Ever since Tom Cruise publicly vowed to eat his newborn’s placenta a few years back, the “afterbirth” organ has gotten a bum rap. But recent evidence suggests that in addition to its long-recognized role in supplying oxygen and nutrients to the growing fetus, the placenta also influences fetal development through epigenetic mechanisms. Now a trio of papers in the journal Epigenetics strengthens the case for placental power.
Birth Weight and GR Promoter Methylation
The first paper, from researchers at Brown University, questioned whether birth weight correlates with promoter methylation of the glucocorticoid receptor (GR) in human placenta (Filiberto et al., Epigenetics, May 2011). Glucocorticoids are steroid hormones that play roles in metabolism and immune function. So the team analyzed GR methylation in 480 human placentas. Here’s what they found:
- Increased promoter methylation of the placental GR gene was associated with a higher-than-average birth weight–a risk factor for obesity, insulin resistance, and cancer later in life.
The researchers speculate that changes in placental gene expression may alter the organ’s metabolic and endocrine function, as well as its ability to transport nutrients, gas, and waste. These changes, in turn, could influence fetal growth and lifelong disease susceptibility.
GR Methylation and Magnesium Deficiency
In the second paper, scientists from Kansai Medical University in Japan also looked at glucocorticoid-related gene methylation, but this time in the offspring of rat mothers fed a magnesium-deficient diet while pregnant (Takaya et al., Epigenetics, May 2011). Magnesium deficiency is known to affect glucocorticoid homeostasis, cause low birth weight, and increase the risk for diabetes. Their major finding:
- When rat moms were fed magnesium-deficient diets, their pups showed increased methylation of the Hsd11b2 promoter in liver. This gene encodes a glucocorticoid-inactivating enzyme.
Previous studies have linked reduced placental Hsd11b2 activity with low birth weight, so this paper reinforces the idea that poor maternal nutrition can alter glucocorticoid levels in the placenta and fetus and thereby influence birth weight. Just like high birth weight, a birth weight that’s too low predisposes offspring to health problems later in life.
Epigenetic Changes to Gene Expression in Twins
And finally, what better way to study epigenetic effects of the intrauterine environment than by looking at newborn monozygotic twins (Gordon et al., Epigenetics, May 2011)? The twins are genetically identical, so any differences in gene expression are likely due to epigenetic variability. When a multinational team of researchers examined genome-wide expression differences in umbilical cord cells of 250 human monozygotic twins, they made some interesting discoveries:
- Monozygotic twins showed gene expression differences at birth.
- Twins with separate placentas showed more differences than those who shared a placenta.
- Genes involved in response to the external environment varied the most in expression between monozygotic twins.
- Variable expression of 41 genes was linked to birth weight, many of which are involved in metabolism and cardiovascular function.
This study suggests that even slight differences in intrauterine environment, such as those experienced by monozygotic twins, can influence gene expression through epigenetic mechanisms.
The take-home: Our first home environment (inside Mom) may be a crucial one for determining our later health, in part through epigenetic changes in the placenta. But no matter what your current health status, we still think Mom deserves flowers on Mother’s Day.
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