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Re: debate
 
Hveragerthi Views: 2,316
Published: 14 y
 
This is a reply to # 1,681,775

Re: debate


 Here is my friends counter to your post.

Re: This is why the body synthesizes what it needs from linoleic acid. But too much arachidonic acid clearly promotes inflammation, which among other things can lead to conditions such as heart disease.

I seriously doubt it. China Study showed that if consumption of arachidonic acid were significantly contributing to heart disease then the trend line for all vascular disease on the bottom graph here wouldn't have had a downwards slope! Raw correlation between ischaemic heart disease mortality age 35-69 (tag M063) and dietary animal fat consumption (tag D053) is also strongly negative: -32%, that is statistically significant (marked by * in the doc).

The original document with these correlations can be downloaded from Oxford web site , see page 223. You may notice the same downwards trends if you look at the rheumatoid arthritis (tag M061), and other inflammatory disease statistics. More animal protein or more animal fat equals less disease in China (except for milk!). More plant food especially wheat = more disease! The trend is very clear-cut and hard to miss.

A few studies in relation to arachidonic acid (AA) and heart health:

http://www.ncbi.nlm.nih.gov/pubmed/20435853

"We therefore conclude that arrhythmias following ischemia-reperfusion injury might originate from mitochondrial depolarization mediated by LOX and AA."


http://www.ncbi.nlm.nih.gov/pubmed/20150962

"Atherosclerosis represents an important chronic inflammatory process associated with several pathophysiological reactions in the vascular wall. The arachidonic acid, released by phospholipase A2, is an important substrate for the production of a group of lipid mediators known as leukotrienes, which induce proinflammatory signaling through the activation of specific BLT and CysLT receptors. The interaction of these substances in the vascular wall determines important morphological alterations like the early lipid retention and the accumulation of foam cells, the development of intimal hyperplasia, and advanced atherosclerotic lesions, and it plays an important role in the rupture of atherosclerotic plaque. Many studies regarding myocardial ischemia and reperfusion show that leukotriene signaling may be involved in the development of ischemic injury. For these, reasons both leukotriene synthesis inhibitors and leukotriene receptor antagonists have been suggested for inducing beneficial effects at different stages of the atherosclerosis process and may represent a new therapeutic target in the treatment of atherosclerotic vessel diseases, in particular in acute coronary syndrome."


http://www.nejm.org/doi/pdf/10.1056/NEJMoa025079

"Variant 5-lipoxygenase genotypes identify a subpopulation with increased atherosclerosis.

The observed diet–gene interactions further suggest that dietary n¡6 polyunsaturated

fatty acids promote, whereas marine n¡3 fatty acids inhibit, leukotriene-mediated

inflammation that leads to atherosclerosis in this subpopulation."

 

 

 

 
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