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Daniel Smith

Publications and source records attributed to Daniel Smith.

3 recordsLinked to original sources

Subcortical volume and white matter integrity abnormalities in major depressive disorder: findings from UK Biobank (N=4446)

BackgroundPrevious reports of altered grey and white matter structure in Major Depressive Disorder (MDD) have been inconsistent. Recent meta-analyses have, however, reported reduced hippocampal grey matter volume in MDD and reduced white matter integrity in several brain regions. The use of different diagnostic criteria, different scanners and imaging sequences may, however, obscure further anatomical differences.\n\nMethodsIn this study, we tested for differences in subcortical grey matter volume and white matter integrity between depressed individuals and controls in a large sample of subjects from the first data release of the UK Biobank imaging study of 4446 individuals, which used consistent diagnostic criteria at a single assessment centre, with a single MRI scanner and protocol.\n\nResultsWhilst we found no significant differences in subcortical volumes, we report significant reductions in depressed individuals versus controls in global white matter integrity, as measured by fractional anisotropy (FA) ({beta} = -0.187, p = 0.017). We also report reductions in FA in association/commissural fibres ({beta} = -0.184, p = 0.019) and thalamic radiations ({beta} = -0.175, p = 0.027). Examining tracts individually, we report tract-specific FA reductions in the left superior longitudinal fasciculus ({beta} = -0.218, pcorrected = 0.012) and superior thalamic radiation ({beta} = -0.258, pcorrected = 0.010) in subjects with depression.\n\nConclusionsOur findings highlight the need for further large adequately-powered studies of depression and provide further evidence for disrupted white matter integrity in the disorder. Future studies would focus on exploring the typical neuro-phenotype in homogenous subgroups of depression.

Neuroscience

High-resolution maps of hunter-gatherer social networks reveal human adaptation for cultural exchange

Are interactions with unrelated and even unknown individuals a by-product of modern life in megacities? Here we argue instead that social ties among non-kin are a crucial human adaptation. By deploying a new portable wireless sensing technology (motes), we mapped social networks in Agta and BaYaka hunter-gatherers in unprecedented detail. We show that strong friendships with non-kin optimize the global efficiency of their social networks thereby facilitating cultural exchange, and that the adaptation for forming friendship ties appears early in development. The ability to extend networks and form strong non-kin ties may explain some human distinctive characteristics such as hypersociality and cumulative culture, and the tendency to exchange ideas with unrelated and unknown individuals in megacities and online social networks.\n\nOne Sentence SummarySocial networks of two hunter-gatherer groups in Congo and the Philippines reveal that friendships are an ancestral adaptation for the exchange of information and culture.

Evolutionary Biology

Genetic and environmental risk for chronic pain and the contribution of risk variants for psychiatric disorders. Results from Generation Scotland: Scottish Family Health Study and UK Biobank

BackgroundChronic pain is highly prevalent worldwide and a significant source of disability, yet its genetic and environmental risk factors are poorly understood. Its relationship with psychiatric illness, and major depressive disorder (MDD) in particular, is of particular importance. We sought to test the contribution of genetic factors and shared and unique environment to risk of chronic pain and its correlation with MDD in Generation Scotland: Scottish Family Health Study (GS:SFHS). We then sought to replicate any significant findings in the UK Biobank study.\n\nMethodsUsing family-based mixed-model analyses, we examined the contribution of genetics and environment to chronic pain using spouse, sibling and household groups as measures of shared environment. We then examined the correlation between chronic pain and MDD and estimated the contribution of genetic factors and shared environment. Finally, we used data from two independent genome-wide association studies to test whether chronic pain has a polygenic risk architecture and examine whether genomic risk of psychiatric disorder predicted chronic pain and whether genomic risk of chronic pain predicted MDD.\n\nResultsChronic pain is a moderately heritable trait (narrow sense heritability = 38.4%) which is more likely to be concordant in spouses and partners (variance explained 18.7%). Chronic pain is positively correlated with depression (rho = 0.13, p = 2.72x10-68) and it shows a tendency to cluster within families for genetic reasons (genetic correlation rho = 0.51, p = 8.24x10-19). Polygenic risk profiles for pain, generated using independent GWAS data, predicted chronic pain in both GS:SFHS (maximum {beta} = 6.18x10-2, p = 4.3x10-4) and UK Biobank (maximum {beta} = 5.68 x 10-2, p < 3x10-4). Genomic risk of MDD is also significantly associated with chronic pain in both GS:SFHS (maximum {beta} = 6.62x10-2, p = 4.3x10-4) and UK Biobank (maximum {beta} = 2.56x10-2, p < 3x10-4).\n\nConclusionsGenetic factors and chronic pain in a partner or spouse contribute substantially to the risk of chronic pain in the general population. Chronic pain is genetically correlated with MDD, has a polygenic architecture and is predicted by polygenic risk of MDD.

Genomics