Perinatal mortality in diabetic versus non-diabetic twin pregnancies, U.S. matched multiple birth data 1995-2000 [16].

<p>HR = Hazard ratio; CI = confidence interval</p>*<p>Hazard ratios adjusted for maternal race, age, education, marital status, parity, smoking, other maternal major illnesses, fetal sex, mode of delivery and twin-cluster level dependence in Cox proportional hazard models.</p>ʃ<p>Gestational age group-specific mortality rates and hazard ratios were calculated using the fetuses-at-risk denominator including all fetuses at risk of death (both born and unborn babies).</p>ʂ<p>P value in test for interaction with diabetes in pregnancy in relation to the risk of perinatal mortality </p

Maternal, pregnancy and newborn characteristics in diabetic versus non-diabetic twin pregnancies in the study population, U.S. 1995-2000 [16].

<p>Data presented are n (%). P values are from Chi-square tests for differences between diabetic and non-diabetic pregnancies.</p>*<p>SGA=Small-for-gestational-age <10^th percentile, LGA=large-for-gestational-age >90^th percentile, according to birth weight percentiles in the study cohort.</p>ʃ<p>Anyone or more of the following conditions: chronic hypertension, heart disease, acute or chronic lung disease, renal disease, genital herpes and RH sensitization.</p>ʂ<p>There were significant numbers (>10%) of missing information on smoking (17.8% missing) and mode of delivery (36.6% missing). The percentages of smokers and caesarean section were based on births without missing information.</p

Neonatal mortality in diabetic versus non-diabetic twin pregnancies, U.S. matched multiple birth data 1995-2000 [16].

<p>HR = Hazard ratio; CI = confidence interval</p>*<p>Hazard ratios adjusted for maternal race, age, education, marital status, parity, smoking, other maternal major illnesses, fetal sex, mode of delivery and twin-cluster level dependence in Cox proportional hazard models.</p>ʃ<p>Gestational age group-specific mortality rates and hazard ratios were calculated using the fetuses-at-risk denominator including all fetuses at risk of death (both born and unborn babies).</p>ʂ<p>P value in test for interaction with diabetes in pregnancy in relation to the risk of neonatal mortality.</p

Data_Sheet_1_Docosahexaenoic acid supplementation in gestational diabetes mellitus and neonatal metabolic health biomarkers.docx

Background and objectiveGestational diabetes mellitus (GDM) “programs” an elevated risk of metabolic dysfunctional disorders in the offspring, and has been associated with elevated leptin and decreased adiponectin levels in cord blood. We sought to assess whether docosahexaenoic acid (DHA) supplementation in GDM affects neonatal metabolic health biomarkers especially leptin and adiponectin.MethodsIn a randomized controlled trial, singleton pregnant women with de novo diagnosis of GDM at 24–28  weeks of gestation were randomized to dietary supplementation of 500 mg DHA per day (intervention, n = 30) until delivery or standard care (control, n = 38). The primary outcomes were cord blood leptin and total adiponectin concentrations. Secondary outcomes included high-molecular-weight (HMW) adiponectin and insulin-like growth factor-1 (IGF-1) concentrations in cord blood, maternal glycemic control post-intervention and birth weight (z score). In parallel, 38 euglycemic pregnant women were recruited for comparisons of cord blood biomarkers.ResultsThere were no significant differences in cord serum leptin, total and HMW adiponectin and IGF-1 concentrations between DHA supplementation and control groups (all p > 0.05). Maternal fasting and 2-h postprandial blood glucose levels at 12–16 weeks post-intervention were similar between the two groups. The newborns in the DHA group had higher birth weight z scores (p = 0.02). Cord blood total and HMW adiponectin concentrations were significantly lower in GDM vs. euglycemic pregnancies.ConclusionDocosahexaenoic acid supplementation at 500  mg/day in GDM women did not affect neonatal metabolic biomarkers including leptin, adiponectin and IGF-1. The results are reassuring in light of the absence of influence on neonatal adipokines (leptin and adiponectin), and potential benefits to fetal growth and development.Clinical Trial Registration: Clinicaltrials.gov, NCT03569501.</p