I needed to disable self sign-ups because I’ve been getting too many spam-type accounts. Thanks.
Premature birth caused by Vitamin A overdose?
A role for the liver in parturition and preterm birth
https://www.oatext.com/pdf/JTS-2-133.pdf
Abstract
Neither the mechanisms of parturition nor the pathogenesis of preterm birth are well understood. Poor nutritional status has been suspected as a major causal factor, since vitamin A concentrations are low in preterm infants. However, even large enteral doses of vitamin A from birth fail to increase plasma concentrations of vitamin A or improve outcomes in preterm and/or extremely low birthweight infants. These findings suggest an underlying impairment in the secretion of vitamin A from the liver, where about 80% of the vitamin is stored in potentially toxic concentrations. Vitamin A accumulates in the liver and breast during pregnancy in preparation for lactation. While essential in low concentration for multiple biological functions, vitamin A in higher concentration can be pro-oxidant, mutagenic, teratogenic and cytotoxic, acting as a highly surface-active, membrane-seeking and destabilizing compound. Regarding the mechanism of parturition, it is conjectured that by nine months of gestation the hepatic accumulation of vitamin A (retinol) from the liver is such that mobilization and secretion are impaired to the point where stored vitamin A compounds in the form of retinyl esters and retinoic acid begin to spill or leak into the circulation, resulting in amniotic membrane destabilization and the initiation of parturition. If, however, the accumulation and spillage of stored retinoids reaches a critical threshold prior to nine months, e.g., due to cholestatic liver disease, which is common in mothers of preterm infants, the increased retinyl esters and/or retinoic acid rupture the fetal membranes, inducing preterm birth and its complications, including retinopathy, necrotizing enterocolitis and bronchopulmonary dysplasia. Subject to testing, the model suggests that measures taken prior to and during pregnancy to improve liver function could reduce the risk of adverse birth outcomes, including preterm birth.
Conclusion
In 1953 Peter Medawar raised the question: “How does the pregnant mother contrive to nourish within itself, for many weeks or months, a fetus that is an antigenically foreign body?” [75]. In other words, why does the mother fail to reject her fetus as a foreign piece of tissue? The suggestion offered here is that the mother does not reject but rather ejects the fetus, normally at around 37 weeks of gestation, as the result of a biochemical rather than an immunological mechanism. Parturition at term is hypothesized to represent an active process of ejection of the fetus associated with the hepatic accumulation and spillage of stored retinoids due to mild liver dysfunction, which progressively weaken the fetal membranes until they rupture at around the ninth month of gestation. Based on this template for parturition at term, it is further proposed that spontaneous preterm birth is similarly due to more severe liver dysfunction and to concentrations of retinyl esters and retinoic acid that exceed the threshold for inducing rupture of the fetal membranes before 37 weeks of gestation.
The model could be tested by determining whether 1) preterm newborns have significantly lower serum retinol (ROL) concentrations than term newborns, but higher concentrations of retinoic acid (RA), a higher percent retinyl esters (RE), and a higher RE:ROL ratio; 2) mothers of preterm newborns have higher liver enzyme levels than mothers of term neonates; and 3) an increased percentage of REs as a fraction of total serum retinol (>10%) is a strong predictor of preterm birth. Subject to further testing in prospective studies, periodic monitoring of changes in maternal retinoid profiles throughout pregnancy could provide a biomarker for the early identification of impending adverse birth outcomes, which could be useful in prevention.
Approaches to the management of pregnancies resulting in preterm birth and its complications suggested by the retinoid toxicity hypothesis could involve the adoption of measures taken prior to and after conception to improve liver function through dietary and lifestyle changes.
This is fascinating. Three of my four babies were born (naturally, at home) three weeks early. I know exactly when they were conceived, and so I knew that it was three weeks early to the day for each of them - we joked that I "cooked" my babies quickly. But they were not actually "cooked" - three of them had fairly severe feeding issues at birth, and all have tongue-tie/lip-tie and other minimal midline defects. They could definitely have used some more time in utero!
My fourth baby was born only two weeks early, and I now wonder if this is because I began a Walsh protocol during my pregnancy with her: large amounts of Vitamins B6/P-5-P, and zinc...which I now hypothesize have worked so well for my own health issues largely because they were protecting me from some of the effects of Vitamin A toxicity.
My first was 2 weeks early, and very skinny but fully formed. I was "less healthy" during that preg: I had headaches and kidney problems. That baby had acne and colic.
My second preg was healthier, a few days late, and she slept better and had better skin.