|No it's not fish oil that's going to save your a** from dying of heart attack. It's vitamin A! 25,000IU/day for those who are already suffering from atherosclerotic lesions and heard disease could do the trick.|
In the atherosclerotic patients, the provision of extra vitamin A supplementation resulted in significant decrease in IL-17 gene expression (-47%) in fresh cell, 18% in PHA activated cells and 35% in ox-LDL activated cells (p<0.05 for all).
RORc gene expression (indicative of the progression of atherosclerosis) in fresh cells as well as ox-LDL activated cells decreased significantly after vitamin A supplementation in atherosclerotic patients (p=0.0001 for both).
|Figure 1: IL-17 & RORc levels in LDL- and PHA activated cells relative to baseline (Mottaghi. 2014)|
In vivo, it has been demonstrated that retinoic acid (RA) enhances TGF-β and Foxp3 expression and will thus decrease the differentiation of the rampant Th17 cells and downregulate their IL-17 production (Mucida. 2007) The exact underlying mechanism is not that important in this context, what is important though, is the fact that it worked in fresh cells (see above) and in phytohemagglutinin (PHA) activated cells, i.e. immune cells on a rampage that have been activated by the bean-lectin phytohemagglutinin (the reason you should never eat raw beans).
Apropos rampage, it's worth noticing that the provision of extra vitamin A led to a significant reduction in RORc gene activity and thus atherosclerotic potential in both, the already active, and activated Th-17 cells of the atherosclerotic subjects, and the PHA- and LDL-activated Th-17 cells of the healthy subjects - in conjunction with the increase in RORc in the placebo group (see Figure 1), this observation provides convincing evidence that vitamin A can also protect healthy individuals from developing atherosclerosis.
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- Mottaghi, Azadeh, et al. "Vitamin A supplementation reduces IL‐17 and RORc gene expression in atherosclerotic patients." Scandinavian Journal of Immunology (2014).
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