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• W2531963913 startingPage "265" @default.
• W2531963913 abstract "Pregnancy sickness is widespread yet its etiology is poorly understood. It is almost certainly endocrine in origin and most likely a product of placental hormones, with human chorionic gonadotropin being the strongest candidate. It has long been known that greater levels of nausea and vomiting during pregnancy are associated with a lower incidence of spontaneous abortion, yet the causal mechanisms remain unclear. One current popular explanation is that nausea and vomiting during pregnancy is fetoprotective, inducing aversions to foods, especially meat, dairy and seafoods, which may carry toxins, pathogens or mutagens. However, most spontaneous abortions arise from genetic or epigenetic defects that are present at or near conception. Moreover, measurements of human chorionic gonadotropin (hCG) at the time of implantation, particularly its hyperglycosylated isoform, accurately predict subsequent spontaneous abortion. Thus the developmental fate of most embryos is fixed before the onset of the symptoms of pregnancy sickness. An alternative explanation for the link between pregnancy sickness and spontaneous abortion is the embryo quality hypothesis: high quality embryos are both more likely to produce the biochemical antecedents of pregnancy sickness and avoid spontaneous abortion. Recent work has shown that the link between pregnancy sickness and spontaneous abortion grows stronger with maternal age, dramatically so in mothers 35 or older. This reflects the parallel rise in the incidence of autosomal aneuploidies with maternal age. The link between pregnancy sickness and spontaneous abortion exists not because nausea and vomiting during pregnancy is fetoprotective, but because nausea and vomiting is an index of a high quality embryo. Pregnancy sickness is not adaptive per se, but the result of an antagonistic pleiotropy over thyroid function, where embryos use hCG to modulate maternal thyroid hormone production during gestation. Embryos benefit from the thyroid hormone production that is key to neurodevelopment, but produce maternal nausea and vomiting as a by-product. Pregnancy sickness, however, may still serve to protect embryo quality but by a different mechanism that posited under the MEPH. Embryo quality is protected by calibrating the dietary intake of a micronutrient – iodine – critical to neuromotor development. For most humans over most of our evolutionary history, iodine has been in short supply, and iodine deficiency is still the most common source of cognitive impairment across the globe. Thus it is of interest that the food aversions most commonly associated with pregnancy sickness, to meat, dairy and seafoods, are also the chief dietary sources of iodine. There is a further intriguing property about iodine: both too little and too much during early pregnancy are damaging to embryo brain development. Given that pregnancy sickness is closely linked to iodine intake and thyroid function (hypothyroidism is associated with lower levels of nausea and vomiting, hyperthyroidism with more), an obvious interpretation emerges. The previously described link between diet and pregnancy sickness – pregnancy sickness is less likely when plants and particularly corn/maize are the sole food staples – arises not because plant food staples are safe, as previously suggested, but because these foods are iodine poor and may, in addition, be goitrogenic. Pregnancy sickness, which reduces the dietary intake of iodine, is clearly maladaptive under conditions of iodine deficiency and hypothyroidism. Conversely, higher levels of pregnancy sickness induced by hyperthyroidism may protect embryos from the inimical effects of excessive dietary iodine during early gestation by reducing the intake of iodine rich foods." @default.
• W2531963913 created "2016-10-28" @default.
• W2531963913 creator A5034492151 @default.
• W2531963913 date "2017-03-01" @default.
• W2531963913 modified "2023-09-27" @default.
• W2531963913 title "Embryo quality: the missing link between pregnancy sickness and pregnancy outcome" @default.
• W2531963913 cites W124264984 @default.
• W2531963913 cites W1506357063 @default.
• W2531963913 cites W1518197206 @default.
• W2531963913 cites W1529934215 @default.
• W2531963913 cites W1544653202 @default.
• W2531963913 cites W1554239135 @default.
• W2531963913 cites W1557598671 @default.
• W2531963913 cites W1574694350 @default.
• W2531963913 cites W1859434745 @default.
• W2531963913 cites W1894082044 @default.
• W2531963913 cites W1919851123 @default.
• W2531963913 cites W1927245176 @default.
• W2531963913 cites W1962079618 @default.
• W2531963913 cites W1963586502 @default.
• W2531963913 cites W1963706156 @default.
• W2531963913 cites W1965773879 @default.
• W2531963913 cites W1965846999 @default.
• W2531963913 cites W1966227297 @default.
• W2531963913 cites W1966247480 @default.
• W2531963913 cites W1966587454 @default.
• W2531963913 cites W1967375819 @default.
• W2531963913 cites W1968533034 @default.
• W2531963913 cites W1968846073 @default.
• W2531963913 cites W1969123608 @default.
• W2531963913 cites W1970976609 @default.
• W2531963913 cites W1972651008 @default.
• W2531963913 cites W1973043651 @default.
• W2531963913 cites W1974138625 @default.
• W2531963913 cites W1975030943 @default.
• W2531963913 cites W1979770327 @default.
• W2531963913 cites W1981345584 @default.
• W2531963913 cites W1982496257 @default.
• W2531963913 cites W1986617857 @default.
• W2531963913 cites W1987154880 @default.
• W2531963913 cites W1987184305 @default.
• W2531963913 cites W1987524953 @default.
• W2531963913 cites W1987867715 @default.
• W2531963913 cites W1988311791 @default.
• W2531963913 cites W1988635100 @default.
• W2531963913 cites W1989308516 @default.
• W2531963913 cites W1989607389 @default.
• W2531963913 cites W1990085978 @default.
• W2531963913 cites W1992651294 @default.
• W2531963913 cites W2000522767 @default.
• W2531963913 cites W2002516057 @default.
• W2531963913 cites W2006221629 @default.
• W2531963913 cites W2008196442 @default.
• W2531963913 cites W2009146699 @default.
• W2531963913 cites W2009421523 @default.
• W2531963913 cites W2009589648 @default.
• W2531963913 cites W2010274639 @default.
• W2531963913 cites W2011231458 @default.
• W2531963913 cites W2011596446 @default.
• W2531963913 cites W2012416051 @default.
• W2531963913 cites W2013189085 @default.
• W2531963913 cites W2014889514 @default.
• W2531963913 cites W2016408036 @default.
• W2531963913 cites W2016535214 @default.
• W2531963913 cites W2017089706 @default.
• W2531963913 cites W2023553902 @default.
• W2531963913 cites W2023829594 @default.
• W2531963913 cites W2024500037 @default.
• W2531963913 cites W2029824662 @default.
• W2531963913 cites W2031239437 @default.
• W2531963913 cites W2031402418 @default.
• W2531963913 cites W2032548799 @default.
• W2531963913 cites W2033710020 @default.
• W2531963913 cites W2036156801 @default.
• W2531963913 cites W2038401300 @default.
• W2531963913 cites W2040592347 @default.
• W2531963913 cites W2041889235 @default.
• W2531963913 cites W2042516581 @default.
• W2531963913 cites W2044772422 @default.
• W2531963913 cites W2045297515 @default.
• W2531963913 cites W2046327875 @default.
• W2531963913 cites W2046619214 @default.
• W2531963913 cites W2047594495 @default.
• W2531963913 cites W2047821864 @default.
• W2531963913 cites W2048649139 @default.
• W2531963913 cites W2049729828 @default.
• W2531963913 cites W2049881308 @default.
• W2531963913 cites W2050440171 @default.
• W2531963913 cites W2050889783 @default.
• W2531963913 cites W2052211882 @default.
• W2531963913 cites W2054145268 @default.
• W2531963913 cites W2054621569 @default.
• W2531963913 cites W2056036126 @default.
• W2531963913 cites W2058597096 @default.
• W2531963913 cites W2058735882 @default.
• W2531963913 cites W2059060185 @default.
• W2531963913 cites W2062585754 @default.
• W2531963913 cites W2064143957 @default.

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