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jessellivermore

03/31/20 11:24 AM

#258861 RE: smarterer #258764

smarter..

I don't have all the answers to your very good questions...Amarin's lawyers here from Covington..top litigation firm in the USA..The fact this Federal judge failed to listen to their arguments make me very suspicious that she had a hidden agenda..

Her decision is so patently convoluted and wrong that there are only a number of possibility..She was on drugs...She was being paid off...she is not intelligent enough to be making decisions that result in wins and losses in the billions..and she has no right being the judge in this case.
To reverse the PTO opinion on the obviousness of the 889 trig and LDL patent issue she would need clear and convincing evidence the PTO made an error...

What is the error I do not believe the PTO used "Mori" a trial reported in an Australian nutritional journal...Not peer reviewed or probably even known about by most members of the medical profession. Mori is vague involving 59 mildly obese males ages about 49yo and morbidities not clear...The 59 were divided into three groups so that only 19 0f the enrollees were on EPA..Nineteen more on DHA and the rest on olive oil. The stated purpose of the study was to determine if EPA and DHA had different effects on blood lipids..The trial ran for six weeks..Results: Fifty-six men aged 48.8 ± 1.1 y completed the study. Relative to those in the olive oil group, triacylglycerols fell by 0.45 ± 0.15 mmol/L (˜20%; P = 0.003)( aside the measuring of trigs in clinical medicine is trig levels in Mg/DL) so this study is little confusing) in the DHA group and by 0.37 ± 0.14 mmol/L (˜18%; P = 0.012) in the EPA group (both EPA and DHA lowered trigs DHA slightly more than EPA). Neither EPA nor DHA had any effect on total cholesterol. LDL, HDL, and HDL2 cholesterol were not affected significantly by EPA, but HDL3 cholesterol decreased significantly (6.7%; P = 0.032)( this is important because the author does not emphasize that EPA would be expected to raise LDL and the author completely overlooks this) and does not ignore EPA the fact EPA did lower HDL3 which would likely increase CVD event risk according to thinking in 2000 . Although HDL cholesterol was not significantly increased by DHA (3.1%), HDL2 cholesterol increased by ˜29% (P = 0.004).(again the author notes that DHA increased LDL cholesterol by 8% (P = 0.019).because it was thought at that time that HDL-was good cholesterol and that would be a positive for DHA. Adjusted LDL particle size increased by 0.25 ± 0.08 nm (P = 0.002) with DHA but not with EPA. In this case larger ldl particle sizes is known to decrease CVD event risk. EPA supplementation increased plasma and platelet phospholipid EPA but reduced DHA. DHA supplementation increased DHA and EPA in plasma and platelet phospholipids. Both EPA and DHA increased fasting insulin significantly. EPA, but not DHA, tended to increase fasting glucose, but not significantly so.

Conclusions: EPA and DHA had differential effects on lipids, fatty acids, and glucose metabolism in overweight men with mild hyperlipidemia

It is clear from this article the author summing up would have concluded that DHA and not EPA would obviously have cut the risk of CVD events more than EPA would.

":>) JL