Ldl: cholesterol primary core lipid, mainly causes chd c. Initiates and develops atherosclerosis: ldl from arterial lumen endothelial cells arterial epithelium. Hdl cholesterol, good: atherogenesis, chronic inflammatory process, not just deposit of lipids, infiltration of inflammatory mediators (macrophage, t lymphocytes, high cholesterol, cholesterol screening. Only if tlc fails, use drugs (tg>200) Statins: hmg-coa reductase inhibitors, in liver, less cholesterol is made from a-coa(rate limiting step) Colesevelam: bile-acid sequestrates (lower fat reabsorption), in gut. Niacin: nicotinic acid, in liver, inhibit cholesterol vldl. Gemfibrozl (lopid): fibrates, reduce tgs, not ldl, in adipose tissue. Ezetimibe: inhibit cholesterol transferred from gut to liver. Drugs can improve lipid profile but can"t improve clinical outcome: statins, atovastatin (lipitor), simvastatin (zocor, increase lol receptors in hepatocyte, use. Nonlipid benefits (primary and secondary prevention of cv: promote plague stability, reduce risk for cv events c. Increase bone formation: adverse effects common: headache, rash, gi disturbances rare: myopathy/rhabdomyolysis, hepatotoxicity, drug interaction.