The findings, published in Cell Metabolism, used mouse models to investigate how changes to the environmental factors in the womb are linked to the risk of metabolic diseases in not only to the mother's own offspring but also the grandoffspring.
Led by Josep Jiménez-Chillarón, of the Hospital Sant Joan de Déu in Spain, the team looked at the patterns of gene expression in mice, finding that for pregnant mice that are malnourished —experiencing a 50% caloric restriction during the last week of pregnancy— that their offspring were at first growth restricted and had low birth weight, but also went on to become obese and diabetic as they aged.
Strikingly, in a domino effect, the offspring of the growth-restricted males also inherited a predisposition to metabolic abnormalities, said the team.
"Current dogma proposes that the vast majority of epigenetic modifications in the sperm and eggs are erased precisely to avoid transmission of environmentally derived changes. But our data suggest that a few environmentally induced epigenetic modifications may be passed and stably maintained in the next generation," says Jiménez-Chillarón. "This may contribute, in part, to the transmission of diabetes risk from parents to offspring."
This opens up the possibility that predisposition for some complex diseases might be inherited independently from one's genetic sequence, said the team.
However, Jiménez-Chillarón noted that it is important not to fall into the temptation of 'blaming' one's parents (or even grandparents) for disease: "Our view is that we inherit some predisposition, but it is our own lifestyle that will determine whether inherited risk will truly translate into disease. Hence, a healthy lifestyle is the best way to prevent any potentially inherited or newly acquired obesity or diabetes predisposition."