Archive for July, 2014

 

HealthTap’s Video Chatting Doctors Want to End Your WebMD Meltdowns

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HealthTap

“On the internet,” says Ron Gutman, “every headache becomes a brain tumor in four clicks or less.”

For Gutman and his colleagues in the world of health tech, this has become a running joke, a cheeky nod to just how far the human imagination can wander after a quick search of benign symptoms. But there’s more than a little truth to it. The fact is: the sheer abundance of health information online makes consulting Dr. Google an altogether flawed—and at times terrifying—first step toward getting better.

Ron Gutman.

Ron Gutman. Alex Washburn/WIRED

So, in 2010, Gutman launched HealthTap, an online service that makes it just as easy to get answers to your health questions from a real, trusted doctor. The company started as a kind of beefed-up question-and-answer site, where users can get free responses to their medical queries from thousands of peer-reviewed doctors, and it grew exponentially, serving over 100 million people with some 1.9 billion doctor answers after just a few years.Now, Gutman is taking things one step further. On Wednesday, his company announced the launch of HealthTap Prime, a new service that gives subscribers unlimited access to live videoconferences with actual doctors for $99 a month, plus $10 for every additional family member.

With Prime, HealthTap is feeding the rapidly growing demand for telemedicine services. According to the research firm IHS, revenue from companies entering this space is expected to grow to $1.9 billion in 2018, a huge leap from the $240 million the industry made in 2013. That’s driven in part by the Affordable Care Act, which champions the use of telehealth technologies in an effort to drive down Medicare and Medicaid costs and improve patient outcomes.

Revenue from telemedicine companies is expected to grow to $1.9 billion in 2018, a huge leap from the $240 million the industry made in 2013.

It’s also a reaction to the growing awareness that many patients are wasting their money on costly and unnecessary tests and doctor visits. One 2009 study by Thomson Reuters found that “unnecessary care”—including unnecessary tests meant to safeguard providers from liability—accounted for $250 billion to $325 billion in annual healthcare spending.

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HealthTap

While telemedicine may never replace traditional in-person care, it does hold the promise of reducing such extraneous doctor visits, making care less costly and more convenient for both the patient and the provider. And as wearable devices and other at-home monitoring tools become more sophisticated, the scope of care that can be delivered virtually will only expand.Several companies are already going after a piece of this massive pie. American Well and Teladoc have begun partnering with insurance companies to offer subscribers telemedicine services as an added benefit in their coverage, and others, like Doctors on Demand, backed by television’s Dr. Phil McGraw, are targeting patients first. Because the field is so new, says Forrester analyst Peter Mueller, there’s still ample room for competition in the space. “I don’t think anyone’s got a lock on the market,” says Mueller, who focuses on health technology. “People are still playing around with models, and this is definitely an interesting one.”

More Than a Video Conferencing Tool

But for Gutman, HealthTap is the only company addressing patient needs from the moment they have a question about a symptom to the virtual consultation and, if necessary, all the way through to diagnosis and prescription. That means with Prime, HealthTap is simultaneously taking on giants like WebMD, major insurers with their own telemedicine programs, and the established healthcare system as we know it. “A lot of people who are starting to do telemedicine services take Skype, put it in a wrapper, have doctors here, patients there, put it in the app store, and they’re done,” he says. “That’s not healthcare. That’s a feature.”

In designing the app, Gutman and his team wanted to make Prime more than just a video conferencing tool. Anyone can access HealthTap’s free database of doctor answers, but only Prime subscribers can pose follow up questions, visible only to them and the community of doctors. HealthTap also creates a personalized feed for Prime users. Similar to Facebook’s News Feed, it generates doctor answers users might be interested in and doctor-approved articles that might pertain to them, based on each user’s personal health records.

HealthTap is taking on giants like WebMD, major insurers with their own telemedicine programs, and the established healthcare system as we know it.

HealthTap’s Video Chatting Doctors Want to End Your WebMD Meltdowns | Business | WIRED.

Butler County Sheriff Richard Jones said Friday that he sent a letter to Mexican President Enrique Pena Nieto, charging him for all the illegals in his jail.

What happened next? The Ohio sheriff told Dana Loesch: “The federal government sends me a letter and said I violated a treaty of like, 1790.”

When Loesch asked for more information, Jones continued: “I sent him a bill for the prisoners that are in my jail. They came here illegally. I’ve not gotten any money from them, but I billed them so much. And I’ll tell you what I got in return: my life was threatened.”

Jones said he got a call from the FBI saying there were three sheriffs in the country that were going to be killed by the drug cartels, and he was one of the three.

Ohio Sheriff Richard Jones appears on TheBlaze TV's 'Dana' with Dana Loesch July 25, 2014. (Photo: TheBlaze TV)

Butler County Sheriff Richard Jones appears on TheBlaze TV’s ‘Dana’ with Dana Loesch July 25, 2014. (Photo: TheBlaze TV)

Jones has also written a letter to President Barack Obama, “asking and pleading with him not to bring these people here to the state of Ohio, and to secure our borders.”

“We’ve had horrendous crimes here in this community,” Jones said. “We had a senior citizen, an elderly lady, molested by a teenager that came over from Mexico. We had another one molested — an eight year old girl. We’ve had drugs pouring in, more so than before the government said the borders were sealed. And we’re being run over by the drug dealers coming to this community. The violence has increased, and we’re a long way from the borders.”

Jones said his county spends eight to ten million dollars each month on welfare programs, which he called “free stuff,” and said that’s “some of the reason that they come here.”

“It’s a terrible, terrible tragedy,” Jones said. “People’s lives are being threatened. It’s in the state of Ohio, for crying out loud. We’re not in Arizona; we’re not in California.”

Jones said the administration is making it “too easy” for those wishing to harm America to cross into the United States.

“They’re going to walk in with backpacks. They’re going to put some dirty bombs together, [and] they’re going to do something really terrible. It’s too easy,” Jones said. “We don’t know who they are. They don’t have vaccinations. Our jails are full. They hit and run. It’s totally out of control, and it’s gotten worse just in the past twelve months.”

 

Here’s What Happened After an Ohio Sheriff Sent a Bill to the Mexican President for the Illegals in His Jail | Video | TheBlaze.com.

‘Confused Cats Against Feminism’ Tumblr Is Just What The Internet Needed.

When Akihiko Takahashi was a junior in college in 1978, he was like most of the other students at his university in suburban Tokyo. He had a vague sense of wanting to accomplish something but no clue what that something should be. But that spring he met a man who would become his mentor, and this relationship set the course of his entire career.

Takeshi Matsuyama was an elementary-school teacher, but like a small number of instructors in Japan, he taught not just young children but also college students who wanted to become teachers. At the university-affiliated elementary school where Matsuyama taught, he turned his classroom into a kind of laboratory, concocting and trying out new teaching ideas. When Takahashi met him, Matsuyama was in the middle of his boldest experiment yet — revolutionizing the way students learned math by radically changing the way teachers taught it.

Instead of having students memorize and then practice endless lists of equations — which Takahashi remembered from his own days in school — Matsuyama taught his college students to encourage passionate discussions among children so they would come to uncover math’s procedures, properties and proofs for themselves. One day, for example, the young students would derive the formula for finding the area of a rectangle; the next, they would use what they learned to do the same for parallelograms. Taught this new way, math itself seemed transformed. It was not dull misery but challenging, stimulating and even fun.

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Credit Photo illustration by Andrew B. Myers. Prop stylist: Randi Brookman Harris.

Takahashi quickly became a convert. He discovered that these ideas came from reformers in the United States, and he dedicated himself to learning to teach like an American. Over the next 12 years, as the Japanese educational system embraced this more vibrant approach to math, Takahashi taught first through sixth grade. Teaching, and thinking about teaching, was practically all he did. A quiet man with calm, smiling eyes, his passion for a new kind of math instruction could take his colleagues by surprise. “He looks very gentle and kind,” Kazuyuki Shirai, a fellow math teacher, told me through a translator. “But when he starts talking about math, everything changes.”

Takahashi was especially enthralled with an American group called the National Council of Teachers of Mathematics, or N.C.T.M., which published manifestoes throughout the 1980s, prescribing radical changes in the teaching of math. Spending late nights at school, Takahashi read every one. Like many professionals in Japan, teachers often said they did their work in the name of their mentor. It was as if Takahashi bore two influences: Matsuyama and the American reformers.

Takahashi, who is 58, became one of his country’s leading math teachers, once attracting 1,000 observers to a public lesson. He participated in a classroom equivalent of “Iron Chef,” the popular Japanese television show. But in 1991, when he got the opportunity to take a new job in America, teaching at a school run by the Japanese Education Ministry for expats in Chicago, he did not hesitate. With his wife, a graphic designer, he left his friends, family, colleagues — everything he knew — and moved to the United States, eager to be at the center of the new math.

As soon as he arrived, he started spending his days off visiting American schools. One of the first math classes he observed gave him such a jolt that he assumed there must have been some kind of mistake. The class looked exactly like his own memories of school. “I thought, Well, that’s only this class,” Takahashi said. But the next class looked like the first, and so did the next and the one after that. The Americans might have invented the world’s best methods for teaching math to children, but it was difficult to find anyone actually using them.

It wasn’t the first time that Americans had dreamed up a better way to teach math and then failed to implement it. The same pattern played out in the 1960s, when schools gripped by a post-Sputnik inferiority complex unveiled an ambitious “new math,” only to find, a few years later, that nothing actually changed. In fact, efforts to introduce a better way of teaching math stretch back to the 1800s. The story is the same every time: a big, excited push, followed by mass confusion and then a return to conventional practices.

The trouble always starts when teachers are told to put innovative ideas into practice without much guidance on how to do it. In the hands of unprepared teachers, the reforms turn to nonsense, perplexing students more than helping them. One 1965 Peanuts cartoon depicts the young blond-haired Sally struggling to understand her new-math assignment: “Sets . . . one to one matching . . . equivalent sets . . . sets of one . . . sets of two . . . renaming two. . . .” After persisting for three valiant frames, she throws back her head and bursts into tears: “All I want to know is, how much is two and two?”

Today the frustrating descent from good intentions to tears is playing out once again, as states across the country carry out the latest wave of math reforms: the Common Core. A new set of academic standards developed to replace states’ individually designed learning goals, the Common Core math standards are like earlier math reforms, only further refined and more ambitious. Whereas previous movements found teachers haphazardly, through organizations like Takahashi’s beloved N.C.T.M. math-teacher group, the Common Core has a broader reach. A group of governors and education chiefs from 48 states initiated the writing of the standards, for both math and language arts, in 2009. The same year, the Obama administration encouraged the idea, making the adoption of rigorous “common standards” a criterion for receiving a portion of the more than $4 billion in Race to the Top grants. Forty-three states have adopted the standards.

The opportunity to change the way math is taught, as N.C.T.M. declared in its endorsement of the Common Core standards, is “unprecedented.” And yet, once again, the reforms have arrived without any good system for helping teachers learn to teach them. Responding to a recent survey by Education Week, teachers said they had typically spent fewer than four days in Common Core training, and that included training for the language-arts standards as well as the math.

Carefully taught, the assignments can help make math more concrete. Students don’t just memorize their times tables and addition facts but also understand how arithmetic works and how to apply it to real-life situations. But in practice, most teachers are unprepared and children are baffled, leaving parents furious. The comedian Louis C.K. parodied his daughters’ homework in an appearance on “The Late Show With David Letterman”: “It’s like, Bill has three goldfish. He buys two more. How many dogs live in London?”

The inadequate implementation can make math reforms seem like the most absurd form of policy change — one that creates a whole new problem to solve. Why try something we’ve failed at a half-dozen times before, only to watch it backfire? Just four years after the standards were first released, this argument has gained traction on both sides of the aisle. Since March, four Republican governors have opposed the standards. In New York, a Republican candidate is trying to establish another ballot line, called Stop Common Core, for the November gubernatorial election. On the left, meanwhile, teachers’ unions in Chicago and New York have opposed the reforms.

The fact that countries like Japan have implemented a similar approach with great success offers little consolation when the results here seem so dreadful. Americans might have written the new math, but maybe we simply aren’t suited to it. “By God,” wrote Erick Erickson, editor of the website RedState, in an anti-Common Core attack, is it such “a horrific idea that we might teach math the way math has always been taught.”

The new math of the ‘60s, the new new math of the ‘80s and today’s Common Core math all stem from the idea that the traditional way of teaching math simply does not work. As a nation, we suffer from an ailment that John Allen Paulos, a Temple University math professor and an author, calls innumeracy — the mathematical equivalent of not being able to read. On national tests, nearly two-thirds of fourth graders and eighth graders are not proficient in math. More than half of fourth graders taking the 2013 National Assessment of Educational Progress could not accurately read the temperature on a neatly drawn thermometer. (They did not understand that each hash mark represented two degrees rather than one, leading many students to mistake 46 degrees for 43 degrees.) On the same multiple-choice test, three-quarters of fourth graders could not translate a simple word problem about a girl who sold 15 cups of lemonade on Saturday and twice as many on Sunday into the expression “15 + (2×15).” Even in Massachusetts, one of the country’s highest-performing states, math students are more than two years behind their counterparts in Shanghai.

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The new math of the ’60s, the new, new math of the ’80s and today’s Common Core math all stem from the idea that the traditional way of teaching math simply does not work.

Adulthood does not alleviate our quantitative deficiency. A 2012 study comparing 16-to-65-year-olds in 20 countries found that Americans rank in the bottom five in numeracy. On a scale of 1 to 5, 29 percent of them scored at Level 1 or below, meaning they could do basic arithmetic but not computations requiring two or more steps. One study that examined medical prescriptions gone awry found that 17 percent of errors were caused by math mistakes on the part of doctors or pharmacists. A survey found that three-quarters of doctors inaccurately estimated the rates of death and major complications associated with common medical procedures, even in their own specialty areas.

One of the most vivid arithmetic failings displayed by Americans occurred in the early 1980s, when the A&W restaurant chain released a new hamburger to rival the McDonald’s Quarter Pounder. With a third-pound of beef, the A&W burger had more meat than the Quarter Pounder; in taste tests, customers preferred A&W’s burger. And it was less expensive. A lavish A&W television and radio marketing campaign cited these benefits. Yet instead of leaping at the great value, customers snubbed it.

Only when the company held customer focus groups did it become clear why. The Third Pounder presented the American public with a test in fractions. And we failed. Misunderstanding the value of one-third, customers believed they were being overcharged. Why, they asked the researchers, should they pay the same amount for a third of a pound of meat as they did for a quarter-pound of meat at McDonald’s. The “4” in “¼,” larger than the “3” in “⅓,” led them astray.

But our innumeracy isn’t inevitable. In the 1970s and the 1980s, cognitive scientists studied a population known as the unschooled, people with little or no formal education. Observing workers at a Baltimore dairy factory in the ‘80s, the psychologist Sylvia Scribner noted that even basic tasks required an extensive amount of math. For instance, many of the workers charged with loading quarts and gallons of milk into crates had no more than a sixth-grade education. But they were able to do math, in order to assemble their loads efficiently, that was “equivalent to shifting between different base systems of numbers.” Throughout these mental calculations, errors were “virtually nonexistent.” And yet when these workers were out sick and the dairy’s better-educated office workers filled in for them, productivity declined.

The unschooled may have been more capable of complex math than people who were specifically taught it, but in the context of school, they were stymied by math they already knew. Studies of children in Brazil, who helped support their families by roaming the streets selling roasted peanuts and coconuts, showed that the children routinely solved complex problems in their heads to calculate a bill or make change. When cognitive scientists presented the children with the very same problem, however, this time with pen and paper, they stumbled. A 12-year-old boy who accurately computed the price of four coconuts at 35 cruzeiros each was later given the problem on paper. Incorrectly using the multiplication method he was taught in school, he came up with the wrong answer. Similarly, when Scribner gave her dairy workers tests using the language of math class, their scores averaged around 64 percent. The cognitive-science research suggested a startling cause of Americans’ innumeracy: school.

Most American math classes follow the same pattern, a ritualistic series of steps so ingrained that one researcher termed it a cultural script. Some teachers call the pattern “I, We, You.” After checking homework, teachers announce the day’s topic, demonstrating a new procedure: “Today, I’m going to show you how to divide a three-digit number by a two-digit number” (I). Then they lead the class in trying out a sample problem: “Let’s try out the steps for 242 ÷ 16” (We). Finally they let students work through similar problems on their own, usually by silently making their way through a work sheet: “Keep your eyes on your own paper!” (You).

By focusing only on procedures — “Draw a division house, put ‘242’ on the inside and ‘16’ on the outside, etc.” — and not on what the procedures mean, “I, We, You” turns school math into a sort of arbitrary process wholly divorced from the real world of numbers. Students learn not math but, in the words of one math educator, answer-getting. Instead of trying to convey, say, the essence of what it means to subtract fractions, teachers tell students to draw butterflies and multiply along the diagonal wings, add the antennas and finally reduce and simplify as needed. The answer-getting strategies may serve them well for a class period of practice problems, but after a week, they forget. And students often can’t figure out how to apply the strategy for a particular problem to new problems.

How could you teach math in school that mirrors the way children learn it in the world? That was the challenge Magdalene Lampert set for herself in the 1980s, when she began teaching elementary-school math in Cambridge, Mass. She grew up in Trenton, accompanying her father on his milk deliveries around town, solving the milk-related math problems he encountered. “Like, you know: If Mrs. Jones wants three quarts of this and Mrs. Smith, who lives next door, wants eight quarts, how many cases do you have to put on the truck?” Lampert, who is 67 years old, explained to me.

She knew there must be a way to tap into what students already understood and then build on it. In her classroom, she replaced “I, We, You” with a structure you might call “You, Y’all, We.” Rather than starting each lesson by introducing the main idea to be learned that day, she assigned a single “problem of the day,” designed to let students struggle toward it — first on their own (You), then in peer groups (Y’all) and finally as a whole class (We). The result was a process that replaced answer-getting with what Lampert called sense-making. By pushing students to talk about math, she invited them to share the misunderstandings most American students keep quiet until the test. In the process, she gave them an opportunity to realize, on their own, why their answers were wrong.

Lampert, who until recently was a professor of education at the University of Michigan in Ann Arbor, now works for the Boston Teacher Residency, a program serving Boston public schools, and the New Visions for Public Schools network in New York City, instructing educators on how to train teachers. In her book, “Teaching Problems and the Problems of Teaching,” Lampert tells the story of how one of her fifth-grade classes learned fractions. One day, a student made a “conjecture” that reflected a common misconception among children. The fraction 5 / 6, the student argued, goes on the same place on the number line as 5 / 12. For the rest of the class period, the student listened as a lineup of peers detailed all the reasons the two numbers couldn’t possibly be equivalent, even though they had the same numerator. A few days later, when Lampert gave a quiz on the topic (“Prove that 3 / 12 = 1 / 4 ,” for example), the student could confidently declare why: “Three sections of the 12 go into each fourth.”

Over the years, observers who have studied Lampert’s classroom have found that students learn an unusual amount of math. Rather than forgetting algorithms, they retain and even understand them. One boy who began fifth grade declaring math to be his worst subject ended it able to solve multiplication, long division and fraction problems, not to mention simple multivariable equations. It’s hard to look at Lampert’s results without concluding that with the help of a great teacher, even Americans can become the so-called math people we don’t think we are.

Among math reformers, Lampert’s work gained attention. Her research was cited in the same N.C.T.M. standards documents that Takahashi later pored over. She was featured in Time magazine in 1989 and was retained by the producers of “Sesame Street” to help create the show “Square One Television,” aimed at making math accessible to children. Yet as her ideas took off, she began to see a problem. In Japan, she was influencing teachers she had never met, by way of the N.C.T.M. standards. But where she lived, in America, teachers had few opportunities for learning the methods she developed.

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Credit Photo illustration by Andrew B. Myers. Prop stylist: Randi Brookman Harris. Butterfly icon by Tim Boelaars.

American institutions charged with training teachers in new approaches to math have proved largely unable to do it. At most education schools, the professors with the research budgets and deanships have little interest in the science of teaching. Indeed, when Lampert attended Harvard’s Graduate School of Education in the 1970s, she could find only one listing in the entire course catalog that used the word “teaching” in its title. (Today only 19 out of 231 courses include it.) Methods courses, meanwhile, are usually taught by the lowest ranks of professors — chronically underpaid, overworked and, ultimately, ineffective.

Without the right training, most teachers do not understand math well enough to teach it the way Lampert does. “Remember,” Lampert says, “American teachers are only a subset of Americans.” As graduates of American schools, they are no more likely to display numeracy than the rest of us. “I’m just not a math person,” Lampert says her education students would say with an apologetic shrug.

Consequently, the most powerful influence on teachers is the one most beyond our control. The sociologist Dan Lortie calls the phenomenon the apprenticeship of observation. Teachers learn to teach primarily by recalling their memories of having been taught, an average of 13,000 hours of instruction over a typical childhood. The apprenticeship of observation exacerbates what the education scholar Suzanne Wilson calls education reform’s double bind. The very people who embody the problem — teachers — are also the ones charged with solving it.

Lampert witnessed the effects of the double bind in 1986, a year after California announced its intention to adopt “teaching for understanding,” a style of math instruction similar to Lampert’s. A team of researchers that included Lampert’s husband, David Cohen, traveled to California to see how the teachers were doing as they began to put the reforms into practice. But after studying three dozen classrooms over four years, they found the new teaching simply wasn’t happening. Some of the failure could be explained by active resistance. One teacher deliberately replaced a new textbook’s problem-solving pages with the old worksheets he was accustomed to using.

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Teachers primarily learn to teach by recalling their memories of having been taught, about 13,000 hours of instruction during a typical childhood — a problem since their instruction wasn’t very good.

Much more common, though, were teachers who wanted to change, and were willing to work hard to do it, but didn’t know how. Cohen observed one teacher, for example, who claimed to have incited a “revolution” in her classroom. But on closer inspection, her classroom had changed but not in the way California reformers intended it to. Instead of focusing on mathematical ideas, she inserted new activities into the traditional “I, We You” framework. The supposedly cooperative learning groups she used to replace her rows of desks, for example, seemed in practice less a tool to encourage discussion than a means to dismiss the class for lunch (this group can line up first, now that group, etc.).

And how could she have known to do anything different? Her principal praised her efforts, holding them up as an example for others. Official math-reform training did not help, either. Sometimes trainers offered patently bad information — failing to clarify, for example, that even though teachers were to elicit wrong answers from students, they still needed, eventually, to get to correct ones. Textbooks, too, barely changed, despite publishers’ claims to the contrary.

With the Common Core, teachers are once more being asked to unlearn an old approach and learn an entirely new one, essentially on their own. Training is still weak and infrequent, and principals — who are no more skilled at math than their teachers — remain unprepared to offer support. Textbooks, once again, have received only surface adjustments, despite the shiny Common Core labels that decorate their covers. “To have a vendor say their product is Common Core is close to meaningless,” says Phil Daro, an author of the math standards.

Left to their own devices, teachers are once again trying to incorporate new ideas into old scripts, often botching them in the process. One especially nonsensical result stems from the Common Core’s suggestion that students not just find answers but also “illustrate and explain the calculation by using equations, rectangular arrays, and/or area models.” The idea of utilizing arrays of dots makes sense in the hands of a skilled teacher, who can use them to help a student understand how multiplication actually works. For example, a teacher trying to explain multiplication might ask a student to first draw three rows of dots with two dots in each row and then imagine what the picture would look like with three or four or five dots in each row. Guiding the student through the exercise, the teacher could help her see that each march up the times table (3×2, 3×3, 3×4) just means adding another dot per row. But if a teacher doesn’t use the dots to illustrate bigger ideas, they become just another meaningless exercise. Instead of memorizing familiar steps, students now practice even stranger rituals, like drawing dots only to count them or breaking simple addition problems into complicated forms (62+26, for example, must become 60+2+20+6) without understanding why. This can make for even poorer math students. “In the hands of unprepared teachers,” Lampert says, “alternative algorithms are worse than just teaching them standard algorithms.”

No wonder parents and some mathematicians denigrate the reforms as “fuzzy math.” In the warped way untrained teachers interpret them, they are fuzzy.

When Akihiko Takahashi arrived in America, he was surprised to find how rarely teachers discussed their teaching methods. A year after he got to Chicago, he went to a one-day conference of teachers and mathematicians and was perplexed by the fact that the gathering occurred only twice a year. In Japan, meetings between math-education professors and teachers happened as a matter of course, even before the new American ideas arrived. More distressing to Takahashi was that American teachers had almost no opportunities to watch one another teach.

In Japan, teachers had always depended on jugyokenkyu, which translates literally as “lesson study,” a set of practices that Japanese teachers use to hone their craft. A teacher first plans lessons, then teaches in front of an audience of students and other teachers along with at least one university observer. Then the observers talk with the teacher about what has just taken place. Each public lesson poses a hypothesis, a new idea about how to help children learn. And each discussion offers a chance to determine whether it worked. Without jugyokenkyu, it was no wonder the American teachers’ work fell short of the model set by their best thinkers. Without jugyokenyku, Takahashi never would have learned to teach at all. Neither, certainly, would the rest of Japan’s teachers.

The best discussions were the most microscopic, minute-by-minute recollections of what had occurred, with commentary. If the students were struggling to represent their subtractions visually, why not help them by, say, arranging tile blocks in groups of 10, a teacher would suggest. Or after a geometry lesson, someone might note the inherent challenge for children in seeing angles as not just corners of a triangle but as quantities — a more difficult stretch than making the same mental step for area. By the end, the teachers had learned not just how to teach the material from that day but also about math and the shape of students’ thoughts and how to mold them.

If teachers weren’t able to observe the methods firsthand, they could find textbooks, written by the leading instructors and focusing on the idea of allowing students to work on a single problem each day. Lesson study helped the textbook writers home in on the most productive problems. For example, if you are trying to decide on the best problem to teach children to subtract a one-digit number from a two-digit number using borrowing, or regrouping, you have many choices: 11 minus 2, 18 minus 9, etc. Yet from all these options, five of the six textbook companies in Japan converged on the same exact problem, Toshiakira Fujii, a professor of math education at Tokyo Gakugei University, told me. They determined that 13 minus 9 was the best. Other problems, it turned out, were likely to lead students to discover only one solution method. With 12 minus 3, for instance, the natural approach for most students was to take away 2 and then 1 (the subtraction-subtraction method). Very few would take 3 from 10 and then add back 2 (the subtraction-addition method).

But Japanese teachers knew that students were best served by understanding both methods. They used 13 minus 9 because, faced with that particular problem, students were equally likely to employ subtraction-subtraction (take away 3 to get 10, and then subtract the remaining 6 to get 4) as they were to use subtraction-addition (break 13 into 10 and 3, and then take 9 from 10 and add the remaining 1 and 3 to get 4). A teacher leading the “We” part of the lesson, when students shared their strategies, could do so with full confidence that both methods would emerge.

By 1995, when American researchers videotaped eighth-grade classrooms in the United States and Japan, Japanese schools had overwhelmingly traded the old “I, We, You” script for “You, Y’all, We.” (American schools, meanwhile didn’t look much different than they did before the reforms.) Japanese students had changed too. Participating in class, they spoke more often than Americans and had more to say. In fact, when Takahashi came to Chicago initially, the first thing he noticed was how uncomfortably silent all the classrooms were. One teacher must have said, “Shh!” a hundred times, he said. Later, when he took American visitors on tours of Japanese schools, he had to warn them about the noise from children talking, arguing, shrieking about the best way to solve problems. The research showed that Japanese students initiated the method for solving a problem in 40 percent of the lessons; Americans initiated 9 percent of the time. Similarly, 96 percent of American students’ work fell into the category of “practice,” while Japanese students spent only 41 percent of their time practicing. Almost half of Japanese students’ time was spent doing work that the researchers termed “invent/think.” (American students spent less than 1 percent of their time on it.) Even the equipment in classrooms reflected the focus on getting students to think. Whereas American teachers all used overhead projectors, allowing them to focus students’ attention on the teacher’s rules and equations, rather than their own, in Japan, the preferred device was a blackboard, allowing students to track the evolution of everyone’s ideas.

Japanese schools are far from perfect. Though lesson study is pervasive in elementary and middle school, it is less so in high school, where the emphasis is on cramming for college entrance exams. As is true in the United States, lower-income students in Japan have recently been falling behind their peers, and people there worry about staying competitive on international tests. Yet while the United States regularly hovers in the middle of the pack or below on these tests, Japan scores at the top. And other countries now inching ahead of Japan imitate the jugyokenkyu approach. Some, like China, do this by drawing on their own native jugyokenkyu-style traditions (zuanyan jiaocai, or “studying teaching materials intensively,” Chinese teachers call it). Others, including Singapore, adopt lesson study as a deliberate matter of government policy. Finland, meanwhile, made the shift by carving out time for teachers to spend learning. There, as in Japan, teachers teach for 600 or fewer hours each school year, leaving them ample time to prepare, revise and learn. By contrast, American teachers spend nearly 1,100 hours with little feedback.

It could be tempting to dismiss Japan’s success as a cultural novelty, an unreproducible result of an affluent, homogeneous, and math-positive society. Perhaps the Japanese are simply the “math people” Americans aren’t. Yet when I visited Japan, every teacher I spoke to told me a story that sounded distinctly American. “I used to hate math,” an elementary-school teacher named Shinichiro Kurita said through a translator. “I couldn’t calculate. I was slow. I was always at the bottom of the ladder, wondering why I had to memorize these equations.” Like Takahashi, when he went to college and saw his instructors teaching differently, “it was an enlightenment.”

Learning to teach the new way himself was not easy. “I had so much trouble,” Kurita said. “I had absolutely no idea how to do it.” He listened carefully for what Japanese teachers call children’s twitters — mumbled nuggets of inchoate thoughts that teachers can mold into the fully formed concept they are trying to teach. And he worked hard on bansho, the term Japanese teachers use to describe the art of blackboard writing that helps students visualize the flow of ideas from problem to solution to broader mathematical principles. But for all his efforts, he said, “the children didn’t twitter, and I couldn’t write on the blackboard.” Yet Kurita didn’t give up — and he had resources to help him persevere. He went to study sessions with other teachers, watched as many public lessons as he could and spent time with his old professors. Eventually, as he learned more, his students started to do the same. Today Kurita is the head of the math department at Setagaya Elementary School in Tokyo, the position once held by Takahashi’s mentor, Matsuyama.

Of all the lessons Japan has to offer the United States, the most important might be the belief in patience and the possibility of change. Japan, after all, was able to shift a country full of teachers to a new approach. Telling me his story, Kurita quoted what he described as an old Japanese saying about perseverance: “Sit on a stone for three years to accomplish anything.” Admittedly, a tenacious commitment to improvement seems to be part of the Japanese national heritage, showing up among teachers, autoworkers, sushi chefs and tea-ceremony masters. Yet for his part, Akihiko Takahashi extends his optimism even to a cause that can sometimes seem hopeless — the United States. After the great disappointment of moving here in 1991, he made a decision his colleagues back in Japan thought was strange. He decided to stay and try to help American teachers embrace the innovative ideas that reformers like Magdalene Lampert pioneered.

Today Takahashi lives in Chicago and holds a full-time job in the education department at DePaul University. (He also has a special appointment at his alma mater in Japan, where he and his wife frequently visit.) When it comes to transforming teaching in America, Takahashi sees promise in individual American schools that have decided to embrace lesson study. Some do this deliberately, working with Takahashi to transform the way they teach math. Others have built versions of lesson study without using that name. Sometimes these efforts turn out to be duds. When carefully implemented, though, they show promise. In one experiment in which more than 200 American teachers took part in lesson study, student achievement rose, as did teachers’ math knowledge — two rare accomplishments.

Training teachers in a new way of thinking will take time, and American parents will need to be patient. In Japan, the transition did not happen overnight. When Takahashi began teaching in the new style, parents initially complained about the young instructor experimenting on their children. But his early explorations were confined to just a few lessons, giving him a chance to learn what he was doing and to bring the parents along too. He began sending home a monthly newsletter summarizing what the students had done in class and why. By his third year, he was sending out the newsletter every day. If they were going to support their children, and support Takahashi, the parents needed to know the new math as well. And over time, they learned.

To cure our innumeracy, we will have to accept that the traditional approach we take to teaching math — the one that can be mind-numbing, but also comfortingly familiar — does not work. We will have to come to see math not as a list of rules to be memorized but as a way of looking at the world that really makes sense.

The other shift Americans will have to make extends beyond just math. Across all school subjects, teachers receive a pale imitation of the preparation, support and tools they need. And across all subjects, the neglect shows in students’ work. In addition to misunderstanding math, American students also, on average, write weakly, read poorly, think unscientifically and grasp history only superficially. Examining nearly 3,000 teachers in six school districts, the Bill & Melinda Gates Foundation recently found that nearly two-thirds scored less than “proficient” in the areas of “intellectual challenge” and “classroom discourse.” Odds-defying individual teachers can be found in every state, but the overall picture is of a profession struggling to make the best of an impossible hand.

Most policies aimed at improving teaching conceive of the job not as a craft that needs to be taught but as a natural-born talent that teachers either decide to muster or don’t possess. Instead of acknowledging that changes like the new math are something teachers must learn over time, we mandate them as “standards” that teachers are expected to simply “adopt.” We shouldn’t be surprised, then, that their students don’t improve.

Here, too, the Japanese experience is telling. The teachers I met in Tokyo had changed not just their ideas about math; they also changed their whole conception of what it means to be a teacher. “The term ‘teaching’ came to mean something totally different to me,” a teacher named Hideto Hirayama told me through a translator. It was more sophisticated, more challenging — and more rewarding. “The moment that a child changes, the moment that he understands something, is amazing, and this transition happens right before your eyes,” he said. “It seems like my heart stops every day.”

 

Why Do Americans Stink at Math? – NYTimes.com.

Chickens Share Backyards and Pests With Dogs, Cats

LOS ANGELES — Jul 30, 2014, 9:51 AM ET

By SUE MANNING Associated Press

Associated Press

The popular push for locally produced food has spawned flocks of backyard chickens in urban neighborhoods nationwide, but people may not realize that feasting on fresh eggs can mean subjecting their more typical household pets to pain from a new pest that hitches a ride on hens.

The poultry flea has been added to a list of parasites, venomous insects and other bothersome pests that take a bite out of dogs and cats every summer, veterinarians said. These bloodsucking pests are different from the most common fleas in the U.S. because they embed their tiny bodies into an animal’s flesh. Poultry fleas aren’t known to transmit disease but can cause infection when they sink into skin.

“You see them on pets that are around environments with chickens, which are becoming more common now that so many people have backyard flocks,” said Dr. Julie Meadows from the Community Practice Service at University of California, Davis, Veterinary Medical Teaching Hospital.

via Chickens Share Backyards and Pests With Dogs, Cats – ABC News.

Running for as little as five minutes a day could significantly lower a person’s risk of dying prematurely, according to a large-scale new study of exercise and mortality. The findings suggest that the benefits of even small amounts of vigorous exercise may be much greater than experts had assumed.

 

In recent years, moderate exercise, such as brisk walking, has been the focus of a great deal of exercise science and most exercise recommendations. The government’s formal 2008 exercise guidelines, for instance, suggest that people should engage in about 30 minutes of moderate exercise on most days of the week. Almost as an afterthought, the recommendations point out that half as much, or about 15 minutes a day of vigorous exercise, should be equally beneficial.

 

But the science to support that number had been relatively paltry, with few substantial studies having carefully tracked how much vigorous exercise is needed to reduce disease risk and increase lifespan. Even fewer studies had looked at how small an amount of vigorous exercise might achieve that same result.

 

So for the new study, published Monday in The Journal of the American College of Cardiology, researchers from Iowa State University, the University of South Carolina, the Pennington Biomedical Research Center in Baton Rouge, La., and other institutions turned to a huge database maintained at the Cooper Clinic and Cooper Institute in Dallas.

 

For decades, researchers there have been collecting information about the health of tens of thousands of men and women visiting the clinic for a check-up. These adults, after completing extensive medical and fitness examinations, have filled out questionnaires about their exercise habits, including whether, how often and how speedily they ran.

 

From this database, the researchers chose the records of 55,137 healthy men and women ages 18 to 100 who had visited the clinic at least 15 years before the start of the study. Of this group, 24 percent identified themselves as runners, although their typical mileage and pace varied widely.

 

The researchers then checked death records for these adults. In the intervening 15 or so years, almost 3,500 had died, many from heart disease.

 

But the runners were much less susceptible than the nonrunners. The runners’ risk of dying from any cause was 30 percent lower than that for the nonrunners, and their risk of dying from heart disease was 45 percent lower than for nonrunners, even when the researchers adjusted for being overweight or for smoking (although not many of the runners smoked). And even overweight smokers who ran were less likely to die prematurely than people who did not run, whatever their weight or smoking habits.

 

As a group, runners gained about three extra years of life compared with those adults who never ran.

 

Remarkably, these benefits were about the same no matter how much or little people ran. Those who hit the paths for 150 minutes or more a week, or who were particularly speedy, clipping off six-minute miles or better, lived longer than those who didn’t run. But they didn’t live significantly longer those who ran the least, including people running as little as five or 10 minutes a day at a leisurely pace of 10 minutes a mile or slower.

 

“We think this is really encouraging news,” said Timothy Church, a professor at the Pennington Institute who holds the John S. McIlHenny Endowed Chair in Health Wisdom and co-authored the study. “We’re not talking about training for a marathon,” he said, or even for a 5-kilometer (3.1-mile) race. “Most people can fit in five minutes a day of running,” he said, “no matter how busy they are, and the benefits in terms of mortality are remarkable.”

 

The study did not directly examine how and why running affected the risk of premature death, he said, or whether running was the only exercise that provided such benefits. The researchers did find that in general, runners had less risk of dying than people who engaged in more moderate activities such as walking.

 

But “there’s not necessarily something magical about running, per se,” Dr. Church said. Instead, it’s likely that exercise intensity is the key to improving longevity, he said, adding, “Running just happens to be the most convenient way for most people to exercise intensely.”

Anyone who has never run in the past or has health issues should, of course, consult a doctor before starting a running program, Dr. Church said. And if, after trying for a solid five minutes, you’re just not enjoying running, switch activities, he added. Jump rope. Vigorously pedal a stationary bike. Or choose any other strenuous activity. Five minutes of taxing effort might add years to your life

 

Running 5 minutes a day can extend life, study says.

5 servings  day

Fruits, Veggies May Have Their Limits in Boosting Lifespan – WebMD.

diopathic disease is defined as one that develops without any apparent or known causes. That is the term used for fibromyalgia, autoimmune diseases, including lupus and chronic fatigue syndrome. While many of these diseases have recognizable signs and symptoms, the lack of causality haunts medical schools, doctors, practices and hospitals. The only ones benefiting from lifelong symptom treatments associated with chronic fatigue syndrome, lupus, autoimmune disease, or fibromyalgia are the pharmaceutical companies who sell billions in medication to treat them. A long list of pain medications, sleep-aids, anti-depressants, and anti-inflammatories are not sufficient because the diagnosis is incorrect. Instead, let’s look at what the possible causes are to these diseases.

An Overview of Fibromyalgia Symptoms

A Conventional Scientific Overview of CFS (Chronic Fatigue Syndrome) and Fibromyalgia Causatives

Below, is a quick list of idiopathic disease causes — we will give a clinical review and explanation as to what takes place.

  • Brain abnormalities
  • Genetic factors (HPA) axis
  • A hyper-reactive immune system
  • Viral or other infectious agents like (Chronic Lyme disease Complex)
  • Psychiatric or emotional conditions

Are Genetics to Blame?

Chronic Fatigue Syndrome and fibromyalgia have been linked with genes involved in the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system. These genes regulate response to trauma, injury, and other stressful events. Our ten years of clinical experience shows that while such traumas could play a role in the etiology (the trigger to exhibiting symptoms) of the disease, they are unlikely the conditions’ causes.

What is the Hypothalamic-Pituitary-Adrenal Axis (HPA)? Does Lyme Disease Play a Role?

HPA makes up a multi-set of direct influences and feedback interactions among the hypothalamus, the pituitary gland (a pea-shaped structure located below the hypothalamus), and the adrenal, also called “suprarenal,” glands which are small, conical organs on top of the kidneys.

The interactions among these organs constitute the HPA-axis, a major part of the neuroendocrine system. From here, the body regulates reactions to stress, as well as processes such as digestion, the immune system, mood, emotions, sexuality, as well as energy. Infectious disease, such as chronic Lyme disease complex, impacts the HPA-axis via neurotoxins that compete for the same receptor sites used by the HPA-axis.

In fact, such infections can bring about identical symptoms of some idiopathic diseases listed above and many of the symptoms associated therewith. This should bring our attention to chronic Lyme Disease complex, which is composed of a number of infections and neurotoxins that bring about even more symptoms than those listed earlier in this article.

Does HPA Affect Fibromyalgia and Chronic Fatigue Syndrome?

Abnormal levels of certain chemicals regulated in the HPA axis area of the brain system have been proposed as a cause of Chronic Fatigue Syndrome and also have some influence in fibromyalgia. This system controls important functions, including sleep, stress response, and depression. Of particular interest to researchers are the chemicals and other factors listed below that are controlled by the HPA-axis.

The HPA-axis is involved in the neurobiology of mood disorders and functional illnesses, including anxiety disorder, bipolar disorder, insomnia, post-traumatic stress disorder, borderline personality disorder, ADHD, major depressive disorder, burnout, chronic fatigue syndrome, fibromyalgia, irritable bowel syndrome and alcoholism. Antidepressants, which are routinely prescribed for many of these illnesses, serve to regulate HPA-axis function. All of these conditions and their symptoms are commonly seen in chronic Lyme disease patients that contain a host of infections and neurotoxins that block serotonin receptors in the brain.

Can Chronic Lyme Disease Complex or Infectious Disease Affect HPA?

Patients may have contracted an infection at any point in their lifetime. However, the symptoms of chronic Lyme disease complex or its coinfections may remain unseen or dormant until the individual is weakened by a trauma or trigger. This could be anything from childbirth or a car accident to the death of a loved one, a divorce or even a vaccine, as seen among children with weakened immune systems.

In the etiology of chronic infectious disease, the traumatic event is a trigger, but not the cause of autoimmune disease, Chronic Fatigue Syndrome, or fibromyalgia. Nevertheless, treating these triggers is critically important to the new patient’s care. What we find is that infection and not genetic defects are at the root of HPA-axis disruption in the brain itself.

The Major Impact of Epigenetic Changes

A number of studies have found that alterations in genes are caused by infections involving immune function, intracellular communication and energy transfer. Researchers have identified many different genes in patients with Chronic Fatigue Syndrome that relate to blood disease, immune system function, and infection.

However, despite these identifications, there is no clear pattern to them and it is quite possible that it is the infections alone that are altering these genes and are responsible for impacting mental and emotional health as well. It is very possible that the infections can alter these genes that impact mental and emotional health as well.

Important Neurotransmitters Changed By Neurotoxins Competing For Receptor Sites

Some patients with Chronic Fatigue Syndrome have abnormally high levels of serotonin, a neurotransmitter (chemical messenger in the brain), and also show deficiencies in dopamine, an important neurotransmitter associated with feelings of reward. In some cases there is also a demonstrable imbalance between norepinephrine and dopamine.

A number of studies on Chronic Fatigue Syndrome have shown patients have lower cortisol levels, a stress hormone produced by the adrenal glands. It has been suggested that such cortisol deficiencies are responsible for Chronic Fatigue Syndrome patients having impaired or weakened responses to psychological or physical stresses like worry, infection, or exercise. However, administering replacement cortisol improves symptoms only in some patients. Why? Infection and their toxins (neurotoxins) must be cleared before hormone replacement can begin to be effective in these patients. It is also common for these patients to have thyroid, testosterone and cortisol issues.

Idiopathic Diseases at Root of Myriad Psychological Disorders Including Sleep-Related Ailments

Evidence suggests that certain CFS, fibromyalgia, and autoimmune patients have disturbed circadian rhythms (disorder of the sleep-wake cycle), which is regulated by the so-called circadian clock, a nerve cluster in the HPA-axis. These are commonly seen in chronic Lyme disease complex along with a number of other neurological symptoms.

A mentally or physically stressful event, such as a viral infection, may disrupt natural circadian rhythms. An inability to reset these rhythms results in a perpetual cycle of sleep disturbances. Medications that improve sleep can be very helpful for certain patients with Chronic Fatigue Syndrome, fibromyalgia and autoimmune diseases. But, until the infections are cleared and hormones are rebalanced, long-term improvement is unlikely, as the patient is likely to relapse.

Psychological, personality and social factors are strongly associated with Chronic Fatigue Syndrome, fibromyalgia, and autoimmune disease like lupus. There is a distinct complex relationship between physical and emotional factors.

What Specific Infections are Responsible

Because most of the features of Chronic Fatigue Syndrome resemble those of a lingering viral illness, many researchers have focused on the possibility that a virus or some other infectious agent, in some cases, causes the syndrome.

We have clinically determined that these patients usually have a group of viral, bacterial, parasitic and fungal infections that make up what we call Lyme Disease Complex. Some patients may or may not have actual Lyme disease but may have another type of tick-borne illness along with a host of co-infections that have brought about immunological, hormonal, and neuroendocrine changes.

Still, not all Chronic Fatigue Syndrome patients show signs of infection. And although experts have long been divided on whether infections play any role in this disorder at all, it does seem clear that subtypes of both viral and non-viral Chronic Fatigue Syndrome exist. That being said, researchers have seemingly overlooked the complexity of mute-infections, multi-toxins and heavy metal components that complicate these conditions, making them extremely difficult to diagnose on a case-to-case basis. When a complex of infections exists, they can affect the activation and replication of each other via biofilm communities. To be certain, most patients are never tested thoroughly and correctly for all the infections that make up chronic Lyme disease complex.

Infections Looking Like the Cause

The theory for Chronic Fatigue Syndrome having a viral cause is not based on hard evidence, rather, on an ever-growing series of observations. Chronic Fatigue Syndrome, as well as Fibromyalgia and Autoimmune disease patients, are often found with elevated levels of antibodies to many organisms that cause fatigue and other Chronic Fatigue Syndrome symptoms. Such organisms include those that cause Lyme disease, Candida (“yeast infection”), herpes virus type 6 (HHV-6), human T cell lymph tropic virus (HTLV), Epstein-Barr, measles, coxsackie B, cytomegalovirus, or parvovirus.

Many of these infectious agents are very common; however, none have emerged as a definitive cause of CFS. Well-designed studies of patients who met strict criteria for CFS without any known cause have not found an increased incidence of any specific infection(s).

In up to 80% of cases, CFS starts suddenly with a flu-like condition. In the U.S., there have been reports of cluster outbreaks of CFS occurring within the same household, workplace, and community (but most have not been confirmed by the Centers for Disease Control and Prevention). However, most cases of CFS occur sporadically in individuals and do not appear to be contagious. These all have the pattern of infections and more importantly, complexes of infections taking over the patient’s immune system, which is clearly seen in the depressed CD57 markers found in almost all of this population.

Infection Complexes Leading to Immune System Abnormalities and Immuno-Compromised States

CFS is sometimes referred to as “Chronic Fatigue Immune Dysfunction Syndrome.” In many cases, studies have detected many immune system irregularities. Some components appear to be over-reactive, while others appear to be under-reactive, but no consistent picture has emerged to explain CFS as a disease of the immune system in conventional medical practices. Chronic Lyme disease patients almost always have depressed CD57 marker called the striker panel and this is almost never run on chronic fatigue patients when they go to their doctor. Almost 100% of the time we find decreased key immune function in all CFS patients because we are running the correct diagnostics.

Autoimmunity Overlaps with Other Conditions

The risk profile for CFS is similar to the risk profiles for a number of autoimmune diseases. Studies are inconsistent with regards to the presence of auto-antibodies (antibodies that attack the body’s own tissues) in CFS, so the disease is unlikely to be due to auto-immunity, making it more likely connected to infectious disease. In Lyme disease patients, we typically see that the patient was diagnosed at one time or another with several autoimmune diseases, but almost certainly the previous physicians were confused. If you have any questions or would like to learn more about customized treatment options, contact us.

– See more at: http://www.envita.com/lyme-disease/finally-one-link-established-chronic-fatigue-syndrome-cfs-lupus-fibromyalgia-autoimmune-disease-chronic-lyme-disease#sthash.7GQKVYib.dpuf

Idiopathic disease is defined as one that develops without any apparent or known causes. That is the term used for fibromyalgia, autoimmune diseases, including lupus and chronic fatigue syndrome. While many of these diseases have recognizable signs and symptoms, the lack of causality haunts medical schools, doctors, practices and hospitals. The only ones benefiting from lifelong symptom treatments associated with chronic fatigue syndrome, lupus, autoimmune disease, or fibromyalgia are the pharmaceutical companies who sell billions in medication to treat them. A long list of pain medications, sleep-aids, anti-depressants, and anti-inflammatories are not sufficient because the diagnosis is incorrect. Instead, let’s look at what the possible causes are to these diseases.

An Overview of Fibromyalgia Symptoms

A Conventional Scientific Overview of CFS (Chronic Fatigue Syndrome) and Fibromyalgia Causatives

Below, is a quick list of idiopathic disease causes — we will give a clinical review and explanation as to what takes place.

  • Brain abnormalities
  • Genetic factors (HPA) axis
  • A hyper-reactive immune system
  • Viral or other infectious agents like (Chronic Lyme disease Complex)
  • Psychiatric or emotional conditions

Are Genetics to Blame?

Chronic Fatigue Syndrome and fibromyalgia have been linked with genes involved in the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system. These genes regulate response to trauma, injury, and other stressful events. Our ten years of clinical experience shows that while such traumas could play a role in the etiology (the trigger to exhibiting symptoms) of the disease, they are unlikely the conditions’ causes.

What is the Hypothalamic-Pituitary-Adrenal Axis (HPA)? Does Lyme Disease Play a Role?

HPA makes up a multi-set of direct influences and feedback interactions among the hypothalamus, the pituitary gland (a pea-shaped structure located below the hypothalamus), and the adrenal, also called “suprarenal,” glands which are small, conical organs on top of the kidneys.

The interactions among these organs constitute the HPA-axis, a major part of the neuroendocrine system. From here, the body regulates reactions to stress, as well as processes such as digestion, the immune system, mood, emotions, sexuality, as well as energy. Infectious disease, such as chronic Lyme disease complex, impacts the HPA-axis via neurotoxins that compete for the same receptor sites used by the HPA-axis.

In fact, such infections can bring about identical symptoms of some idiopathic diseases listed above and many of the symptoms associated therewith. This should bring our attention to chronic Lyme Disease complex, which is composed of a number of infections and neurotoxins that bring about even more symptoms than those listed earlier in this article.

Does HPA Affect Fibromyalgia and Chronic Fatigue Syndrome?

Abnormal levels of certain chemicals regulated in the HPA axis area of the brain system have been proposed as a cause of Chronic Fatigue Syndrome and also have some influence in fibromyalgia. This system controls important functions, including sleep, stress response, and depression. Of particular interest to researchers are the chemicals and other factors listed below that are controlled by the HPA-axis.

The HPA-axis is involved in the neurobiology of mood disorders and functional illnesses, including anxiety disorder, bipolar disorder, insomnia, post-traumatic stress disorder, borderline personality disorder, ADHD, major depressive disorder, burnout, chronic fatigue syndrome, fibromyalgia, irritable bowel syndrome and alcoholism. Antidepressants, which are routinely prescribed for many of these illnesses, serve to regulate HPA-axis function. All of these conditions and their symptoms are commonly seen in chronic Lyme disease patients that contain a host of infections and neurotoxins that block serotonin receptors in the brain.

Can Chronic Lyme Disease Complex or Infectious Disease Affect HPA?

Patients may have contracted an infection at any point in their lifetime. However, the symptoms of chronic Lyme disease complex or its coinfections may remain unseen or dormant until the individual is weakened by a trauma or trigger. This could be anything from childbirth or a car accident to the death of a loved one, a divorce or even a vaccine, as seen among children with weakened immune systems.

In the etiology of chronic infectious disease, the traumatic event is a trigger, but not the cause of autoimmune disease, Chronic Fatigue Syndrome, or fibromyalgia. Nevertheless, treating these triggers is critically important to the new patient’s care. What we find is that infection and not genetic defects are at the root of HPA-axis disruption in the brain itself.

The Major Impact of Epigenetic Changes

A number of studies have found that alterations in genes are caused by infections involving immune function, intracellular communication and energy transfer. Researchers have identified many different genes in patients with Chronic Fatigue Syndrome that relate to blood disease, immune system function, and infection.

However, despite these identifications, there is no clear pattern to them and it is quite possible that it is the infections alone that are altering these genes and are responsible for impacting mental and emotional health as well. It is very possible that the infections can alter these genes that impact mental and emotional health as well.

Important Neurotransmitters Changed By Neurotoxins Competing For Receptor Sites

Some patients with Chronic Fatigue Syndrome have abnormally high levels of serotonin, a neurotransmitter (chemical messenger in the brain), and also show deficiencies in dopamine, an important neurotransmitter associated with feelings of reward. In some cases there is also a demonstrable imbalance between norepinephrine and dopamine.

A number of studies on Chronic Fatigue Syndrome have shown patients have lower cortisol levels, a stress hormone produced by the adrenal glands. It has been suggested that such cortisol deficiencies are responsible for Chronic Fatigue Syndrome patients having impaired or weakened responses to psychological or physical stresses like worry, infection, or exercise. However, administering replacement cortisol improves symptoms only in some patients. Why? Infection and their toxins (neurotoxins) must be cleared before hormone replacement can begin to be effective in these patients. It is also common for these patients to have thyroid, testosterone and cortisol issues.

Idiopathic Diseases at Root of Myriad Psychological Disorders Including Sleep-Related Ailments

Evidence suggests that certain CFS, fibromyalgia, and autoimmune patients have disturbed circadian rhythms (disorder of the sleep-wake cycle), which is regulated by the so-called circadian clock, a nerve cluster in the HPA-axis. These are commonly seen in chronic Lyme disease complex along with a number of other neurological symptoms.

A mentally or physically stressful event, such as a viral infection, may disrupt natural circadian rhythms. An inability to reset these rhythms results in a perpetual cycle of sleep disturbances. Medications that improve sleep can be very helpful for certain patients with Chronic Fatigue Syndrome, fibromyalgia and autoimmune diseases. But, until the infections are cleared and hormones are rebalanced, long-term improvement is unlikely, as the patient is likely to relapse.

Psychological, personality and social factors are strongly associated with Chronic Fatigue Syndrome, fibromyalgia, and autoimmune disease like lupus. There is a distinct complex relationship between physical and emotional factors.

What Specific Infections are Responsible

Because most of the features of Chronic Fatigue Syndrome resemble those of a lingering viral illness, many researchers have focused on the possibility that a virus or some other infectious agent, in some cases, causes the syndrome.

We have clinically determined that these patients usually have a group of viral, bacterial, parasitic and fungal infections that make up what we call Lyme Disease Complex. Some patients may or may not have actual Lyme disease but may have another type of tick-borne illness along with a host of co-infections that have brought about immunological, hormonal, and neuroendocrine changes.

Still, not all Chronic Fatigue Syndrome patients show signs of infection. And although experts have long been divided on whether infections play any role in this disorder at all, it does seem clear that subtypes of both viral and non-viral Chronic Fatigue Syndrome exist. That being said, researchers have seemingly overlooked the complexity of mute-infections, multi-toxins and heavy metal components that complicate these conditions, making them extremely difficult to diagnose on a case-to-case basis. When a complex of infections exists, they can affect the activation and replication of each other via biofilm communities. To be certain, most patients are never tested thoroughly and correctly for all the infections that make up chronic Lyme disease complex.

Infections Looking Like the Cause

The theory for Chronic Fatigue Syndrome having a viral cause is not based on hard evidence, rather, on an ever-growing series of observations. Chronic Fatigue Syndrome, as well as Fibromyalgia and Autoimmune disease patients, are often found with elevated levels of antibodies to many organisms that cause fatigue and other Chronic Fatigue Syndrome symptoms. Such organisms include those that cause Lyme disease, Candida (“yeast infection”), herpes virus type 6 (HHV-6), human T cell lymph tropic virus (HTLV), Epstein-Barr, measles, coxsackie B, cytomegalovirus, or parvovirus.

Many of these infectious agents are very common; however, none have emerged as a definitive cause of CFS. Well-designed studies of patients who met strict criteria for CFS without any known cause have not found an increased incidence of any specific infection(s).

In up to 80% of cases, CFS starts suddenly with a flu-like condition. In the U.S., there have been reports of cluster outbreaks of CFS occurring within the same household, workplace, and community (but most have not been confirmed by the Centers for Disease Control and Prevention). However, most cases of CFS occur sporadically in individuals and do not appear to be contagious. These all have the pattern of infections and more importantly, complexes of infections taking over the patient’s immune system, which is clearly seen in the depressed CD57 markers found in almost all of this population.

Infection Complexes Leading to Immune System Abnormalities and Immuno-Compromised States

CFS is sometimes referred to as “Chronic Fatigue Immune Dysfunction Syndrome.” In many cases, studies have detected many immune system irregularities. Some components appear to be over-reactive, while others appear to be under-reactive, but no consistent picture has emerged to explain CFS as a disease of the immune system in conventional medical practices. Chronic Lyme disease patients almost always have depressed CD57 marker called the striker panel and this is almost never run on chronic fatigue patients when they go to their doctor. Almost 100% of the time we find decreased key immune function in all CFS patients because we are running the correct diagnostics.

Autoimmunity Overlaps with Other Conditions

The risk profile for CFS is similar to the risk profiles for a number of autoimmune diseases. Studies are inconsistent with regards to the presence of auto-antibodies (antibodies that attack the body’s own tissues) in CFS, so the disease is unlikely to be due to auto-immunity, making it more likely connected to infectious disease. In Lyme disease patients, we typically see that the patient was diagnosed at one time or another with several autoimmune diseases, but almost certainly the previous physicians were confused. If you have any questions or would like to learn more about customized treatment options, contact us.

– See more at: http://www.envita.com/lyme-disease/finally-one-link-established-chronic-fatigue-syndrome-cfs-lupus-fibromyalgia-autoimmune-disease-chronic-lyme-disease#sthash.7GQKVYib.dpuf

Fibromyalgia Breakthrough – Treat The Causes, Not Just The Symptoms.

 

diopathic disease is defined as one that develops without any apparent or known causes. That is the term used for fibromyalgia, autoimmune diseases, including lupus and chronic fatigue syndrome. While many of these diseases have recognizable signs and symptoms, the lack of causality haunts medical schools, doctors, practices and hospitals. The only ones benefiting from lifelong symptom treatments associated with chronic fatigue syndrome, lupus, autoimmune disease, or fibromyalgia are the pharmaceutical companies who sell billions in medication to treat them. A long list of pain medications, sleep-aids, anti-depressants, and anti-inflammatories are not sufficient because the diagnosis is incorrect. Instead, let’s look at what the possible causes are to these diseases.

An Overview of Fibromyalgia Symptoms

A Conventional Scientific Overview of CFS (Chronic Fatigue Syndrome) and Fibromyalgia Causatives

Below, is a quick list of idiopathic disease causes — we will give a clinical review and explanation as to what takes place.

  • Brain abnormalities
  • Genetic factors (HPA) axis
  • A hyper-reactive immune system
  • Viral or other infectious agents like (Chronic Lyme disease Complex)
  • Psychiatric or emotional conditions

Are Genetics to Blame?

Chronic Fatigue Syndrome and fibromyalgia have been linked with genes involved in the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system. These genes regulate response to trauma, injury, and other stressful events. Our ten years of clinical experience shows that while such traumas could play a role in the etiology (the trigger to exhibiting symptoms) of the disease, they are unlikely the conditions’ causes.

What is the Hypothalamic-Pituitary-Adrenal Axis (HPA)? Does Lyme Disease Play a Role?

HPA makes up a multi-set of direct influences and feedback interactions among the hypothalamus, the pituitary gland (a pea-shaped structure located below the hypothalamus), and the adrenal, also called “suprarenal,” glands which are small, conical organs on top of the kidneys.

The interactions among these organs constitute the HPA-axis, a major part of the neuroendocrine system. From here, the body regulates reactions to stress, as well as processes such as digestion, the immune system, mood, emotions, sexuality, as well as energy. Infectious disease, such as chronic Lyme disease complex, impacts the HPA-axis via neurotoxins that compete for the same receptor sites used by the HPA-axis.

In fact, such infections can bring about identical symptoms of some idiopathic diseases listed above and many of the symptoms associated therewith. This should bring our attention to chronic Lyme Disease complex, which is composed of a number of infections and neurotoxins that bring about even more symptoms than those listed earlier in this article.

Does HPA Affect Fibromyalgia and Chronic Fatigue Syndrome?

Abnormal levels of certain chemicals regulated in the HPA axis area of the brain system have been proposed as a cause of Chronic Fatigue Syndrome and also have some influence in fibromyalgia. This system controls important functions, including sleep, stress response, and depression. Of particular interest to researchers are the chemicals and other factors listed below that are controlled by the HPA-axis.

The HPA-axis is involved in the neurobiology of mood disorders and functional illnesses, including anxiety disorder, bipolar disorder, insomnia, post-traumatic stress disorder, borderline personality disorder, ADHD, major depressive disorder, burnout, chronic fatigue syndrome, fibromyalgia, irritable bowel syndrome and alcoholism. Antidepressants, which are routinely prescribed for many of these illnesses, serve to regulate HPA-axis function. All of these conditions and their symptoms are commonly seen in chronic Lyme disease patients that contain a host of infections and neurotoxins that block serotonin receptors in the brain.

Can Chronic Lyme Disease Complex or Infectious Disease Affect HPA?

Patients may have contracted an infection at any point in their lifetime. However, the symptoms of chronic Lyme disease complex or its coinfections may remain unseen or dormant until the individual is weakened by a trauma or trigger. This could be anything from childbirth or a car accident to the death of a loved one, a divorce or even a vaccine, as seen among children with weakened immune systems.

In the etiology of chronic infectious disease, the traumatic event is a trigger, but not the cause of autoimmune disease, Chronic Fatigue Syndrome, or fibromyalgia. Nevertheless, treating these triggers is critically important to the new patient’s care. What we find is that infection and not genetic defects are at the root of HPA-axis disruption in the brain itself.

The Major Impact of Epigenetic Changes

A number of studies have found that alterations in genes are caused by infections involving immune function, intracellular communication and energy transfer. Researchers have identified many different genes in patients with Chronic Fatigue Syndrome that relate to blood disease, immune system function, and infection.

However, despite these identifications, there is no clear pattern to them and it is quite possible that it is the infections alone that are altering these genes and are responsible for impacting mental and emotional health as well. It is very possible that the infections can alter these genes that impact mental and emotional health as well.

Important Neurotransmitters Changed By Neurotoxins Competing For Receptor Sites

Some patients with Chronic Fatigue Syndrome have abnormally high levels of serotonin, a neurotransmitter (chemical messenger in the brain), and also show deficiencies in dopamine, an important neurotransmitter associated with feelings of reward. In some cases there is also a demonstrable imbalance between norepinephrine and dopamine.

A number of studies on Chronic Fatigue Syndrome have shown patients have lower cortisol levels, a stress hormone produced by the adrenal glands. It has been suggested that such cortisol deficiencies are responsible for Chronic Fatigue Syndrome patients having impaired or weakened responses to psychological or physical stresses like worry, infection, or exercise. However, administering replacement cortisol improves symptoms only in some patients. Why? Infection and their toxins (neurotoxins) must be cleared before hormone replacement can begin to be effective in these patients. It is also common for these patients to have thyroid, testosterone and cortisol issues.

Idiopathic Diseases at Root of Myriad Psychological Disorders Including Sleep-Related Ailments

Evidence suggests that certain CFS, fibromyalgia, and autoimmune patients have disturbed circadian rhythms (disorder of the sleep-wake cycle), which is regulated by the so-called circadian clock, a nerve cluster in the HPA-axis. These are commonly seen in chronic Lyme disease complex along with a number of other neurological symptoms.

A mentally or physically stressful event, such as a viral infection, may disrupt natural circadian rhythms. An inability to reset these rhythms results in a perpetual cycle of sleep disturbances. Medications that improve sleep can be very helpful for certain patients with Chronic Fatigue Syndrome, fibromyalgia and autoimmune diseases. But, until the infections are cleared and hormones are rebalanced, long-term improvement is unlikely, as the patient is likely to relapse.

Psychological, personality and social factors are strongly associated with Chronic Fatigue Syndrome, fibromyalgia, and autoimmune disease like lupus. There is a distinct complex relationship between physical and emotional factors.

What Specific Infections are Responsible

Because most of the features of Chronic Fatigue Syndrome resemble those of a lingering viral illness, many researchers have focused on the possibility that a virus or some other infectious agent, in some cases, causes the syndrome.

We have clinically determined that these patients usually have a group of viral, bacterial, parasitic and fungal infections that make up what we call Lyme Disease Complex. Some patients may or may not have actual Lyme disease but may have another type of tick-borne illness along with a host of co-infections that have brought about immunological, hormonal, and neuroendocrine changes.

Still, not all Chronic Fatigue Syndrome patients show signs of infection. And although experts have long been divided on whether infections play any role in this disorder at all, it does seem clear that subtypes of both viral and non-viral Chronic Fatigue Syndrome exist. That being said, researchers have seemingly overlooked the complexity of mute-infections, multi-toxins and heavy metal components that complicate these conditions, making them extremely difficult to diagnose on a case-to-case basis. When a complex of infections exists, they can affect the activation and replication of each other via biofilm communities. To be certain, most patients are never tested thoroughly and correctly for all the infections that make up chronic Lyme disease complex.

Infections Looking Like the Cause

The theory for Chronic Fatigue Syndrome having a viral cause is not based on hard evidence, rather, on an ever-growing series of observations. Chronic Fatigue Syndrome, as well as Fibromyalgia and Autoimmune disease patients, are often found with elevated levels of antibodies to many organisms that cause fatigue and other Chronic Fatigue Syndrome symptoms. Such organisms include those that cause Lyme disease, Candida (“yeast infection”), herpes virus type 6 (HHV-6), human T cell lymph tropic virus (HTLV), Epstein-Barr, measles, coxsackie B, cytomegalovirus, or parvovirus.

Many of these infectious agents are very common; however, none have emerged as a definitive cause of CFS. Well-designed studies of patients who met strict criteria for CFS without any known cause have not found an increased incidence of any specific infection(s).

In up to 80% of cases, CFS starts suddenly with a flu-like condition. In the U.S., there have been reports of cluster outbreaks of CFS occurring within the same household, workplace, and community (but most have not been confirmed by the Centers for Disease Control and Prevention). However, most cases of CFS occur sporadically in individuals and do not appear to be contagious. These all have the pattern of infections and more importantly, complexes of infections taking over the patient’s immune system, which is clearly seen in the depressed CD57 markers found in almost all of this population.

Infection Complexes Leading to Immune System Abnormalities and Immuno-Compromised States

CFS is sometimes referred to as “Chronic Fatigue Immune Dysfunction Syndrome.” In many cases, studies have detected many immune system irregularities. Some components appear to be over-reactive, while others appear to be under-reactive, but no consistent picture has emerged to explain CFS as a disease of the immune system in conventional medical practices. Chronic Lyme disease patients almost always have depressed CD57 marker called the striker panel and this is almost never run on chronic fatigue patients when they go to their doctor. Almost 100% of the time we find decreased key immune function in all CFS patients because we are running the correct diagnostics.

Autoimmunity Overlaps with Other Conditions

The risk profile for CFS is similar to the risk profiles for a number of autoimmune diseases. Studies are inconsistent with regards to the presence of auto-antibodies (antibodies that attack the body’s own tissues) in CFS, so the disease is unlikely to be due to auto-immunity, making it more likely connected to infectious disease. In Lyme disease patients, we typically see that the patient was diagnosed at one time or another with several autoimmune diseases, but almost certainly the previous physicians were confused. If you have any questions or would like to learn more about customized treatment options, contact us.

– See more at: http://www.envita.com/lyme-disease/finally-one-link-established-chronic-fatigue-syndrome-cfs-lupus-fibromyalgia-autoimmune-disease-chronic-lyme-disease#sthash.7GQKVYib.dpuf

diopathic disease is defined as one that develops without any apparent or known causes. That is the term used for fibromyalgia, autoimmune diseases, including lupus and chronic fatigue syndrome. While many of these diseases have recognizable signs and symptoms, the lack of causality haunts medical schools, doctors, practices and hospitals. The only ones benefiting from lifelong symptom treatments associated with chronic fatigue syndrome, lupus, autoimmune disease, or fibromyalgia are the pharmaceutical companies who sell billions in medication to treat them. A long list of pain medications, sleep-aids, anti-depressants, and anti-inflammatories are not sufficient because the diagnosis is incorrect. Instead, let’s look at what the possible causes are to these diseases.

An Overview of Fibromyalgia Symptoms

A Conventional Scientific Overview of CFS (Chronic Fatigue Syndrome) and Fibromyalgia Causatives

Below, is a quick list of idiopathic disease causes — we will give a clinical review and explanation as to what takes place.

  • Brain abnormalities
  • Genetic factors (HPA) axis
  • A hyper-reactive immune system
  • Viral or other infectious agents like (Chronic Lyme disease Complex)
  • Psychiatric or emotional conditions

Are Genetics to Blame?

Chronic Fatigue Syndrome and fibromyalgia have been linked with genes involved in the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system. These genes regulate response to trauma, injury, and other stressful events. Our ten years of clinical experience shows that while such traumas could play a role in the etiology (the trigger to exhibiting symptoms) of the disease, they are unlikely the conditions’ causes.

What is the Hypothalamic-Pituitary-Adrenal Axis (HPA)? Does Lyme Disease Play a Role?

HPA makes up a multi-set of direct influences and feedback interactions among the hypothalamus, the pituitary gland (a pea-shaped structure located below the hypothalamus), and the adrenal, also called “suprarenal,” glands which are small, conical organs on top of the kidneys.

The interactions among these organs constitute the HPA-axis, a major part of the neuroendocrine system. From here, the body regulates reactions to stress, as well as processes such as digestion, the immune system, mood, emotions, sexuality, as well as energy. Infectious disease, such as chronic Lyme disease complex, impacts the HPA-axis via neurotoxins that compete for the same receptor sites used by the HPA-axis.

In fact, such infections can bring about identical symptoms of some idiopathic diseases listed above and many of the symptoms associated therewith. This should bring our attention to chronic Lyme Disease complex, which is composed of a number of infections and neurotoxins that bring about even more symptoms than those listed earlier in this article.

Does HPA Affect Fibromyalgia and Chronic Fatigue Syndrome?

Abnormal levels of certain chemicals regulated in the HPA axis area of the brain system have been proposed as a cause of Chronic Fatigue Syndrome and also have some influence in fibromyalgia. This system controls important functions, including sleep, stress response, and depression. Of particular interest to researchers are the chemicals and other factors listed below that are controlled by the HPA-axis.

The HPA-axis is involved in the neurobiology of mood disorders and functional illnesses, including anxiety disorder, bipolar disorder, insomnia, post-traumatic stress disorder, borderline personality disorder, ADHD, major depressive disorder, burnout, chronic fatigue syndrome, fibromyalgia, irritable bowel syndrome and alcoholism. Antidepressants, which are routinely prescribed for many of these illnesses, serve to regulate HPA-axis function. All of these conditions and their symptoms are commonly seen in chronic Lyme disease patients that contain a host of infections and neurotoxins that block serotonin receptors in the brain.

Can Chronic Lyme Disease Complex or Infectious Disease Affect HPA?

Patients may have contracted an infection at any point in their lifetime. However, the symptoms of chronic Lyme disease complex or its coinfections may remain unseen or dormant until the individual is weakened by a trauma or trigger. This could be anything from childbirth or a car accident to the death of a loved one, a divorce or even a vaccine, as seen among children with weakened immune systems.

In the etiology of chronic infectious disease, the traumatic event is a trigger, but not the cause of autoimmune disease, Chronic Fatigue Syndrome, or fibromyalgia. Nevertheless, treating these triggers is critically important to the new patient’s care. What we find is that infection and not genetic defects are at the root of HPA-axis disruption in the brain itself.

The Major Impact of Epigenetic Changes

A number of studies have found that alterations in genes are caused by infections involving immune function, intracellular communication and energy transfer. Researchers have identified many different genes in patients with Chronic Fatigue Syndrome that relate to blood disease, immune system function, and infection.

However, despite these identifications, there is no clear pattern to them and it is quite possible that it is the infections alone that are altering these genes and are responsible for impacting mental and emotional health as well. It is very possible that the infections can alter these genes that impact mental and emotional health as well.

Important Neurotransmitters Changed By Neurotoxins Competing For Receptor Sites

Some patients with Chronic Fatigue Syndrome have abnormally high levels of serotonin, a neurotransmitter (chemical messenger in the brain), and also show deficiencies in dopamine, an important neurotransmitter associated with feelings of reward. In some cases there is also a demonstrable imbalance between norepinephrine and dopamine.

A number of studies on Chronic Fatigue Syndrome have shown patients have lower cortisol levels, a stress hormone produced by the adrenal glands. It has been suggested that such cortisol deficiencies are responsible for Chronic Fatigue Syndrome patients having impaired or weakened responses to psychological or physical stresses like worry, infection, or exercise. However, administering replacement cortisol improves symptoms only in some patients. Why? Infection and their toxins (neurotoxins) must be cleared before hormone replacement can begin to be effective in these patients. It is also common for these patients to have thyroid, testosterone and cortisol issues.

Idiopathic Diseases at Root of Myriad Psychological Disorders Including Sleep-Related Ailments

Evidence suggests that certain CFS, fibromyalgia, and autoimmune patients have disturbed circadian rhythms (disorder of the sleep-wake cycle), which is regulated by the so-called circadian clock, a nerve cluster in the HPA-axis. These are commonly seen in chronic Lyme disease complex along with a number of other neurological symptoms.

A mentally or physically stressful event, such as a viral infection, may disrupt natural circadian rhythms. An inability to reset these rhythms results in a perpetual cycle of sleep disturbances. Medications that improve sleep can be very helpful for certain patients with Chronic Fatigue Syndrome, fibromyalgia and autoimmune diseases. But, until the infections are cleared and hormones are rebalanced, long-term improvement is unlikely, as the patient is likely to relapse.

Psychological, personality and social factors are strongly associated with Chronic Fatigue Syndrome, fibromyalgia, and autoimmune disease like lupus. There is a distinct complex relationship between physical and emotional factors.

What Specific Infections are Responsible

Because most of the features of Chronic Fatigue Syndrome resemble those of a lingering viral illness, many researchers have focused on the possibility that a virus or some other infectious agent, in some cases, causes the syndrome.

We have clinically determined that these patients usually have a group of viral, bacterial, parasitic and fungal infections that make up what we call Lyme Disease Complex. Some patients may or may not have actual Lyme disease but may have another type of tick-borne illness along with a host of co-infections that have brought about immunological, hormonal, and neuroendocrine changes.

Still, not all Chronic Fatigue Syndrome patients show signs of infection. And although experts have long been divided on whether infections play any role in this disorder at all, it does seem clear that subtypes of both viral and non-viral Chronic Fatigue Syndrome exist. That being said, researchers have seemingly overlooked the complexity of mute-infections, multi-toxins and heavy metal components that complicate these conditions, making them extremely difficult to diagnose on a case-to-case basis. When a complex of infections exists, they can affect the activation and replication of each other via biofilm communities. To be certain, most patients are never tested thoroughly and correctly for all the infections that make up chronic Lyme disease complex.

Infections Looking Like the Cause

The theory for Chronic Fatigue Syndrome having a viral cause is not based on hard evidence, rather, on an ever-growing series of observations. Chronic Fatigue Syndrome, as well as Fibromyalgia and Autoimmune disease patients, are often found with elevated levels of antibodies to many organisms that cause fatigue and other Chronic Fatigue Syndrome symptoms. Such organisms include those that cause Lyme disease, Candida (“yeast infection”), herpes virus type 6 (HHV-6), human T cell lymph tropic virus (HTLV), Epstein-Barr, measles, coxsackie B, cytomegalovirus, or parvovirus.

Many of these infectious agents are very common; however, none have emerged as a definitive cause of CFS. Well-designed studies of patients who met strict criteria for CFS without any known cause have not found an increased incidence of any specific infection(s).

In up to 80% of cases, CFS starts suddenly with a flu-like condition. In the U.S., there have been reports of cluster outbreaks of CFS occurring within the same household, workplace, and community (but most have not been confirmed by the Centers for Disease Control and Prevention). However, most cases of CFS occur sporadically in individuals and do not appear to be contagious. These all have the pattern of infections and more importantly, complexes of infections taking over the patient’s immune system, which is clearly seen in the depressed CD57 markers found in almost all of this population.

Infection Complexes Leading to Immune System Abnormalities and Immuno-Compromised States

CFS is sometimes referred to as “Chronic Fatigue Immune Dysfunction Syndrome.” In many cases, studies have detected many immune system irregularities. Some components appear to be over-reactive, while others appear to be under-reactive, but no consistent picture has emerged to explain CFS as a disease of the immune system in conventional medical practices. Chronic Lyme disease patients almost always have depressed CD57 marker called the striker panel and this is almost never run on chronic fatigue patients when they go to their doctor. Almost 100% of the time we find decreased key immune function in all CFS patients because we are running the correct diagnostics.

Autoimmunity Overlaps with Other Conditions

The risk profile for CFS is similar to the risk profiles for a number of autoimmune diseases. Studies are inconsistent with regards to the presence of auto-antibodies (antibodies that attack the body’s own tissues) in CFS, so the disease is unlikely to be due to auto-immunity, making it more likely connected to infectious disease. In Lyme disease patients, we typically see that the patient was diagnosed at one time or another with several autoimmune diseases, but almost certainly the previous physicians were confused. If you have any questions or would like to learn more about customized treatment options, contact us.

– See more at: http://www.envita.com/lyme-disease/finally-one-link-established-chronic-fatigue-syndrome-cfs-lupus-fibromyalgia-autoimmune-disease-chronic-lyme-disease#sthash.7GQKVYib.dpuf

Rebecca Ehalt may have missed her dog while away in Europe, but it’s clear that her pet schnauzer missed her so much that it knocked the poor pooch off her feet — literally.

 

Ehalt visited her family’s home in Pennsylvania earlier this week from Slovenia, where she’s currently living, for a wedding reception that her parents had planned for Ehalt and her husband. Upon returning, she reunited with her 9-year-old schnauzer, Casey, whom she hadn’t seen in two years.

Video: After two years apart, a dog finally reunited with his owner, only to pass out from the overwhelming joy. Carson Daly reports from the Orange Room.

The video shows Casey excitedly jumping on Ehalt and attempting to smother her with kisses. But the happiness at Ehalt’s return is eventually a bit too much for her, and the little pooch wobbles a little bit before passing out on the ground.

Ehalt, who uploaded the video to YouTube on Thursday, conceded that the reaction might be because the absence felt much longer to her pup. Their two-year separation “in fairness is 14 years in dog years,” she wrote in the caption with the video.

“I think the video really says it,” Ehalt’s sister, Rachel Abbett, told TODAY.com about the reunion.

As for the high-pitched noises Casey makes, that’s apparently normal for schnauzers. “Anyone who’s familiar with the breed knows they’re a little higher pitched,” Abbett said.

Though Abbett said they’ve never seen Casey faint before and that they were initially worried about her, Casey was given a clean bill of health after a visit to the vet Friday morning — a happy ending to an even happier video.

via Dog faints after being reunited with owner after 2 years apart – Pets – TODAY.com.

It was surprising when scientists discovered a new part of the human body earlier this year, but understandable that it had gone undetected for so long given that it’s only 15 microns thick (it’s in the eye). But another, larger part of the human body will now need to be added to anatomy books.

A ligament has been hiding in the knees of most — but not all — people.

A French surgeon in 1879 speculated that an additional ligament might be located in the front of the knee, but it wasn’t until 134 years later that Belgian knee surgeons have identified it.

The newly identified knee ligament, which was thought to exist for more than a century but just recently proven, is called anterolateral ligament. (Image source:

The newly identified knee ligament, which was thought to exist for more than a century but just recently proven, is called anterolateral ligament. (Image source: University Hospitals Leuven)

For four years, Dr. Steven Claes and Dr. Johan Bellemans, orthopedic surgeons with the University Hospitals Leuven, researched ACL tear repairs and “pivot shift” issues — when the knee gives out — that seemed to be related.

Claes and Belleman’s found the new anterolateral ligament (ALL) in 97 percent (40 of the 41) of cadaver knees they studied. Further research showed this “pivot shift” was the result of an ALL injury.

The discovery of ALL clarifies what the study authors called in their abstract a “long-standing enigma” regarding a ligament connecting the femur with the anterolateral tibia.

The new find was published in the Journal of Anatomy.

Going forward, Claes and Bellemans are trying to develop a surgical technique to correct ALL injuries.

via New Human Body Part Discovered — But Not Everyone May Have It | TheBlaze.com.

Wait, you mean not everyone has out-of-body experiences at their own will?

 

It was apparently a surprise for a University of Ottawa graduate student studying psychology that it was unusual for her to be able to will herself out of her body, as she claims she can do.

 

Scientists monitored activity in the woman's brain using functional MRI while she willed herself out of her body. (Photo credit: Shutterstock)

Scientists monitored activity in the woman’s brain using functional MRI while she willed herself out of her body. (Photo credit: Shutterstock)

 

According to a case study published in the journal Frontiers in Human Neuroscience, the woman not only described what this was like but researchers studied her brain while she had an “extra-corporeal experience.”

 

The 24-year-old was an undergraduate when she learned that having an out-of-body experience was not necessarily the norm.

 

“She appeared surprised that not everyone could experience this,” the study authors wrote.

 

She first remembers willing herself out of her body when she was in preschool, using it as a “distraction during the time kids were asked to nap.” As she grew up, she assumed “everyone could do it.”

 

When in such a state she said she could see herself in the air above her body. She could watch herself move but was aware that her “real” body was not moving.

 

“I feel myself moving, or, more accurately, can make myself feel as if I am moving. I know perfectly well that I am not actually moving,” she told the researchers. “There is no duality of body and mind when this happens, not really. In fact, I am hyper-sensitive to my body at that point, because I am concentrating so hard on the sensation of moving. I am the one moving – me – my body. For example, if I ‘spin’ for long enough, I get dizzy. I do not see myself above my body. Rather, my whole body has moved up. I feel it as being above where I know it actually is. I usually also picture myself as moving up in my mind’s eye, but the mind is not substantive. It does not move unless the body does.”

 

In the case study, researchers conducted tests that included MRI analysis and questionnaires. What they found was that the brain during such “extra-corporeal experiences” exhibited activation in areas that are consistent with other studies about out-of-body experiences, which neurologists had associated with hallucinations.

 

These images show activated areas of the brain while the woman was supposedly having an out-of-body experience. (Image source: Andra M. Smith and Claude Messier/University of Ottawa/Frontiers in Human Neuroscience)

These images show activated areas of the brain while the woman was supposedly having an out-of-body experience. (Image source: Andra M. Smith and Claude Messier/University of Ottawa/Frontiers in Human Neuroscience)

 

Here are a couple bullets of some of the specific observations made of her brain:

 

  • The results suggest that the ECE reported here represents an unusual type of kinesthetic imagery that shares some features of previously described out-of-body experiences and some features of more typical motor imagery.

  • The cerebellum also shows strong activation that is consistent with the participant’s report of the impression of movement during the ECE. There are also left middle and superior orbital frontal gyri activations, structures often associated with action monitoring.

The researchers called the woman’s experience “a novel one,” as she was healthy, young and didn’t have any brain abnormalities.

 

They acknowledged that there are limitations to the study in that it only relies on one woman’s account. However, they wrote that due to her level of detail and unusual descriptions, “we are inclined to take her report at face value.”

Overall, the authors believe this woman’s experience could mean that others have such an ability to will themselves out of their bodies as well, but, perhaps like this woman, they don’t report it because they think it is normal and widely experienced. The researchers also wondered whether if it is an ability held by infants and children that is lost and forgotten without practice.

Scientists Scanned Woman’s Brain During ‘Out-of-Body Experience’ and This Is What They Found | TheBlaze.com.

9 Things to Know About Reviving the Recently Dead

By Greg Miller

In 1986, a two-and-a-half year-old girl named Michelle Funk fell into a stream and drowned. By the time paramedics found her, she hadn’t been breathing for more than an hour. Her heart was stopped. In other words, she was dead. Somewhat inexplicably, the paramedics continued to work on her, and so did doctors in the emergency room. Then, three hours after she died, Michelle Funk took a breath and her heart fluttered back into action.

Funk’s case inspired David Casarett to go to medical school, with plans to become an ER doctor. He wanted to bring people back to life. Casarett is now an associate professor of medicine at the University of Pennsylvania. In his new book, Shocked: Adventures in Bringing Back the Recently Dead, he explores the history, science, and moral hazards of reviving the recently dead.

jacket-image-SHOCKED

Casarett is enthusiastic about the emerging technologies that are allowing doctors to save patients who would have been a lost cause in the very recent past. But these technologies come at a cost, he writes. They may restore life, but whether it’s a life worth living is another matter.

As inspired as he was by Funk’s near-miraculous revival, Casarett has also seen heartbreaking cases in which patients were revived with heroic efforts—only to languish, unresponsive, in an ICU for weeks while their families agonize over how long to maintain life support. Those cases caused Casarett to abandon his plans to become an ER doc. He now focuses on easing the suffering of patients near the end of life as a palliative care and hospice doctor.

Here are a few things he’d like you to know about reviving the dead.

Be glad you weren’t recently deceased in the 18th century

In the 1700s, Good Samaritans in several European cities began to take a keen interest in reviving people who appeared to have drowned. Their methods seem dubious today: throwing the no-longer breathing person onto a trotting horse or dunking them in freezing water, tickling the back of the throat with a feather, blowing tobacco smoke into the rectum, or administering a good whipping.

But not all these methods are totally without scientific grounding, Casarett writes. The up and down motion of a trotting horse could move the diaphragm and chest walls in and out enough to force air in and out of the lungs and stimulate some circulation, not unlike CPR. And tobacco smoke contains nicotine, which prompts the brain to release epinephrine, which in turn increases the rate and strength of the heart’s contractions. In fact, epinephrine is a key item in modern day crash carts.

“Some of the techniques they tried back then were bizarre, but some of them actually turned out to be direct ancestors of things we use today,” Casarett said. “Mouth-to mouth resuscitation was pioneered, as far as I can tell, in Amsterdam in the late 18th century, and it’s still a mainstay of resuscitation today.”

If you want to die and live to tell about it, go somewhere cold

Casarett recounts several remarkable tales of people who defied the odds by coming back to life after an hour or more without breathing and without a pulse. A young Swedish woman, for example, survived 80 minutes trapped under the ice in a frozen stream. In all these cases, the person was somewhere cold.

That’s not a coincidence. When cells are deprived of oxygen and nutrients, they soon begin to self-destruct. Cold delays this process by reducing cells’ metabolic needs. That allows the brain and other organs to escape damage for far longer than they would have otherwise. “If this happened at room temperature, there’s virtually no chance they would have survived, at least not cognitively intact,” Casarett said.

“Today, some of the most exciting work in resuscitation medicine involves making people cold,” he said.

Otherwise, try Pittsburgh

Indeed, a clinical trial underway at the University of Pittsburgh Medical Center will put this idea to the test in trauma patients. Only in dire cases where massive blood loss has caused cardiac arrest, doctors will replace the patient’s blood with ice-cold saline solution in hopes of buying time to repair the wounds before cells and organs begin to break down. There’s been some ethical discussion about the trial because the patients will be unconscious and therefore unable to give informed consent (people can request a bracelet that would let doctors know they wish to opt out).

Casarett says he’s not familiar enough with the details of the trial to comment on the ethical issues, but he’s fascinated by the science behind it. In Shocked, he describes some of the experiments with dogs and pigs that laid the foundation for the trial. “This isn’t just a half-baked idea, it has a pretty strong basis in molecular biology,” he said.

“If you’re going to get in an accident anywhere in the U.S. in the next few years, I would try to have it happen in Pittsburgh,” Casarett said. “You’d have a chance of getting what may become the standard of care in the next five or ten years.”

The squirrels have secrets

Hibernation is the way animals like bears and squirrels ramp down their metabolism to survive winter. If humans could be put in a similar state of suspended animation, it might be an alternative to putting them on ice (or replacing their blood with freezing saline) to preserve the brain and other organs.

For all its advantages, cooling patients has its disadvantages too: It makes it harder to restore a normal heart rhythm and it requires a lot of equipment, making it difficult to use outside a hospital. A chemical that could do the same thing might be more effective and more widely useful, Casarett says.

In researching Shocked, he visited the labs of scientists trying to understand the biochemical changes that occur when animals like squirrels, mice, and lemurs (the only known hibernating primates) enter a hypometabolic state. It’s still early days, but Casarett says it’s not too crazy to imagine a future in which crash carts and ambulances carry a drug derived from a compound found in hibernating animals. “Imagine a drug that could do everything that buckets of ice could do, but could do it much more quickly in a single injection,” he said. “That would be the goal.”

Don’t waste your money on cryonics

The most lively chapter in Shocked recounts Casarett’s visit to a cryonics convention, where he meets people willing to pony up $200,000 to put their bodies on ice after they die, in hopes that scientists will eventually come up with a cure for whatever killed them.

“I had expected to be in a room full of freaks and geeks, and certainly some people were completely nuts, but I was surprised by the degree to which some people were really very knowledgeable,” he said.

He was impressed by scientific talks on how to cool a recently deceased body as quickly as possible and how to freeze it without the formation of ice crystals, which can tear tissue apart and throw electrolyte concentrations out of whack.

All in all, however, he left unconvinced that cryonauts will be successfully frozen and reanimated anytime soon. “I can think of a lot of other ways to spend that money,” he said.

Kiss the dummy and shock strangers

Blowing into someone’s mouth and pumping on their chest during CPR helps get a little bit of oxygen into their blood and circulate it until an ambulance arrives. It saves lives, and Casarett wants everyone to take a course and practice on Annie, the ubiquitous CPR training dummy.

Even people who don’t know CPR can save the life of someone in cardiac arrest with an automated electronic defibrillator (AED). These devices can detect an abnormal heart rhythm and issue voice commands to guide even a novice user to apply an electric shock to correct it. Together, more people trained in CPR and more AEDs in public places, constitute a strategy for what Casarett calls crowdsourced survival.

We’re not there yet, though. A colleague of his at Penn has found that AEDs are more common in rich areas of Philadelphia than in lower income neighborhoods. And California’s Supreme Court recently ruled that big box retailers like Target aren’t obligated to have an AED in their stores.

Resuscitation doesn’t work like you see on TV

The biggest difference between resuscitation as shown on TV medical dramas and reality is the likelihood of success, Casarett says. “On TV they make it look much easier and more effective than it is in real life.” He notes that one study in the 1990s actually tried to quantify this: the researchers found that 75 percent of people who received CPR in several TV medical dramas survived, compared to less than 30 percent in real life.

Another difference: Recently revived people often throw up. That’s because when you’re unconscious, your muscles relax, including the sphincter muscle at the bottom of your esophagus that normally keeps your stomach contents from coming back up. Relax that muscle in someone lying on their back while another person is pounding on their chest, and… it’s easy to understand why the recently revived often have some spitting up to do. “That’s something you usually don’t see on television,” Casarett said.

Dying isn’t as simple as it used to be

The line between alive and dead is getting blurrier thanks to advances in technology, Casarett writes. “Several emergency room physicians I talked to told me that even five years ago, when confronted with a cardiac arrest patient, you would run through the routine, do what you could, and then it would be pretty clear at some point that you’d exhausted your bag of tricks and there was nothing else you could do,” Casarett said. But now there are more and more things to try.

For example, extracorporeal membrane oxygenation machines can withdraw the blood of a patient in heart failure, oxygenate it, and pump it back into the body, keeping them alive—or something like it. “That line is getting more difficult to define because of all these technologies,” Casarett said.

Coming back from the dead comes at a cost

Restoring life may be getting easier, but the quality of that life can be questionable, especially when a revived patient never regains consciousness. “It’s not a chance to say goodbye or even grieve, it just draws out the dying process,” Casarett said. And then there’s the issue no one likes to talk about, the financial costs, which can run to more than $20,000 a day.

As medical science marches forward, we can expect more incredible stories of revival, Casarett writes. But we also have to expect more hard decisions about the emotional and financial costs of these new technologies, and what kind of life—and death—they’ll provide.

 

9 Things to Know About Reviving the Recently Dead | Science | WIRED.

A Toronto doctor who specializes in the treatment of tropical diseases says it’s unlikely a recent outbreak of the deadly Ebola virus in West Africa could spread to North America.

Dr. Jay Keystone, who works in the tropical diseases unit of Toronto General Hospital, was interviewed Wednesday on CBC Radio’s Metro Morning.

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A woman puts on a protective mask to protect against SARS at a wash station at the entrance to North York General Hospital in Toronto in May 2003. (Kevin Frayer/Canadian Press)

He said the SARS outbreak in 2003 that killed more than 40 people in Toronto helped improve how we identify, treat and contain infections diseases. He said such measures are lacking in countries affected by the current Ebola outbreak: Guinea, Liberia and Sierra Leone

As of July 23, the number of Ebola cases in West Africa reached 1,201, with 672 deaths, according to the World Health Organization.

The fast-acting Ebola virus, which first appeared in 1976, produces a violent hemorrhagic fever that leads to internal and external bleeding. The infection is transmitted by direct contact with blood, bodily fluids, and tissues of infected people or animals.

Though there is no vaccine and no specific treatment for Ebola, Keystone said there are a number of measures travellers to the region can take to protect themselves.

Here’s what Keystone told Metro Morning guest host David Common:

How does a person contract Ebola?

“They usually acquire it from close contact with blood and body fluids, and that means someone coughs in your face, you handle a body or you look after someone and don’t have ideal infection-control methods. You get the virus on your hands, you touch your nose, your mouth.”

What symptoms do Ebola patients show?

“It looks like the flu: fever, headache, sore throat, muscle aches and pains. That’s in the first few days. And then vomiting, diarrhea and the really serious part of the illness — that is the hemorrhage part — really doesn’t occur until toward the end of the first week.”

Once a patient is hemorrhaging, can they be saved?

“It all depends on the quality of medical care. Most Ebola outbreaks have occurred in villages, in mission hospitals where essentially they have a very poor level of health care and very poor infection control methods. The mortally rate in this outbreak … is about 60 per cent. So you can survive. The better the care, more likely you are to survive but there’s no antibiotic or anti-viral agent to treat this disease.”

Why has this outbreak been so bad?

“First, there’s a lot of cross-border travel. Whereas most other outbreaks have been isolated in the middle of virtually nowhere. Also, people in these countries don’t trust the government. They don’t believe in the infection. They hide their cases. If someone dies, they take [the body] home. And unfortunately the funeral procedures where you touch the body, and handle the body, markedly increases your risk. These cases are now more in central areas, cities rather than tiny villages. All of those reasons I think have compounded to make this a much greater outbreak.”

Doctors treating patients in Africa have died. Foreign doctors have been infected. Should we be worried about Ebola making its way to Canada?

“I don’t think we need to be worried. Health-care providers, paramedics, the people who deal with the situation first-hand, I think we’re the ones who have greatest risk. You have to remember since 1976 when this virus was first described, there are less than a handful of cases of [patients] who’ve gone to North American or European countries and very rarely is there secondary transmission. And that’s because we have much better public health, infrastructure and certainly better methods of isolating [patients]. SARS was a perfect wake-up call and Ebola is following that … our health-care system improved dramatically after SARS.”

What do doctors in West Africa need to do to control the outbreak now?

“Mostly it’s case finding. And that’s the biggest problem. Someone comes in ill, they go back to their village and other people are infected but no one knows about it. The problem is they don’t have enough personnel to follow up carefully and also people are hiding cases. It’s all about case finding, surveillance, making the diagnosis, isolating the individuals and using appropriate isolation procedures. That will help, but it’s going to take a long time given what’s going on there.

What should people travelling to West Africa know and do to protect themselves?

“The most important thing is to try and stay away from people who are ill. You won’t get Ebola unless the individual you’re in contact with is sick. So if someone is well, you’re not going to get it. So you just need to have a heightened awareness that this is going on and wash your hands frequently, certainly before meals. [Ebola is spread through] direct contact, it’s not someone walking into a room with someone with Ebola and getting the infection. Ebola generally is not aerosolized, meaning it doesn’t go well into the air.”

 

Ebola virus: What you need to know to protect yourself – Toronto – CBC News.