In patients with moderate hypertriglyceride- mia, it is reasonable to reduce both atherogenic VLDL and associated risk factors by nonpharma- cological means where possible. This can best be achieved by identification and treatment of the multiple underlying causes of elevated triglyc- erides (eg, lifestyle causes, secondary disorders, and triglyceride-raising drugs).S4.5.2-1 Triglyceride- raising drugs include oral estrogens, tamoxifen, raloxifene, retinoids, immunosuppressive drugs (cyclosporine, sirolimus, tacrolimus), beta blockers, interferon, atypical antipsychotic drugs, protease inhibitors, thiazide diuretics, glucocorticoids, rosi- glitazone, bile acid sequestrants, L-asparaginase, and cyclophosphamide. 2. Most patients with severe hypertriglyceride- mia have multiple ASCVD risk factors and are at enhanced risk of developing atherosclerotic This risk is conveyed by atherogenic VLDL plus other factors, such as obesity, metabolic syndrome, and hyperglycemia. Although chylomicronemia per se may not be ath- erogenic, in most patients it associates with other For this reason, initiation of statin therapy is reasonable. We stress that statins alone cannot prevent increasing levels of triglycerides in the face of secondary causes (see Recommendation 1) from triggering acute hypertriglyceridemic pancreatitis. Indeed, in the pregnant woman with severe hypertriglyceride- mia, statins are not part of the treatment regimen because they are not recommended at the pres- ent time in pregnancy. (See Section 5., Statin Safety and Statin-Associated Side Effects. )3. Epidemiological studies show that patients with moderate hypertriglyceridemia generally are at increased risk of ASCVD.S4.5.2-2 S4.5.2-4 Few studies that primarily recruited patients with hypertriglyceri- demia have been carried out with triglyceride-low- ering drugs. Statin therapy reduces VLDL similarly to and statin trials include hypertriglyc- eridemic patients. 