Background: Very little is known about how much choline is needed in pregnancy, but it is well documented that choline plays several important physiological roles—including in fetal cognitive development and regulation of inflammation. Despite little evidence regarding optimal intakes, it is of concern that most (> 90%) pregnant people consume less choline than is recommended and that the functional consequences of these low intakes for mother and offspring have not been well defined in human pregnancy. Knowing this, the aim of this dissertation was to assess the impact of varied maternal choline intake on maternal inflammation and adolescent offspring cognition. Methods: This work comprises three studies, two epidemiological and one long-term follow-up of an experimental feeding trial. In our epidemiological work, we analyzed data from Project Viva (697 participants, U.S.A.) and APrON (1251 participants, C.A.). We assessed maternal diet via Food Frequency Questionnaire (Viva) and 24-hour recall (APrON), and inflammatory markers via (Interleukin-6 (IL-6), Tumor Necrosis Factor-α, C-Reactive Protein (CRP) (Viva) or high sensitivity CRP (APrON) in maternal blood. We used regression models to assess relationships between choline intake and inflammatory markers, considering interactions with other methyl donor nutrients. In our long-term follow-up, we used Cambridge Cognition’s CANTAB to assess memory in the 21 14-year-old children of women who consumed 480 vs. 930 mg choline/d during their third trimester of pregnancy. Results: Project Viva data showed that higher choline intake in conjunction with higher methyl donor nutrient intake was associated with lower IL-6 (e.g. betaine, β interaction =-0.08, 95% CI = -0.14, -0.02). APrON data revealed that participants with higher choline intakes had reduced odds of elevated inflammation (hs-CRP >5 mg/L) compared to those with lower intakes (e.g. intake > 700 vs. 200 mg/d OR = 0.07, 95% CI 0.02-0.15). Lastly, experimental evidence from the long-term cognitive follow-up task revealed superior spatial memory in participants in the 930 mg/d group (vs the 480 mg/d group; p = 0.057), but no differences between groups on non-spatial memory tasks. Conclusions: These results provide novel evidence regarding the importance of prenatal choline intake for maternal inflammation and offspring cognition and highlight concerns about current low intakes. Future directions should include replication of these findings and exploration of the potential contribution of choline’s anti-inflammatory effects to the findings in adolescent cognition.