Quote:
Originally Posted by hackskii  Snip......
Arachidonic Acid: How it Creates Disease
However, the natural and more likely chemical conversion of dietary LA will go on to be converted into Arachidonic acid, a 20 carbon long chain fatty acid that is also found in animal products, specifically red meat, dairy and eggs. Arachidonic acid (AA) will lead to PG2 series of chemical mediators, which are pro-inflammatory, contribute to platelet aggregation and increased constriction of the vessels. The platelet aggregation and vessels changes if also coupled with a poor diet- which would favour low nutrients and high blood lipids- can contribute to an increased CVD risk. AA can also create thromboxanes of the 2 series, specifically thromboxane A2 (TXA2) which is a more potent vasoconstrictor and promotes platelet aggregation. In addition, eicosanoid metabolites from AA such as prostaglandin E2 (PGE2), leukotriene B4, 12-hydroxyeicosatetraenoic acid and TXA2 have all been positively linked to carcinogenesis. |
This appears to be the only attempt at providing some medical reference. Again, it fails to be in a study where they actually gave AA to a human. My counter for it is a simple supplementation study where they gave 1,500mg of AA daily for 50 days to human subjects. For the record, this is officially the 4th time you have ignored this information and tried to present it as fact yet again.
The effect of dietary arachidonic acid on platelet function, platelet fatty acid composition, and blood coagulation in humans.
Nelson GJ, Schmidt PC, Bartolini G, Kelley DS, Kyle D.
Western Human Nutrition Research Center, ARS, USDA, San Francisco, California 94129, USA.
Arachidonic acid (AA) is the precursor of thromboxane and prostacyclin, two of the most active compounds related to platelet function. The effect of dietary AA on platelet function in humans is not understood although a previous study suggested dietary AA might have adverse physiological consequences on platelet function. Here normal healthy male volunteers (n = 10) were fed diets containing 1.7 g/d of AA for 50 d. The control diet contained 210 mg/d of AA. Platelet aggregation in the platelet-rich plasma was determined using ADP, collagen, and AA. No statistical differences could be detected between the aggregation before and after consuming the high-AA diet. The prothrombin time, partial thromboplastin time, and the antithrombin III levels in the subjects were determined also. There were no statistically significant differences in these three parameters when the values were compared before and after they consumed the high-AA diet. The in vivo bleeding times also did not show a significant difference before and after the subjects consumed the high-AA diet. Platelets exhibited only small changes in their AA content during the AA feeding period.
The results from this study on blood clotting parameters and in vitro platelet aggregation suggest that adding 1.5 g/d of dietary AA for 50 d to a typical Western diet containing about 200 mg of AA produces no observable physiological changes in blood coagulation and thrombotic tendencies in healthy, adult males compared to the unsupplemented diet. Thus, moderate intakes of foods high in AA have few effects on blood coagulation, platelet function, or platelet fatty acid composition.