Diabetes Health Talk

Potential blockbuster diabetes medication from Bristol-Myers Squibb appears free from heart-related side effects that have plagued similar treatments, federal health officials said Monday.

Despite low rates of heart attacks and related problems in testing, the Food and Drug Administration will still ask an outside panel to scrutinize the company’s safety data at a meeting Wednesday.

Bristol-Myers and partner AstraZeneca have asked the FDA to approve Onglyza to reduce blood sugar levels in patients with type 2 diabetes. The drug uses a chemical reaction similar to Merck’s Januvia and would compete against the blockbuster medication, which had sales of $1.4 billion last year.

The drug is part of a new wave of medications taking aim at the U.S. diabetes market, which has grown to more than $5 billion as the disease becomes more prevalent.

Analyst estimates of Onglyza’s market potential vary, given its similarity to a more established drug. Sales estimates range from $300 million per year to more than $1 billion.

Shares of New York-based Bristol-Myers climbed 36 cents, or 1.7 percent, to close at $21.02 Monday. U.S.-traded shares of London-based AstraZeneca rose $1.87, or 5.8 percent, to $34.25.

Regulators have begun demanding more rigorous safety testing of diabetes drugs since a 2007 analysis suggested GlaxoSmithKline’s blockbuster pill Avandia could increase heart risks.

Under guidelines issued last year, FDA requires companies to test diabetes drugs on more high-risk patients, including the elderly, to detect potential heart problems. Detecting heart risks connected with diabetes drugs is challenging because patients with the disease are already at risk of heart problems.

Because Bristol-Myers and AstraZeneca conducted their studies before the guidelines were released, their testing “was not designed to prospectively measure cardiovascular risk,” agency reviewers noted. As a result the FDA said there is “insufficient information” to determine if some heart problems were related to the drug, according to briefing documents posted online.

Type 2 diabetes typically worsens over time as less and less insulin is produced by the pancreas. Usually, treatment for type 2 diabetes starts with lifestyle changes and a diabetes pill, such as metformin. Sulfonyureas and thiazolidinediones are other types of diabetes pills that can be considered, but both can cause weight gain, and sulfonyureas can cause more episodes of hypoglycemia (low blood glucose) than metformin.

Liraglutide is a new injectable diabetes medicine. It is now under development as a possible alternative to available diabetes pills. Researchers are performing studies to find out how liraglutide compares to other diabetes medicines.

Why did the researchers do this particular study?
The researchers wanted to compare the effectiveness and safety of adding liraglutide, glimepiride (a sulfonylurea), or a dummy pill to metformin treatment for people with type 2 diabetes.

Who was studied?
The study included more than 1,000 adults with type 2 diabetes who had been taking either one type of diabetes pill or more than one type of diabetes pill for more than 3 months.

How was the study done?
Participants received liraglutide injections, glimepiride pills, or dummy pills in combination with metformin for 26 weeks. Researchers measured the participants’ A1C and body weight at the start and end of the study and collected information about whether they experienced nausea or hypoglycemia while on the treatments.

What did the researchers find?
Adding liraglutide to metformin provided better diabetes control than metformin alone. The liraglutide-metformin combination controlled blood glucose as well as and caused less weight gain and hypoglycemia than a combination of glimepiride and metformin. Liraglutide caused more nausea than glimepiride, but the nausea declined over time.

What are the implications of the study?
Adding liraglutide to metformin may be a good treatment option for patients whose diabetes is not adequately controlled with metformin alone, especially when weight gain and hypoglycemia are a concern.

When a state judge ruled late last year that qualified nurses are the only school personnel who can give insulin shots to children with diabetes, he exacerbated an enormous problem.

Although I do not have kids, I would be upset at this ruling. I would probably hire a nurse to go to school and give my kids their insulin shots.

Most California schools do not have full-time nurses. Now, the parents of an estimated 15,000 diabetic children are scrambling — pushing school districts to hire nurses, driving to schools to administer the insulin shots and in some cases choosing home schooling.

Many doctors and diabetes advocates are outraged. Scores of lay people — babysitters, siblings, grandparents — regularly administer insulin, and they see no reason why trained, nonmedical school staff, like teachers or clerks, should not be allowed to help students. They fear the massive shortage of school nurses means children are not getting insulin shots in a timely manner. And they say diabetes is being used as a political tool to force school districts to hire more nurses — an unlikely scenario given the state’s $42 billion budget deficit.

“It’s untenable to expect nurses to be the sole provider of insulin in schools,” said Dr. Darrell Wilson, a pediatric endocrinologist at Stanford University and the Lucile Packard Children’s Hospital. “To say that only a nurse can do this is spectacularly unnecessary. This is not a complicated procedure.”

In 2007, a class-action lawsuit against the California Department of Education produced an agreement that allowed nonmedical personnel to administer insulin injections to students if no nurse was available.

New study shows Avandia and Actos doubles a women with Diabetes type-2 risk of bone fractures.

Scientists already knew the two caused bone fractures in certain women, but were unsure of the magnitude.

Sonal Singh of North Carolina’s Wake Forest University School of Medicine.

Singh and colleagues at Wake Forest, working with researchers at Britain’s University of East Anglia, based their findings on a pooled analysis of 10 previous clinical studies lasting at least a year involving 14,000 patients.

They concluded that if TZDs were used by diabetic women aged around 70 for a year, one additional fracture would occur among every 21 women. Among younger women, around age 56, use of the drugs would lead to one extra fracture for every 55 women.

Always be sure to ask your doctor or health care physician of your medications and side effects. Also ask if those side effects need to be addressed, such as additional calcium, in this case. Before starting any new medications or supplements, herbal remedies and minerals, discuss those with your doctor. There may be adverse reactions between then that may increase your sypmptos or have unwanted side effects you hadn’t counted on.

If you need additional calcium, that is easily remedied, by adding more low-fat milk and cheese to your diet, or vitamin D pills or getting just ten minutes more sunshine per day (with your sunscreen and protective covering. ). Exercise is also important to stop bone loss or calcium leaching from your body. Just a ten minute walk a day is all it takes to get started with healty bones.

Scientists at the Diabetes Center at University of California San Francisco say two drugs that are already on the market to treat cancer patients could help people living with Type-1 diabetes.

Results from a new study performed with non-obese diabetic mice show that treating mice with either of the drugs before the on-set of Type-1 diabetes prevented the development of the disease.

“This was a therapy that was working in animals that had already developed the disease. The second surprise for us was that we didn’t have to treat continuously. We could treat for a limited time, a couple of months and then stop the treatment,” explained Dr. Jeffrey Bluestone.

The disease went into permanent remission in 80 percent of the mice.

Bluestone says the challenge now is to set up a trial for humans.

“These drugs in cancer patients have had some side effects,” he warned.

They’re side effects that cancer patients facing a life threatening disease are more likely to endure than diabetics who are generally healthy except for a lack of insulin.

UCSF doctors say if everything goes well with funding they may be able to set up a trial in about a year.

Bluestone warns that these results came from a mouse study, and there are always challenges in going from mouse to man.

The widespread problem of children failing to take their medication for a range of life-threatening illnesses is to be tackled as part of a new university research project.

The first phase of the study will be to look at methods previously tried to address the problem and to talk to three groups of school-age children — five to seven year olds, 10 to 12-year-olds and 15 to 17-year-olds — and their parents about their experiences of the healthcare system and medication. They will also interview a range of healthcare professionals including GPs, hospital paediatricians, community paediatricians and pharmacists, nurses and GP practice managers and secretaries about the issues they face in communicating their services to young people. Lastly, they will consult with other stakeholder groups including patient groups such as Asthma UK and Epilepsy Action and healthcare-related organisations such as the Royal College of Practice Nurses.

During the second phase they will design a new strategy that can be embedded within the whole range of healthcare services for children — this may include encouraging children and parents to write down their concerns or questions as a driver for their consultation with their GP and giving health practitioners a range of extra resources targeted specifically at supporting younger patients.

Dr Monica Lakhanpaul, Community Paediatrician and Senior Lecturer in Child Health at The University of Leicester, said: “We are fully aware that children may not take medicines sometimes prescribed to them by health professionals.

“Reasons for this vary — children and families may not receive information that facilitates their understanding of why they are taking their medicine and therefore not understand its importance; they may not understand how to take the medicine or the health professionals may not prescribe the type of medication that children could take easily, eg tablets instead of liquids.

“We wish to find out why — and why not — children take their medicine and use this information to develop a tool allowing health professionals to work together with children and parents and carers to improve the medicine they are prescribed. 
 
“A very important element of the study is to gain views from a number of different perspectives i.e from parents/carers, health professionals and children themselves.”
Lecturers at The University of Leicester are key collaborators in the study. Dr Hitesh Pandya is able to provide experience of working with families who are seen in the hospital and Dr Lakhanpaul, a Community Paediatrician, works with children who are managed out of hospital and who, in most cases, will not have a nurse or doctor giving their medication but need to take responsibility within the home or school environment.
 
Dr Lakhanpaul added: “Another advantage at Leicester is that we can provide access to a multi-ethnic community who are often under-represented in research studies. It is important to have perspectives from individuals from different socio-economic and cultural backgrounds. We hope to achieve this by involving families from Leicestershire.”

A drug designed to specifically hit a protein linked to the life-extending benefits of a meager diet can essentially trick the body into believing food is scarce even when it isn’t, suggests a new report in the November Cell Metabolism.

The drug called SRT1720, which acts through the protein SIRT1, enhances running endurance in exercised mice and protects the animals against weight gain and insulin resistance even when they eat a high-fat diet, the researchers report. The drug works by shifting the metabolism to a fat-burning mode that normally takes over only when energy levels are low.

The findings bolster the notion that SIRT1 may be a useful target in the fight again metabolic disorders, including obesity and type 2 diabetes. It also helps lay to rest a long-standing controversy in the scientific world over the metabolic benefits of the red wine ingredient known as resveratrol. Resveratrol also acts on SIRT1, but its influence on other metabolic actors had left room to question exactly how it works.

” There has been a lot of controversy in the field about resveratrol action,” said Johan Auwerx of Ecole Polytechnique Fédérale de Lausanne. “We find that the majority of the biology of resveratrol can be ascribed to SIRT1.” While SIRT1 might not explain all of resveratrol’s effects, the new results suggest that the central metabolic protein is responsible for about “80 percent of the picture,” he said.

The researchers had conducted earlier studies to demonstrate many of the benefits of resveratrol. To further explore the underlying pathways responsible in the new study, they ran essentially the same experiments with the more potent and specific SIRT1-activating compound SRT1720 developed by the company Sirtris Pharmaceuticals, Inc.

The researchers found that a low dose of SRT1720 partially protected mice from gaining weight on a high-fat diet after 10 weeks of treatment. At higher doses, the drug completely prevented weight gain in the animals. SRT1720 also improved blood sugar tolerance and insulin sensitivity and endowed the animals with greater athletic ability.

” SIRT1720 made the animals run twice as long,” Auwerx said. That improvement was seen only when the researchers specifically exercised the animals. Their voluntary activity actually declined in the study as they hunkered down to save energy.

They found further evidence that the SIRT1 activator acts as a calorie-restriction mimetic that favors the use of fat stores by promoting the direct modification of multiple SIRT1 targets. It also induces chronic metabolic adaptations that involve the indirect activation of AMPK, an enzyme that regulates skeletal muscle glucose and the metabolism of fatty acids.