What’s the Cause of Heart Disease?

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Despite its obsessive focus on cholesterol levels as the ultimate arbiter of cardiovascular disease, most of the medical field agrees that plenty of other factors also contribute: tobacco usage, psychosocial stress, activity level, and genetic predispositions. In short, a diverse set of lifestyle and genetic factors are consistently associated with cardiovascular disease. This is accepted in the ancestral health community, just as it’s accepted in the mainstream medical community, but the question remains — why? Why does stress contribute to heart disease? How does smoking tobacco increase the risk of heart disease? Why are both the sedentary and the overtrained at a higher risk for heart disease?

Well, as I’m (and others are) quite fond of saying, inflammation is most likely the ultimate cause of heart disease, and all those factors — even some of the genetic ones — are mediated by inflammation. When you get down to it, any explanation of the links between smoking and heart disease, stress and heart disease, exercise and heart disease, cholesterol and heart disease, and even genetics and heart disease must include inflammation to be accurate. As I’ll briefly discuss in the following post, each of these lifestyle and even genetic factors exert much (if not most) of their influence on heart disease via their effects on inflammation.

Let’s explore the evidence for the inflammatory roots of heart disease and continue our discussion of inflammation.


The most common form of tobacco ingestion is smoking — the inhalation of smoked emitted by the burning of dried tobacco. Now, some would argue that it’s the modern processing of tobacco that makes smoking it so bad for us, and that unprocessed tobacco is more benign and results in less heart disease. Or that it’s the modern diet that makes smoking so harmful (see the traditional Kitavans with their moderate smoking habit and apparent lack of heart disease). That’s probably true on some level, but it’s not really within the scope of today’s post. So when I refer to “smoking,” I mean the kind of mass market cigarettes that smokers in the industrialized world use: your Marlboros, your Camels, your Lucky Strikes. The kind that is linked to heart disease.

Plenty of studies show that inhaling incredibly hot, burnt tobacco plant material acutely increases inflammation, quitting immediately lowers inflammation, and recent review (PDF) of the literature specifically causally connects smoking-related inflammation and heart disease. One study even showed that smoking heaps acute inflammatory stress on atherosclerotic plaque, thus increasing the chance of a rupture. And when your atherosclerotic plaque ruptures, or breaks off, the resulting thrombus can lodge itself in the artery and block the blood flow. That, my friends, is a garden-variety heart attack caused by inflammation. Does it get much more cut and dry than that?

It’s also worth noting that smokeless tobacco ingestion, while far from benign, is associated with lower inflammatory markers and less heart disease than smoking.

Stress and Other Psychosocial Factors

Stress comes in many guises nowadays. While Grok had to deal with a few acute, undoubtedly intense psychological stressors, like facing down an opponent or a large animal bearing imposing claws and teeth, he probably didn’t experience the type of chronic, persistent psychological stress “enjoyed” by modern man. We know that psychosocial stress induces a physiological inflammatory response, and just like chronic exercise, chronic psychosocial stress can probably lead to chronic inflammation.

Studies consistently show that folks with higher amounts of psychosocial stress and depression display elevated C-reactive protein and IL-6 levels, both markers of inflammation. They’re also heavier and more likely to be diabetic, which are absolutely confounding factors, but the inflammation/stress association holds even when you account for the other variables. Teasing out cause and effect is probably impossible, but we know that stress, obesity, heart disease, and inflammation are all linked. A further clue may be found among people with anxiety disorders characterized by a heightened inflammatory response to psychosocial stress; commonly, this population experiences a “pro-inflammatory state” and hypertension, both of which are predictors of future cardiovascular disease. Another study found that certain psychosocial factors, like anger and cynicism, were linked to progression of cardiovascular disease.

For a further look at this, check out “The Great Cholesterol Con” by Malcolm Kendrick, who thinks stress is the primary cause of heart disease. I wouldn’t go that far, but it, along with the inflammatory response it engenders, plays a big role. This review paper attempts to explain how psychosocial stress-induced inflammation might lead to heart disease.

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