Skip to main content
. 2022 Jul 22;13:855265. doi: 10.3389/fpsyt.2022.855265

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.

a

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.