Hypertension during pregnancy may affect kids` health
Posted on Wednesday, 27th February 2013
Mild maternal hypertension early in pregnancy actually benefits the fetus, but that late-pregnancy hypertension has negative health consequences for the child, a new study has found.
The study, conducted by researchers from the Centre for Social Evolution at the Department of Biology, University of Copenhagen, is based on more than 750,000 births in Denmark, with follow-up data on children`s hospital diagnoses for up to 27 years.
"It has been known for some time now that pregnancy-induced hypertension can lead to more serious toxic conditions ( preeclampsia ), but it has puzzled biologists why such a medical condition that can be quite dangerous for both mother and child has not previously been removed by natural selection in our stoneage ancestors," said Professor Jacobus Boomsma, Director of the Centre for Social Evolution and coordinator of the study.
"However, evolutionary theory also emphasizes that paradoxes of this kind can be due to genetic parent-offspring conflicts, so we set out to test whether we could find statistical evidence for that type of explanation," he stated.
The results clearly indicate that mothers with minor increases in blood pressure in the first trimester of pregnancy have babies that enjoy generally better health than children of mothers who never get a hypertension diagnosis during pregnancy.
The difference was between 10 and 40 percent fewer diagnoses across all disease categories during the 27 years of available follow-up data, a result that has never been documented before.
However, when hypertension continues or starts later in pregnancy, this advantage shifts to a ca. 10 percent disadvantage in terms of an increased risk of acquiring a diagnosis in the Danish public health data bases.
Child mortality during the first year of life showed the same trend. In spite of this risk being very low in Denmark, no children of mothers with early pregnancy-induced hypertension died, whereas the mortality risk of children born to mothers with hypertension late in pregnancy was above average.
Parent-offspring-conflict theory maintains that father-genes in the placenta will have a tendency to `demand` a somewhat higher level of nutrition for the fetus than serves the interests of mother-genes. It argues that father genes that somehow manage to enhance maternal blood pressure will likely be met by maternal genes compensating this challenge.
Both types of genes are 50/50 represented and thus likely to find a `negotiated` balance while creating an optimally functioning placenta. However, when the pull of paternal genes cannot quite be managed by maternal counterbalances, there is a risk of elevated blood pressure to develop and persist, leading to late occurring pregnancy complications and compromised offspring health.
The results obtained are consistent with the idea that some deep fundamental conflicts lay buried in our genes right from the moment of conception. Imprinted genes are prime suspects for mediating such conflicts as they `remember` which parent they come from.
"Molecular biologists have recently found many such genes in mice and man, and they are particularly expressed in the placenta as the theory predicts. Our study therefore suggests that further research to test whether different patterns of pregnancy-induced hypertension are indeed related to paternal or maternal imprints would be highly worthwhile," said PhD student Birgitte Hollegaard, who did the analyses together with EU Marie Curie Postdoctoral Fellow Sean Byars.
The authors of the study hope these results will help build bridges between their evolutionary inspired public health analyses and established clinical praxis.
"Ultimately we are not only interested in the fundamental science aspects of genome level reproductive conflicts, but also in seeing some of these findings being made more directly useful, for example by adjusting pregnancy monitoring schemes to take long term risks for offspring health into account," Jacobus Boomsma concluded.