious now, doesn't it?

"Understanding how best to define and measure optimum nutrition will make the application of new technologies to allow each person to optimize their own nutrition a much more realistic possibility than it is today," says Joyce C. McCann, study co-author. "If the principles of the theory, as demonstrated for vitamin K and selenium can be generalized to other vitamins and minerals, this may provide the foundation needed."

McCann and research colleagues of the Nutrition and Metabolism Center at Children's Hospital Oakland Research Institute in Oakland, California compiled and assessed several general types of scientific evidence. Testing whether selenium-dependant proteins that are essential from an evolutionary perspective are more resistant to selenium deficiency than those less essential, they discovered an astoundingly sophisticated array of mechanisms at cellular and tissue levels. In instances where selenium was limited, these mechanisms protected essential selenium-dependant proteins at the expense of those nonessential. Fascinating, too, was how mutations in selenium-dependant proteins lost on modest selenium deficiency result in traits shared by age-related diseases that include heart disease, cancer, and loss of immune or brain function.

Selenium plays a role in the functioning of the thyroid gland and in every cell requiring thyroid hormone. Dietary selenium stems from nuts, cereals, meat, mushrooms, fish, and eggs, with high levels also founding Brazil nuts, kidney, tuna, crab, and lobster. However, the report supports the daily intake of a multi-vitamin that includes selenium.

Gerald Weissmann, M.D, Editor-in-Chief of the FASEB Journal had this to say: "This paper should settle any debate about the importance of taking a good, complete, multivitamin every day... As this report shows, taking a multivitamin that contains selenium is a good way to prevent deficiencies that, over time, can cause harm in ways that we are just beginning to understand."

Partial to a particular multivitamin, Methuselites? Comment below!</br></br>



Reference:

"How Vitamins and Minerals May Prevent Age-Related Diseases." Science Daily. Science Daily LLC, 31 May 2011. Web. 31 May 2011. http://www.scienceda...10531115323.htm.




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Heart attacks and strokes, once thought to be the plague of wealthy countries, have become the burden of developing nations worldwide. The aim of polypill is to change that. The first international polypill study published on the 25th of May suggests the extreme effectiveness of a pill that could significantly reduce the burden of cardiovascular disease, taken with an ease that is as "automatic as brushing your teeth".

Data was analyzed from 378 people with a raised risk of cardiovascular disease. Half were given the polypill and half a placebo. About a third of the participants were British, a third Dutch and a third Indian. Specifically, overall systolic blood pressure was reduced from a pre-trial average of 134 mmHg to 124; while 'bad' LDL cholesterol came down from 3.7 mmol/L to 2.9.

Professor Anthony Rodgers of the George Institute for Global Health in Australia, who led the study, said:

"The results show a halving in heart disease and stroke can be expected for people taking this polypill long-term... We are really excited about this - it is a step closer to providing the polypill to patients."

The polypill concept has actually been around for decades but news from the 2009 American College of Cardiology annual conference forced the medical community and the public to sit up and take notice. One of the pioneers of the polypill, Professor Malcolm Law of the Wolfson Institute of Preventive Medicine in London states: "We have long advocated the polypill as a safe and effective way of greatly reducing the incidence of heart attacks and strokes in the population... This study shows that it's possible to make such a product that is effective and doesn't have adverse side effects."

The polypill such as the one used in The Indian Polycap Study would be easily affordable and reduce the cost of doctor's appointments, blood and cholesterol tests, and treatments greatly, making it ideal for the developing world where risk of heart attack and stroke abound and where proper medication may not be in supply or are too heavy a financial burden. "These drugs are off-patent and cost pennies," says Law. "You might be talking in terms of 50p a day. There's no way it's going to drain resources."

The 412 volunteers in the 2009 study all had a relatively low risk of heart attack and stroke, though each had at least one risk factor, be it high blood pressure, smoking habit or obesity. But in a higher risk population, "the pill might be expected to reduce rates of heart attack and stroke by around a staggering 75%", Law said. The volunteers who were given Polycap saw their blood pressure drop from six to seven points for both systolic and diastolic levels, cutting risk of heart disease by 62% and risk of stroke by 48% based on results of other studies that showed risk reduction from cutting blood pressure levels, and at no increase of side effects.

The Co-principal investigator on a 2011 study from the National Heart and Lung Institute at Imperial College London states: "The polypill idea is really simple: make it easier for people to get the medication they need by giving them just one polypill to take each day, rather than lots of different pills that may need to be taken at different times. It's likely that combining medications in one polypill could enable people in low-income countries to have easy access to cheap preventive medication."

A Department of Health spokesman said: "We welcome any evidence that contributes to providing the best treatment for people with cardiovascular disease."

"It is also important to remember that changes made to a person's lifestyle such as stopping smoking, eating healthily and taking regular exercise have far reaching health benefits that will not be reaped from medication, including reduction in the risk of developing diabetes and cancer."

Though the benefits are substantial, Associate Professor Anushka Patel, of The George Institute for Global Health noted, "Previous studies could not measure polypill side effects reliably, which is really important...This trial was reassuring in that we did not see unexpected problems. We did show previous studies had underestimated polypill side effects considerably - in the short-term about 1 in 6 people have a side effect. Most were mild but about 1 in 20 overall stopped treatment due to side effects."

Evidently, the benefits are not as massive as researchers initially suggested; side effects were also not as rare as what was first thought. This indicates that treatment is best targeted to those at higher risk.

"This heralds a more balanced, measured approach than the initial hype around the polypill," said Professor Otavio Berwanger, Hospital do Coração, Sao Paolo. "It is not a panacea. It is a really promising part of an overall package that should include measures to tackle the major causes of heart disease and cancer ie. smoking, poor diet and physical inactivity."


</br></br></br>References:

PILL Collaborative Group 2011 An International Randomised Placebo-Controlled Trial of a Four-Component Combination Pill ("Polypill") in People with Raised Cardiovascular Risk. PLoS ONE 6(5): e19857. doi:10.1371/journal.pone.0019857

The Indian Polycap Study (TIPS) Nicholas Wald,Malcolm Law The Lancet - 5 September 2009 ( Vol. 374, Issue 9692, Page 781 ) DOI: 10.1016/S0140-6736(09)61584-1

Adams, Stephen. "10 P Polypill 'halves Heart Disease and Stroke Risk'" The Telegraph. Telegraph Media Group, 26 May 2011. Web. 6 June 2011. http://www.telegraph...roke-risk.html.

First International Trial Shows Polypill Halves Predicted Heart and Stroke Risk - Cancer Benefit Also Now Expected." The George Institute for Global Health. The George Institute, 26 May 2011. Web. 6 June 2011. http://www.georgeins...-and-stroke-ris.

Boseley, Sarah. "New Trials Launch of a Daily Polypill Which Could Potentially save Millions of Lives." Sarah Boseley's Global Health Blog. Guardian News and Media, 17 May 2010. Web. 6 June 2011. http://www.guardian....roke-prevention.




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"People think that inflammation drives cancer, but they never understood the mechanism," says Michael P. Lisanti, M.D., Ph.D., Professor and Chair of Stem Cell Biology & Regenerative Medicine at Jefferson Medical College of Thomas Jefferson University.

"What we found is that cancer cells are accelerating aging and inflammation, which is making high-energy nutrients to feed cancer cells."

The researchers' findings were published in Cell Cycle journal in three separate papers online June 1st.

What exactly makes a tumor grow and how can it be stopped? Focusing on this longstanding conundrum, scientists from the Kimmel Cancer Center at Jefferson shed new light on how cancer cells speed up the aging of local connective tissue cells to cause inflammation, in turn providing fuel for the tumor to grow and even metastasize. Understanding the mechanisms of this process - similar to how brain and muscle cells interact with the body - could be useful in new drug development for treatment and prevention of cancers.

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"We are all slowly rusting, like the Tin-Man in the Wizard of Oz," Dr. Lisanti said. "And there is a very similar process going on in the tumor's local environment." In normal aging, DNA is damaged and the body deteriorates because of oxidative stress, which is interestingly induced by cancer cells in normal connective tissue in order to seep vital nutrients from it. Autophagy, the stress response induced by cancer cells in nearby cells that allow the cancer cells to be fed and grown, were previously discovered by Dr. Lisanti and his team. However, it was still unclear exactly how the cancer cells induced this stress. Even more puzzling was defining the relationship between the connective tissue and the way in which this 'energy' was transferred.

"Nobody fully understands the link between aging and cancer," says Dr. Lisanti, who used pre-clinical models and tumors from breast cancer patients to study these mechanisms.

"[A]s you age, your whole body becomes more sensitive to this parasitic cancer mechanism, and the cancer cells selectively accelerate the aging process via inflammation in the connective tissue..." which explains why cancer ravages a spectrum of ages but becomes more prevalent with age.

One of the three published papers reveals a gene expression pattern associated with lethal tumors also associated with normal aging as well as Alzheimer's disease. As a matter of fact, these aging and Alzheimer's disease signatures can also identify which breast cancer patients will undergo metastasis. The researchers found that oxidative stress is a common catalyst for both dementia and cancer cell spreading.

"If lethal cancer is a disease of "accelerated aging" in the tumor's connective tissue, then cancer patients may benefit from therapy with strong antioxidants and anti-inflammatory drugs," states Dr. Lisanti. "Antioxidant therapy will "cut off the fuel supply" for cancer cells," as well as have a natural anti-inflammatory affect on the body.
</br></br></br>References:

"Cancer Cells Accelerate Aging and Inflammation in the Body to Drive Tumor Growth." E! Science News. E! Science News, 27 May 2011. Web. 13 June 2011. http://esciencenews....ve.tumor.growth.

How Blood Vessels Feed Tumors. Adapt. Betsy Mason. Wired Science. Wired.com © 2010 Condé Nast Digital, 16 Apr. 2009. Web. 13 June 2011. http://www.wired.com.../04/tumorvideo/.



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CEO Dave Gobel describes the dynamic evolution of Methuselah Foundation in this interview with cool blogger Aaron Keefe, published on his blog Pondr. In this interview, we learn about Dave's motivation for founding the Methuselah Foundation, the economics of the budding longevity funding industry, and the strategic course of the Methuselah Foundation.
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For those who don't know much about you and your background, could you tell us how you got to where you are now as the CEO of the Methuselah Foundation?

I got to be the CEO of the foundation because I founded it in 2001, incorporated the foundation. Then in 2003 Aubrey de Grey and I met and that's when we began operations after all the government administrivia got established. So that's how.
What got me interested in longevity is really a couple of things. I guess around 1994, a good friend was going downhill on a sled and ended up running up into a tree and becoming a quadriplegic. I have a serious streak of do-good-ism and it was frustrating to me to not be able to do anything. My background was in software entrepeneurship and what did I know about medicine or anything like that... So that was the start of my path down a medical, philanthropic path.
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How about the concept of longevity in particular? What motivated you to pursue that?

I was around 46 or 47 when I began to realize that we were all on a one-way ride so I began to think about the typical stuff like supplements, exercise, diet and so forth. And because of an engineering, entrepreneurial mindset, I'm a voracious reader and read everything there was on the topics. I'm also a firm believer in a very simple manufacturing concept: it's much better to fix a problem before there's a problem.

Every step along the way where the problem where it gets worse, it gets 10 times more expensive to repair it until you need a heart transplant and you're talking about multiple hundreds of thousands of dollars. But if you could pre-keep the atherosclerosis from happening than none of those costs and pains and suffering and so forth occur. So with that mindset, I began to look for what was in the literature and began the process of education.

Along the way, another family friend got diagnosed with leukemia and this person was unable to be treated with the treatment she needed because she was unable to fit the profile for the trial that would potentially benefit her. In any case, when she got to the point of severe straits, they were able to take her on as a, I guess, charity case that would not mess up their statistics so she got the operation, a bone marrow transplant, and from what I understand the operation was a success, but the trauma of the operation killed her. That made me very, very angry. Not at anybody, but at a system, that cannot decide whether what is the actual question: Your money or your life?

People have their feet in both canoes and it's a tension that's horrible. I understand it, I accept that it exists, but there needs to be ways to change the paradigm instead of continuing to fiddle with the paradigm around the edges. In other words, we're being laced on the outside of a medical system that everyone knows is messed up and isn't going to do anything.

So about longevity - if you can prevent these things from happening or you can reverse what's already happened, than you're doing two things: you're preventing diseases that would have occurred from ever occurring, or at worse, they're going to happen a whole lot later and in combination with the relatively fast advance of what I'll call the digital medical personalized world incorporating genomics and mathometrics genome chips and all that stuff, that if you could put those diseases back, you would not die in the meantime and have the opportunity to take advantage of those things.
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Who do you think are the most prolific longevity-funding organizations?

If by 'prolific' you mean having the highest impact, then I would say organizations such ourselves, the Methuselah Foundation and SENS foundation because the impact that we've had, we believe plays a significant part in changing the way people think about longevity from "It would be wrong to extend the lifespan", "The idea of becoming immortal is wrong" (which of course we've never publicized) "The world is over-populated", "We're going to ruin the earth with all these people"...

Changing the conversation from "It'll never happen, and if it could happen, it would be wrong" to "It's inevitable that it will happen". We think that's a very powerful contribution that we've been able to make to the conversation.

What are you doing this year that is new?

Well, we've actually been doing it for a couple of years, but we haven't been saying much about it because we are highly judicious about it, and that is we have a small but targeted investment fund that is called the Methuselah Life Science fund and we were the founding investor in Organovo. We were the ones who also suggested that instead of immediately trying to create bypass grafts, which is an excellent thing to do but very, very expensive, that they should commercialize the printer. Well, they took that idea on board and went ahead and did it, after we helped them get formed and funding.

So what will be new this year is we will probably fund or help fund an additional longevity-oriented company. When these companies succeed, and so far all the companies we've invested in so far are doing just then, then there's liquidity in that.
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What are one or two key tactical activities that we might see in the next year?

We're going to raise the profile of the NewOrgan Prize and we're going to be adding a component to that prize which would talk about tissue preservation where, let's say that there's an organ that's going to be engineered - let's call it a kidney - the kidney's been either engineered or harvested. So the prize will be for a technology (people typically think of cryogenics) that would allow the emergence of organ and macro-tissue banking. So that, I think, is a reasonably near-term, we'll call it a 5 year timeline where the outcome desire is an industry where if a kidney is needed, there's going to be a kidney and options among kidneys to help provide optimal matching, not just "here's a kidney; take it or leave it".

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To be clear, the goal in 5 years is actually have a functional replacement kidney and the company to manufacture these?

No, the goal is to have an organ-banking technology so that an organ or tissues can be stored for a month at least. So let's say you're a police officer and someone shot you and you need a liver. Those are hard to get, just ask Mr. Jobs how hard those are to get on demand. But if there was a bank, you would have a selection of them. So there's a thing called a blood bank, a sperm bank, a cord blood bank, and that needs to be raised to the size of about a heart or a kidney. And if you can do that, all of a sudden, there is a huge benefit that occurs and in addition to providing for organs on demand instead of hoping and praying, it lowers costs, and it will also benefit tissue engineering because if you think about it, if you're building a biological construct, you don't want it to begin to rot before you finish it.

That's why it's a two-phase prize. The first phase is organ/tissue banking, probably cryogenics, but who knows. The second phase is whole-new organs; I expect that would be won within 10 years. We'll be raising that profile. We will probably announce an investment or the start up of another longevity oriented company and we also have a group of donors called The 300 and we told them that we would do the appropriate thing and erect a monument to their incredible support and so we're going to announce that we've acquired some land where that will go and it's a very cool location-- I'll leave it at that!
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Photography: John Lambert Pearson
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Karoshi is the Japanese term for "death from overwork", literally occupational sudden death-- the major medical causes being heart attack and stroke due to stress at work and often without previous signs of illness. In a country where employees were known to work 12+ hours a day six or seven days of the week and often working unpaid overtime hours, it doesn't come as a surprise that Japan is one of the few countries that reports Karoshi as a separate category in national statistics. Japan broke a record in the financial year of 2006-07 when around 355 workers fell ill from overwork, and of them, 147 typically died of heart attack or stroke. The statistic was Japan's highest figure, a 7.6% increase from the previous year in spite of government efforts to cut hours. But with Japanese employees putting in an average of 1,780 hours annually, not including unpaid overtime, the campaign to pre-empt karoshi would have to overcome some big obstacles.

Kenichi Uchino, a 30 year old Toyota employee, shortly before he died, collapsed at work at 4 am after more than 80 hours of overtime a month for six months, told his wife he was happiest when asleep.

From the Scientific American under the article "Can Work Kill?":

"A 1998 survey of 526 Japanese men, aged 30 to 69, supported the idea that long working hours can be hazardous to a man's health. The subjects of the study included men who had been hospitalized with a heart attack as well as healthy men of similar ages and occupations. The results were striking: Men from both groups who put in more than 11 hours of work on an average day were 2.4 times more likely to have a heart attack than were men who worked "just" seven to nine hours a day."

Let's take Sweden: In 1996 a Swedish study explored not just working hours and its correlation to health, but working conditions. More than 12,500 employed men over a period of 14 years were observed and evaluated by the psychological and physical demands of each individual man's occupation. Age, exercise habits, smoking history, medical history, educational level and social class of each were collected. The results? Those with low control over the demands of their jobs were 1.8 times more likely to die from heart disease than those with more control were. Those with low-level social support from co-workers were 2.6 times more vulnerable to cardiovascular death.

2,465 Danish bus drivers were observed in an earlier study. The intensity of traffic on the drivers' routes were linked to a two-fold increase in the risk of heart attack and death. Lack of social support only served to compound the problem. A seven-year study of 500 Swedish men implicated job strain as a predictor of mortality--high demands and low control combined to explain this effect. A related Italian study of 99,029 railway workers found that the particular combination of high job responsibility and minimal physical activity was associated with an increased risk of heart attack.

An American study assessed stress, personality, and psychological strain by questionnaire among 73 males with a mean age of 23 years old, 73% of whom worked full-time. Anxiety was positively associated with role ambiguity in the work place, as well as depression and resentment. Anxiety was also positively related to heart rate, the relationship between anxiety and work load greatest among Type A personalities.

High mental demands, low personal control and inadequate social support are the particularly worrisome factors of how overwork exacts its toll on the mind and body, and by extension, longevity.

Though more research is required to verify these observations, we do know that mental stress heightens adrenaline and cortisone blood levels, two of the so-called stress hormones while psychological stress raises heart rate and blood pressure. It can also induce arrhythmia, or abnormal heart pumping rhythm. Platelets in the blood can also be activated by stress, triggering clots that can block diseased coronary arteries.
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Photography: Eye Ubiquitous
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Perhaps one of the better approaches to work can be found in France, where despite comparatively short workweeks, French employees regularly top productivity surveys. Though less time is spent at the office than their American and Japanese counterparts, when they are in the office, their time is used more efficiently. Perhaps cutting the number of hours you give yourself to complete tasks will help you get them done in a more timely manner, getting you home to your family, friends and mental "happy place" faster. As the French say: À Votre Santé!
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References:

Simon, Harvey B. "Can Work Kill?" Scientific American 10.2 (1999): 44-46. Scribd.com. Scribd Inc. Web. 20 June 2011.http://www.scribd.co...health-passions.

Alex. "Avoiding Karoshi." Geekpreneur. New Media Entertainment, Ltd. V2, 23 July 2008. Web. 20 June 2011.
http://www.geekprene...voiding-karoshi.





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If you were faced with your own mortality, if you found out that you had a short time to live, what would you wish could have been different in your life? What regrets might you have? All too often, you might find yourself engulfed - drowning, even - in the minutiae of life without pausing every now and then to contemplate where you really are and more importantly, who you've become. Are you brave enough to strive to get to a point of feeling fulfilled with both?

Bronnie Ware, writer of the blog Inspiration and Chai, seems to be one of those eternally sunlit figures that seeks nothing but the good for others. After years of working in palliative care with patients sent home to live out their last days in peace, Bronnie found herself asking the same questions of the individuals she cared for. She noted reoccurring themes in responses over the years.
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I wish I had the courage to live a life true to myself, not the life others expected of me.

"When people realise that their life is almost over and look back clearly on it, it is easy to see how many dreams have gone unfulfilled."

Remarkably this was the most common regret her patients expressed to her. Expectations from our family, friends, colleagues, and even the expectations we perceive from society that continue to oppose the concept of contentment in life may cause us to swerve from what truly brings us happiness. Battling against our own ideas of what we should be: wealthy, prominent, "successful" may be one of the most difficult hurdles to overcome in this pursuit as well.

"It is very important to try and honour at least some of your dreams along the way. From the moment that you lose your health, it is too late. Health brings a freedom very few realise, until they no longer have it."

</br></br>I wish I didn't work so hard.Sadly, all of Ms. Ware's male patients felt deep regret for living so much of their lives in the hamster wheel of work, having been part of a generation where most female patients were not the family breadwinners.

Interestingly, a worldwide survey of happiness reveals that beyond a certain income level (that which covers your basic needs), happiness is not contingent on money. According to the research, happiness in wealthier countries is now far more dependant on closer personal relationships, good health and job satisfaction. "We always think if we just had a little bit more money, we'd be happier," says Catherine Sanderson, a psychology professor at Amherst College, "but when we get there, we're not." "Once you get basic human needs met, a lot more money doesn't make a lot more happiness," notes Dan Gilbert, a psychology professor at Harvard University and the author of the book Stumbling on Happiness.

Indeed, the more you make, the more you want. The more you have, the less effective it is at bringing you joy, and that seeming paradox has long bedeviled economists.

Simplifying your lifestyle will free you of a lot of time and money spent in maintaining a lifestyle that the world deems as "successful". It is entirely possible to not require the income that you may think you need. By doing this, more time and energy can be focused on new experiences, opportunities, and the relationships you want to cultivate. And it's the relationships that matter.

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(To be continued...)
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References:

Ware, Bronnie. "Regrets of the Dying." Inspiration and Chai. Mountain Tracks 2009. Web. 23 June 2011.
http://inspirationan...-the-Dying.html.

Futrelle, David. "Can Money Buy Happiness?" CNNMoney. Cable News Network, 18 July 2006. Web. 23 June 2011. http://money.cnn.com...82225/index.htm.




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I had a stick of CareFree gum, but it didn't work. I felt pretty good while I was blowing that bubble, but as soon as the gum lost its flavor, I was back to pondering my mortality.
- Mitch Hedberg
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The Thinker, Auguste Rodin; San Francisco
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At some point(s) in our lives, the idea of our own mortality strikes us and we may be forced to ask ourselves some pretty intimidating questions like:

What have I done in my life? How will I be remembered? Has my life stood for something?

And perhaps we aren't prepared with the right answer. Perhaps we shoulder the weight and continue on with more awareness of how precious our life is and the time that we have to truly live it.

This second installment on aspects of human thinking when faced with mortality is on a few more common expressions of some who were sadly forced to recognized death as a fast-approaching outcome, but who were fortunate to have a sympathetic ear to talk to before the end. These voices are the patients of Bronnie Ware, former palliative care nurse and writer of the blog Inspiration and Chai.
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I wish I had the courage to express my feelings.

Relationships --marriages in particular-- can cause one to habitually suppress the way he/she feels in order to maintain a modicum of peace. Unfortunately this may cause one to develop heavy emotions of bitterness and resentment, perhaps even eventually leading to illness. In 1971, a research team from the University of Michigan recruited 192 couples aged 35-69 years from Tecumseh, Michigan and followed them closely over 17 years. Each couple was individually interviewed about their methods for dealing with anger in marriage. Asked to imagine their mate shouting at them for something that they thought was not their fault, they were to describe how the would normally respond.
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Photo Credit: Getty Images
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Based on whether they communicated their anger and resolved conflicts, the couples were placed into four groups: Group 1 where both spouses affectively communicated their anger when they felt unfairly accused by the other; Groups 2 and 3 where one mate communicated and the other suppressed anger; Group 4 where both partners suppressed their anger and sulked. The researchers discovered that early death was twice as likely to occur in Group 4 where both partners suppressed their anger, compared to Groups 1-3.

Affective communication is crucial in maintaining healthy relationships, and allowing yourself the freedom to express your emotions in a constructive and reasonable manner will contribute greatly to a healthy mind, meaningful relationships, and by extension your longevity.
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I wish I stayed in touch with my friends.

"It is common for anyone in a busy lifestyle to let friendships slip. But when you are faced with your approaching death, the physical details of life fall away," writes Bronnie Ware.
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Photo credit: Vera Sytch
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Because of the typically hectic Western lifestyle so many of us are accustomed to, friendships often fade over shorter and shorter periods of time. We get so wrapped up with our own lives that we tend to overlook the most loyal, admirable, best people we know. According to Ms. Ware, many had "deep regrets about not giving friendships the time and effort that they deserved", and in the face of death, many suffered to fully comprehend the loss.

"It is all comes down to love and relationships in the end. That is all that remains in the final weeks: love and relationships."

</br>I wish I had let myself be happier."This is a surprisingly common one. Many did not realise until the end that happiness is a choice. They had stayed stuck in old patterns and habits."

Studies on what makes people happy conclude that material possessions and high achievements actually don't have much to contribute to the state of happiness. When you break it down, it's all about your outlook on life and the quality of your relationships.
Human beings are inherently creatures of habit; most acquire and stay within a pretty narrow pattern or set of habits. Fear of change leaves many pretending, to themselves and others, that they are content with the way things are when deep down there may be hidden longings for a different way of life. Unfortunately, those that reach the end of their lives with a true sense of satisfaction for the life they led have become a rarity.

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Ms. Ware summarizes it all with these simple words: Life is a choice. It is YOUR life. Choose consciously, choose wisely, choose honestly. Choose happiness.

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References:

Ware, Bronnie. "Regrets of the Dying." Inspiration and Chai. Mountain Tracks 2009. Web. 23 June 2011.
http://inspirationan...-the-Dying.html.

Paddock, Catherine. "Suppressing Anger in Marriage Linked to Shorter Life." Medical News Today. MediLexicon International Ltd., 28 Jan. 2008. Web. 30 June 2011.
http://www.medicalne...icles/95322.php.





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Rapamycin - an immunosuppressant drug used to prevent organ rejection in transplantation - has been found to reverse a very rare, fatal genetic disease called Hutchinson-Gilford progeria syndrome, characterized by very rapid, dramatic appearance of aging.
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Remember our friend and Mprize Lifespan Achievement winner, Dr. David Z. Sharpe? He and his team have already proven that Rapamycin extends the lifespan in healthy mice and now researchers are hoping to uncover new insights into treating progeria and other diseases related to aging.

Published in the journal Science Translational Medicine, a new study finds that Rapamycin can reverse the defects from skin cells of patients with progeria (namely, decreased growth, deformities in their membranes, and early death) by enhancing the cells' ability to degrade the protein progerin, accumulated in excessive amounts in progeria patients who suffer with issues typically linked with old age: balding, joint pain, hardened skin, hip dislocation, heart disease, and not to mention arteriosclerosis that leads to higher chances of heart attack and stroke.
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Cells taken from progeria patients were treated with the Rapamycin.
Top image shows a toxic protein called progerin (green) spread evenly throughout the cells.
Bottom displays the treated cells with the concentrated protein removed much more effectively.
Credit: Science/AAAS

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The findings may have relevance beyond the treatment of this rare genetic disease. Progerin accumulation in normal cells, though not nearly as concentrated as those of progeria sufferers, may still be a factor of the aging process.

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Previous research has shown that cellular maintenance failure is a key component of aging. Associate professor of neurology at Harvard Medical School and one of the authors of the paper, Dimitri Krainc indicates that age-related diseases like Parkinson's and Alzheimer's also result in defects of the "trash-removal" system of the cells. In simpler terms: Failure of cellular maintenance is a key component of aging.

"With normal aging... you start accumulating by-products of normal cell functions," says Krainc. Though this study only focused on the effects of Rapamycin on progerin, it may also help clean up other toxic proteins as well.

Dr. David Sinclair, Mprize competitor and director of the Paul F. Glenn Laboratories for the Biological Mechanisms of Aging at Harvard Medical School, hopes that "the study increases the search for molecules to replace Rapamycin" so as not to have the immunosuppressant side effects. Such alternatives could be a major step forward in the fight against aging.

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References:

Scaffidi P, Gordon L, Misteli T (2005) The Cell Nucleus and Aging: Tantalizing Clues and Hopeful Promises. PLoS Biol 3(11): e395. doi:10.1371/journal.pbio.0030395
http://dx.doi.org/10...al.pbio.0030395.

Vezena, Kenrick. "Drug Reverses 'Accelerated Aging' in Human Cells." Technology Review. MIT Technology Review, 29 June 2011. Web. 1 July 2011.
http://www.technolog...ne/37916/?p1=A1.




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Jewelers, machinists, and chocolatiers. What do these have in common? Just decades-old 3-D printing technology to make custom pieces without having to form molds. Now leading figures in regenerative therapies are using cutting edge 3-D bioprinting to construct living tissue, and perhaps even whole human organs.

In laboratories worldwide, luminaries in biology, chemistry, medicine, and engineering are working on the routes toward one audacious, spectacular goal: to print a functioning human kidney, liver, or heart using a patient's own cells.

Anthony Atala, NewOrgan Prize Scientific Advisory board member and Director of the Wake Forest Institute for Regenerative Medicine, envisions what he calls "the Dell computer model" where a surgeon could order up "this hard drive, with this much memory..." Except that he/she would be talking about specs for living tissue instead of electronics. What an amazing time we live in!

"The possibilities for this kind of technology are limitless," said Lawrence Bonassar, whose lab at Cornell University has printed vertebral tissue that tested well in mice. "Everyone has a mother or brother or uncle, aunt, grandmother who needs a meniscus or a kidney or whatever, and they want it tomorrow. ... The promise is exciting."


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Organovo's NovoGen MMX Bioprinterâ„¢
Photo Credit: Organovo
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Researchers have already printed skin and vertebral disks and put them into living bodies (yet to be human bodies) but a few types of printed replacement parts such as blood vessels and arterial structures for use in coronary bypass surgeries could be ready for use in human trials in as little as two to five years. In fact, on December 8, 2010 Organovo announced the release of data on the world's very first fully bioprinted blood vessels from their NovoGen MMX Bioprinter.

"These vessels are the world's first arteries made solely from cells of an individual person," said Keith Murphy, Chief Executive Officer of Organovo. "Our results show the power of the NovoGen bioprinting technology to create tissue starting only with cells."

Aortic valves are the focus of Jonathan Butcher's lab at Cornell University, with the hopes of printing replacement valves for children with heart disease. Every method of bioprinting differs slightly from one lab to the next. Check out how it's done at Cornell!

"If the federal government created a 'human organ project' and wanted to make the kidney, I literally think it could happen in 10 years," says chemical engineer Keith Murphy, co-founder of Organovo, a firm that makes and works with high-end bioprinters and a major investment of Methuselah Foundation. "But that would require a massive commitment of people [and] resources", he said.

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That's why we at Methuselah Foundation ask you to see the scale of good that this technology can bring to humanity. We ask for the commitment to help realize the goal of making an organ available when the need arises, extending the lives of countless people all over the world. Donate today!

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References:

Berkowitz, Bonnie. "3-D Printers May Someday Allow Labs to Create Replacement Human Organs." The Washington Post National. The Washington Post, 9 May 2011. Web. 4 July 2011.
http://www.washingto...0WbG_story.html.

http://www.organovo.com/






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A tissue-engineered small intestine in mice that mimics the intestinal structures of a natural intestine was successfully created by researchers from The Saban Research Institute of Children's Hospital LA on July 5, 2011 in Los Angeles, California. This is a significant milestone toward someday applying this regenerative medicine technique to human beings.
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Tracy Grikscheit, MD The Saban Research Institute of Children's Hospital Los Angeles
(Photo: Business Wire)

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Published as "A Multicellular Approach Forms a Significant Amount of Tissue-Engineered Small Intestine in the Mouse" in the July issue of Tissue Engineering Part A and led by Tracy C. Grisksheit, MD, she explains: "In this paper, we are able to report that we can grow tissue-engineered intestine in a mouse model, which opens the doors of basic biology to understand how to grow this tissue better."

Those "doors of basic biology" may lead to solutions for Grikscheit's (a pediatric surgeon) for her more vulnerable patients-- premature newborns. These infants are at increased risk for a type of gastrointestinal disease of an unknown cause called necrotizing enterocolitis (NEC) which happens when the intestine is injured. NEC is the most common gastrointestinal emergency in neonates and primarily occurs in premature infants. Unfortunately, rates of prematurity are increasing and so are the numbers of children with NEC.

"The small intestine is an exquisitely regenerative organ. The cells are constantly being lost and replaced over the course of our entire lives," Grikscheit explains.

"Why not harness that regenerative capacity to benefit these children?"

Why not? Fantastic question. It is crucial to treat NEC early on to prevent bacteria from leaking into the abdomen, potentially threatening the lives of the infants; often the only solution is surgical removal of the small intestine, leaving the baby dependant on intravenous feeding which puts them at risk for liver damage. Transplants are possible but only as a short-term solution, with only 50% chance the grafted intestine will last past the 5th year of the child's life.

So Griksheit and her research team pressed forward for better options, taking advantage of regenerative techniques. They took samples of intestinal tissue from mice, comprised of the muscle cells and epithelial cells that make up the layers of tissue, then transplanted the cell mixture within the abdomen on biodegradable polymers or "scaffolding"--a word that you will read time and time again in regenerative medical procedures. And voila: brand new engineered small intestines developed and consisted of all the cell types found in the native intestine. The transplanted cells were ingeniously labeled green so that the scientists could identify which cells were provided.
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Illustration of the intestinal tissue regeneration process
Photo: University of Southern California
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"What is novel about this research is that this tissue-engineered intestine contains every important cell type needed for functional intestine. For children with intestinal failure, we are always looking for long-term, durable solutions that will not require the administration of toxic drugs to ensure engraftment. This tissue-engineered intestine, which has all of the critical components of the mature intestine, represents a truly exciting albeit preliminary step in the right direction," said Henri Ford, MD, Vice President and Surgeon-in-Chief at Children's Hospital Los Angeles.


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References:

Kavanagh, Ellin. "Children's Hospital Los Angeles Researchers Engineer Small Intestine in Lab Research Experiments." Children's Hospital Los Angeles. Children's Hospital Los Angeles, 5 July 2011. Web. 7 July 2011.
http://www.chla.org/...t=10861741¬oc=1.

"PIBBS Research Faculty Directory." University of Southern California. University of Southern California. Web. 7 July 2011. http://www.usc.edu/p...rikscheit_t.htm.
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June 9, 2011 - A synthetic trachea made up of a 36 year old patient's own cells was implanted,
saving his life and allowing him to breathe easy, cancer-free
(Photo Credit: David Green)
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"He was condemned to die," said Paolo Macchiarini, a professor of regenerative surgery who carried out the procedure at Sweden's Karolinska University Hospital. "We now plan to discharge him [Friday]."

For the first time in surgical history, on June 9th 2011, an entirely synthetic and permanent trachea was successfully transplanted using a patient's own cells. An Eretrian man from Iceland, Andemariam Teklesenbet Beyene, left Karolinska University Hospital in Huddinge, Stockholm Friday breathing through a trachea engineered with cells that came from his own body, not one transplanted from a cadaver's throat.

As a 36 year old father of two and student of geology at the University of Iceland in Reykjavik, Beyene never imagined that he would suffer from an advanced case of tracheal cancer, experiencing the excruciating difficulty of malignant tumors expanding to about six centimeters in length, almost completely blocking his windpipe and choking off his oxygen supply.

It had reached a point where Dr. Paolo Macchiarini of Karolinska University Hospital decided that there was no time to wait for a donor trachea and assembled a team to build one with Beyene's own cells. With the successful transplantation of cadaver-based windpipes in 10 patients, he had good reason to feel emboldened. But tracheas from cadavers that are so relied on by patients like Beyene are in very short supply and those who are fortunate enough to receive one face risk of rejection and a life-time of immunosuppressant drugs that also inconveniently include a number of side effects. With a synthetic trachea built from his own cells, Beyene can breathe easy--without the use of the immune-suppressing drugs.

"It makes all the difference," said Dr. Macchiarini. "If the patient has a malignant tumor in the windpipe, you can't wait months for a donor to come along."

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So how did they do it? Scientiest Alexander Seifalian of University College London built the trachea with a glass tube as a base with the precise dimensions of Beyene's trachea, obtained from three-dimensional images. A medical plastic called polyethylene glycol was then used to build a scaffold around it. Because of the plastic's porous nature, stem cells can grow into it, induced by the hormones applied by the scientists to persuade them to differentiate into the bony cells- the cells normally found in the lining and exterior of the trachea. Then it's "popped" into the oven-like bioreactor where after the two days it takes for the cells to grow and proliferate, it's ready for implantation. From beginning to end, the entire process took less than a week's time.

The operation marks another step forward for the field of regenerative medicine and "further validates the fact that these technologies may have a role in treating larger numbers of patients in the future," said Dr. Anthony Atala, director of the Institute for Regenerative Medicine at Wake Forest University School of Medicine in Winston-Salem, N.C.

48 hours after the procedure, the appropriate cells were shown by imaging and other studies to populate the artificial windpipe which had begun to function like a natural one. Beyene's immune system did not reject it because the cells came from his own body. In fact, he no longer has cancer and is expected to have a normal life expectancy, the doctors said. His speedy recovery is quite a testament to the mission of making fresh body parts for transplantation or treatment from one's own cells and more immediately, it offers a viable option for thousands who suffer from tracheal cancer or other life-threatening conditions that affect the trachea.

Dr. Macchiarini says he plans to use the same windpipe-transplant technique on three more patients, two from the U.S. and a nine-month-old child from North Korea who was born without a trachea.

Regenerative therapies are saving more and more lives but there is yet so much ground to cover before much more complex organs like the heart with its many different cell types can be built from a patient's own cells. We plead you to help us get there faster! Join the New Organ Network for free. Create a profile, build a network of your friends and family. Show that you care!

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References:

Naik, Gautam. "Lab-Made Trachea Saves Man." Wall Street Journal Health. Dow Jones & Company, Inc, 8 July 2011. Web. 8 July 2011.
http://online.wsj.co...cleTabs=article.

Cevallos, Marissa. "Transplanted Trachea, Born in Lab, Is One of Several Engineered-organ Success Stories." Los Angeles Times Booster Shots. Los Angeles Times, 8 July 2011. Web. 8 July 2011.
http://www.latimes.c...0,2121263.story.




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Alright. We do a lot of gushing about Organovo. But you know what? With it walking the precipice of cutting-edge, revolutionary technology called bio-printing and its quite impressive strides thus far, we think gushing of geyser-like proportions is warranted... necessary, even. Consider this: Since the founding of Organovo just four years ago, the company has raised over $2 million from private investors and has already developed the bioprinting technology that lays down patterned, cultured cells in a supporting structure of a jello-like hydrogel in a 3-D structure. Which is... you know... phenomenal. And just three years after its founding, Organovo's NovoGen MMX Bioprinter was named one of Time Magazine's Best Inventions of 2010. If you don't think that's impressive, then you can just stop reading here.
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Their dynamic momentum, with considerable help from the Methuselah Foundation since their beginning has led to the reality of bio-engineered blood vessels and the ambitious plans for kidneys, livers, and other vital organs that are now under way. Armed with a new and, more importantly, stable source of revenue, Organovo is going through expansion of laboratory space to accommodate the size of its ambition! How brilliant is that?! But where's the moolah coming from?

"Our dance card was full at BIO for partnering meetings, and we've got a spectrum of big and small, U.S., Japanese, British, and Swiss pharma companies at the table," CEO Keith Murphy writes.

"The response to what we're doing has really been tremendous. People can really use what we have in Oncology, Diabetes, Fibrosis, and other areas where a 3-D [tissue structure] is relevant."

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Murphy has identified a burgeoning market among pharmaceuticals by forming what he calls 3-D "constructs" of diseased or dysfunctional human cells to be used as models for new drug testing. These models react to drug compounds much as they would in the body because the cell matrix enables each cell to interact with adjoining cells (just as it does in the body!). So by producing living human tissue outside the body, the company is making it possible for pharmaceutical researchers to test an experimental compound's toxicity in a manner that mimics the reaction within a living organism.
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With that in view, two partnership agreements with pharmaceutical companies as well as one made with a regenerative company have been "signed, sealed, delivered" and several other companies are in the works for the same. By the end of this year, Murphy writes, more partnership deals expect to be signed.

"One of the things that's been good about the past six months is that the promise of our technology is holding true," Murphy says. "The constructs we're creating robustly build [blood vessels] with collagen, so the blood vessel grows stronger over time. The next challenge is getting to greater and greater vascularization of the construct. The emerging story is going to be, 'Who can make thicker tissues with more blood vessels inside?' "

As Keith Murphy says, creating a made-to-order liver or pancreas in just a few weeks "could happen in 10 years." The applications continue to advance rapidly. The industry is gaining in heat and momentum. Even in the world of investment, Louis Basenese's recent recommendation allowed White Cap Report readers to pocket 140% gains in just seven months. Numbers don't lie and progress is measured in numbers. The public deserves to know that technology like this not only exists outside of science fiction novels, but that we are actively pursuing the day when a complex organ such as a heart or a liver can be printed by a patient's own cells. Everyone who cares for their own health (and that of their family and friends) deserves to have the opportunity to support this endeavor. (Hint: Think NewOrgan Prize.)


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References:

Bigelow, Bruce V. "Organovo's Bio-Printing Technology Yields Unanticipated Revenue from Pharma Partners." Xconomy | San Diego. Xconomy Inc., 13 July 2011. Web. 14 July 2011.
http://www.xconomy.c...rma-partners/2/.

Fritz, Justin. "Need a New Liver? Just Hit "Print"." Wall Street Daily. The White Cap Research Group, LLC, 21 June 2011. Web. 14 July 2011. http://www.wallstree...t-human-organs/.




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Still from "How To Live Forever" where Jack LaLanne offers director Mark Wexler some exercise advice

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This is Mark- the guy to the right. It was a genuine pleasure to chat with Mark. He seems to be one of those real, empathic film makers who work passionately to dignify diverse personalities through film (and is willing to travel the world and live off a suitcase to do it). How to Live Forever, like the rest of his documentaries, stems from a hugely personal time in his life. And, well, what's the use in us trying to convey the message of the movie? The trailer does it so much better than we ever could.

• Can you tell me about the "A-ha" moment when you realized that you wanted to make this film?

When I turned 50 my mom passed away and soon thereafter, my AARP card arrived in the mail and it got me thinking "Hmm, maybe there's a way to tack more time in. Maybe there's a way to extend my life, maybe add a whole new chapter to my life or chapters." So I have a lot of things I want to do and I thought there might be a way to add more time so that set me out on this journey all over the world, initially talking to scientists about how one might extend one's life. And then it sort of opened up into talking to a variety of people from philosophers to scientists to centenarians, all sorts of different people about how they're living long and ways that I can live longer. You know, calorie restrictors- the gamut.

I started out the film thinking that I would talk to scientists who would tell me to eat more blueberries, take these supplements and that would give you x amount of years, etc. And I got to talking to people. One of the takeaways from the movie is that it's not only the length of one's life but also the quality of living and being able to appreciate it-- I think it's equally important as adding years. So I do still want more years but that may not be the primary goal at this point.

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Poster design by Kajsa Björs
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• How did you map out your course of documenting the world's oldest people? How did you know where to start?

At first I knew I wanted to go to the longevity hotspots of the world and I knew one was probably Okinawa, Japan. And I knew that Iceland male life expectancy was long. And there were basically several characters around the world; a guy I filmed named Buster was a 101 year old marathon runner, who was smoking several cigarettes a day and drinking beer still. So I was looking for unusual and quirky characters and my journey around the world involved talking to these centenarians who were unusual for living a long time. So not only was there the longevity hot spots in the world, but the characters, the people-- that's what brought me all over the place.
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• How long was your journey for?

It took me about 4 years in total to make the film. Some of that, maybe a year and a half in the editing room. And you know, I was cruising the internet, I was talking to people a lot, I would interview someone and ask if they knew someone who knew about calorie restriction and they'd refer me to someone else. There were a lot of referrals but also research, which I love. A lot of it had to be researched well otherwise I'd go halfway across the world and if things didn't happen exactly the way I wanted, that would have been a very expensive mistake.

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Not everyone we filmed got into the movie, unfortunately, but the movie will have a great extra section just because there are so many interesting characters. We interviewed a 90 year old surgeon who is still performing heart surgery, we interviewed a guy who still flies kites at 100 years old (above) -- he builds these amazing kites and still flies them. These are all quite interesting characters who, I think, shared a great sense of humor; the glass is always half full; they have a very positive outlook on life. It was so inspirational to be around these people to be in their presence and they have a sort of inner serenity that is very appealing. I had a great time making the movie because I got to be around these people.

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One of those inspirational figures is SENS' own Aubrey de Grey! Who is apparently quite adept at rowing a gondola.

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• It's clear that the inspiration for your documentaries hugely stem from your personal experiences and values - I think that takes a very special kind of courage; after making How to Live Forever, what are your conclusions about life extension and the world's pursuit of youth and vigor?

We come from a youth-obsessed culture and I think that's one of the things I love about Japan, especially Okinawa-- elders are really worshipped there and I think there's a lot to learn from older people. I would love to live longer but I also I want to live well.

AI think all the worry about living longer may age me quicker than just enjoying what I have now. I think there are technologies right around the corner that will extend life significantly and that will affect all of society and I think that's very exciting to realize. But I think there may be consequences good and bad that we can't imagine that will affect our world, everyone's world. I also think that as a baby boomer, all of us are interested in packing in more, living longer.

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• What would you like the audience to come away with?

The subject of aging can be difficult- but most people came away with feeling uplifted and optimistic about where they are in the life cycle so I was happy to impart that to audiences. I hope the movie is thought-provoking and entertaining -- it's also a particularly funny movie. So I was happy to be able to do that. I think having a purpose in life is really key. In Japan there is this thing call ihi kai which is a reason to get up and do your thing-- I think that's key and I think that's something to nurture. I think we lose that. In Western culture a lot of people retire early and they lose their purpose. And that purpose doesn't necessarily mean you have to have a job- you know, it can be a hobby that keeps one interested in life. I think people who retire often feel rudderless and that of course affects their health and longevity.

I didn't expect young people to be interested in the movie- I honestly thought it would only interest baby boomers, people beyond their 40s. But I was surprised to see that young people really enjoyed it, were into it, and I'm pleased by that.

At first I worried that Methuselah Foundation was just all about the numbers- you know, just being alive as long as one can - but I'm glad to know that it's about having the best quality of life for as long as one can.

So make sure to pre-order your DVDs so you won't miss out on this awesome documentary-- it releases on August 23rd!

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This handout picture taken in 2010 and released to Reuters on July 12, 2011 shows
a bioengineered tooth unit grown by researchers at Tokyo University of Science, using mouse stem cells.
REUTERS/Dr. Takashi Tsuji/Tokyo University of Science/Handout


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Here's something to nosh on-- a team of Japanese researchers led by Professor Takashi Tsuji from Tokyo University of Science have constructed teeth out of mouse stem cells and successfully transplanted them into mice!

The team removed two varieties of stem cells from the molar teeth of mice and placed them in a mold to grow in the laboratory, thus controlling its formation - the shape and length of the teeth. Afterwards, the whole tooth units were transplanted into the lower jaws of one-month-old mice. On average, it took 40 days for the transplanted teeth to fuse with the mice's jaw bones and tissues. Able to detect even the nerve fibers growing in the new teeth, the scientists were able to conduct a very thorough study.

The outcome: The mice with the regenerated teeth were able to eat and chew normally with no complications.

"The bioengineered teeth were fully functional... there was no trouble (with) biting and eating food after transplantation," writes Masamitsu Oshima, assistant professor at the Research Institute for Science and Technology, Tokyo University of Science.

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Oral photographs (upper) and micro-CT (lower) images showing occlusion of natural (left) and bioengineered teeth (right).
Image credit: PLoS ONE 6(7): e21531. doi:10.1371/journal.pone.0021531

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The researchers hope that this step will contribute in the development of new human organs grown from a patient's own cells.
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"It is important to develop technologies for the culture of the bioengineered organ... for the realization of future organ replacement regenerative therapy," Professor Takashi Tsuji wrote in his reply to questions from Reuters.

Reminiscing about the 2010 US research that led to the construction of an artificial lung that allowed lab rats to breathe for several hours, Tsuji emphasized the necessity of locating the right "seed cells" for reparative therapy. In this case, entire tooth units could be grown because the stem cells were taken from molar teeth of mice, where they later grew into enamel, dental bones and other parts that comprised a regular tooth unit.

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References:

Lyn, Tan Ee. "Experts Grow Whole Tooth Units Using Mouse Stem Cells." Reuters. Thomson Reuters, 12 July 2011. Web. 20 July 2011.
http://www.reuters.c...E76B4EI20110712.

Braconnier, Deborah. "Stem Cells Grow Fully Functional New Teeth." Medical XPress. Medical Xpress, 13 July 2011. Web. 20 July 2011.
http://medicalxpress...onal-teeth.html.



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"She turned me into a newt!"
"A newt?"
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"I got better."

- Monty Python and the Holy Grail (1975)
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Armed with the stunning ability to regenerate limbs, eyes, hearts, spinal cords, intestines, and even its upper and lower jaws, newts are the masters of regeneration. Thanks in part to the initial illuminating studies of Italian biologist Lazzaro Spallanzani conducted over 200 years ago, we've known for a while that newts and salamanders had this special gift.

As science and technology progressed, biologists learned more about the ability of the cells at the site of the injury to de-differentiate, rapidly reproduce and differentiate again to grow a new organ or limb. But it's always been unclear the lengths these abilities could stretch to.

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In a study spanning 16 years, Panagiotis Tsonis, along with his team, concludes that the healing ability of newts remain unaffected by injury and age, debunking 250 years of scientific theory about a fundamental element of tissue regeneration - that age and repeated amputation negatively affect regeneration.

As director of the University of Dayton's Center for Tissue Regeneration and Engineering at Dayton (TREND), Tsonis believes that his discovery will benefit the progressive field of regeneration research, bringing biologists and the medical community one step closer to a complete understanding of the mechanism behind newt regeneration. One day, he believes, humans will be fully able to replicate the process for themselves.

Tsonis' mentor and co-author of the study Goro Eguchi set up the experiment in 1994, after collecting several Japanese fire-bellied newts (Cynops pyrrhogaster), successfully keeping them in captivity, and over time anesthetising the newts and carefully removing the lenses from their eyes. The team focused on the newt's lens for is unique in that it can be removed entirely and regenerates in a completely enclosed environment after the incision in the cornea heals within a day.

To remove the lens, a small nick to the cornea was made, which quickly sealed, forming a protective environment so that the lens could regenerate without the disruption of any outside influence. And do you know how many times he did this? 18 times in total, with newts that were estimated to be at least 14 years old when collected, making them 30 by the end of the study.

The outstanding thing: The 17th and 18th regenerated lenses of each newt were virtually identical to intact lenses from full-grown newts!

With these repeated surgeries throughout a span of 16 years, and with the oldest newts regenerating their lens as well as the young ones, the team proved the long-held belief that regeneration capabilities are adversely affected with age to be false.

"We are still a long way from relating this to humans, but what this shows is that the newt is an excellent source for finding answers to regeneration, particularly as it relates to old age," Tsonis said. "The newt not only has good regeneration properties, but it has the ability to protect and preserve regeneration."

If you haven't seen him explain newt regeneration himself, check it out here!
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A lens on a young newt that has never undergone regeneration (left) is practically identical to the 17th regenerated lens on an aged newt (right).

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"I expected to see regeneration in the final trials, but this good? Even I was surprised a little. It was a perfect lens," Tsonis said. "As a biologist, I can say this is the biggest discovery in regeneration research involving newts in 250 years."

The next step? Discover how newts keep their regenerative potential in their ageing tissues so that the new understanding can be applied to human medicine. It won't be an easy task, since newts and salamanders are notoriously difficult to work with in captivity, but Tsonis's group are working hard and remain optimistic. "Our findings... are of paramount importance to the field of regeneration and ageing," Egochi writes.

"We and others have invested a lot of effort to develop these techniques. Many important questions can now be addressed to understand why newts do what they do and how to apply it to regenerative medicine. After all, this animal does everything that regenerative medicine seeks to achieve!"

Join in our efforts to incentivize and accelerate progress in regenerative medicine! Haven't joined our NewOrgan Network? Sign up for free and get your friends and family on board, too.

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References:

Eguchi, Eguchi, Nakamura, Yadav, Milan & Tsonis. 2011. "Regenerative capacity in newts is not altered by repeated regeneration and ageing". Nature Communications. http://dx.doi.org/10.1038/ncomms1389

"Ageless Regeneration." University of Dayton News. University of Dayton, 12 June 2100. Web. 20 July 2011. http://www.udayton.e...on_research.php.

Young, Ed. "Newt Healing Factors Unaffected by Age and Injury." Discover. Kalmbach Publishing Co., 12 July 2011. Web. 22 July 2011. http://blogs.discove...age-and-injury/.



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Though cancer cells seem to rebel against orderly cell life and death, breaking all the rules like a misfit, growing wildly and dangerously, there is actually a balance between a cancer cell's fiery metabolism and skyrocketing levels of cellular stress--it is dependant on a hyperactive metabolism to fuel its rapid growth as well as antioxidant enzymes to rein in potentially toxic reactive oxygen species (ROS) generated by such high metabolic demand.

Now a study from scientists at the Broad Institute and Massachusetts General Hospital (MGH) reveals a novel compound that successfully but selectively blocks this response to oxidative stress in cancer cells, sparing normal cells. In fact, its effectiveness surpasses even a chemotherapy drug currently used for breast cancer. The compound? It's actually derived from the fruit of a pepper plant native to southern India and Southeast Asia, a compound called plant-based piperlongumine or PL. Cancer cells are killed by jamming the machinery that dissipates high oxidative stress and the resulting ROS. Because of their more modest metabolism, normal cells maintain low levels of ROS, making high levels of the anti-oxidant enzymes unnecessary once they pass a certain threshold.

"Piperlongumine targets something that's not thought to be essential in normal cells," said Stuart L. Schreiber, a senior co-author and director of the Broad's Chemical Biology Program. "Cancer cells have a greater dependence on ROS biology than normal cells."

Some of the best discoveries in history are found by accident, and Sam w. Lee and Anna MAndinova, both senior co-authors from the Cutaneous Biology Research Center (CBRC) at MGH certainly weren't looking for a ROS inhibitor when they found PL. Their target was in the tumor suppressor gene p53, mutated in more than haf of all cancer types. They were looking for something to increase the levels of the properly functioning p53 gene. A promising signal for PL occurred, but they only assumed it worked by the enhancement of the p53 gene. When PL induced cancer cell death independent of the p53's activity as the tumor suppressor gene, they sat up and took notice. PL was tested in normal cells - they weren't killed.
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"The novelty of this compound was that it was able to recognize cancer cells from normal cells," said Mandinova, a Broad associate member and a faculty member at MGH and Harvard Medical School. "It has a mode of action that targets something especially important to the cancer cell."

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And yet another surprise- after the Proteomics Platform's quantitative analysis identified the target of PL, they found an indirect process on which cancer cells depend, in the stead of the assumed oncogene (a protein encoded by a cancer-causing gene being inhibited). There is a small number of new cancer drugs that target oncogenes directly, but they may not be the only promising new direction for treating cancers. See, cancer genes don't act alone and PL exploits a dependency developed after oncogenes transform normal cells into cancer cells.

"Our studies suggest that piperlongumine's ROS-associated mechanism is especially relevant to the transformed cancer cell," said co-author Andrew M. Stern, associate director of Novel Therapeutics at the Broad. "And this in part may underlie the observed selectivity of PL."

The scientists tested PL against cancer and normal cells engineered to develop cancer in mice injected with human bladder, lung, breast, or melanoma cancer cells. The PL inhibited tumor growth but showed no toxicity in normal mice. The tougher test of mice that spontaneously developed breast cancer revealed PL blocking both tumor growth and metastasis, whereas the chemotherapy drug paclitaxel (Taxol), even at high levels, proved less effective.
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"This compound is selectively reducing the enzyme activity involved in oxidative stress balance in cancer cells, so the ROS level can go up above the threshold for cell death," said Lee, a Broad associate member and associate director of CBRC at MGH. "We hope we can use this compound as a starting point for the development of a drug so patients can benefit."

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Much more work needs doing to gain a better understanding of how the ROS process differs between normal and cancer cells before the launch of clinical trials. Further studies will focus on different forms of cancer and their genotypes, or genetic information. So while the authors remain cautious, they're hopeful.

"Our next set of goals is to learn if there are specific cancer genotypes that will be more sensitive to this compound than others," said Alykhan F. Shamji, associate director of the Broad's Chemical Biology Program. "We hope our experiments will help be predictive of whether patients with the same genotypes in their tumors would respond the same way. It would help us to pick the right patients."

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Reference:

Cooney, Elizabeth. "Taking out a Cancer's Co-dependency." Broad Institute News and Multimedia. Broad Institute, 13 July 2011. Web. 25 July 2011. http://www.broadinst...e.org/news/2979.





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Jessica McConnell Burt / George Washington University

Researcher Chet Sherwood, holding a chimpanzee brain
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"We are very weird animals," said Emory University anthropologist Todd Preuss at the Yerkes National Primate Research Center in Atlanta, who wasn't involved in the study. "Among neuroscientists, the assumption has been that species are all the same, but this shows there is something really unusual about the late-life biology of the human species."

It's estimated that as much as one in every five people in the US will be over the age of 65 by 2030, more than twice the number of elderly just a decade ago, according to the US Administration on Aging. Unfortunately for us, unlike chimpanzees and other primates, elderly humans are vulnerable to a host of neurodegenerative diseases such as Alzheimer's--the hope of researchers is that understanding the basic biology of the brain can lead to new treatment and measures to postpone the mental demise of aging.

In this study, the first direct comparison of humans to chimps, a team of brain-scanning scientists led by George Washington University anthropologist Chet Sherwood find that chimps don't experience such memory loss and that humans are uniquely afflicted by this oddity of longevity. They used MRI technology to scan and measure changes in five crucial brain structures involved in memory, reasoning and mental processing, and overall brain volume and density. Measurements were compared from 87 adult human brains (that's, ahem, a lot of brains) ranging from 22 - 88 years of age with brain volumes of 99 adult chimps ranging from coinciding 10 - 51 years of age. The gray matter of neurons and white matter of connecting neural fibers were also measured. Chimps' brains were found to only weigh a third as much as the average 3 lb human brain. The 3 lb human brain was found to shrink by up to a surprising 15% in later years.

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The results? "We found no age-related changes in chimpanzees," said Dr. Sherwood. The human brains lost significant volume over time while the chimpanzees' remained intact with age. But what humans eventually won't have in brain volume, they make up for with longevity-- a human being can expect to live up to 80 years or more, almost twice the normal lifespan of a chimpanzee in the wild.

"It seems that this is the cost," said Dr. Sherwood. "We experience more extensive atrophy in the brain that results in this obvious shrinkage, of a kind that is not seen even in our closest relatives, chimpanzees."

"We were most surprised that chimpanzees, who are separated from humans by only 6-8 million years of independent evolution, did not more closely resemble the human pattern of brain aging," said Sherwood. "It was already known that macaque monkeys, separated from humans by about 30 million years, do not show humanlike, widespread brain atrophy in aging."

"This is an excellent example of research that has implications for societal benefits," said NSF Physical Anthropology Program Officer Kaye Reed. "While Dr. Sherwood and colleagues are interested in the evolutionary significance of brain differences between chimpanzees and humans, the results of this research can be used as a basis to explore degenerative brain diseases, such as Alzheimer's, in a medical context."

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References:

Hotz, Robert L. "Brain Shrinkage: It's Only Human." The Wall Street Journal | Health. Dow Jones & Company, Inc, 26 July 2011. Web. 30 July 2011. http://online.wsj.co...4286877908.html.



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If you've ever been struck with painful, almost total immobility because of your back or neck, then you know how excruciating it can be. Millions every year haul themselves to doctors for treatment and become part of a statistic for a broad category of illness called degenerative disc disease, a leading cause of disability worldwide. But now Cornell engineers in Ithaca are working in collaboration with doctors at Weill Cornell Medical College on a bio-engineered spinal implant that could someday spell relief for these millions.

"We've engineered discs that have the same structural components and behave just like real discs," says Lawrence Bonassar, Ph.D, associate professor of biomedical engineering and mechanical engineering, together with Roger Härtl, M.D., associate professor of neurosurgery at Weill Cornell Medical College and chief of spinal surgery at NewYork-Presbyterian Hospital/Weill Cornell Medical Center.
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"The hope is that this promising research will lead to engineered discs that we can implant into patients with damaged discs."

This new research will be published online Aug. 1, 2011 in the Proceedings of the National Academy of Sciences. Their other colleagues on the paper are Robby Bowles, Cornell Ph.D. '11, and Harry Gebhard, M.D., of Weill Cornell Medical College. 40-60 percent of American adults suffer from chronic back or neck pain annually and though there might be a surgery called a discectomy (removing the spinal disk and fusing the vertebrate bones to stabilize the spine), they are for those diagnosed with severe degenerative disc disease or herniated discs. But the patient's back will not likely feel the same as before.(Bonassar Lab)
From left, a natural rat IVD compared with a tissue engineered IVD.

"Bone or metal or plastic implants are complicated structures which come with a mechanical risk of the structures moving around, or debris from the metal or plastic particles accumulating in the body from wear and tear," says Härtl.

From a biological perspective, the new discs could create a "huge advantage" over traditional implants because of how they integrate and mature with the vertebrae. This major surgery would become less invasive, safer and come with fewer long-term side effects, he says.

How'd they do it? Focusing on the regeneration and analysis of musculoskeletal tissue, Bonasser and colleagues engineered artificial discs of two polymers- collagen, which wraps around the exterior and a hydrogel alginate in the middle. These were seeded with cells that repopulate the structures with new tissue. Extraordinarily, though artificial implants today degrade over time, the researchers are finding that the implants actually improve as they mature in the body due to the cell growth. Now that's progress!

"Our implants have maintained 70 to 80 percent of initial disc height. In fact, the mechanical properties get better with time," says Bonassar.

The scientists began collaborating on the project in 2006, first funded by an Ithaca-Weill seed grant. Since then, the project has moved into animal testing stages and has received several awards and accolades, a $325,000 grant from Switzerland's AOSpine foundation and $100,000 in support from NFL Charities.

Isn't this fantastic news? Regenerative breakthroughs are growing in frequency and affectiveness-- help us get there faster!

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Reference:

Ju, Anne. "Back, Neck Pain Sufferers Could Find Relief with Cornell-developed Spinal Disc Implants." Cornell University | Chronicle Online. Cornell University, 1 Aug. 2011. Web. 2 Aug. 2011.
http://www.news.corn...VDimplants.html.



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We're all interested in living a healthy, long life. For those of us who really mean it, our lifestyle reflects the discipline, restraint, and healthy moderation we think it takes to achieve a vibrant 100 years of life (at least). If you fit that category, reading things like "People who live to 95 or older are no more virtuous than the rest of us in terms of their diet, exercise routine or smoking and drinking habits" may be a bit of an irritation. Yes, you did just read that and we did just quote from a study conducted by researchers of Albert Einstein College of Medicine of Yeshiva University published yesterday, August 3, 2011 in the online edition of Journal of American Geriatrics Society entitled "Lifestyle Factors of People with Exceptional Longevity". Feeling a little grumpy? Bear with me.

The age-old debate between Nature and Nurture rages on in the field of healthy life extension research-- you can guess which side this study seems to lean more towards. "Nature" in this case comes in the form of protective longevity genes while "nurture" represents lifestyle behaviors and habits. This study, involving a few hundred centenarians, suggests that one's genes may play more of an important role in living an exceptionally long life than one's way of living.

The centenarians indulged in smoking and drinking just as much as their shorter-lived contemporaries. Their diets followed the same vein as others in the general population and they were just as likely to be overweight, perhaps even exercising less than the average person. What gives?

Senior author of the study, Nir Barzilai, M.D., the Ingeborg and Ira Leon Rennert Chair of Aging Research and Director of the Institute for Aging Research at Einstein, together with his colleagues, interviewed 477 independent Ashkenazi Jews aged 95 or older, a group more genetically homogenous than other populations. In this manner, the identification of genetic differences contributing to life span would be simplified. This population was questioned about current habits as well as their lifestyle in earlier years.

Now these researchers were intent on peering into the mystery of longevity through wide lenses--data collected in the 1970s were used to compare the long-lived group with another group of some 3,000 individuals from the general population born around the same time but generally didn't get to make it 95 years of age.

To put it plainly: What they found was that people who lived to 95+ did not seem to have healthier lifestyles than those who died younger. Check out these numbers: 43% male centenarians reported exercising regularly at moderate intensity compared with 57% of men of the other group. Almost 30% of the long-lived females were smokers, a bit higher than the 26% in the comparison population who smoked. With the men, that percentage was significantly higher at 60% of the centenarian group compared to the 74% of their shorter-lived counterparts. About 24% of the men in the older group drank alcohol on a daily basis whereas 22% made that a habit from the younger group.

However, men and women from both groups were just as likely to be overweight. But there was one difference. Centenarians were less likely to be obese with only 4.5% of men in the older group compared to the 12% of the other male subjects. A similar pattern was found among women. When asked why they believed they had lived so long, most did not attribute their advanced age to lifestyle habits. 20% believed that physical activity played a role, 19% claimed a positive attitude, 12% to a busy or active life, 15% for less smoking and drinking, 8% believed it was good luck, and 6% attributed their longevity to religion or spirituality.

One finding that came as no surprise from the study was that about a third of the centenarians reported having many long-lived family members and relatives--previous studies of Ashkenazi Jews have helped locate a gene variant in the population that causes significantly elevated levels of HDL or "good" cholesterol in the centenarians that appeared to confer resistance Alzheimer's and heart disease. For those of us who can't claim the gene variant, there is potential good news, Dr. Barzilai says. There is a drug currently being developed that has the same effect on HDL as that particular gene.

"In previous studies of our centenarians, we've identified gene variants that exert particular physiology effects, such as causing significantly elevated levels of HDL or 'good' cholesterol," said Dr. Barzilai, who is also professor of medicine and of genetics at Einstein. "This study suggests that centenarians may possess additional longevity genes that help to buffer them against the harmful effects of an unhealthy lifestyle...We're identifying genes that play a role in aging and then we can design drugs to mimic their actions."

While longevity genes may protect centenarians from bad habits, healthy lifestyle choices remain critical for the vast majority of the population. The U.S. Census Bureau estimates there were nearly 425,000 people aged 95 and older living in the U.S. in 2010 − a fraction (.01) of the 40 million U.S. adults 65 and over.

"Although this study demonstrates that centenarians can be obese, smoke and avoid exercise, those lifestyle habits are not good choices for most of us who do not have a family history of longevity," said Dr. Barzilai. "We should watch our weight, avoid smoking and be sure to exercise, since these activities have been shown to have great health benefits for the general population, including a longer lifespan."

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References:

O' Connor, Anahad. "Centenarians Have Plenty of Bad Habits Too." The New York Times Health. The New York Times Company, 4 Aug. 2011. Web. 4 Aug. 2011.
http://well.blogs.ny...bad-habits-too/.

Newman, Kimberly. "Lifestyles of the Old and Healthy Defy Expectations." EurkAlert! AAAS, the Science Society, 3 Aug. 2011. Web. 4 Aug. 2011.
http://www.eurekaler...o-lot072811.php.



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A blood-borne immune factor present in elderly mice contributes to signs of mental decline when injected into young mice. By inhibiting this blood-born immune factor, youthfulness is restored in old mice, implying that it may be possible to change some of the symptoms of aging in the brain by altering the levels of immune factors in the blood.

The hippocampus, an important sea-horse shaped component of the brain that plays a role in memory, spatial memory, and navigation, loses function and ceases to produce new neurons as it ages. Though this deterioration can be partially reversed when animals regularly exercise thereby stimulating circulation and releasing chemicals and metabolites into the blood, Tony Wyss-Coray of Stanford University School of Medicine wondered if there was a blood-borne element that might contribute to these changes.

Published in August 31, 2011 in Nature, his study implies that it may be possible to change some of the aging symptoms of the brain by altering the levels of immune factors in the blood.

By stitching the flank of a young mouse to the flank of an old one, Wyss-Coray and colleagues formed a conjoined-twin effect, allowing the blood of both mice to mingle. They found that the young animals showed a decline in neurogenesis while the old ones showed new growth as compared to young and old stitched to partners of similar age.

"There seemed to be rejuvenation in the old brain," said Wyss-Coray.

So the researchers extracted only blood plasma devoid of the cells of old mice and injected into the young mice. They saw a similar decline in neurogenesis. It appeared as though an extracellular blood protein was responsible. These mice were then administered a battery of memory tests and mazes. The mice with old blood plasma did not form as robust memories and did not remember the solution to a maze as well as normal young mice--similar impairments found in old mice.

In order to identify the element in the plasma that caused this effect, comparisons were made on the concentrations of blood proteins in the conjoined animal; of six candidate proteins whose levels that changed after the mice were stitched together, CCL11 or eotaxin, a chemokine, demonstrated the most significant change.

"The factor [CCL11] is a surprising character," said Richard Ransohoff from the Cleveland Clinic Lerner College of Medicine. "It's a chemokine that has zero prior neurobiology," he added. Known only for its role in attracting eosinophils or immune cells that play a major role in allergy and asthma, when the researchers injected this chemokine into young mice, a decrease in new neuron formation was observed. This effect was then reversed with an injection of a CCL11-blocking antibody! Observing too how CCL11 fluctuates with age, Wyss-Coray and researchers saw that its blood-levels elevated in mice and in humans with age.

Wyss-Coray agrees that this study opens a floodgate of new questions. But he's encouraged by the possibilities. For example, "if we could rejuvenate or maintain the brain in general," he said, it might delay some of the detrimental effects that cause dementia or Alzheimer's.

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References:

S. A. Villeda et al., "The ageing systemic milieu negatively regulates neurogenesis and cognitive function," Nature, 477:90-96, doi:10.1038/nature10357, 2011.




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When chemotherapy proved ineffective for 65-year-old William Ludwig, a retired corrections officer from New Jersey a year ago, he signed up to be the first to receive treatment in a bold experiment at the University of Pennsylvania. By then, his life was draining away, as he put it. He thought he had nothing to lose.

The research team, led by Dr. Carl June, removed a billion of William's T-cells (white blood cells that fight viruses and tumors) and engineered them with new genes that reprogram the cells to attack his cancer. A disabled form of H.I.V. -1, the virus that causes AIDS, was employed to transport cancer-fighting genes into the patient's own T-cells. In essence, the team trained Ludwig's own immune system to kill cancer cells. The process is detailed in The New England Journal of Medicine as well as in Science Translational Medicine.

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There were no reactions at first but after 10 days, he shook with chills, his temperature skyrocketed while his blood pressure plummeted--William had so rapidly become ill that the doctors moved him into intensive care, warning him that he might die. Fearing the worst, his family gathered at the hospital.

Fast forward a few weeks later. No fever. No leukemia.

All traces of leukemia vanished. No leukemic cells were to be found in his blood or bone marrow; his CT scan was clean. The doctors calculate that the treatment destroyed up to two pounds of cancer cells. One year later, and William is still in complete remission. Before the treatment, there were days when he could barely get out of bed. Now he revels on the green of gulf and works on his yard.

"I have my life back," says William.

"It's great work," said Dr. Walter J. Urba of the Providence Cancer Center and Earle A. Chiles Research Institute in Portland, Ore. He called the patients' recoveries remarkable, exciting and significant. "I feel very positive about this new technology. Conceptually, it's very, very big."

Though Ludwig's doctors do not claim that he is cured, as it is too soon to tell - the research has far to go and the treatment is still experimental and unavailable outside of clinical studies - the treatment has obviously helped Ludwig tremendously. This may be a turning point in the long struggle to develop effective gene therapies to combat cancer. And not just for leukemia--other cancers may also be vulnerable to this breakthrough approach.

Two other chronic lymphocytic leukemia patients were also treated in the experiment; one had a partial remission--his disease lessened but did not completely go away. Another, like William, experienced complete remission. All three were at an advanced stage of the disease, ran out of chemotherapy options, and were not candidates for bone-marrow transplantation.

Dr. Carl June said the results stunned even him and his colleagues, Dr. David L. Porter, Bruce Levine and Michael Kalos. Of course they had hoped to see some benefit of the experimentation, but had not dreamed of seeing complete, prolonged remissions in the patients. When Mr. Ludwig began running fevers, the doctors did not initially realize that it was a sign that his T-cells were furiously battling with his leukemia.

Dr. Walter J. Urba said he thinks the approach would ultimately be used against other types of cancer along with leukemia and lymphoma though he cautions that "For patients today, we're not there yet." And he added the usual scientific caveat: To be considered valid, the results must be repeated in more patients, and by other research teams.

But what profound hope we have for this to be validated!

When Ludwig entered the trial, Dr. June said that he was "almost dead". The trial was Phase 1, meaning that the main goal was to find out if the treatment was safe, and if so, at what doses. Ludwig thought that if the trial study could give him six months to a year, it would be worth it, but even if it didn't help him personally, he felt that it would still be worth helping the study.

"I feel wonderful," Mr. Ludwig said in an interview. "I walked 18 holes on the golf course this morning."

William Ludwig was tremendously week before the study, suffering repeated bouts of pneumonia and wasting away. Now, he is full of energy. He has gained 40 pounds. He and his wife bought an R.V., in which they travel with their grandson and nephew.

"I feel normal, like I did 10 years before I was diagnosed," Mr. Ludwig said. "This clinical trial saved my life."


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Reference:

Grady, Denise. "An Immune System Trained to Kill Cancer." The New York Times | Health. The New York Times Company, 12 Sept. 2011. Web. 14 Sept. 2011.
http://www.nytimes.c...f=health&src=me.



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Credit: Teresa Kelly


Our friend and scientific advisory board member Anthony Atala of the Wake Forest University for Medicine discussed the advances of regenerative medicine in the fourth installment of The University of Rhode Island's Honors Colloquium. The lecture began with a progress report for the new field of regenerative medicine and, reminding the audience that it was only in a few decades ago in 1954 that surgeons transplanted an organ into a human for the first time in history, it's astonishing that as 2012 quickly approaches, medical science has progressed to allow organs such as kidneys, uteruses, bladders, urethras, and even the skin to regrow.

"Is this science fiction?" Atala asks. "Not really. We see it in biology all the time."

He outlined the process a surgeon goes through to regenerate an organ--the easiest organs being flat, such as the skin. For the larger, tubular organs such as the kidney and liver, that happens to be a different, much more difficult ball game.

For skin regeneration, the surgeon simply extracts a bit of cells the size of less than half a postage stamp from the patient. Then, after being mixed with a solution to keep the cells alive, the cells are then sprayed back onto the patient. Should the patient be immobile, he would be scanned by a machine and his cells delivered to a bio-printer. The printer would produce a sticky sheet of gel cells to be administered to the patient to help regenerate his skin.

Nearing the end of his presentation, Atala played a short clip of an interview with former patient Luke M., whose surgery was performed 10 years ago. A new bladder was engineered for him out of his own cells. Prior to the operation, he said he was faced with a lifetime of dialysis. He could barely get out of bed, constantly missed school, and couldn't play basketball with his friends without feeling faint.

"After surgery, I was able to do more things, like wrestle in high school," said Luke, proudly. "I even became captain of the team. Because they used my own cells to build this bladder, I got it for life. So I'm all set."

Atala reminded the audience how 50 years ago, the iron lung was thought to be revolutionary technology. Now, we look back on it and think "Boy, wasn't that primitive?" The goal of medical science is to keep pushing forward and breaking boundaries, he said, so that in the next 50 years, people can look back on his technology and find it primitive as well.

"My goal tonight was to make this look easy to you," he stated. "But I assure you, the work we do is anything but easy. We still have many challenges ahead, but the promise this field holds is to try and make our patients better."


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Reference:

Delande, Kimberly. "Colloquium Speaker Addresses Future of Organ Regeneration through Technology." The Good 5¢ Cigar. College Media Network, 5 Oct. 2011. Web. 6 Oct. 2011.
http://www.ramcigar....06#.ToyEoJxZhG8.




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[ImmInst]

"We are at the cusp of a revolution in medicine and biotechnology that will radically increase not just our life spans but also, and more importantly, our health spans. That is, we will live longer and with a higher quality of life. [We] will examine the fascinating new technologies that will allow doctors to repair or replace worn-out body parts, re-engineer our bodies, and take preventative measures that will radically lengthen our lives." -Sonia Arrison, 100+ Chapter 2: How Science and Technology Will Increase Life Span

With her new book 100 Plus, Sonia Arrison introduces us to the people and the innovations that are transforming our lives while bringing to the fore a very comprehensive picture of how life-extending discoveries will impact our personal, social, and economic spheres. After a decade of research and writing experience on the breakthrough advances in science and biotechnology, Arrison's wide-angle approach to healthy life extension is both sparklingly informative and thought-provoking.

What will your life look like after reaching your 100th year? Will over-population be a major issue? How will living longer and with more vigor affect your family life, your personal belief system, even your finances? Her work is a fantastic attempt in addressing these questions.

Peter Thiel graces 100 Plus with the following words in his foreward:
"Arrison's book begins with a history of the many great men and women of the past who sought human longevity. She surveys he current generation of scientists and technologists who promise to usher in a new era, demonstrating that aging is a foe that can be hobbled and potentially even beaten. From here Arrison goes to the heart of things by directly confronting opposition to longer and healthier lives and outlining the extraordinary economic, social, and cultural changes that will happen as the world wakes up from history..."

The Methuselah Foundation team is voraciously reading 100 Plus with growing excitement for Arrison's well-informed candor and refreshing perspective on the advances of healthy life extension technologies that cover a wide range of angles.

And as if you needed more reason to go read this book as soon as you can get your hands on it, CEO Dave Gobel had this to say about it from his Amazon review:

"The best thing about 100+ is that it documents the increases in healthy longevity that are already happening right now. Refreshingly, it treats widely held cultural and religious values with legitimate respect, without resorting to the typical elitist/dismissive tone others have taken. 100+ carefully covers new ground on topics that I've not seen covered in detail before - such as how longevity will affect the future of childbearing and the family - based on little known trends and science happening right now. This book is also the best survey of the field of life extension to date, giving useful and actionable insights on such topics as population growth, the environment, economics, medical trials and advances in biotech without burdening the reader with red-herring issues like immortality or demonizing the "opposition". The book is an easy and compelling read and even though I've read extensively on the subject, each page of 100+ offers up new facts with real value - no filler or arm waving here! Highly recommended."

Now how's that for a review? Pick it up, read it, think about it, and tell us how it's affected the way you think about living to see a healthy 100... and beyond!

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Reference:

Arrison, Sonia. 100 Plus. New York: Basic, 2011. Print.




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When you think about old age, what comes to mind? Most people associate old age with disability and cognitive and physical impairment but researchers from the University of Pittsburgh and Children's Hospital of Pittsburgh of UPMC have found that old age is not synonymous with impairment and disability. According to the study published by the Public Library of Science in the online journal PLoS ONE, exceptional cognitive and physical function in old age leaves behind a tell-tale immunologic fingerprint.

"Our study indicates that getting older does not necessarily mean that the immune system gets weaker, as many of us assumed," says lead investigator Abbe N. de Vallejo, Ph.D., associate professor of pediatrics and immunology at University of Pittsburgh School of Medicine. "The immune system is dynamic, and the changes it undergoes over time very much influence function."

Previous studies showed that immune cells called T-cells become more like natural killer (NK) cells, which typically targets virus-infected cell and tumor cells. For this new study, the team collected blood samples from a body of 140 participants who had been followed in the Cardiovascular Health Study for nearly 20 years and were 78-94 years old. Only two were younger than 82--the average age of the group was 86. The researchers gathered information about the participants' health and function, medical history, hospitalizations, self-rated health, and cognitive and physical function assessments via standardized tests.
A closer look at the new study revealed that those who were most physically and cognitively resilient had a dominant pattern of stimulatory NK receptors on the surface of the T-cell. These unusual T-cells can be activated directly through these NK receptors in a manner independent of the conventional ones. The functionally resilient elders also have a distinct profile of blood proteins called cytokines that reflect an immune-enhancing environment.
The group that showed mild health impairment had a dominant pattern of inhibitory NK receptors on their T-cells, with a cytokine profile indicating a pro-inflammatory environment. Both of these immunologic features might suggest greater susceptibility to illness.
"These findings indicate that there is remodeling or adaptation of the immune system as we age that can be either protective or detrimental," Dr. de Vallejo said. "Now we have an immunological fingerprint that can identify individuals who are more likely to stay physically and cognitively well."

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References:
"Exceptional Cognitive and Physical Health in Old Age Leaves Immunologic Fingerprint, Study Finds." Science Daily. Science Daily, 21 Oct. 2011. Web. 25 Oct. 2011. http://www.scienceda...11021125808.htm.
Abbe N. Vallejo, David L. Hamel, Robert G. Mueller, Diane G. Ives, Joshua J. Michel, Robert M. Boudreau, Anne B. Newman. NK-Like T Cells and Plasma Cytokines, but Not Anti-Viral Serology, Define Immune Fingerprints of Resilience and Mild Disability in Exceptional Aging. PLoS ONE, 2011; 6 (10): e26558 DOI: 10.1371/journal.pone.0026558

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In what is the first conviction under the U.S. federal statute outlawing black-market organ sales, a Brooklyn man named Levy Izhak Rosenbaum pleaded guilty Thursday to brokering three illegal kidney transplants for at least $120,000 each (a huge markup) and conspiring to arrange yet another sale. He boasted on tape that he actually handled "quite a lot" during the decade-long scheme.
At 60 years of age, Rosenbaum is but one of 46 people arrested in 2009 in a massive federal corruption probe dubbed "Operation Big Rig" that ensnared dozens of officials, politicians, community and religious leaders involved in organ sales, money laundering, and political corruption over an investigative period of 10 years.
From January 2006 to February 2009, Rosenbaum conspired to obtain kidneys from paid donors in exchange for payments of $120,000, $150,000 and $140,000 from three recipients of the organs.
"Rosenbaum admitted he was not new to the human kidney business when he was caught brokering what he thought was a black-market deal," U.S. Attorney Paul Fishman said in a release.

"A black market in human organs is not only a grave threat to public health, it reserves lifesaving treatment for those who can best afford it at the expense of those who cannot [...] We will not tolerate such an affront to human dignity."

Rosenbaum faces up to 20 years in prison when he's sentenced February 2. He agreed to forfeit $420,000 he received in connection with the three transplants and admitted that he invented cover stories and fictitious relationships between donors and recipients so doctors wouldn't know a kidney was being sold.
His black market involvement was exposed with the help of Solomon Dwek, a cooperating criminal defendant who helped prosecutors develop charges against defendants in the "Operation Big Rig" case. Posed as an employee of Dwek and claiming that her uncle needed a transplant, an undercover agent met with Rosenbaum in mid-February 2008. He told them that it was illegal to buy and sell organs but that he had been "doing this a long time" and explained that he would help the recipient and donor concoct a false story to support the appearance of a legitimate donation, Fishman said. Rosenbaum also claimed he would be in charge of "babysitting" the donor after the person arrived from overseas.
"I am what you call a matchmaker," he told the snitch. "I've never had a failure."
During Thursday's plea, Rosenbaum admitted that he typically located Israelis who were willing to be paid for giving up their kidneys and that he was responsible for travel arrangements for the donor to the United States along with their accomodations pre- and post-operation. He arranged for blood samples and helped each paid donor and recipient fabricate stories to fool hospital staff. His lawyers noted that the surgeries took place in "prestigious American hospitals and were performed by experienced and expert" surgeons.
He remains free on bail and under house arrest pending sentencing scheduled for February 2, 2012.
Methuselah Foundation's New Organ Prize not only serves to catalyze progress in tissue and organ regeneration but it also aims to make the crimes of the black market a thing of the past. In a future where an individual in need of an organ can have one made with their own cells, the market for organs exploited from the disadvantaged and weak will eventually shrink and disappear altogether.
We at Methuselah Foundation echo the words of Attorney Fishman: "We will not tolerate such an affront to human dignity."
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Reference:
Golson, Jennifer. "Brooklyn Man Who Sold Kidneys on Black Market Pleads Guilty." Thomson Reuter News and Insight. Thomson Reuters, 28 Oct. 2011. Web. 28 Oct. 2011.
http://newsandinsigh..._pleads_guilty/.
Photo Credit: Tony Kurdzuk | The Star-Ledger


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The October 28, 2011 issue of the journal Cell reports that researchers at Weill Cornell Medical College have uncovered the biochemical signals in mice that trigger generation of new lung alveoli, the countless tiny champagne grape-like sacs within the lung where oxygen exchange takes place. The team claim that they have taken an important step forward in their quest to "turn on" lung regeneration. This research may effectively treat millions suffering from respiratory disorders.
It's common knowledge in the biomedical industry that mice have the ability to regenerate and even expand the capacity of one lung if the other is missing--this study identifies the specific molecular triggers behind this adaptive process. The researchers believe these findings are quite relevant to human beings.
Dr. Shahin Rafii, the Arthur B. Belfer Professor of Genetic Medicine and co-director of the Ansari Stem Cell Institute at Weill Cornell Medical College and this study's lead investigator said "Several adult human organs have the potential upon injury to regenerate to a degree, and while we can readily monitor the pathways involved in the regeneration of liver and bone marrow, it is much more cumbersome to study the regeneration of other adult organs, such as the lung and heart."

"It is speculated, but not proven, that humans have the potential to regenerate their lung aveoli until they can't anymore, due to smoking, cancer, or other extensive chronic damage," says Dr. Rafii, who is also an investigator at the Howard Hughes Medical Institute. "Our hope is to take these findings into the clinic and see if we can induce lung regeneration in patients who need it, such as those with chronic obstructive pulmonary disease (COPD)."

Dr. Rafii and his colleagues previously uncovered growth factors that control regeneration in the liver and bone marrow. In both cases, they found that endothelial cells produce the key inductive growth factors, described as "angiocrine factors". The current lung study revealed the same phenomenon: Blood vessel cells in the lungs jump-start alveoli regeneration. "Blood vessels are not just the inert plumbing that carries blood. They actively instruct organ regeneration," says Dr. Rafii. "This is a critical finding. Each organ uses different growth factors within its local vascular system to promote regeneration."
In the study, the left lungs of mice were removed for Dr. Bi-Sen Ding to examine the biochemical process of the remaining lung's regeneration. According to a prior investigation by Dr. Crystal, once the left lungs were removed, the right lungs regenerated by 80%. It replaced the majority of the lost alveoli. They discovered that when the left lung is removed, receptors on endothelial cells in the lung that respond to basic fibroblast growth factor and vascular endothelial growth factor is triggered.
Research lead Dr. Shafin Rafii explained: "Several adult human organs have the potential upon injury to regenerate to a degree, and while we can readily monitor the pathways involved in the regeneration of liver and bone marrow, it is much more cumbersome to study the regeneration of other adult organs, such as the lung and heart [...]"
Co-author Dr. Ronald G. Crystal said "There is no effective therapy for patients diagnosed with COPD. Based on this study, I envision a day when patients with COPDD and other chronic lung diseases may benefit from treatment with factors derived from lung blood vessels that induce lung regeneration."
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Reference:
Rattue, Grace. "Lung Regeneration May Be A Reality Soon." Medical News Today. Medical News Today, 1 Nov. 2011. Web. 2 Nov. 2011. http://www.medicalne...cles/236928.php.


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[niner]

"Soon" is a relative term... It isn't the word I'd use. I'd guess ten years at the earliest.