Do statins increase the risk for diabetes?

According to a new study published in the Lancet:

Statin therapy is associated with a slightly increased risk of development of diabetes, but the risk is low both in absolute terms and when compared with the reduction in coronary events. Clinical practice in patients with moderate or high cardiovascular risk or existing cardiovascular disease should not change.

In this meta-analysis of 13 statin trials, statin therapy was associated with a 9% increased risk for incident diabetes. Statin therapy was associated with a 9% increased risk for incident diabetes

Stay tuned, because this article is likely to generate some very interesting discussions regarding the use of statins. You may have heard the phrase, "statins should be in drinking water." How about the idea of creating a super cardiovascular pill that includes a statin, aspirin, beta blocker, and ACE inhibitor?

Maybe the bigger question is regarding the use of statins for patients who have normal cholesterol levels but who have elevated hs-CRP levels (suggesting systemic inflammation which may lead to cardiovascular disease, even if your lipid levels are normal). I'm referring to the JUPIPTER study published in the New England Journal of Medicine and the recent FDA-approved indication for Crestor (rosuvastatin).

Specifically, this includes men 50 years of age and older and women 60 years of age and older who have an elevated amount of a substance known as high sensitivity C-reactive protein in their blood and at least one additional traditional cardiovascular risk factor such as smoking, high blood pressure, a family history of premature heart disease, or low amounts of high-density lipoprotein or HDL cholesterol, the so-called “good cholesterol.”

Click here to read the entire Lancet article titled, "Statins and risk of incident diabetes: a collaborative meta-analysis of randomised statin trials"

Misguided health article on CNN about CRP

CNN has a story that has a misguided title (in my opinion). The story is titled, "Study suggests C-reactive protein doesn't cause heart disease." If we focus on causality, we may be missing the boat.

C-reactive protein (CRP) may not cause heart disease, but it may be a marker of underlying inflammation. Chronic inflammation may lead to coronary heart disease (CHD). If that's all true, then the title of the story can be misguiding. We often think in terms of cause and effect. If you have blood stasis (not moving), then you can form a blood clot. Cause and effect. So, if cardiovascular inflammation causes CHD, can you have inflammation without an elevation in CRP? Can you also develop CHD without any inflammation if you also have really high cholesterol levels? I think we're learning that the pathophysiology of CHD is not as simple as we learned about in medical school.

Well, if CRP doesn't cause heart disease, so what? What if CRP is an indicator of heart disease? That's the real question. It may not have a causal relationship, but that statement may be misguiding.

The JUPITER study published in the New England Journal of Medicine (NEJM) showed that a cholesterol-lowering drug Crestor (rosuvastatin) significantly reduced the incidence of major cardiovascular events in healthy-appearing patients who had low and normal cholesterol levels. This was such a groundbreaking study that it stirred significant controversy about CRP and the high-sensitivity CRP (hs-CRP).

CNN quotes the lead author of the JUPITER study in this story as "Another leading CRP researcher who isn't so sure about the findings published in the Journal of the American Medical Association (JAMA)." Dr. Paul M. Ridker, the director of the Center for Cardiovascular Disease Prevention at Brigham and Women's Hospital, in Boston, Massachusetts, said: "A null Mendelian randomization may not mean very much... While it does not support causality, I don't think most genetic statisticians believe it excludes a causal pathway either."

Are you familiar with Mendelian Randomization and Genetic Association Studies? Good, me too. The JAMA studied used this as one of its steps: " A mendelian randomization study for the most associated single-nucleotide polymorphism (SNP) in the CRP locus in our data together with published data on CRP variants with CHD let us assess the potential causal association of CRP with CHD." Did you catch all that? Good, me too.

Dr. Ridker argues that clinicians should still measure hs-CRP for the following reasons:

• A, it predicts vascular risk even when cholesterol is low and other risk factors are absent, and,
  
• B, because we have clinical trial data demonstrating that if you have an increased level of [hs-CRP], you will live longer and have fewer heart attacks and strokes if you take a statin.

Dr. Ridker goes on to say: "I have always felt that CRP is a good clinical biomarker of inflammation (and high vascular risk) but that it is inflammation that is likely to be causal for atherosclerosis, not CRP itself." To read the CNN story, click here.