Adolescent age moderates genetic and environmental influences on parent-adolescent positivity and negativity: Implications for genotype-environment correlation.
We examined how genotype-environment correlation processes differ as a function of adolescent age. We tested whether adolescent age moderates genetic and environmental influences on positivity and negativity in mother-adolescent and father-adolescent relationships using parallel samples of twin parents from the Twin and Offspring Study in Sweden and twin/sibling adolescents from the Nonshared Environment in Adolescent Development Study. We inferred differences in the role of passive and nonpassive genotype-environment correlation based on biometric moderation findings. The findings indicated that nonpassive gene-environment correlation played a stronger role for positivity in mother- and father-adolescent relationships in families with older adolescents than in families with younger adolescents, and that passive gene-environment correlation played a stronger role for positivity in the mother-adolescent relationship in families with younger adolescents than in families with older adolescents. Implications of these findings for the timing and targeting of interventions on family relationships are discussed.
Adolescent alcohol abuse is associated with adverse outcomes in early adulthood, but differences in familial status and structure and household and community environments correlate with both adolescent drinking and adverse adult outcomes and may explain their association. We studied drinking-discordant twin pairs to evaluate such confounds to ask: Will between-family associations replicate in within-family comparisons?
With longitudinal data from >3,000 Finnish twins, we associated drinking problems at age 18½ with 13 outcomes assessed at age 25; included were sustained substance abuse, poor health, physical symptoms, early coital debut, multiple sexual partners, life dissatisfaction, truncated education, and financial problems. We assessed associations among twins as individuals with linear regression adjusted for correlated observations; within-family analyses of discordant twin pairs followed, comparing paired means for adult outcomes among co-twins discordant for adolescent problem drinking. Defining discordance by extreme scores on self-reported problem drinking at age 18½ permitted parallel analyses of twins as individuals and discordant twin pairs. Alternate definitions of pair-wise discordance and difference score correlations across the entire twin sample yielded supplementary analyses.
All individual associations were highly significant for all definitions of discordance we employed. Depending on definitions of discordance, 11 to 13 comparisons of all drinking-discordant twin pairs and 3 to 6 comparisons of discordant monozygotic (MZ) twin pairs replicated between-family associations. For most outcomes, effect size attenuated from individual-level analysis to that within discordant MZ twin pairs providing evidence of partial confounding in associations reported in earlier research. The exception was the General Health Questionnaire (GHQ); at age 25, GHQ-12 had equivalent associations with age 18½ Rutgers Alcohol Problem Index across all comparisons.
Our analyses control for shared family background, and, partly or fully, for shared genes, to yield within-family replications and more compelling evidence than previously available that adolescent alcohol abuse disrupts transitions into early adulthood.
The aims of the present study were to evaluate the contribution of the genetic and environmental factors to the risk of teenage childbearing, and to study whether life style, socio-economic conditions, and personality traits could explain possible familial effects. We linked two population-based registers: the Swedish Twin Register and the Swedish Medical Birth Register. The study covers female twin pairs born between 1953 and 1958, having their first infant before the age of 30 years (n = 1885). In order to separate familial effects from other environmental influences, and genetic effects from shared environmental effects, only complete twin pairs with known zygosity were included, in all 260 monozygotic and 370 dizygotic twin pairs. We used quantitative genetic analyses to evaluate the importance of genetic and environmental effects for liability to teenage childbearing. Logistic regression analyses were used to estimate the effects of life style, socio-economic situation, and personality on the probability of teenage childbearing, and to study whether psychosocial factors could explain possible familial effects. Fifty-nine percent (0-76%) of the variance in being a teenage mother was attributable to heritable factors; 0% (0-49%) was due to shared environmental factors; and 41% (23-67%) was explained by non-shared environmental factors. Thus, the data were consistent with the hypothesis that the familial aggregation of teenage childbearing is completely explained by genetic factors, although the alternative hypothesis that familial aggregation is entirely explained by shared environmental factors cannot be ruled out. Significant effects of smoking habits, housing conditions, and educational level were found in relation to liability to teenage childbearing. However, the familial effects on risk of teenage childbearing were not mediated through similarities in life style and socio-economic factors. When studying risk factors for teenage childbearing, it is recommended to include life style and socio-economic variables as well as information about family history of teenage childbearing. Twin Research (2000) 3, 23-27.
We analyzed questionnaire survey responses in a cohort of 30,344 twins in Sweden, 280 of whom became inpatients due to neurosis within the subsequent 10 years. As a group, they differed substantially in their reported health profile from the survey responders who were not admitted for psychiatric treatment. When subclassified into anxiety, depressive, and other neuroses, these were indistinguishable from each other regarding self-perceived health and personality traits. Women were more likely to be hospitalized for neurosis. These mental and social antecedents for both anxiety and depression are in keeping with the concept of a shared diathesis which is supported by neurophysiological, treatment and genetic epidemiological studies.
Clinically significant anxiety symptoms are prevalent among the elderly, yet knowledge about the longitudinal course of anxiety symptoms in later life remains scarce. The goals of this study were to (a) characterize age trajectories of state anxiety symptoms in the second half of life, and (b) estimate genetic and environmental contributions to individual differences in the age trajectory of state anxiety. This study was based on data from 1,482 participants in the Swedish Adoption/Twin Study of Aging who were aged 50 and older at their first occasion (512 complete twin pairs, 458 singletons) and had up to 6 measurement occasions spanning 11 years. Consistent with life span developmental theories of age-related emotional change, anxiety symptom levels declined during the transition from midlife to the mid-60s, followed by a mild increase that gradually plateaued in the 80s. There were substantial individual differences in the age trajectory of anxiety. After accounting for effects of sex, cohort, mode of testing, and proximity to death, this longitudinal variation was partitioned into biometric sources. Nonshared environmental variance was highest in the late 60s and declined thereafter, whereas genetic variance increased at an accelerated pace from approximately age 60 onward. There was no evidence for effects of rearing or other shared environment on anxiety symptoms in later life. These findings highlight how the etiology of anxiety symptoms changes from midlife to old age.
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Cites: Twin Res Hum Genet. 2007 Jun;10(3):423-3317564500
Cites: Acta Genet Med Gemellol (Roma). 1991;40(1):7-201950353
It has been suggested that certain health behaviours, such as smoking, may operate as mediators of the well-established inverse association between IQ and mortality risk. Previous research may be afflicted by unadjusted confounding by socioeconomic or psychosocial factors. Twin designs offer a unique possibility to take genetic and shared environmental factors into account. The aim of the present national twin study was to determine the interrelations between IQ at age 18, childhood and attained social factors and smoking status in young adulthood and mid-life. We studied the association between IQ at age 18 and smoking in later life in a population of 11 589 male Swedish twins. IQ was measured at military conscription, and data on smoking and zygosity was obtained from the Swedish Twin Register. Information on social factors was extracted from censuses. Data on smoking was self-reported by the twins at the age of 22-47 years. Logistic regression models estimated with generalised estimating equations were used to explore possible associations between IQ and smoking among the twins as individuals as well as between-and within twin-pairs. A strong inverse association between IQ and smoking status emerged in unmatched analyses over the entire range of IQ distribution. In within-pair and between-pair analyses it transpired that shared environmental factors explained most of the inverse IQ-smoking relationship. In addition, these analyses indicated that non-shared and genetic factors contributed only slightly (and non-significantly) to the IQ-smoking association. Analysis of twin pairs discordant for IQ and smoking status displayed no evidence that non-shared factors contribute substantially to the association. The question of which shared environmental factors might explain the IQ-smoking association is an intriguing one for future research.
Autism spectrum disorders (ASDs) have been suggested to represent the extreme end of a normal distribution of autistic like traits (ALTs). However, the evidence of this notion is inconclusive.
To study whether there are similar genetic and/or environmental etiologies behind ASDs and ALTs.
A nationwide twin study.
Consenting parents of all Swedish twins aged 9 and 12 years, born between July 1, 1992, and December 31, 2001 (n = 19 208), were interviewed by telephone to screen for child psychiatric conditions, including ASDs.
Two validated cutoffs for ASDs, 2 cutoffs encompassing the normal variation, and 1 continuous measure of ALTs were used with DeFries-Fulker extreme-end analyses and standard twin study methods.
We discerned a strong correlation between the 4 cutoffs and the full variation of ALTs. The correlation was primarily affected by genes. We also found that the heritability for the 4 cutoffs was similar.
We demonstrate an etiological similarity between ASDs and ALTs in the normal variation and, with results from previous studies, our data suggest that ASDs and ALTs are etiologically linked.
The present study addresses the issue of differential heritability with increasing severity of parent-reported internalizing and externalizing behavior problems assessed by the Child Behavior Checklist. The sample includes 526 identical and 389 fraternal same-sexed twin pairs from five national birth cohorts, aged 5-6, 8-9, and 12-15 years. Heritability (h2), common environment (c2), and changes in these parameters as a function of proband score were analyzed by multiple regression models (Cherny et al., 1992). Internalizing and externalizing behavior showed significant heritability. A small increment in h2 and a reduction of c2 with increasing severity of externalizing behavior were independent of sex and age. For internalizing behavior h2 increased and c2 declined with increasing severity for the 5-6 and 8-9 year olds. Logarithmic transformation of scores lowered h2 and increased c2, particularly for externalizing behavior. The changes in heritability with severity were nonsignificant for the transformed variables.
We performed a whole-genome expression study to clarify the nature of the biological processes mediating between inherited genetic variations and cognitive dysfunction in schizophrenia.
Gene expression was assayed from peripheral blood mononuclear cells using Illumina Human WG6 v3.0 chips in twins discordant for schizophrenia or bipolar disorder and control twins. After quality control, expression levels of 18,559 genes were screened for association with the California Verbal Learning Test (CVLT) performance, and any memory-related probes were then evaluated for variation by diagnostic status in the discovery sample (N = 190), and in an independent replication sample (N = 73). Heritability of gene expression using the twin design was also assessed.
After Bonferroni correction (p
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Cites: Am J Hum Genet. 2000 Aug;67(2):369-8210880296
In 1975 and again in 1981, all adult twins in the population-based Finnish Twin Cohort were administered postal questionnaires yielding data on self-reported frequency and quantity of alcohol use. The longitudinal results provide information on the age-to-age stability of social drinking patterns among 13,404 (twin) individuals aged 18 to 43 at baseline; model-fitting the cross-temporal consistency of the twins' reported alcohol use yields unique estimates of the contribution of genetic and environmental factors to their individual age-to-age stabilities. Mean consumption levels did not change between 1975 and 1981. Patterns of social drinking were more stable in older (aged 24-43 at baseline) than younger (aged 18-23 at baseline) adult twins, and were more stable among men than women. Heritabilities were significant at both baseline and follow-up for all three alcohol measures in both genders and both age groups, with a median magnitude of 0.48. Both longitudinal genetic and environmental covariances were significant, and both were generally higher among older pairs. Genetic covariances (median magnitude = 0.68) were significantly higher than environmental covariances (median = 0.36). Analyses of absolute changes in alcohol use revealed heritable influences on the disposition to change. We conclude that genes contribute to both consistency and change in patterns of alcohol use from early to midadulthood.
