Editors' ChoiceEpigenetics

You are what your great grandmother ate

See allHide authors and affiliations

Science Translational Medicine  29 Jun 2016:
Vol. 8, Issue 345, pp. 345ec102
DOI: 10.1126/scitranslmed.aag2113

It has long been understood that what we eat contributes directly to our risk of developing diseases from obesity to diabetes to heart disease. An emerging question in this field is whether our own poor dietary choices can affect the health of our offspring through diet-driven epigenetic modifications in the germline. Now, Saben et al. provide provocative evidence that overnutrition in mothers can have lasting effects through second and even third generations to female offspring via transgenerational inheritance of mitochondrial dysfunction. The authors fed female mice a high-fat/high-sugar diet to initiate the metabolic syndrome in mothers, and then followed germline transmission of mitochondrial dysfunction through the next three generation of female progeny that were instead maintained on a “healthy” chow diet. Despite consumption of a normal diet, the first, second, and third generations of female offspring from mothers with poor nutrition developed mitochondrial dysfunction in skeletal muscle. Also, the expression of key proteins involved in mitochondrial dynamics was significantly altered in germ line cells of the first and second generation progeny. Although all in mice, this study suggests the powerful impact that epigenetic regulation can potentially have on disease phenotypes and encourages mothers to seek more nutritious choices—if not for themselves, then for their generations to come.

J. L. Saban et al., Maternal metabolic syndrome programs mitochondrial dysfunction via germline changes across three generations. Cell Rep. 10.1016/j.celrep.2016.05.065 (2016). [Full Text]

Stay Connected to Science Translational Medicine

Navigate This Article