Recent studies of healthy individuals indicate that a single meal high in saturated fat will cause immediate increases in triglycerides, oxidative stress, and inflammation, which causes corresponding post-meal worsening of endothelial dysfunction, vasoconstriction, and systolic blood pressure. Post-prandial hyperlipemia, manifest as elevated levels of triglycerides, chylomicrons, and remnant lipoproteins, causes oxidative stress and inflammation, and independently potentiates the adverse effects of post-prandial hyperglycemia. These elevated and protracted post-meal lipid levels are common manifestations of insulin resistance and the metabolic syndrome.
Triglycerides are traditionally measured in the fasting state—typically the lowest triglyceride level of the day. Two large recently published cohort studies involving over 40,000 individuals found that post-prandial hypertriglyceridemia was associated with increased risk of CV events, whereas fasting triglyceride level was not. Post-prandial triglyceride levels are also directly related to angiographic progression of coronary and carotid atherosclerosis. Subanalyses of 3 randomized trials showed that lowering levels of elevated triglycerides by 20% to 40% reduced CAD rates by approximately 30% to 40%.