HD, I am always impressed with your great attention to detail and in depth research with of course data to support your statements.
From the scientific standpoint comparisons between two agents in patient populations are usually considered valid only when head to head studies designed to compare such agents have been conducted.
As there are no head to head studies comparing the efficacy of L vs V in either the Marine or Anchor population, any comparative statements that ensue are mainly inferences that are hypothesis generating. The major sources of such "comparative " inferences stem from meta-analysis on the one hand or analyzing the TG lowering efficacy from the Marine and Anchor type populations for each V and L on the other. I believe your statements stem from the latter approach. In the meta-analysis area I believe that DHA has been suggested to be more efficacious than EPA. Meta analyses as you know are plagued with variations in populations, different baseline TG levels, differences in Omega3 doses, different duration of studies, differences in concomitant lipid lowering agents etc etc. Of interest over the last several years Brinton, Balantyne, Hayes et al at different Lipid Meetings have used the Phase 3 Trials for both V and L where the dose of these agents are similar and the baseline TG levels are known, to draw these inferences - very much as you have done !! HD, I believe that you are in good company, although I can sense JL frowning as I write this.
In fact as you correctly stated that the baseline TG in Marine was in the 600s whereas the baseline TG in the L Phase 3 was slightly above 800. When the Marine TG lowering efficacy of V is analyzed with baseline TG exceeding 750, a 45% lowering in TG is observed and when V is combined with Statins, an intriguing even more robust TG lowering of 65% is observed ( the latter effect has hitherto-fore not been demonstrated with V ). With the inherent limitations in mind, your statements are not only valid but have certainly been articulated by many Lipid experts over the years.
Ins more important note, JL is very accurate in having stated (for a long time ) that athero-inflammation may be the common denominator underlying CVE. There have been some recent analyses of Statin trials where pleotropic effects have been implicated in the genesis of Statin benefits. Patients who manifest TG in the 200 plus range often with underlying Type 2 DM and the Metabolic Syndrome Phenotype - the elevated TG levels and low HDL may be the clinical signal of significant underlying inflammatory processes. The lipids may just be epi-phenomena of a very turbulent underlying process of endothelial dysfunction and inflammation. In fact most Myocardial Infarcts (MI) occur with only about 50% occlusion of Coronary vessels soon prior the MI event. Hence plaque rupture has been incriminated in such Acute MI events resulting in the sudden and dramatic 100% occlusion. Plaque stability has been a prominent subject of both basic science and clinical research in recent years. The publications that have been posted by JL, Zumantu and others ( Authors Preston Mason - Harvard ; and Madoff et al UCLA ) have beautifully demonstrated in vitro and in vivo basic science and Clinical studies of the favorable effect of EPA on cellular processes in the basic science area which has been complemented by clinical studies on the measurement of the Fibrous Cap of Coronary Plaques in the clinical area. It is the sum total of all this data that suggests that the TG lowering effect of EPA may literally be scratching the surface of its potential benefits. The authors of Jelis pointed to the potential Pleotropic effects of EPA when a meager 5% decrease in TG was associated with a significant 19% reduction in CVE.
My apologies if a great deal of this has been rehashed by others on this board. I read comments of posters only intermittently:
The likes of JL, HD, VBru, AV, Whalatane, Zumantu, and others have been real fun to read.
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