Atherosclerosis
Atherosclerosis is an ongoing inflammatory response. Recent advances in basic science have established a fundamental role for inflammation in mediating all stages of this disease from initiation through progression and, ultimately, the life-threatening complications of atherosclerosis. These new findings provide important links between risk factors and the mechanisms of atherogenesis. Clinical studies have shown that this emerging biology of inflammation in atherosclerosis applies directly to human patients. Elevation in markers of inflammation predicts outcomes of patients with acute coronary syndromes, independently of myocardial damage. In addition, low-grade chronic inflammation, as indicated by levels of the inflammatory marker C-reactive protein, prospectively defines risk of atherosclerotic complications, thus adding to prognostic information provided by traditional risk factors. Moreover, certain treatments that reduce coronary risk also limit inflammation. In the case of lipid lowering with statins, this anti-inflammatory effect does not appear to correlate with reduction in low-density lipoprotein levels.
In a 2025 report issued by the Journal of the American College of Cardiology, the authors said that the high-sensitivity C-reactive protein (hsCRP) blood test that measures CRP, a known inflammatory marker that increases in response to inflammation in the body, can determine whether a person is at risk of developing cardiovascular disease.20 This is essentially what we have been claiming here regarding vitamin D, inflammation, and CVD. Of course, the American College of Cardiology may not like the solution to most CVD at all, which is safe, inexpensive (mostly free) vitamin D. For my personal situation for more than twenty years I have requested a CRP test to determine if there is inflammation anywhere. There isn’t, so I don’t worry about heart disease.
