In addition to what others have mentioned, chronic heavy ethanol consumption engages three different enzymatic pathways to metabolize the ethanol to acetaldehyde and eventually acetate to be oxidized to ATP.

In light or casual drinkers, their stomach contains alcohol dehydrogenase (ADH) which initiates the breakdown of ethanol to acetaldehyde - note that men have more ADH than women which contributes to their naive tolerance of ethanol and eating food allows more time for your stomach ADH to function. "It's not a myth, folks."

After that is where the dose makes the poison. In the liver we use a hepatic isoform of ADH to break down what the stomach could not, but if the hepatic ADH is overwhelmed we use the microsomal ethanol oxidizing system, or MEOS. The MEOS is our 'overdrive' that helps compensate for heavy alcohol consumption but as a result produces a high degree of free radical byproducts that can lead to cell damage in the liver. Over years of consistent MEOS activity and damage you see the cellular dysfunction characteristic of cirrhosis.