The associated clinical information provided by the NSWBTRC is important for analysis of the phenotypic characteristics and determining whether detected differences reflect susceptibility to, or are consequences of, alcohol use. Having toxicology reports at time of death potentially allows attribution of pathology to alcohol-induced neuroadaptations or exposure effects. In terms of covariates, the NSWBTRC alcohol research cohorts are developed to only include cases that do not have a history of illicit drug abuse, apart from tobacco smoking. It is estimated that 80% of alcoholics smoke tobacco, and neuroimaging (Durazzo et al., 2014) and animal studies (Tong et al., 2015) suggest that tobacco smoke has additive or synergistic effects with alcohol on alcohol-related brain disorders (ARBD). However, in a recent pathological study, all the atrophy seen in ARBD, and largely in white matter, was centrally attributable to alcohol (McCorkindale et al., under review). The consideration of smoking status and volume is a relatively recent trend in alcohol research, with most research to date comparing cases with high levels of alcohol abuse, or specific organ damage (e.g., cirrhosis), to normal controls. Our
