Fat cells as Inflammation Factories

The headline called it “the new” science behind America’s deadliest diseases. WSJ reporter Laura Landro was talking about inflammation and its role in causing human disease.

Now, you all know my reaction when a prestigious newspaper features a founding principle of this blog. Well, let’s just say it felt awfully nice.

A brief Mandrola review of inflammation is in order:

First: Acute Inflammation is normal, and required for life. It’s the name given to a series of complex and protective responses of the body’s tissue when invaded or injured. Think about what happens when your skin is infected: A symphony of cells and chemical messengers rush to the scene to wall off and defeat the invader. You know it’s happening because the area turns red, warm, swollen and painful. If enough inflammation occurs, fibrosis (scar) replaces normal tissue. That’s okay on the skin; but it’s not so good for organs like the heart and brain.

Second: Inflammation becomes problematic when it becomes chronic. Imagine the damage done when the inflammatory system stays turned on for too long. Even at low levels, circulating chemical messengers of inflammation turn the body on itself. In their role of walling off and destroying, inflammatory messengers tell blood vessels to thicken, blood cells to get sticky and scar tissue to infiltrate organs. This chronic process causes heart disease, stroke, Alzheimer’s disease, Cancer and many more.

Ms. Landro is right: Excess inflammation lies at the core of human disease.

But this important mainstream media article does far more than review the damaging role of excess inflammation. Ms. Landro adds two other important facts to the conversation:

Obesity’s Role: The mistake made by many is to consider fat as an inert physical impairment. Meaning, it does its damage by chronically increases the work done by the heart and body. This wear-and-tear thesis greatly underestimates the badness of fat. It turns out that fat cells…

…“act like small factories to churn out molecules known as cytokines, which set inflammation in motion”, says Peter Libby, chief of the division of cardiovascular medicine at Brigham and Women’s Hospital in Boston and a professor at Harvard Medical School.

This is such an important message. Patients and doctors need to emphasize the dangers of fat cells. Fat doesn’t just harm us because of physics; they harm us through biochemistry—through inflammation.

Treating excess inflammation: Here’s where a cyclist and advocate for healthy choices quivers with delight. Thus far, the ‘free lunch’ therapies—taking an anti-inflammation pill—have not been curative. (Though statins help in patients with established artery inflammation.) What works for chronic inflammation? Attention to nutrition. Ms. Landro reviews the growing body of science behind the role of nutrition and inflammation. Can you guess which foods soothe, and which ones inflame? I’ll help. Think real versus man-made.

It turns out that eating whole grains, cold-water fish, vegetables, nuts and fruit are considered by many experts to be “anti-inflammation” diets. While these real foods may help soothe the inflammatory system—perhaps by reducing fat cells—man-made processed food drives fat storage. The white things, like potatoes, donuts and pasta, feed and grow the hotbeds of inflammation—the fat cells.

My only criticism of the nicely done article is the lack of mention of exercise. Oodles of studies show that ‘normal’ levels of exercise—and its chief effect, fitness—lowers markers of inflammation. The way exercise lowers inflammation are obvious: by reducing fat, by lowering blood pressure, by improving sleep, by enhancing sugar metabolism, to name just a few.

Even without the mention of exercise, I loved this piece. In the struggle to help our patients, and our nation, with the epidemic of obesity, new ideas and sticky messages are critical.

The concept that fat cells are factories of inflammation and that good health choices help slow their output is one that I will be using—and liking/tweeting.

Progress?

Maybe?

JMM