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 aim of this study was to examine the effects of genetic and environment influences and sex on injury involvement using two sets of Finnish twin data. The younger participants were 955 twins born between 1983 and 1987, aged 20 to 24 years. The older participants were 12,428 twins born between 1930 and 1957, aged 33 to 60 years. Within-twin correlations in monozygotic and dizygotic twins suggested that genetic effects play no role in injury involvement among young twins, but do have some effect at older ages. The results indicated that environmental factors have greater importance in injury involvement than genetic factors in the younger twin data set (FT12), whereas in a middle-aged (33-60 years) twin data set, genetic effects explained about quarter of the variance in injury involvement. Sex was a strong contributing factor, with males being generally more prone to injuries than females.
Overweight in children and adolescents has reached dimensions of a global epidemic during recent years. Simultaneously, information and communication technology use has rapidly increased.
A population-based sample of Finnish twins born in 1983-1987 (N = 4098) was assessed by self-report questionnaires at 17 y during 2000-2005. The association of overweight (defined by Cole's BMI-for-age cut-offs) with computer and cell phone use and ownership was analyzed by logistic regression and their association with BMI by linear regression models. The effect of twinship was taken into account by correcting for clustered sampling of families. All models were adjusted for gender, physical exercise, and parents' education and occupational class.
The proportion of adolescents who did not have a computer at home decreased from 18% to 8% from 2000 to 2005. Compared to them, having a home computer (without an Internet connection) was associated with a higher risk of overweight (odds ratio 2.3, 95% CI 1.4 to 3.8) and BMI (beta coefficient 0.57, 95% CI 0.15 to 0.98). However, having a computer with an Internet connection was not associated with weight status. Belonging to the highest quintile (OR 1.8 95% CI 1.2 to 2.8) and second-highest quintile (OR 1.6 95% CI 1.1 to 2.4) of weekly computer use was positively associated with overweight. The proportion of adolescents without a personal cell phone decreased from 12% to 1% across 2000 to 2005. There was a positive linear trend of increasing monthly phone bill with BMI (beta 0.18, 95% CI 0.06 to 0.30), but the association of a cell phone bill with overweight was very weak.
Time spent using a home computer was associated with an increased risk of overweight. Cell phone use correlated weakly with BMI. Increasing use of information and communication technology may be related to the obesity epidemic among adolescents.
Little is known about the associations of serum fatty acids with lipoprotein profile and the underlying genetic and environmental etiology of these relationships. We aimed to analyze the phenotypic association of serum n-6 and n-3 polyunsaturated (PUFAs), monounsaturated (MUFAs) and saturated (SFAs) fatty acids (relative proportion to total fatty acids) with lipids and lipoproteins, and to quantify common genetic and environmental factors determining their covariation.
Two cohorts of healthy Finnish twins were assessed in young adulthood. Data were available for 1269 individual twins including 561 complete pairs. Serum metabolites were measured by nuclear magnetic resonance spectroscopy. Bivariate quantitative genetic models were used to decompose the phenotypic covariance between the pairs of traits into genetic and environmental components.
Among the strongest correlations observed, serum total n-6 PUFAs and linoleic acid were inversely (max. r=-0.65) and MUFAs positively (max. r=0.63) correlated with triglycerides and very low-density lipoprotein (VLDL) particle concentration, particularly with large VLDL (for n-6 PUFAs) and medium VLDL (for MUFAs). Genetic factors significantly contributed to their covariance with bivariate heritability estimates ranging from 44% to 56% for n-6 PUFAs and 58% to 66% for MUFAs. Genetic correlations with lipid traits were moderate to high (max. rA=-0.59 and 0.70 for n-6 PUFAs and MUFAs, respectively). Statistically significant, but substantially weaker phenotypic correlations of total n-3 PUFAs, docosahexaenoic acid (DHA) and SFAs with lipoprotein profile were not decomposed into their genetic and environmental components.
Shared genetic factors are important in explaining why higher concentrations of serum n-6 PUFAs and lower concentrations of serum MUFAs strongly associate with lower triglyceride and VLDL particle concentrations.
Little is known about the relationship between growth and lipoprotein profile. We aimed to analyze common genetic and environmental factors in the association of height from late childhood to adulthood and pubertal timing with serum lipid and lipoprotein subclass profile.
A longitudinal cohort of Finnish twin pairs (FinnTwin12) was analyzed using self-reported height at 11-12, 14, 17 years and measured stature at adult age (21-24 years). Data were available for 719 individual twins including 298 complete pairs. Serum lipids and lipoprotein subclasses were measured by proton nuclear magnetic resonance spectroscopy. Multivariate variance component models for twin data were fitted. Cholesky decomposition was used to partition the phenotypic covariation among traits into additive genetic and unique environmental correlations.
In men, the strongest associations for both adult height and puberty were observed with total cholesterol, low-density lipoprotein cholesterol, intermediate-density lipoprotein cholesterol, and low-density lipoprotein particle subclasses (max. r = -0.19). In women, the magnitude of the correlations was weaker (max. r = -0.13). Few associations were detected between height during adolescence and adult lipid profile. Early onset of puberty was related to an adverse lipid profile, but delayed pubertal development in girls was associated with an unfavorable profile, as well. All associations were mediated mainly by additive genetic factors, but unique environmental effects cannot be disregarded.
Early puberty and shorter adult height relate to higher concentrations of atherogenic lipids and lipoprotein particles in early adulthood. Common genetic effects behind these phenotypes substantially contribute to the observed associations.
The genetic component of alcohol use disorder is substantial, but monozygotic twin discordance indicates a role for nonheritable differences that could be mediated by epigenetics. Despite growing evidence associating epigenetics and psychiatric disorders, it is unclear how epigenetics, particularly DNA methylation, relate to brain function and behavior, including drinking behavior.
The authors carried out a genome-wide analysis of DNA methylation of 18 monozygotic twin pairs discordant for alcohol use disorder and validated differentially methylated regions. After validation, the authors characterized these differentially methylated regions using personality trait assessment and functional MRI in a sample of 499 adolescents.
Hypermethylation in the 3'-protein-phosphatase-1G (PPM1G) gene locus was associated with alcohol use disorder. The authors found association of PPM1G hypermethylation with early escalation of alcohol use and increased impulsiveness. They also observed association of PPM1G hypermethylation with increased blood-oxygen-level-dependent response in the right subthalamic nucleus during an impulsiveness task.
Overall, the authors provide first evidence for an epigenetic marker associated with alcohol consumption and its underlying neurobehavioral phenotype.
Comment In: Am J Psychiatry. 2015 Jun;172(6):499-50125982661
We analyzed prevalence and stability of attitudes endorsing sexual abstinence ideals from late adolescence into early adulthood and studied associations of these attitudes with religiosity and alcohol abstinence in a sexually liberal Nordic society. Our population-based sample of Finnish twins permitted comparisons of co-twins concordant for religiosity but discordant for drinking to evaluate the association of sexual abstinence ideals with alcohol abstinence, controlling for household environment. From age 17 to 24, endorsement of sexual abstinence as a romantic ideal declined from 25% to 15%. Religiosity and alcohol abstinence correlated, both separately and together, with endorsing sexual abstinence. Abstinence ideals were associated with literal belief in fundamental tenets of the Bible. The association of sexual abstinence ideals with alcohol abstinence was confirmed in within-family comparisons of co-twins discordant for drinking but concordant for religiosity. Alcohol-abstinent twins were significantly more likely than their non-alcohol-abstinent twin siblings to endorse sexual abstinence ideals; that result suggests the association of sexual abstinence ideals with abstaining from alcohol is not explained by unmeasured confounds in familial background and structure. Our longitudinal results and analyses of discordant twins suggest that attitudes toward sexual abstinence ideals are embedded within other conservative attitudes and behaviors.
Assortative mating by body height and weight is well established in various populations, but its causal mechanisms remain poorly understood. We analyzed the effect of phenotypic assortment and social homogamy on spousal correlations for body height and body mass index (BMI, kg/m(2)). Our data derived from a questionnaire administered to the adult Finnish Twin Cohort in 1990 (response rate 77%) yielding results from 922 monozygotic and 1697 dizygotic adult twin pairs who reported information about their body height and weight and that of their spouses. Assortative mating was evident for body height and BMI. For body height, the effects of social homogamy (0.24 in men and 0.29 in women) and phenotypic assortment (0.27 and 0.28, respectively) were about the same. For BMI, the effect of social homogamy was stronger (0.31 in men and 0.28 in women) than the effect of phenotypic assortment (0.13 in both men and women). When assortative mating was taken into account, shared environmental factors had no effect on phenotypic variation in body height or BMI. Our results show that assortative mating needs to be considered in population genetic studies of body height and weight.
We explored correlates of the Eating Disorder Inventory subscales Body Dissatisfaction (BD) and Drive for Thinness (DT) and genetic and environmental influences on these traits.
In a population-based sample of 4,667 Finnish twins aged 22-27 years, we conducted twin modeling to explore genetic and environmental contributions to body dissatisfaction and drive for thinness. Logistic regression was used for the correlational analysis.
Various eating and body size-related factors and psychosomatic symptoms were significantly associated with high body dissatisfaction and drive for thinness in both genders. In women, early puberty onset, early initiation of sexual activity, and multiple sex partners were statistically significant risk factors of body dissatisfaction. In gender-specific univariate twin models, additive genes accounted for 59.4% (95% confidence interval [CI] = 53.2-64.7%) of the variance in body dissatisfaction and for 51.0% (95% CI = 43.7-57.5%) of the variance in drive for thinness among females, but for none of the variance among males.
There are very distinct gender differences in the heritability patterns of body dissatisfaction and drive for thinness in young adults.
In contrast to many phenotypes that have been studied using twin designs, substance use shows considerable evidence of environmental influence. Accordingly, specifying the relevant environments and understanding the nature of their effects is an important research priority. Twin studies also have demonstrated that the importance of genetic and environmental influences varies across development for a variety of behavioral outcomes, including substance use. Here, we report analyses exploring moderating effects associated with parenting and peer characteristics on adolescent smoking and drinking, measured at ages 14 and 17. We find significant evidence of moderating effects associated with two dimensions of parenting (parental monitoring and time spent in activities with parents) on adolescent smoking, measured at two time points across development, but no moderating effects on adolescent drinking. Genetic influences on smoking increased, and common environmental effects decreased, as adolescents reported less parental monitoring and spending more time with their parents. Conversely, we find evidence that adolescent drinking is more strongly influenced by peer characteristics. The importance of genetic predispositions was increased among adolescents who reported more friends who used alcohol. These analyses illustrate the importance of incorporating measured aspects of the environment into genetically informative twin models to begin to understand how specific environments are related to various outcomes. Furthermore, they illustrate the importance of using a developmental perspective to understand how specific influences may vary across different ages, and across different phenotypes.