Normal rise of triglycerides in pregnancy occurs due to increased estrogen which increases liver VLDL secretion and decreased lipoprotein lipase activity ( an enzyme involved with triglyceride metabolism ) which leads to decreased clearance of triglycerides. In the first trimester there is an increase in ovarian estrogen which increases triglycerides. In the 2nd and 3rd trimester there is increased ovarian and placental estrogen which increases triglycerides. There are some genetic defects that can increase triglycerides in pregnancy which are decreased lipoprotein lipase, increased APOC3, and decreased APOC2 which are involved with chylomicron metabolism ( chylomicrons carry triglycerides after a meal that contained fat while VLDL carries triglycerides produced by the liver from carbs in the fasting state ). Drugs that decrease triglycerides in pregnancy are fibrates, omega 3 fatty acids, and niacin and they are category C. Women with gestational diabetes mellitus have higher triglycerides which is further increased in pregnancy, but women with gestational diabetes mellitus will have lower LDL-C than women with no gestational diabetes mellitus, and increase in HDL-C will not be as robust. Women with increased triglycerides and increased waist circumference represent a phenotype with greater cardiovascular risk. There is no association between pregnancy and the hyperlipidemia of pregnancy and sbsequent coronary disease. The lipid changes of pregnancy are accentuated in women with FH. The only lipid abnormality requiring treatment during pregnancy is hypertriglyceridemia, which is associated with increased risk for preeclampsia and pancreatitis.