Nutrients, Vol. 18, Pages 424: The First 1000 Days: Maternal Nutrient Intake—A Window of Opportunity for Pulmonary Hypertension—A Narrative Review
Nutrients doi: 10.3390/nu18030424
Authors:
Alina-Costina Luca
Solange Tamara Roșu
Cosmin Diaconescu
Dana Elena Mîndru
Cristina Gavrilovici
Adriana Vizireanu
Viorel Țarcă
Eduard Vasile Roșu
Elena Țarcă
The first 1000 days of life, starting from conception to a child’s second birthday, constitute a pivotal period for fetal lung and pulmonary vascular development. Maternal nutrition during this period plays an important role in fetal growth, immune programming and organ development, including that of the pulmonary system. This narrative review consolidates evidence linking maternal nutrition and early-life nutrient intake during this period with the development of pulmonary hypertension in the newborn. We examine the influence of both nutrient deficiencies and excesses on fetal lung and vascular development. We performed a structured search of PubMed and Embase (conducted from February 2025 to March 2025) and screened reference lists. Twenty-eight peer-reviewed studies were included, comprising human clinical and observational evidence and studies on animal models. The findings suggest that imbalances in maternal diet can disrupt placental function, induce inflammation, and trigger epigenetic alterations, all contributing to pulmonary vascular dysfunction and increased pulmonary hypertension susceptibility in neonates. Notably, maternal undernutrition and thiamine deficiency during lactation have been directly linked to pulmonary hypertension in infants. Conversely, high-fat diets and excessive polyphenol intake have been associated with adverse fetal cardiovascular remodeling. While current evidence is primarily derived from animal models and observational studies, it highlights the urgent need for targeted nutritional strategies and clinical trials during pregnancy. Although human causality is unproven for most exposures, studying maternal nutrition in the first 1000 days could offer a cost-effective method for reducing the burden of pediatric pulmonary hypertension and its long-term consequences and for prospective trials aimed at preventing early-life pulmonary vascular disease.
The first 1000 days of life, starting from conception to a child’s second birthday, constitute a pivotal period for fetal lung and pulmonary vascular development. Maternal nutrition during this period plays an important role in fetal growth, immune programming and organ development, including that of the pulmonary system. This narrative review consolidates evidence linking maternal nutrition and early-life nutrient intake during this period with the development of pulmonary hypertension in the newborn. We examine the influence of both nutrient deficiencies and excesses on fetal lung and vascular development. We performed a structured search of PubMed and Embase (conducted from February 2025 to March 2025) and screened reference lists. Twenty-eight peer-reviewed studies were included, comprising human clinical and observational evidence and studies on animal models. The findings suggest that imbalances in maternal diet can disrupt placental function, induce inflammation, and trigger epigenetic alterations, all contributing to pulmonary vascular dysfunction and increased pulmonary hypertension susceptibility in neonates. Notably, maternal undernutrition and thiamine deficiency during lactation have been directly linked to pulmonary hypertension in infants. Conversely, high-fat diets and excessive polyphenol intake have been associated with adverse fetal cardiovascular remodeling. While current evidence is primarily derived from animal models and observational studies, it highlights the urgent need for targeted nutritional strategies and clinical trials during pregnancy. Although human causality is unproven for most exposures, studying maternal nutrition in the first 1000 days could offer a cost-effective method for reducing the burden of pediatric pulmonary hypertension and its long-term consequences and for prospective trials aimed at preventing early-life pulmonary vascular disease. Read More
