From Arthritis to Zoster

If we want to understand the myriad and mysterious ways of our immune systems, sometimes we have to connect the dots. For practitioners of Western medicine, that occasionally means throwing off the shackles of dogma and embracing a new concept.

Way back in the 1990s, while performing autopsies on individuals who died following heart attacks, scientists discovered bacteria in the walls of some victims’ coronary arteries. More specifically, the bacteria – along with the inflammation they precipitated – were found in plaques, those thickened areas that cause “hardening” of the arteries and that eventually occlude the vital conduits that carry blood and oxygen to the heart muscle.

It was an interesting finding, one which led some researchers to suggest that coronary artery disease – like peptic ulcer disease (another heretical notion, at first) – might be an infectious illness. However, statin drugs were rapidly becoming de rigueur for “informed” physicians, so much of the conjecture connecting infectious organisms with coronary artery disease fell quickly by the wayside.

Aggressively marketed as both prevention and cure for all vascular ills, statins grew in popularity – not coincidentally becoming a major source of revenue for pharmaceutical firms – and they are now part of the “standard of care” for dealing with any condition that is even remotely associated with cardiovascular disease: hypercholesterolemia, hypertension, diabetes, evil spirits…some experts now recommend that even our children should be taking these drugs.

Alas, there is a tiny, irritating fly in the ointment. Despite the “take-statins-for-everything” message that is continuously smeared across American television screens and that is slathered liberally over the pages of medical journals, it is actually inflammation – the perennial companion of a vigilant immune system – that is the perpetrator of cardiovascular disease. Study after study has implicated inflammation in the genesis of atherosclerosis and its nasty outcomes. Indeed, not long ago, high-sensitivity C-reactive protein, an indicator of vascular inflammation, was added to the array of blood tests that physicians can use to determine a person’s risk for coronary artery disease and heart attack.

This is not to say that aberrant lipid levels don’t play some role in heart attacks and strokes; they clearly do. However, our reliance on these markers – and our reflexive attempt to “normalize the numbers” at all costs – has been less than universally effective for preventing heart attacks…which was the hope of statin advocates when these medications first became vogue.

Research continues to reinforce the role of inflammation, a direct result of immunologic reactivity, in this all-too-common disease.

One might wonder when some research dollars will be spent on identifying the immunologic factors that lead to heart attacks and strokes. What trigger or triggers, for example, stimulate the macrophages in our arterial walls to ingest packets of low-density lipoproteins (LDLs), transform into foam cells, and release cytokines that encourage other immune cells to damage the linings of our vessels? In fact, are low-density lipoproteins really one of the root causes of cardiovascular disease, as statin proponents tell us, or are they merely another marker for an as yet unidentified inflammatory process?

These questions (and so many others) should interest responsible scientists, for a clearer understanding of the basic mechanisms behind coronary artery disease might lead to cheaper, safer preventive measures that would save a lot of lives and a lot of healthcare dollars.

In the case of coronary artery disease, we seem to have stepped once more to the verge of issues that were initially examined by curious people nearly two decades ago, but that were buried beneath avalanches of misinformation proffered by the moneymakers. Our pursuit of real answers is too often thwarted by profiteers.

To date, no one has thoroughly explored the association between immunity, inflammation and cardiovascular disease. Such an effort would apparently be unseemly, as it might just threaten the economic machine that is the statin market. I could be mistaken about that, though: I recently read an article attesting to a statin drug’s ability to lower the levels of inflammatory markers in people at risk for heart disease. So it won’t be long before statins are marketed as top-notch anti-inflammatories, too.

Thus, as long as we keep peddling statins to physicians and an unsuspecting public – promoting the drugs as panacea – we may not need real answers to all of those nagging questions.

After all, once dogma gets rolling, it has a lot of inertia.