A recent study, conducted on lab mice, has shown that the way a baby is born could have a long-term impact on their metabolic health.
Stress hormones produced during labor have a protective effect on a baby’s ability to metabolize fats. In addition, the researchers found that many of the genes and hormones essential to adaptive metabolism are not ready until just before spontaneous birth.
The stress of laboring has previously been shown to help the baby transition to extra-uterine life, and metabolic function is just another benefit of that stress. This led to the conclusion that waiting for labor to begin on its own, and then allowing baby to experience at least some labor, should have a beneficial effect on the baby’s life-long metabolism.
Glucocorticoids, a kind of stress hormone, cause the body to produce a protein called PPARa in the fetal liver. PPARa prepares the liver to metabolize fats from milk after birth. This is crucial because, without it, the liver continues to expect to metabolize the sugar-rich placental diet, as it did in utero.
Human babies can become very sick when their liver is not prepared to process milk, but this is rare. The researchers indicate that the main application of this study is in the prevention of diseases developed later in life — such as obesity, Type 2 diabetes and fatty liver disease.
So, the stress hormones produced late in pregnancy and during labor directly stimulate the production of the protein PPARa, which prepares the baby to get energy from fat-rich milk instead of sugar-rich placental nourishment — but that’s not all.
The study found that PPARa also triggers a chain reaction that eventually activates other genes involved in fat-burning.
Babies whose livers are not adequately prepared to consume a higher-fat diet, suggests research, will become stressed from years of processing normal human milk and then a human diet. This can lead to metabolic disorders, such as those listed above.
One researcher said these stress hormones — crucial to the baby’s metabolic development — are also responsible for inducing labor in the mother.
In fact, glucocorticoids is sometimes used to speed fetal lung maturation in babies at risk for premature birth. In these cases, doctors are trying to mimic the body’s processes to signal specific growth in the baby. Another recent study (also using mice) points to development of the fetal lungs as the trigger of spontaneous labor.
Allowing labor to begin on its own protects a baby from being born developmentally too early — even if that just means a few extra days for some hormones, or their receptor sites, to gain rank.
Case in point: Labor inductions often fail because it is physiologically too early for labor. Oxytocin is the hormone that makes your uterus contract. No oxytocin, no contraction — no contraction, no labor.
When a person is chemically induced at the hospital, fake oxytocin is given to get contractions going. Sometimes this works just fine. But often times, it doesn’t work very well at all.
One of the reasons for this is that oxytocin receptor sites on the uterus build up over the course of your pregnancy, notably at the very end. Your doctor may think you are ready, you may be essentially at your due date, but if your body isn’t ready — it’s not time yet.
The effects of a ‘premature’ induction of labor like this are immediately apparent. With the immaturity of receptor sites and gene expression in the fetal liver, the effects can be much slower to appear, say authors of the study.
We know that the receptor sites on the liver are most numerous just before birth (Speirs et al., 2004) and that these receptor sites play an important role in the development of the fetus and its preparation for birth (Cole et al., 1995). We also know that stress during labor causes the release of the hormones that the receptor sites are waiting for (Barlow et al., 1974).
So, (in the case of the liver) a baby born too early — without enough receptor sites or without stress hormones to attach to those receptor sites — would appear to be at a much heightened risk for metabolic disorders, both immediately and in the future.
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