Age Matters in Weight Gain: Overweight at Young Age Takes Toll

Being overweight, especially from a young age, appears to lead to a bigger heart later in life, a condition that has been linked to serious heart problems and even death, according to research being presented at the American College of Cardiology's 62nd Annual Scientific Session.

Results of this longitudinal study found that people who carry excess weight over their lifetime are much more likely to have increases in left ventricular mass and relative wall thickness -- both strong and independent predictors of cardiovascular morbidity and mortality. In this instance, timing is indeed everything; the earlier someone becomes overweight, the greater the increase in the heart's mass later in life.

"Being overweight in your 20s can have detrimental effects on the heart 40 years in the future, especially if you keep the weight on over the years," said Arjun K. Ghosh, MBBS, MRCP (U.K.), MSc, clinical research fellow at the International Centre for Circulatory Health of Britain's National Heart and Lung Institute and at the U.K. Medical Research Council's Unit for Lifelong Health and Aging and the study's lead investigator, on behalf of the full study team.

"It's probably the wrong attitude to think 'I know I'm overweight now, but I'll lose the weight later' because the longer you spend overweight, the greater the weight of your heart muscle. And we know from other studies that even if we take away or account for high blood pressure, diabetes or other risk factors for heart disease, somebody with a bigger heart muscle is more likely to have a heart attack, die or have other problems, such as stroke."

Researchers tracked the body mass index (BMI) of 1,653 men and women at different points in their lives to examine the effects of being overweight on the structure of the heart. BMI is a simple measure of the body's fat using a calculation of weight to height. People who were considered overweight, with a BMI of 25 to 29.9, or obese, with a BMI of 30 or above, had the heaviest hearts. Dr. Ghosh said few, if any, studies have been able to look at this question over such a long duration. He and his team drew from 44 years of data. Strikingly, the heart was 7 percent heavier for those who were overweight beginning in their 20s compared to those who only became overweight in their 60s.

"Our findings add to the wealth of evidence that obesity and being overweight from a young age is not good and provide yet another reason why we need to focus on preventing obesity and promoting a healthy lifestyle," he said. "Being overweight is a significant risk factor for heart disease, and worldwide, people seem to be becoming overweight at younger and younger ages."

Dr. Ghosh said previous research demonstrates that it is difficult to go back to and maintain a normal weight once someone has become overweight. As such, prevention of becoming overweight in the first place should be the aim. This is especially relevant amid the growing obesity epidemic, even among children. One in three school-aged children in North America are now overweight and this upward trend shows no signs of slowing, which means more children are entering adulthood carrying excess weight.

Individuals included in this study are participants in the Medical Research Council National Survey of Health and Development (or the 1946 British birth cohort), which is the longest running birth cohort study in the United Kingdom. Between ages 60 and 64, participants underwent echocardiography, an ultrasound of the heart, to allow researchers to measure the size of the heart muscle and their BMI was calculated. BMI and other cardiovascular risk factors had previously been measured at 20, 26, 36, 43 and 53 years of age. Higher BMI from 20 years onward was associated with increased heart muscle mass, with those with higher BMIs at each time point having heavier hearts at age 60-64 years of age. These associations remain after researchers adjusted for related risk factors, e.g., high blood pressure, diabetes and sex.

Two previous analyses of cardiac health indicators in the same study cohort revealed that people with diabetes are at greater risk of heart problems the longer they had diabetes and that a sharp spike in blood pressure during midlife, not just crossing a certain threshold, such as becoming hypertensive, can increase a person's risk of heart disease later in life. Both were presented at ACC.12.

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'Switch' Critical to Wound Healing Identified

Scientists from A*A*STAR's Institute of Medical Biology (IMB) have identified a molecular "switch" that controls the migration of skin cells necessary for wounds to close and heal. This is especially significant for diabetics and other patients who suffer from chronic wounds, wounds that do not heal or take years to do so, which are vulnerable to infections and could lead to amputations. This switch mechanism may hold the key to developing therapeutics that will reduce or prevent chronic wounds.

The scientists discovered that a tiny "micro-RNA" molecule, called miR-198, controls several different processes that help wound healing, by keeping them switched off in healthy skin. When skin is wounded, the manufacture of miR-198 quickly stops and the levels of miR-198 drop, switching on many wound healing processes.

In the non-healing wounds of diabetics, miR-198 does not disappear and wound healing remains blocked. This therefore identifies miR-198 as a potential diagnostic biomarker for non-healing wounds.

These findings were recently published in the journal Nature. The research leading to this discovery was carried out in collaboration with A*STAR's Bioinformatics Institute (BII), National University Hospital (NUH), Singapore and Jnana Sanjeevini Diabetes Center, Bangalore, India.

Importance of this discovery

Chronic wounds in patients with diabetes are a major global health burden and the most common cause of lower extremity amputations. In Singapore, diabetes is the fifth most common medical condition diagnosed and one in nine people aged 18 to 69 has diabetes. Unfortunately, chronic wounds are currently poorly understood and insufficiently treated. Chronic wounds also tend to affect the elderly and disabled patients, especially those confined to a wheelchair or bed-bound.

Dr. Prabha Sampath said, "Moving forward, we hope to translate this research into improved patient outcomes. We can now build on this research, to see how we can modulate the defective switch in chronic wounds by targeting miR-198 and its interacting molecules, to develop new strategies for treating chronic wounds."

Professor Birgitte Lane, Executive Director of IMB, said, "This switch appears to be an entirely new regulatory component in wound healing, and probably a very important one. Poor wound healing is a major healthcare burden, and this discovery is particularly timely in the face of aging populations and the sharp global rise in diabetes. The finding gives us a platform from which to develop therapies that could significantly reduce chronic wounds and improve healthcare."

An FSTL1-miR-198 molecular 'see-saw' switch

The information necessary to expressmicroRNA-198 (miR-198) and follistatin-like 1 (FSTL1) protein are found in a single "message" produced by the cell. However, miR-198 and FSTL1 protein cannot be produced at the same time -- it can only be one or the other. These two molecules also have opposite roles: miR-198 (found in unwounded skin) inhibits skin cell migration and wound healing, whereas FSTL1 protein (expressed after injury) promotes skin cell migration and wound healing. A regulatory switch dictates their expression, and hence controls the "see-saw" between inactive resting skin cells and the cell migration necessary for wound healing.

Dr. Sampath and her team showed that healthy unwounded skin contained high levels of miR-198 but no FSTL1 protein. They demonstrated that these high levels of miR-198 prevent skin cell migration by suppressing several genes, such as PLAU, LAMC2 and DIAPH1, which are needed for different aspects of the wound healing process. However upon injury, miR-198 is switched off in the wound by a signal from transforming growth factor β1 (TGF-β1). This allows FSTL1 to now be made instead, and the skin migration genes to be unblocked, promoting migration of skin cells into the wound area to drive skin wound healing.

The scientists further examined skin samples of chronic non-healing ulcer wounds from patients with diabetes mellitus. They observed that, unlike healthy skin that had been injured, there remained high levels of miR-198 (inhibiting skin cell migration and wound healing) and an absence of FSTL1 protein (promoting skin cell migration upon wounding), indicating that this "switch" is defective in chronic wounds.

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'Brewing' New Medicines?

Researchers employing a century-old observational technique have determined the precise configuration of humulones, substances derived from hops that give beer its distinctive flavor.
That might not sound like a big deal to the average brewmaster, but the findings overturn results reported in scientific literature in the last 40 years and could lead to new pharmaceuticals to treat diabetes, some types of cancer and other maladies.
"Now that we have the right results, what happens to the bitter hops in the beer-brewing process makes a lot more sense," said Werner Kaminsky, a University of Washington research associate professor of chemistry.
Kaminsky is the lead author of a paper describing the findings, published this month in the journal Angewandte Chemie International Edition.
There is documentation that beer and its bittering acids, in moderation, have beneficial effects on diabetes, some forms of cancer, inflammation and perhaps even weight loss.

Kaminsky used a process called X-ray crystallography to figure out the exact structure of those acids, humulone molecules and some of their derivatives, produced from hops in the brewing process. That structure is important to researchers looking for ways to incorporate those substances, and their health effects, into new pharmaceuticals.
Humulone molecules are rearranged during the brewing process to contain a ring with five carbon atoms instead of six. At the end of the process two side groups are formed that can be configured in four different ways - both groups can be above the ring or below, or they can be on opposite sides.
Which of the forms the molecule takes determines its "handedness," Kaminsky said, and that is important for understanding how a particular humulone will react with another substance. If they are paired correctly, they will fit together like a nut and bolt.
If paired incorrectly, they might not fit together at all or it could be like placing a right hand into a left-handed glove. That could produce disastrous results in pharmaceuticals.
Kaminsky cited thalidomide, which has a number of safe uses but was famously used to treatmorning sickness in pregnant women in the late 1950s and early 1960s before it was discovered to cause birth defects. Molecule "handedness" in one form of the drug was responsible for the birth defects, while the orientation of molecules in another form did not appear to have the negative effects.
To determine the configuration of humulones formed in the brewing process, coauthors Jan Urban, Clinton Dahlberg and Brian Carroll of KinDex Therapeutics, a Seattle pharmaceutical firm that funded the research, recovered acids from the brewing process and purified them.
They converted the humulones to salt crystals and sent them to Kaminsky, who used X-ray crystallography - a technique developed in the early 20th century - to determine the exact configuration of the molecules.
"Now that we know which hand belongs to which molecule, we can determine which molecule goes to which bitterness taste in beer," Kaminsky said.
The authors point out that while "excessive beer consumption cannot be recommended to propagate good health, isolated humulones and their derivatives can be prescribed with documented health benefits."
Some of the compounds have been shown to affect specific illnesses, Kaminsky said, while some with a slight difference in the arrangement of carbon atoms have been ineffective.
The new research sets the stage for finding which of those humulones might be useful in new compounds to be used as medical treatments.

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Risk Of Type 2 Diabetes Increased By Binge Drinking By Causing Insulin Resistance

Binge drinking causes insulin resistance, which increases the risk of Type 2 diabetes, according to the results of an animal study led by researchers at the Diabetes Obesity and Metabolism Institute at the Icahn School of Medicine at Mount Sinai. The authors further discovered that alcohol disrupts insulin-receptor signaling by causing inflammation in the hypothalamus area of the brain.

The results are published in the journal Science Translational Medicine.
"Insulin resistance has emerged as a key metabolic defect leading to Type 2 diabetes and coronary artery disease (CAD)," said Christoph Buettner, MD, PhD, senior author of the study and Associate Professor of Medicine (Endocrinology, Diabetes and Bone Disease). "Someone who regularly binge drinks even once a week, over many years, may remain in an insulin resistant state for an extended period of time, potentially years," said Dr. Buettner.
In this study, researchers treated rats with alcohol for three consecutive days to simulate human binge drinking.

A control group received the same amount of calories. Once alcohol was no longer detectable in blood, glucose metabolism was studied through either glucose-tolerance tests or through controlled-insulin infusions. The rats treated with alcohol were found to have higher concentrations of plasma insulin than the control group, suggesting that insulin resistance may have been the cause of the impaired glucose tolerance.
High plasma insulin levels are a major component of the metabolic syndrome, a group of risk factors that occur together and increase the risk for Type 2 diabetes, coronary artery disease, and stroke.

"Previously it was unclear whether binge drinking was associated with an increased risk for diabetes, since a person who binge drinks may also tend to binge eat, or at least eat too much. Our data show for the first time that binge drinking induces insulin resistance directly and can occur independent of differences in caloric intake," said Claudia Lindtner, MD, first author of the study and an Associate Researcher of Medicine, Endocrinology, Diabetes and Bone Disease at the Icahn School of Medicine.

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Do Gender And Ethnicity Alter Childhood Risk For Metabolic Syndrome?

Metabolic syndrome is more likely to affect children who are obese than overweight or non-overweight and who have other characteristics associated with the disorder, such as high blood pressure or insulin resistance. A new comprehensive and systematic review of the medical literature on metabolic syndrome in children that probed deeper to evaluate the risk associated with gender, ethnicity, and geography was published in Metabolic Syndrome and Related Disorders, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers. The article is available on the Metabolic Syndrome and Related Disorders website.

Amanda Friend, MBChB, Leone Craig, PhD, and Steve Turner, MD, University of Aberdeen, Scotland, assessed data from 85 studies and reported their findings in the article "The Prevalence of Metabolic Syndrome in Children: A Systematic Review of the Literature." Overall, the prevalence of metabolic syndrome increased substantially when comparing groups of overweight or obese children to whole populations of youths.

The authors found significant differences in metabolic syndrome prevalence for boys versus girls and for older compared to younger children. Some evidence suggested that there may also be an association between ethnicity and region of the world where a child lives and the prevalence of metabolic syndrome - a possible link that warrants further study.
"The authors should be lauded for their comprehensive and careful review of a group that has been largely ignored, which is children," says Ishwarlal (Kenny) Jialal, MD, PhD, Editor-in-Chief of the Journal and Director of the Laboratory for Atherosclerosis and Metabolic Research and Professor of Internal Medicine at the University of California, Davis Medical Center (Sacramento). "They clearly show that increasing age, male sex, and adiposity are risk factors for metabolic syndrome in children. They also emphasize the need for future studies to confirm the reported increased prevalence in certain ethnic groups."

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Joslin Scientists Find First Human IPSC From Patients With Maturity Onset Diabetes Of The Young

Joslin scientists report the first generation of human induced pluripotent stem cells from patients with an uncommon form of diabetes, maturity onset diabetes of the young (MODY). These cells offer a powerful resource for studying the role of genetic factors in the development of MODY and testing potential treatments. The findings appear in the Journal of Biological Chemistry.

Human induced pluripotent stem cells (hiPSCs) are adult cells that have been genetically reprogrammed to exhibit the characteristics of embryonic stem cells, including the ability to differentiate into specialized cell types. The generation of hiPSCs, which was first reported in 2006, was a major scientific breakthrough with the potential to increase understanding of many diseases and aid in drug development.

Maturity onset diabetes of the young (MODY) is a form of diabetes that mainly affects individuals age 25 or younger and accounts for about 1 to 5 percent of all diabetes cases in the United States. Unlike type 1 and type 2 diabetes, which are polygenic and result from alterations in genetic and environmental factors, MODY is a monogenic disease that results from mutations in a single gene. To date, eight types of MODY and eleven MODY genes have been identified. Some types of MODY produce only mild symptoms and are often treated solely with oral diabetic medications.

Joslin Diabetes Center is one of a limited number of research institutes with the capability to generate hiPSCs from patients with diabetes. The cells used to produce the hiPSCs were obtained from patients with five different types of MODY at Joslin Diabetes Center and Haukeland University Hospital, Bergen, Norway. The MODY-hiPSCs are morphologically, molecularly and functionally indistinguishable from human pluripotent stem cells (hPSCs).

As a monogenic disease, MODY provides "a valuable opportunity to directly study in more detail the genetic mechanisms underlying the disease and not be influenced by other factors, such as insulin resistance," says senior author Rohit N. Kulkarni, M.D., Ph.D., a Principal Investigator in the Section on Islet Cell and Regenerative Biology at Joslin and Associate Professor of Medicine at Harvard Medical School.
The scientists will first induce the MODY-hiPSCs to differentiate towards beta cells and in the process learn more about the potential blocks in their ability to differentiate. Using the iPSC-derived beta cells, they plan to study how MODY genes regulate the insulin secretory function. "Generating hiPSCs is an important step forward because we cannot obtain beta cells from living patients. These cells will allow us to do many experiments that otherwise would not be possible," says Dr. Kulkarni.

The scientists also plan to explore ways to correct the genetic defect and use the beta cells derived from the "repaired" hiPSCs to test various treatments. "If we find medications that improve beta cell function, we can go back to the clinic and use them to treat patients," says Dr. Kulkarni. "It will allow us to tailor treatments to a patient's unique characteristics and provide personalized medicine to diabetes patients."

 

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Type 3 Diabetes.....Alzheimer's?

Just in case you need another reason to cut back on junk food, it now turns out that Alzheimer’s could well be a form of diet-induced diabetes. That’s the bad news.

The good news is that laying off soda, doughnuts, processed meats and fries could allow you to keep your mind intact until your body fails you. We used to think there were two types of diabetes: the type you’re born with (Type 1) and the type you “get.” That’s called Type 2, and was called “adult onset” until it started ravaging kids. Type 2 is brought about by a combination of factors, including overeating, American-style.

The idea that Alzheimer’s might be Type 3 diabetes has been around since 2005, but the connection between poor diet and Alzheimer’s is becoming more convincing, as summarized in a cover story in New Scientist entitled “Food for Thought: What You Eat May Be Killing Your Brain.” (The graphic — a chocolate brain with a huge piece missing — is creepy. But for the record: chocolate is not the enemy.)

The studies [1] are increasingly persuasive, and unsurprising when you understand the role of insulin in the body. So, a brief lesson. We all need insulin: in non-diabetics, it’s released to help cells take in the blood sugar (glucose) they need for energy. But the cells can hold only so much; excess sugar is first stored as glycogen, and — when there’s enough of that — as fat. (Blood sugar doesn’t come only from sugar, but from carbohydrates of all kinds; easily digested carbohydrates flood the bloodstream with sugar.)

Insulin not only keeps the blood vessels that supply the brain healthy, it also encourages the brain’s neurons to absorb glucose, and allows those neurons to change and become stronger. Low insulin levels in the brain mean reduced brain function. Type 1 diabetes, in which the immune system destroys insulin-producing cells in the pancreas, accounts for about 10 percent of all cases.

Type 2 diabetes is chronic or environmental, and it’s especially prevalent in populations that overconsume hyperprocessed foods, like ours. It’s tragically, increasingly common — about a third of Americans have diabetes or pre-diabetes — and treatable but incurable. It causes your cells to fail to retrieve glucose from the blood, either because your pancreas isn’t producing enough insulin or the body’s cells ignore that insulin. (That’s “insulin resistance”; stand by.)

Put as simply as possible (in case your eyes glaze over as quickly as mine when it comes to high school biology), insulin “calls” your cells, asking them to take glucose from the bloodstream: “Yoo-hoo. Pick this stuff up!” When the insulin calls altogether too often — as it does when you drink sugar-sweetened beverages and repeatedly eat junk food — the cells are overwhelmed, and say, “Leave me alone.” They become resistant. This makes the insulin even more insistent and, to make matters worse, all those elevated insulin levels are bad for your blood vessels.

Diabetes causes complications too numerous to mention, but they include heart disease, which remains our No. 1 killer. And when the cells in your brain become insulin-resistant, you start to lose memory and become disoriented. You even might lose aspects of your personality. In short, it appears, you develop Alzheimer’s. A neuropathologist named Alois Alzheimer noticed, over a century ago, that an odd form of protein was taking the place of normal brain cells.

How those beta amyloid plaques (as they’re called) get there has been a mystery. What’s becoming clear, however, is that a lack of insulin — or insulin resistance — not only impairs cognition but seems to be implicated in the formation of those plaques. Suzanne de la Monte, a neuropathologist at Brown University, has been working on these phenomena in humans and rats. When she blocked the path of insulin to rats’ brains, their neurons deteriorated, they became physically disoriented and their brains showed all the signs of Alzheimer’s.

The fact that Alzheimer’s can be associated with low levels of insulin in the brain is the reason why increasing numbers of researchers have taken to calling it Type 3 diabetes, or diabetes of the brain.[2] Let’s connect the dots: We know that the American diet is a fast track not only to obesity but to Type 2 diabetes and other preventable, non-communicable diseases, which now account for more deaths worldwide than all other causes combined.

We also already know that people with diabetes are at least twice as likely to get Alzheimer’s, and that obesity alone increases the risk of impaired brain function. What’s new is the thought that while diabetes doesn’t “cause” Alzheimer’s, they have the same root: an over consumption of those “foods” that mess with insulin’s many roles. (Genetics have an effect on susceptibility, as they appear to with all environmental diseases.)

“Sugar is clearly implicated,” says Dr. de la Monte, “but there could be other factors as well, including nitrates in food.” If the rate of Alzheimer’s rises in lockstep with Type 2 diabetes, which has nearly tripled in the United States in the last 40 years, we will shortly see a devastatingly high percentage of our population with not only failing bodies but brains.

Even for the lucky ones this is terrible news, because 5.4 million Americans (nearly 2 percent, for those keeping score at home) have the disease, the care for which — along with other dementias — will cost around $200 billion this year. Gee. That’s more than the $150 billion we’ve been saying we spend annually on obesity-related illnesses. So the financial cost of the obesity pandemic just more than doubled.

More than 115 million new cases of Alzheimer’s are projected around the world in the next 40 years, and the cost is expected to rise to more than a trillion of today’s dollars. (Why bother to count? $350 billion is bad enough.) The link between diet and dementia negates our notion of Alzheimer’s as a condition that befalls us by chance. Adopting a sane diet, a diet contrary to the standard American diet (which I like to refer to as SAD), would appear to give you a far better shot at avoiding diabetes
in all of its forms, along with its dreaded complications.

There are, as usual, arguments to be made for enlisting government help in that struggle, but for now, put down that soda!

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Red Wine Could Mask Testosterone Levels, Experts Warn

Red wine could give athletes and players a boost in the sports arena by increasing the amount of performance-enhancing hormone testosterone in their bodies, according to researchers from London's Kingston University.

However not only could the beverage help them to trophy success, it could also allow them to beat anti-doping tests. A team led by Professor Declan Naughton, from the University's School of Life Sciences, found that red wine might reduce the amount of testosterone excreted by the body, which could distort the findings of drug tests taken from urine samples.

Testosterone is a naturally-occurring steroid hormone present in both men and women. It can increase muscle mass, boost stamina and speed up recovery. Sportspeople, however, are prohibited from taking it, or a synthetic version of it, to try to gain a competitive edge.

Although red wine is not a banned substance away from the sports field, Professor Naughton's team has referred its findings to the World Anti-Doping Agency because of the newly-discovered side effect of potential change to the amount of testosterone in the body.

"Previous research has shown the effect over-the-counter anti-inflammatory drugs can have on enzymes," Professor Naughton explained. "Since many of these drugs are derived from plants, we decided to look at the effect particular foods and beverages can have on enzymes involved in testosterone excretion. We chose green tea and then red wine because both have a huge variety of natural molecules and we wanted to see if they affected the amount of testosterone excreted in urine."

The team found that a compound in red wine, known as quercetin, partially blocked the action of an enzyme called UGT2B17, which looks for testosterone and then sends a message to the kidneys to excrete it.

Professor Naughton stressed that the research had so far been conducted in test tube experiments and had yet to be trialled on humans. "A full clinical study would be needed to determine the effects on people but, if the same results were found, it would confirm that compounds in red wine can reduce the amount of testosterone in urine and give a boost to testosterone levels," he explained.

The effect of red wine on an individual would vary because of factors such as weight, fitness, health and diet, making it hard to estimate how much was needed to improve performance, Professor Naughton said.

Teetotallers are not exempt from the effects. In fact, the alcohol content of red wine has very little impact because non-alcoholic molecules are responsible for inhibiting testosterone excretion.

The team also found the results were the same for red wine extract in supplement form. The active compounds such as quercetin are found in many foodstuffs as well as supplements.

The findings have been published in leading international journal Nutrition. The research follows an earlier study from Professor Naughton's team which showed that green and white tea could also inhibit testosterone excretion.

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Link Between Creativity and Mental Illness Confirmed in Large-Scale Swedish Study

People in creative professions are treated more often for mental illness than the general population, there being a particularly salient connection between writing and schizophrenia. This according to researchers at Karolinska Institutet, whose large-scale Swedish registry study is the most comprehensive ever in its field.

Last year, the team showed that artists and scientists were more common amongst families where bipolar disorder and schizophrenia is present, compared to the population at large. They subsequently expanded their study to many more psychiatric diagnoses -- such as schizoaffective disorder, depression, anxiety syndrome, alcohol abuse, drug abuse, autism, ADHD, anorexia nervosa and suicide -- and to include people in outpatient care rather than exclusively hospital patients.

The present study tracked almost 1.2 million patients and their relatives, identified down to second-cousin level. Since all were matched with healthy controls, the study incorporated much of the Swedish population from the most recent decades. All data was anonymized and cannot be linked to any individuals.

The results confirmed those of their previous study, that certain mental illness -- bipolar disorder -- is more prevalent in the entire group of people with artistic or scientific professions, such as dancers, researchers, photographers and authors. Authors also specifically were more common among most of the other psychiatric diseases (including schizophrenia, depression, anxiety syndrome and substance abuse) and were almost 50 per cent more likely to commit suicide than the general population.

Further, the researchers observed that creative professions were more common in the relatives of patients with schizophrenia, bipolar disorder, anorexia nervosa and, to some extent, autism. According to Simon Kyaga, Consultant in psychiatry and Doctoral Student at the Department of Medical Epidemiology and Biostatistics, the results give cause to reconsider approaches to mental illness.

"If one takes the view that certain phenomena associated with the patient's illness are beneficial, it opens the way for a new approach to treatment," he says. "In that case, the doctor and patient must come to an agreement on what is to be treated, and at what cost. In psychiatry and medicine generally there has been a tradition to see the disease in black-and-white terms and to endeavour to treat the patient by removing everything regarded as morbid."

The study was financed with grants from the Swedish Research Council, the Swedish Psychiatry Foundation, the Bror Gadelius Foundation, the Stockholm Centre for Psychiatric Research and the Swedish Council for Working Life and Social Research.

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Most-Used Diabetes Drug Works in Different Way Than Previously Thought

A team, led by senior author Morris J. Birnbaum, MD, PhD, the Willard and Rhoda Ware Professor of Medicine, with the Institute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine, University of Pennsylvania, found that the diabetes drug metformin works in a different way than previously understood. Their research in mice found that metformin suppresses the liver hormone glucagon's ability to generate an important signaling molecule, pointing to new drug targets. The findings were published online this week in Nature.

For fifty years, one of the few classes of therapeutics effective in reducing the overactive glucose production associated with diabetes has been the biguanides, which includes metformin, the most frequently prescribed drug for type 2 diabetes. The inability of insulin to keep liver glucose output in check is a major factor in the high blood sugar of type 2 diabetes and other diseases of insulin resistance.

"Overall, metformin lowers blood glucose by decreasing liver production of glucose," says Birnbaum. "But we didn't really know how the drug accomplished that."

Imperfectly Understood

Despite metformin's success, its mechanism of action remained imperfectly understood. About a decade ago, researchers suggested that metformin reduces glucose synthesis by activating the enzyme AMPK. But this understanding was challenged by genetic experiments in 2010 by collaborators on the present Nature study. Coauthors Marc Foretz and Benoit Viollet from Inserm, CNRS, and Université Paris Descartes, Paris, found that the livers of mice without AMPK still responded to metformin, indicating that blood glucose levels were being controlled outside of the AMPK pathway.

Taking another look at how glucose is regulated normally, the team knew that when there is no food intake and glucose decreases, glucagon is secreted from the pancreas to signal the liver to produce glucose. They then asked if metformin works by stopping the glucagon cascade.

The Nature study describes a novel mechanism by which metformin antagonizes the action of glucagon, thus reducing fasting glucose levels. The team showed that metformin leads to the accumulation of AMP in mice, which inhibits an enzyme called adenylate cyclase, thereby reducing levels of cyclic AMP and protein kinase activity, eventually blocking glucagon-dependent glucose output from liver cells.

From this new understanding of metformin's action, Birnbaum and colleagues surmise that adenylate cyclase could be a new drug target by mimicking the way in which it is inhibited by metformin. This strategy would bypass metformin's affect on a cell's mitochondria to make energy, and possibility avoid the adverse side effects experienced by many people who take metformin, perhaps even working for those patients resistant to metformin.

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Treatment For Gastrointestinal Conditions May Be Improved By Targeting Neurotransmitter

Selective targeting of the neurotransmitter that differentially affects brain cells that control the two distinct functions of the pancreas may allow for new medication therapies for conditions like diabetes, dyspepsia and gastro-esophageal reflux, according to Penn State College of Medicine researchers.
"This study differs from what's been reported

previously about brain neurons that control the gastrointestinal tract," said R. Alberto Travagli, professor, Department of Neural and Behavioral Sciences, and lead investigator. "It provides further support to the idea that separate nerve pathways regulate the diverse functions of organs along the upper gastrointestinal tract."
The pancreas has two functional parts: one that releases digestive enzymes, and one that releases hormones like insulin and glucagon. The vagus nerve, which originates in the brain, regulates both of these pancreatic functions. This nerve detects chemical and biological changes that occur along the gastrointestinal tract and interprets and integrates these signals before sending appropriate responses back to the organs. In the brain, these signals tell the nerves controlling each specific organ what the proper response is -- for example, digestive processes and insulin release -- according to the signals detected in the GI tract.
Neurotransmitters in the brain and in organs like the pancreas control the nerve networks that receive these signals. Neurotransmitters are chemicals released from nerves that allow them to communicate with each other as well as with organs of the body. One of these neurotransmitters is glutamate, which acts on specific proteins called receptors that are present on the nerve cells. There are different classes and types of receptors that glutamate can act upon; one major class of these receptors is metabotropic glutamate receptors (mGluRs). This class is further divided into three subgroups -- I, II or III -- depending on their location and function on the nerve cells.
"The aim of this study was to investigate how these mGluRs are organized on nerve synapses -- the specialized structures that allow a signal to pass from one cell to another cell," Travagli said. "The second aim of the study was to see whether pancreatic insulin and enzyme secretions are controlled by different types of vagal motoneurons -- the cells of the nervous system that control motor functions of the pancreas through the vagus nerve."
Group II and III mGluRs are present in synapses that can either excite or inhibit the vagal nerve cells that send signals to the pancreas, and different outcomes can be seen depending on which group of mGluRs glutamate acts upon. When glutamate acts upon either group II or group III mGluR, insulin secretion is decreased. Pancreatic enzyme secretion is increased only by activation of group II mGluR by glutamate.
"The data shows mGluRs on brainstem vagal nerve circuits that regulate pancreatic functions are organized in a very specific manner," Travagli said. "This type of separation in their organization may allow for development of selective drugs that target very specific vagal neurocircuits in patients with such conditions as gastrointestinal reflux disorders, functional dyspepsia, gastroparesis and pancreatic exocrine or endocrine dysfunctions."

Related articles

• Treatment For Gastrointestinal Conditions May Be Improved By Targeting Neurotransmitter (medicalnewstoday.com)
• In T2 Diabetes, Which Comes First: High Insulin Levels or Insulin Resistance? (diabeticmediterraneandiet.com)
• Targeting neurotransmitter may help treat gastrointestinal conditions (sciencedaily.com)

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Pig That Models Human Diseases Such As Obesity, Diabetes, And Cardiovascular Disease Gets International Attention

A detailed annotation of the genome of T.J. Tabasco, a pig from the University of Illinois South Farms, is the outcome of over 10 years of work by an international consortium. It is expected to speed progress in both biomedical and agricultural research. U of I Vice President for Research Lawrence Schook said that the College of ACES played a crucial role in getting the work started.

Funding that came through ACES allowed Schook and others to put together the Swine Genome Sequencing Consortium, an alliance of university, industry, and government laboratories in the U.S., Europe, and Asia. The USDA committed 10 million dollars to the project. Today the project includes scientists from more than 50 research groups.
Schook said that the project has three main objectives: (1) to serve as a blueprint for understanding evolution and domestication, (2) to advance research on animal production and health, and (3) to explore ways to use the pig in biomedical applications.
The first publication, which just appeared in Nature, focuses on the pig's evolution. Researchers compared the reference genome from T.J. Tabasco with genomes of wild and domestic pigs from Europe and Asia (including archaeological and museum samples), and to human, mouse, dog, horse, and cow genomes.
"The pig is interesting because the wild boar still exists," Schook explained. "We could look at domestication, and we also looked at speciation. From an evolutionary perspective, these Sus species diverge in a very short time."
The researchers traced the domestic pig back to Southeast Asia. From there, it spread across Eurasia. The glaciation period separated the pigs into two groups about one million years ago. Today they are almost sub-species. "However, their chromosome structures have stayed very similar," Schook noted.
Pigs were independently domesticated in western Eurasia and East Asia 10,000 to 15,000 years ago. There is evidence that as the early European settlers moved around, they bred the domesticated females with wild boars.
Pigs in Central and South America are thought to have originated on the Iberian Peninsula. In a paper soon to be published in Heredity, the researchers tracked how these pigs adapted to different climates, altitudes, and diets.
As well as providing insights into how the pig evolved, the genome sequencing provides valuable new tools for animal breeding. One is a DNA test that can identify individual pigs that are less susceptible to certain diseases or have a genetic predisposition to fattening rapidly, eating less, and bearing many offspring.
On the biomedical side, researchers will build on ongoing efforts to use the pig to model human diseases, including lifestyle diseases such as obesity, diabetes, and cardiovascular disease. The sequencing identified 112 genes in pigs that are also responsible for diseases in people, suggesting that pigs could be used for drug testing.
Another direction is to use pigs as a source of organs for humans. Schook mentioned islet cells for diabetics as an example.
"Human transplant of eyelets doesn't work because there's not enough cells in a single pancreas," he explained. "If you could have an animal source, even if they get rejected, they're plentiful."
Clearly, there are a plenitude of exciting possibilities for future research. "For me, the next phase is looking at this concept of epigenomics - of how the environment affects gene expression," Schook said.

Related articles

• Scientists Sequence Entire Pig Genome in Breakthrough That Could Combat Human Disease (medicaldaily.com)
• Pig genome helps us understand why they eat crappy things (southofheaven.typepad.com)
• Pig That Models Human Diseases Such As Obesity, Diabetes, And Cardiovascular Disease Gets International Attention (medicalnewstoday.com)

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Gene Variations Linked To Higher Risk Of Bipolar Disorder

Scientists from the Florida campus of The Scripps Research Institute (TSRI) have identified small variations in a number of genes that are closely linked to an increased risk of bipolar disorder, a mental illness that affects nearly six million Americans, according to the National Institute of Mental Health.

"Using samples from some 3,400 individuals, we identified several new variants in genes closely associated with bipolar disorder," said Scripps Florida Professor Ron Davis, who led the new study, which was published recently by the journal Translational Psychiatry.
A strong tendency towards bipolar disorder runs in families; children with a parent or sibling who has bipolar disorder are four to six times more likely to develop the illness, according to the National Institute of Mental Health.
While the genetic basis for bipolar disorder is complex and involves multiple genes, it appears to be associated with a biochemical pathway known as cyclic adenosine monophosphate (cAMP) signaling system. The Davis laboratory and others have previously shown that the cAMP signaling plays a critical role in learning and memory processes. The new study focused on this signaling pathway.
"As far as I know, this has not been done before - to query a single signaling pathway," said Davis. "This is a new approach. The idea is if there are variants in one gene in the pathway that are associated with bipolar disorder, it makes sense there would be variants in other genes of the same signaling pathway also associated with the disorder."
The new study examined variations in 29 genes found in the two common types of bipolar disorder - bipolar disorder I (the most common form and the most severe) and bipolar disorder II. Genes from a total of 1,172 individuals with bipolar disorder I; 516 individuals with bipolar disorder II; and 1,728 controls were analyzed.
Several statistically significant associations were noted between bipolar disorder I and variants in the PDE10A gene. Associations were also found between bipolar disorder II and variants in the DISC1 and GNAS genes.
Davis noted that the location of PDE10A gene expression in the striatum, the part of the brain associated with learning and memory, decision making and motivation, makes it especially interesting as a therapeutic target.

Related articles

• Gene Variations Linked To Higher Risk Of Bipolar Disorder (medicalnewstoday.com)
• Scientists pinpoint gene variations linked to higher risk of bipolar disorder (eurekalert.org)
• Scientists pinpoint gene variations linked to higher risk of bipolar disorder (sciencedaily.com)
• Replicating risk genes in bipolar disorder (eurekalert.org)

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Better Therapies For Cardiovascular Disease May Be Product Of Protein Tug Of War

Two proteins are in a tug of war that determines how much the body makes of superoxide, a highly reactive and potentially destructive product of oxygen that's dramatically elevated in cardiovascular disease, researchers report.
Their finding indicates an antiulcer drug just may help the body reduce excessive levels.
Hsp90 and Hsp70 are both heat shock proteins but appear to have opposite effects on reactive oxygen species production, said Dr. David J.R. Fulton, Interim Director of the Vascular Biology Center at the Medical College of Georgia at Georgia Health Sciences University.
"Our studies show that Hsp90 promotes the activity of Nox enzymes, the source of reactive superoxide and all of the reactive oxygen species that descend from it, while Hsp70 has an opposing action that inhibits Nox," Fulton said.
When researchers gave Hsp90 inhibitors, the binding of Nox enzymes to Hsp90 was reduced, its binding to Hsp70 increased and reactive oxygen species production decreased. The inhibitors also reduced reactive oxygen species production in blood vessels from obese mice, where it contributes to the loss of elasticity and narrowing that are hallmarks of cardiovascular disease. While Hsp90 inhibition was known to suppress inflammation and reduce cardiovascular damage, just how it made these positive changes was unknown.
The yin and yang the researchers found points toward a targeted therapy that should give Hsp70 the edge, said Dr. Feng Chen, postdoctoral fellow. Chen is first author of the study in the American Heart Association journal Arteriosclerosis, Thrombosis and Vascular Biology.
Hsp90 inhibitors are used to treat cancer, which depends on Hsp90 to support rapid cell division. But they also target proteins that help blood vessels relax, such as nitric oxide synthase, so probably are not a good choice in cardiovascular disease. "Cardiovascular disease is a chronic disease, and we want to minimize negative side effects while providing protection," Fulton said.
In this case, a better approach appears to be directly increasing the expression of Hsp70 with a drug such as geranylgeranylacetone, or GGA, an antiulcer drug used in Japan with relatively few side effects, Chen said. When the MCG researchers treated human aortic vascular smooth muscle cells with the drug, for example, Hsp70's binding to Nox increased while Nox's ability to generate superoxide decreased.
Next steps include looking at whether this increased expression of Hsp70 actually translates to healthier blood vessels in a cardiovascular model. "If we can upregulate Hsp70 without affecting nitric oxide synthase, it should," said Fulton, the study's corresponding author.
Hsp70 and 90 are chaperones that guide protein folding in different ways and can influence more than just whether Nox enzymes are stable or degraded. Hsp70 levels are regulated by the molecule heat shock factor, which is bound to and repressed by Hsp90. That's one reason why Hsp90 inhibitors increase Hsp70 levels.
Reactive oxygen species are not all bad, the researchers noted. At normal levels, they aid cell signaling and homeostasis as well as the mounting of an immune response. However, excessive levels associated with chronic inflammation are thought to accelerate cardiovascular disease. "A little bit is good; you want a well-honed immune system to fend of pathogens," Fulton said. "Chronic inflammation is the problem."
The researchers completed their studies in normal and diabetic mice - diabetes increases the risk of cardiovascular disease by at least 50 percent - as well as the saphenous, or major superficial leg veins, of patients with cardiovascular disease.

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Link Between Vitamin D Deficiency And Type 1 Diabetes

A study led by researchers from the University of California, San Diego School of Medicine has found a correlation between vitamin D3 serum levels and subsequent incidence of Type 1 diabetes. The six-year study of blood levels of nearly 2,000 individuals suggests a preventive role for vitamin D3 in this disease. The research appears the December issue of Diabetologia, a publication of the European Association for the Study of Diabetes (EASD).
"Previous studies proposed the existence of an association between vitamin D deficiency and risk of and Type 1 diabetes, but this is the first time that the theory has been tested in a way that provides the dose-response relationship," said Cedric Garland, DrPH, FACE, professor in UCSD's Department of Family and Preventive Medicine.
This study used samples from millions of blood serum specimens frozen by the Department of Defense Serum Registry for disease surveillance. The researchers thawed and analyzed 1000 samples of serum from healthy people who later developed type 1 diabetes and 1000 healthy controls whose blood was drawn on or near the same date but who did not develop type 1 diabetes. By comparing the serum concentrations of the predominant circulating form of vitamin D - 25-hydroxyvitamin D (25(OH)D) - investigators were able to determine the optimal serum level needed to lower an individual's risk of developing type 1 diabetes.
Based mainly on results of this study, Garland estimates that the level of 25(OH)D needed to prevent half the cases of type 1 diabetes is 50 ng/ml. A consensus of all available data indicates no known risk associated with this dosage.
"While there are a few conditions that influence vitamin D metabolism, for most people, 4000 IU per day of vitamin D3 will be needed to achieve the effective levels," Garland suggested. He urges interested patients to ask their health care provider to measure their serum 25(OH)D before increasing vitamin D3 intake.
"This beneficial effect is present at these intakes only for vitamin D3," cautioned Garland. "Reliance should not be placed on different forms of vitamin D and mega doses should be avoided, as most of the benefits for prevention of disease are for doses less than 10,000 IU/day."

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Electronic Medical Records

Living in the digital age has brought around new technologies that revolutionize the health care industry. In a day and age where you can keep the contents of your entire computer on something the size of a stick of gum, doctors and healthcare professionals are now pushing for their patients to carry thumb-drives with Electronic Medical Records on it. I know being a Diabetic I carry a thumb-drive with all my medical information on it so that way if I have a medical emergency, doctors and emergency response teams will have my whole history right there at their fingertips. Electronic medical Records Software is typically easy to use and there are companies that will even maintain these records for you. One such company that provides these services is Optimus ERM they offer:

ADT and Resident Information

The Electronic Chart (eChart)

Point-of-Care (POC) Documentation

Automated MDS

Integrated Electronic Heath Records

Fully Integrated Billing and Financial System

Electronic Control Center (eCC)—Management Dashboard

CPOE Physician Order Module

eMAR and eTAR (Electronic Medication Administration Records and Electronic Treatment Administration Records)

Pharmacy and Lab Interfaces

Physician Full Clinical Module

Complete Support for Integrated CCRC Campuses

Full Therapy (Rehab) Module that is Integrated with Resident Clinical Records

I strongly urge everyone to at least get one and update it with your current records and place one in a safety deposit box or on your keychain, you never know when it will save your life.

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Type 2 Diabetes May Increase The Risk Of Barrett's Esophagus

Patients with Type 2 Diabetes may face an increased risk for Barrett's Esophagus (BE), regardless of other risk factors including smoking, alcohol consumption, obesity and gastroesophageal reflux disease (GERD), according to research unveiled at the American College of Gastroenterology's (ACG) 77th Annual Scientific meeting in Las Vegas.
The study, "Diabetes Mellitus Increases the Risk of Barrett's Esophagus: Results from A Large Population Based Control Case Study," suggests that, "if you have diabetes, your risk for Barrett's esophagus (BE) may be almost doubled ," said co-investigator, Prasad G. Iyer, M.D., of the Mayo Clinic College of Medicine. He said this risk may be higher in men with diabetes likely because men tend to carry more fat in the abdomen compared to women who tend to carry weight around the hips and thighs.
Type 2 diabetes is the most is the most form of diabetes, with millions of Americans living with the disease. Barrett's esophagus is a condition in which the tissue lining the esophagus is replaced by tissue that is similar to the lining of the intestine. No signs or symptoms are associated with Barrett's esophagus but it is commonly found in people with GERD. About 5 to 10 percent of patients with chronic GERD will develop Barrett's esophagus.
Performing a population-based control study using the United Kingdom's General Practice Research Database (GPRD) (a primary care database containing more than 8 million patients), the researchers identified 14,245 Barrett's esophagus cases and 70,361 controls without Barrett's esophagus. Cases were more likely than controls to have ever smoked and consumed alcohol; and the prevalence of Type 2 diabetes before Barrett's esophagus diagnosis was higher in cases than controls. The mean BMI was also higher in cases than in controls both at baseline and over the study period.
Obesity is associated with an increased risk of Barrett's esophagus and esophageal cancer, but it is "unclear" if this is caused from a mechanical and/or metabolic effects such as hyperinsulinemia, according to investigators, who aimed to determine if there is an epidemiologic link between Type 2 diabetes and Barrett's esophagus after adjusting for known risk factors including obesity, smoking, alcohol use and GERD.
"Interestingly, we found that among the study cohort, if you had diabetes there was a twofold increase in your risk for Barrett's esophagus," explained Dr. Iyer. "When we stratified the results by gender, the association of Type 2 diabetes with Barrett's esophagus was stronger in males compared to females, which may reflect the different fat distributions in men and women."
Dr. Iyer said that while this study is retrospective - and further prospective studies are needed to better understand the link between Barrett's Esophagus and Type 2 Diabetes - the results do offer valuable and potentially life-saving insight to patients and health care providers: "if you lose weight your risk for Barrett's esophagus and esophageal cancer may decrease." Dr. Iyer suggested patients who are overweight, particularly if they carry their excess weight in their belly, talk to their physicians about their risk for Barrett's Esophagus and whether they should undergo screening through an upper endoscopy.

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New Depression Treatment Avoids Cognitive Side-Effects

Magnetic Seizure Therapy (MST) may be an effective treatment for the 30% of depression patients who do not receive benefits from conventional treatment.
The treatment was analyzed by a team of experts from the Monash Alfred Psychiatry Research Centre (MAPrc). Their research was published in two leading journals:Psychiatry Research: Neuroimaging and Depression and Anxiety.
Depressive disorders are very common and potentially disabling, said MAPrc Deputy Director Professor Paul Fitzgerald, study leader. He added that one fifth of all Australians are affected with depression at some time in their lives.
Professor Fitzgerald explained:

"Electroconvulsive Therapy (ECT) is one of the only established interventions for treatment resistant depression. But use of ECT is limited due to the presence of memory-related side effects and associated stigma.

This caused the MAPrc experts to start their observations on new treatment strategies. MST is a method that stimulates the brain that may have comparable outcomes to ECT, except with no unwanted reactions.
A previous report in Archives of General Psychiatry indicated that a treatment using magnetic currents to stimulate the brain induced remission in individuals with treatment-resistant depression.
Fitzgerald revealed:

"In MST, a seizure is induced through the use of magnetic stimulation rather than a direct electrical current like ECT. Magnetic fields are able to pass freely into the brain, making it possible to more precisely focus stimulation."

MST will better alleviate symptoms of depression without the memory difficulties that people experience with ECT, by not using direct electrical currents and inducing a stimulation that is more focal.
This therapy is only accessible in a few locations worldwide, as the research has just only begun. In Australia, the MAPrc is the only centre where trials are being conducted.
Results from the study showed that MST led to a remarkable decrease in depression symptoms:

• 40% of subjects showed overall improvement
• 30% of subjects showed some improvement

The patients did not report any cognitive side effects from this therapy.
"MST shows antidepressant efficacy without apparent cognitive side effects." Fitzgerald said.
However, further trials need to be conducted in order to have better insight on the best conditions for stimulation, as well as to compare MST to already existing treatments, such as ECT.
Large-scale randomized controlled trials are necessary to correctly assess the differences between MST and ECT. A substantial amount of research needs to be carried out before official statements can be made about the effectiveness of this therapy.
Funding from beyondblue and the NHMRC has been given to Professor Fitzgerald and his colleagues to conduct a large-scale trial on MST as a potential treatment for depression

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Oraquick–The Next Step in Testing

What is OraQuick?

OraQuick^® is the first FDA-approved oral swab in-home test for HIV-1 and HIV-2. It's an oral swab test that doesn't require blood. It's completely private. And it's based on the same HIV test that healthcare professionals have used since 2004.

With OraQuick, you have the comfort of getting your test results in the privacy of your own home. It's the only at-home oral HIV test approved by the FDA.

Trusted

Adapted from a clinically proven, FDA-approved test. With over 20 million tests sold, healthcare professionals have used it since 2004.

Confidential

You can call our Support Center any time. Our trained customer service representatives are available 24/7 ready to answer your questions.

Private

You take the test in the privacy of your own home.

Fast

You get results in 20 minutes.

Oral

OraQuick is an oral test. You just swipe your gums. There's no blood involved.

The OraQuick Test Kit includes:

1. Step-by-step directions
2. An oral swab test stick and tube with solution
3. Information booklets on HIV and testing
4. Package Insert containing information about the test

How Oral Testing Works

Most people assume that blood is involved in HIV testing. But with OraQuick an oral swab is used for testing and requires no blood. By collecting oral fluid from your gums, you collect fluid similar to that used in blood testing.

So the OraQuick Test detects antibodies for HIV, not the virus itself.

You just gently swipe the test swab along your upper gums once and your lower gums once. Then you insert the swab inside the test tube provided and get your results in just 20 minutes.

Safe and approved by the FDA for use by adults (17 years of age or older), OraQuick is the first and only HIV test that delivers your results with all the comforts and privacy of home.

A Name You Can Trust

For two decades, OraSure Technologies has been a leader in the development, manufacture and distribution of oral diagnostic and collection devices.

OraSure products are sold around the world to clinical laboratories, hospitals, clinics, community-based organizations and other public and governmental health organizations and agencies. With our products, healthcare providers can deliver critical information to their patients, empowering them to make decisions that will help improve and protect their health.

Where to Buy

OraQuick is available for purchase here at OraQuick.com or at fine retailers near you. If you do not see your favorite retailer listed below, please contact the retailer directly for product purchase or store location information.

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A direct link is not available at this time. For purchase or store location information, please contact the retailer directly.

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Available only in the U.S. through OraQuick.com or at authorized national retailers.

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Patch that could replace insulin jabs for diabetics

A stick-on patch that blasts insulin through the skin could banish the need for daily injections for many diabetics.

The high-tech electronic patch contains enough insulin to last the patient several days.

When a hand-held device, called a sonic applicator, is held over the patch, it fires sound waves that open up the pores in the skin and force the drug into the bloodstream more quickly.

Initial trials suggest the patch, called the U-Strip, can deliver insulin into the blood as quickly and effectively as a needle

The patch, called the U-Strip, has undergone initial trials in the U.S. involving around 100 people who have insulin-dependent diabetes.

The results suggest the patch can deliver insulin into the blood as quickly and effectively as a needle.

A larger trial, involving more than 500 patients, is now being planned and, if successful, the revolutionary device could become available in the UK within the next three years.

Diabetes affects around 2.8 million Britons. It occurs when the pancreas either stops producing insulin altogether, or its output drops sharply.

Insulin helps muscles absorb sugar from the blood to burn as a source of fuel.

Without the right levels of insulin, the disease can cause irreversible damage to the kidneys, eyes, nerves, heart and major arteries.

Many patients must test their blood sugar several times a day, and need insulin jabs for the rest of their lives in order to maintain adequate levels of the hormone.

Experts believe many would have better glucose control if there was an easier way to take their insulin.

A survey last year by the charity Diabetes UK showed one in three sufferers hid their condition from others and often failed to test their blood sugar levels or missed insulin jabs in case they drew attention to themselves.

Diabetes affects around 2.8 million Britons. It occurs when the pancreas either stops producing insulin altogether, or its output drops sharply

The sound wave patch could be a painless and more discreet alternative.

Drug-releasing skin patches are already widely used in hormone replacement therapy for the menopause and to help smokers quit.

Most work by allowing the active drug to gradually ‘seep’ through the skin.

But this technology only works with drugs made up of small molecules. Getting bigger molecules, such as those found in insulin, through the skin has been a major stumbling block.

But as the sound waves hit the skin, they prise open sweat glands and hair follicles which provide a direct route through to the bloodstream.

The patient usually wears the patch on their upper arm and places the hand-held sonic applicator — about the size of a mobile phone — directly over it.

At the press of a button, it produces a burst of sound waves that propel the insulin through the pores of the skin and into the bloodstream in a matter of seconds.

The device can hold different amounts of insulin, allowing it to be tailored to each patient, and contains a computer chip so that doctors can programme exactly how much insulin needs to be delivered into the body.

As with insulin injections, this has to be done several times a day to keep blood glucose levels under control. But the patch is waterproof and stays on the skin 24 hours a day, even during showers or baths.

The U.S. firm behind the new technology, Pennsylvania-based Transdermal Specialties Inc., says the smart patch can transmit the data wirelessly to a computer so it can be forwarded to the patient’s doctor.

Commenting on the development, Libby Dowling, clinical advisor for Diabetes UK, said: ‘Anything that makes daily life for people with diabetes easier is a good thing, and we will watch the developments of this technology with interest.’

_____________________________________________________

Meanwhile, scientists have developed a diabetes ‘vaccine’ made from the body’s own immune cells.

The injection appears to prevent type 1 diabetes by halting the damage that leads to the pancreas being unable to produce insulin.

Scientists hope the treatment, which has so far only been tested on mice, could eventually be used to ‘immunise’ at-risk children and adolescents.

Those with a family history of the disease would be one of the main target groups, as diabetes has a strong genetic link.

The condition causes the immune system to attack insulin-producing cells in the pancreas.

The reason remains a mystery, but one theory is that the process can be triggered by viral infection.

Some research points to enteroviruses — these cause diarrhoea and vomiting, but can also infect the pancreatic cells, triggering the immune system to attack them.

The jab works by harnessing cells called macrophages to protect against this attack.

Normally these cells are responsible for the damage associated with type 1 diabetes, but experts at the Karolinska Institute in Stockholm have found a way of converting macrophages into ‘good’ cells.

They inject a molecule that ‘tells’ the cells to protect rather than destroy, and so shield the pancreas from other immune system attacks.

The team tested the injection on mice that were genetically susceptible to diabetes.

After 12 weeks, only 25 per cent had developed diabetes, compared with 83 per cent of mice not given the jab.

The scientists now hope to use the injection in human trials.

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