Sipping, an early form of alcohol initiation, is associated with aspects of psychopathology and personality that reflect long-term risk for harmful alcohol use. In the Adolescent Brain and Cognitive Development cohort (N = 11,872), sipping by age 9–10 was concurrently associated with impulsivity, other aspects of externalizing, and prodromal schizophrenia symptoms. Still, these associations were cross-sectional in nature, leaving open the possibility that these features of psychopathology and personality might not reflect long-term risk for alcohol consumption and related harm across development. Here, we attempted to replicate baseline concurrent associations across three waves of data to extend concurrent associations to prospective ones. Most cross-sectional associations replicated across waves, such that impulsivity, other aspects of externalizing, reward sensitivity (e.g., surgency, sensation seeking), and prodromal schizophrenia symptoms were associated with increased odds of having sipped alcohol by the age of 12. Nevertheless, not all concurrent associations replicated prospectively; impulsigenic features did not reflect long-term risk for sipping. Thus, some psychopathology features appeared to reflect stable risk factors, whereas others appeared to reflect state-dependent risk factors. All told, sipping might not reflect long-term risk for harmful alcohol use, and the nature of sipping may change across development.

Recently, Macgregor et al. (2009) demonstrated significant associations of ADH polymorphisms with reactions to alcohol and alcohol consumption measures in an Australian sample. The aim of the present study was to replicate these findings in a Dutch sample. Survey data on alcohol phenotypes came from 1,754 unrelated individuals registered with the Netherlands Twin Register. SNPs in the ADH gene cluster located on chromosome 4q (n = 491) were subdivided in seven gene sets: ADH5, ADH4, ADH6, ADH1A, ADH1B, ADH1C and ADH7. Within these sets associations of SNPs with alcohol consumption measures, age at onset variables, reactions to alcohol and problem drinking liability were examined. Of the original 38 SNPs studied by Macgregor et al. (2009), six SNPs were not available in our dataset, because one of them had a minor allele frequency < .01 (rs1229984) and five could not be imputed. The remaining SNP associations with alcohol phenotypes as identified by Macgregor et al. (2009) were not replicated in the Dutch sample, after correcting for multiple genotype and phenotype testing. Significant associations were found however, for reactions to alcohol with a SNP in ADH5 (rs6827292, p = .001) and a SNP just upstream of ADH5 (rs6819724, p = .0007) that is in strong LD with rs6827292. Furthermore, an association between age at onset of regular alcohol use and a SNP just upstream of ADH7 (rs2654849, p = .003) was observed. No significant associations were found for alcohol consumption and problem drinking liability. Although these findings do not replicate the earlier findings at the SNP level, the results confirm the role of the ADH gene cluster in alcohol phenotypes.