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Critical supply chain issues with nutrition and oxygen can cause preterm delivery or even death before a baby is ever born, raising the risk of cardiovascular disease for both the mother and the kid for the rest of their lives.
Researchers have found that a midgestational spike in the hormone leptin, which we often link with hunger control, produces significant blood vessel malfunction and restricts the baby’s growth in preeclampsia, a condition that puts both mother and baby at danger.
Preeclampsia is known to cause an increase in leptin synthesis by the placenta about 20 weeks into a pregnancy, but the effects have not yet been determined.
According to experts, vascular physiologist in the Department of Physiology at the Medical College of Georgia and corresponding author of the study published in the journal Hypertension, “it’s kind of emerging as a marker of preeclampsia.”
The placenta, a transitory organ that helps the mother nourish and oxygenate her unborn child, as well as fat cells, create leptin, which is mostly produced by fat cells.
In a healthy pregnancy, leptin levels gradually rise, although it’s unclear exactly what leptin is doing in this situation, even properly. There is some evidence that it functions as a natural nutrition sensor during reproduction or as a means to promote the formation of new blood vessels and/or growth hormone for normal development.
In a healthy pregnancy, leptin levels gradually rise, although it’s unclear exactly what leptin is doing in this situation, even properly. There is some evidence that it functions as a natural nutrition sensor during reproduction or as a means to promote the formation of new blood vessels and/or growth hormone for normal development.
For the first time, a new study examining the effects demonstrates that an increase in leptin causes endothelial dysfunction, which causes blood vessels to contract, lose their capacity to relax, and limit a baby’s growth.
The impact of the midgestation leptin rise was nearly the same when researchers suppressed the precursor for the potent, natural blood vessel dilatant nitric oxide, as occurs in hypertension.
