Table 4.
Results from regression models relating omega-6:omega3 metrics and pro-inflammatory cytokines (N = 68).
TNF-α | IL-6 | |||
---|---|---|---|---|
β (SE) | p | β (SE) | p | |
Models Considering ΣOmega-6:ΣOmega-3 | ||||
Model 1: Without Covariates | ||||
Omega-6:omega-3 | 0.03 (0.02) | 0.21 | 0.11 (0.12) | 0.39 |
Model 2: With Covariates | ||||
Omega-6:omega-3 | 0.10 (0.12) | 0.39 | 0.01 (0.10) | 0.94 |
Fatty acid supplement statusa | −0.09 (0.14) | 0.51 | 0.02 (0.14) | 0.91 |
Pre-pregnancy BMI | 0.44 (0.11) | <0.001 | 0.46 (0.13) | <0.001 |
Models Considering AA:EPA | ||||
Model 3: Without Covariates | ||||
AA:EPA | 0.43 (0.12) | 0.001 | 0.32 (0.11) | 0.004 |
Model 4: With Covariates | ||||
AA:EPA | 0.22 (0.16) | 0.16 | 0.08 (0.14) | 0.58 |
Fatty acid supplement statusa | 0.01 (0.15) | 0.94 | −0.01 (0.17) | 0.99 |
Pre-pregnancy BMI | 0.37 (0.12) | 0.002 | 0.40 (0.12) | 0.001 |
AA, Arachidonic Acid; EPA, Eicosapentaenoic Acid; TNF-α, Tumor Necrosis Factor-alpha; IL-6, Interleukin-6.
0 = not taking a fish oil or fatty acid supplement, 1 = taking a fish oil or fatty acid supplement. BMI, body mass index. Results of these regression models suggest that while the ratio of AA-to-EPA was associated with greater TNF-α and IL-6 in models that did not considered covariates, these associations were no longer significant after controlling for pre-pregnancy BMI and whether the individual was taking a fatty acid supplement.