Prenatal high-dose pyridoxine may prevent hypertension and syndrome X in-utero by protecting the fetus from excess glucocorticoid activity.
The increased risk for hypertension, insulin resistance syndrome, and coronary events associated with small-for-gestational-age birth, has plausibly been attributed to excessive prenatal exposure to glucocorticoids; this may up-regulate glucocorticoid activity throughout life by permanently decreasing expression of hippocampal glucocorticoid receptors crucial for feedback control of cortisol secretion. Since pyridoxal phosphate is a safe physiological antagonist of glucocorticoid activity, it is proposed that prenatal supplementation with high-dose pyridoxine may counteract the adverse impact of glucocorticoids on fetal growth, as well as on subsequent cardiovascular risk.
McCarty
M F
MF
Pantox Laboratories, San Diego, California, USA.
D004305:Dose-Response Relationship, Drug; D005260:Female; D005333:Fetus / Q000187:drug effects* / Q000378:metabolism; D005938:Glucocorticoids / Q000037:antagonists & inhibitors*; D006801:Humans; D006973:Hypertension / Q000517:prevention & control*; D007231:Infant, Newborn; D007232:Infant, Newborn, Diseases / Q000517:prevention & control*; D007236:Infant, Small for Gestational Age; D017566:Microvascular Angina / Q000517:prevention & control*; D011247:Pregnancy; D011736:Pyridoxine / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*
D005938:Glucocorticoids; D011736:Pyridoxine