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 .
Dietary alpha-linolenic acid decreases C-reactive protein, serum amyloid A and interleukin-6 in dyslipidaemic patients.
BACKGROUND Inflammation plays an important role in the pathogenesis of coronary artery disease . We examined whether dietary supplementation with alpha-linolenic acid ( ALA , 18:3n-3 ) affects the levels of inflammatory markers in dyslipidaemic patients . METHODS We recruited 76 male dyslipidaemic patients ( mean age=51+/-8 years ) following a typical Greek diet . They were r and omly assigned either to 15 ml of linseed oil ( rich in ALA ) per day ( n=50 ) or to 15 ml of safflower oil ( rich in linoleic acid ( LA , 18:2n-6 ) ) per day ( n=26 ) . The ratio of n-6:n-3 in linseed oil supplemented group was 1.3:1 and in safflower oil supplemented group 13.2:1 . Dietary intervention lasted for 3 months . Blood lipids and C-reactive protein ( CRP ) , serum amyloid A ( SAA ) , and interleukin-6 ( IL-6 ) levels were determined prior and after intervention . CRP and SAA were measured by nephelometry and IL-6 by immunoassay . RESULTS Dietary supplementation with ALA decreased significantly CRP , SAA and IL-6 levels . The median decrease of CRP was 38 % ( 1.24 vs. 0.93 mg/l , P=0.0008 ) , of SAA 23.1 % ( 3.24 vs. 2.39 mg/l , P=0.0001 ) and of IL-6 10.5 % ( 2.18 vs. 1.7 pg/ml , P=0.01 ) . The decrease of inflammatory markers was independent of lipid changes . Dietary supplementation with LA did not affect significantly CRP , SAA and IL-6 concentrations but decreased cholesterol levels . CONCLUSIONS Dietary supplementation with ALA for 3 months decreases significantly CRP , SAA and IL-6 levels  in dyslipidaemic patients . This anti-inflammatory effect may provide a possible additional mechanism for the beneficial effect of plant n-3 polyunsaturated fatty acids in primary and secondary prevention of coronary artery disease
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 .