AI Article Synopsis

  • The Barker Hypothesis suggests that a poor environment in the womb can lead to restricted fetal growth and a higher risk of diseases related to metabolism and heart health later in life.
  • A new statistical model using genomic SEM software was developed to analyze the genetic influences on birthweight and cardiometabolic traits by separating contributions from mothers and their offspring.
  • Research from the Norwegian HUNT study, involving data from over 15,000 mother-child pairs, provided evidence of maternal effects on blood pressure and genetic overlap between birthweight and glucose levels, indicating strong genetic ties between these traits and offering new insights beyond environmental factors.

Article Abstract

The Barker Hypothesis posits that adverse intrauterine environments result in fetal growth restriction and increased risk of cardiometabolic disease through developmental compensations. Here we introduce a new statistical model using the genomic SEM software that is capable of simultaneously partitioning the genetic covariation between birthweight and cardiometabolic traits into maternally mediated and offspring mediated contributions. We model the covariance between birthweight and later life outcomes, such as blood pressure, non-fasting glucose, blood lipids and body mass index in the Norwegian HUNT study, consisting of 15,261 mother-eldest offspring pairs with genetic and phenotypic data. Application of this model showed some evidence for maternally mediated effects of systolic blood pressure on offspring birthweight, and pleiotropy between birthweight and non-fasting glucose mediated through the offspring genome. This underscores the importance of genetic links between birthweight and cardiometabolic phenotypes and offer alternative explanations to environmentally based hypotheses for the phenotypic correlation between these variables.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9823066PMC
http://dx.doi.org/10.1007/s10519-022-10116-9DOI Listing

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