Challenges of linking early-life conditions and disease susceptibility.

Einstein FH.

Diabetes. 2012 May;61(5):981-2.

Since David Barker first raised concerns about the impact of poor maternal nutrition and fetal growth restriction on the infant’s long-term health (1,2), the obesity epidemic has shifted attention to the long-term effects of maternal over-nutrition and hyperglycemia in pregnancy (rev. in 3). Currently, one in five women is obese at the start of pregnancy and 2–10% are diagnosed with gestational diabetes mellitus (4). With the new diagnostic criteria for gestational diabetes mellitus, this number is expected to rise to ?18% of pregnant women worldwide (5,6). Despite these foreboding increases, we still have limited insight into the underlying mechanisms that link in utero conditions to later susceptibility for chronic disease. The inability to assess intrauterine exposures is one significant barrier to progress in this area. The discovery of a marker or profile that would more precisely measure fetal exposure to adverse conditions could ultimately help to identify infants at increased risk for age-related diseases and target preventative strategies specifically to at-risk individuals. In this edition of Diabetes, Bouchard et al. (7) tackle this problem in their investigation of placental changes in cytosine methylation associated with maternal glucose tolerance. At the same time, their work exemplifies some of the common challenges in epigenomic research.
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