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P1-34 Can associations between prenatal nutrition and body mass index be explained by common genetic variants? Findings from the Dutch hunger winter families study
  1. L H Lumey1,
  2. A Vaarhorst2,
  3. A D Stein3,
  4. B Heijmans2
  1. 1Columbia University, New York, USA
  2. 2Leiden Univ Med Ctr, Leiden, The Netherlands
  3. 3Emory University, Atlanta, Georgia, USA


Genome wide association (GWAS) studies have identified single nucleotide polymorphisms (SNPs) related to body mass index (BMI: kg/m2). Associations have also been reported between fetal malnutrition and BMI. We use the circumstances of the Dutch Hunger Winter of 1944–1945 to further examine these relations. We studied 348 adult men and women born in affected cities in the western Netherlands who had been exposed to famine during pregnancy, 294 born before or after the famine as time-controls, and 305 same-sex unexposed siblings of above groups as family controls. Mean age at examination was 58 years. We evaluated common variants in the FTO, TMEM18, MC4R, GNPDA2, BDNF, SEC16B, NEGR1, SH2B1, SFRS10, MTCH2, and KCTD15 genes related to BMI. A genetic risk score was calculated for each individual by summing the number of risk alleles in these genes. Scores were also weighted using recent GWAS estimates of gene specific changes in BMI per risk allele. Institutional ethics committees gave the appropriate approvals for the study. Genetic risk scores had a mean of 11.4 (SD 2.2) and were not related to prenatal famine. Adult BMI was 1.34 units higher among famine exposed (95% CI 0.73 to 1.94) and further adjustments for risk score had little effect. There was no statistical interaction between famine exposure and genetic risk scores with regard to BMI outcomes. Analyses with weighted risk scores confirm these patterns. Common genetic variants related to BMI do not explain the association between prenatal famine and adult BMI in our study population.

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