Larrydip (observing your convention):
They measured serum levels, which may not mean much of anything, at least in the stroke context.
Also it is not clear what the people actually ate: "Serum linoleic acid and n3 polyunsaturated fatty
acids reflect diet, whereas serum saturated fatty acid and monounsaturated fatty acid do not because
of metabolic conversion of other fatty acids that obscures the relationship of these fatty acids in
the serum and diet."
The worst is that they say things that are patently false: "Finally, linoleic acid also reduces
platelet aggregation..." Omega 6s convert to arachidonic acid, and that is a major factor in
platelet aggregation. For example: "Platelet aggregation was induced by collagen
(1. µg/ml) or arachidonic acid (1 mM). These agonists were added to the cuvettes 3 min after
addition of SNC or SNP." Go to elsevier.nlindex.httOpen ↗ for this study.
There are plenty more like it. It seems that in some people, the omega 6s are kept in the serum
more than in other people. In those other people, the linoleic omega 6 get metabolized to
arachidonic acid, then risk of stroke increases. The idiots who did this study are real losers
Larry, so I guess you feel quite comfortable in their company.
And of course, the usual qualifications:
"The present study has certain limitations. First, dehydration of polyunsaturated fatty acids during
preservation at -80°C may be a potential problem. Subsample analysis, however, demonstrated that
there were no material changes in serum n3 or n6 polyunsaturated fatty acid composition between the
1990 and 1998 values. Furthermore, mean values of fatty acids were similar to those reported in our
previous studies in which the serum samples were preserved at -80°C for only 3 months until
analysis.17,25 Second, the serum samples were nonfasting, and the time of blood collection may
affect fatty acid composition. However, subsample analysis revealed no significant difference in
serum fatty acid composition between fasting and nonfasting samples. Third, the generalizability of
the present data to Western countries is unknown. The proportion of stroke subtypes in the present
study was 38% for hemorrhagic strokes, 48% for lacunar infarctions, 10% for large-artery occlusive
infarctions, and 4% for embolic infarctions, which were similar to previous reports among Japanese,
whereas those in Western countries were 15% to 20%, 15% to 25%, 50% to 60%, and 10%, respectively.31
Because ischemic stroke was mostly lacunar infarction among Japanese and large-artery occlusive
infarction among whites, the present study implies the importance of linoleic acid in the prevention
of lacunar stroke. A potential effect on large-artery occlusive infarction was uncertain because of
the limited number of cases.
In conclusion, our observational study suggests that serum linoleic acid may protect against
ischemic stroke and lacunar infarction, possibly because of lowering of blood pressure levels and
improvement in small-vessel circulation via reduced platelet aggregation and enhanced erythrocyte
deformability. This finding implies the potential importance of dietary intake of linoleic acid for
the prevention of ischemic stroke. A clinical trial is necessary to confirm the causality between
linoleic acid intake and risk of ischemic stroke."
I wouldn't trust these guys to give the birds in my back yard nutritional advice.
These kinds of studies demonstrate how screwed up things are in the "dietary science" field today,
not much more.
Larry (no nothing) Hoover posted:
"This study compares actual body composition data....not dietary measures, but fatty acid
composition of stroke victims and controls. The type of stroke is very clearly defined.....and the
only significant relationships in hemorrhagic stroke and fatty acids are in monounsaturated and omega-
6 classes. Look at table 2 (cause I know you have trouble reading):
stroke.ahajournals.org2086Open ↗
e87567a16d6f2a7906f6f43eeda"