Fetal and Neonatal Programming: Evidence and Clinical Implications

Abstract

Fetal and neonatal programming is the phenomenon describing deviations from normal developmental patterns. These deviations can increase risks for diseases later in life and are an example of phenotypic plasticity seen throughout nature. For instance, infants born with low birth weight, as a marker of an unfavorable intrauterine environment, are programmed differently and may have an increased risk for multiple diseases in adulthood. These risks include coronary heart disease, increased insulin resistance, hypertension, and imbalances in the immune system. This article discusses mechanisms responsible for fetal and neonatal programming. We also introduce possible changes to current clinical management and practices that reflect the current findings of fetal and neonatal programming.

Impact of elevated peak serum estradiol levels during controlled ovarian hyperstimulation on the birth weight of term singletons from fresh IVF-ET cycles

“…Although maximizing follicular response during COH is important, it is more important to minimize the risks of OHSS and LBW associated with supraphysiologic E 2 levels, especially given the correlation between LBW and adult cardiovascular disease, diabetes, and dyslipidemia [31][32][33]. While there has been a recent shift towards frozen embryo transfer cycles in the name of improved endometrial physiology, it is plausible that conservative stimulation protocols with autologous, fresh transfer offer the same benefits, provided serum E 2 levels are carefully monitored.…”

Prenatal Hypoxia Reduces Mitochondrial Protein Levels and Cytochrome c Oxidase Activity in Offspring Guinea Pig Hearts

“…32 Briefly, frozen left and right cardiac ventricles of prenatally NMX and HPX offspring hearts were pulverized with mortar and pestle and 30 to 50 mg homogenized in ice-cold mitochondrial isolation buffer (250 mmol/L sucrose, 5 mmol/L HEPES, 1 mmol/L EDTA, pH 7.5) in a Next Advance Bullet Blender (Averill Park, NY) for 5 minutes and centrifuged at 4 C at 500g to remove the cellular debris. The supernatant fractions were centrifuged at high speed (12.5 Â 1000g) to generate an enriched mitochondrial pellet fraction.…”

“…[1][2][3][4] Fetal HPX has been shown to alter signaling mechanisms of multiple fetal organs such as the heart, 5-9 brain, 10,11 liver, [12][13][14][15][16] and skeletal muscle. 16 Chronic intrauterine HPX has been shown to contribute to permanent changes in cardiovascular function of the offspring through programming.…”

Perinatal programming and cardiomyocyte aging

“…Интенсивные исследования последних десятиле-тий позволили идентифицировать дополнительные факторы, способствующие программированию за-болеваний, которые включают изменение питания в перинатальный период, воздействие на плод глю-кокортикоидов и гипоксии [48,49]. Показано, что ве-роятность развития метаболических и сердечно-сосу-дистых заболеваний увеличивается не только на фоне малой массы тела при рождении, но и при большой (более 5 000) массе тела [50].…”

“…Таким образом, вероятно, внутриутробная гипок-сия связана с развитием в последующей жизни муль-тиорганной патологии через механизм перинаталь-ного программирования [48].…”