U.S. sees diabetes rates skyrocket

By Agence France-Presse Thursday, November 15, 2012 20:56 EST

HHS

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The United States saw a dramatic rise in the number of adults suffering from diabetes between 1995 and 2010, according to official statistics released Thursday.

The prevalence of the disease increased by at least 50 percent in 42 of the country’s 50 states. In 18 of those, the rate at least doubled, according to a study by the Centers for Disease Control and Prevention.

“Regionally, we saw the largest increase in diagnosed diabetes prevalence in the South, followed by the West, Midwest, and Northeast,” said Linda Geiss, lead author of the report.

The states that saw the highest rise in cases included Oklahoma (226 percent), Kentucky (158 percent), Georgia (145 percent), Alabama (140 percent) and Washington (135 percent).

In 1995, only three states along with the District of Columbia — home of the nation’s capital, Washington — and Puerto Rico had a diagnosed diabetes prevalence of at least six percent.

But by 2010, all 50 US states recorded a prevalence of more than six percent, said Ann Albright, who heads the CDC’s Division of Diabetes Translation.

“These rates will continue to increase until effective interventions and policies are implemented to prevent both diabetes and obesity,” she said in a statement. More than a third of American adults are obese.

Type 2 diabetes, which accounts for 90-95 percent of all diabetes cases in the United States, could be prevented by making lifestyle changes, the statement said.

The CDC, together with its partners, is working on initiatives to prevent type 2 diabetes and minimize complications in those already diagnosed with the disease.

The study used data from an annual telephone survey of health behaviors and conditions of US adults aged 18 and older.

 

http://www.rawstory.com/rs/2012/11/15/u-s-sees-diabetes-rates-skyrocket/

OHSU research suggests America may over-vaccinate

 

 

PORTLAND, Ore. –A new study published in the New England Journal of Medicine this week by Oregon Health & Science University researchers suggests that timelines for vaccinating and revaccinating Americans against disease should possibly be reevaluated and adjusted. The study shows that in many cases, the established duration of protective immunity for many vaccines is greatly underestimated. This means that people are getting booster shots when their immunity levels most likely do not require it. The results are published in the November 8 edition of the journal

 

“The goal of this study was to determine how long immunity could be maintained after infection or vaccination. We expected to see long-lived immunity following a viral infection and relatively short-lived immunity after vaccination, especially since this is the reasoning for requiring booster vaccinations. Surprisingly, we found that immunity following vaccination with tetanus and diphtheria was much more long-lived than anyone realized and that antibody responses following viral infections were essentially maintained for life,” explained Mark Slifka, Ph.D. Slifka serves as an associate scientist at the Vaccine and Gene Therapy Institute with joint appointments at the Oregon National Primate Research Center and the department of molecular microbiology and immunology in the OHSU School of Medicine.

 

The research also reconfirmed a previous finding by Slifka and his colleagues: that the duration of immunity after smallpox vaccination is much longer than previously thought. In that earlier study published in the journal Nature Medicine in 2003, these OHSU researchers observed surprisingly long-lived antiviral antibody responses but they were unable to measure the slow rate of decline. In this current study, they demonstrate that this type of immunity is maintained with a calculated half-life of 92 years – a number that is substantially longer than the estimate of only 3 to 5 years of immunity following vaccination that was previously proposed by experts at the Centers for Disease Control and Prevention.

 

“Another example is the tetanus vaccine,” said Slifka. “Doctors are told that vaccination is effective for a period of 10 years – but after that, people should be revaccinated. Based on our studies and the work of others, once a person has received their primary series of vaccinations they are likely to be protected for at least three decades. Indeed, other countries such as Sweden have changed their vaccination policies and doctors are advised to offer tetanus revaccination only once every 30 years.” Importantly, this has not resulted in any increase in the number of tetanus cases in Sweden and demonstrates first-hand that switching from the 10-year to 30-year policy is safe and effective. Taking this small step in vaccination scheduling could save hundreds of millions of dollars on health care here in the US.”

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Common cold virus can cause polio in mice when injected into muscles

Contact: Becky Levine Levin005@mc.duke.edu 919-684-4148 Duke University Medical Center

Common cold virus can cause polio in mice when injected into muscles

DURHAM, N.C. — Virologists at Duke University Medical Center have discovered that, under the right conditions, a common cold virus closely related to poliovirus can cause polio in mice.

The researchers injected a cold virus called Coxsackievirus A21 into mice that were engineered to be susceptible to this particular virus. However, instead of developing a cold, the mice unexpectedly displayed paralytic symptoms characteristic of polio. The researchers determined that administering the virus directly into muscles, instead of the virus’s normal home in the nasal cavity, was critical for development of polio.

The findings challenge traditional views as to what defines a poliovirus, said Matthias Gromeier, M.D., a Duke virologist and senior author of the study.

“In principle, Coxsackieviruses could cause polio in humans,” said Gromeier. “We are in the process of eradicating polio worldwide, but if we eliminate the poliovirus and cease polio vaccinations, our immune systems wouldn’t produce antibodies against polio, and Coxsackievirus could theoretically fill the niche of eradicated polio” he said.

Results of the study will be published in the Sept. 6, 2004, issue of the Proceedings of the National Academy of Sciences.

Until now, it has been widely accepted that Coxsackievirus and poliovirus cause distinct illnesses because they bind to different docking sites, called receptors, on host cell surfaces. The current study turned that belief on its head, said Gromeier. Poliomyelitis has long been regarded as the signature of poliovirus, a virus that recognizes and binds to the CD155 receptor. However, the mice were genetically engineered to have only the Coxsackie A21 receptor, called ICAM-1, and they did not have the poliovirus receptor. Still, when the mice were injected with Coxsackievirus, it initiated infection through the ICAM-1 receptor, and caused symptoms of polio.

The manner in which the mice were infected with Coxsackievirus facilitated its unusual behavior inside the body, the study showed. The mice were injected with Coxsackievirus into their calf muscles, an unusual route of entry. Following the injection, the mice began to display symptoms of polio, including an abnormal gait, dropfoot, and lower hind limb paresis.

The researchers were left wondering how this intramuscular portal of entry could affect the virus’s ability to access the types of cells normally infected by polio.

In studying the virus’ action within infected mice, they found that the virus traveled from the calf muscle where it was injected to the central nervous system along “motor neuron axons.” Such axons extend from the central nervous system to muscles throughout the body and convey commands for muscle movement. The site in the muscle where axons physically attach is called a neuromuscular junction. These junctions likely served as the cold virus’ portal of entry into the nervous system.

“We gave the coxsackievirus a distinct advantage by injecting it directly into muscle, where it had direct access to the kinds of nerve cells polio normally attacks,” said Gromeier. “The resulting polio symptoms were milder than those caused by the poliovirus, but it was polio nonetheless.”

Such a subtle change in entry mode significantly changed the virus’ behavior, and therein lies one of the greatest dangers associated with viruses, said Gromeier.

Viruses are extremely adaptable and they can alter themselves dramatically based upon their environment. Coxsackievirus A21 is one of a large group of cold viruses that are genetically very similar to polioviruses.

“Our study reveals how similar these viruses actually are,” he said. “It is fascinating that a minor change such as injection site may cause a harmless cold virus to attack the central nervous system.”

Gromeier’s team is now collaborating with the Centers for Disease Control to test numerous Coxsackievirus samples from patients around the world. Their goal is to determine which genetic features of the Coxsackievirus induce polio and under what conditions.

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Study pinpoints effects of different doses of an ADHD drug; Finds higher doses may harm learning

MADISON – New research with monkeys sheds light on how the drug methylphenidate may affect learning and memory in children with attention deficit hyperactivity disorder.

The results parallel a 1977 finding that a low dose of the drug boosted cognitive performance of children with ADHD, but a higher dose that reduced their hyperactivity also impaired their performance on a memory test.

“Many people were intrigued by that result, but their attempts to repeat the study did not yield clear-cut results,” says Luis Populin, an associate professor of neuroscience at the University of Wisconsin-Madison School of Medicine and Public Health.

Populin was senior author of the new study exploring the same topic, now available in the early access section of the Journal of Cognitive Neuroscience, published last week. In the study, three monkeys were taught to focus on a central dot on a screen, while a “target” dot flashed nearby. The monkeys were taught that they could earn a sip of water by waiting until the central dot switched off, and then looking at the location of the now-vanished target dot.

The system tests working (short-term) memory, impulsiveness and willingness to stick with the task, as the monkeys could quit “working” at any time, says Populin. The study used different doses of methylphenidate — the generic name for Ritalin — that were comparable to the range of clinical prescriptions for ADHD.

According to the Centers for Disease Control, almost 5 percent of American children are taking medications for ADHD.

Strikingly, dosage had a major and unexpected impact. “At a low dose, the performance scores improved because the monkeys could control their impulses and wait long enough to focus their eyes on the target. All three were calmer and could complete a significantly larger number of trials,” says Populin, who collaborated with Jeffrey Henriques and graduate student Abigail Rajala on the study.

At the higher dose, “performance on the task is impaired,” Populin says,  “but the subjects don’t seem to care, all three monkeys continued making the same errors over and over.” The monkeys stayed on task more than twice as long at the higher dose, even though they had much more trouble performing the task.

Although ADHD drugs are commonly thought to improve memory, “If we take the accuracy of their eye movements as a gauge of working memory, memory was not helped by either dose,” says Populin. “It did not get better at the lower dose, and there actually was a small negative effect at the higher dose.”

Memory is at the root of many intellectual abilities, but it can be affected by many factors, says Bradley Postle, a professor of psychology at UW-Madison.

Postle, an expert on working memory who was not involved in the study, says methylphenidate affects the brain’s executive function, “which can create an internal environment that, depending on the dose, is either more or less amenable to memory formation and/or retention. If you can concentrate, and are able to process information without being interrupted by distracting thoughts or distractions in your environment, you will perform much better on a memory test. Apparently, the lower dose of methylphenidate helped create the conditions for success without actually improving memory itself.”

Monkeys are not people, but monkeys in the study still reminded him of school children, Populin says.

“They made premature movements, could not wait to look at the target before they could be rewarded for doing so. It’s like a kid where the teacher says, ‘When you complete the task, raise your hand.’ But he can’t wait, even if he knows that by responding prematurely he will not get rewarded,” he says.

The study results had another parallel with daily life, Populin says. Drug dosages may be set high enough to reduce the characteristic hyperactivity of ADHD, “but some children say that makes them feel less creative and spontaneous; more like a robot. If learning drops off as it did in our study, that dose may not be best for them. Our monkeys actually did act like robots at the higher doses, keeping at it for up to seven hours even though their performance was so low.”

The logical way forward would involve a similar study with people diagnosed with ADHD, Populin says. With millions of children, and an increasing number of adults, taking medicines for the condition, “We have to be very careful about finding the right spot on the dose curve, or we may get changes in behavior that we don’t want.  People think these drugs help improve memory, but our data say, ‘No, your memory is not getting better.’ At the higher dose, you get a behavioral improvement at a price, and that price is cognitive ability.”