Subgroup analysis revealed that increasing dietary ALA tends to elevate CRP concentration  in healthy subjects .
However , the null effect of ALA supplementation on other inflammatory markers was not changed in various subgroups , indicating that the results are stable .
Meta-regression results revealed a negative relationship between the effect size on CRP and its baseline concentration .
No significant publication bias was observed for all inflammatory markers as suggested by funnel plot and Begg ’s test .
Conclusion Our meta- analysis did not find any beneficial effect of ALA supplementation  on reducing inflammatory markers including TNF , IL-6 , CRP , sICAM-1 , and sVCAM-1 .
However , in healthy subjects  , ALA supplementation might increase CRP concentration
Purpose The aim of the current meta- analysis was to investigate the effect of increasing dietary ALA intake on the blood concentration of inflammatory markers including tumor necrosis factor ( TNF ) , interleukin 6 ( IL-6 ) , C-reactive protein ( CRP ) , soluble intercellular adhesion molecule-1 ( sICAM-1 ) , and soluble vascular cell adhesion molecule-1 ( sVCAM-1 )  in adults .
Inflammation markers predict zinc transporter gene expression in women with type 2 diabetes mellitus.
The pathology of type 2 diabetes mellitus ( DM ) often is associated with underlying states of conditioned zinc deficiency and chronic inflammation . Zinc and omega-3 polyunsaturated fatty acids each exhibit anti-inflammatory effects and may be of therapeutic benefit in the disease . The present r and omized , double-blind , placebo-controlled , 12-week trial was design ed to investigate the effects of zinc ( 40 mg/day ) and α-linolenic acid ( ALA ; 2 g/day flaxseed oil ) supplementation on markers of inflammation [ interleukin (IL)-1β , IL-6 , tumor necrosis factor (TNF)-α , C-reactive protein ( CRP ) ] and zinc transporter and metallothionein gene expression in 48 postmenopausal women with type 2 DM . No significant effects of  zinc or ALA supplementation were observed on inflammatory marker concentrations or fold change in zinc transporter and metallothionein gene expression . Significant increases in plasma zinc concentrations were observed over time in the groups supplemented with zinc alone or combined with ALA ( P=.007 and P=.009 , respectively ) . An impact of zinc treatment on zinc transporter gene expression was found ; ZnT5 was positively correlated with Zip3 mRNA ( P<.001 ) only in participants receiving zinc , while zinc supplementation abolished the relationship between ZnT5 and Zip10 . IL-6 predicted the expression levels and CRP predicted the fold change of the ZnT5 , ZnT7 , Zip1 , Zip7 and Zip10 mRNA cluster ( P<.001 and P=.031 , respectively ) . Fold change in the expression of metallothionein mRNA was predicted by TNF-α ( P=.022 ) . Associations among inflammatory cytokines and zinc transporter and metallothionein gene expression support an interrelationship between zinc homeostasis and inflammation in type 2 DM
Subgroup analysis revealed that increasing dietary ALA tends to elevate CRP concentration  in healthy subjects .
However , the null effect of ALA supplementation on other inflammatory markers was not changed in various subgroups , indicating that the results are stable .
Meta-regression results revealed a negative relationship between the effect size on CRP and its baseline concentration .
No significant publication bias was observed for all inflammatory markers as suggested by funnel plot and Begg ’s test .
Conclusion Our meta- analysis did not find any beneficial effect of ALA supplementation  on reducing inflammatory markers including TNF , IL-6 , CRP , sICAM-1 , and sVCAM-1 .
However , in healthy subjects  , ALA supplementation might increase CRP concentration
Purpose The aim of the current meta- analysis was to investigate the effect of increasing dietary ALA intake on the blood concentration of inflammatory markers including tumor necrosis factor ( TNF ) , interleukin 6 ( IL-6 ) , C-reactive protein ( CRP ) , soluble intercellular adhesion molecule-1 ( sICAM-1 ) , and soluble vascular cell adhesion molecule-1 ( sVCAM-1 )  in adults .