Alcohol consumption has been shown to be consistently associated with an increased risk of pancreatitis, and plausible biological mechanisms have been identified for the effect [see [171]]. In particular, the metabolites of alcohol, such as acetaldehyde and fatty acid ethyl esters, may initiate and/or enhance pancreatic injury. Alcohol may also attenuate or augment inflammatory cell activation, leading to fibrosis in the pancreas [38;172-175]. All these mechanisms come into place especially with heavy consumption. Thus, the meta-analysis of Irving and colleagues cited above found that, compared with non-drinkers, alcohol consumption of two or fewer drinks per day (<= 24 g pure alcohol/day) was almost identical to the risk of non-drinkers (RR=1.0, 95% CI: 0.8-1.2; P=0.887). Drinking 3 to 4 drinks was associated with only marginally significant higher risk than for abstention (RR=1.2, 95% CI: 1.0-1.5, P=0.059), but overall the dose-response relationship increased monotonically (see Table 3).
