Commentaries: on Lea Pulkkinen's "Longitudinal Study and School Reform"Developmental Research as Impetus for School Reform
In: European psychologist, Band 9, Heft 3, S. 143-144
ISSN: 1878-531X
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In: European psychologist, Band 9, Heft 3, S. 143-144
ISSN: 1878-531X
In: European psychologist, Band 12, Heft 3, S. 240-241
ISSN: 1878-531X
In: Twin research and human genetics: the official journal of the International Society for Twin Studies (ISTS) and the Human Genetics Society of Australasia, Band 19, Heft 2, S. 163-165
ISSN: 1839-2628
We offer a brief sketch of an overlooked early twin researcher, Arvo Johannes Lehtovaara (1905–1985), Professor of Psychology at the University of Jyväskylä, 1939–1952, and the University of Helsinki, 1952–1970, with background notes on his mentor, Eino Kaila.
In: The Journal of sex research, Band 51, Heft 2, S. 197-207
ISSN: 1559-8519
In: Twin research, Band 5, Heft 5, S. 366-371
ISSN: 2053-6003
In: Twin research, Band 2, Heft 4, S. 274-285
ISSN: 2053-6003
In: Twin research and human genetics: the official journal of the International Society for Twin Studies (ISTS) and the Human Genetics Society of Australasia, Band 10, Heft 1, S. 25-32
ISSN: 1839-2628
AbstractWe enrolled more than 3500 same-sex twins from 5 consecutive Finnish birth cohorts into a longitudinal study as each cohort reached age 16. Twins completed the Psychopathic Deviate (Pd) Scale of the Minnesota Multiphasic Personality Inventory at baseline, Sensation Seeking Scale items as each cohort reached age 17, and later, at average ages 18.5 and 25, the Rutgers Alcohol Problem Index (RAPI). Using raw maximum likelihood estimation, we fit a Cholesky model to the 4 variables assessed at 4 ages across the 4 twin types; we estimated genetic and environmental influences on the stability of alcohol problems across development and the genetic and environmental contributions to predictive correlations between adolescent personality and later alcohol-related behavior problems. With one exception, the phenotypic, genetic, and environmental correlations were very similar for males and females. The exception was that the lagged associations of Pd and RAPI reflect a higher genetic correlation among males than females and a higher environmental correlation among females than males. Our analyses suggest that developmental changes underlying variation in alcohol problems from late adolescence to early adulthood differ for males and females. In males, the main change is decreased variation due to shared environmental effects; the magnitude of genetic effects is stable over time, and the high genetic correlation, .95, suggests that the same genetic influences are important at both ages. Among females, in contrast, genetic influences decline in magnitude from age 18 to 25, and at least part of the genetic effect evident at age 25 differs from the genetic effect evident at age 18.
In: Twin research and human genetics: the official journal of the International Society for Twin Studies (ISTS) and the Human Genetics Society of Australasia, Band 21, Heft 6, S. 502-506
ISSN: 1839-2628
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.
In: Twin research, Band 7, Heft 3, S. 261-274
ISSN: 2053-6003
In: Twin research and human genetics: the official journal of the International Society for Twin Studies (ISTS) and the Human Genetics Society of Australasia, Band 12, Heft 3, S. 261-268
ISSN: 1839-2628
AbstractWe investigated prospectively whether physical activity level in adolescence predicts use of alcohol and illicit drugs in early adulthood. We studied 4,240 individual twins (1,870 twin pairs). We classified those who consistently reported frequent leisure physical activity at ages 16, 17 and 181/2 as persistent exercisers, those exercising less than three times monthly as persistently inactive, and all others as occasional exercisers. To control for familial confounds, within-family analyses compared activity-substance use associations in co-twins discordant for baseline physical activity. Individual-based analyses showed no clear association between baseline physical activity and subsequent weekly alcohol consumption. However, weekly alcohol intoxication (OR = 1.9,p= .002) and problems due to alcohol use (OR = 2.0,p< .001) were more common among persistently inactive participants. After excluding those reporting weekly intoxication at baseline, the risk for alcohol intoxication remained elevated among women occasionally (OR = 2.4,p= .017) or persistently (OR = 5.8,p< .001) inactive at baseline, but this association was not replicated within discordant twin pairs. Individual-based analyses showed that drug use in adulthood was more common among those persistently physically inactive in adolescence (OR = 3.7,p< .001) in comparison to those persistently active. This finding was replicated within discordant twin pairs. Among those with no drug experience during adolescence, persistent inactivity (OR = 1.9,p= .007) increased risk for drug use. We conclude that persistent physical inactivity in adolescence may increase the risk of later problems due to excess alcohol use. Sedentary lifestyle predicts illicit drug use even when controlling for familial factors.
In: Twin research and human genetics: the official journal of the International Society for Twin Studies (ISTS) and the Human Genetics Society of Australasia, Band 8, Heft 3, S. 232-244
ISSN: 1839-2628
AbstractThe role of co-twin dependence (twins' closeness or reliance on the co-twin) was examined as a moderator of genetic and environmental influences on alcohol use in adolescence and early adulthood in a large longitudinal population-based study of Finnish twins (FinnTwin16). The associations between co-twin dependence and alcohol use were studied first at an individual level in adolescence (n = 3362) and early adulthood (n = 2912). Then, maximum likelihood models were fit to the two waves of data from same-sex twin pairs to assess the differences and changes in genetic and environmental influences on alcohol use (abstinence, drinking frequency, intoxication frequency); N = 1342 pairs in adolescence, and N = 1078 pairs in early adulthood. Overall, no significant associations were found between co-twin dependence and individual alcohol use. However, co-twin dependence importantly modulated genetic effects on drinking habits, especially in adolescence, but also in early adulthood. Co-twin–dependent twins reported greater similarity in their alcohol-related behavior across all alcohol-use measures at both time points, and the role of genes and environments varied according to co-twin dependence. Shared environmental factors explained most of the variation in drinking among co- twin–dependent twins in adolescence and contributed to drinking to intoxication during early adulthood. In contrast, among co-twin–independent twin pairs, genetic variance contributed significantly to all alcohol-use measures at both time-points. An interdependent sibling relationship is an important modifier of drinking habits, and it appears to reduce the impact of inherited liabilities on alcohol-related behavior especially in adolescence.
In: Twin research and human genetics: the official journal of the International Society for Twin Studies (ISTS) and the Human Genetics Society of Australasia, Band 15, Heft 6, S. 714-719
ISSN: 1839-2628
Objectives: The aim of the present study was to examine the role of genetic and environmental factors in the phenotypic variance of bruxism in a large population-based cohort of young adult twins in Finland.Methods: The material of the present study derives from the FinnTwin16 cohort study consisting of five birth cohorts of twin pairs born in 1975–1979 who completed a questionnaire (at mean age 24, range 23–27 years) with data on frequency of sleep-related bruxism in 2000–2002. We used quantitative genetic modeling, based on the genetic similarity of monozygotic and dizygotic twins, to estimate the most probable genetic model for bruxism, based on decomposition of phenotypic variance into components: additive genetic effects (A), dominant genetic effects (D), and non-shared environmental effects (E).Results: On average, 8.7% experienced bruxism weekly, 23.4% rarely, and 67.9% never, with no significant gender difference (p = .052). The best fitting genetic model for bruxism was the AE-model. Additive genetic effects accounted for 52% (95% CI 0.41–0.62) of the total phenotypic variance. Sex-limitation model revealed no gender differences.Conclusions: Genetic factors account for a substantial proportion of the phenotypic variation of the liability to sleep-related bruxism, with no gender difference in its genetic architecture.
In: Twin research, Band 6, Heft 2, S. 106-118
ISSN: 2053-6003
In: Twin research and human genetics: the official journal of the International Society for Twin Studies (ISTS) and the Human Genetics Society of Australasia, Band 9, Heft 3, S. 431-437
ISSN: 1839-2628
AbstractIn the population-based FinnTwin16 study, proportions of genetic and environmental factors contributing to muscle dissatisfaction and muscle-enhancing substance use were assessed in 319 pairs of twin brothers: 141 monozygotic (MZ) and 178 dizygotic (DZ) pairs. In addition there were 86 twin individuals from pairs in which only one co-twin responded. Of all respondents, 30% experienced high muscle dissatisfaction. The corresponding proportion of muscle-enhancing substance use was 10%. The subjects were similar in age (23.8 years, 95% confidence interval [CI] 23.76–23.84), body mass index (23.7, 95% CI 23.5–23.9), and waist circumference (84.5 cm, 95% CI 83.7–85.2), independent of their muscle dissatisfaction or muscle-enhancing substance use status and independent of their zygosity. The MZ polychoric correlation for muscle dissatisfaction was .39 (95% CI .17–.58) and .27 for DZ pairs (95% CI .07–.46). The MZ tetrachoric correlation for muscle-enhancing substance use was .65 (95% CI .28–.87) and .56 for DZ pairs (95% CI .26–.78). The AE model, where additive genetic factors (A) accounted for 42% (95% CI .23–.59) and unique environmental factors (E) 58% (95% CI .41–.77) of the liability, provided the best fit for muscle dissatisfaction. The CE model, where common environmental factors (C) accounted for 60% (95% CI .37–.77) and unique environmental factors (E) 40% (95% CI .23–.63) of the liability, provided the best fit for muscle-enhancing substance use. Both genetic and unique (nonfamilial) environmental factors are involved in muscle dissatisfaction in the population. Nongenetic factors (both familial and non-familial) appear to best explain the use of muscle-enhancing substances.
In: Twin research, Band 4, Heft 1, S. 25-29
ISSN: 2053-6003
AbstractSex differences in the heritability of self-reported body-height in two Finnish twin cohorts were studied by using sex-limitation models. The first cohort was born in 1938–1949 (N = 4873 twin pairs) and the second in 1975–1979 (N = 2374 twin pairs). Body-height was greater in the younger cohort (difference of 3.1 cm for men and 2.9 cm for women). The heritability estimates were higher among men (h2 = 0.87 in the older cohort and h2 = 0.82 in the younger cohort) than women (h2 = 0.78 and h2 = 0.67, respectively). Sex-specific genetic factors were not statistically significant in either cohort, suggesting that the same genes contribute to variation in body height for both men and women. The stronger contribution of environmental factors to body-height among women questions the hypothesis that women are better buffered against environmental stress, at least for this phenotype.