If you have recently been tested for C-Reactive Protein (CRP) and your doctor says you now should take a statin drug despite the fact that your cholesterol levels are fine, you are not alone. Within the last year, the media picked up on the story that high C-Reactive Protein is an even better predictor of heart disease than high cholesterol. The logic goes like this: if you have heart disease, you're almost certain to be prescribed a statin. If you don't have heart disease, but you have elevated CRP, an indicator for future heart disease, then that's almost like having heart disease, and you should take a statin drug. Never mind that your cholesterol levels will be driven down into the danger zone.
Drug companies are already hard at work trying to come up with a drug that will lower the concentration of CRP in your blood. Their reasoning is the same as their reasoning for cholesterol: if a high concentration of CRP is associated with heart disease, then reducing the concentration will surely defend against heart disease.
However, fortunately for CRP, we now have a very high-tech new cutting edge method to test the hypothesis that a substance causes a particular disease. It's a powerful and elegant new tool, and it depends upon genetic sequencing. What is especially good about this method is that you don't have to give to thousands of people a drug (i.e, that reduces CRP) that might be doing them harm, which is what's necessary if you're going to do a placebo-controlled study of a new drug.
The method, termed "Mendelian randomization," relies on knowledge of the gene sequence associated with a particular substance, such as CRP. All you need to do is to sequence that gene for hundreds of thousands of people, something that is now relatively straightforward, and it does nothing to interfere with their well-being. You can then use statistics to determine which alternative patterns of that gene are associated with higher or lower concentrations of CRP in the blood. Now you just have to look at how the two groups (low and high CRP tendencies) distribute over heart disease incidence.
This method was applied very successfully in a study involving over 100,000 people. These people were monitored over the course of nearly twenty years, and their genetic signatures for CRP were compared with their heart disease risk. Results are reported in a 2009 article in the Journal of the American Medical Assocation . The New York Times picked up on the story, and you can read about it here: (C-Reactive Protein Exonerated) .
The results of the study revealed that CRP does not cause heart disease! Apparently, its concentration goes up in response to the changes in the blood vessels that lead to heart disease. It might even be protective against heart disease. I.e., if heart disease were a fire, then CRP could be the water hose rather than the match. Its concentration would go up in order to defend against whatever else is causing the damage to the vessels.
Now here's where it gets interesting. Suppose cholesterol is the same as CRP? I think it can not be ruled out that high cholesterol is a response rather than a cause. If the kind of test that was applied to CRP can be applied to cholesterol (e.g., if there aren't technical issues that make it infeasible for cholesterol) then I think someone ought to perform this test. I'm certain that Big Pharma will never fund such a study, however, since they have thoroughly convinced the medical community and the public at large that cholesterol causes heart disease. They have nothing to prove, and everything to lose, if they turn out to be wrong about cholesterol and heart disease.
The next section will examine the theory that heart disease results from a response to an infectious agent. We will show that, if this is true, then cholesterol plays a crucial role in fighting the infection. Statin drugs, by reducing the bio-availability of cholesterol, interfere with this protective response.