In adults with hypercholesterolemia, cascade screening often identifies other family members with elevated LDL-C (Section 4.2.). However even moderate hypercholesterolemia can accelerate development of atherosclerosis.S4.4.4.2-4 Sec- ondary causes of elevated cholesterol hypothyroidism (TSH), obstructive liver disease (liver panel), renal disease and nephrosis (creatinine and urine analysis) as well as dietary and medication history should be addressed Elevations of LDL-C persisting af- ter excluding secondary causes suggests genetic forms of hypercholesterolemia. Young adults who experience prolonged exposure to hyperlipidemia prior to age 55 are shown to have significantly increased risk of coro- nary heart disease.S4.4.4.2-6 Intensive lifestyle change has the potential to reduce the hyperlipidemia and associ- ated ASCVD risk factor burden. A smaller group, but even at higher risk, are young adults with persistent, moderate hypercholesterolemia (LDL-C 160-189 mg/dL), especially when risk-enhanc- ing factors, such as a family history of premature AS- CVD, are present. Since there is increased probability of genetic FH in this LDL-C range, clinical judgment would suggest that these high risk young adults will benefit from long-term statin therapyS4.4.4.2-7 (Section 4.2.). In- deed, it has been shown that those with higher LDL-C can gain as much or more benefit from cholesterol re- duction as do those with lower pretreatment LDL-C but at higher risk.S4.4.4.2-8,S4.4.4.2-9 In young adults without phenotypically severe hy- percholesterolemia, risk assessment should begin by estimation of lifetime risk.S4.4.4.2-10 The pooled cohort equations (PCE) can be used to estimate lifetime risk starting at age 21 years (see Section 4.4.2.). This information can inform a focused risk discussion designed to improve high-risk lifestyle behaviors in- cluding tobacco use, sedentary lifestyle and/or poor When young adults with hyper- cholesterolemia or multiple risk factors are identified, lifestyle intervention is indicated. 