Category: Diabetes News

Researchers in Jerusalem have identified a possible cure for Type 1 diabetes in the form of a signal that activates regeneration of pancreatic beta cells, which are responsible for producing insulin. The research team claims that the discovery could pave the way for treating Type 1 diabetes by restoring or increasing pancreatic beta cell function.

The study, which took place over a period of several years, was led by Professor Yuval Dor with the Hebrew University of Jersualem Institute for Medical Research Israel-Canada. Also working on the project were researchers with the Hadassah University Medical Center, and Roche, a research-focused pharmaceuticals company. The study was funded by the Juvenile Diabetes Research Foundation.

“Our work shows that as the glucose level is increased in the blood, it tells the beta cells to regenerate,” said Professor Dor. “It’s not blood glucose per se that is the signal, but the glucose-sensing capacity of the beta cell that’s the key for regeneration.”

The research shows for the first time that high glucose levels in the blood are a trigger that initiates the regeneration of pancreatic beta cells. These cells are attacked by the immune systems of individuals with Type 1 diabetes; the destruction of the cells means that the individual cannot produce as much insulin, resulting in a disruption in the body’s handling of blood glucose. The glucose cannot be absorbed into cells and used for energy, so the patient must receive insulin injections, usually several times a day, to compensate for lowered insulin production. To reverse the effects of Type 1 diabetes, the pancreatic beta cells need to be regenerated and enlarged.

The research team used diabetic mice to study the effects of elevated blood glucose levels on individuals with Type 1 diabetes. They found that diabetic mice with elevated blood glucose levels had regenerated more beta cells than did the mice without diabetes, which seems to suggest that glucose is a key component in the regeneration of beta cells. The research also showed that glucokinase, an enzyme that senses the presence of glucose, is an important compound in activating the beta cell regeneration process.

“This means that the more work that beta cells are required to do, the more of themselves they make,” said Shay Porat, a graduate student who spearheaded the study along with Noa Weinberg, another student. As existing beta cells found it more difficult to keep up with their work load, they initiated the regeneration of more beta cells.

As the study demonstrated the central role that glucokinase plays in beta cell regrowth, it could pave the way for therapeutics that manage the levels of that enzyme and encourage existing beta cells to replicate.

Even more exciting, the research could lead to therapies that prevent the immune system from destroying the beta cells in the first place, which would constitute a cure for Type 1 diabetes.

According to Professor Aaron Hanukoglu with Tel Aviv University’s Sackler Medical School, “The incidence of Type 1 has been rising persistently for several decades in many countries around the world including Israel, and many research groups are trying to find a cure or prevention for this chronic disease. This Jerusalem research on mice is very elegant and laborious, and if proven true in humans, it may lead to development of therapeutic measures for regeneration of pancreatic beta cells and a cure to juvenile-onset diabetes.”

The Screen Actors Guild is awarding Mary Tyler Moore, known for her roles in 60s and 70s television with “The Dick Van Dyke Show” and “The Mary Tyler Moore Show” as well as her work in promoting diabetes research, with the lifetime achievement award.

Moore, now 74, also works as a producer and has suffered from Type 1 diabetes herself. The Screen Actors Guild announced that Moore will be presented with the lifetime achievement award in at its yearly television and film awards ceremony in January 2012. Moore has won seven Emmys for her roles in television. She was also nominated for an Oscar for her role in the 1980 film “Ordinary People.”

Moore’s big break came when she was cast as Laura Petrie, wife of Dick Van Dyke in the 60s sitcom named after him. She was 23 at the time. Moore later produced and starred in “The Mary Tyler Moore Show,” playing a single career woman working at a news station.

“Mary Tyler Moore won our hearts as Laura Petrie and Mary Richards, our respect as her production company became synonymous with quality television, our awe as she tackled difficult subject matter in film and on Broadway, and our admiration she turned her public recognition into a catalyst to draw attention to critical and deeply personal health and social issues,” said Ken Howard, national president of the Screen Actors Guild. The Guild represents over 125,000 actors working across film, television, commercials, and video games. Moore will be presented with the award on January 29, when the Guild will also honor the best performances in film and television at their annual awards ceremony.

At the age of 33, around the time she was working on “The Mary Tyler Moore Show,” Moore was diagnosed with Type 1 diabetes. “When the doctor said I had diabetes, I conjured images of languishing on a chaise longue nibbling chocolates,” she said of her initial diagnosis. “I have no idea why I thought this.” Moore quickly learned that living with diabetes meant managing insulin levels with injections and finger prick tests.

Although she admits that having Type 1 diabetes limits spontaneity, Moore still uses insulin injections and refuses to use a pump that automatically administers insulin. She admits that planning is important with this approach to living with diabetes: “You’ve got to always plan. It is a fact of life that if someone invites you out to dinner you have to think, ‘What are they going to be doing when they serve you dinner? How quickly are they going to get it on the table from the time I arrive? When should I take my shot? What should I eat of what’s available?'”

Moore says that she carries a syringe loaded with insulin wherever she goes; if her insulin levels drop too low, she isn’t squeamish about giving herself a shot. She does say that she’s impressed by how well the younger generations approach handling diabetes — much better than she did when she was younger.

Moore was named as the international chairwoman of the Juvenile Diabetes Research Fund and has used her position to raise funds for research and to promote diabetes awareness. In honor of Moore’s efforts with the JDRF, the organization established a research initiative called “Forever Moore,” which supports the Fund’s Academic Research and Development and its Clinical Development Program. The program works toward developing new therapies for Type 1 diabetics from research into diabetes.

A recent study has found that insulin pump therapy may be more cost effective than frequent daily insulin injections in Type 2 diabetics who require large doses of insulin throughout the day.

According to Phyllis Wolff-McDonagh, DNP, a certified diabetes instructor, pump therapy was less expensive over the long term because the insulin was absorbed more efficiently than with injections. Wolff-McDonagh presented the findings at the annual American Association of Diabetes Educators meeting; the study analyzed results from Type 2 diabetics with heavy insulin requirements, over 150 units per day. In those patients, insulin pumps saved over $12,000 in a four year period.

Type 1 diabetics have long used insulin pumps to supplement their bodies’ insulin deficiencies. Few studies have been conducted on the efficacy of insulin pumps for Type 2 diabetics; however, the existing research shows that they appear to be at least as effective in regulating hemoglobin A1c levels as multiple daily insulin injections; in some cases, insulin pumps have actually been more effective. None of the previous research has considered the cost of injections versus the cost of pumps.

In Wolff-McDonagh’s new study, the researchers studied medical records of 15 adults who ranged in age from 40 to 64. All of the patients had begun using insulin pumps within the seven years prior to the study; all had failed to achieve HbA1c levels under 8% even though they had undertaken multiple insulin injections every day for at least a year.

The results of the study showed that the mean HbA1c level in the participants dropped from 9.4% at the beginning of the study to 8.2% after one year. The participants showed an average increase in body mass index from 38.6kg/m2 at the beginning of the study to 40kg/m2 after one year. Previous research into both Type 1 and Type 2 diabetes have shown similar increases in body weight associated with improved blood glucose regulation; the weight gain is thought to be associated with a reduction in glycosuria, or the excretion of glucose in the urine.

To analyze the cost of using the pumps, the study participants were separated into three groups according to their level of basal insulin use through multiple daily injections; the low-insulin group used less than 100 units per day, the moderate group used 100-150 units per day, and the heavy-insulin group used over 150 units per day. In calculating costs, the researchers took into account the cost of insulin and supplies such as syringes and pumps.

For patients who received four injections per day, the cost was $525 per year, or $2,100 for four years. The cost of pump therapy included $5,250 for the pump plus $1,500 per year for pump supplies, equaling $11,250 over a four year period.

The cost efficiency of pump therapy varied according to the dosage of the patients. For low-dose patients, injections were less expensive than pumps, with the former costing $9,172 for four years versus $14,994 for the latter. For moderate insulin users, the costs were about the same at $22,380 for injections and $23,002 for pump therapy. For heavy insulin users, pumps were much less expensive at $28,826 versus $41,100 for injections. Dr. Wolff-McDonagh added that since insulin pumps afford more efficient glycemic control, they may also ultimately be cheaper for moderate insulin users.

Pump therapy is not popular among Type 2 diabetics because reimbursement is uncommon. To determine eligibility for receiving a pump, Medicare looks at C-peptide levels, which Wolff-McDonagh believes should change: “Medicare needs to re-look at this, but before that can happen, large randomized controlled studies need to be done to see what happens over long periods of time,” she said.

Today, almost 26 million Americans — adults and children — have been diagnosed with diabetes. By 2025, that number is projected to rise to 438 million individuals around the world, which would be about 7.8% of the world’s adult population. Combating the rise of diabetes involves multifaceted strategies but promoting a healthy diet is one of the most effective ways of reducing the numbers of the disease. Two recent studies have shown that a common food source can aid in the fight against diabetes, suggesting that including almonds in the diet of a Type 2 diabetic can help to regulate blood sugar and cholesterol levels.

The first study, published in the journal Metabolism, discovered that study participants, who had Type 2 diabetes, had a 30% decrease in their blood glucose levels after consuming a meal high in carbohydrates when they ate an ounce of almonds immediately before the meal. Those who did not have Type 2 diabetes showed a 7% decrease in blood glucose levels when they consumed the same amount of almonds and ate the same meal. The participants also fasted overnight and were then separated into two random groups; one group received a meal without almonds and the other group received a meal that included almonds. Among the Type 2 diabetics in the group that received the meal with almonds, blood sugar levels were shown to be reduced after the meal.

A second, smaller pilot study was conducted with some of the same participants to determine whether regular almond consumption had an effect on blood sugar levels. Participants with Type 2 diabetes were randomly separated into two groups of six to seven subjects; one group ate an ounce of almonds five days a week for 12 weeks. The other group ate two cheese sticks at the same frequency and for the same time period. The almonds and cheese sticks were similar in nutritional properties: the almonds contained 163 calories, 0g carbohydrates, and 14g fat, while the cheese sticks had 160 calories, 0g carbohydrates, and 12g of fat. Other than the almonds and cheese sticks, the two groups ate a very similar diet.

The study found that the group who regularly consumed almonds showed a 4% decrease in levels of hemoglobin A1c (HbA1c), which is a measure of blood sugar levels. They also showed a 4% reduction in body mass index, or BMI, over the group that ate cheese sticks for the period of the study.

Another study published in the journal Diabetes Care discovered that nuts (such as almonds) helped Type 2 diabetics in maintaining healthy cholesterol and blood sugar levels in men and postmenopausal women.

“Both of these studies further deepen our understanding of the benefits of almond consumption for those with Type 2 diabetes,” said Karen Lapsley, Ph.D. “Those with diabetes are faced with many challenges with their disease management, which is why we are always energized when new research is published that supports our understanding of almonds’ role in helping alleviate some of the difficulties.” Lapsley is also the Chief Science Officer for the Almond Board of California.

A one-ounce serving of almonds offers 3.5 grams of fiber, 13 grams of unsaturated fat and only 1 gram of saturated fat. The studies demonstrate that almonds make a healthy food choice for Type 2 diabetics, helping them to maintain blood glucose levels. The studies show that consumption of almonds provides benefits for Type 2 diabetics both in the long and short term, making them an excellent choice for anyone coping with diabetes.

A study that analyzed over 3,400 French adults over a period of 14 years found that those with Type 2 diabetes who received insulin treatment had a significantly increased risk of death.

According to Dr. Emilie Bérard, an epidemiology researcher at the University Hospital Center in Toulouse, France, patients with diabetes who were “treated with insulin at baseline were at increased risk of all-cause mortality.” Dr. Bérard spoke at the yearly meeting of the European Society of Cardiology, adding that the data “provides further information to the debate on the risks and benefits of increasing hypoglycemic treatments.”

The study adjusted for factors that may have affected the outcomes of the data. Even after the adjustments were made, the study found that diabetics who received treatment with insulin were five times more likely to die over the 14 year period of the study than the study participants who did not have diabetes. Those who received insulin were also 1.5 to 2.2 times more likely to die than diabetics who were treated with other hypoglycemic drugs such as metformin or sulfonylurea. The relative risk of death for diabetic patients who were treated with insulin was nearly double that of diabetic patients who did not recieve any treatment at all — the latter group was about 2.8 times more likely to suffer death than patients without diabetes.

Dr. Lars Rydén, a professor of medicine at the Uppsala University in Sweden, cautioned against taking the study’s findings at face value. The study was “on the right track,” according to Dr. Rydén, but its findings must also “be taken with a grain of salt.”

“The results indicate something, but we need further studies,” continued Dr. Rydén. He commented that a major potential flaw in Dr. Bérard’s findings were that it used several adjusting factors in a fairly small sample group of only 171 diabetic patients. “I think [the analysis] is on the edge of controlling for too many things in a small number of people, which led to extremely wide confidence intervals,” said Dr. Rydén.

The findings were also questioned because the participants did not undergo an evaluation of their A1c levels when the study began in 1995 and 1996. According to Dr. Bérard, this means that the adjusted analysis could not account for the varying quality of diabetes control that the patients may have received at baseline. Dr. Bérard speculated that the insulin treatment could have caused a higher rate of hypoglycemia which lead to a higher mortality rate, it could have caused increased weight gain, or it could be indicative of more serious cases of diabetes. It may have also stimulated the sympathetic nervous system, which could have promoted atherosclerosis and triggered vasoconstriction.

The study analyzed data collected from a random sample of 3,403 French adults who were aged between 34 and 64. The study began in 1995 and 1996 and was a part of the MONICA (Multinational Monitoring of Trends and Developments in Cardiovascular Disease) project, a large study sponsored by the World Health Organization. Of the study sample group, 171 participants had diabetes, with 123 on a hypoglycemic regimen and 48 who were not being treated for diabetes at all.

Dr. Bérard’s team analyzed the participants’ data 14 years after their first assessment and found that the mortality rates varied widely, from 7% in the group without diabetes to 33% in the group who were treated with insulin; those who were not receiving hypoglycemic treatment at the beginning of the study had a 23% mortality rate.

For decades, scientists have been trying to identify the molecules that activate beta cell growth in the fight against diabetes. Once these molecules are identified, scientists could develop therapeutics that target them. One research team, funded by the Juvenile Diabetes Research Fund in collaboration with pharmaceutical manufacturer Hoffman-La Roche, recently made significant headway in this area of diabetes research by discovering a protein responsible for beta cell growth as well as a compound that activates it. The team’s findings were published in the journal Cell Metabolism.

The research team was led by Markus Stoffel, M.D., Ph.D., professor at the Swiss Federal Institute of Technology in Zurich, Switzerland a recipient of the Juvenile Diabetes Research Fund’s Gerold & Kayla Grodsky Basic Research Scientist Award. The team is hopeful that its findings will prove to be significant progress in the effort to develop new therapeutics that can be used to regenerate beta cells.

The team’s findings build on research that they conducted five years ago. In that previous research, Dr. Stoffel’s team discovered that a protein known as Tmem27 is found on the surface membranes of beta cells — the insulin-producing cells located in the islets of Langerhans in the pancreas. They found that higher concentrations of Tmem27 on beta cells were linked to increased mass of the islets of Langerhans in mice. Additionally, they discovered that cleaving Tmem27 leaves it totally inactive.

“We hypothesized that if we could prevent Tmem27 from being cleaved and increase the levels of this protein, we could get more beta cell growth,” said Dr. Stoffel. “This observation gave us the rationale to look for what was inactivating Tmem27.”

Once Dr. Stoffel’s team discovered that cleaving Tmem27 de-activated it, they set about searching for molecules that could be responsible for the process. They zeroed in on Bace2, an enzyme protein that can also be found on the surface membrane (or plasma membrane) of beta cells. To confirm their theories, the team analyzed mice and found that those with lower levels of Bace2 had larger islets and a greater number of beta cells in the pancreas through the process of cell regeneration, or proliferation. The mice with lowered levels of Bace2 were also more efficient at removing glucose from the bloodstream than were the mice that had Bace2.

The team’s next goal was to demonstrate the growth of beta cells by inhibiting Bace2. They worked with the scientists of therapeutic company Hoffman-La Roche, who developed an inhibiting compound that prevented Bace2 activity. When the mice were given the compound, their Bace2 was inhibited and their beta cells began to regenerate. Additionally, it was discovered that Bace1, a chemically similar compound to Bace2, does not cleave the Tmem27 protein. Bace1 may be linked to a variety of other diseases, including Alzheimer’s disease and Down syndrome, but since it does not cleave Tmem27, the door is open for anti-diabetes therapeutics that inhibit Bace2 specifically. Research to develop inhibitors for Bace1 is already underway by several companies.

In addition to the identification of a possible target for anti-diabetes therapeutics, the research that Dr. Stoffel’s team conducted may also pave the way for the development of new tests to determine the presence of Tmem27 fragments in the bloodstream, which could be used as a measure of the number of beta cells present in the pancreas.

A joint study conducted by the Scripps Research Institute and the Dana-Farber Cancer Institute at Harvard University has discovered a new type of anti-diabetic therapeutic that works by targeting a particular molecular switch.

The findings set the stage for the development of new anti-diabetic therapeutics that will have drastically reduced adverse side effects compared to current anti-diabetics such as Avandia (rosiglitazone), which will be discontinued from sale this fall amid concerns that it increases the risk of heart attack.

The results of the new study were published in the journal Nature. It describes a newly-discovered compound called SR1664 and was led by Patrick R. Griffin with the Department of Molecular Therapeutics at Scripps Florida, Theodore Kamenecka, the associate scientific director of medicinal chemistry at Scripps Florid, and Bruce Spiegelman, a professor of cell biology at Dana-Farber Cancer Institute.

“In this study, we demonstrate that we have discovered novel compounds that work effectively through a unique mechanism of action on a well-validated clinical target for diabetes,” stated Griffin. “This unique mechanism of action appears to significantly limit side effects associated with marketed drugs. This study is a great example of interdisciplinary, inter-institutional collaboration with chemistry, biochemistry, structural biology, and pharmacology.”

“It appears that we may have an opportunity to develop entire new classes of drugs for diabetes and perhaps other metabolic disorders,” says Spiegelman.

The study is a follow-up on research that the authors published last year in the same journal, Nature. That research suggested that the development of insulin resistance in humans could be caused by a mechanism linked to obesity. The research found that a protein called PPARG affects the normal function of several genes when it undergoes phosphorylation, or the addition of a phosphate group to the protein. The kinase Cdk5, an enzyme involved in multiple sensory pathways, is responsible for causing the phosphorylation of PPARG.

The researchers’ new study confirms what they suspected in their original research: blocking Cdk5 from acting on PPARG could be the basis of effective anti-diabetes therapies. The SR1664 compound discovered in the newer research binds to PPARG but does not activate the transcription of genes.

Griffin’s team is cautious about being overly optimistic in their report on the side effects of anti-diabetes treatment with SR1664. However, the research did clearly demonstrate that this type of treatment causes fewer side effects in mice than medications such as Avandia, which can cause weight gain or increased plasma volume.

In the study, the researchers treated diabetic mice with both Avandia and with SR1664. While both groups showed improved blood glucose levels, the mice treated with Avandia also displayed more fluid retention and weight gain soon after beginning treatment. The mice treated with SR1664, on the other hand, showed neither. The researchers also tested SR1664 in cell cultures for its effect on bone formation and fat generation in bone cells, both side effects of Avandia and other therapies. SR1664 caused no such side effects.

Although SR1664 will likely not be used directly as a drug, its discovery will allow researchers to develop similar compounds that can be used to treat diabetes. “With data in hand showing that our compounds are as efficacious as the currently marketed PPARG modulators, while demonstrating a significant improvement of side effects in limited studies, we are now advancing newer compounds with improved pharmaceutical properties into additional studies,” says Griffin.

Are you one of the millions who finds it hard to get up and exercise regularly? You’re definitely not alone, and new research shows that those who tend to stay active may have been born with different genes. For years, diet and exercise have been prescribed as the best way to stay in shape and maintain one’s health, but a lack of motivation to exercise could be the result of an unlucky drawing in the genetic lottery.

The research was conducted by Professor Gregory Steinberg and his team at McMaster University in Canada. The team was studying health mice that had been specifically bred for the study; some of the mice had two genes removed which are essential in exercise. The two genes are responsible for controlling a protein called AMP-activated protein kinase, or AMPK. The enzyme is “switched on” when an organism such as a mouse or human exercises.

“Mice love to run,” said Professor Steinberg, who is the associate professor of medicine at the Michael G. DeGroote School of Medicine as well as the Canada Research Chair in Metabolism and Obesity. Steinberg described how the removal of the two exercise genes caused an immediate change in the physical capabilities of the mice: “While the normal mice could run for miles, those without the genes in their muscle could only run the same distance as down the hall and back. It was remarkable. The mice looked identical to their brothers or sisters but within seconds we knew which ones had the genes and which one didn’t.”

Those mice lacking the genes that controlled AMPK had decreased mitochondria — the powerhouses that provide energy to cells — and a subsequent dysfunction in the ability of the muscle cells to utilize glucose to generate energy.

“When you exercise you get more mitochondria growing in your muscle. If you don’t exercise, the number of mitochondria goes down,” says Steinberg. “By removing these genes we identified the key regulator of the mitochondria is the enzyme AMPK.”

While there are many research teams around the world studying AMPK and its implications, Professor Steinberg’s team is the first to outline the importance of its role in exercise. Their findings are published in the Proceedings of the National Academy of Sciences.

According to Professor Steinberg, the team’s findings have important implications for individuals who find it difficult to exercise, including disabled people, asthmatics and the obese. When regular physical exercise is neglected over a long-term period, additional complications such as diabetes and heart disease can occur.

“As we remove activity from our lives due to emerging technology, the base level of fitness in the population is going down and that is reducing the mitochondria in people’s muscles. This in turn makes it so much harder for people to start exercising,” says Professor Steinberg. With the lack of exercise required in our modern lives, and the subsequent reduction of mitochondria in our cells, our risk of developing serious complications has risen as industrial technology has taken over and reduced the need for frequent physical exertion.

Steinberg says that he rides his bicycle or runs to work to stay in shape: “It is the only way that I can manage to make sure I stay fit.” Regular exercise has a variety of health benefits, from reducing weight and fighting illnesses and disease to improving mood, increasing energy levels and encouraging healthy sleep patterns.

According to a new study, a variety of lifestyle factors may independently affect an individual’s chance of developing Type 2 diabetes. Such risk factors include diet, exercise, weight, and alcohol and tobacco use.

The researchers found that individuals were less likely to develop Type 2 diabetes if they had healthy lifestyles overall, even if they had family histories of diabetes or were overweight. In addition, each positive lifestyle choice reduced their chances of developing the disease.

“There are implications certainly for individuals to take one step at a time toward a healthy lifestyle,” said Jared Reis with the National Heart, Lung, and Blood Institute, located in Bethesda, Maryland, and an author on the study. “There is certainly benefit for those who may have a tough time with losing weight if they adopt these other healthy lifestyle factors” such as getting more exercise, eating a healthier diet, and eliminating smoking and alcohol.

The study analyzed data from over 200,000 Americans; the data was collected through surveys that the participants filled out themselves and it asked questions about their health in the years 1995 and 1996. At that time, most of the participants were older aged, in their 50s or 60s; however, none had diabetes at the start of the study.

The researchers followed up with those participants ten years later, asking whether they had developed diabetes since the first survey. On average, one in 10 men and one in 13 women had developed Type 2 diabetes since the beginning of the study.

Researchers then looked back at the data collected during the first survey, breaking down the questions according to five categories: body mass index (BMI), exercise, diet, and the use of alcohol and tobacco. According to the results, each healthy behavior that appeared on the survey, such as getting regular exercise or stopping smoking, reduced the participant’s risk of developing diabetes, even when accompanied by other unhealthy lifestyle choices.

As such, a participant who ate a well-rounded diet and avoided unhealthy fats and low-quality refined grains had a lower risk of developing diabetes even if he or she exercised little, smoked cigarettes and drank alcohol regularly.

The results proved consistent even among those who had a family history of diabetes, which put them at a higher risk overall.

The study found that normal weight women who answered positively to adopting healthy lifestyle choices, such as eating healthy, getting regular exercise, and avoiding alcohol and tobacco were 84% less likely to develop diabetes than overweight women who engaged in the opposite unhealthy activities. Similarly, men who made healthy choices were 72% less likely to develop diabetes compared with their less healthy peers.

Although the data pointed to the fact that healthy choices could counteract the risk of developing diabetes, the researchers noted that weight was still the most important determining factor in the development of diabetes.

“While the message is that all these things matter… the number one top-of-the-list take-home is, don’t be overweight in the first place,” said Dr. Lawrence Phillips, an endocrinologist at Emory University in Atlanta. “It’s important not to confuse the baby with the bathwater here,” added Phillips, who was not involved with the study.

While the study is encouraging in its predictions that healthy choices reduce the risk of diabetes, it cannot prove definitively that removing alcohol, tobacco or saturated fats can reduce any one individual’s risk of developing the disease.

Good news for diabetics who love the calming and relaxing influence of yoga — a recent study suggests that yoga classes could help Type 2 diabetics lose some weight and, more importantly, help regulate their blood sugar levels. The study was published in the journal Diabetes Care.

The study was conducted on 123 middle-aged and older adults, and it showed that the patients who participated in yoga classes as a type of supplemental treatment for their existing diabetes care lost a few pounds over the three-month period of the study. In addition, their average blood glucose levels held at a steadier level than the control group of Type 2 diabetics who did not add yoga sessions to their diabetes care.

The study participants who took yoga classes several times a week — 60 of them in all — showed an average decrease in body mass index, or BMI, from 25.9 to 25.4. On the BMI scale, the “overweight” range is from 25 to 30.

While the findings were encouraging in suggesting yoga as a form of supplemental treatment for diabetes, they did not suggest that yoga should replace the typical exercise regimen that is prescribed for Type 2 diabetics.

Shreelaxmi V. Hegde with the Srinivas Institute of Medical Science and Research Center in Mangalore, India was the lead researcher on the study. According to Hedge, although yoga showed some positive benefits, Type 2 diabetics would benefit even more from vigorous exercise such as running.

“In our study the effect of yoga on BMI (body mass index) and blood sugar control was marginal,” said Hegde. “But, it should be noted that yoga controlled the blood sugar levels which otherwise rose in the control group.”

The study also found signs of decreased oxidative stress in the group that participated in yoga. Oxidative stress is the condition where free radicals — dangerous leftovers from cellular energy production — increase to levels that the body cannot handle. Oxidative stress, when present over long periods of time, is known to contribute to the development of several chronic diseases.

The research team studied the participants’ bloodstreams for the presence of chemicals that are indicative of oxidative stress. These results showed that the presence of these chemicals was reduced by an average of 20 percent in the group that took yoga classes.

According to Hedge, if this reduction in oxidative stress could be maintained over a long period of time, the patient could lower his or her risk of developing diabetes complications, including heart disease, kidney disease, and nerve damage. However, more research is needed to determine whether yoga could actually be used to curb oxidative stress in the long term.

In the meantime, Hedge has a theory on why yoga could reduce oxidative stress: yoga stimulates the parasympathetic nervous system, or the part of the nervous system responsible for unconscious activities such as breathing and digestion.

Hedge did state that the type of yoga used in the study was a gentle form that excluded certain poses because they could exacerbate the patients’ complications. However, some yoga classes provide a more intense workout that could be dangerous to those with potential complications while being more beneficial to individuals who can handle the extra stress. Many hospitals and community centers around the U.S. are beginning to offer yoga classes tailored specifically for those with chronic illnesses such as cancer and diabetes, as well as yoga classes for older individuals who want to stay in shape.