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Background: Studies have shown a correlation between language abilities and alcohol use; however, results are inconsistent. A recent study using a discordant twin design showed an association between early child language development and later alcohol use behaviors; i.e., the twin with more advanced language abilities was more likely to try alcohol earlier in adolescence (Latvala et al., 2014). The authors suggested that this could result from better socialization of individuals with greater language abilities, which could lead to more opportunities for alcohol experimentation. The findings by Latvala et al. raise interesting questions, but the study has limitations, and replication is needed.Method: We aimed to replicate and build upon these results utilizing 488 same sex twin pairs from the Colorado Longitudinal Twin Study, a longitudinal sample with quantitative measures of language abilities starting when the twins were 14 months old.Results: We found no significant correlations between a latent measure of child language abilities or measures of general cognitive ability at ages 14, 20, and 24 months and a latent alcohol use variable at ages 17 and 22 years.Conclusion: Our results did not replicate the association between early language ability and later alcohol use reported by Latvala et al. Possible reasons for differing results across samples, including varying cultural norms as well as differences in educational attainment, peer influences, and novelty seeking, were discussed. [ABSTRACT FROM AUTHOR]

Social processes are associated with depression, particularly understanding and responding to others, deficits in which can manifest as callousness/unemotionality (CU). Thus, CU may reflect some of the genetic risk to depression. Further, this vulnerability likely reflects the neurological substrates of depression, presenting biomarkers to capture genetic vulnerability of depression severity. However, heritability varies within brain regions, so a high-resolution genetic perspective is needed. We developed a toolbox that maps genetic and environmental associations between brain and behavior at high resolution. We used this toolbox to estimate brain areas that are genetically associated with both depressive symptoms and CU in a sample of 258 same-sex twin pairs from the Colorado Longitudinal Twin Study (LTS). We then overlapped the two maps to generate coordinates that allow for tests of downstream effects of genes influencing our clusters. Genetic variance influencing cortical thickness in the right dorsal lateral prefrontal cortex (DLFPC) sulci and gyri, ventral posterior cingulate cortex (PCC), pre-somatic motor cortex (PreSMA), medial precuneus, left occipital-temporal junction (OTJ), parietal-temporal junction (PTJ), ventral somatosensory cortex (vSMA), and medial and lateral precuneus were genetically associated with both depression and CU. Split-half replication found support for both DLPFC clusters. Meta-analytic term search identified "theory of mind", "inhibit", and "pain" as likely functions. Gene and transcript mapping/enrichment analyses implicated calcium channels. CU reflects genetic vulnerability to depression that likely involves executive and social functioning in a distributed process across the cortex. This approach works to unify neuroimaging, neuroinformatics, and genetics to discover pathways to psychiatric vulnerability.