Exercise behavior, cardiorespiratory fitness, and obesity are strongly influenced by genetic factors. By studying young adult twins, we examined to what extent these interrelated traits have shared genetic and environmental etiologies. We studied 304 twin individuals selected from the population-based FinnTwin16 study. Physical activity was assessed with the Baecke questionnaire, yielding three indexes: sport index, leisure-time index, and work index. In this study, we focused on sport index, which describes sports participation. Body composition was determined using dual-energy X-ray absorptiometry and cardiorespiratory fitness using a bicycle ergometer exercise test with gas exchange analysis. The Baecke sport index was associated with high maximal oxygen uptake adjusted for lean body mass (Vo(2max)[adj]) (r = 0.40), with low body fat percentage (BF%) (r = -0.44) and low waist circumference (WC) (r = -0.29). Heritability estimates for the key traits were as follows: 56% for sport index, 71% for Vo(2max)[adj], 77% for body mass index, 66% for WC, and 68% for BF%. The association between sport index and Vo(2max) was mostly explained by genetic factors (70%), as were both the association between sport index and BF% (71%) and that between sport index and WC (59%). Our results suggest that genetic factors explain a considerable part of the associations between sports participation, cardiorespiratory fitness, and obesity.
We estimated genetic and environmental variance of BMI among 7245 non-pregnant MZ and DZ pairs of the same sex from the population-based Finnish Twin Cohort. The contributions of additive genetic effects, shared and non-shared environmental effects on age-adjusted BMI-variance were estimated by LISREL structural equation models. Genetic effects contribute 72% in men and 66.4% in non-pregnant women of total variance, while 27.8% of variance among men and 33.6% among women is due to non-shared environmental effects. Shared environmental effects were nonsignificant (0% for women and 0.2% for men). Similar values were obtained for hereditary and non-shared environmental effects, when shared environmental effects were not included in the model. The inclusion of pregnant women did not substantially change heritability estimates.
Eighteen pairs of monozygotic twins discordant for long-term occupational exposure to organic solvents were examined for disturbances of cardiovascular reflexes. All of the subjects were asymptomatic, and considered themselves healthy. No significant differences were observed between the exposed and the nonexposed twins. The finding suggests that occupational solvent exposure at these particular levels is unlikely to cause disturbances of the autonomic nervous function.
Genetic influences on variability of body weight and onset of menarche are well known. To investigate the genetic and environmental contributions to the association of body weight with onset of menarche, we studied Finnish twins from consecutive birth cohorts (the FinnTwin16 study) ascertained from the national population registry, which identifies nearly 100% of all living twins. Baseline questionnaires were mailed to the twins within 60 days of their sixteenth birthday and later to older sibs of the twins. Pairwise response rates (approximately 85% across gender and zygosity) and 30 months of data collection yielded results from 1283 twin pairs. The questionnaires included a survey of health habits and attitudes, a symptom checklist, MMPI personality scales, and a survey of relationships with parents, peers, and the co-twin. Age at menarche was reported by 468 monozygotic (MZ) girls, 378 girls from like-sex dizygotic (FDZ) pairs, 434 girls from opposite-sex (OSDZ) pairs, and 141 older female sibs of the twins. The one-month test-retest reliability of age at menarche in an independent sample (N = 136) of 16-year-olds from a national survey was 0.96. Girls from OSDZ pairs had a significantly higher mean age at menarche (13.33 yr) than FDZ girls (13.13 yr) (difference, 0.20 yr; 95% confidence interval, 0.05-0.35). The MZ correlation for age at menarche was 0.75, the DZ correlation was 0.31, and the sib-twin correlation was 0.32. A bivariate twin analysis of age at menarche and body mass index (wt/ht2) indicated that 37% of the variance in age at menarche can be attributed to additive genetic effects, 37% to dominance effects, and 26% to unique environmental effects. The correlation between additive genetic effects on age at menarche and body mass index was 0.57, indicating a substantial proportion of genetic effects in common.
We studied the cumulative incidence, concordance rate and heritability for diabetes mellitus in a nationwide cohort of 13,888 Finnish twin pairs of the same sex. The twins were born before 1958 and both co-twins were alive in 1967. Data on diabetes were derived through computerized record linkage from death certificates, the National Hospital Discharge Register and the National Drug Register. Records were reviewed in order to assign a diagnostic category to the 738 diabetic patients identified. Of these patients 109 had Type 1 (insulin-dependent) diabetes, 505 Type 2 (non-insulin-dependent) diabetes, 46 gestational diabetes, 24 secondary diabetes, 38 impaired glucose tolerance and 16 remained unclassified. The cumulative incidence of diabetes was 1.4% in men and 1.3% in women aged 28-59 years and 9.3% and 7.0% in men and women aged 60 years and over, respectively. The cumulative incidence did not differ between monozygotic and dizygotic twins. The concordance rate for Type 1 diabetes was higher among monozygotic (23% probandwise and 13% pairwise) than dizygotic twins (5% probandwise and 3% pairwise). The probandwise and pairwise concordance rates for Type 2 diabetes were 34% and 20% among monozygotic twins and 16% and 9% in dizygotic twins, respectively. Heritability for Type 1 diabetes was greater than that for Type 2 where both genetic and environmental effects seemed to play a significant role.
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.
To study twin resemblance for weight change (delta wt) and to assess the consistency of body mass index (BMI) over 6 years.
6 year follow-up based on identical mailed questionnaires in 1975 (baseline) and in 1981 (follow-up).
5967 same-sexed non-pregnant Finnish twin pairs aged 18-54 in 1975 (1106 male and 862 female monozygotic (MZ) and 2430 male and 1569 female dizygotic (DZ) pairs).
Intra-pair correlations of delta wt and BMI, estimates of genetic and environmental components of variance of delta wt and BMI.
Unadjusted mean delta wt was +2.0 (s.d. = 4.6) kg among MZ and 2.1 (4.9) kg among DZ male individuals. Corresponding values among MZ and DZ female individuals were +1.5 (4.4) kg and +1.7 (4.4) kg, respectively. Age and initial BMI together explained 8.0% of the male and 2.3% of the female phenotypic variance of delta wt. The intraclass correlations for delta wt (adjusted for age and initial BMI) for all pairs were 0.29 and 0.07 for MZ and DZ men and 0.25 and 0.05 for MZ and DZ women, respectively. The BMI of the twins increased slightly during the follow-up compared to the baseline values (23.9 (2.7) for MZ and 24.1 for DZ men and 23.0 (3.3) for MZ and 23.2 (3.42) for DZ women). The intra-class correlations for BMI at baseline (0.69 for MZ and 0.34 for DZ men and 0.67 for MZ and 0.29 for DZ women) were almost identical with the correlations at follow-up (0.67 for MZ and 0.32 for DZ men and 0.69 for MZ and 0.29 for DZ women). The intra-class correlations for both BMI and delta wt were consistently higher among pairs living together than among pairs living apart at baseline and at follow-up in both zygosity groups (MZ and DZ). Among pairs living apart at baseline, the longitudinal model for BMI showed that the correlation between genetic effects at baseline and at follow-up was very high (> 0.9 in all age groups among both genders). The correlations for environmental effects ranged from 0.50 to 0.67 during the follow-up period.
Weight changes in adults over a 6-year period appear to be determined by environmental effects rather than genetic factors. However, the genetic component in BMI is considerable and stable over time. Shared environment is likely to contribute to the resemblance of both delta wt and BMI among adult twin pairs, especially among MZ pairs.
We investigated whether BMI predicts type 2 diabetes in twins and to what extent that is explained by common genetic factors.
This was a population-based twin cohort study. Monozygotic (n = 4,076) and dizygotic (n = 9,109) non-diabetic twin pairs born before 1958 answered a questionnaire in 1975, from which BMI was obtained. Information on incident cases of diabetes was obtained by linkage to nationwide registers until 2005.
Altogether, 1,332 twins (6.3% of men, 5.1% of women) developed type 2 diabetes. The HR for type 2 diabetes increased monotonically with a mean of 1.22 (95% CI 1.20-1.24) per BMI unit and of 1.97 (95% CI 1.87-2.08) per SD of BMI. The HRs for lean, overweight, obese and morbidly obese participants were 0.59, 2.96, 6.80 and 13.64 as compared with normal weight participants. Model heritability estimates for bivariate variance due to an additive genetic component and non-shared environmental component were 75% (men) and 71% (women) for BMI, and 73% and 64%, respectively for type 2 diabetes. The correlations between genetic variance components (r (g)) indicated that one fifth of the covariance of BMI and type 2 diabetes was due to shared genetic influences. Although the mean monozygotic concordance for type 2 diabetes was approximately twice the dizygotic one, age of onset of diabetes within twin pair members varied greatly, irrespective of zygosity.
A 28-year follow-up of adult Finnish twins showed that despite high trait heritability estimates, only a fraction of covariation in BMI and incident type 2 diabetes was of genetic origin.
This study identifies, in genetically informative data, familial and socioregional environmental influences on abstinence from alcohol at age 16.
Data are from FinnTwin 16, a population-based study of five consecutive birth cohorts of Finnish twins (N = 5,747 twin individuals), yielding 2,711 pairs of known zygosity. Measures of alcohol use, embedded into a health-habits questionnaire, were taken from earlier epidemiological research with nontwin Finnish adolescents. The questionnaire was administered sequentially to all twins as they reached age 16. Separate questionnaires, including measures of alcohol use and screening questions for alcohol problems, were received from 5,243 of the twins' parents.
Abstinence from alcohol to age 16 exhibits very significant familial aggregation, largely due to nongenetic influences. Abstinence rates are influenced by socioregional variation, sibling interaction effects and parental drinking patterns. Sibling and parental influences are greater in some regional environments than in others: the relative likelihood that a twin abstains, given that the co-twin does, or that both parents do, is shown to be modulated by socioregional variation.
Environmental contexts affect the likelihood of maintaining abstinence from alcohol to midadolescence, and socioregional variation modulates influences of siblings and parents. The results illustrate how genetically informative data can inform prevention research by identifying target variables for intervention efforts.
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.
To study genetic and environmental factors affecting body mass index (BMI) and BMI phenotypic correlations across adolescence.
Prospective, population-based, twin cohort study.
We used twin modeling in 2413 monozygotic and same-sex and opposite-sex dizygotic Finnish twin pairs born in 1983-1987 and assessed using self-report questionnaires at 11-12, 14 and 17 years of age.
Heritability of BMI was estimated to be 0.58-0.69 among 11-12- and 14-year-old boys and girls, 0.83 among 17-year-old boys and 0.74 among 17-year-old girls. Common environmental effects shared by siblings were 0.15-0.24 among 11-12- and 14-year-old boys and girls but no longer discernible at 17 years of age. Unique environmental effects were 0.15-0.23. Additive genetic factors explained 90-96% of the BMI phenotypic correlations across adolescence, whereas unique environmental factors explained the rest. Common environment had no effect on BMI phenotypic correlations.
The genetic contribution to BMI is strong during adolescence, and it mainly explains BMI phenotypic correlations across adolescence. Common environmental factors have an effect on BMI during early adolescence, but that effect disappears by late adolescence.
Cites: Twin Res. 2003 Oct;6(5):361-7614624720
Cites: Twin Res. 2002 Oct;5(5):366-7112537860
Cites: Obes Rev. 2004 May;5 Suppl 1:4-10415096099
Cites: N Engl J Med. 1990 May 24;322(21):1483-72336075
The purpose was to examine whether maximal walking speed, maximal isometric knee extensor strength, and leg extensor power share genetic or environmental effects in common. The data was collected from 103 monozygotic and 114 dizygotic female twin pairs aged 63-76 years. Maximal walking speed over 10 m was measured in the laboratory corridor using photocells for timing. Isometric knee extensor strength and leg extensor power were measured using an adjustable dynamometer. The genetic models showed that strength, power, and walking speed had a genetic effect in common which accounted for 52% of the variance in strength, 36% in power, and 34% in walking speed. Strength and power had a non-shared environmental effect in common explaining 13% of variation in strength and 14% in power. The remaining variance was accounted for by trait-specific effects. Some people may be more prone to functional limitation in old age due to their genetic disposition, but this does not rule out that changes in the lifestyle of predisposed subjects may also have a major effect. Approximately half of the variation in each trait was explained by environmental effects, which suggests the importance of the physical activity to improve performance and prevent functional limitation.
The rise in body mass index (BMI) during adulthood increases the risk for metabolic disorders, functional limitations and disability in old age. This twin study examined prospectively whether genetic and environmental influences on women's BMI also account for mobility 29 years later.
The sample consisted of 103 monozygotic and 114 dizygotic pairs of twin sisters reared together. Body mass index was initially evaluated in 1975, when the women were aged 42.6+/-3.4 years, and was followed-up in 1981, 1990, 2001 and 2004. Mobility was evaluated using the standardised 6-minute walking test in 2001, when the women were aged 68.6+/-3.2 years, and followed-up 3 years later. An investigation was made into how genetic and environmental influences on adult BMI accounted for mobility in old age using a genetic latent growth modelling approach.
During the follow-up period, BMI increased by 17%. Midlife BMI was a significant predictor of mobility 29 years later. Genetic influences on BMI level and its rate-of-change accounted for 37% and 25% respectively, of the genetic influences on mobility later in life. The corresponding environmental influences on BMI level and its rate-of-change were 35% and 22%.
Genes predisposing to higher BMI across middle age increase the risk for poorer mobility in old age. Identifying those genes could lead to interventions targeted at preventing obesity and mobility loss later in life. However, modification of environmental factors, eg exercise and nutrition, remain the most feasible ways of influencing BMI and mobility across the life span.
Cognitive deficits in alcohol dependence (AD) have been observed, poorer verbal ability being among the most consistent findings. Genetic factors influence both cognitive ability and AD, but whether these influences overlap is not known.
A subset of 602 monozygotic (MZ) and dizygotic (DZ) twins from FinnTwin16, a population-based study of Finnish twins, was used to study the associations of verbal ability with DSM-III-R diagnosis and symptoms of AD, the maximum number of drinks consumed in a 24-h period, and the Rutgers Alcohol Problem Index (RAPI) scores. These twins, most of them selected for within-pair discordance or concordance for their RAPI scores at age 18.5 years, were studied with neuropsychological tests and interviewed with the Semi-Structured Assessment for the Genetics of Alcoholism (SSAGA) in young adulthood (mean age 26.2 years, range 23-30 years).
All alcohol problem measures were associated with lower scores on the Vocabulary subtest of the Wechsler Adult Intelligence Scale - Revised (WAIS-R), a measure of verbal ability. In bivariate genetic models, Vocabulary and the alcohol problem measures had moderate heritabilities (0.54-0.72), and their covariation could be explained by correlated genetic influences (genetic correlations -0.20 to -0.31).
Poorer verbal ability and AD have partly overlapping biological etiology. The genetic and environmental influences on the development of cognitive abilities, alcohol problems and risk factors for AD should be studied further with prospective longitudinal designs.
Twin studies integrate genetic and environmental (including physical environment and life-style) information by comparing monozygotic and dizygotic twins for the occurrence of disease. Our objectives were to compare cancer incidence in twins with national rates and to estimate both the probability that co-twins of affected twins may develop cancer and the importance of genetic predisposition and environment in cancer development. The nationwide record linkage of the Finnish Twin Cohort Study, the Finnish Cancer Registry and the Central Population Register allowed the follow-up of 12,941 same-sexed twin pairs for incident primary cancers from 1976 to 1995. Zygosity was determined by use of a validated questionnaire in 1975. Methods included calculation of standardized incidence ratios and concordances and fitting of structural equation models. A total of 1,613 malignant neoplasms occurred in the cohort. The overall cancer incidence among twins resembled that among the general population. Monozygotic co-twins of affected twins were at 50% higher risk than were dizygotic co-twins. Based on genetic modeling, inherited genetic factors accounted for 18% (95% confidence interval 4-32%) of the liability in inter-individual variation in the risk of overall cancer, while non-genetic factors shared by twins accounted for 7% (0-16%) and unique environmental factors for 75% (65-85%). Our results appear to exclude a contribution greater than one-third for genetic predisposition in the development of cancer in the general population, thus pointing to the earlier confirmed substantial role of environment.
The problems of differentiation between environmental and genetic influences on the development of multiple sclerosis are well known. Twin studies may provide valuable information on this question. However, most published twin series are selected and no through clinical twin studies based on epidemiologic series have been carried out. In this study, all available same-sex twin pairs with clinically definite multiple sclerosis derived from the Finnish Twin Cohort of 15815 pairs were studied by clinical evaluation, magnetic resonance imaging, and visual and auditory evoked responses. The mean length of follow-up of the pairs after the onset of symptoms of multiple sclerosis was 20 years. Two of the seven monozygotic pairs were concordant; one was definitely so, and in the other, the co-twin of the index case had, in addition to clinical findings, white matter changes suggestive of multiple sclerosis in magnetic resonance imaging and abnormal visual evoked responses. All six dizygotic pairs were discordant. The frequency of the HLA antigen DR2 in probands (69%) was significantly increased, but the distribution among the healthy subjects and patients showed nonsignificant differences. The results indicate a genetic influence on the susceptibility to multiple sclerosis, although still unknown genetic determinants are possible involved.
Like other atopic diseases, hay fever is known to cluster in families. This clustering is due either to effects of a shared family environment or to genetic inheritance. By comparing the occurrence of hay fever among monozygous (MZ) and dizygous (DZ) twin pairs, we were able to estimate the contribution of genetic and environmental factors in the development of hay fever.
A questionnaire mailed to a nationwide sample of 2483 families with 16-year-old twins furnished data for the cumulative incidence of physician-diagnosed hay fever among these adolescents and their parents.
Among the 1765 twin pairs with data available for analysis, hay fever was reported for 14.1% of boys (95% CI=12.4-15.8%) and 10.0% of girls (95% CI=8.6-11.4%). The MZ twin pairs (probandwise concordance rate=60.3%, 95% CI =52-68%) were significantly more concordant for hay fever than were DZ twin pairs (31.5%, 95% CI=26-36%). Genetic factors accounted for 74-82% of the interindividual variability in liability to hay fever, variation in shared family environment for 7% at most, and unique (individual) environment for 18%.
Familial occurrence of hay fever is mainly due to genes predisposing to the trait. Environmental exposures shared in common by family members but varying between families appear to account for at most a modest proportion of the variability in risk of developing hay fever.
Some health related psychosocial correlates of the Eysenck neuroticism scale were examined in a questionnaire study of 1501 monozygotic (MZ) and 3455 dizygotic (DZ) male twin pairs representing the adult male twin population in Finland. In analyses of the individuals, 34% of the variance in neuroticism was associated to: psychological variables (stress of daily activities, life satisfaction, quality of sleep, and extroversion - the explanatory rate of this variable set was 30%), psychotropic drugs (5%), alcohol use (4%), and smoking (2%). Neuroticism was also associated to social, life change, and medical variables. In pairwise analyses, the heritability estimate (h2) was 0.54 for pairs living together and 0.39 for pairs living apart. It seems that heritability estimates are confounded by the closer intrapair relationship between members of MZ than DZ pairs. In pairwise analyses, 23% of the intrapair difference of neuroticism in MZ pairs was associated to intrapair differences in the aforementioned variables. The following explanatory rates were found: psychological variables, 21%; psychotropic drugs, 2%; alcohol use, 2%; and smoking, 1%. Neuroticism of pairs discordant for background variables showed similar intrapair differences as between individuals in the following variables: service vs farming work, use of alcohol, use of antacids, hypertension, heavy physical work, quality of sleep, changes of workplace for negative reasons, smoking, and use of tranquillizers. It appears that in Finland environmental factors explain at least 61% of the variability in neuroticism, and that factors determining neuroticism are also associated to health related behavior such as smoking, use of alcohol and psychotropic drugs.
The contribution of hereditary factors in basal cell carcinoma of the skin has not been well defined at the population level. We aimed to assess the hereditary component in basal cell carcinoma by comparing its occurrence in monozygotic and dizygotic twin pairs. The Finnish Twin Cohort, comprising 12,941 adult, like-sex twin pairs with established zygosity and resident in Finland in 1975, was linked with the Finnish Cancer Registry. We identified 335 twin pairs in which at least one twin had basal cell carcinoma diagnosed between 1953 and 1996. Standardized incidence ratios, concordances, tetrachoric correlations and pairwise relative risks were computed by standard methods. Components of variance in liability were estimated by structural equation modelling. There was an elevated risk of basal cell carcinoma for the co-twin of a diseased twin, but no difference in risk by zygosity. During the prospective follow-up in 1976-96, the probandwise concordance was 7.7% in monozygotic and 7.0% in dizygotic pairs. Model fitting indicated that genetic factors were not needed to account for the distribution of basal cell carcinoma in twin pairs. These results confirm the major role of environmental factors in the aetiology of basal cell carcinoma.