Several biologic mechanisms have been proposed to explain the observed increased risk of pancreatic cancer related to heavy alcohol consumption. Alcohol may initiate inflammatory responses that result in overt chronic pancreatitis or diabetes mellitus, perhaps via induction of mitogenic stimuli [22, 23]. Alcohol consumption also may lead to asymptomatic chronic pancreatitis that then leads to pancreatic cancer [66–71], although the prevalence of the history of pancreatitis is small in the overall population of pancreatic cancer patients. In addition, oxidative and non-oxidative pancreatic damage due to metabolism of alcohol can initiate inflammatory and fibrotic cascades that may result in subsequent carcinogenesis [22]. Further detailed study of alcohol consumption, including dose, duration, and pattern of exposure, is needed to discern the biologic mechanisms that are important in pancreatic cancer development.
