A number of studies appear to have found a link between low levels of folate in the diet, a high intake of alcohol, and the onset of cancer – specifically bowel cancer . One study even found that men with a high alcohol/low folate lifestyle had a five-fold increase in bowel cancer risk, compared to those who stayed off the sauce and ate more folate-rich foods.

Adding to the pile, researchers in the Netherlands found alterations in methylation at certain DNA regions in bowel cancers taken from patients with a high alcohol and low folate diet. And experiments on rats have shown that acetaldehyde, the byproduct of alcohol, might actually block the methyltransferase enzymes that stick methyl groups onto DNA.

The evidence certainly points towards a role for alcohol in disrupting DNA methylation. But that’s not the only epigenetic mark we know about. There’s also methylation and acetylation of histones – the proteins that package DNA. These modifications act as a ‘code’, telling the cell whether specific genes should be switched on or off. Does alcohol have any impact on these?

So far, the evidence is limited, but Shivendra Shukla and his colleagues have found some initial hints that the histone code may also be disrupted by boozing. For example, rats given “acute in vivo” doses of alcohol (a.k.a. binge drinking) show changes in the pattern of histone methylation in cells in the liver, lungs and spleen. And experiments on liver cells grown in the lab show that alcohol induces changes in histone methylation that in turn cause changes in the patterns of gene activity.

So we know that alcohol can have an impact on epigenetic states, which may be the trigger for cancer. But many people drink – and some of them drink a lot – yet not all of them develop cancer. What’s the explanation?