Medicool's
Unique MultiVitamin
for Diabetics

  

Click To See The Latest Products For People With Diabetes

Click for Current News

You are currently in the News Archive

Click for Free offers
2004 | 2005 | 2006 | 2007
STUDY FINDS MEDITERRANEAN DIET CUTS RISK OF DIABETES BY 83%

DATE: June 27, 2008

The Mediterranean diet, with abundant quantities of virgin olive oil, gives strong protection against diabetes, a study has shown.

The diet, which includes high quantities of fruit, vegetables and wholegrain pulses and cereals is already known to protect against cardiovascular disease and, according to some research, against Alzheimer's disease. Now scientists in Spain have found that it also gives a defence against the epidemic of diabetes associated with growing rates of obesity and consumption of high-fat fast food. Researchers who monitored the eating habits of 13,000 graduates from the University of Navarra for eight years from 1999 to 2007 found those who stuck closely to a Mediterranean diet had an 83 per cent lower risk of developing diabetes than those who ate less healthy food.

Those who followed the diet most rigorously had more risk factors for diabetes, such as being older, having a family history of the disease and a history of smoking. Yet they were less likely to develop the disease. This suggests the protective effect of the diet may be substantial, the authors report in the British Medical Journal. Professor Martinez-Gonzalez and colleagues from the University of Navarra, say: "Substantial protection against diabetes can be obtained with the traditional Mediterranean diet, rich in olive oil, vegetables, fruit, nuts, cereals, legumes and fish, but relatively low in meat and dairy products." As well as having high levels of antioxidant vitamins, which mop up free radicals - damaging substances in the blood thought to be linked to cancer and arterial damage - the diet also lowers cholesterol and blood pressure, risk factors for heart disease. People who eat a Mediterranean diet are less likely to be obese, have a lower risk of breast and bowel cancer and half the rate of lung disease. A study also showed it reduced the risk of Alzheimer's by 40 per cent.


DIABETES EPIDEMIC - GETTING WORSE

DATE: June 20, 2008

Every day in the United States, 4,100 new cases of diabetes are diagnosed. The Centers for Disease Control and Prevention predicts that one in three Americans born in 2000 will develop diabetes. These alarming rates have sparked new educational campaigns to help prevent type 2 diabetes, the most common form of the disease, which is closely tied to being overweight. The growing problem also seems to be shaping the food aisles.

In the past four years, nearly 6,000 new sugar-free products hit store shelves, according to Lynn Dornblaser, a new-product analyst with Mintel, a market research company in Chicago. Beyond sugar-free, new diabetes-friendly foods are showing up in supermarkets, including snack bars, shakes and cereals that are promoted to people with diabetes. Despite the growing popularity of “diabetic foods,” however, some experts believe the marketing simply perpetuates a myth. “What is a diabetic food?” asked dietitian Hope Warshaw, a certified diabetes educator and author of “Diabetes Meal Planning Made Easy” (American Diabetes Association, $14.95). “There are no special foods that people with diabetes need to eat. We do a disservice to people by having them think they need to run out and buy special foods.” Warshaw said the nutrition recommendations for people with diabetes are the same as the general public — no rigid diet and no need to limit your selections to sugar-free foods. Sugar? Yes, people with diabetes can still have sugar. The no-sugar myth is one of the biggest misconceptions about diabetes, according to a new book “16 Myths of a Diabetic Diet” (American Diabetes Association, $14.95), by registered dietitians Karen Chalmers and Amy Campbell. This informative and easy-to read book busts the most common myths about diabetes and cleverly compares the old and new methods for managing diabetes. “Gone are the days when sugar is strictly off limits,” said co-author Campbell in a phone interview. “All carbohydrates break down into glucose in the same way. Your body doesn’t recognize whether the carbohydrate is a cookie, slice of bread or a potato.”

Sugar has always been intrinsically linked to diabetes. In fact, the disorder was once called “sugar diabetes” and people mistakenly believed that eating too much sugar was the cause. For years, people with diabetes were advised to avoid sweets because they were thought to overload the blood with glucose much faster than starches. Now researchers recognize that sugar has an impact on blood glucose that is similar to other carbohydrates. It’s much more important to keep track of total carbohydrates than to focus on avoiding sugar, Campbell said. “Totally eliminating sugar is unnecessary and impossible.” Even if all carbohydrates affect blood glucose levels in similar ways, they do differ nutritionally. Experts still advise choosing more starches or “complex” carbs — whole grains, fruits, vegetables and legumes — in place of concentrated sweets or “simple” carbs. Sugary foods and beverages can add a lot of empty calories and make it more difficult to manage your weight. Sweets also are typically high in fat, which can aggravate heart disease risk. However, instead of feeling guilty about eating sugar and trying to avoid it at all costs, Campbell encourages people with diabetes to find ways to fit reasonable portions into their eating plan — and enjoy them. Sugar-free options (particularly beverages) may help with calorie control, but they’re no longer a mandate for diabetes. Some may not even provide a significant advantage, said Chalmers.

Many sugar-free candies, cookies, cakes and ice creams contain nearly the same amount of calories and carbohydrates as their real sugar counterparts. That’s particularly true for sugar-free foods made with polyols or sugar alcohols (such as sorbitol, mannitol and xylitol). Although it has been many years since the nutrition guidelines for diabetes have changed, people still hold on to the belief that sugar is forbidden. Even some physicians still tell newly diagnosed patients to “stay away from sugar,” said Chalmers. Unfortunately, that’s often the only message they’re left with, she said. Instead, Chalmers encourages people to sit down with a certified diabetes educator and get the updated facts. She said the goal is to “fit diabetes into your lifestyle rather than fitting your lifestyle into your diabetes.” Finding ways to fit in favorite foods is the new mantra. Even the concept of a “diabetic diet” is a thing of the past. Now experts say people with diabetes should follow the same healthful eating plan as the rest of us — with an emphasis on whole grains, fruits and vegetables, lean protein and “good” fats. Moving beyond the myths, according to Campbell and Chalmers in their book, is the best way to manage diabetes and ensure you continue to enjoy the pleasures of the table.

DIABETES COOKBOOKS

It’s a myth that people with diabetes should only use diabetic cookbooks and recipes, according to “16 Myths of a Diabetic Diet.” Nonetheless, you’ll still find an endless array on bookstore shelves. Here are some of the best selections that keep the focus on flavor, all recently published by the American Diabetes Association.

  • “The All-Natural Diabetes Cookbook: The Whole Food Approach to Great Taste and Healthy Eating,” by Jackie Newgent.
  • “The Healthy Carb Diabetes Cookbook: Favorite Foods to Fit Your Meal Plan,” by Jennifer Bucko and Lara Rondinelli.
  • “Trim & Terrific Diabetic Cooking,” by Holly Clegg.

PESTICIDE EXPOSURE MAY INCREASE RISK OF DIABETES

DATE: June 13, 2008

Licensed pesticide applicators who used chlorinated pesticides on more than 100 days in their lifetime were at greater risk of diabetes, according to researchers from the National Institutes of Health (NIH). The associations between specific pesticides and incident diabetes ranged from a 20 percent to a 200 percent increase in risk, said the scientists with the NIH's National Institute of Environmental Health Sciences (NIEHS) and the National Cancer Institute (NCI).

"The results suggest that pesticides may be a contributing factor for diabetes along with known risk factors such as obesity, lack of exercise and having a family history of diabetes," said Dale Sandler, Ph.D., chief of the Epidemiology Branch at the NIEHS and co-author on the paper. "Although the amount of diabetes explained by pesticides is small, these new findings may extend beyond the pesticide applicators in the study," Sandler said. Some of the pesticides used by these workers are used by the general population, though the strength and formulation may vary. Other insecticides in this study are no longer available on the market, however, these chemicals persist in the environment and measurable levels may still be detectable in the general population and in food products. For example, chlordane, which was used to treat homes for termites, has not been used since 1988, but can remain in treated homes for many decades. More than half of those studied in the National Health and Nutrition Examination Survey in 1999-2002 had measurable evidence of chlordane exposure. "This is not cause for alarm," added Sandler "since there is no evidence of health effects at such very low levels of exposure."

Overall, pesticide applicators in the highest category of lifetime days of use of any pesticide had a small increase in risk for diabetes (17 percent) compared with those in the lowest pesticide use category (0-64 lifetime days). New cases of diabetes were reported by 3.4 percent of those in the lowest pesticide use category compared with 4.6 percent of those in the highest category. Risks were greater when users of specific pesticides were compared with applicators who never applied that chemical. For example, the strongest relationship was found for a chemical called trichlorfon, with an 85 percent increase in risk for frequent and infrequent users and nearly a 250 percent increase for those who used it more than 10 times. In this group, 8.5 percent reported a new diagnosis of diabetes compared with 3.4 percent of those who never used this chemical. Trichlorfon is an organophosphate insecticide classified as a general-use pesticide that is moderately toxic. Previously used to control cockroaches, crickets, bedbugs, fleas, flies and ticks, it is currently used mostly in turf applications, such as maintaining golf courses.

"This is one of the largest studies looking at the potential effects of pesticides on diabetes incidence in adults," said Freya Kamel, Ph.D., a researcher in the intramural program at NIEHS and co-author in the paper appearing in the May issue of the American Journal of Epidemiology. "It clearly shows that cumulative lifetime exposure is important and not just recent exposure," said Kamel. Previous cross-sectional studies have used serum samples to show an association between diabetes and some pesticides.

Diabetes occurs when the body fails to produce enough insulin to regulate blood sugar levels or when tissues stop responding to insulin. Nearly 21 million Americans have diabetes. The cause of diabetes continues to be a mystery, although genetics and environmental factors such as obesity and lack of exercise appear to play roles.

To conduct the study, the researchers analyzed data from more than 30,000 licensed pesticide applicators participating in the Agricultural Health Study, a prospective study following the health history of thousands of pesticide applicators and their spouses in North Carolina and Iowa. The 31,787 applicators in this study included those who completed an enrollment survey about lifetime exposure levels, were free of diabetes at enrollment, and updated their medical records during a five-year follow-up phone interview. Among these, 1,171 reported a diagnosis of diabetes in the follow-up interview. The majority of the study participants were non-Hispanic white men.

Researchers compared the pesticide use and other potential risk factors reported by the 1,171 applicators who developed diabetes since enrolling in the study to those who did not develop diabetes. Among the 50 different pesticides the researchers looked at, they found seven specific pesticides — aldrin, chlordane, heptachlor, dichlorvos, trichlorfon, alachlor and cynazine — that increased the likelihood of diabetes among study participants who had ever been exposed to any of these pesticides, and an even greater risk as cumulative days of lifetime exposure increased.

All seven pesticides are chlorinated compounds, including two herbicides, three organochlorine insecticides and two organophosphate pesticides.

"The fact that all seven of these pesticides are chlorinated provides us with an important clue for further research," said Kamel. Previous studies found that organochlorine insecticides such as chlordane were associated with diabetes or insulin levels. The new study shows that other types of chlorinated pesticides, including some organophosphate insecticides and herbicides, are also associated with diabetes. The researchers also found that study participants who reported mixing herbicides in the military had increased odds of diabetes compared to non-military participants.


NEW SIGNAL PATHWAY IMPORTANT IN DIABETES RESEARCH

DATE: June 06, 2008

Scientists at Karolinska Institutet in Sweden and Miami University have discovered that cells in the pancreas cooperate -- signal -- in a way hitherto unknown. The discovery can eventually be of significance to the treatment of diabetes. The aim of the project was to find out how the healthy body regulates glucose concentrations in the blood. Scientists have known for a long time that glucose is regulated with the help of hormones in the pancreas, which is to say that pancreatic beta cells produce insulin, which reduces sugar levels, and that alpha cells produce glucagon, which boosts them. This glucose balance must be kept within a very narrow interval, and we need both insulin and glucagon to remain in good health.

"A person with low blood sugar levels feels poorly and faint; a person with excessively high blood sugar levels gets diabetes," says Per-Olof Berggren, professor of experimental endocrinology at Karolinska Institutet and the leader of this study. Much more is known about insulin secretion than glucagon secretion, and so Professor Berggren's team focused on the latter. They discovered that alpha cells also secreted glutamate, which facilitates glucagon release and makes it more efficient. The scientists are working on the hypothesis that when glucose levels are raised in a healthy person, the beta cells become active and start to release insulin, which reduces sugar concentrations in the blood, upon which the alpha cells then start to secrete glucagon and glutamate. In this context, glutamate acts as a positive signal that tells the alpha cells that it is time to accelerate the production of glucagon to prevent glucose levels from falling too low. "It's this signal pathway that is our discovery," says Professor Berggren. "This interaction between beta cells and alpha cells is crucial for normal blood sugar regulation."

The discovery also means that when the beta cells fail to produce insulin properly, as is the case in diabetes, the alpha cells' signal path is also blocked, which upsets the glucose balance even more. The team hope that their discovery of the signal pathway will eventually give new impetus to clinical diabetes research. "Maybe we'll be able to achieve better blood sugar regulation in diabetes patients if we target more the glucagon/glutamate rather than just the insulin", says Professor Berggren.


NEW EVIDENCE FOR CAUSE OF TYPE 1 DIABETES DISCOVERED

DATE: May 29, 2008

Scientists at Washington University School of Medicine in St. Louis working with diabetic mice have examined in unprecedented detail the immune cells long thought to be responsible for type 1 diabetes. Researchers were able to examine the immune cells from isolated insulin-making structures in the pancreas known as the islets of Langerhans. They caught the immune cells, known as dendritic cells, "red-handed": carrying insulin and fragments of insulin-producing cells known as beta cells. This can be the first step toward starting a misdirected immune system attack that destroys the beta cells, preventing the body from making insulin and causing type 1 diabetes.

The results, reported online in The Proceedings of the National Academy of Sciences, push scientists a step closer to finding ways to treat this condition. "Now that we've isolated dendritic cells from the pancreas, we can look at why they get into the pancreas and determine which of the materials that they pick up are most critical to causing this form of diabetes," says senior author Emil R. Unanue, M.D., the Paul and Ellen Lacy Professor of Pathology. "That may allow us to find ways to inhibit dendritic cell function in order to block the disorder." The American Diabetes Association estimates that 1 million to 2 million Americans suffer from type 1 diabetes, which is also called juvenile diabetes because it frequently develops in children. Patients require insulin injections to survive because the immune system has destroyed the islets of Langerhans, which contain the body's only beta cells. The insulin these cells make is required for the critical task of regulating blood sugar levels.

Scientists detected dendritic cells in the islets years ago. Dendritic and other antigen-presenting cells are the sentinels of the immune system: They pick up bits of protein from around the body and present them to lymphocytes to initiate an immune system reaction. The lymphocytes lead immune attacks against foreign invaders like bacteria and viruses and eliminate them, clearing infections. But when interaction between an antigen-presenting cell and a lymphocyte leads to a part of the body being mistakenly identified as alien, the resulting attack harms the body, causing autoimmune diseases. Although dendritic cells' presence in the islets and their ability to summon immune attacks made them likely suspects in type 1 diabetes, they were challenging to isolate from the pancreas for closer examination.

"They're very tiny and there are only about 5 to 10 of them per islet, each of which contains approximately a thousand cells," explains Unanue. "So the senior postdoctoral researcher in the lab who did this work, Boris Calderon, had to develop some sophisticated cellular assays to pick them up." Calderon, M.D., found indications that the cells were carrying granules of insulin and pieces of proteins from beta cells on their cell surfaces. To test whether this cargo carried by the dendritic cells had the potential to trigger an immune attack on beta cells, Calderon exposed the dendritic cells to lymphocytes taken from diabetic mice. The lymphocytes were activated by the dendritic cells of the islets and switched into attack mode.

In a separate line of research, Unanue's lab has learned that dendritic cells in the pancreas may normally have beneficial effects on the health of beta cells. They've shown that when dendritic cells are absent from the pancreas, the beta cells are smaller, an indication that they're not as healthy. "We think these dendritic cells aren't in the pancreas by accident," says Unanue. "We believe that in the normal individual they help maintain the health of beta cells. But in a person with autoimmune diabetes, they appear to start the problems that destroy beta cells." The key distinction likely lies in a group of proteins called the major histocompatibility complex (MHC). Two decades ago, Unanue and Paul Allen, Ph.D., the Robert L. Kroc Professor of Pathology and Immunology, showed that the MHC provides the stage on which antigen-presenting cells show bits of protein or peptides to other immune system cells. Scientists believe autoimmune conditions like type 1 diabetes are caused by differences in what the MHC binds to and how it presents that material to immune attack cells. In support of this theory, Unanue's laboratory and that of Michael Gross, Ph.D., Washington University professor of chemistry, have collaboratively shown that the genes that encode the MHC proteins in the diabetic mouse are unique and bind to a set of very characteristic peptides. In addition to studying what protein fragments carried by dendritic cells are essential for causing type 1 diabetes, Unanue and others are working to learn how genetic variations in the MHC alter the chances that the immune system will mistakenly attack the body.


GASTRIC BYPASS SURGERY RESTORES SEXUAL FUNCTION IN MORBIDLY OBESE MEN

DATE: May 23, 2008

Losing weight may help resolve erectile dysfunction in obese men, according to research presented today at the 103rd Annual Scientific Meeting of the American Urological Association (AUA). Morbid obesity can cause sexual dysfunction independent of other common confounders, including diabetes, hypertension and smoking. In this study from researchers in Boston and Philadelphia, sexual function was normalized in some men who underwent gastric bypass surgery for weight loss. Researchers presented data to reporters during a special press conference on May 19, 2008.

“This study shows that weight loss and other risk factors which are alleviated by weight loss may be keys to restoring sexual function,” said Anthony Y. Smith, M.D. “These results give men another reason to improve their health by losing weight.”

In this study, 95 patients undergoing gastric bypass surgery for weight loss completed the Brief Sexual Inventory (BSI) pre- and post-operatively. On average, BSI scores improved in all categories, including sexual drive, erectile function, ejaculatory function, problem assessment and sexual satisfaction. The amount of weight lost predicted the degree of improvement in all areas of the survey. Results were then compared to data from the Olmstead County Study of Urinary Health Status Survey, a community-based prospective study often used as a baseline for study comparison. After an average of 67 percent weight loss post-bypass, BSI scores were comparable to patients in the Olmstead Study.

Gastric bypass surgery, a procedure that reduces the body’s caloric intake, can be used to induce significant weight loss in the obese. Calorie reduction is accomplished by making the stomach smaller and bypassing part of the stomach and small intestines so that fewer calories are absorbed. The patient feels full faster and learns to reduce the amount of food that he/she eats.


RESEARCH REVEALS DEMENTIA RISK FOR MEN & WOMEN

DATE: May 16, 2008

Men are more likely to develop Alzheimer's if they have a stroke, while women are more at risk if they are depressed, research suggested. A low level of education is also thought to influence the chance that both sexes will develop the disease.

A study of almost 7,000 people over the age of 65 examined a range of environmental and health factors to see how they affected progression of dementia. None of the people had dementia at the start of the study but 2,882 (42%) were classed as having mild cognitive impairment (MCI). This means they were starting to show signs of decline and did not perform highly on tests examining their level of recall.

The group, drawn from the French cities of Bordeaux, Dijon and Montpellier, was followed up after two years and again two years later. Men and women with MCI were more likely to be depressed and to be taking anticholinergic drugs, which are used to treat a range of conditions including incontinence, travel sickness and stomach cramps. Recent research has suggested some of these drugs can cause elderly people to experience greater decline in their thinking skills.

The study said men with MCI "were also more likely to have a higher body mass index, diabetes and stroke, whereas women were more likely to have poor subjective health, to be disabled, to be socially isolated, and to suffer from insomnia." The authors said: "Some potentially reversible risk factors for progression to dementia were identified, which were not the same for men and women. These factors should be taken into account in the development of gender-specific clinical intervention programmes for MCI."

The study was published in the Journal of Neurology, Neurosurgery and Psychiatry.


PATHWAY THAT CONTROLS THE PRODUCTION OF BLOOD SUGAR BEING UNRAVELED IN NEW STUDY

DATE: May 09, 2008

Peter Light, Alberta Heritage Foundation for Medical Research senior scholar and associate professor in the U of A Department of Pharmacology, has co-authored an article in the April 10 edition of the prestigious international science magazine, Nature. The paper showcases the discovery of a novel signaling pathway between the gut, the brain and the liver, and lowers blood sugar when activated.

In collaboration with University of Toronto diabetes researcher Tony Lam, Light was able to advise on experiments that showed the presence of fat in the small intestine activates a subset of nerves that send a signal to the brain, which in turn instructs the liver to lower blood-sugar production. "It is almost like a remote-control device which has a direct line to the brain," said Light. "It is like the gut has the brain on speed dial."

Light, whose research focuses on the effects of fats on insulin secretion in the pancreas, says although scientists have known that the brain and liver were involved in lowering blood sugar, this is the first time a direct link has been discovered. "This means if you can target this pathway in the gut, you may be able to regulate blood-sugar levels, which represents a novel approach to treating Type 2 diabetes," he said

Scientists around the world are in a race to discover new and effective ways to lower blood-sugar levels in people who are obese or who have diabetes because of the resulting risk of severe complications from high blood sugar, including heart attack, stroke, blindness, erectile dysfunction, foot problems and amputations. "The next set of experiments will look to determine what types of fats trigger this mechanism and what types of neurons are involved in this pathway to be able to target them with a variety of drugs," said Light. "Once you've established that signaling pathway, you can start looking at molecular targets for specific drugs. "The nice thing is, because it is in the gut, it is very amenable for some localized oral treatment."

Light adds that the discovery of this direct neural pathway opens up an avenue to discover the possible causes of Type 2 diabetes. "Is the whole mechanism dampened in an obese or Type 2 diabetic state?" said Light. "It could well be that if you have a diet high in fats going into the gut, it could just desensitize those neurons and they will not fire off any more."


RED WINE - POTENTIAL BENEFIT FOR DIABETES

DATE: May 02, 2008

New research suggests that resveratrol, a chemical commonly found in red wine, has the ability to lower blood sugar levels, but might also have certain yet-to-be-understood side effects. This research will be presented at the American Association of Clinical Endocrinologists (AACE) 17th Annual Meeting & Clinical Congress by Kimberly Martin, MD, and mentor, Dr. F. Ismail-Beigi, on Friday, May 16th, at the Walt Disney World Dolphin Resort in Orlando.

Resveratrol is a naturally occurring chemical found in grapes that has been reported to have cardioprotective, anti-inflammatory, anti-viral, and glucose-lowering properties. The effect of resveratrol on lowering blood glucose in diabetic rats has been reported by several investigators in the past.

Their results have shown that resveratrol improves glycemia by stimulating glucose transport in certain tissues including the skeletal muscle that expresses the insulin-sensitive Glut4 isoform of glucose transporters. However, the research by Drs. Martin and Ismail-Beigi shows that in cells expressing the Glut1 isoform, resveratrol blocks glucose transport by binding and inhibiting the Glut1 transporter. This may be of importance because certain cells and tissues, including brain, retina, placenta, and red blood cells express large amounts of this transporter. Hence, the presumed inhibition of the Glut1 transporter in these tissues in-vivo may have undesired and negative effects on their normal function.

"It's exciting to see resveratrol's glucose-lowering effect in diabetic experimental animals," Dr. Martin said. "However, studies are currently underway in our laboratory to determine whether the agent inhibits glucose transport in the brain of normal and diabetic animals."


GUM DISEASE CAN CONTRIBUTE TO MORE HARM THAN JUST TO YOUR TEETH

DATE: April 25, 2008

'Watch your mouth,'' the saying goes, and science is turning up ever more reasons to heed that advice literally. According to the editors of Consumer Reports, preventing gum disease (periodontitis), the leading cause of adult tooth loss, is gaining new urgency as research shows that gum disease can contribute to illnesses such as diabetes, heart disease, stroke and pneumonia.

The culprit, scientists believe, is a spillover of bacteria and inflammatory agents from the mouth into the bloodstream, which bustles them off to the rest of the body. CR health experts explain that related problems include these:

Diabetes. Gum disease and diabetes behave with yin-yang synergy. Because diabetes can affect circulation, it can restrict blood flow to the gums. That along with suppressed immunity in patients with diabetes can create the perfect setup for periodontitis. Recent research has suggested that treating periodontal disease can improve blood-sugar control. CR reports that some major insurance companies already offer patients with diabetes extended coverage for periodontal treatments.

Heart disease. Consumer Reports says that having gum disease can increase the risk of heart disease, a study found. Other data show that adults with the highest levels of some oral bacteria have thicker carotid arteries, a predictor of heart attack and stroke; and people who suffer from angina and heart attacks have higher levels of certain oral bacteria. Plus, oral bacteria provoke inflammation, which might increase levels of white blood cells and C-reactive protein. That protein, found in the blood, has been linked to heart disease. A March 2007 New England Journal of Medicine study of 120 patients found that aggressive treatment of periodontal disease was linked to improved circulation. In a recent trial, periodontal therapy reduced patients' C-reactive protein levels.

Pneumonia. Poor oral hygiene has been shown to contribute to fatal pneumonias in hospital patients and nursing-home residents. In those settings, lax oral hygiene can foster a buildup of bacteria capable of causing respiratory infection.

A patient placed on a respirator, for instance, is susceptible to breathing those bacteria, causing pneumonia. Institutions can avoid such infections by practicing stringent oral hygiene, including swabbing patients' mouths with plaque-inhibiting rinses containing chlorhexidine (Peridex, PerioGard).

CR concludes that taking care of the mouth and teeth can help stave off periodontal disease and possibly other serious illnesses.

ABCs of oral care

Eat a diet high in calcium and vitamins C and D. Avoid sugary foods: When oral bacteria ferment sugar, they create tooth-eroding acids.

Brush teeth twice a day and floss daily to remove plaque and bacteria.

See a dentist twice yearly for checkups (including an oral-cancer exam). Those who smoke or have periodontal disease or diabetes might need cleaning and checkups every three to four months.

USEFUL INFO Recent research has suggested that treating periodontal disease can improve blood-sugar control, important for people with diabetes.

Visit the Consumer Reports Web site at www.consumerreports.org


VIITAMIN D MIGHT HELP PROTECT AGAINST TYPE 1 DIABETES DEVELOPMENT

DATE: April 18, 2008

A review of the evidence shows a strong role for vitamin D supplements given in childhood protecting against the development of type 1 diabetes in later life. The higher the dose, the greater the protection. Further research is needed to find out the formulation, dose and duration of supplementation that will afford most protection.

Type 1 diabetes is an autoimmune disease in which the body destroys the insulin-producing cells in the pancreas, leaving the patient dependent upon insulin injections to control blood glucose levels. The disease is not well understood, but often starts in childhood and is most common among those of European descent, affecting around 2 million people in Europe and North America. What is more, those in Northern latitudes are more likely to be affected; a child in Finland is 400 times more likely to have type 1 diabetes than a child in Venezuela. The disease is increasing at a rate of about three percent per year and it has been predicted that by 2010 there will be 40 percent more cases of type 1 diabetes than there were in 2000. There is, therefore, an urgent need for better understanding of what causes type 1 diabetes.

Previous research has suggested that vitamin D supplementation in childhood might protect against type 1 diabetes and other autoimmune diseases like multiple sclerosis and rheumatoid arthritis. Vitamin D is obtained either from within the body, by exposure to sunlight, or from the diet. In some northern areas, children are short of vitamin D because of a lack of sunlight. There is also little vitamin D in breast milk. Therefore, vitamin D supplements have been recommended for infants but the uptake and dosage of these is variable. Researchers in Manchester, UK, have carried out a review of research on vitamin D supplementation and later development of type 1 diabetes, to determine whether this might be a useful way of helping protect children from the disease.

The researchers looked for high quality clinical trials that compared the risk of type 1 diabetes among those taking vitamin D with those who did not take it. They found five such trials, covering 6455 individuals in several European countries.

Overall, children given vitamin D supplementation had a 30 percent reduced risk of developing type 1 diabetes compared to children who did not receive supplements. There was also a dose response effect. Those who had been diagnosed with rickets, which is a sure sign of vitamin D deficiency, went on to be the most likely to develop type 1 diabetes. And those who received the most regular and higher doses of vitamin D had the lowest risk of type 1 diabetes.

The mechanism by which vitamin D supplementation may protect against type 1 diabetes remains unclear. However, there are vitamin D receptors on both insulin-producing cells and immune cells, suggesting that the vitamin plays a role in their healthy function. The study does not prove a cause and effect relationship between vitamin D and protection against diabetes. A further long-term trial designed specifically to address this question is now needed. Further investigation is also needed into how much vitamin D is needed, and for how long, to gain maximum protection.


SCIENTISTS AT MASSACHUSETTS GENERAL HOSPITAL HAVE INITIATED A CLINICAL TRIAL TO REVERSE TYPE 1 DIABETES

DATE: March 21, 2008

The trial is exploring whether the promising results from the laboratory of Denise Faustman, MD, PhD, can be applied in human diabetes. Faustman's previous studies have shown that mice with a form of diabetes that closely resembles type 1 diabetes in humans can be cured. In the animal studies, a commonly used vaccine that provides protection against tuberculosis, called Bacillus Calmette-Guerin (BCG) was used effectively to deplete the abnormal immune cells that attack and destroy the insulin producing cells of the pancreas. The first step in the human study, which is currently enrolling volunteers, is to determine whether the same strategy using BCG vaccination can be used to modify the abnormal autoimmune cells that are present in type 1 diabetes, sometimes called "juvenile-onset" diabetes.

"We are pleased to be starting human clinical trials," said Faustman. "Human trials take time, but we are making the step from curing diabetes in mice to determining whether it will work in men and women with diabetes."

Type 1 diabetes usually starts during childhood or adolescence and can cause a variety of severe complications including kidney failure, loss of vision, amputations, heart disease, and strokes. It occurs when a person's immune system attacks and destroys the insulin-producing cells in the pancreas. In the absence of insulin, which is necessary for sugar and other nutrients to enter cells, blood sugar levels rise. The risk for developing complications is closely linked to the elevated blood sugar levels over time. If blood sugar levels are well controlled, the long-term complications can largely be avoided. However, the so-called intensive therapy that is required to maintain near-normal sugar levels requires life-long demands on the patient, including frequent blood sugar monitoring and at least 3 daily injections of insulin or use of an insulin pump, along with restrictive diets. Insulin doses must be adjusted based on blood sugar levels, dietary factors, and anticipated exercise. Thus, a cure for diabetes has been highly sought after and has attracted much research interest.

The clinical trial is using the BCG vaccine for several reasons. BCG has been used safely for nearly 80 years as a tuberculosis vaccine. It is now being used in the human trial because it causes a low-grade inflammatory reaction, which in the mouse model of autoimmune diabetes lead to the destruction of the abnormal autoimmune cells.

David M. Nathan, MD, director of the MGH Diabetes Center, who is leading the human study at MGH, provides context, "This is the very first step in what is likely to be a long process in achieving a cure. We first need to determine whether the abnormal autoimmune cells that underlie type 1 diabetes can be knocked out with BCG vaccination, as occurred in the mouse studies."

www.mgh.harvard.edu


VITAMIN D MAY CUT RISK OF DIABETES IN CHILDREN

DATE: March 14, 2008

Giving young children vitamin D supplements may reduce their risk of developing type 1 diabetes later in life, research suggests.

Children who took supplements were around 30% less likely to develop the condition than those who did not. Type 1 diabetes results from the immune system destruction of pancreatic cells which produce the hormone insulin. The study, by St Mary's Hospital for Women and Children, in Manchester England, appears in Archives of Disease in Childhood.

Type 1 diabetes is most common among people of European descent, with around two million Europeans and North Americans affected. It is becoming increasingly common, and it is estimated that the number of new cases will rise by 40% between 2000 and 2010. The Manchester team pooled data from five studies examining the effect of vitamin D supplementation. Not only did the use of supplements appear to reduce the risk, the effect was dose dependent - the higher and more regular the dose, the lower the likelihood of developing the disease.

Previous research has found that people newly diagnosed with type 1 diabetes have lower concentrations of vitamin D than those without the condition. Studies have also found that type 1 diabetes is more common in countries where exposure to sunlight - which enables the body to manufacture vitamin D - is lower. For instance, a child in Finland was 400 times more likely to develop the disease than a child in Venezuela. Separate research has linked low levels of vitamin D and sunlight to other autoimmune disorders, including multiple sclerosis and rheumatoid arthritis. Further evidence of vitamin D's role comes from the fact that pancreatic beta cells and immune cells carry receptors or docking bays for the active forms of the vitamin.

It is thought that vitamin D helps to keep the immune system healthy, and may protect cells from damage caused by chemicals which control inflammation. Dr Victoria King, of the charity Diabetes UK, said: "Much more research, in particular controlled trials which compares the results when one group of people are given vitamin D supplements and one group is not, are needed before we can confirm a concrete association between vitamin D and type 1 diabetes."

Governnment experts in the UK recommend vitamin D supplementation for at least the first two years of a child's life, although the Chief Medical Officer for England has suggested supplements for the first five years is a good idea.


GROWING EVIDENCE SHOWS THAT SURGERY MAY EFFECTIVELY CURE TYPE 2 DIABETES

DATE: March 07, 2008

A new article published in a special supplement to the February issue of Diabetes Care by a leading expert in the emerging field of diabetes surgery points to the small bowel as the possible site of critical mechanisms for the development of diabetes.

The study's author, Dr. Francesco Rubino of NewYork-Presbyterian Hospital/Weill Cornell Medical Center, presents scientific evidence on the mechanisms of diabetes control after surgery. Clinical studies have shown that procedures that simply restrict the stomach's size (i.e., gastric banding) improve diabetes only by inducing massive weight loss. By studying diabetes in animals, Dr. Rubino was the first to provide scientific evidence that gastrointestinal bypass operations involving rerouting the gastrointestinal tract (i.e., gastric bypass) can cause diabetes remission independently of any weight loss, and even in subjects that are not obese.

"By answering the question of how diabetes surgery works, we may be answering the question of how diabetes itself works," says Dr. Rubino, who is a professor in the Department of Surgery at Weill Cornell Medical College and chief of gastrointestinal metabolic surgery at NewYork-Presbyterian/Weill Cornell.

Dr. Rubino's prior research has shown that the primary mechanisms by which gastrointestinal bypass procedures control diabetes specifically rely on the bypass of the upper small intestine -- the duodenum and jejunum. This is a key finding that may point to the origins of diabetes.

"When we bypass the duodenum and jejunum, we are bypassing what may be the source of the problem," says Dr. Rubino, who is heading up NewYork-Presbyterian/Weill Cornell's Diabetes Surgery Center.

In fact, it has become increasingly evident that the gastrointestinal tract plays an important role in energy regulation, and that many gut hormones are involved in the regulation of sugar metabolism. "It should not surprise anyone that surgically altering the bowel's anatomy affects the mechanisms that regulate blood sugar levels, eventually influencing diabetes," Dr. Rubino says.

While other gastrointestinal operations may cure diabetes as an effect of changes that improve blood sugar levels, Dr. Rubino's research findings in animals show that procedures based on a bypass of the upper intestine may work instead by reversing abnormalities of blood glucose regulation.

In fact, bypass of the upper small intestine does not improve the ability of the body to regulate blood sugar levels. "When performed in subjects who are not diabetic, the bypass of the upper intestine may even impair the mechanisms that regulate blood levels of glucose," says Dr. Rubino. In striking contrast, when nutrients' passage is diverted from the upper intestine of diabetic patients, diabetes resolves.

This, he explains, implies that the upper intestine of diabetic patients may be the site where an abnormal signal is produced, causing, or at least favoring, the development of the disease.

How exactly the upper intestine is dysfunctional remains to be seen. Dr. Rubino proposes an original explanation known in the scientific community as the "anti-incretin theory."

Incretins are gastrointestinal hormones, produced in response to the transit of nutrients, that boost insulin production. Because an excess of insulin can determine hypoglycemia (extremely low levels of blood sugar) -- a life-threatening condition -- Dr. Rubino speculates that the body has a counter-regulatory mechanism (or "anti-incretin" mechanism), activated by the same passage of nutrients through the upper intestine. The latter mechanism would act to decrease both the secretion and the action of insulin.

"In healthy patients, a correct balance between incretin and anti-incretin factors maintains normal excursions of sugar levels in the bloodstream," he explains. "In some individuals, the duodenum and jejunum may be producing too much of this anti-incretin, thereby reducing insulin secretion and blocking the action of insulin, ultimately resulting in Type 2 diabetes."

Indeed, in Type 2 diabetes, cells are resistant to the action of insulin ("insulin resistance"), while the pancreas is unable to produce enough insulin to overcome the resistance.

After gastrointestinal bypass procedures, the exclusion of the upper small intestine from the transit of nutrients may offset the abnormal production of anti-incretin, thereby resulting in remission of diabetes.

In order to better understand these mechanisms, and help make the potential benefits of diabetes surgery more widely available, Dr. Rubino calls for prioritizing research in diabetes surgery. "Further research on the exact molecular mechanisms of diabetes, surgical control of diabetes and the role played by the bowel in the disease may bring us closer to the cause of diabetes."

Today, most patients with diabetes are not offered a surgical option, and bariatric surgery is recommended only for those with severe obesity (a body mass index, or BMI, of greater than 35kg).

"It has become clear, however, that BMI cut-offs can no longer be used to determine who is an ideal candidate for surgical treatment of diabetes," says Dr. Rubino.

"There is, in fact, growing evidence that diabetes surgery can be effective even for patients who are only slightly obese or just overweight. Clinical trials in this field are therefore a priority as they allow us to compare diabetes surgery to other treatment options in the attempt to understand when the benefits of surgery outweigh its risks. Clinical guidelines for diabetes surgery will certainly be different from those for bariatric surgery, and should not be based only on BMI levels," he notes.

"The lesson we have learned with diabetes surgery is that diabetes is not always a chronic and relentless disease, where the only possible treatment goal is just the control of hyperglycemia and minimization of the risk of complications. Gastrointestinal surgery offers the possibility of complete disease remission. This is a major shift in the way we consider treatment goals for diabetes. It is unprecedented in the history of the disease," adds Dr. Rubino.

Type 2 diabetes, which accounts for 90 to 95 percent of all cases of diabetes, is a growing epidemic that afflicts more than 200 million people worldwide.

At a time when diabetes is growing epidemically worldwide, Dr. Rubino says that finding new treatment strategies is a race against time. "At this point, missing the opportunity that surgery offers is not an option."

In addition to having performed landmark studies in the field of diabetes surgery, Dr. Rubino was the principal organizer of an influential Diabetes Surgery Summit, held in Rome in March 2007. This international consensus conference helped establish the field, making international recommendations for the use of surgery and creating an International Diabetes Surgery Task Force. Dr. Rubino serves as a founding member.

For more information, patients may call (866) NYP-NEWS.


STEM CELL RESEARCH MAKING PROGRESS TOWARD DIABETES PREVENTION AND CURE

DATE: February 29, 2008

Stem Cell Research Making Progress Toward Diabetes Prevention and Cure

Researchers at a small San Diego biotech company have devised a procedure for turning human embryonic stems cells into insulin-producing cells inside mice. Numerous researchers have been trying to figure out how to convert embryonic stem cells into insulin-producing cells that could be used to treat diabetics. But progress has been slow because scientists don't know the recipe for stimulating immature stem cells to differentiate into the highly specialized pancreatic islet cells, the cells that are destroyed in Type 1 diabetes. The new work, by researchers at the privately held biotech firm Novocell, is important because it suggests one method for doing this that might work in humans: "It is proof that you can take embryonic stem cells for the first time and take them all the way through to become pancreas cells" that release insulin, says lead researcher Emmanuel Baetge, head scientist at Novocell. The company hopes to devise a human treatment based on the process in a few years

Harvard University stem-cell researcher Douglas Melton called the finding "one more step in a long and important process" toward devising human stem-cells treatments. But he cautions it is "not yet" a breakthrough. The Novocell researchers have been grinding away on figuring out how to transform stem cells into insulin-producing cells for six years. In previous papers, they found they could take proprietary embryonic stem cells in the test tube and convert them into pancreas precursor cells by adding and subtracting a variety of growth-promoting proteins. But they were not able to quite make the final step and transform the cells into healthy insulin-producing cells, at least in the test tube. So instead, they transplanted their immature human pancreas cells into mice. "We said, 'Something is wrong; we don't have the right environment. Lets transplant the cells and see what happens,'" says Baetge. Lo and behold, after a month, the cells started to become functional and produce insulin. Some unknown signals inside the mice had stimulated them to convert into mature insulin-makers. To prove that the new cells were functional, the researchers then destroyed the mouse's own insulin-producing cells using a toxin that didn't kill the transplanted cells. The mice didn't get diabetes, confirming that the new cells worked, according to the report in Nature Biotechnology.

Novocell hopes a similar procedure might also work for treating human diabetes. But much work remains before any clinical trial could begin. The first step will be to purify the mix of precursor cells injected into the mice to pinpoint the exact cell type responsible for becoming insulin cells. Safety is another huge concern; researchers will need to provide evidence that the new cells won't turn into something else beside insulin cells once implanted inside people--such as a tumor. The company also needs to devise a method for efficiently making large quantities of the precursor cells. Nonetheless, "I do think that a procedure like this could work in people," says Harvard University stem-cell expert Kevin Eggan. "I don't think that there is any reason to doubt the validity" of the finding. In theory, the new research could dovetail nicely with the surprising findings late last year by Japanese and American scientists that ordinary skin cells can be re-programmed to turn into embryonic stem cells. These findings raise the possibility of future stem-cell treatments that do not involve the destruction of embryos. But whatever the source of stem cells for future therapies, scientists will still need recipes for making them into particular cell types used for treatment--such as the protocol Novocell has developed. "It is certainly a huge breakthrough, but there is a long way to go [before using the re-programmed] cells as a substitute for embryonic stem cells," says Baetge. Some researchers worry that the Novocell finding, while solid, is a bit of a black box. "This doesn't really teach us very much. Something happens [inside the mice], but we don't know anything about what. At the end of the day we didn't learn very much," says Vanderbilt University stem-cell researcher Mark A. Magnuson. He called converting a stem cell into pancreatic beta cells a "phenomenally complex" process. While stem cells hold huge promise, "we are not anywhere near close to new therapies for years," he says.


GLUCOSE TESTING IN DIABETIC DIALYSIS PATIENTS NOT ACCURATE

DATE: February 22, 2008

The standard test for measuring blood sugar control in people with diabetes is not accurate in those on kidney hemodialysis, according to new research at Wake Forest University Baptist Medical Center.

Wake Forest investigators reported in Kidney International that the hemoglobin A1c test (HbA1c) underestimates true glucose control in hemodialysis patients and could give false comfort to patients and physicians. Hemodialysis, in which blood is passed through an artificial kidney machine for cleansing, is used in cases of kidney failure. "These results suggest that the nearly 200,000 diabetic hemodialysis patients in the United States who use this test may not be receiving optimal care for their blood sugar," said Barry I. Freedman, M.D., senior author and a professor of internal medicine and nephrology. Diabetic dialysis patients who believe their blood sugars are in the ideal range may still have unacceptably high blood sugars. "This was a surprise to the nephrology community," said Freedman. "The test we've all come to accept as 'the gold standard' has proven to be inaccurate in this patient population."

HbA1c measures the percentage of hemoglobin (a protein in red blood cells) that has reacted with glucose. This measure, also known as glycosylated hemoglobin, reflects blood sugar control over the previous 30-120 days. This study evaluated 307 patients with diabetes - 258 with end-stage kidney disease on hemodialysis and 49 who did not have kidney failure. The researchers compared the standard HbA1c test with a newer test (glycated albumin, or GA) that measures the amount of blood sugar that has reacted with albumin, a protein in the plasma. The GA test reflects blood sugar control over the previous three to four weeks. Blood samples were also analyzed to determine recent blood sugar levels. Compared to those without kidney failure, diabetic patients on hemodialysis had higher blood sugars and GA levels, despite paradoxically lower HbA1c results. The relationship between GA and HbA1c differed between diabetic dialysis patients and those without kidney disease, demonstrating that the HbA1c did not accurately reflect blood sugar control in those on hemodialysis.

Researchers believe the major reason for the discrepancy is that HbA1c depends on red blood cell survival and these cells don't live as long in hemodialysis patients. Most dialysis patients have anemia requiring treatment with medications that stimulate red blood cell production (erythropoietin). The current study confirmed a report in Japanese patients and is the first to demonstrate the inaccuracy of the HbA1c in black and white dialysis patients. The Wake Forest researchers will soon determine whether these concerns also apply to patients on peritoneal dialysis and to people with kidney disease not yet on dialysis. Controlling blood sugar is important because high levels are risk factors for developing hardening of the arteries (atherosclerosis) and lead to higher rates of kidney disease, heart attack, stroke, nerve damage and blindness. People with diabetes who undergo hemodialysis are at especially high risk. About one out of four diabetic dialysis patients (23 percent) in the U.S. will die from cardiovascular and infection complications during their first year on dialysis, and only 31 percent survive five years.

"Control of blood sugar improves outcomes of diabetic patients, so accurate assessment is critical," said Freedman. "This study supports the GA test as a more accurate measure of long-term blood sugar control among diabetic patients who are on hemodialysis." The GA test is not currently available in the United States. Freedman said that until it is available, doctors and patients should be aware that the HbA1c underestimates glucose control and is affected by both erythropoietin administration and the hemoglobin concentration. The research is sponsored by Asahi Kasei Pharma Corporation (Tokyo), manufacturer of the GA test. Co-investigators were Todd Peacock, B.S., Zak K. Shihabi, Ph.D., Anthony J. Bleyer, M.D., Emily L. Dolbare, M.D., Joyce R. Byers, R.N., Mary Ann Knovich, M.D., Jorge Calles-Escandon, M.D., and Gregory R. Russell, M.S., all with Wake Forest.

Wake Forest University Baptist Medical Center is an academic health system comprised of North Carolina Baptist Hospital and Wake Forest University Health Sciences, which operates the university's School of Medicine. U.S. News & World Report ranks Wake Forest University School of Medicine 18th in primary care and 44th in research among the nation's medical schools. It ranks 35th in research funding by the National Institutes of Health. Almost 150 members of the medical school faculty are listed in Best Doctors in America.


STUDY CONFIRMS LINK BETWEEN FAST-FOOD CONSUMPTION AND AN INCREASE IN METABOLIC RISK FACTORS

DATE: February 15, 2008

Otherwise-healthy adults who eat two or more servings of meat a day - the equivalent of two burger patties - increase their risk of developing metabolic syndrome by 25 percent compared with those who eat meat twice a week, according to research published in /Circulation: Journal of the American Heart Association./

Metabolic syndrome is a cluster of cardiovascular disease and diabetes risk factors including elevated waist circumference, high blood pressure, elevated triglycerides, low levels of high-density lipoprotein (HDL or "good") cholesterol and high fasting glucose levels. The presence of three or more of the factors increases a person's risk of developing diabetes and cardiovascular disease. But it's not just meat that adds inches to the waist, increases blood pressure and lowers HDL - "it's fried foods as well," said Lyn M. Steffen, Ph.D., M.P.H., R.D., co-author of the study and an associate professor of epidemiology at the University of Minnesota. Dairy products, by contrast, appeared to offer some protection against metabolic syndrome. Steffen said that, "Fried foods are typically synonymous with commonly eaten fast foods, so I think it is safe to say that these findings support a link between fast-food consumption and an increase in metabolic risk factors."

The findings emerged from an analysis of dietary intake by 9,514 participants in the Atherosclerosis Risk In Communities (ARIC) study. ARIC is a collaborative study funded by the National Heart, Lung, and Blood Institute. Unlike other researchers who have investigated relationships between nutrients and cardiovascular risk, "we specifically studied food intake. When making recommendations about dietary intake it is easier to do so using the framework of real foods eaten by real people," Steffen said. Researchers assessed food intake using a 66-item food frequency questionnaire. From those responses, they categorized people by their dietary preferences into a Western-pattern diet or a prudent-pattern diet. In general, the Western-pattern diet was heavy on refined grains, processed meat, fried foods, red meat, eggs and soda, and light on fish, fruit, vegetables and whole grain products. Prudent diet eating patterns, by contrast, favored cruciferous vegetables (e.g., cabbage, radish and broccoli), carotenoid vegetables (e.g., carrots, pumpkins, red pepper, cabbage, broccoli and spinach), fruit, fish and seafood, poultry and whole grains, along with low-fat dairy.

Researchers also assessed associations with individual food items: fried foods, sweetened beverages (regular soda and fruit drinks), diet soda, nuts and coffee.

After nine years of follow-up, 3,782 (nearly 40 percent) of the participants had three or more of the risk factors for metabolic syndrome. At baseline, participants were 45 to 64 years old - ages at which many people gain weight. Steffen said that weight gain over the years of follow-up might explain some of the cases of metabolic syndrome. But "after adjusting for demographic factors, smoking, physical activity and energy intake, consumption of a 'Western' dietary pattern was adversely associated with metabolic syndrome," she said. "One surprising finding was while it didn't increase the risk of metabolic syndrome, there was no evidence of a beneficial effect of consuming a prudent diet either. I had expected to find a beneficial effect because we have seen that in other studies." When Steffen and colleagues analyzed the results by specific foods, they found that meat, fried foods and diet soda were all significantly associated with increased risk of metabolic syndrome, but consumption of dairy products was beneficial. The study did not address the mechanisms involved in the increased risk of metabolic syndrome seen with certain foods, but Steffen speculated that "it may be a fatty acid mechanism since saturated fats are a common link and certainly overweight and obesity are contributing to the development of metabolic syndrome." She also said more research on the relationship between diet soda and its association to metabolic syndrome is needed.

The fact that 60.5 percent of the ARIC population had metabolic syndrome at the start of the study or developed it during nine years of follow-up is troubling, researchers said. Steffen said the study's results are clear: Too much meat, fried foods and diet soda, do not add up to a healthy life.

American Heart Association dietary guidelines for healthy Americans age 2 and older include:

  • Limit saturated fat, trans fat, cholesterol and sodium in the diet.
  • Minimize the intake of food and beverages with added sugars.
  • Eat a diet rich in vegetables, fruits and whole-grain foods.
  • Select fat-free and low-fat dairy.
  • Eat fish at least twice per week.
  • Emphasize physical activity and weight control.
  • Avoid use of and exposure to tobacco products.
  • Achieve and maintain healthy cholesterol, blood pressure and blood glucose levels.

MAYO CLINIC STUDY FINDS ASSOCIATION BETWEEN DIABETES AND PANCREATIC CANCER

DATE: February 08, 2008

A new Mayo Clinic study found that 40 percent of pancreatic cancer patients are diagnosed with diabetes prior to their pancreatic cancer diagnosis. The onset of diabetes appears to be many months (in some cases up to two years) prior to cancer diagnosis. This information provides researchers an important clue for earlier detection of pancreatic cancer. The study was published in last month's issue of Gastroenterology.

"Our previous studies have shown an association between recent diagnoses of diabetes and pancreatic cancer," says Suresh Chari, M.D., a Mayo Clinic gastroenterologist and the study's lead author. "We are now quite convinced that in most patients with pancreatic cancer the diabetes is caused by the cancer and not the other way around. Our next step is to identify a biomarker for pancreatic cancer-induced diabetes in order to screen patients with new-onset diabetes for early pancreatic cancer and provide surgical treatment as quickly as possible." More than 33,000 people die each year from pancreatic cancer, the fourth-leading cause of cancer death in the United States. Patients with this cancer seldom exhibit disease-specific symptoms until the cancer is at an advanced stage and surgery is no longer an option. Therefore, fewer than 5 percent of pancreatic cancer patients survive five years after diagnosis. This study reviewed the medical records of 736 patients with pancreatic cancer and 1,875 healthy individuals with fasting blood glucose data in their medical record. Dr. Chari's team found that 40 percent of pancreatic cancer patients were diagnosed with diabetes, while only 20 percent of the healthy individuals had fasting blood glucose levels in the diabetic range.

Type 2 diabetes is far more common than pancreatic cancer-induced diabetes. According to a previous study authored by Dr. Chari, only one in 125 patients over age 50 with new-onset diabetes will be diagnosed with pancreatic cancer. Dr. Chari's team continues work in identifying the differences between pancreatic cancer-induced diabetes and regular type 2 diabetes. The goal of the research is to cost-effectively screen for pancreatic cancer using a blood test that can identify individuals who have new-onset diabetes and are more likely to have pancreatic cancer. This will allow for earlier detection and increased opportunity for successful surgical treatment. Other members of the Mayo Clinic research team included Cynthia Leibson, Ph.D., Kari Rabe, Lawrence Timmons, Jeanine Ransom, Mariza de Andrade, Ph.D., and Gloria Petersen, Ph.D. As part of this ongoing research, a clinical trial studying the role of high resolution secretin-enhanced CT scan to diagnose early pancreatic cancer in patients at high risk for pancreatic cancer is currently in progress at Mayo Clinic in Rochester, Minn. Eligible participants must be 50 years or older, must have received a diagnosis of diabetes within the past two years, and must have at least one of the following: no family history of diabetes, abdominal discomfort or pain, weight loss, or elevated serum CA 19-9. The Mayo Clinic website: www.mayoclinic.com


WHOLE GRAIN FOODS MIGHT REDUCE DIABETES RISK

DATE: February 01, 2008

Many have touted whole grain foods as a way to prevent type 2 diabetes, and a new review finds a reduction in risk for people who consume a diet high in unrefined grains. However, the authors caution that more research is necessary before scientists can confirm a causal relationship. "At the moment, because there is only weak evidence, no definite conclusion can be drawn concerning the protective effect of whole grain foods for the development of type 2 diabetes," said lead review author Marion Priebe. Refined cereal food products remove the nutrient- and fiber-rich bran and germ of the grain, leaving only the starchy inner parts. A decrease in consumption of whole grain cereals over the last decade, occurring at the same time as an increase in type 2 diabetes, has lead to the theory that there is a connection between the two.

Priebe, a nutritionist and epidemiologist at the Center for Medical Biomics, University Medical Center Groningen in the Netherlands, and colleagues reviewed 12 studies that examined relationships between whole grain intake and type 2 diabetes. These studies consisted of a single randomized controlled clinical trial and 11 prospective studies. The review appears in the latest issue of The /Cochrane Library/, a publication of The Cochrane Collaboration, an international organization that evaluates medical research. Systematic reviews draw evidence-based conclusions about medical practice after considering both the content and quality of existing medical trials on a topic. In the prospective studies, researchers followed groups of people without diabetes over long periods to see whether those who consumed more whole grain foods were less likely to get the disease than other participants were. These studies consistently showed a reduction of risk for the disease in those with a high intake of whole grain foods or cereal fiber.

Two of the studies that looked at the effect of whole grain consumption on weight, an important diabetes risk factor, found only a slight improvement.Scientists consider evidence from prospective studies to be weaker than that from randomized controlled trials. Other factors, like an overall healthy lifestyle, can also influence the development of type 2 diabetes and it is not possible to completely correct for known and possibly unknown factors in this study design. In randomized controlled trials, which are more difficult to perform, researchers can exclude or control for other influences on the development of the disease.Priebe said she was surprised that only one randomized trial on this topic exists: "As type 2 diabetes mellitus is reaching epidemic proportions and diet is considered as a modifiable risk factor, it is important to have a sound knowledge of which kinds of food can contribute to the prevention of this disease and to identify gaps in this knowledge."

Osama Hamdy, M.D., medical director of the Clinical Obesity Program at the Joslin Diabetes Center in Boston, said the kinds of data used within the review are troubling. He said that studies about diabetes prevention should be randomized controlled trials over long durations. Although the concept of a whole grains-rich diet as a possible diabetes preventative is interesting, he said, none of the review studies would enable any kind of cause-and-effect conclusion. "This is an additional piece of information that tells us diets rich in whole grains will probably do some good in the prevention of type 2 diabetes," Hamdy said. "It is not a shortcut to tell you exactly what you need. It is just more support of a concept that has been around for a long time." "Whole grain foods are rich in dietary fiber and nutrients and they are recommended to be consumed together with plenty of fruit and vegetables for a healthy diet," Priebe said. The findings of this review are in line with those recommendations." The Cochrane Collaboration is an international nonprofit, independent organization that produces and disseminates systematic reviews of health care interventions and promotes the search for evidence in the form of clinical trials and other studies of interventions. Visit www.cochrane.org for more information.


STUDY BACKS SURGERY FOR OBESE PATIENTS WITH DIABETES

DATE: January 25, 2008

Preliminary research indicates that obese patients with type 2 diabetes who had gastric banding surgery lost more weight and had a higher likelihood of diabetes remission compared to patients who used conventional methods for weight loss and diabetes control, according to a study in the a January 23 issue of The Journal of the American Medical Association.

"Obesity and type 2 diabetes are likely to be the 2 greatest public health problems of the coming decades. The conditions are strongly linked, with the increased prevalence of diabetes correlating with the increased prevalence of obesity," the authors write. Weight control is perhaps the most important aspect of type 2 diabetes management. Recent evidence indicates that improvement in blood glucose control is related to the degree of weight loss. Currently available lifestyle and pharmacological strategies provide only small to modest levels of weight loss, a problem compounded by patients with diabetes experiencing greater difficulty in losing weight than those without diabetes. Significant sustained weight loss as a result of bariatric surgery has never been formally studied as a treatment for type 2 diabetes in obese participants, according to background information in the article.

John B. Dixon, M.B.B.S., Ph.D., of Monash University, Melbourne, Australia, and colleagues conducted a 2-year trial involving 60 obese participants (body mass index [BMI] greater than 30, less than 40) to compare surgically induced weight loss with conventional therapy for the management of type 2 diabetes. Patients were randomized to receive either conventional diabetes therapy with a focus on weight loss by lifestyle change or laparoscopic adjustable gastric banding with conventional diabetes care. Of the 60 patients enrolled, 55 (92 percent) completed the 2-year follow-up. The researchers found that remission of type 2 diabetes was achieved by 26 study participants (43 percent) at two years, with 22/30 (73 percent) from the surgical program and 4/30 (13 percent) from the conventional-therapy program. This represented 76 percent and 15 percent remission rates for those in the surgery and conventional-therapy groups, respectively. Greater percentage of weight loss at two years and lower baseline HbA1c values (hemoglobin used primarily to identify the average plasma glucose concentration) were independently associated with remission, but percentage of weight loss alone explained most of the variance.

"After 2 years, the surgical group displayed a 5 times higher remission rate and 4 times greater reduction in HbA1C values than the conventional-therapy group," the authors write. The surgical group achieved an average 20.7 percent body weight loss at two years, compared with 1.7 percent among the conventional-therapy group, representing a loss of 62.5 percent of excess weight (using BMI of 25 as ideal weight) in the surgical group compared with 4.3 percent in the conventional-therapy group. There were no serious complications in either group. "An important finding of this study is that degree of weight loss, not the method, appears to be the major driver of glycemic improvement and diabetes remission in obese participants. This has important implications, as it suggests that intensive weight-loss therapy may be a more effective first step in the management of diabetes than simple lifestyle change. This study shows that few participants achieved remission with a body weight loss of less than 10 percent, a level expected to produce important health benefits," the researchers add. "While caution is required in interpreting the longer-term benefits of surgery and weight loss, this study presents strong evidence to support the early consideration of surgically induced loss of weight in the treatment of obese patients with type 2 diabetes," they conclude.


ARTHRITIS AND CANCER TREATMENT SEEN PROMISING IN THE TREATMENT OF DIABETES

DATE: January 18, 2008

An antibody used in the treatment of certain cancers an rheumatoid arthrities may be a promising treatment for diabetes say researchers at the Yale School of Medicine.

The boffins conducted a test on mice using the antibody, rituximab (anti-CD20), which depletes B cells that have been found to play a role in autoimmune diseases by interacting with T cells of the immune system.

T cells destroy insulin-producing cells directly in the pancreas, leading to type 1 diabetes.

Li Wen, senior research scientist in the division of endocrinology, said that the study showed that once B cells were depleted, regulatory cells can emerge.

"Our paper shows, for the first time, that after successful B cell depletion, regulatory cells emerge that can continue to suppress the inflammatory and autoimmune response even after the B cells return," Wen said.

"Even more strikingly, we found that these regulatory cells include both B and T cells."

To find if B cell depletion might prove to be a therapy for type 1 diabetes, Wen and her colleague at Yale, Mark Shlomchik, M.D., professor of laboratory medicine and immunobiology, engineered mice predisposed to diabetes and had the human version of CD20, the molecule rituximab targets, on the surface of their B cells.

They then treated the rodents with a mouse version of rituximab to deplete B cells in them either before diabetes onset, or within days of diagnosis with diabetes.

During the course of the study the researchers noted that treatment with the drug significantly delayed diabetes onset in pre-diabetic mice by 10- to 15-weeks.

The equivalent period for humans would be approximately 10 to 15 years.

Of the 14 mice that already had diabetes, five stopped needing insulin for two to five months.

"These studies suggest that B cells can have dual roles in diabetes and possibly other autoimmune diseases. The B cells might promote disease initially, but after being reconstituted following initial depletion with rituximab, they actually block further disease. This means that multiple rounds of medication to deplete the B cells might not be necessary or even advisable," Shlomchik added.

The study is published in the Journal of Clinical Investigation.


HEART RISK FACTOR CONTROL WORSE IN DIABETIC WOMEN

DATE: January 11, 2008

Deaths from cardiovascular disease are declining among men with diabetes, but not women, and poorer control of blood pressure and cholesterol levels may be to blame, a new study suggests.

Among diabetic patients with existing cardiovascular disease, Dr. Assiamira Ferrara of Kaiser Permanente in Oakland, California and colleagues found, women were 5.4 percent less likely than men to have systolic blood pressures at recommended levels, and 5.9 percent less likely to have their "bad" LDL-cholesterol under control.

"Women with diabetes should be more concerned about their risk of developing cardiovascular disease," Ferrara told Reuters Health in an interview, adding that diabetic women should make sure that their doctor is doing the appropriate screening for blood pressure and cholesterol and keeping these two parameters under control.

Over the past 25 years, Ferrara and her colleagues note, deaths from cardiovascular disease among men with and without diabetes have fallen. While women overall are also experiencing a decline in deaths from heart disease, women with diabetes are not, they explain in the medical journal Diabetes Care.

To determine if gender differences in control of heart disease risk factors might help explain this disparity, the researchers looked at 8,821 men and women with diabetes belonging to 10 different managed care plans in the U.S. About one-third had a history of cardiovascular disease.

Among people with no heart or blood vessel disease, there was no difference in the percentage of men and women who had their blood sugar, blood pressure or LDL cholesterol under control.

But for those who did have cardiovascular disease, 41.2 percent of men had systolic blood pressure (the top number in a blood pressure reading) of 140 mm/Hg or greater, compared to 46.6 percent of women. And 22.4 percent of men had LDL-cholesterol levels above the recommended 3.35 mmol/l, compared to 28.3 percent of women. Women whose LDL levels were too high were 9 percent less likely than their male counterparts to be receiving intensive medication to lower their LDL.

Given that better LDL-cholesterol and blood pressure control is known to reduce heart disease-related mortality among people with diabetes, the researchers say, "more intense treatment in women with diabetes offers the opportunity to reduce the observed gap between men and women with diabetes in the reduction of CVD mortality."

By Anne Harding
SOURCE: Diabetes Care, January 2008.


RISK OF TYPE 2 DIABETES MAY BE INCREASED BY LACK OF DEEP SLEEP

DATE: January 04, 2008

Scientists from the University of Chicago suggest that not getting quality sleep may increase a person's risk of developing diabetes. The researchers say a disturbed night's sleep may lead to high blood sugar levels, weight gain and, eventually, even type 2 diabetes because the body becomes unable to recognise normal insulin signals. It is already known that the deepest form of sleep, known as slow-wave sleep, affects a person's metabolism and previous studies have also shown an association with diabetes and a lack of sleep. The research team led by Dr. Esra Tasali, who wanted to test the impact of sleep quality on blood glucose control, conducted a study involving nine healthy and slim men and women. The volunteers were first monitored for two consecutive nights in order to establish what their normal sleep patterns were, then on the following three nights, the research team woke them with a loud noise when they drifted into deep sleep.

The team discovered after injecting the volunteers with glucose and measuring their daytime blood sugar levels and insulin response, that eight of them had developed insulin resistance even though the overall amount of sleep they had remained unchanged. Dr. Tasali says strategies should be considered to improve sleep duration and quality as a potential intervention to prevent or delay the development of type 2 diabetes. Tasali says the alarming rise in the prevalence of type 2 diabetes associated with an ageing population and increased obesity, indicates the importance of understanding the factors that promote its development. Dr. Tasali says restricting sleep duration in healthy young adults results in decreased glucose tolerance and the current data indicates that not only reduced sleep duration but also reduced sleep quality may play a role in diabetes risk. Dr. Tasali also says as chronic shallow sleep and diabetes are typical factors associated with ageing, more research is needed to find out if age-related changes in sleep quality contribute to such metabolic changes. The study appears in the Proceedings of the National Academy of Sciences.