The most fascinating article on Scurvy that you will read this week.

Scott and Scurvy I had been taught in school that scurvy had been conquered in 1747, when the Scottish physician James Lind proved in one of the first controlled medical experiments that citrus fruits were an effective cure for the disease. From that point on, we were told, the Royal Navy had required a daily dose of lime juice to be mixed in with sailors' grog, and scurvy ceased to be a problem on long ocean voyages. But here was a Royal Navy surgeon in 1911 apparently ignorant of what caused the disease, or how to cure it. Somehow a highly-trained group of scientists at the start of the 20th century knew less about scurvy than the average sea captain in Napoleonic times. Scott left a base abundantly stocked with fresh meat, fruits, apples, and lime juice, and headed out on the ice for five months with no protection against scurvy, all the while confident he was not at risk. What happened? [...] In the second half of the nineteenth century, the cure for scurvy was lost. The story of how this happened is a striking demonstration of the problem of induction, and how progress in one field of study can lead to unintended steps backward in another. An unfortunate series of accidents conspired with advances in technology to discredit the cure for scurvy. What had been a simple dietary deficiency became a subtle and unpredictable disease that could strike without warning. Over the course of fifty years, scurvy would return to torment not just Polar explorers, but thousands of infants born into wealthy European and American homes. And it would only be through blind luck that the actual cause of scurvy would be rediscovered, and vitamin C finally isolated, in 1932.

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One parasite to rule them all - Wolbachia protects against mosquito-borne diseases

This is an updated version of the first post I wrote this year. The scientists in question were looking at ways of recruiting bacteria in the fight against mosquito-borne diseases, such as dengue fever. They've just published new results that expand on their earlier experiments. Mosquitoes are incredibly successful parasites and cause millions of human deaths every year through the infections they spread. But they are no match for the most successful parasite of all - a bacterium called Wolbachia. It infects around 60% of the world's insect species and it could be our newest recruit in the fight against malaria, dengue fever and other mosquito-borne infections. Wolbachia doesn't usually infect mosquitoes but Scott O'Neill from the University of Queensland is leading a team of researchers who are trying to enlist it. Earlier this year, they published the story of their first success. They had developed a strain that not only infects mozzies, but halves the lifespans of infected females. Now, as the year comes to an end, they're back with another piece of good news - their life-shortening bacteria also guard the mosquitoes from other infections. It protects them against a species of Plasmodium, related to the parasite that causes malaria in humans, as well as the viruses responsible for dengue fever and Chikungunya. Infected insects are less likely to carry parasites that cause human disease, and those that do won't live long enough to spread them. It's a significant double-whammy that could have a lot of potential in controlling mosquito-borne diseases. Using Wolbachia for biological control makes sense because the bacterium uses many self-serving strategies that allow it to spread like wildfire. And because it's transmitted in the eggs of infected females, all of its strategies involve screwing over male insects, whose sperm are useless to it. Sometimes it kills males outright before they're even born. Sometimes, it turns them into females. In other subtler cases, it ensures that infected males can only mate successfully with infected females. If they try to breed with uninfected ones, the embryos die at an early stage of development. This strategy is known as "cytoplasmic incompatibility". It gives infected females (who can produce living young with any male they like) a competitive advantage over uninfected females, who can only start the next generation with uninfected males. Once Wolbachia gets a foothold in a population, massive swathes of it eventually become carriers. This is exactly what O'Neill's strain does - it induces complete cytoplasmic incompatibility. Once introduced into a natural population, it should invade with tremendous zest. The strain also halves the lifespan of the Aedes aegypti mosquito. This might seem like a flimsy victory, but it's an important one. Once an individual sucks up a mouthful of infected blood, it takes two weeks for any parasites or viruses they've drink to reproduce in their gut and travel back to their salivary glands. Only then do they become infectious. This means that mosquitoes only really pose a threat to human health once they're old and they are fairly short-lived insects anyway. Any technique that slashes their already limited lifespan will have a huge impact on controlling the diseases they carry. Even though Wolbachia lowers a female's lifespan, they don't hurt her egg-laying ability, or kill her off before she gets a chance to breed. So a Wolbachia-based approach would never drive a mosquito to extinction - it would just kill older individuals before they become capable of spreading disease. Now, O'Neill's team, led by Luciano Moreira, have found that their Wolbachia recruits have a second advantage - they stop mosquitoes from becoming vectors for the viruses and parasites that cause human disease. The bacterium almost entirely prevented infections by dengue virus, even if it was injected directly into their bodies. Even after five generations of breeding with wild mosquitoes, the offspring of the Wolbachia carriers still resisted dengue virus. Moreira found similar results for the Chikunguya virus. He also pitted his Wolbachia­-carrying mozzies against Plasmodium gallinaceum, a parasite that infects birds, but is closely related to P.falciparum that causes human malaria. A week after the mosquitoes had fed on contaminated blood, Moreira found 26 times less Plasmodium DNA in insects defended by Wolbachia, and the number of individuals that could potential transmit the parasite had halved. Wolbachia sets the mosquito's immune system on high-alert, switching on a few important immune system genes. Even if any viruses or parasites slip through, it's possible the bacterium outcompetes them for important nutrients like fatty acids and cholesterol. The viruses responsible for dengue and Chikunguya need cholesterol from their host to replicate themselves and Plasmodium needs a loan of fatty acids. But Wolbachia demands these molecules too and Moreira thinks it may simply be better at fighting for them. So far, so promising, but O'Neill acknowledges that there's a lot of work to be done before his strain of Wolbachia can prove its worth for human health. So far, he has only shown that it interferes with infection by P.gallinaceum and not the Plasmodium species that causes human malaria. Likewise, he has only shown that Wolbachia does the job in the A.aegypti mosquito, rather than Anopheles gambiae, the main vector for human malaria. Then there are the practical aspects. It's likely that Wolbachia's anti-male strategies will allow lab-infected mosquitoes to rapidly spread the bacterium. Certainly, earlier studies have found that Wolbachia can infect an entire laboratory population of mosquitoes within just a few generations. But that still needs to be tested, first in contained greenhouse settings and then later in field experiments. Computer models will also help to understand whether releasing infected mosquitoes will make a sizeable dent in the wild population, how long that would take, and whether resistant strains would eventually evolve. Reference: Moreira et al. 2009. A Wolbachia Symbiont in Aedes aegypti Limits Infection with Dengue, Chikungunya, and Plasmodiu. Cell DOI: 10.1016/j.cell.2009.11.042 More on mosquitoes: Life-shortening bacteria vs. dengue mosquitoes Genetically-modified mosquitoes fight malaria by outcompeting normal ones Size matters for mosquitoes but medium-sized males do better Bacterial smells have potential for trapping pregnant mosquitoes Mosquitoes harmonise their buzzing in love duets

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Was Recent U.S. Stock Market Drop Accompanied by More Heart Attacks? Duke Studies Relationship

A novel report explores the possible relationship between fluctuations in the stock market and the incidence of local heart attacks. The results were presented at the annual scientific meeting of the American College of Cardiology by a team of researchers from Duke University Medical Center. The initial data analysis showed an increased incidence of heart attacks from the Duke Databank for Cardiovascular Disease from January 2008 to July 2009. After conducting a comprehensive analysis looking specifically at the relationship with the stock market during that time, there was a trend between increased heart attacks with stock market declines. However, when results were adjusted to account for a known seasonal increase in heart attacks during winter months, the relationship was less clear. “In the unadjusted findings we saw a strong trend,” says Christopher O’Connor, MD, Director of the Duke Heart Center and senior author of the paper. “However, previous studies have not done these analyses with a seasonal correction. Previous research has shown that myocardial infarctions (MIs) occur more frequently during winter months than summer months. When we corrected for seasonality, we learned the time of year could be impacting our results.” After the U.S. suffered a severe economic crisis in the fall of 2008, the Duke researchers designed a pilot, single site observational study to explore whether the economic crisis and stock market volatility impacted cardiovascular (CV) event rates. Few studies have explored how economic trends impact cardiovascular events, explains Mona Fiuzat, PharmD, a researcher at Duke and the study’s lead investigator. During preliminary analysis, when the data were plotted against the daily NASDAQ opening values during the decline period, it revealed an inverse relationship between heart attacks and stock markets. “You can see the visual pattern,” says Fiuzat. “During the period that the NASDAQ was declining, the MI rates were increasing.” However, when more rigorous testing was used to specifically test the correlation with stock market values and eliminate the seasonable variability, the research question could no longer be answered. “The stock market declined during the winter, and previous studies show more MIs occur during the winter,” says Fiuzat. ”Therefore, we can’t say definitively that there is an association. There is the possibility that there is no relationship.” Fiuzat and O’Connor say the study had other limitations, including its sample size, its regional bias, and the large variability of MI events within the Duke database. They plan to conduct a larger study over a longer period of time, to determine whether a relationship between the stock market and heart attack rates exists.

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Breast Cancer Prognosis and Occult Lymph Node Metastases, Isolated Tumor Cells, and Micrometastases

Background The prognostic relevance of isolated tumor cells and micrometastases in lymph nodes from patients with breast cancer has become a major issue since the introduction of the sentinel lymph node procedure. We conducted a systematic review of this issue. Methods Studies published from January 1, 1977, until August 11, 2008, were identified by use of MEDLINE, EMBASE, and the Cochrane Library. A total of 58 studies (total number of patients = 297 533) were included and divided into three categories according to the method for pathological assessment of the lymph nodes: cohort studies with single-section pathological examination of axillary lymph nodes (n = 285 638 patients), occult metastases studies with retrospective examination of negative lymph nodes by step sectioning and/or immunohistochemistry (n = 7740 patients), and sentinel lymph node biopsy studies with intensified work-up of the sentinel but not of the nonsentinel lymph nodes (n = 4155 patients). We used random-effects meta-analyses to calculate pooled estimates of the relative risks (RRs) of 5- and 10-year disease recurrence and death and the multivariably corrected pooled hazard ratio (HR) of overall survival of the cohort studies. Results In the cohort studies, the presence (vs the absence) of metastases of 2 mm or less in diameter in axillary lymph nodes was associated with poorer overall survival (pooled HR of death = 1.44, 95% confidence interval [CI] = 1.29 to 1.62). In the occult metastases studies, the presence (vs the absence) of occult metastases was associated with poorer 5-year disease-free survival (pooled RR = 1.55, 95% CI = 1.32 to 1.82) and overall survival (pooled RR = 1.45, 95% CI = 1.11 to 1.88), although these endpoints were not consistently assessed in multivariable analyses. Sentinel lymph node biopsy studies were limited by small patient groups and short follow-up. Conclusion The presence (vs the absence) of metastases of 2 mm or less in diameter in axillary lymph nodes detected on single-section examination was associated with poorer disease-free and overall survival.

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Women die more often than men from heart disease: study

Women die more often than men from heart disease because they are not systematically given the same treatment and tests, according to a French study unveiled here Tuesday. The study, carried out on 3,000 women in the French region of Franche-Comte in 2006 and 2007, found that those hospitalized after suffering a cardiac attack were less frequently given an angiograph to study the heart's vessels. The technique involves dilating a coronary artery, and often a small stent is then inserted to keep the artery open.

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Oral contraceptive pills could help women live longer; cut heart disease, cancer risks: Study

Contraceptive pills used by women for birth-control could help them lead a longer life with lesser risk of major life-threatening conditions like heart disease and cancer, says a new study. The study conducted in more than 46,000 women over a period of 40 years showed that contraceptive pills users were less likely to die of heart [...]

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Years of Smoking Associated with Lower Parkinson’s Risk, Not Number of Cigarettes Per Day

Researchers have new insight into the relationship between Parkinson’s disease and smoking. Several studies have shown that smokers have a lower risk of developing Parkinson’s disease. A new study published in the March 10, 2010, online issue of Neurology®, the medical journal of the American Academy of Neurology, shows that smoking for a greater number of years may reduce the risk of the disease, but smoking a larger number of cigarettes per day may not reduce the risk. “These results could guide the development of studies on various tobacco components with animal models to help understand the relationship between smoking and Parkinson’s disease,” said study author Honglei Chen, MD, PhD, of the National Institute of Environmental Health Sciences in Research Triangle Park, N.C. “Research to reveal the underlying chemicals and mechanisms is warranted; such studies may lead to a better understanding of the causes of Parkinson’s disease. However, given the many adverse consequences of smoking, no one would suggest smoking in order to prevent Parkinson’s disease.” The study involved 305,468 AARP members age 50 to 71 . . . Current smokers were 44 percent less likely to develop Parkinson’s disease than people who had never smoked. People who had smoked in the past and quit were 22 percent less likely to develop Parkinson’s than people who had never smoked. . . . People who smoked for 40 or more years were 46 percent less likely to develop Parkinson’s disease than people who never smoked. Those who smoked for 30 to 39 years were 35 percent less likely to have the disease than nonsmokers. In contrast, those who smoked for one to nine years were only eight percent less likely to get the disease. The risk of developing Parkinson’s disease did not change based on how many cigarettes a person smoked per day. Chen noted that studies have shown that smoking is not associated with a slower progression of the disease once Parkinson’s develops or a reduced risk of death, so he said there is no evidence to support the use of nicotine or other smoking-related chemicals in treating the disease.

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Jamie Dukes talks about his battle with obesity

Vinnie Iyer Jamie Dukes, a former NFL offensive lineman who entered the league as an undrafted free agent, played for the Falcons, Packers and Cardinals in a 10-year career (1986-95). Now working as an analyst for the NFL Network, Dukes is passionate about an issue that affects him and many other retired players—battling obesity and the major health issues it can cause. Dukes, 45, talked to Sporting News' Vinnie Iyer about the problem, the solution he found for himself and how he's spreading the word about this issue. Sporting News: How does obesity develop into a problem for retired NFL linemen? Jamie Dukes: As a lineman, you're trained to maintain body mass, so you gorge yourself to stay at 290 or more pounds over the course of your career. When you're retired, not working out as much as you used to, taking on responsibilities like being a father, you realize your weight is getting progressively worse. There are no six and seven hours in the gym anymore. For me, 12 years after I finished playing, I was a biscuit away from 400 pounds. SN: How did you overcome the problem? JD: I had some teammates who passed away—Reggie White from sleep apnea, Ricky Bryan from a heart attack—that were directly related to being overweight. I tried all the diets, and I would lose 15 pounds here and there, but then would come a family vacation and I put it all back on again. I then heard about the gastric band procedure, and since July 16, 2008, it's helped me lose 110 pounds. SN: How does the gastric band work? JD: It's a numbers game, really. The procedure sets up a silicone band around the stomach, so it closes up more quickly. I used to consume 10-12 ounce portions, and now they're much smaller. It sends a sensation to your brain that you're full, so you're unable to consume large quantities. You can still eat all the foods you like, just less of them. You don't have issues with feeling hungry. It's just a 30-minute procedure, and I've had no medical issues. SN: How have you spread the word about your success? JD: Many former players contacted me after watching me on television, melting away the pounds right in front of their eyes. There's a lot of disability that comes with being obese, and a lot of guys have knee or other joint replacements. Literally, they want help taking off the weight that their lower body is carrying. SN: Is there something players can do to prevent this during their active career? JD: We all make a deal to play this game. It's not when they're playing or right when guys retire—that's when they're most physically fit. It's after that when those muscles turn into fat. SN: Have a good story on how you've inspired another former player? JD: I was at the Super Bowl, and the Saints were honoring one of their great former linebackers, Rickey Jackson. New Orleans is about to celebrate this victory, and he asked me "Tell me, what you done to lose all that weight?" It speaks volumes. It was so stunning to me, with his team right there, winning a championship, that was the first thing we talked about. SN: Do you consider yourself the leader of this cause? JD: I'm not the first player to recognize this problem. I'm just trying to do my part. With my Put Up Your Dukes foundation, it's there to help those who haven't connected the dots that a lot of what they're going through comes from what I call a disease of excess. SN: So is it more wishful thinking with other weight-loss solutions? JD: It's all about going from supersized consumption to eating in moderation. There are different ways to go about just shutting it off and keep from being overweight. SN: How about fighting this problem from a young age? JD: Childhood obesity is big issue, and through the NFL's Play 60 program, we're trying to get kids more involved in getting in enough physical activity every day. It's not good that P.E. is being pulled out of a lot of schools. With Xbox and other video games, more kids are on the couch moreoften. We've got to work to get them back outside. Vinnie Iyer is a writer for Sporting News. E-mail him at viyer@sportingnews.com.

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Studies: Intense treatment doesn't help diabetics

Key results from a landmark federal study are in, and the results are disappointing for diabetics: Adding drugs to drive blood pressure and blood-fats lower than current targets did not prevent heart problems, and in some cases caused harmful side effects. A decade ago, the federal government launched the three-part study to see whether intensely lowering blood sugar, blood pressure, or fats in the blood would reduce heart attacks and strokes in diabetics. The first piece of the study - about blood sugar - was stopped two years ago, when researchers saw more instead of less risk with that approach. Now, the other two parts of the study are in. What should diabetics do? Focus on healthy diets and lifestyles, and take tried-and-true medicines that doctors recommend now to control health risks, said several experts, including Dr. Clyde Yancy, a Baylor University cardiologist and president of the American Heart Association. The studies were presented Sunday at an American College of Cardiology conference and published on the Internet by the New England Journal of Medicine. They involve people with Type 2 diabetes - the most common form and the one rising because of the obesity epidemic. Diabetics have more than double the risk of dying of heart attacks or strokes than people without the disease.

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Protecting Your Liver With Fibromyalgia & Chronic Fatigue Syndrome

Did you know one of the hazards of fibromyalgia and chronic fatigue syndrome is liver damage? These conditions don't directly attack your liver, but the medications we take can do a lot of damage. Anti-inflammatories (NSAIDs) and narcotics, especially those containing acetaminophen (such as Vicodin), send a constant stream of toxins through your liver. This means that the liver has to work extra hard, and that can take a toll. I've known this academically for a long time, but I recently came face-to-face with this very real complication of long-term medication use -- in a blood test last fall, my liver enzymes were through the roof. My doctor said I was at risk for developing fatty liver, with can lead to cirrhosis. Now that scared the heck out of me! I can't really say I was surprised, but I was certainly shaken out of the "it won't happen to me" state of mind. I've had heavy NSAID use since I was 13, when I was put on a daily dose of 1600 mg of Motrin (ibuprofen) for on-going pain from an earlier back injury. A year later, it was upped to 2400 mg. I stayed on that for a couple of years, until Motrin became available over the counter. I continued taking it then, but less frequently and in smaller doses. In my 20s, I also took a lot of Tylenol (acetaminophen) for carpal tunnel disorder. Since my fibromyalgia symptoms started about 4 years ago, I'd been on Relafen (nabumetone), a prescription NSAID, at the maximum daily dosage. Add in the occasional Vicodin, and my liver's been racing to keep up. A couple months ago, I cut out the daily Relafen. I've taken some Aleve (naproxen sodium) and a little more Vicodin than usual, but I've tried hard not to medicate unless I really needed to. My doctor re-checked my liver enzymes recently, and one is normal and the other is only slightly elevated, so that's good news. The bad news is that my muscles have been tight, hard and spasmodic. (I should note that fibromyalgia is not considered an inflammatory condition, and much of my problems with inflammation are from myofascial pain syndrome and autoimmune thyroid disease.) So I have 2 issues to deal with -- I need to get my muscle pain and inflammation under control, and I also need to protect my liver. For pain and inflammation, I'm stepping up my use of some treatments, including: Acupuncture Massage Heat and/or ice Epsom salt baths I'm also trying to use my diet to lower inflammation. Here's more information about that: Your Diet for Managing Symptoms Dr. Weil's Anti-Inflammatory Food Pyramid To protect my liver, I'm taking an herbal supplement called milk thistle. While it's not a scientifically proven or FDA-approved treatment, milk thistle is a traditional remedy that's believed to help your liver process toxins. I'm also considering a detox diet. As I often do, I turned to Cathy Wong, About.com's Guide to Alternative Medicine, for more information about protecting my liver. Here are some great articles from her: Fighting Fatty Liver What You Need to Know About a Detox Diet I'll be getting my liver enzymes checked on a regular basis to make sure they stay down. If you have a drug history that's anything like mine, it might be wise to ask your doctor about getting a liver function test periodically. Have you had abnormal liver tests or liver problems because of medications? How bad has it gotten? What have you done to counter it? Do you get your liver enzymes checked regularly? Leave your comments below! Learn more or join the conversation! NEWSLETTER | FORUM | BIO | TWITTER | FACEBOOK Photo © A.D.A.M. Protecting Your Liver With Fibromyalgia & Chronic Fatigue Syndrome originally appeared on About.com Fibromyalgia & Chronic Fatigue Syndrome on Thursday, March 11th, 2010 at 06:00:17. Permalink | Comment | Email this

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