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Background Mindfulness-based therapies have been shown to be effective in treating depression and reducing cognitive biases. Anxiety sensitivity is one cognitive bias that may play a role in the association between mindfulness and depressive symptoms. It refers to an enhanced sensitivity toward symptoms of anxiety, with a belief that these are harmful. Currently, little is known about the mechanisms underpinning the association between mindfulness, depression, and anxiety sensitivity. The aim of this study was to examine the role of genetic and environmental factors in trait mindfulness, and its genetic and environmental overlap with depressive symptoms and anxiety sensitivity. Methods Over 2,100 16-year-old twins from a population-based study rated their mindfulness, depressive symptoms, and anxiety sensitivity. Results Twin modeling analyses revealed that mindfulness is 32% heritable and 66% due to nonshared environmental factors, with no significant influence of shared environment. Genetic influences explained over half of the moderate phenotypic associations between low mindfulness, depressive symptoms, and anxiety sensitivity. About two-thirds of genetic influences and almost all nonshared environmental influences on mindfulness were independent of depression and anxiety sensitivity. Conclusions This is the first study to show that both genes and environment play an important role in the etiology of mindfulness in adolescence. Future research should identify the specific environmental factors that influence trait mindfulness during development to inform targeted treatment and resilience interventions. Shared genetic liability underpinning the co-occurrence of low mindfulness, depression, and anxiety sensitivity suggests that the biological pathways shared between these traits should also be examined. [ABSTRACT FROM AUTHOR]

Background Separation anxiety disorder ( SAD) and separation anxiety symptoms ( SA) have been studied both epidemiologically and genetically; however, large between-studies discrepancies emerge relative to the role of genetic, shared-, and nonshared environmental influences on these conditions. Methods Based upon available literature, 18 cohorts and 31,859 subjects belonging to twin samples in Europe, the United States, and Australia were included in three meta-analytic estimations of: the standardized variance components of etiological influences on SAD/ SA, and on the effect of sex and rater. Results Meta-analytic estimations carried out on all cohorts showed that within-family (genetic 43% and shared environmental 17%) factors explain most of individual differences for SAD/ SA. Meta-heritability estimates were higher among females (.52) than males (.26), whereas nonshared environmental effects were stronger for the latter (.74) than for the former (.41). When SAD/ SA was rated by parents, the shared environmental influences were higher than those obtained with self-assessment instruments (.23 versus .05), but this may reflect an age difference between subsamples. Conclusions A shared environmental effect is present and important in SAD/ SA. Our results support at an etiological level the involvement of parents in treating SAD/ SA in children, and the provision of specific strategies to parents to manage their own anxiety. Depression and Anxiety 00:1-8, 2012. © 2012 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Background Cognitive biases have long been hypothesized to influence the development and maintenance of symptoms of internalizing problems. Anxiety sensitivity represents one such bias and refers to sensitivity to the physical and emotional symptoms of anxiety and the belief that these are harmful. Twin studies indicate a role for both environmental and genetic influences on anxiety sensitivity. However, little work has been done specifying environments or genes involved in this phenotype. In light of this, we looked at the association between stressful life events, the serotonin transporter gene polymorphism (5HTTLPR), and anxiety sensitivity in a longitudinal sample of adolescents. Methods Stressful life events and anxiety sensitivity were measured in over 1,500 individuals at three time points (mean ages 15, 17, and 20 years). 5HTTLPR was genotyped in 1,109 participants. Results There was consistent evidence for an association between stressful life events and both anxiety sensitivity and change in anxiety sensitivity over time. Although the effect of independent stressful life events was relatively short lived, dependent stressful life events were associated with anxiety sensitivity over time. There was no evidence for a main effect of 5HTTLPR on anxiety sensitivity. 5HTTLPR genotype did not moderate the effect of stressful life events on anxiety sensitivity. Conclusions The current study extends previous work by showing that stressful life events, independent of the individual, explained change in cognitions associated with anxiety and depression. This effect does not, however, appear to be moderated by genotype. [ABSTRACT FROM AUTHOR]