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.
The nature of the association between body height and educational attainment found in previous studies remains to be clarified. The aim of this study was to examine factors contributing to this association by using a large Finnish twin data set (8798 adult twin pairs) gathered by questionnaire in 1981. A bivariate twin analysis was used to determine whether the genetic and environmental factors behind body height and educational attainment correlate with each other. A high heritability was found for body height (h2 = 0.78 in men and h2 = 0.75 in women), and a moderate heritability for education (h2 = 0.47 and h2 = 0.43, respectively). Shared environmental effects were also important in body height (c2 = 0.12 in men and c2 = 0.11 in women) and education (c2 = 0.36 and c2 = 0.43, respectively). A high correlation (r(c) = 0.77 in men, r(c) = 0.58 in women) of shared environmental factors education and body height, and weaker correlations (r = 0.11 and r = 0.08, respectively) of unshared environmental factors were found. The correlation of genetic factors between these two characteristics was not statistically significant. The results suggest that the association between body height and education is due mainly to nongenetic family factors.
Leptin is involved in the regulation of body weight, but the relative role of genetic and environmental influences on inter-individual variation in leptin levels is unknown.
To investigate the genetic and environmental contributions to the association of body mass index (BMI) with serum leptin levels, 58 monozygotic (MZ, 27M, 31F), and 74 like-sexed dizygotic (DZ, 32M, 42F) Finnish twin pairs aged 50--76 y were studied.
Serum leptin levels, weight, height, hip and waist measurements.
Women had higher mean leptin levels (16.8+/-9.5 ng/ml), and more overall variability in leptin levels than men (6.4+/-3.5 ng/ml; P
Molecular epidemiological studies confirm a substantial contribution of individual genes to variability in susceptibility to disease and death for humans. To evaluate the contribution of all genes to susceptibility and to estimate individual survival characteristics, survival data on related individuals (eg twins or other relatives) are needed. Correlated gamma-frailty models of bivariate survival are used in a joint analysis of survival data on more than 31,000 pairs of Danish, Swedish and Finnish male and female twins using the maximum likelihood method. Additive decomposition of frailty into genetic and environmental components is used to estimate heritability in frailty. The estimate of the standard deviation of frailty from the pooled data is about 1.5. The hypothesis that variance in frailty and correlations of frailty for twins are similar in the data from all three countries is accepted. The estimate of narrow-sense heritability in frailty is about 0.5. The age trajectories of individual hazards are evaluated for all three populations of twins and both sexes. The results of our analysis confirm the presence of genetic influences on individual frailty and longevity. They also suggest that the mechanism of these genetic influences may be similar for the three Scandinavian countries. Furthermore, results indicate that the increase in individual hazard with age is more rapid than predicted by traditional demographic life tables.
This study examined the stability and change over time in genetic and environmental influences on walking ability among older women. Maximal walking speed over 10 m and 6-min walking endurance test were measured under standard conditions at baseline and 3 years later. At both times, 63 monozygotic (MZ) and 67 dizygotic (DZ) twin pairs were measured for walking speed and 58 MZ and 56 DZ pairs for walking endurance. Participants were twin sisters reared together and aged 63-75 years at baseline. Genetic and environmental influences were examined using longitudinal genetic modelling. The results showed that walking speed was preserved from baseline to follow-up. Genetic influences on walking speed were also similar at baseline (56%) and follow-up (60%). Walking endurance declined from baseline to follow-up, while genetic influences for walking endurance increased from baseline (40%) to follow-up (60%). Most of the genetic influences identified at baseline were also present at follow-up for walking speed (r(g)=0.72) and endurance (r(g)=0.71). In conclusion, among relatively healthy older women, genetic influences on walking speed and endurance were moderate at baseline, while at 3-year follow-up a moderate increment was observed in walking endurance. Newly expressed genetic influences were recognized at follow-up.
Sleeptalking is usually benign but chronic cases in adults may relate to psychopathology. We hypothesize substantial genetic influences in the liability to sleeptalking and an association between sleeptalking and psychiatric disorders. In 1990 a questionnaire sent to the Finnish Twin Cohort yielded responses from 1298 monozygotic and 2419 dizygotic twin pairs aged 33-60 years. We used structural equation modelling to estimate genetic and environmental components of variance in the liability to sleeptalking. Register data on hospitalization and long-term antipsychotic medication were used to assess psychiatric comorbidity. The occurrence of childhood and adult sleeptalking was highly correlated. A gender difference was only seen in adults, with sleeptalking being more common in males than in females. The proportion of total phenotypic variance in liability to sleeptalking attributed to genetic influences in childhood sleeptalking was 54% (95% CI, 44-62%) in males and 51% (43-58%) in females, and for adults it was 37% (27-46%) among males and 48% (40-56%) among females. An association with psychiatric comorbidity was found only in adult sleeptalking, and it was highest in those with adult-onset sleeptalking (odds ratio, 3.77; 95% CI, 2.32-6.17). Sleeptalking is quite a persistent trait, also being common in adults. There are substantial genetic effects on sleeptalking both in childhood and as adults, which appear to be highly correlated. In adults psychiatric comorbidity is about twice as common in those with frequent sleeptalking, compared to those with infrequent or no sleeptalking, but most cases of sleeptalking are not associated with serious psychopathology.