Breastfeeding practice in mothers with eating disorders

The purpose of this study was to compare the prevalence of breastfeeding in women with anorexia nervosa, bulimia nervosa, binge eating disorder and eating disorders not otherwise specified - purging subtype, with mothers with no eating disorders during the first 6 months after birth. The study is based on the Norwegian Mother and Child Cohort Study conducted at the Norwegian Institute of Public Health. Questionnaire-based information on eating disorder diagnoses and breastfeeding in 39 355 women was used to estimate the risk of cessation of breastfeeding with Cox proportional hazards regression. Almost all women (98%) initially breastfeed their infants, with no statistically significant difference between the eating disorders subgroups and women with no eating disorders. However, the risk of early cessation before 6 months post-partum increased for all subgroups of mothers with eating disorders, compared with mothers with no eating disorders. After adjusting for maternal body mass index, age, education, birthweight and pre-term birth, only mothers with anorexia nervosa [hazard ratios (HR), 2.35; 95% confidence interval (CI) 1.22-4.53] and eating disorder not otherwise specified-purging subtype (HR, 1.95; 95% CI 1.08-3.53) had increased risk for cessation of breastfeeding There were no differences in the risk of cessation of exclusive breastfeeding. These results show that some eating disorders may influence mothers' early feeding practices and indicate that additional support may be necessary to assist women with anorexia nervosa in maintaining breastfeeding

Gestational thyroid hormone concentrations and risk of attention-deficit hyperactivity disorder in the Norwegian Mother, Father and Child Cohort Study

Background: Maternal thyroid function plays an important role in foetal brain development; however, little consensus exists regarding the relationship between normal variability in thyroid hormones and common neurodevelopmental disorders, such as attention-deficit hyperactivity disorder (ADHD). Objective: We sought to examine the association between mid-pregnancy maternal thyroid function and risk of clinically diagnosed ADHD in offspring. Methods: We conducted a nested case–control study in the Norwegian Mother, Father and Child Cohort Study. Among children born 2003 or later, we randomly sampled singleton ADHD cases obtained through linkage with the Norwegian Patient Registry (n = 298) and 554 controls. Concentrations of maternal triiodothyronine (T3), thyroxine (T4), T3-Uptake, thyroid-stimulating hormone (TSH) and thyroid peroxidase antibody (TPO-Ab) were measured in maternal plasma, collected at approximately 17 weeks' gestation. Indices of free T4 (FT4i) and free T3 (FT3i) were calculated. We used multivariable adjusted logistic regression to calculate odds ratios and accounted for missing covariate data using multiple imputation. We used restricted cubic splines to assess non-linear trends and provide flexible representations. We examined effect measure modification by dietary iodine and selenium intake. In sensitivity analyses, we excluded women with clinically significant thyroid disorders (n = 73). Results: High maternal T3 was associated with increased risk of ADHD (5th vs 1st quintile odds ratio 2.27, 95% confidence interval 1.21, 4.26). For FT4i, both the lowest and highest quintiles were associated with an approximate 1.6-fold increase in risk of ADHD, with similar trends found for T4. The FT4i association was modified by dietary iodine intake such that the highest risk strata were confined to the low intake group. Conclusions: Both high and low concentrations of maternal thyroid hormones, although within population reference ranges, increase the risk of ADHD in offspring. Increased susceptibility may be found among women with low dietary intake of iodine and selenium

Iodine Intake is Associated with Thyroid Function in Mild to Moderately Iodine Deficient Pregnant Women

Background: Studies indicate that mild to moderate iodine deficiency in pregnancy may have a long-term negative impact on child neurodevelopment. These effects are likely mediated via changes in maternal thyroid function, since iodine is essential for the production of thyroid hormones. However, the impact of iodine availability on thyroid function during pregnancy and on thyroid function reference ranges are understudied. The aim of this study was to investigate the association between iodine intake and thyroid function during pregnancy. Design: In a population-based pregnancy cohort including 2910 pregnant women participating in The Norwegian Mother and Child Cohort Study, we explored cross sectional associations of maternal iodine intake measured (1) by a food frequency questionnaire and (2) as iodine concentration in a spot urine sample, with plasma thyroid hormones and antibodies. Results: Biological samples were collected in mean gestational week 18.5 (standard deviation 1.3) and diet was assessed in gestational week 22. Median iodine intake from food was 121 μg/day (interquartile range 90, 160), and 40% reported use of iodine-containing supplements in pregnancy. Median urinary iodine concentration (UIC) was 59 μg/L among those who did not use supplements and 98 μg/L in the women reporting current use at the time of sampling, indicating mild to moderate iodine deficiency in both groups. Iodine intake as measured by the food frequency questionnaire was not associated with the outcome measures, while UIC was inversely associated with FT3 (p = 0.002) and FT4 (p < 0.001). Introduction of an iodine-containing supplement after gestational week 12 was associated with indications of lower thyroid hormone production (lower FT4, p = 0.027, and nonsignificantly lower FT3, p = 0.17). The 2.5th and 97.5th percentiles of TSH, FT4, and FT3 were not significantly different by groups defined by calculated iodine intake or by UIC. Conclusion: The results indicate that mild to moderate iodine deficiency affect thyroid function in pregnancy. However, the differences were small, suggesting that normal reference ranges can be determined based on data also from mildly iodine deficient populations, but this needs to be further studied. Introducing an iodine-containing supplement might temporarily inhibit thyroid hormone production and/or release

Exploration of different methods to assess dietary acrylamide exposure in pregnant women participating in the Norwegian Mother and Child Cohort Study (MoBa)

We assessed dietary exposure to acrylamide in 119 pregnant Norwegian women. The aim of the study was to explore three different methods for estimation of long-term intake of acrylamide and whether it is possible by a food frequency questionnaire (FFQ) to identify pregnant women with high exposure to acrylamide. Acrylamide excreted as mercapturic acid metabolites in 24-h urine was used as an evaluation tool. Food consumption was assessed by an FFQ and by a 4-day weighed food diary (FD). Acrylamide intake was also estimated by a probabilistic approach based on 2 days from the FD. Primarily, acrylamide concentrations reported from analyses of Norwegian foods were used. The dietary exposure to acrylamide estimated as ¿g/kg bw/day (median and 95 percentile) was 0.48 (0.92) by the FFQ, 0.41 (0.82) by the FD and 0.42 (0.70) by the probabilistic approach. The amount of acrylamide excreted as urinary metabolites (median and 95 percentile) was 0.16 ¿g/kg bw/24-h (0.50) in non-smokers, corresponding to a dietary exposure of approximately 0.30 ¿g/kg bw/day (0.91). Linear regression of acrylamide excreted as urinary metabolites identified crisp bread and potato crisps as significant independent predictors, along with cooking oil and onion/garlic. Dietary exposure to acrylamide calculated by FFQ, FD and probabilistic modelling were comparable. The comparison of FFQ acrylamide estimates with levels of urinary acrylamide metabolites showed that the MoBa FFQ was able to identify participants with high dietary acrylamide exposure. Our findings facilitate future studies on acrylamide exposure and health outcomes in the MoBa stud