Friday, August 05, 2016 9:01:24 AM
After the morning sell off I put a stop in at $3.20 and was closed out. I was impressed with the buying. I'm watching for a new entry.
I'll be spending some time doing a real-time portfolio on my seeking alpha profile (under Steven Giardino). I realize no one does that. Everyone would rather tell you what they did after the fact and try to appear as good as possible. I don't need or want to do that. Tired of the phoniness.
The main point behind my AMRN short thesis only continues to gather support the more I research these omega 3 studies, including higher dose. I also think you guys have discounted the benefits of DHA too much. Vas having exactly 0% of that molecule. I've found numerous contradictions in AMRN's own papers, saying LDL-C probably doesn't matter and then in the next breath saying their Vas is better than other supps and scripts because they lose DHA, which raises LDL (somewhat--but not so much the type of LDL most associated with CVD -- though personally I think that's a symptom rather than a cause of CVD anyway).
AVII, I would liken your color charts and declarations of correlating higher EPA concentrations with things like "53% reduction in MACE" to the DCVax-Direct slides done by NWBO :). How about you add a note in there that says "btw, this 53% reduction was based on comparing 22 events with 10 events from a total population of over 18,000 subjects." Anyway I think your % for Vas are incorrect? I don't know, where did you get those %s? This shows the concentration by ug/mg:
http://www.fda.gov/downloads/AdvisoryCommittees/CommitteesMeetingMaterials/Drugs/EndocrinologicandMetabolicDrugsAdvisoryCommittee/UCM370985.pdf
And on that point (of NWBO), this reminds me much of so many cancer vaccine trials and theories behind them. "But look at the amazing HR in THIS subgroup! And this one! Let's do studies targeting *these* patients." Fail, fail, fail fail... Lots of brilliant researchers left scratching their heads. The problem is correlation does not imply causation. Even when it *really* looks like it does.
For example, you see demographic studies that show high fish eating pops that have low MI. You assume it's the EPA/DHA. Or especially the EPA. You're already far from the original correlation. Especially because you've completely dropped the DHA, but also because it was fish, not fish oil... But anyway, people often stop looking beyond that correlation and assume causation. But then there are things like:
And you can keep going from there. Lots of overlooked *other* correlations that probably *do* imply causation.
Japanese have low incidence of MI compared with western countries, though it's been steadily on the rise. Can you think of anything else besides fish consumption that may have lent itself to low MI rates in the past, and why that may be changing? How about obesity? Exercise habits? Overall dietary habits (% carbs, esp sugar, refined flour, vegetable consumption, etc). You just stop at fish and say that's why? I think a lifetime of fish consumption will help, but 2 - 6 years of fish oil--or rather, high dose EPA only, is a crap shoot. You really have nothing but some relatively very small subgroup data from the JELIS study to back up your hypothesis.
When I look at the whole picture, and even in the JELIS study see that patients with 4 risk factors, 1,220 patients per group, showed *no significant difference* in event rates (0.5% RRR and 0.1% ARR), I'm more than suspicious.
You can't hide with 1,612 events.
I would rather invest in IMUC.
More to write, but no time right now.
Jmo
GL
(will let you guys know when I re-short)
"Think for yourselves and let others enjoy the privilege to do so, too."
-Voltaire
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