After 10 weeks of Se supplementation, a higher percentage of women in the Se group had pulsatility index (PI) of <1.45) () than of those in the placebo group. However, no comparison was made of the birth weight of babies in both groups.
The mean Edinburgh Postnatal Depression Scale (EPDS) score in the selenium supplemented group was significantly lower than the control group (8.8 + 5.1 vs. 10.7 + 4.4, )
Se supplementation, compared with placebo, resulted in a significant reduction in fasting plasma glucose, serum insulin levels, and homeostasis model of assessment- (HOMA-) insulin resistance and a significant increase in quantitative insulin sensitivity check index
Se supplementation downregulated gene expression of tumour necrosis factor alpha (TNF-α) and transforming growth factor beta (TGF-β) and upregulated gene expression of VEGF in lymphocytes of patients with GDM
Se supplementation did not cause any significant difference in the adiponectin level (which is inversely related to insulin resistance) from 12 to 35 weeks of gestation ()
Se supplementation resulted in upregulation of peroxisome proliferator-activated receptor-γ () and glucose transporter 1 () in lymphocytes of patients with GDM.
Se supplementation increased breastmilk Se concentration (), did not change breastmilk glutathione peroxidase activity, significantly increased the concentration of polyunsaturated fatty acids (), mainly linoleic acid (), and decreased the concentration of saturated fatty acids in breast milk ()
The proportion of women with detectable HIV-1 RNA in breast milk increased in Se supplemented (36.4%) than placebo (27.5%) group. The effect was more in primiparas.
Se supplementation significantly lowered risk of preterm delivery (relative risk (RR) 0.32, 95% confidence interval (CI) 0.11–0.96) compared to placebo. Se supplementation caused no effect on HIV-disease progression in pregnant women.
Se supplementation lowered TPO Ab titres during the postpartum period compared to controls (323.2 ± 44 vs. 621.1 ± 80 kIU/litre) (). Postpartum thyroid dysfunction and permanent hypothyroidism were significantly lower in selenium supplemented population compared with controls (28.6 vs. 48.6%, ; and 11.7 vs. 20.3%, ).
From 36 weeks’ gestation to 6 months’ postpartum, Se supplementation decreased Tg Ab [19.86 (11.59–52.60) IU/ml; ] in a thyroiditis positive population but it increased in the control group (151.03 ± 182.9 IU/ml; ). TPO Ab also decreased on Se supplementation (255.00 (79.00–292.00) IU/ml; ) but increased in the control group (441.28 ± 512.18 IU/ml; ) during the same period.
Low-dose Se supplementation in pregnant women with mild-to-moderate deficiency had no effect on TPO Ab concentration from 12 to 35 weeks of gestation but tended to change thyroid function in TPO Ab + ve women in late gestation (35 weeks): reduced TSH (2.10 (1.83, 2.38) vs. 2.50 (2.24, 2.79) mU/l, ), reduced FT4 (10.54 (9.83,11.25) vs. 11.67 (11.03 vs. 12.31) pmol/l, )
Se supplementation did not affect TPO Ab or TSH level in pregnant women. During late gestation (35 weeks), serum FT4 levels were lower in the selenium-treated women compared to controls (10.54 vs. 10.82 pmol/l, ).
There was no incidence of preeclampsia in the treated group, but 4.7% (n = 3) of women in the control group suffered from preeclampsia (statistically nonsignificant)
Se supplementation significantly lowered the concentration of soluble vascular endothelial growth factor receptor 1 (sFlt-1), which is a biomarker of preeclampsia, among the Se deficient women. However, the difference in the concentration of other biomarkers was not significant.
