Weight, exercise, smoking & sleep

Visceral fat and insulin resistance drive the whole atherogenic pattern — high triglycerides, low HDL, small dense LDL, high ApoB. Losing visceral fat improves all of them, and even modest loss helps. GLP-1 drugs (semaglutide, tirzepatide) improve the metabolic profile, and SELECT showed semaglutide cut cardiovascular events ~20% in overweight patients without diabetes — a genuine new lever (though only partly via weight). None of this is a licence to skip proven LDL-lowering. Evidence ●●●●○

Aerobic plus resistance training modestly lowers triglycerides and raises HDL, and has a large effect on insulin sensitivity, blood pressure, and plaque stability. Aim for ~150 minutes/week of moderate activity, ideally with both zone-2 endurance and something that builds VO₂ max. It doesn't lower LDL much directly — its value is metabolic and vascular, protecting the artery wall rather than moving the LDL number.

Smoking is one of the most potent accelerators of plaque and rupture — quitting is among the highest-yield things a person can do for their arteries, full stop. Alcohol raises triglycerides, and the old 'red wine is heart-healthy' story has largely collapsed — there's no cardiac threshold worth chasing. Poor sleep and sleep apnoea worsen blood pressure, insulin resistance, and inflammation; chronic stress feeds the same fire via cortisol and inflammation. These move plaque biology directly.