Excellently argued take on the CVD epidemic. It still is an epidemic as cardiovascular disease firmly remains the top cause of premature death.

Two aspects are most often overlooked in the epidemiological debate about CVD and attempts to associate it causally with whatever coincides with its trends. First, the randomness of MACEs (major adverse cardiovascular events) and, second, their most upstream cause.

The current consensus is that chronic low-grade inflammation is the trigger that creates the “vascular theatre” in which MACEs ultimately play out. That is, chronic inflammation damages the innermost lining of the arteries, the endothelium, which then becomes more prone to atherosclerotic plaque development. Not all plaques cause heart attacks or strokes, it’s typically the so-called vulnerable ones. Once they “break”, exposure of their inner core to the bloodstream sets off a cascade of thrombus formation, dislocation, downstream blockage, etc. If fibrinolysis kicks in in time, everything is fine, if it doesn’t then voila there is a heart attack or stroke.

Funnily though, these cascades happen unnoticed in most people at some time. Only when all the right conditions are met, will a MACE occur. It’s a random effect. The chance for it to happen depend largely on the presence and degree of all its prerequisites.

Why am I explaining this? Because all the potential causes that you mention play a role in inflammation. Reducing any one or more of those will lower the chances of a MACE to happen. So, for any given individual we can’t say which lever has the largest effect on preventing or postponing a MACE. That’s why the best game plan is to reduce as much as possible any of the prerequisites. In that sense, your “best lines of defence” is a very sensible approach to avoiding heart attacks and strokes.