Endocrine, week 2

It’s the week of long names and rare diseases. Hyperlipidemia, hypercholestremia, hypertriglyceridemia, each congenital in nature but rare (at least for the most part). The fact is that the complex “hyper” fatty acid diseases really are part of the larger backdrop that has helped define how fatty acids affect vascular health and lead to atherosclerosis. The connection here, as it is with so many other diseases we’ve covered up to this point, is that the disease process involved in the pathogenesis of atherosclerosis is a combination of genetics, lifestyle and environmental triggers that lead to an eventual disease state.

Part of the week’s objectives involved an analysis of student lipid profiles. I have to admit that I was nervous. Given that I am one of the older students in the class, I somehow expected my lipid profile to be out of the norm (the glaring outlier in the analysis), especially when compared to all the younger punks students in the class. This fortunately wasn’t the case and my “bad” fat (my low density lipoprotein (LDL)) was low and my “good” fat (my high density lipoprotein (HDL)) was high. Furthermore, the ratio of Cholesterol to HDL was under the target range of 4.0. All good news, but what does it really mean? Given my age, total cholesterol, HDL, lifestyle factors and BP, I can use a model to estimate a 10 year risk of coronary artery disease in myself. The model is known as the Framingham CVD Risk Assessment (there is a calculator available here at the National Cholesterol Education Program if you’re curious about your own risk of developing coronary artery disease). My ten year risk of coronary artery disease is <1% … and I think I can live with that (at least for the moment).


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