Effects of Mediterranean Diet During Pregnancy on the Onset of Overweight or Obesity in the Offspring: A Randomized Trial

Abstract

Abstract Background/Objectives Maternal diet during pregnancy could represent a potential target for pediatric overweight/obesity prevention. Mediterranean Diet (MD) is one of the healthiest dietary models exerting protective effects against excess weight. To date, the evidence on the MD-effects during pregnancy for the prevention of childhood overweight/obesity are scarce and based on observational studies. The Mediterranean Diet during Pregnancy (PREMEDI) trial has been designed to evaluate the efficacy of a nutritional counseling aimed at promoting MD-adherence during pregnancy on the occurrence of overweight or obesity at 24 months in the offspring. Methods The PREMEDI was a randomized-controlled, parallel groups, prospective trial. 104 women in their first trimester of pregnancy were randomly assigned to standard obstetrical and gynecological care alone (CT group, n=52) or plus a nutritional counseling promoting MD (MD group, n=52). 5 women in the MD arm and 2 women in the CT arm were lost to follow-up. Women enrolled in the MD group were provided 3 session of nutritional counseling (one session for trimester). The primary outcome was the proportion of overweight or obesity at 24 months. Other outcomes included maternal MD-adherence, maternal weight gain, and epigenetic modulation of genes involved in metabolic pathways. Results A lower proportion of overweight or obesity was observed at 24 months in children of MD-arm mothers compared to those in the CT arm (6% vs. 33%, absolute risk difference=-27%, 95%CI -41% to -12%, intention to treat analysis, p<0.001; number needed to treat 3, 95%CI 2 to 8). This effect was associated with a higher DNA methylation rate of the leptin gene in cord blood (30.4% [1.02 SD] vs. 16.9% [2.99 SD], MD vs. CT arm, p<0.0001). Conclusions MD during pregnancy is an effective strategy to prevent pediatric overweight/obesity at 24 months. This effect could be mediated, at least in part, by an epigenetic modulation of leptin expression.