M Camille Hoffman1, Robert Freedman2, Amanda J Law3, Alena M Clark4, Sharon K Hunter5. 1. Department of Obstetrics and Gynecology, Division of Maternal Fetal Medicine, University of Colorado Denver School of Medicine, Mail Stop F-546, Anschutz Medical Center, Aurora, CO, 80045, USA; Department of Psychiatry, University of Colorado Denver School of Medicine, Mail Stop F-546, Anschutz Medical Center, Aurora, CO, 80045, USA. Electronic address: Camille.Hoffman-Shuler@cuanschutz.edu. 2. Department of Psychiatry, University of Colorado Denver School of Medicine, Mail Stop F-546, Anschutz Medical Center, Aurora, CO, 80045, USA. Electronic address: Robert.Freedman@cuanschutz.edu. 3. Department of Obstetrics and Gynecology, Division of Maternal Fetal Medicine, University of Colorado Denver School of Medicine, Mail Stop F-546, Anschutz Medical Center, Aurora, CO, 80045, USA; Department of Psychiatry, University of Colorado Denver School of Medicine, Mail Stop F-546, Anschutz Medical Center, Aurora, CO, 80045, USA; Department of Cell and Developmental Biology, University of Colorado Denver School of Medicine, Mail Stop F-546, Anschutz Medical Center, Aurora, CO, 80045, USA; Department of Medicine, University of Colorado Denver School of Medicine, Mail Stop F-546, Anschutz Medical Center, Aurora, CO, 80045, USA. Electronic address: Amanda.Law@cuanschutz.edu. 4. Department of Nutrition and Dietetics, Campus Box 93, University of Northern Colorado, Greeley, CO, 80639, USA. Electronic address: alena.clark@unco.edu. 5. Department of Psychiatry, University of Colorado Denver School of Medicine, Mail Stop F-546, Anschutz Medical Center, Aurora, CO, 80045, USA. Electronic address: Sharon.Hunter@cuanschutz.edu.
Abstract
BACKGROUND & AIMS: Maternal gestational infection is a well-characterized risk factor for offsprings' development of mental disorders including schizophrenia, autism, and attention deficit disorder. The inflammatory response elicited by the infection is partly directed against the placenta and fetus and is the putative pathogenic mechanism for fetal brain developmental abnormalities. Fetal brain abnormalities are generally irreversible after birth and increase risk for later mental disorders. Maternal immune activation in animals models this pathophysiology. SARS-CoV-2 produces maternal inflammatory responses during pregnancy similar to previously studied common respiratory viruses. METHOD: Choline, folic acid, Vitamin D, and n-3 polyunsaturated fatty acids are among the nutrients that have been studied as possible mitigating factors for effects of maternal infection and inflammation on fetal development. Clinical and animal studies relevant to their use in pregnant women who have been infected are reviewed. RESULTS: Higher maternal choline levels have positive effects on the development of brain function for infants of mothers who experienced viral infections in early pregnancy. No other nutrient has been studied in the context of viral inflammation. Vitamin D reduces pro-inflammatory cytokines in some, but not all, studies. Active folic acid metabolites decrease anti-inflammatory cytokines. N-3 polyunsaturated fatty acids have no effect. CONCLUSIONS: Vitamin D and folic acid are already supplemented in food additives and in prenatal vitamins. Despite recommendations by several public health agencies and medical societies, choline intake is often inadequate in early gestation when the brain is forming. A public health initiative for choline supplements during the pandemic could be helpful for women planning or already pregnant who also become exposed or infected with SARS-CoV-2.
BACKGROUND & AIMS: Maternal gestational infection is a well-characterized risk factor for offsprings' development of mental disorders including schizophrenia, autism, and attention deficit disorder. The inflammatory response elicited by the infection is partly directed against the placenta and fetus and is the putative pathogenic mechanism for fetal brain developmental abnormalities. Fetal brain abnormalities are generally irreversible after birth and increase risk for later mental disorders. Maternal immune activation in animals models this pathophysiology. SARS-CoV-2 produces maternal inflammatory responses during pregnancy similar to previously studied common respiratory viruses. METHOD: Choline, folic acid, Vitamin D, and n-3 polyunsaturated fatty acids are among the nutrients that have been studied as possible mitigating factors for effects of maternal infection and inflammation on fetal development. Clinical and animal studies relevant to their use in pregnant women who have been infected are reviewed. RESULTS: Higher maternal choline levels have positive effects on the development of brain function for infants of mothers who experienced viral infections in early pregnancy. No other nutrient has been studied in the context of viral inflammation. Vitamin D reduces pro-inflammatory cytokines in some, but not all, studies. Active folic acid metabolites decrease anti-inflammatory cytokines. N-3 polyunsaturated fatty acids have no effect. CONCLUSIONS: Vitamin D and folic acid are already supplemented in food additives and in prenatal vitamins. Despite recommendations by several public health agencies and medical societies, choline intake is often inadequate in early gestation when the brain is forming. A public health initiative for choline supplements during the pandemic could be helpful for women planning or already pregnant who also become exposed or infected with SARS-CoV-2.
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