Metabolic syndrome (MS) is a clustering of cardiometabolic risk factors that is considered a predictor of cardiovascular disease, type 2 diabetes and mortality. There is no consistent evidence on whether the MS construct works in the same way in different populations and at different stages in life. We used confirmatory factor analysis to examine if a single-factor-model including waist circumference, triglycerides/HDL-c, insulin and mean arterial pressure underlies metabolic syndrome from the childhood to adolescence in a 6-years follow-up study in 174 Swedish and 460 Estonian children aged 9 years at baseline. Indeed, we analyze the tracking of a previously validated MS index over this 6-years period. The estimates of goodness-of-fit for the single-factor-model underlying MS were acceptable both in children and adolescents. The construct stability of a new model including the differences from baseline to the end of the follow-up in the components of the proposed model displayed good fit indexes for the change, supporting the hypothesis of a single factor underlying MS component trends. A single-factor-model underlying MS is stable across the puberty in both Estonian and Swedish young people. The MS index tracks acceptably from childhood to adolescence.
Major psychiatric disorders including alcohol use disorder are considered multigenic and the smallness of effects of individual genes may be attributed to either complex biological mechanisms or geneenvironment interactions. The latter explanation is highlighted by the relatively fast changes in secular trends and in cohort effects on alcohol use disorder. Interactions of candidate gene variants with birth cohort have been found in the Estonian Children Personality Behaviour and Health Study, a longitudinal investigation from 1998 with a sample highly representative of birth cohorts within a region. Such interactions regarding initiation of alcohol use or alcohol use disorder have been revealed for e.g., 5-HTTLPR, VMAT1, OXR and NRG1, and suggest that rapid alterations in the socioeconomic environment promote changes in the genetic vulnerability to environmental risks factors such as alcohol.
Suicide is complex phenomenon with multiple causes and underlying processes which is an equally great challenge for contemporary science and our society in general. Several models have been proposed to explain suicide and several studies aimed at delineating the factors and processes playing a role in its background. The most wellknown and widely accepted risk factors of suicidal behaviour deal mainly with psychological and socioeconomic factors, however, we know less about the biological, neurochemical and genetic correlates and contributors of suicidality. Suicidality has been associated with impulsive aggression, and the majority of suicides are committed by depressive patients. Recently an increasing number of studies point to an association between certain types of suicidal behaviour. The suggestion that conflicting results may be due to inhomogenous suicidal samples indicates that different phenotypes of suicides may have profoundly different underlying factors e ven on the biochemical and genetic level. Research shows that the s allele of the 5-HTTLPR is associated with violent completed suicides. This polymorphism has also been related to affective disorders, however, evidence supports that the association between suicide and the s allele is independent of the association between the 5-HTTLPR and depression. The s allele is also associated with several traits, such as impulsive aggression, hopelessness and affective temperaments, which may serve as important endophenotypes in delineating the genetic background of different types of suicidal behaviour. Expanding our knowledge and understanding of the role of the serotonergic system in suicidal behaviour may lead to better recognition of suicide and of the prodromal symptoms of suicidal behaviour and may also play an important role in developing drugs with a potential to reduce suicidality.
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