Excessive omega 6 intake promotes oxidative modification of LDL cholesterol, a primary driver of atherogenesis, and most individuals exhibit an omega 6 to omega 3 ratio exceeding 20 to 1. But LDL is mainly produced by our liver and serves essential physiological roles such as hormone synthesis and cellular repair, its atherogenic potential depends on both oxidative state and particle phenotype. Oxidized, small dense LDL particles (pattern B) readily infiltrate the arterial intima and accelerate plaque formation. Therefore, clinical strategies should aim to minimize LDL oxidation and shift the lipoprotein profile toward larger, more buoyant LDL particles (pattern A), which are less likely to contribute to cardiovascular pathology.