I've found that I can often increase compliance with statins by having pt take them 3x/week or QOD.  I try this often especially in my secondary prevention group. I understand "any statin is better than none", but do data support this approach?   -- any is better than none! No rct with this but yes data supports every other day but that is observational..what about vascepa in reducing CAD risk both primary and secondary risk? Vascepa is now the first and only drug approved by the FDA as an adjunct to maximally tolerated statin therapy to reduce the risk of myocardial infarction, stroke, coronary revascularization, and unstable angina requiring hospitalization in adult patients with elevated triglyceride (TG) levels (≥150 mg/dL) and established cardiovascular disease or diabetes mellitus and two or more additional risk factors for cardiovascular diseaseReduce it trial---The big trial which showed all the promise used mineral oil as a placeboAND then we have evaporate trial—which showed steady plaqueThe groups didn’t start off the same!When you do an RCT- everything is random and therefor EVERYTHING IS EQUAL—but that idnt happen. And yes the people were blinded but they don’t say that the people reading the CT was blindedThe placebo group had higher CRP and dramatically worse cholesterol panels after taking mineral oilThen most recently we have the strength it trial- which showed no difference and should have had high bioavailability! Like LDL that went up 50 points in the placebo group!! That shouldn’t happen!What about fibrates for triglycerides > 400 or 500 to prevent complications like pancreatitis? No – no- no- no evidence for fibrates, period, throw them away. DRUGECTOMY for everyoneGiven evidence is only for patient to age 79, what do you recommend for patients over 79 with high lipids or on who are on a statin if concern for risk of negative cognitive effects of statins in this group?   Remember 5 years or less to live. stop the statin. And the cognitive declinePlease comment on lipophilic vs hydrophilic statins and possible detrimental effects on cognition.If cognitive risk is so small, why is there a black-box warning? It makes it difficult to convince the patient to take a statin when they read this warning.ano M, Bell KL, Galasko D, et al. A randomized, double-blind, placebo-controlled trial of simvastatin to treat Alzheimer disease. Neurology 2011;77(6):556-563.In this multicenter trial, the authors gave simvastatin or placebo to 406 patients with mild to moderate Alzheimer disease, aged at least 50 years, with a Mini-Mental State Examination score between 12 and 26, who otherwise would not have been taking a statin. Simvastatin was no better than placebo in slowing cognitive deterioration in patients with mild to moderate Alzheimer disease. (LOE = 1b)Steenland K, Zhao L, Goldstein FC, Levey AI. Statins and cognitive decline in older adults with normal cognition or mild cognitive impairment. J Am Geriatr Soc 2013;61(9):1449-55.These researchers serially assessed approximately 3500 elderly patients for 3.4 years. The elders did not have dementia at baseline and approximately one third were using a statin. After 3.4 years of follow-up, the rate of cognitive decline among statin users was comparable with that of nonusers. https://www.ahajournals.org/doi/10.1161/circ.128.suppl_22.A10589Results: Significantly higher proportional reporting ratios (PRRs) were observed for lipophilic statins, which more readily cross the blood-brain barrier, (range: 1.48-3.50) compared to hydrophilic statins (range: 0.68-1.60). However, fluvastatin, lovastatin, and pitavastatin (lipophilic) had relatively few adverse reports in the AERS database. The signal of higher risk of cognitive dysfunction was observed for the lipophilic statin atorvastatin (PRR = 2.68, 95% confidence interval: 2.52-2.85) followed by simvastatin (PRR = 2.20, 95% confidence interval: 2.02-2.40).Conclusions: Inconsistent(continued)