Friday, February 12, 2016

Proinflammatory HDL Results from Oxidized Lipid [Linoleic Acid] Mediators...

 " the pathogenesis of both idiopathic and associated types of pulmonary arterial hypertension [PAH]"

The funny thing about search engines is that once you find to the correct terms to look for, you start learning things very quickly.
"...In this study, we have demonstrated a “pathologic HDL phenotype” in subjects with PAH. This observation may reasonably be expected in our subjects with APAH as related to connective-tissue diseases; however, a similar magnitude of HDL dysfunction was noted in the IPAH cohort. This effect was further compounded by a significant increase in the normal proinflammatory influence of LDL in both PAH cohorts, as reflected by the increased LII [LDL Inflammatory Index] values. A 25–50-fold increase in plasma levels of oxidation products of both arachidonic acid [AA] (HETEs) and linoleic acid [LA] (HODEs) therein suggested a significant increase in “oxidant stress” contributing to the proinflammatory HDL dysfunction in PAH..."
So high blood pressure results from having high levels of the oxidative by-products of omega-6 fats. Oxidized LDL, also discussed in this study, is one of the primary signs of atherosclerosis, which causes much heart disease.  The oxidized fat in oxidized LDL, is, not surprisingly, LA.

Well, we know what causes that massive increase in oxidative products of LA and AA.

I wonder if it's as easy to fix here as it is with fatty liver?

It's certainly worth a shot...

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