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Background: Anxiety in parents is associated with anxiety in offspring, although little is known about the mechanisms underpinning these intergenerational associations. We conducted the first genetically sensitive study to simultaneously examine the effects of mother, father and child anxiety symptoms on each other over time. Method: Adoptive parent and child symptoms were measured at child ages 6, 7 and 8 years from 305 families involved in the Early Growth and Development Study, using a prospective adoption design. Children were adopted at birth to non-relatives and composite data on internalising problems within birth families were used as a proxy measure of offspring inherited risk for anxiety. Structural equation models were fitted to the data to examine prospective associations between adoptive mother, father and child symptoms, whilst accounting for individuals’ symptom stability over time. Results: Child anxiety symptoms at age 7 predicted adoptive mothers’ anxiety symptoms at age 8. No mother-to-child or child-to-father effects were observed. These results were consistent in sensitivity analyses using only paternal offspring reports and using a second measure of child anxiety symptoms. Fathers’ anxiety symptoms at child age 6 prospectively predicted child symptoms, but only when paternal offspring reports were included in the model. Composite data on birth family internalising problems were not associated with child anxiety symptoms. Conclusions: Results show environmentally mediated associations between parent and child anxiety symptoms. Results support developmental theories suggesting that child anxiety symptoms can exert influence on caregivers, and mothers and fathers may play unique roles during the development of child symptoms. Further research is needed on the role of genetic transmission associated with anxiety symptoms in biologically related families. In the meantime, researchers and clinicians should strive to include fathers in assessments and consider the effects of child symptoms on caregivers.
1Depression is more frequent among individuals exposed to traumatic events. 2 Both trauma exposure and depression are heritable. However, the relationship 3 between these traits, including the role of genetic risk factors, is complex and poorly 4 understood. When modelling trauma exposure as an environmental influence on 5 depression, both gene-environment correlations and gene-environment interactions 6 have been observed. The UK Biobank concurrently assessed Major Depressive 7 Disorder (MDD) and self-reported lifetime exposure to traumatic events in 126,522 8 genotyped individuals of European ancestry. We contrasted genetic influences on 9 MDD between individuals reporting and not reporting trauma exposure (final sample 10 size range: 24,094-92,957). The SNP-based heritability of MDD was greater in 11 participants reporting trauma exposure (24%) than in individuals not reporting trauma 12 exposure (12%), taking into account the strong, positive genetic correlation observed 13 between MDD and reported trauma exposure. The genetic correlation between MDD 14and waist circumference was only significant in individuals reporting trauma 15 exposure (r g = 0.24, p = 1.8x10-7 versus r g = -0.05, p = 0.39 in individuals not 16 reporting trauma exposure, difference p = 2.3x10 -4 ). Our results suggest that the 17 genetic contribution to MDD is greater when additional risk factors are present, and 18 that a complex relationship exists between reported trauma exposure, body 19 composition, and MDD. 20 21
Twin studies have shown that emotional problems (anxiety and depression) in childhood and adolescence are moderately heritable (~20–50%). In contrast, DNA-based ‘SNP heritability’ estimates are generally <15% and non-significant. One notable feature of emotional problems is that they can be somewhat transient, but the moderate stability seen across time and across raters is predominantly influenced by stable genetic influences. This suggests that by capturing what is in common across time and across raters, we might be more likely to tap into any underlying genetic vulnerability. We therefore hypothesised that a phenotype capturing the pervasive stability of emotional problems would show higher heritability. We fitted single-factor latent trait models using 12 emotional problems measures across ages 7, 12 and 16, rated by parents, teachers and children themselves in the Twins Early Development Study sample. Twin and SNP heritability estimates for stable emotional problems (N = 6110 pairs and 6110 unrelated individuals, respectively) were compared to those for individual measures. Twin heritability increased from 45% on average for individual measures to 76% (se = 0.023) by focusing on stable trait variance. SNP heritability rose from 5% on average (n.s.) to 14% (se = 0.049; p = 0.002). Heritability was also higher for stable within-rater composites. Polygenic scores for both adult anxiety and depression significantly explained variance in stable emotional problems (0.4%; p = 0.0001). The variance explained was more than in most individual measures. Stable emotional problems also showed significant genetic correlation with adult depression and anxiety (average = 52%). These results demonstrate the value of examining stable emotional problems in gene-finding and prediction studies.
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