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type 2 diabetes

Blood Sugar Control for Diabetes: Asking the Heart Questions

Posted on by Dr. Francis Collins

Glucose testing

Credit: Thinkstock

When most people think about risk factors for cardiovascular disease, they likely think of blood pressure readings or cholesterol levels. But here’s something else that should be high on that list: diabetes. That’s because people with diabetes are roughly twice as likely to die of heart disease than other folks [1]. Yet the issue of how best to help such people lower their cardiovascular risks remains a matter of intense debate. Some studies have suggested that part of the answer may lie in tightly controlling blood sugar (glucose) levels with a strict regimen of medications and monitoring [2]. Other research has shown that the intense effort needed to keep blood glucose levels under tight control might not be worth it and may even make things worse for certain individuals [3].

Now, a follow up of a large, clinical trial involving nearly 1,800 U.S. military veterans with type 2 diabetes—the most common form of diabetes—provides further evidence that tight blood glucose control may indeed protect the cardiovascular system. Reporting in The New England Journal of Medicine [4], researchers found a significant reduction in a composite measure of heart attacks, strokes, heart failure, and circulation-related amputations among the vets who maintained tight glucose control for about five and a half years on average. What’s particularly encouraging is most of the cardiovascular-protective benefit appears to be achievable through relatively modest, rather than super strict, reductions in blood glucose levels.


Taking a New Look at Artificial Sweeteners

Posted on by Dr. Francis Collins

Packets of artificial sweetenersDiet sodas and other treats sweetened with artificial sweeteners are often viewed as guilt-free pleasures. Because such foods are usually lower in calories than those containing natural sugars, many have considered them a good option for people who are trying to lose weight or keep their blood glucose levels in check. But some surprising new research suggests that artificial sweeteners might actually do the opposite, by changing the microbes living in our intestines [1].

To explore the impact of various kinds of sweeteners on the zillions of microbes living in the human intestine (referred to as the gut microbiome), an Israeli research team first turned to mice. One group of mice was given water that contained one of two natural sugars: glucose or sucrose; the other group received water that contained one of three artificial sweeteners: saccharin (the main ingredient in Sweet’N Low®), sucralose (Splenda®), or aspartame (Equal®, Nutrasweet®). Both groups ate a diet of normal mouse chow.


Global Health: Time to Pay Attention to Chronic Diseases

Posted on by Dr. Francis Collins

Graph of projected deaths by cause in low income countries

Caption: Projected deaths (in millions) by cause in low-income countries. Note increase in non-communicable diseases (orange).
Credit: Adapted from Beaglehole R, Bonita R. Lancet. 2008 Dec 6;372(9654):1988-96.

Greetings from China. I’m here in Shanghai with other biomedical research leaders for two major meetings. The first one, which is the topic of my blog today, is on global health. So, you might expect there to be a lot of talk about malaria, influenza, MERS-CoV, Ebola virus, sleeping sickness, dengue fever, tuberculosis, HIV/AIDS, and other infectious diseases. And those are most certainly topics of intense interest to NIH and our colleagues around the world. But this particular meeting is about a different kind of global health threat that’s becoming a rapidly growing problem: chronic diseases.

While infectious diseases remain a significant problem in the developing world, cancer, heart disease, obesity, diabetes, and other non-communicable diseases are now among the fastest growing causes of death and disability around the globe. In fact, nearly three-quarters of the 38 million people who died of chronic diseases in 2012 lived in low- or middle-income countries [1].


It’s Spring! A Great Time for Cycling, Running, Walking, and Working Out!

Posted on by Dr. Francis Collins

People with their bikes at NIH

Caption: My wife Diane Baker and I, enjoying last year’s NIH Bike to Work Day.
Credit: NIH

Happy Bike to Work Day! I really wish that I could take part in the festivities on the National Institutes of Health (NIH) campus in Bethesda, MD as I have in past years, but NIH-related travel is keeping me away from my trusty bike.

So, let me take a moment to commend all of the enthusiastic cyclists at NIH, along with everyone else out there who’s doing everything you can to get and stay physically fit.  Here at NIH, we are particularly well situated to know the facts: taking charge of your health by participating in an exercise program and eating the right foods is among the most important investments you can make in your future.


DNA Analysis Finds New Target for Diabetes Drugs

Posted on by Dr. Francis Collins

ATCG's with a silhouette of people
Credit: Jane Ades, National Human Genome Research Institute, NIH

Type 2 diabetes (T2D) tends to run in families, and over the last five years the application of genomic technologies has led to discovery of more than 60 specific DNA variants that contribute to risk. My own research laboratory at NIH has played a significant role in this adventure. But this approach doesn’t just provide predictions of risk; it may also provide a path to developing new ways of treating and preventing this serious, chronic disease that affects about 26 million Americans.

In an unprecedented effort aimed at finding and validating new therapeutic targets for T2D, an international team led by NIH-funded researchers recently analyzed the DNA of about 150,000 people across five different ancestry groups. Their work uncovered a set of 12 rare mutations in the SLC30A8 gene that appear to provide powerful protection against T2D, reducing risk about 65 percent—even in the face of obesity and other risk factors for the disease [1].


Introducing AMP: The Accelerating Medicines Partnership

Posted on by Dr. Francis Collins

Pie charts showing AMP targets reducing failures due to efficacy

Caption: Lack of efficacy currently accounts for more than half of all drug failures in Phase II clinical studies (left). If AMP’s target validation efforts improve efficacy by 90% (right), the success rate will rise significantly.

It would seem like there’s never been a better time for drug development. Recent advances in genomics, proteomics, imaging, and other technologies have led to the discovery of more than a thousand risk factors for common diseases—biological changes that ought to hold promise as targets for drugs.

But this deluge of new opportunities has to be put in context: drug development is a terribly difficult business. To the dismay of researchers, drug companies, and patients alike, the vast majority of drugs entering the development pipeline fall by the wayside. The most distressing failures occur when a drug is found to be ineffective in the later stages of development—in Phase II or Phase III clinical studies—after years of work and millions of dollars have already been spent [1]. Why is this happening? One major reason is that we’re not selecting the right biological changes to target from the start.


Metabolomics: Taking Aim at Diabetic Kidney Failure

Posted on by Dr. Francis Collins

Patients with red tubes attached to their arms

iStock
Caption: Dialysis is often used to treat kidney failure related to diabetes.

My own research laboratory has worked on the genetics of diabetes for two decades. One of my colleagues from those early days, Andrzej Krolewski, a physician-scientist at the Joslin Diabetes Center in Boston, wondered why about one-third of people with type 2 diabetes eventually develop kidney damage that progresses to end-stage renal disease (ESRD), but others don’t. A stealthy condition that can take years for symptoms to appear, ESRD occurs when the kidneys fail, allowing toxic wastes to build up. The only treatments available are dialysis or kidney transplants.


More Beta Cells, More Insulin, Less Diabetes

Posted on by Dr. Francis Collins

Artist redition of a liver, WAT fat, and BAT fat cells combining with green dots representing betatrophin combining to induce pancreatic cells

Caption: Betatrophin, a natural hormone produced in liver and fat cells, triggers the insulin-producing beta cells in the pancreas to replicate
Credit: Douglas Melton and Peng Yi

Type 2 diabetes (T2D) has arguably reached epidemic levels in this country; between 22 and 24 million people suffer from the disease. But now there’s an exciting new development: scientists at the Harvard Stem Cell Institute have discovered a hormone that might slow or stop the progression of diabetes [1].

T2D is the most common type of diabetes, accounting for about 95% of cases. The hallmark is high blood sugar. It is linked to obesity, which increases the body’s demand for more and more insulin. T2D develops when specific insulin-producing cells in the pancreas, called beta cells, become exhausted and can’t keep up with the increased demand. With insufficient insulin, blood glucose levels rise. Over time, these high levels of glucose can lead to heart disease, stroke, blindness, kidney disease, nerve damage, and even amputations. T2D can be helped by weight loss and exercise, but often oral medication or insulin shots are ultimately needed.


Meet Alex—Before and After NIH Clinical Trial

Posted on by Dr. Francis Collins

Photo of an infant with mottled skin adjacent to a photo of young man with clear skin being examined by a female doctor.

Caption: Alex, then and now, with Dr. Goldbach-Mansky
Credit: Kate Barton and Susan Bettendorf (NIH)

Alex Barton recently turned 17. That’s incredible because Alex was born with a rare, often fatal genetic disease and wasn’t expected to reach his teenage years.

When Alex was born, he looked like he’d been dipped in boiling water: his skin was bright red and blistered. He spent most of his time sleeping. When awake, he screamed in agony from headaches, joint pain, and rashes. After a torturous 14 months, a rheumatologist told his mother that Alex suffered from Neonatal-Onset Multisystem Inflammatory Disease (NOMID). The doctor showed her a brief and scary paragraph in a medical text. Kate Barton, Alex’s mother, admitted that it “knocked her over like a freight train.”


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