Objectives: This study tested whether mothers with maternal hypothyroidism have increased odds of CHD in their offspring, and examined the relationship between CHD, maternal thyroid function, and nausea and vomiting in pregnancy. Background: Maternal hypothyroidism increases the risk for foetal demise and prematurity and can have a negative impact on neurodevelopment. Prior studies have postulated a relationship between maternal thyroid function, CHD, and maternal nausea and vomiting in pregnancy. Methods: A cross-sectional case–control study was conducted over a 17-month period to obtain a history of maternal thyroid status and nausea and vomiting in pregnancy. Paediatric echocardiograms were evaluated for CHD by a blinded paediatric cardiologist. Logistic regression analysis was performed to examine the association between CHD and maternal hypothyroidism. Results: Of the 998 maternal–child pairs, 10% (98/998) of the mothers reported a history of prenatal hypothyroidism. The overall prevalence of CHD in the study sample was 63% (630/998). Mothers with a history of hypothyroidism were significantly more likely to have offspring with CHD compared with mothers without a history of hypothyroidism (72 versus 62%; p=0.04). The adjusted odds ratio (95% confidence interval) of CHD in offspring associated with reported maternal hypothyroidism was 1.68 (1.02–2.78). Conclusion: This study suggests that maternal hypothyroidism is a risk factor for the development of CHD. Further prospective investigations are necessary to confirm this association and delineate pathogenic mechanisms.

Nutrient insults in early pregnancy, such as nutrient deprivation during famines, are often associated with an unfavourable outcome. Suboptimal nutrition in the early stage of gestation has been linked to a number of adverse effects on fetal growth and development. Historically, nausea and vomiting in pregnancy (NVP) was an important contributor to pregnancy-related mortality; indeed, Charlotte Bronte died from starvation and dehydration after suffering very severe NVP 4 months into her first pregnancy (Gaskell, 1858). Although NVP seldom now progresses to be life-threatening, it affects the majority of pregnant women, and potentially presents a challenge to nutrient intake in the most vulnerable period of development. Symptoms range from mild (nausea only) to severe (a level of vomiting that restricts nutrient intake and ultimately threatens metabolic and electrolyte balance). Although NVP has been documented for thousands of years, its cause has not yet been satisfactorily elucidated, but seems to be related to endocrinological changes. Pregnant women also frequently report dietary cravings and aversions during pregnancy which can be linked to both the incidence and severity of NVP. Paradoxically, NVP appears to be positively associated with a favourable outcome of pregnancy, including increased birth weight and gestational age. The mechanisms by which NVP favours the outcome of pregnancy are not known. They may be related to women increasing their nutrient intake to alleviate symptoms, improving the quality of their diet or reducing energy expenditure. Alternatively, adaptation to a reduced nutrient intake might stimulate the expression of growth factors and affect placentation or metabolism, thus favouring fetal growth when NVP resolves.