We’ve all experienced inflammation in our bodies. We get a paper cut and a finger becomes inflamed at that spot—it seems for days on end—before healing. We twist an ankle and the area becomes red and swollen (inflamed); but a little ice, rest, elevation and over time the area is as good as new.

In this sense, inflammation is a good thing. It’s the body’s natural defense and indicates a healthy immune system response when injuries or infections occur.

But what happens when our WHOLE BODY becomes inflamed? I’m not talking about an autoimmune disease that exhibits itself in specific areas of the body—such as psoriasis, celiac disease, or rheumatoid arthritis—and makes itself known for all to see, a sort of medical shout out that says, “Look here! This is runaway inflammation.”

I’m talking about a silent killer—chronic inflammation. Recently, I had a routine medical check-up with my primary care physician and, as part of the process, blood was drawn and specific lab results were reported. One of the things my doctor looked at was my C-reactive protein lab result. He was happy to see it within normal limits and made sure to comment on that since that’s an indicator of chronic infection and one of the indicators for heart disease.

For many years, cardiologists have focused on heart disease as a plumbing repair issue—clogged arteries due to cholesterol build-up that narrows and then blocks those arteries near the heart must be cleared. In the early years of modern cardiac disease management, it was believed that the cholesterol we eat caused the build-up in our arteries.

In later years, it was discovered that certain fats we eat (saturated fats and trans fats, specifically) caused the body to make much more cholesterol than necessary. Hence, the popularity of cholesterol-lowering drugs such as Lipitor and the advancement of procedures to unblock clogged arteries. In this sense, cardiologists became sophisticated “Roto-Rooter” plumbers.

Recently, a series of interesting articles reported an evolving science that indicates there is much more involved regarding cardiac disease than the idea of clogged pipes (arteries).

The studies that shed light on this evolving science indicate that a possible primary cause of coronary artery disease is chronic inflammation—a so-called systemic inflammation that causes scar tissue in our arteries that begin to trap fatty particles (cholesterol) from our blood. That’s why my physician was happy to see my C-reactive protein lab result within normal limits.

Presently, there is a clinical trial of a new drug called Canakinumab, a drug that reduces systemic—or low-grade, total body—inflammation. The clinical trial is called the Canakinumab Anti-Inflammatory Thrombosis Outcomes Study (CANTOS). The study results indicate that this drug lowers heart attack risks independent of cholesterol-lowering medications, like the statin drug Lipitor.

Patients on Canakinumab experienced an astounding 30% decrease in the need for invasive and expensive bypass surgeries and angioplasty procedures. This represents a whole new level of cardiac disease prevention and brings in a third tier of heart attack prevention (the first two measures being the importance of diet and exercise, and then the additional layer of protection with cholesterol-lowering statin drugs).

An interesting additional benefit of this drug was a documented decrease in cancer risk by 50%. Researchers now question if the idea of reducing systemic inflammation throughout the body may not only prevent the onset of cardiac disease but also become a cancer prevention measure. This has stimulated a whole new area of cancer research, but it’s too early to get excited about that possibility at this point.

It should be noted that since Canakinumab lowers the body’s immune system response, this drug may have a detrimental effect by increasing the risk of common infections becoming more serious, and even fatal, events. So, the benefits of this new therapy will have to outweigh the possible disadvantages, and further research may discover ways to minimize the infection-related risks.

Thoughts? Comments? I’d love to hear them!