Over recent years there has been increasing awareness that parental exposures to lifestyle and environmental toxins can increase the risk of non-communicable diseases such as obesity and metabolic syndrome in the next generation. Studies in rodent models have shown that this transgenerational transmission of disease occurs down both the maternal (oocyte) and paternal (sperm) line. The most studied example is obesity where oocytes from obese mothers have altered metabolic parameters which are associated with impaired embryo development and alterations in fetal growth trajectories. This appears likely to be mediated through metabolic sensor proteins that link metabolic dysfunction to altered epigenetics marks in both DNA and histones. Similarly, obesity in males induces oxidative stress, which signals a cascade of perturbations including to DNA methylation as well as changes in microRNA signatures. This paradigm that the environment of the gametes and early embryo can influence long term development also has implications for clinical IVF where this occurs in the laboratory. Further elucidations of the pathways involved in this amplification of disease into the next generation will be essential for the development of effective interventions that can break this cycle.