In summary, a prerequisite for the development of alcoholic pancreatitis would be the specific individual predisposition present in patients with late-onset idiopathic chronic pancreatitis. Furthermore, because the reported prevalence of chronic pancreatitis in patients with heavy alcohol consumption is markedly higher than the prevalence of late-onset idiopathic pancreatitis in the general population, the authors conclude that, in predisposed patients, alcohol consumption promotes the development of pancreatitis and accelerates the manifestation of symptoms and complications. This concept explains the observation that only a minority of severe alcoholics develop chronic pancreatitis. Conversely, in postmortem studies, a substantial proportion of older individuals without premortem evidence of pancreatic disease and no excessive alcohol history have pancreatic morphologic alterations resembling chronic pancreatitis. Thus, in the general population, a considerable number of asymptomatic "carriers," together with an undetected high prevalence of late-onset idiopathic chronic pancreatitis, may exist. In these persons, alcohol consumption might amplify and accelerate preexisting asymptomatic idiopathic pancreatic damage. As a consequence, in a dose-dependent manner, alcohol may lead to an earlier onset of or induce clinically apparent pancreatitis in persons who otherwise might never have had symptoms during their lives.