When you think of heart disease, heart attacks probably come to mind first. Like most things biological, however, there’s more to the story. The most common sort of heart failure is actually caused by a process whereby the walls of the heart thicken and slow down. This is often called diastolic heart failure or cardiac hypertrophy.

For about three-quarters of a century, the leading cause of death in America and much of the West has been heart disease. Cancer comes in second on this terrible list. In the 1800s and before, the leading causes were infectious diseases like influenza or tuberculosis. Thanks to sanitation and vaccination, the pathogens that cause these diseases have been rendered near harmless.

When you think of heart disease, heart attacks probably come to mind first. Like most things biological, however, there’s more to the story. The most common sort of heart failure is actually caused by a process whereby the walls of the heart thicken and slow down. This is often called diastolic heart failure or cardiac hypertrophy.

Like any machine that works 24 hours a day every day, the moving parts of the heart suffer damage and begin to wear out. The cells of the heart swell up, increasing the total mass of the heart and decreasing its efficiency. There are scenarios where an enlarged heart indicates a healthy heart—like that of an athlete—but physiologically, the two processes are quite different.

A paper published this year in the journal Science by researchers from the Harvard Stem Cell Institute has shown that a protein called GDF11 may be closely related to this decline in functionality. GDF11 circulates in much higher concentrations in the bodies of young mice as well as humans, and decreases as we age. There obviously existed a correlation, though causation was not clear.

That changed with this study, titled Restoring Systemic GDF11 Levels Reverses Age-Related Dysfunction in Mouse Skeletal Muscle, led by Doctors Richard Lee and Amy Wagers. I’ve written about this study before, but it deserves a lot more attention, as its consequences are so important.

It demonstrated that the decrease in GDF11 is directly linked to hypertrophy. The flip side of this discovery is the real news here. The study showed that increasing levels GDF11 in the bloodstream causes shrinking of the heart back to healthy size. GDF11, which stands for growth differentiation factor 11, or bone morphogenic protein 11, is the name of a protein in the very important transforming growth factor (TGF-β) family.

Researchers observed and measured the heart size of old mice versus old mice that had had blood from younger mice introduced into their circulatory systems. Before the treatment, the old mice had larger hearts due to the inflammatory action I mentioned above. After the treatment of young blood, however, the hearts of the old mice began to resemble young, healthy hearts.

The results are astonishing. Not even the researchers who proposed the study believed they would see anything this drastic and promising. In an interview about the study, Dr. Wagers said that, “When we started these experiments, I actually was thinking that there would not be a response. We had been using similar kinds of approaches in other tissues, regenerative tissues, tissues that we know have the capacity to heal themselves after they’ve been injured. But the heart is not well known for doing that, and so I was quite convinced that there would be no response. When I saw the dramatic difference in heart size that was very apparent after this exposure of an old animal to young blood, it was very clear that we had to figure out what was going on.”

That’s not the end of the story involving GDF11, however. The Harvard Stem Cell Institute released a second paper that showed GDF11 also led to improved neurogenesis and cerebral vasculature. The GDF11 protein appears to be another piece of the puzzle in terms of understanding the aging process and ultimately, how to stop it.

This one protein may not be the fountain of youth itself, but it presents exciting possibilities. The problem of delivery method could be approached in a few ways. Obviously, there is injection, but that would only provide short-term benefits. One solution that would actually be achievable much sooner than it sounds would be to engineer and implant GDF11-producing cells near the heart or brain. These cells would maintain the higher levels of this intriguing protein where it’s need most. I’m speaking with several important scientists about this therapy right now and will have more news for you in the future

Sincerely,

Patrick Cox

To learn more about the new research driving Patrick's investigations at his Transformational Technology Alert letter for Mauldin Economics, click here.