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Background: Whereas the adverse effects of severe iodine deficiency during pregnancy are well documented, the effects of mild-to-moderate deficiency are not well established.Objectives: We aimed to explore whether iodine nutrition and timing of iodine supplement initiation are associated with thyroid function in pregnant and postpartum women.Methods: In this cohort study, 137 pregnant women were enrolled and followed up at gestational weeks (GWs) 18 and 36, and 3 and 6 mo postpartum. Thyroid function tests [thyroid-stimulating hormone (TSH), free triiodothyronine (fT3), and free thyroxine (fT4)], urinary iodine and creatinine concentration (UIC:Cr), and iodine intake (including iodine supplement use) were measured at each time point. The associations between thyroid hormone concentrations and UIC:Cr, iodine intakes, and iodine supplement use were estimated using multiple generalized estimating equation models.Results: The median UIC at GW18 was 94 μg/L, indicating mild-to-moderate iodine deficiency. UIC:Cr (β; 95% CI) per 100 μg/g was negatively associated with fT3 (-0.191; -0.331, -0.051) and fT4 (-0.756; -1.372, -0.141) concentrations. Iodine intake (β; 95% CI) per 100 μg/d was positively associated with TSH (0.099; 0.022, 0.177), and negatively associated with fT3 (-0.084; -0.0141, -0.027) and fT4 (-0.390; -0.599, -0.182) concentrations. Compared with no use of supplement, those initiating an iodine-containing supplement prepregnancy and continuing through pregnancy had lower TSH (estimated means) (1.35 compared with 1.68 mIU/L, P = 0.021), and higher fT3 (4.48 compared with 4.28 pmol/L, P = 0.035) and fT4 (15.2 compared with 14.4 pmol/L, P = 0.024) concentrations.Conclusions: Lower iodine availability during pregnancy and postpartum was associated with lower TSH, and higher fT3 and fT4 concentrations. The use of an iodine-containing supplement that was initiated prepregnancy and continuing through pregnancy was associated with lower TSH, and higher fT3 and fT4 concentrations, which may suggest improved thyroid function. These findings support the notion that optimization of iodine intake should start before pregnancy.This trial was registered at clinicaltrials.gov as NCT02610959. [ABSTRACT FROM AUTHOR]

Background: Maternal seafood intake during pregnancy is associated with child neurodevelopment. No randomized controlled trials (RCTs) have examined the effect of maternal lean fish consumption during pregnancy on child neurodevelopment.Objectives: The objective of the study was to examine the effect of increased maternal cod intake during pregnancy on infant general and socio-emotional development in the first year of life, and whether any effects observed were mediated by maternal iodine status.Methods: In an RCT, 133 pregnant women (≤19 weeks of gestation) were randomly assigned to receive 200 g cod fillet twice weekly (intervention) or to continue with their habitual diet (control) for 16 wk. The mothers completed the developmental screening questionnaires Ages and Stages Questionnaire, 2nd edition (ASQ-2) and Ages and Stages Questionnaire: Social-Emotional (ASQ:SE) when the infants were 3, 6, and 11 mo old. We compared scores between groups using linear mixed-effects models and examined whether iodine status postintervention mediated the effect on child development.Results: We found no difference between infants in the intervention and control groups on total ASQ-2 scores (P = 0.633), but a difference on the ASQ:SE scores in favor of the intervention group (20.9 and 20.5 in the intervention group and 26.1 and 26.8 in the control group for 3 and 6 mo, respectively; P = 0.020). There was no difference in change of the scores between the groups over time (P = 0.946). The effect of group on the total ASQ:SE scores was not mediated via maternal urinary iodine concentration postintervention (β = -1.03, SE = 0.68, P = 0.126).Conclusions: Our results provide no evidence for an effect of increased cod intake during pregnancy on general child development in the first year of life, but there was a positive effect on socio-emotional problems. More studies are needed to define the role of fish consumption during pregnancy and the effects on child neurodevelopment.This trial was registered at clinicaltrials.gov as NCT02610959. [ABSTRACT FROM AUTHOR]

Background: Data from recent meta-analyses question an association between dietary intake of saturated fatty acids (SFAs) and risk of cardiovascular disease (CVD). Moreover, the prognostic effect of dietary SFA in patients with established CVD treated with modern conventional medication has not been extensively studied. Objective: We investigated the associations between self-reported dietary SFA intake and risk of subsequent coronary events and mortality in patients with coronary artery disease (CAD). Methods: This study included patients who participated in the Western Norway B-Vitamin Intervention Trial and completed a 169-item semiquantitative food-frequency questionnaire after coronary angiography. Quartiles of estimated daily intakes of SFA were related to risk of a primary composite endpoint of coronary events (unstable angina pectoris, nonfatal acute myocardial infarction, and coronary death) and separate secondary endpoints (total acute myocardial infarction, fatal coronary events, and all-cause death) with use of Cox-regression analyses. Results: This study included 2412 patients (81% men, mean age: 61.7 y). After a median follow-up of 4.8 y, a total of 292 (12%) patients experienced at least one major coronary event during follow-up. High intake of SFAs was associated with a number of risk factors at baseline. However, there were no significant associations between SFA intake and risk of coronary events [age- and sex-adjusted HR (95% CI) was 0.85 (0.61, 1.18) for the upper vs. lower SFA quartile] or any secondary endpoint. Estimates were not appreciably changed after multivariate adjustments. Conclusions: There was no association between dietary intake of SFAs and incident coronary events or mortality in patients with established CAD. [ABSTRACT FROM AUTHOR]

Background: Vitamin B12 and folate are essential micronutrients important for normal infant growth and development., Objectives: The aims were to describe vitamin B12 and folate status in pregnant females and their infants according to commonly used status cutoffs and examine the associations between maternal status, maternal supplement use, and breastfeeding and infant status., Methods: Pregnant females were recruited at 18 wk gestation in Bergen, Norway. Maternal vitamin B12 and folate status were measured at gestational weeks 18 (n = 136) and 36 (n = 116), and infant status was measured at ages 3 (n = 73) and 6 (n = 74) mo., Results: At gestational weeks 18 and 36, respectively, 4.4% and 2.6% of the mothers had plasma cobalamin concentrations <148 pmol/L, 0.7% and 6.9% had methylmalonic acid (MMA) concentrations >0.26 μmol/L, and 3.7% and 30% had folate concentrations <10 nmol/L. None of the females had total homocysteine (t-Hcy) concentrations >13 μmol/L or 3 combined indicator of vitamin B12 (cB12) < -0.5. At 3 and 6 mo, respectively, 4.1% and 5.4% of the infants had cobalamin concentrations <148 pmol/L, 63% and 74% had t-Hcy concentrations >6.5 μmol/L, 59% and 66% had MMA concentrations >0.26 μmol/L, and 47% and 60% had cB12 > -0.5. None of the infants had folate concentrations <10 nmol/L. Several of the vitamin B12 biomarkers in infants were associated with maternal vitamin B12 status during pregnancy. Breastfed infants had lower vitamin B12 status (as indicated by plasma cobalamin, t-Hcy, and cB12) than nonbreastfed infants at both 3 and 6 mo. Use of supplements during pregnancy was associated with better vitamin B12 status among infants at 3 and 6 mo, as indicated by infants' cobalamin and t-Hcy concentrations., Conclusions: Subclinical vitamin B12 deficiency among infants was common and associated with maternal vitamin B12 status during pregnancy and breastfeeding. Among the mothers, an increase in biochemical folate deficiency was discovered toward the end of gestation. Further studies are needed to investigate clinical consequences. This trial was registered at clinicaltrials.gov as NCT02610959., (Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.)