Metformin is a drug that shows up in discussion here every so often. It is thought to be a calorie restriction mimetic, recapitulating some of the metabolic changes caused by the practice of calorie restriction. Its effects on life span in laboratory animals are up for debate and further accumulation of evidence – the results are on balance more promising than the generally dismal situation for resveratrol, but far less evidently beneficial than rapamycin. Like rapamycin, metformin isn’t something you’d want to take as though it were candy, even if the regulators stood back to make that possible, as the side effects are not pleasant and potentially serious.

I should note as an aside that while ongoing research into the effects of old-school drugs of this nature is certainly interesting, it doesn’t really present a path to significantly enhanced health and longevity. It is a pity that such research continues to receive the lion’s share of funding, given that the best case outcome is an increase in our knowledge of human metabolism, not meaningful longevity therapies. Even if the completely beneficial mechanism of action is split out from the drug’s actions – as seems to be underway for rapamycin – the end results will still only be a very modest slowing of aging. You could do better by exercising, or practicing calorie restriction.

For the billions in funding poured into these drug investigation programs, there should be a better grail at the end of the road – such as that offered by the SENS vision of rejuvenation biotechnology. Targeted repair of the biological damage of aging is a far, far better strategy than gently slowing the pace of damage accumulation through old-style drug discovery programs. This is a biotechnology revolution: time to start acting like it.

Anyway, aside done, let me point you to a recent open access review on metformin: the interesting work that won’t really be in any way relevant to the future of your longevity, but which I’ll wager has raised more funding as an object of study than the entire present extant SENS program and directly related scientific studies:

Metformin, an oral anti-diabetic drug, is being considered increasingly for treatment and prevention of cancer, obesity as well as for the extension of healthy lifespan. Gradually accumulating discrepancies about its effect on cancer and obesity can be explained by the shortage of randomized clinical trials, differences between control groups (reference points), gender- and age-associated effects and pharmacogenetic factors. Studies of the potential antiaging effects of antidiabetic biguanides, such as metformin, are still experimental for obvious reasons and their results are currently ambiguous.

…

The wave of interest, with periodical decays and increasing surges, was associated with the attempts to use antidiabetic biguanides [such as metformin] to control body weight and tumor growth. Another facet of the situation is that almost 45 years ago these drugs were suggested to promote longevity. Over the last years, the expanding bodies of relevant evidence, which mainly related to metformin, started to merge and occupy increasing place in current literature. The objective of the present essay is to attract more attention to accumulating inconsistencies. The first two sections of the essay, which are related to obesity and cancer, are based mostly on clinical data. The third section, which is related to aging or, rather, antiaging, is based predominately on experimental evidence obtained in rodents. Clearly, obesity and cancer have numerous interrelationships with aging, [however], we will separate these aspects for the sake of clarity in discussing the relevant effects of metformin.

See what you think; it makes for an interesting read – and includes a table of results from a number of life span studies that are, indeed, all over the map. It somewhat reinforces the point that unambiguous success in extending healthy life is not going to arrive from this quarter. Think SENS, not drug discovery – what will come from the drug discovery clade is a slow, grinding, and expensive cataloging of the fine details of genetics, metabolism, and aging in mammals.

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Following on from a recent post on the involution of the thymus in adults, the process by which it ceases to generate immune cells and atrophies, here is a another paper that considers some of the possible paths to interventions that maintain the thymus into old age. Given experiments in mice showing that transplant of a young thymus extends life, this seems worthy of further investigation: “The thymus is the primary organ for T-cell differentiation and maturation. Unlike other major organs, the thymus is highly dynamic, capable of undergoing multiple rounds of almost complete atrophy followed by rapid restoration. The process of thymic atrophy, or involution, results in decreased thymopoiesis and emigration of naïve T cells to the periphery. Multiple processes can trigger transient thymic involution, including bacterial and viral infection(s), aging, pregnancy and stress. Intense investigations into the mechanisms that underlie thymic involution have revealed diverse cellular and molecular mediators, with elaborate control mechanisms. This review outlines the disparate pathways through which involution can be mediated, from the transient infection-mediated pathway, tightly controlled by microRNA, to the chronic changes that occur through aging.”

Link: http://www.ncbi.nlm.nih.gov/pubmed/22539280

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An article from the Wellcome Trust: “Researchers have been engineering cartilage in the laboratory for 15 years or more, but as yet the tissues they have created don’t function properly in human joints. [Researchers] are taking a new approach to try to bridge the gap between laboratory-created cartilage and the tissue our bodies make. … Biological texts show that these lab-grown tissues have the appearance, texture, and protein and mineral components of bone and cartilage. But once they are tested in an animal, these tissues simply don’t behave quite like the natural tissues they are supposed to replicate. … Joints are remarkable feats of engineering, but efforts to grow them in the lab have focused mostly on their biology. … Biologists attempting to create cartilage and bone over the past 15 years have typically tested the mechanical properties of their laboratory-grown tissue – for example, whether it is rubbery and resilient enough when pressure is applied. … Just because biological tests indicate a tissue looks like bone and feels like bone, doesn’t actually mean it is bone … This is where an engineering perspective becomes important. To look at how close a match these laboratory-generated tissues really are to native bone and cartilage, [researchers] supplemented the biological analyses with engineering tests, such as bio-Raman microspectroscopy. … You shine a laser on the material, and the way the light scatters gives you an idea of the bonds between its components. Different mineral types form different bonds, so you get a much more precise picture of what is actually present. … If a lab-grown tissue seems from some tests to be the real thing but isn’t really, then it won’t behave like it once it has been implanted in a human body. … [The researchers aim] to use an engineering approach to create a whole osteochondral interface in which bone and cartilage transition seamlessly into each other like they do in the body. … That’s the only way it will effectively transmit loads to the underlying bone. And because bone will heal, it will heal the construct into the joint.”

Link: http://www.wellcome.ac.uk/News/2012/Features/WTVM054966.htm

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For some years researchers have been investigating the mechanisms of limb and organ regrowth in lower animals like salamanders, with an eye to finding out how easy or hard it would be to recreate those same capabilities in mammals – such as we humans. Do we retain the core mechanisms, lying dormant in our biochemistry, or have they been completely lost? Time and ongoing research will tell.

But these are not the only areas of regrowth wherein researchers might learn something of interest to regenerative medicine. Consider that elk regularly regrow their antlers, for example – not a simple organ by any means. Further down the scale of impressiveness, we might consider the many higher animals that regularly regrow feathers or coats of hair. Is there anything in their biochemistry that might be discovered and adapted to cause humans to regenerate in situations where they normally do not?

If you buy into the argument that salamander biochemistry is worth investigation, then it’s hard to reject similar investigations in other species capable of the lesser forms of regrowth mentioned above. An open access paper is presently doing the rounds on this topic; you can read the summary in the release, or look at the paper itself:

Physiological Regeneration of Skin Appendages and Implications for Regenerative Medicine

The concept of regenerative medicine is relatively new, but animals are well known to remake their hair and feathers regularly by normal regenerative physiological processes. Here, we focus on 1) how extrafollicular environments can regulate hair and feather stem cell activities and 2) how different configurations of stem cells can shape organ forms in different body regions to fulfill changing physiological needs.

Regenerative medicine has great potential. The main challenge is how to elicit and harness the power of regeneration. Currently, the major issues are how to obtain stem cells, how to pattern stem cells into organized tissues and organs, and how to deliver stem cell products to patients. Although human beings have very limited powers of regeneration, many animals have robust regenerative powers, distilled and selected over millions of years of evolution. Here, we review fundamental principles of regenerative biology learned from nature in the hope that they can be applied to help the progress of regenerative medicine.

…

Using the episodic regeneration of skin appendages as a clear readout, we have the opportunity to understand and modulate the behavior of adult stem cells and organ regeneration at a level heretofore unknown. Through this work, we hope to be able to establish or improve the stem cell environment so it can be applied to regenerative medicine.

In conclusion, we think it will be very productive to learn how nature manages the physiological regeneration process. This is a reprogramming process in which the genetic and epigenetic events converge to generate complex functional forms, depending on the physiological need in different parts of the body and at different stages of life. Principles learned from regenerative biology can then be applied toward regenerative medicine.

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Maria Konovalenko of the Science for Life Extension Foundation here reports on the recent Genetics of Aging and Longevity Conference, held last month in Moscow and attracting researchers in the field from around the world.

It has been a while since I’ve posted my blog updates. The reason was the Genetics of Aging and Longevity conference. I have been involved in preparations of this meeting since December and the last month before the event was especially tough. Anyway, the conference turned out to be pretty good. I was surprised to hear so many good responses and impressions from the attendees and the speakers, so I am proud to say that the meeting was a success. The talks were superb, a lot of new and even unpublished data, a lot of discussions during the breaks and meals. I saw quite many people walking around with burning eyes – from excitement of science, of course) Some of those eyes are in the photos below. I believe this was a ground braking event on life extension topic in Russia, a truly unique gathering of minds. The more meetings like this we have, the more attention they get in the media, the better chances we have to live longer.

The post includes a great many photographs of folk from the aging research community; browse through if you are interested in putting faces to the names you read about in the science press. Konovalenko concludes with this note:

Quite a lot of researchers said that we are on the verge of a breakthrough in the area of life extension. Maybe we have already discovered something fantastic, but haven’t yet realized it’d effective for people. Even if we have a drug that slows aging down, we still need a panel of biomarkers to prove the effect. I do hope we will have both the breakthrough and the markers soon.

I’ll point you to something I said a while back about concrete and conferences:

I’m a fan of the “concrete and conferences” metric for measuring the health of science. Two side effects of increasing research funding in a field are new buildings at universities and research centers (the “concrete” part of the metric) and new gatherings of researchers (the conferences). Both of these symptoms are also fairly easy to track. The more of both, the better, with new buildings indicating more money entering the system than new conferences.

More conferences generally indicates a larger population of researchers with budgets, interest in the field, and progress in their laboratories to talk about.

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You might recall research published last near on NRG-1 levels in naked mole-rats. Here is an update: “The typical naked mole rat lives 25 to 30 years, during which it shows little decline in activity, bone health, reproductive capacity and cognitive ability. … Naked mole rats have the highest level of a growth factor called NRG-1 in the cerebellum. Its levels are sustained throughout their life, from development through adulthood. … NRG-1 levels were monitored in naked mole rats at different ages ranging from a day to 26 years. The other six rodent species have maximum life spans of three to 19 years. The cerebellum coordinates movements and maintains bodily equilibrium. The research team hypothesized that long-lived species would maintain higher levels of NRG-1 in this region of the brain, with simultaneous healthy activity levels. Among each of the species, the longest-lived members exhibited the highest lifelong levels of NRG-1. The naked mole rat had the most robust and enduring supply. … In both mice and in humans, NRG-1 levels go down with age … The strong correlation between this protective brain factor and maximum life span highlights a new focus for aging research, further supporting earlier findings that it is not the amount of oxidative damage an organism encounters that determines species life span but rather that the protective mechanisms may be more important.”

Link: http://www.mysanantonio.com/life/health/article/The-secret-of-long-life-may-be-in-a-naked-mole-rat-3543091.php

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An update on the LysoSENS research project from the SENS Foundation, which aims to discover and adapt bacterial enzymes to break down the damaging buildup of unwanted metabolic byproducts in the aging body: “SENS Foundation-funded research shows that expression of a modified microbial enzyme protects human cells against 7-ketocholesterol toxicity, advancing research toward remediation of the foam cell and rejuvenation of the atherosclerotic artery. … Atherosclerotic cardiovascular disease is the principal cause of ischaemic heart disease, cerebrovascular disease, and peripheral vascular disease, making it the root of the leading cause of morbidity and mortality worldwide. Atherosclerosis begins with the entrapment and oxidation of low-density lipoprotein (LDL) cholesterol in the arterial endothelium. As a protective response, the endothelium recruits blood monocytes into the arterial wall, which differentiate and mature into active macrophages and engulf toxic oxidized cholesterol products (oxysterols) such as 7-ketocholesterol (7-KC). Although initially protective, this response ultimately leads to atherosclerotic plaque: oxidized cholesterol products accumulate in the macrophage lysosome, and impair the processing and trafficking of native cholesterol and other materials, leading macrophages to become dysfunctional and immobilized … more and more of these disabled “foam cells” progressively accumulate in the arterial wall, generating the fatty streaks that form the basis of the atherosclerotic lesion. Rejuvenation biotechnology can be brought to bear against this disease of aging through the identification, modification, and therapeutic delivery of novel lysosomal enzymes derived from microbes to the arterial macrophage – enzymes which are capable of degrading oxidized cholesterol products. SENS Foundation-funded researchers have been making steady progress in the identification and characterization of candidate enzymes for several years now, and a new report represents a substantial advance in the research: the rescue of cellular oxysterol toxicity by an introduced microbial lysosomal enzyme.”

Link: http://sens.org/node/2737

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New Delhi, May 17: A herbal formulation containing gooseberry, or amla, prescribed in traditional Ayurvedic medicine appears to help fruit flies tolerate high temperatures and starvation, and gain lifespan by a modest 10 per cent, scientists have said.

The scientists said the herbal compound called Amlaka rasayana, claimed by traditional Ayurvedic medicine to increase body strength and enhance longevity, appears to bolster the capacity of fruit flies to withstand heat and starvation stress.

The researchers from the Banaras Hindu University (BHU), the Arya Vaidya Shala, Kottakkal, and Manipal University, published the results of their experiments with fruit flies this week in the international journal PLoS One. While previous studies have explored the physiological effects of amla formulations, the scientists said their results are based on statistical rigour and large sample sizes.

The researchers added tiny amounts of the compound into the meals of fruit flies. The improved heat tolerance is dramatic, said Subhash Lakhotia, a senior zoologist at the BHU and principal investigator of the study.

The flies are typically knocked down after short periods of exposure to temperatures above 38C. The number that collapsed after the exposure was significantly lower among flies that received the herbal supplement than among the flies that did not.

In another experiment, the researchers denied the flies solid food, but allowed them only water. The flies that fed on the herbal supplement had greater tolerance to starvation, more of them surviving, compared to those that did not get the supplement.

While fruit flies have long reigned as model animals for biomedical research, the scientists say the new study establishes the validity of the fruit fly model as a test organism to investigate the scientific basis of Ayurveda.

Flies have been used for years to understand many human diseases, including cancer and neurodegeneration, Lakhotia told The Telegraph. We now have greater confidence to test traditional herbal formulations in fly models of neurodegenerative diseases such as Huntingtons, Alzheimers, or Parkinsons , he said.

The scientists also fed fruit flies a traditional formulation called Rasa-sindoor, an organo-metallic derivative of mercury, and found no effect on the life span or on starvation tolerance, but observed even better heat tolerance than achieved with Amlaka rasayana.

While the experiments on the flies were conducted at the BHU, collaborators at Kottakkal prepared the formulations through standardised recipes. Future studies will be aimed at understanding the physiological effects that such formulations have on the flies, Lakhotia said.

Continue reading here:
Amla passes fruit fly test

The choroid plexus is, amongst other things, a filter for cerebrospinal fluid – you might think of this role as analogous to that of the kidney as a filter for blood, though the two organs are very different in structure at every level, and the choroid plexus also produces the fluid it filters. Like all of the systems in the body and brain, the choroid plexus progressively fails in its function with age, and researchers have reason to believe that this failure contributes to conditions such as Alzheimer’s disease:

An organ in the brain called the choroid plexus apparently plays a critical role in preventing the accumulation of a protein associated with Alzheimer’s disease. The researchers found that the choroid plexus acts as a sort of ‘fishnet’ that captures the protein, called beta-amyloid, and prevents it from building up in the cerebrospinal fluid, which surrounds and bathes the brain and spinal cord. Moreover, tissue in the organ is able to soak up large amounts of the protein and may contain enzymes capable of digesting beta-amyloid.

Levels of beta-amyloid in the brain are more dynamic than their slow buildup over the years implies. You might think of the condition – and indeed the increase in amyloid levels in aging in general – as a slowly progressing imbalance of amyloid creation and clearance mechanisms rather than a slow and irrevocable deposition of amyloid. That in turn implies that a working therapy could quickly reverse all but the latest stages of the disease, when neurons are dying in large numbers.

Do rising brain levels of a plaque-forming substance mean patients are making more of it or that they can no longer clear it from their brains as effectively? … Clearance is impaired in Alzheimer’s disease. We compared a group of 12 patients with early Alzheimer’s disease to 12 age-matched and cognitively normal subjects. Both groups produced amyloid-beta (a-beta) at the same average rate, but there’s an average drop of about 30 percent in the clearance rates of the group with Alzheimer’s. … Scientists calculate this week [that] it would take 10 years for this decrease in clearance to cause a build-up of a-beta equal to those seen in the brains of Alzheimer’s patients. The results have important implications for both diagnosis and treatment.

Here is a more recent paper that reviews what is known of the role of the choroid plexus:

Pathological Alteration in the Choroid Plexus of Alzheimer’s Disease: Implication for New Therapy Approaches

In the recent years, much attention has been directed to the roles of the choroid plexus in the central nervous system (CNS) under both normal and pathological conditions. This specialized ventricular structure has recently emerged as a key player in a variety of processes that monitor and maintain the biochemical and cellular homeostasis of the CNS.

The main role of the choroid plexus is to produce cerebrospinal fluid (CSF) and to maintain the extracellular environment of the brain by monitoring the chemical exchange between the CSF and the brain tissue. This involves the surveying of the chemical and immunological status of the extracellular fluid and the removal of toxic substances as well as important roles in the regenerative processes following traumatic events. In addition to CSF, the plexus produces various peptides which can have nourishing and neuroprotective properties.

…

Morphological alterations of choroid plexus in Alzheimer’s disease (AD) have been extensively investigated. These changes include epithelial atrophy, thickening of the basement membrane, and stroma fibrosis. As a result, synthesis, secretory, and transportation functions are significantly altered resulting in decreased cerebrospinal fluid (CSF) turnover. Recent studies discuss the potential impacts of these changes, including the possibility of reduced resistance to stress insults and slow clearance of toxic compounds from CSF with specific reference to the amyloid peptide.

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FDA Panel Supports Rapid, At-Home HIV Test

Home HIV tests should be sold in retail stores, a U.S. Food and Drug Administration advisory panel urged Tuesday. If approved by the FDA, a mouth-swab test made by OraSure Technologies Inc.and sold commercially to health professionalswould become available over the counter. That way, people could check if they had the virus within the privacy of their own homes. The 20-minute test is 93 percent accurate for positive results and 99.8 percent for negative, according to the manufacturer. About 240,000 Americans are unaware they are HIV positive, and are responsible for between 50 and 70 percent of the 50,000 new infections each year. "There is huge global momentum in support of over-the-counter testing for HIV," Nitika Pant Pai, an assistant professor of medicine at Montreal's McGill University who co-authored an analysis of the effectiveness of an at-home HIV test earlier this year, told HealthDay. "People desire private, discreet options that protect their confidentiality." It's unclear how much the over-the-counter test would cost.

How to Cope With Criticism

You're looking a little pudgy these days. Why didn't you get that promotion? You should be doing a better job with the kids. Why isn't the house cleaner?

Criticism stings. Yes, you're going to feel deflated and defensive, and you're probably going to take it personally. Certainly, it's easier to give than receive. "No one enjoys being criticized, especially if it's unfair," says psychologist Harriet Lerner, author of The Dance of Anger. "Yet how well we respond determines how our relationships go, both at work and at home. A lot is at stake."

It's possible to master the art of coping with criticism, which is important for your well-being: "If you don't learn how to deal with criticism, it'll likely elevate your stress level and compromise your mental and emotional functioning," says psychologist Leon Seltzer, who's based in Del Mar, Calif. "Like everything else, it's best not to let things get to you. That's why learning how to effectively 'process' criticism is so important to happiness and well-being."

Next time you're in the hot seat, try these nine tactics:

1. Breathe. Do what you can to remain calm. Slow your breathing and take a long, deep breath before speaking. When you're on guard, your nervous system quickens, interfering with your ability to appropriately listen and respond.

2. Postpone the conversation if necessary. If deep breaths don't help and you're too riled to engage in a reasonable conversation, trying to listen could actually do more harm than good. Tell the other person that you recognize the conversation's importance, but that you can't have it at that moment. Schedule another time so you can be prepared and ready to talk. [Read more: How to Cope With Criticism]

What Role Do Drugs Play in Determining Longevity?

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Health Buzz: Home HIV Test Backed By FDA Panel

Public release date: 15-May-2012 [ | E-mail | Share ]

Contact: Stephanie Desmon sdesmon1@jhmi.edu 410-955-8665 Johns Hopkins Medical Institutions

Even though hundreds of thousands more people finished grueling 26.2 mile marathons in the United States in 2009 compared to a decade earlier, a runner's risk of dying during or soon after the race has remained very low about .75 per 100,000, new Johns Hopkins research suggests. Men, however, were twice as likely to die as women.

"It's very dramatic when someone dies on the course, but it's not common," says Julius Cuong Pham, M.D., Ph.D., an associate professor of emergency medicine and anesthesiology and critical care medicine at the Johns Hopkins University School of Medicine, and leader of the study published online in The American Journal of Sports Medicine. "There are clearly many health benefits associated with running. It doesn't make you immune, but your risk of dying from running a marathon is very, very low."

Pham and his colleagues found that between 2000 and 2009, 28 people died during or in the 24 hours following, a marathon, most of them men. Half of those who died were over age 45, and all but one in the over-45 group died of heart disease. For younger runners, the cause of death varied widely and included cardiac arrhythmia and hyponatremia, the latter owing to drinking excessive amounts of water.

Marathons have long been considered the pinnacle of endurance sports, but they have become wildly popular in recent years. Pham and colleagues looked at statistics from approximately 300 marathons per year and found that the number of finishers increased dramatically between 2000 and 2009, from 299,018 to 473,354. The researchers said they believe the recent increase in marathon popularity is partially because of increasing awareness of the health benefits gained from regular exercise.

Numerous studies have linked exercise to better physical and mental health, and to longevity, Pham says. Similarly, marathon running has been associated with decreased risks of hypertension, high cholesterol and diabetes. People who run regularly have been found to have lower rates of all-cause mortality and disability.

With so many more people participating, Pham says he expected to find that the pace of marathons would have slowed over time, but the average finishing time also stayed steady at roughly four hours and 35 minutes.

One limitation of the study, however, is that there is no easily available access to data on the number of people who drop out of the races without finishing, which may have artificially kept average finishing times higher.

Pham, a three-time marathoner himself, cautions that people should not think that marathon training or running is risk-free. He noted that studies have shown the yearly incidence of injury in people training for marathons to be as high as 90 percent, with the vast majority of injuries damaging the musculoskeletal system.

Continue reading here:
Death risk for marathoners remains low during or soon after race

Java consumption linked to slightly increased longevity

Web edition : Wednesday, May 16th, 2012

Its the news that coffee addicts have been waiting for: Drinking several cups of coffee every day may help you live longer. A study of more than 400,000 people finds that drinking coffee reduces the risk of death from heart disease, stroke and even infections, researchers report in the May 17 New England Journal of Medicine.

Scientists have long puzzled over the notion that a stimulant could provide a health benefit. Theres been a concern for a long time that coffee could even be detrimental, says study coauthor Neal Freedman, an epidemiologist at the National Cancer Institute in Bethesda, Md. Our results might provide some reassurance for long-term coffee drinkers.

Since the study volunteers werent randomly assigned to drink coffee or not, the research has the limitations of being observational in nature. But with data from 402,260 participants, the results are very powerful and unlikely to be superseded by another coffee study anytime soon, says Roy Ziegelstein, a cardiologist at the Johns Hopkins Bayview Medical Center. This might be as good as it gets, he says.

Freedman and his colleagues analyzed data provided by men and women who completed a detailed questionnaire that included information about coffee intake as part of a medical studyin the mid-1990s. The researchers excluded people who had previously had cancer, heart disease or some other serious illness and recorded the remaining volunteers mortality status through 2008 by checking death records.

During a median follow-up of 13.6 years, people who drank two or more cups of coffee per day were 10 to 16 percent less likely to have died than nondrinkers. A single cup a day provided less apparent benefit. Women seemed to get more out of drinking ample java than men; women who drank six cups of coffee per day had a 15 percent reduced risk of death compared with nondrinkers, while men consuming that much had only a 10 percent reduced risk.

More than two cups a day seemed to offer some protection against death due to heart disease, respiratory ailments and diabetes, while four or more cups a day imparted apparent benefits against stroke and infections.

The researchers accounted for differences between coffee drinkers and nondrinkers such as body mass, smoking status and the consumption of alcohol, red meat, white meat, vitamins, fruits and vegetables.

Caffeine may not play a big role in coffees apparent benefit. Decaffeinated coffee consumption was associated with about the same longevity edge as regular. There are a huge number of chemically active components aside from caffeine in coffee, says Rachel Huxley, an epidemiologist at the University of Minnesota School of Public Health in Minneapolis. Given that the relationship between coffee intake and reduced mortality is not confined to one particular disease suggests that there are a lot of possible mechanisms involved.

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Coffee gives jolt to life span

KENT, Ohio A Kent State University professor received a grant to continue groundbreaking Parkinsons research and seeks participants for a clinical study.

Parkinsons disease affects about 1.5 million Americans and often leads to decreased independence and increased reliance on caregivers and the healthcare system for individuals living with it. However, research conducted by Kent State Universitys Angela Ridgel, Ph.D., shows reduced symptoms of the disease with the use of exercise using motorized bicycles.

Ridgel, Ph.D., an assistant professor in exercise science/physiology at Kent State, recently received a two-year, $390,900 grant from the National Institutes of Health to continue her work to design and test smart motorized bicycles, which could access individual effort, performance, skill level and therapeutic value in order to maximize the benefit.

Ridgel and her research collaborators, Kenneth Loparo at Case Western Reserve University and Fred Discenzo at Rockwell Automation, are seeking people, ages 50 to 79 years old, with a clinical diagnosis of idiopathic Parkinsons disease to partake in a clinical trial that will be held over a one-week period at Kent State. There is no cost for participants.

After we complete this study, we anticipate that participants will be able to move better for a period of time after the exercise, Ridgel said. Furthermore, the information gathered from this research will allow for future exercise recommendations for individuals with Parkinsons disease and other neurological disorders.

For more information or to see if you are a candidate to participate in the clinical study, contact Ridgel at (330)672-7495.

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My Town: KSU Professor Receives Grant for Parkinson’s Research

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Sergey Brin, a co-founder of Google, has contributed $132-million to the battle against Parkinsons disease, support work that is encouraging drug companies to accelerate treatment efforts, Bloomberg writes.

Mr. Brin, 38, began donating to Parkinsons research in 2005, three years before he learned that he carries a flawed gene that gives him a 50 percent change of contracting the progressive brain disease, which afflicts his mother.

His giving, most of it to the Michael J. Fox Foundation for Parkinsons Research, has helped create a database of 7,000 patients DNA and advanced research into the genetic causes of the disease. Pharmaceutical firms Pfizerand GlaxoSmithKline are drawing on that work in pursuing a new class of medicines that could become the first to slow the progress of the disease.

On the basis of their Parkinsons giving, Mr. Brin and his wife, Anne Wojcicki, ranked 25th on The Chronicle of Philanthropys list of 2011 top donors.

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Google’s Sergey Brin Takes Big Role in Parkinson’s Fight

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by WHAS11

WHAS11.com

Posted on May 10, 2012 at 5:50 PM

Updated yesterday at 6:02 PM

LOUISVILLE, Ky. (WHAS11) New research could provide hope for millions of Americans suffering from Alzheimers and Parkinson’s disease.

Every day there is a new challenge for Derek Duncan, 44, of Jeffersontown.

I thought, Im too young, but at the same time I thought at least I know what this is now,” said Derek Duncan.

Duncan has Parkinson’s disease. He started showing symptoms of tremors and balance issues at the age of 38. He takes steps every day to stay healthy and keep up on the latest research.

“If it takes the last breath in my body, we are gonna keep fighting. said Duncan.

New research happening in Louisville could give Parkinson’s patients like Derek and others new hope. The research is centered around a virus sometimes found in Kentucky’s big crop, tobacco.

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Tobacco could provide cure for Parkinson's, Alzheimer's

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Public release date: 11-May-2012 [ | E-mail | Share ]

Contact: Patrik Verstreken 32-497-422-165 VIB (the Flanders Institute for Biotechnology)

Neuroscientist Patrik Verstreken, associated with VIB and KU Leuven, succeeded in undoing the effect of one of the genetic defects that leads to Parkinson’s using vitamin K2. His discovery gives hope to Parkinson’s patients. This research was done in collaboration with colleagues from Northern Illinois University (US) and will be published this evening on the website of the authorative journal Science.

“It appears from our research that administering vitamin K2 could possibly help patients with Parkinson’s. However, more work needs to be done to understand this better,” says Patrik Verstreken.

Malfunctioning power plants are at the basis of Parkinson’s.

If we looked at cells as small factories, then mitochondria would be the power plants responsible for supplying the energy for their operation. They generate this energy by transporting electrons. In Parkinson’s patients, the activity of mitochondria and the transport of electrons have been disrupted, resulting in the mitochondria no longer producing sufficient energy for the cell. This has major consequences as the cells in certain parts of the brain will start dying off, disrupting communication between neurons. The results are the typical symptoms of Parkinson’s: lack of movement (akinesia), tremors and muscle stiffness.

The exact cause of this neurodegenerative disease is not known. In recent years, however, scientists have been able to describe several genetic defects (mutations) found in Parkinson’s patients, including the so-called PINK1 and Parkin mutations, which both lead to reduced mitochondrial activity. By studying these mutations, scientists hope to unravel the mechanisms underlying the disease process.

Paralyzed fruit flies

Fruit flies (Drosophila) are frequently used in lab experiments because of their short life spans and breeding cycles, among other things. Within two weeks of her emergence, every female is able to produce hundreds of offspring. By genetically modifying fruitflies, scientists can study the function of certain genes and proteins. Patrik Verstreken and his team used fruitflies with a genetic defect in PINK1 or Parkin that is similar to the one associated with Parkinson’s. They found that the flies with a PINK1 or Parkin mutation lost their ability to fly.

Upon closer examination, they discovered that the mitochondria in these flies were defective, just as in Parkinson’s patients. Because of this they generated less intracellular energy energy the insects needed to fly. When the flies were given vitamin K2, the energy production in their mitochondria was restored and the insects’ ability to fly improved. The researchers were also able to determine that the energy production was restored because the vitamin K2 had improved electron transport in the mitochondria. This in turn led to improved energy production.

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WILLIAMSTOWN, N.J.–(BUSINESS WIRE)–

Eva & Estela Wear Ur Love (http://www.evaandestela.com), a local, family-owned business, today announced the launch of its line of t-shirts and family apparel designed to raise awareness for multiple sclerosis.

Eva & Estela Wear Ur Love is the entrepreneurial endeavor of Kristen Sitarski-Munoz of Williamstown, NJ. In 2010, Sitarski-Munoz and her husband Ryan faced the simultaneous struggle of job losses and Ryans diagnosis of multiple sclerosis. Determined to overcome both challenges with courage and determination, Sitarski-Munoz created Eva & Estela Wear Ur Love, which is named for the couples two young daughters. The organization designs and sells t-shirts with the messages of family, hope, and love. Five percent of the proceeds will go directly to the Multiple Sclerosis Society.

According to the National Multiple Sclerosis Society, approximately 400,000 Americans have multiple sclerosis, a chronic, unpredictable disease of the central nervous system. Each week, about 200 more people are diagnosed with the disease.

Through the strength of our family unit, we were able to confront the challenges of multiple sclerosis and financial hardships with courage and determination, said Kristen Sitarski-Munoz, Founder & CEO of Eva & Estela Wear Ur Love. The result is Eva & Estela Wear Ur Love, which serves as a reminder to all families to support each other, celebrate each other, and most importantly, Wear Ur Love.

Eva & Estela Wear Ur Love currently offers five lines of t-shirts for infants, children and adults, including: Boys Club Tee, Family Words Design, Girls Club Tee, Heart/Key Tee Design, and the XO Design.

Eva & Estela Wear Ur Love

Eva & Estela Wear Ur Love is a growing, family-owned t-shirt and apparel business created to raise awareness for multiple sclerosis. Eva & Estela Wear Ur Love is the entrepreneurial endeavor of Kristen Sitarski-Munoz of Williamstown, NJ. Sitarski-Munoz and her husband Ryan faced the simultaneous struggle of job losses and Ryans diagnosis of multiple sclerosis. Determined to overcome both challenges with courage and determination, Sitarski-Munoz created Eva & Estela Wear Ur Love in honor of the couples two young daughters. The organization designs and sells t-shirts with the messages of family, hope, and love. Five percent of the proceeds go directly to the Multiple Sclerosis Society. For more information on Eva & Estela Wear Ur Love, please visit: http://www.evaandestela.com.

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By Michelle Fay Cortez – Thu May 10 22:26:00 GMT 2012

The U.S. Food and Drug Administration warned doctors and patients against the use of an unproven procedure known as liberation therapy that some physicians have touted as a treatment for multiple sclerosis.

The procedure uses a balloon-tipped catheter or a metal device called a stent to prop open narrowed blood vessels in the neck and chest that some investigators claim may exacerbate or even cause multiple sclerosis, a degenerative disease of the brain and spinal cord. The therapy has been linked to strokes, migration of the metal stents, damaged veins, blood clots, abdominal bleeding and death, the FDA said in a statement.

The unapproved treatment is used for chronic cerebrospinal venous insufficiency, which some doctors say may worsen multiple sclerosis by hindering blood flow from the brain and spinal cord, the agency said. No studies have conclusively linked multiple sclerosis to the condition and there is no accepted method to diagnose it, the FDA said.

There is no reliable evidence from controlled clinical trials that this procedure is effective in treating MS, said William Maisel, deputy director for science in the FDAs Center for Devices and Radiological Health, who called for study of the link between multiple sclerosis and narrowed veins. Patients are encouraged to discuss the potential risks and benefits of this procedure with a neurologist or another doctor familiar with the procedure, he said in a statement.

Multiple sclerosis, a chronic inflammatory disease, affects about 400,000 Americans, according to National Multiple Sclerosis Society. It stems from damage to the myelin sheath, fatty tissue that protects nerve fibers in the brain and spinal cord used to conduct electrical impulses that control movement.

The condition is currently treated with medications, including Biogen Idec Inc. (BIIB)s Avonex and Tysabri and Teva Pharmaceutical Industries Ltd. (TEVA)s Copaxone.

To contact the reporter on this story: Michelle Fay Cortez in Minneapolis at mcortez@bloomberg.net

To contact the editor responsible for this story: Reg Gale at rgale5@bloomberg.net

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FDA Warns MS Patients Against Unproven Stent Procedure

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By Robert Langreth – Fri May 11 04:00:01 GMT 2012

Sergey Brin, co-founder of Google Inc.

Sergey Brin, co-founder of Google Inc. Photographer: Tony Avelar/Bloomberg

Mark Tuschman via Bloomberg.

Michael J. Fox, actor and Parkinson’s activist of the Michael J. Fox Foundation, center stage, participates in a question and answer session with 23andMe Inc. employees at their offices in Mountainview, California on April 26, 2012. Photographer: Mark Tuschman via Bloomberg.

Michael J. Fox, actor and Parkinson’s activist of the Michael J. Fox Foundation, center stage, participates in a question and answer session with 23andMe Inc. employees at their offices in Mountainview, California on April 26, 2012. Photographer: Mark Tuschman via Bloomberg. Photographer: Mark Tuschman via Bloomberg.

Mark Tuschman via Bloomberg.

Michael J. Fox; actor and Parkinson’s activist of The Michael J. Fox Foundation speaks to Anne Wojcicki, chief executive officer of 23andMe Inc., during a visit to their offices in Mountainview, California on April 26, 2012.

Michael J. Fox; actor and Parkinson’s activist of The Michael J. Fox Foundation speaks to Anne Wojcicki, chief executive officer of 23andMe Inc., during a visit to their offices in Mountainview, California on April 26, 2012. Photographer: Mark Tuschman via Bloomberg.

Sergey Brin, the 38-year-old co- founder of Google Inc. (GOOG), is making strides in his quest to find a cure for Parkinsons, a progressive disease his DNA and family history suggest may afflict him as early as 10 years from now.

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WASHINGTON An experimental treatment for multiple sclerosis has caused death, strokes, nerve damage and abdominal bleeding and has no proven benefits for sufferers of the disease, the Food and Drug Administration warned Thursday.

Known as liberation therapy, the treatment targets chronic cerebrospinal venous insufficiency or CCSVI a narrowing of the veins in the head and neck. It involves inserting balloons or stents into veins to widen them in an attempt to relieve the symptoms of MS.

The FDA received reports in 2011 of a patient who died from bleeding in the brain after undergoing the treatment and another who was left permanently paralyzed by a stroke. Those incidents prompted the formal warning.

Other serious adverse effects from the procedure have been reported in medical journals.

The FDA has not approved any devices for use in liberation therapy, but doctors can offer the procedure to their patients. Doctors and other experts estimate that thousands of Americans have had the treatment, but the exact number is not known, because there is no central registry of patients.

Tim Coetzee, chief researcher for the National Multiple Sclerosis Society, said the link between the condition and MS was not yet well understood, nor were the potential side effects of liberation therapy.

“We’re still determining the risks associated with this,” he said.

MS is an autoimmune disease with a wide range of symptoms that include physical disability and chronic pain. Drugs can treat the symptoms, but there is no cure.

Paolo Zamboni, an Italian researcher, first proposed the link between CCSVI and MS in 2009. Zamboni published research showing that poor blood drainage from the brain and spinal cord aggravated nerve damage caused by MS. Surgically widening veins could help blood flow, he argued, alleviating symptoms of the disease.

Zamboni’s findings seemed to promise an effective treatment for MS and generated widespread interest among patients and doctors. Subsequent research tempered the enthusiasm, and the potential of liberation therapy is still being investigated.

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