Stress causes cortisol levels in the blood to rise, altering the expression and activity of its regulatory agents - corticotropin-releasing hormone (CRH) and 11p-hydroxysteroid dehydrogenase (11pHSD). In this paper, the effects of cortisol, CRH, and 11pHSD on conception and fetal development are analyzed, including review of relevant research, assessment methods, and potential future studies. Within a woman's body the ovaries and the placenta independently control cortisol, CRH, and 11pHSD concentration. However, this hormonal balance can be disrupted by the high cortisol concentration in the blood, consequently decreasing chances of conception and altering fetal development. High pre-conception intraovarian cortisol levels, a low cortisol/cortisone ratio, and oxidative 11pHSD activity have been found to negatively affect fertilization, especially concerning in-vitro procedures. During gestation, high levels of maternal cortisol can increase the amount of placental CRH, potentially effecting substance transport across the womb, altering fetal gene expression, and increasing the risk of abnormalities in mental development, cardiovascular diseases in offspring, or premature birth. These negative stress-related outcomes emphasize the importance of cortisol, CRH, and 11pHSD screening. Several suitable molecular techniques are reviewed in this paper. These include immunoassays, liquid chromatography with tandem mass spectrometry, and the polymerase chain reaction, applied to sal iva, urine, blood plasma, hair, follicular fluid, or amniotic fluid samples. Such screening may play an important role in successful IVF procedures as well as avoiding fetal physiological impairments. However, further investigation is needed regarding the relationship between maternal stress and the concentration of cortisol, CRH and 11pHSD in the ovaries and placenta.
Keywords: maternal stress, cortisol, 11beta-hydroxysteroid dehydro - genase, fetal development, fertilization, laboratory assessment techniques.
