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Could sleep deprivation and changes in maternal microbiota during early pregnancy raise the risk of neural tube and heart malformations?

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Autor(es):
Cavalcante-Silva, Vanessa ; Samama, Marise ; de Oliveira, Allan Chiaratti ; D'Almeida, Vania ; Entezami, Frida ; Tufik, Sergio ; Andersen, Monica L.
Número total de Autores: 7
Tipo de documento: Artigo Científico
Fonte: Medical Hypotheses; v. 204, p. 3-pg., 2025-11-01.
Resumo

Neural tube and heart malformations are major congenital anomalies influenced by genetic and environmental factors, including elevated maternal homocysteine (Hcy) levels. Elevated Hcy levels have been linked to nutritional deficiencies, particularly in folate and cobalamin, as well as with genetic variations in key metabolic enzymes such as methionine synthase (MS), methylenetetrahydrofolate reductase (MTHFR), and cystathionine (3-synthase. We hypothesize that elevated Hcy, which has been associated with impaired fetal development, may be influenced by gut microbiota imbalances and sleep disturbances. The gut microbiota is thought to contribute to Hcy metabolism, partly through the production of essential vitamins such as B12 and folate. In this context, dysbiosis, which may be exacerbated by hormonal changes during pregnancy and by sleep deprivation, reflecting a hypomethylated environment. This hypomethylation can adversely affect gene expression and embryonic and fetal development. Strategies to improve maternal sleep quality and support microbiota health, together with folate supplementation, have been suggested to modulate Hcy levels and potentially benefit pregnancy outcomes and fetal development. (AU)

Processo FAPESP: 20/13467-8 - Relação da apneia obstrutiva do sono e suas comorbidades com a microbiota intestinal: interface com sexualidade e função reprodutiva
Beneficiário:Monica Levy Andersen
Modalidade de apoio: Auxílio à Pesquisa - Temático
Processo FAPESP: 23/08657-0 - Avaliação da associação entre prematuridade, senescência celular e ritmicidade circadiana
Beneficiário:Vânia D'Almeida
Modalidade de apoio: Auxílio à Pesquisa - Regular