The evidence is convergent. Multiple independent sources reach the same conclusion, the underlying mechanism is well-characterized, and even the field's most cautious voices treat it as worth doing.
that was not that long ago alan that people thought hdlc was everything and today thanks to the ctep trials the mrs we now know hdlc is a much more complicated than we ever thought and b probably not something we should be trying to manipulate in an effort to improve outcomes
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Bookmarking — the dossier-vs-overview split is the right call. Most of the time I want overview; sometimes I want receipts.
Would love a "what would change this verdict" RSS feed. Sign me up if it exists.
So as a causal factor, high LDL, and particularly small LDL, is unquestionably a pathologic agent that is worthy of therapeutic lowering, whereas the role of HDL is a bit more complicated. And the removal process is important, there's no question about that. The removal of cholesterol is important. But HDL is also a marker for this other syndrome, and trying to raise HDL cholesterol is not necessarily guaranteed to reduce heart disease risk the same way lowering LDL is.