The notion that environmental influences on phenotype can be mediated by detectable/measurable epigenetic marks is of interest to the biologist, the clinician and the broader community. These molecular epigenetic marks might be valuable as biomarkers of future disease, proving opportunity for preclinical diagnosis. This is dependent, to some extent, on the long term stability of these marks, which is in most cases unknown. This makes their predictive value unclear. I will discuss how the meaning of the word epigenetics has changed over the last ten years and why this has caused confusion. Empirical evidence has altered our view of the importance of DNA methylation in the determination of phenotype.
Over the last fifty years, obesity levels have increased dramatically and changes to adipose tissue and epigenetic marks in adipose tissue have been detected. Whether these marks are drivers of obesity or consequences of obesity is yet to be determined. Moreover, there is some evidence that obesity can be inherited across generations, not just via DNA sequence (genotype) but also via epigenetic marks in the gametes. The idea is that mothers or fathers who have become obese transmit this to their offspring independent of any genetic susceptibility to obesity. The current evidence for this is weak.
I will discuss these ideas using data collected from studies in mice and humans.