Sublime

Astaxanthin

these chemical firefighters knock out free radicals, and then stabilize themselves to end the destructive chain reaction.

This is my starting point with any patient, whether they are like Anahad (with one prominent risk factor) or like me (lots of smaller risk factors). Our first order of business is to reduce the burden of apoB particles, primarily LDLs but also VLDLs, which can be dangerous in their own right. And do so dramatically, not marginally or incrementally.

Adam Appich, master of science, is there with several studies that show how legacy cognitive blindness will forever prevent people from acting in their own best interests.

When I look at a patient’s blood panel for the first time, my eyes immediately dart to two numbers: apoB and Lp(a). I look at the other numbers, too, but these two tell me the most when it comes to predicting their risk of ASCVD. ApoB not only tells me the concentration of LDL particles (which, you’ll recall, is more predictive of disease than the

bearing on the quality of the oil.

This is not an atypical scenario: when a patient comes to me and says their father or grandfather or aunt, or all three, died of “premature” heart disease, elevated Lp(a) is the first thing I look for. It is the most prevalent hereditary risk factor for heart disease, and its danger is amplified by the fact that it is still largely flying under the

While there are seven statins on the market, I tend to start with rosuvastatin (Crestor) and only pivot from that if there is some negative effect from the drug (e.g., a symptom or biomarker). My goal is aggressive: as rationalized by Peter Libby, I want to knock someone’s apoB concentration down to 20 or 30 mg/dL, about where it would be for a chi