Atlas, this best post (14647) I ever read here
. The paper details how EPA works (vs DHA )and confirms EPA's efficay in reducing CV events. I can't see hwo anyone can dispute it or assume anything but incredible success from Amarin's "reduce it" study.
Furthermore any doctor on the panel who hadnt read this prior to ADCOM will be thoroughly embarassed and wish they did.
I just got through reading it(twice)and the ramifications here are astounding ! In fact I just forwarded the paper to my girlfriend who is a RN in one the top rated hospitals for CV / open heart surgery in the country to shove under the nose of an arrogant Card She argued with the other day who claimed he had not heard of Vascepa - and then he attemtped to discount as "just fish oil" from Costco. But what is truly ironic is a good friend had just come back from his annual visit with his Card who is in the same freaking practice with the Card who hadnt yet heard of Vascepa! .. WTF?? This is a true story...
Anyways back to this astounding paper..
There are a lot of key nuggets like these....
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?3 exist as constituents of cell membrane phos- pholipids. DHA is found in all organs and is abundant in nerve tissues, such as the cerebral cortex, hip- pocampus and retina, at concentrations that are several hundred times higher than those of EPA. In contrast, the EPA concentrations are only one-fifth to one-thirtieth of those of DHA in organs other than the brain and retina 36) (Fig. 1). The fact that DHA is present in large quantities in nerve tissue suggests that the physiological roles of EPA and DHA are not necessarily identical and that DHA may not influence the cardiovascular system.
In the EPA-treated subjects, the EPA levels in blood phospholipids rose rapidly, whereas those of DHA decreased slightly. In contrast, the increase in the blood phospholipid DHA levels in the DHA-treated subjects was small, occurring at a mod- erate rate as compared to the increase in EPA, and the EPA levels increased only moderately. Although the mechanisms have not been elucidated, EPA incorpora- tion into blood phospholipids indicates the priority of EPA in the circulatory pool, with DHA being taken up into the extracirculatory pool, implying that EPA and DHA undergo different processes of metabo- lism37) (Fig.2). In a similar 6-week study, 4 g/day of EPA-E (96% purity) or DHA-E (92% purity) was administered in patients with mild hypercholesterol- emia. The EPA-E increased the plasma phospholipid EPA levels and decreased the AA levels, while the DHA levels remained unchanged. In contrast, DHA-E increased the blood phospholipid DHA levels, while the AA levels decreased and the EPA levels slightly increased38) (Fig.3).
And this paragraph... Talks about how EPA us converted into DHA in our body but is seemingly restricted to maintain a specific DHA level in key organs that use DHA like the brain. Another words, you might not have to take supplemental DHA ever. It's says...
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The increase in the blood EPA levels following the DHA administration was considered to have been be due to reverse conversion from DHA. The reverse conversion rate in humans has been calculated to be 1.4%41). Dietary DHA and EPA have been found to downregulate the DPA to DHA conversion rate to 70%, leading to the expectation that EPA administration does not result in an increase in the DHA lev- els36). Given the autonomous functions of DHA in the brain, retina and sperm, restricted DPA to DHA conversion may play a very important role42). In artificially induced ?3-deficiency states, brain tissue membranes resist the decrease in the DHA levels43). ?3 deprivation reduces the blood DHA levels by 89% and the brain DHA levels by 37%44). EPA to DHA conversion may be restricted in order to maintain constant DHA levels for nervous system signaling45). Although the reason for this phenomenon is unknown, the following may be a potential cause.
DHA is abundant in nervous tissue, and the oxidized DHA metab- olite trans-4-hydroxy-2-hexenal (HHE) has been reported to exhibit neural toxicity. The concentration of HHE required for 50% cell death in primary cultures of cerebral cortical neurons is 23 µmol/L46). The extractable HHE level in the hippocampus/parahip- pocampal gyrus of normal control subjects is 11.3 pmol/mg protein47). This suggests that higher DHA levels than required result in nerve toxicity through metabolic oxidization in nerve tissue. If nonphysiological high doses of DHA are administered, the increase in the DHA levels is regulated to prevent high DHA levels in nerve tissue, which may result in saturation.
In summary, the blood EPA levels increase following EPA administration, whereas the DHA and AA levels remain unchanged or decrease. DHA administration results in a substantial increase in the blood DHA levels, with a slight increase in the EPA levels and decrease in the AA levels.
AI
