An old, aspirin-like drug called salsalate could help control blood sugar in people with type 2 diabetes. In the TINSAL-T2D trial, 286 volunteers took pills containing either salsalate or a placebo for nearly a year. Over the course of the trial, those in the salsalate group had lower blood sugar levels, and some were even able to reduce dosages of other diabetes medications they were taking. Experts aren’t exactly sure how salsalate helps control blood sugar, but its effectiveness supports the idea that inflammation plays a role in type 2 diabetes. Although the results are promising, what we really need to know about salsalate (or any new or repurposed drug) is how its long-term benefits and risks stack up against each other. The trial was too small and too short to determine those risks. According to the researchers, such “outcomes require continued evaluation before salsalate can be recommended for widespread use” by people with type 2 diabetes.
A lot is known about diabetes. But a discovery that could change how this disease is treated shows just how much more there is to learn. A team of Harvard Medical School researchers has discovered a hormone called betatrophin made by liver and fat cells that signals the body to make more insulin-producing beta cells. A report of their work appears in this month’s issue of the prestigious scientific journal Cell. In mice with diabetes, experimentally turning on the production of betatrophin inside liver and fat cells caused an increase in beta cells and a dramatic improvement in blood sugar. It will, of course, take much more research in mice—and then in humans—to determine if this newly discovered hormone can serve as a treatment for diabetes. So it’s too soon to get excited that the discovery of betatrophin will translate directly into a new treatment for diabetes. But it is another example of the human body’s power to naturally repair itself.
Beginning in March, 2013, reports started to come out of Eastern China that a new “bird flu” virus was loose and causing infections in humans. The new virus is called H7N9. Should we in the U.S. be worried? Neither I nor anyone I know can give a confident answer to that question. So far the news is reassuring. A report from the U.S. Centers for Disease Control and Prevention (CDC), and another from a team from China in this week’s New England Journal of Medicine, indicate that so far the new H7N9 virus has not clearly spread from one person to another, and has not spread outside of Eastern China. Even so, every public health agency around the world is keeping a close eye on China. That’s because a virus that cannot spread easily from one person to another can change or swap genes—and suddenly be capable of spreading easily.
In the past decade, a remarkable series of experiments from laboratories all over the world has begun to show what causes aging—and how to slow it. In the latest example of such aging research, two of my Harvard Medical School colleagues, cardiologist Richard T. Lee (co-editor in chief of the Harvard Heart Letter) and stem cell biologist Amy Wagers and their teams have found a substance that rejuvenates aging hearts in mice. The researchers joined the circulation of an old mouse with a thick, stiffened heart to that of a young mouse. After four weeks, the heart muscle of the old mouse became dramatically thinner and more flexible. The team then identified a substance called growth differentiation factor 11 (GDF11) as the probable “anti-aging” substance. It’s too soon to tell if this discovery will ever help humans with heart failure. But it reveals that there are substances naturally present in all living things that cause aging and that retard it. By understanding them, we may someday be able to slow aging.
On Monday, Dr. Joseph E. Murray passed away at age 93. A long-time member of the Harvard Medical School faculty, Murray pioneered the field of organ transplantation. This great achievement, for which he was honored with the Nobel Prize in Medicine in 1990, has given the gift of life to hundreds of thousands of people destined to die young. But his success did not come easily. Not only did Murray attempt to do something others judged impossible, but kept trying in the face of sometimes withering criticism from peers. Murray’s team successfully performed the first organ transplant, a kidney donation from one young man to his twin brother. Over the next decade, Murray and his colleagues learned how to quiet the immune system to make it possible to transplant organs between unrelated people.
Sometimes, the Nobel Prize in Physiology or Medicine is awarded for a discovery or invention that already is improving the practice of medicine and saving lives. Sometimes it is awarded for very basic research that might someday affect medical practice and human health. Such is the case with this year’s Nobel Prize in Physiology or Medicine, which was awarded to Sir John Gurdon of Great Britain and Dr. Shinya Yamanaka. If I had to put into one sentence the message of today’s Prize, it would be this: our cells are a lot smarter and more flexible than we once imagined, and capitalizing on that fact could greatly improve the treatment of many human diseases. The work of Gurdon and Yamanaka led the way to today’s work on stem cells, which could someday be used to treat human diseases. The 2012 Nobel Prize in Medicine, like many before it, demonstrates that people with the curiosity and courage to ask what appear to be ridiculous questions, and a society that supports their work, can change our world for the better.
Researchers at Kansas State University have developed a blood test that rapidly detects breast cancer (as well as non-small cell lung cancer) in very early stages, long before symptoms appear or the cancer can be seen by other methods. The experimental test identifies enzyme patterns that differ from one type of cancer to another. According to the researchers, the test can detect very early breast cancers (stages 0 and 1), as well as early lung cancers (stages 1 and 2), within an hour, with 95% accuracy. However, they tested only 32 participants with various stages of breast or lung cancer, as well as 12 people without cancer. Whether finding cancer that early makes a difference for treatment and survival remains to be seen.
This summer, Harvard Health Publications hosted a group of mobile health startup companies, all part of the first Rock Health Boston class. I had the pleasure of attending their end-of-program demonstrations. It was 1) fun and 2) inspiring to see the future of medicine as told by young, savvy, energetic teams. All seven startups have similar goals—using the Web or apps to provide faster, better access to health care and to identify health issues before they become huge problems. Speaking before a standing-room-only crowd of potential investors, reviewers, and friends at the Broad Institute in Cambridge, the companies made polished pitches that had come a long way from those they offered upon their arrival at Harvard Health Publications in June. The seven companies include (in alphabetic order): Home Team Therapy, NeuMitra, NeuroTrack, NoviMedicine, Podimetrics, Reify Health, and RxApps.
Results of a study presented at the annual meeting of the American Society of Clinical Oncology in Chicago indicates that an experimental drug combination could be effective against HER-2-positive breast cancer. The new therapy, called trastuzumab emtansine (T-DM1), combines a monoclonal antibody with a potent chemotherapy agent. The combination is exciting because Herceptin guides the cell-killing chemotherapy agent to HER-2 receptors on breast cancer cells. This focused attack targets cancer cells and largely bypasses healthy cells, which the chemotherapy drug would otherwise damage. In the study, which included nearly 1,000 women with HER-2-positive breast cancer that had spread either within the breast or elsewhere in the body, 65.4% of the women taking T-DM1 were still alive after two year, compared to 47.5% of those on standard treatment for this type of cancer. In addition, women on T-DM1 experienced far fewer side effects.
Some encouraging Alzheimer’s news from Sweden: a vaccine called CAD106 appears to be safe and ramps up the body’s immune system against a protein likely involved in Alzheimer’s. The hope is that this vaccine will slow the progression of Alzheimer’s disease, and possibly even stop it. The vaccine is designed to activate the body’s immune system against beta amyloid, a protein fragment that forms deposits called amyloid plaques between nerve cells in the brain. Three-quarters of those who received CAD106 developed antibodies against beta amyloid protein. Virtually all of them—including those getting the placebo—reported one or more side effects, ranging from inflammation of the nose and throat to headache, muscle pain, and fatigue. None, though, developed meningoencephalitis, an inflammation of brain tissue that derailed work on an earlier version of the vaccine. The next step in the development of CAD106 is a larger clinical trial to confirm the vaccine’s safety and to see if it is effective at slowing the relentless progression of Alzheimer’s disease.