The metabolic pathways for ethanol and fructose (sugar is half fructose) both produce acetaldehydes - but I'd thought that they stayed local to the liver. They *start* there so concentrations will be higher there. The liver's a remarkable organ - the only one that can regrow after damage. Might *that* be why there isn't an associated rise in liver cancer - or is there one? The correlation is there; could it be as simple as spikes in either glucose or insulin coupled with cellular damage from direct contact with ethanol?

Also a semi-non drinker, so I've no particular 'skin' in this game.