This kind of epigenetic research can be applied to any number of genes and related conditions. As such, there is great promise for individuals at risk of a variety of health conditions (with a known genetic basis) with the potential to reverse problems that can be treated using epigenetic drugs. The potential of such drugs to modify behaviour(s) or physical dysfunction is intriguing, although we’re some way off this goal.

However, diet is undoubtedly important in affecting the epigenome and shaping behaviour (see Dining at the Epigenetic Café).  The stressed rat pups of the low-LG-mothers could be calmed by administering a demethylating agent while feeding methionine led to distress in the previously calm high-LG-mother’s offspring. While it has been found to be effective in the treatment of bipolar depression (Carney 1989, British Journal of Psychiatry) methionine has been shown to aggravate schizophrenia (Brune & Himwich 1962, Journal of Nervous and Mental Disease, Israelstam 1967, Journal of Nuclear Medicine).

Seemingly contradictory outcomes are perhaps to be expected at this early stage in unravelling the epigenome’s role as an environmental buffer, given the complex interaction of myriad gene products that control brain function and behaviour. The McGill team were able to establish that feeding methionine to rats changed the balance of methylation in about 300 genes (that’s 1% of the number of genes they examined and there’s about 25,000 in the mammalian genome).

This kind of focus will drive nurture towards becoming a more exact science.  We want to know more about which genes specifically are being epigenetically marked by certain environmental conditions and how long those marks last.  We want to know how subtle an environmental factor can be to still have a measurable effect on the epigenome. Does smiling at your baby or sending your child to the naughty step effect an epigenetic change?

Environmental impacts on the genome, epigenetic marks, can be carried over from one generation to the next and beyond. Studies in mice have shown that the grandmother’s diet can affect the epigenetic state of her grandchildren and their tendency towards obesity (see Dining at the Epigenetic Café and Dining for your Descendants). Waterland and colleagues (2006, European Journal of Human Genetics) think that DNA methylation might in fact be controlling appetite. Feeding a methyl-supplemented diet halted the tendency for an overeating strain of mice to become fatter and fatter over subsequent generations.