There are many meds that require an empty stomach, or no dairy within X hours of dosing, etc. But these are potent synthetics that often "bind" or eradicate, or inhibit various pathways.
Fish oil is a food. And oils/fats compete with each other during a digestive cycle. The EPA is literally diluted out.
It's not so much the EPA/DHA imo as it is getting rid of the saturated mammal fats and trans fats, including hydrogenated oils (like Vegas, with their 0% EPA serum levels, do). Getting rid of bad fats and lowering your sugar and overall caloric intake if your BMI is high will reduce risk of CVD and MACE, *not* heaping a tsp of fish oil a day on top. Even switching over to LA is great, so long as you lose the bad stuff:
LA is the most abundant dietary PUFA and accounts for approximately 90% of dietary omega-6 PUFA intake (63). Taking into consideration the results from RCTs and observational cohort studies, a 2009 American Heart Association scientific advisory concluded that obtaining at least 5-10% of total caloric intake from omega-6 PUFA is associated with a reduced risk of coronary heart disease (CHD) relative to lower intakes (64, 65). A pooled analysis of 11 cohort studies, encompassing 344,696 individuals followed for 4 to 10 years, found that replacing 5% of energy from saturated fatty acids (SFAs) with PUFA was associated with a 13% lower risk of coronary events (95% CI: 0.77, 0.97) and a 26% lower risk of coronary deaths (95% CI: 0.61, 0.89) (66). A 2012 meta-analysis of seven RCTs corroborated this beneficial effect, with an estimated 10% reduction in CHD risk (RR: 0.90, 95% CI: 0.83-0.97) for each 5% energy increase in PUFA consumption (67).
In controlled feeding trials, replacing dietary SFA with PUFA consistently lowers serum total and LDL cholesterol concentrations (68, 69). In fact, LA has been shown to be the most potent fatty acid for lowering serum total and LDL cholesterol when substituted for dietary SFA (70). The mechanisms by which linoleic acid lowers blood cholesterol include (1) the upregulation of LDL receptor and redistribution of LDL-C from plasma to tissue, (2) increased bile acid production and cholesterol catabolism, and (3) decreased conversion of VLDL to LDL (71).
Although dietary LA lowers blood cholesterol levels, supplementation with concentrated sources of LA may have adverse cardiovascular effects in individuals with preexisting CHD (see Disease Treatment).
Omega-3 fatty acids: a-linolenic acid Several prospective cohort studies have examined the relationship between dietary ALA intake and cardiovascular disease (CVD). A 2012 meta-analysis of observational studies evaluated the risk of incident CVD related to dietary consumption or biomarkers of ALA (72). The analysis included 27 studies, 251,049 individuals and 15,327 CVD events (fatal coronary heart disease [CHD], nonfatal CHD, total CHD, and stroke). Overall, the pooled analysis found a moderately lower risk of CVD with higher ALA exposure (Relative Risk [RR]: 0.86; 95% CI: 0.77, 0.97).
Unlike LA, the cardioprotective effects of higher ALA intakes do not appear to be related to changes in serum lipid profiles. A meta-analysis of 14 randomized controlled trials concluded that ALA supplementation had no effect on total cholesterol, LDL cholesterol, or triglyceride levels (73). However, several controlled clinical trials have found that increasing ALA intake decreased serum concentrations of C-reactive protein (CRP), a marker of inflammation that is strongly associated with the risk of cardiovascular events, such as MI and stroke (74-76).
Long-chain omega-3 fatty acids: eicosapentaenoic acid and docosahexaenoic acid Evidence is accumulating that increasing intakes of long-chain omega-3 fatty acids (EPA and DHA) can decrease the risk of cardiovascular disease by (1) preventing arrhythmias that can lead to sudden cardiac death, (2) decreasing the risk of thrombosis (a clot) that can lead to myocardial infarction (MI) or stroke, (3) decreasing serum triglyceride levels, (4) slowing the growth of atherosclerotic plaque, (5) improving vascular endothelial function, (6) lowering blood pressure slightly, and (7) decreasing inflammation (77).
In spite of these possible biological effects, clinical trials have not shown a significant effect of long-chain omega-3 supplementation on major cardiovascular events. A 2006 systematic review and meta-analysis of randomized controlled trials and prospective cohort studies concluded that long-chain omega-3 fatty acids do not significantly reduce the risk of total mortality or cardiovascular events (78). Likewise, a 2012 meta-analysis of secondary prevention trials (20 RCTs, including 68,680 patients) found no significant effect of omega-3 supplements (~1.5 g/day of EPA + DHA for a median of 2 years) on all-cause mortality, cardiac death, sudden death, myocardial infarction, or stroke (79). The same lack of effect was observed in a 2012 systematic review and meta-analysis of RCTs investigating the impact of omega-3 supplementation on inflammatory biomarkers in both healthy and ill individuals (80).
And of course, if you're eating more fish, your getting EPA and 9x the DHA as in supps, but more importantly *aren't* eating crap as much:
A 2012 meta-analysis of 17 cohort studies with 315,812 participants and an average follow-up of 15.9 years calculated the pooled effect of fish consumption on coronary heart disease (CHD) mortality (82). Low (1 serving/week) or moderate fish consumption (2-4 servings/week) had a significant beneficial effect on the prevention of CHD mortality. Specifically, compared with the lowest fish consumption (<1 serving/month or 1-3 servings/month), consumption of 1 serving of fish per week and 2-4 servings/week was associated with a 16% (RR: 0.84, 95% CI: 0.75, 0.95) and 21% (RR: 0.79, 95% CI: 0.67,0.92) lower risk of fatal CHD, respectively.
People that eat fish more tend to be more educated, exercise more, eat more fiber, have lower BMI, better blood glucose levels, etc. The above meta analysis doesn't do the differences justice. They are just more health conscious individuals.
And then there are the limitations of all studies. They provide a correlation, and you must attempt to decipher causation based on it. And imo that's usually not possible. More information is needed. So you can look at all components you can account for across various risk factors, and then compare the results corrected for these. And in this case it appears to me that it's what you *don't eat*, much more than what you do, that makes the difference. But without a doubt, in oncology and cardiology, exercise trumps all. Want to lower you risk of CVD and every cancer out there? Exercise a lot. Then combine that with better dietary habits, eliminating most sat fat and trans fats, while keeping your caloric intake in check, and voila your risk is far lower.
Talk about RRR.. I could take the placebo group of the Vascepa P3 and make them do what I say and they would *destroy* Vas arm. RRR of > 50% for my group.
All jmho ;)
GL
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