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The relationship between the parental genomes in terms of the future growth and development of their offspring is not critical. For the majority of the genome the tissue-specific gene expression and epigenetic status is shared between the parents equally, with both alleles contributing without parental bias. For a very small number of genes the rules change and control of expression is restricted to a specific, parentally derived allele, a phenomenon known as genomic imprinting. The insulin-like growth factor 2 ( Igf2/IGF2 ) is a robustly imprinted gene, important for fetal growth in both mice and humans.  In utero IGF2  exhibits paternal expression, which is controlled by several mechanisms, including the maternally expressing untranslated  H19  gene. In the study by Soubry  et al. , a correlation is drawn between the  IGF2  methylation status in fetal cord blood leucocytes, and the obesity status of the father from whom the active  IGF2  allele is derived through his sperm. These data imply that paternal obesity affects the normal  IGF2  methylation in the sperm and this in turn alters the expression of  IGF2  in the baby.

Fat dads must not be blamed for their children's health problems