Baby Aspirin Recalled After Acetaminophen Discovery

More than 16,000 bottles of baby aspirin are being recalled by Advance Pharmaceutical Inc. after one of the bottles was found to be filled with acetaminophen pills.

The recall covers 120-pill bottles labeled to contain 81-milligram aspirin pills. The bottle discovered by a CVS pharmacist contained 500-mg acetaminophen pills, ABC News reported.

No injuries have been reported, according to Advance Pharmaceutical spokesman Abu Amanatullah.

Doctors said that unknowningly taking acetaminophen instead of baby aspirin could lead to an overdose that results in liver failure, the need for a liver transplant or death, ABC News reported.

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Discovery could someday help people with diabetes make more insulin

Posted May 24, 2013, 3:11 pm

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 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.

For the team’s leader, Dr. Douglas Melton, research on the subject of diabetes is personal as well as professional. In 1993, his six-month-old son was diagnosed with type 1 diabetes. Since then Melton, who is co-director of the Harvard Stem Cell Institute, has turned his considerable research skills to learning how diabetes happens and how it might be cured.

In type 1 diabetes, the body’s immune system attacks the pancreas, a spongy little organ that sits below the stomach. The attack destroys insulin-producing cells in the pancreas, called beta cells. Without enough insulin, muscle cells can’t absorb sugar from the bloodstream. Sugar levels rise in the blood, causing havoc throughout the body. Untreated type 1 diabetes can be deadly. Even with treatment, usually daily injections of insulin, type 1 diabetes often leads to heart disease, vision problems, and nerve problems.

In the more common type 2 diabetes, the muscles resist that action of insulin, causing blood sugar to rise. As the pancreas churns out more and more insulin, the beta cells can eventually become burned out.

Over the years, Melton and his colleagues made a surprising discovery: the pancreas could make new beta cells, even in people with type 1 diabetes. “Old” pancreas cells can divide, forming young ones. Unfortunately, the pancreas isn’t naturally able to make enough new beta cells to make up for those killed by diabetes.

Melton and colleagues reasoned that there might be some chemical signal that prompts beta cells to divide and increase. The Cell paper details their search for and discovery of such a signal in mice. It’s a hormone the team called betatrophin. This hormone, made by liver and fat cells, travels through the blood to the pancreas. There, it prompts existing beta cells to grow and divide, making new beta cells.

In mice with diabetes, turning on the production of betatrophin by 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.

This work is just the latest example of an even larger scientific discovery that has played out over the past two decades. We are learning that the human body has much greater power to naturally repair itself than we once imagined. Scientists all over the world are working to discover ways to stimulate the body’s own natural healing mechanisms, as Dr. Melton and colleagues are doing.

In the United States, this work and other important investigations are threatened by the “sequester,” which is cutting funding for medical research. It would be a shame for an important discovery like Melton’s to languish because of political infighting. Regardless of what you think about federal spending in general, if you share my view that we should not be cutting funding for health research and public health, you could do what I have done. Write your representatives in Congress to restore cuts in medical research.

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Discovery reverses aging of mouse hearts—could it work in humans, too?

Posted May 13, 2013, 12:19 pm

Every living thing is constantly aging. It seems universal and inevitable—a law of nature. Just look in the mirror, or check out your family and friends.

Yet in the past decade, a remarkable series of experiments from laboratories all over the world has begun to challenge that “law.” In both simple animals like worms and in more complicated animals like mice, scientists are discovering what causes aging—and how to slow it. The life spans of several simple animals have been extended greatly by simple biological manipulations. More important, during that extra time alive, the animals remain quite strong and fertile.

The latest example of such aging research was just reported in the prestigious scientific journal Cell by 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. (You can see a video of the researchers discussing their work below.) The discovery could someday lead to a treatment that prevents or reverses the most common kind of heart failure in humans: age-related diastolic dysfunction. There is currently no specific treatment that prevents or reverses this condition.

In diastolic dysfunction, the heart muscle becomes thicker and stiffer. As a result, when blood enters the heart, its muscular walls can’t stretch enough to accept all the blood flowing into it. That means the heart pumps less blood with each beat, making it difficult to circulate blood to every cell in the body. Blood backs up into the lungs, causing difficulty breathing. It also backs up into the rest of the body, causing fatigue and swelling, particularly in the legs and feet. That’s heart failure.

Mice have a similar condition. It develops as the animals get older, just like it does in humans. The team led by Lee and Wagers wondered if something was present in the blood of young mice that kept the heart young. To pursue that possibility, they joined the circulation of an old mouse to that of a young mouse. As a result, the two animals shared the same blood. After 4 weeks, the thickened and stiff heart muscle of the old mouse became dramatically thinner and more flexible.

In other words, it looked like Lee and Wagers’ hunch was right: some substance was present in the blood of young mice that rejuvenates the heart muscle of old mice. Most likely, that substance had been in the blood of the old mice when they were younger, but had decreased as the mice aged.

The team then identified a substance called growth differentiation factor 11 (GDF11) as a good candidate to be the “anti-aging” substance: it was at high levels in the blood of young mice but not old mice. To prove its role, Lee and Wagers gave old mice enough GDF11 so they had the same blood levels of it as young mice. Again, the thickened, stiff heart muscle of the old mice became rejuvenated. So at least in mice, a common kind of aging of the heart could be reversed by a particular anti-aging substance.

Will this discovery in mice offer any help to humans with heart failure? It will take a lot more research to know. It may not work in humans the way it works in mice. It may work in humans, but cause unacceptable side effects. Any beneficial effects might not last.

On the other hand, it also is possible that this substance has anti-aging effects in more organs than just the heart—and not only in mice, but maybe also in humans. So the discovery could have even greater potential than it now appears.

For me, what is important about this study is not whether it will help human health: we just can’t know if it will until much more research is performed.

What I find important is that the work by Lee and Wagers, like a number of studies before it, reveals a remarkable new truth: there are substances naturally present in all living things that cause aging and that retard it. In other words, aging is not a mystical process. Aging is chemistry. By understanding that chemistry, we may someday be able to slow aging.

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