EPA...The Big Picture...
With all due respect to one poster who is championing the "bear side" of the EPA argument...ie that R-I will show marginal or worse CVD risk reduction; and it is possible 4 gms of EPA may actually increase the risk of CVD in a toxic manner. I will try to explain his point of view and where and why IMO he has gone wrong...
The first point is that EPA and DHA on the whole have some similarities, both lower trigs..DHA more so on a per dose basis. The two n-3s (omega-3s) also have many differences...So the questions that need to be answered are 1)is one of them more important in lowering CVD, 2) are they both equally important (the Lovaza issue) in CVD risk or 3) Are they (or one of them) dangerous in high dosage (ie 4gm/day)..
The first observation is that most if not all P's citations deal with "lipid issues"..I am not going to get into characterizing the "strength" of his links, or his interpretations. Lipid issues..ie..trigs,LDL, LDL-C, particle size, HDL-C, VLDL, APO-b, APO-c, remnant particles, oxidized LDL/LDL-C...are fertile fruit for arguments within the CVD arena. LDL-C..the foundation of the multi multi billion dollar statin empire past and present is very weakly grounded and has never offered an explanation on why over 50% of initial AMIs occur in individuals with normal or low LDL-Cs..
So it might be the case that DHA is a better trig lowerer and that elevated trigs constitute a very significant portion of the non-HDL-C fraction (APO-B) and that this is one determinate of CVD risk..It also might be that that EPA actually lowers HDL-C where as DHA does not and HDL-C (the good cholesterol) is thought to offer some CVD risk benefit...
The problem with these arguments is lipids are confusing because they are not really the central characters in the atherosclerosis story..They are at best "extras"...The Korean War played a very important part in the the American doctors formulation of atherosclerosis (AS) and CVD...Prior to WWII AS was not as prevalent in the USA...but the incidence began to climb in the late 1940s...The Korean War in the early 1950s provided a rich supply of young American 19yo males for autopsy. Doctors noted many of those young men had "streaking" of the aortic wall and the streaks were high in cholesterol..The doctors drew what seemed to be an obvious conclusion that AS was simply cholesterol gumming up the arteries the way sludge might accrue in a sewer pipe..and Voila this led to the statin industry...
The real issue which escaped the doctors was that AS is not really a lipid disorder...It is an inflammatory disorder. The rise of AS in the USA was more the effect of the 1940s developing the seed oil "screw extractor"...Which allowed extraction of seed oils fractions of which were highly resistant to oxidation and paved the way for the modern "Super Markets"...Which could not exist without the use of these oils in grains and processed foods because of limitations on "shelf life"..
Fact was these oils are major sources of arachidonic acid (AA)...AA is the major driver of systemic inflammation. Which leads us to chapter two in the n-3 story...
What are we talking about here?..Number one heart attacks do not usually occur because the artery is "gummed up"..They occur secondary to rupture of AS plaques which are the consequences of inflammation..Where as lipids in their various concentrations can influence inflammation the over all sensitivity of the inflammatory system to outside influence is more important than what the drivers are.. The sensitivity is effected by several factors the most important being the "eicosanoid cell and nuclear membrane system"...This system is locally based and present on all cells except erythrocytes. It consists of cell and nuclear membrane receptors..Which control inflammatory sensitivity..AA competes with EPA (and not DHA) for cell membrane and PPAR receptors in a binary way. And it is the balance of these two molecules which largely determines the sensitivity of the inflammatory response. High inflammatory levels lead to AS. .Both AA and EPA are inflammatory, but AA is much much more pro inflammatory..
There are other substances that effect the eicosanoid receptors..notably aspirin, ASAIDs and steroids..The difference between EPA and the others is that EPA alone can actually trigger the release of "good eicosanoids" which promote "well being"..Aspirin does block the release of inflammatory eicosanoids, but destroys the membrane receptors and does not release positive eicosanoids..
So despite the fact that DHA might produce some positive effect s on the lipid profiles its basic structure prevents it from acting on the receptors of the eicosanoid system..And this out weighs any possible benefit in the lipid profiles...Also as far as ODing on EPA because the doses are too high..This flys in the face of all observations which support the notion the higher the EPA/AA ratio the lower the CVD risk..
As far as Vegans or vegetarians I have no problem with the fact they might have low CVD event rates with low EPA and high AA..There are other factors which influence systemic inflammation and caloric restriction is one of them...We are not developing a drug for vegetarians. Our target is the millions of Americans who shop at the super markets and eat too much pizza, burgers and frys, the Colonial's Chicken...and drinks sugar drinks...
":>) JL
