Differences in age at natural menopause by occupation, education, and place of residence were examined using a cross-sectional population sample of Finnish women aged 45-64 years (n = 1,713, response rate 86%). The sample was selected at random from the Finnish Population Register in 1989 (final n = 1,505, 75%). Kaplan-Meier estimates showed the median age at natural menopause to be 51 years for all women (95% confidence interval (CI) 50.6-51.4). The median menopausal age of smokers and nulliparous women was 50 years; that of nonsmokers and women whose first full-term pregnancy occurred before the age of 25 years was 52 years. Differences between occupational and educational groups were statistically significant (Mantel-Cox test for occupation, p 11 years) it was 0.75 (95% CI 0.59-0.96), adjusted to reflect smoking, use of hormones, body mass index, and age at first full-term pregnancy. Sociodemographic variables appear to be associated with age at natural menopause in a representative sample of Finnish women.
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.
The aim was to study whether aerobic fitness measured by a maximal endurance running test at adolescence predicts prevalence of hypertension or blood pressure levels in adulthood. From the 413 (197 slow runners and 216 fast runners) participating in a 2000-meter running test at adolescence in 1976 and responding to a health and fitness questionnaire in 2001, 29 subjects (15 very slow runners and 14 very fast runners) participated in a clinical follow-up study in 2001. Compared to those who were fast runners in adolescence, those who were slow runners tended to have higher age-adjusted risk of hypertension at follow-up (OR 2.7, 95 % CI 0.9 to 7.5; p=0.07). The result persisted after further adjustment for body mass index at follow-up (OR 2.9, 95 % CI 1.0 to 8.3; p=0.05). Diastolic blood pressure was higher for very slow runners at adolescence compared to very fast runners, the age-adjusted mean diastolic blood pressure being 90 mm Hg (95 % CI 86 to 93) vs. 83 mm Hg (95 % CI 80 to 87), age-adjusted p=0.013. High endurance type fitness in adolescence predicts low risk of hypertension and low resting diastolic blood pressure levels in adult men.
Prior studies suggest that certain types of personality are at higher risk for developing depressive disorders. This study examined the relationship between old age depressive symptoms and two middle-age personality dimensions, neuroticism and extraversion.
The present study is part of the Finnish Twin Study on Aging, where altogether 409 female twins who had completed the Eysenck Personality Inventory at the age of 38-51 years were studied for depressive symptoms 28 years later using Center for the Epidemiologic Studies Depression Scale. Logistic regression analysis suitable for dependent data and univariate and Cholesky models for decomposing the genetic and environmental factor were used.
Middle age extraversion protected from later depressive symptoms while neuroticism increased the risk. Twin modeling indicated that the association between neuroticism and depressive symptoms resulted from shared genetic risk factors common to both traits. However, a substantial proportion of the genetic vulnerability was specific to old age depressive symptoms and was not shared with neuroticism. Middle age extraversion had no genetic relationship with old age depressive symptoms.
The relationship between middle age neuroticism and old age depressive symptoms is strong but only partly the result of genetic factors that predispose to both neuroticism and depressive symptoms. Extraversion, by contrast, has no genetic relationship with depressive symptoms experienced in old age.
To evaluate genetic influences on the use and abuse of alcohol, we compared questionnaire measures of the frequency, quantity, and density of social drinking, and the frequency of alcohol-induced passouts self-reported by 879 monozygotic (MZ) and 1940 dizygotic (DZ) pairs of twin brothers, aged 24-49 yr. The measures of frequency, quantity, and density (heavy drinking once or more a month) significantly intercorrelate, and the self-reported alcohol consumption by this sample is satisfactorily stable and consistent with nationwide sales figures. None of the drinking measures was associated with twin type (zygosity), and only density correlated with age. Similarity of drinking habits among twin brothers was evaluated as a function of their genetic resemblance and age, the frequency of their social contact with one another, and the interactions of these terms. The effects were estimated from hierarchical linear regressions of a double-entry data matrix from which each twin's drinking was predicted from that of his twin brother, and that pair's age, zygosity, cohabitation status, and frequency of social contact. Significant genetic variance was found for each of the drinking measures with heritability estimates ranging from 0.36 to 0.40. Co-twins in more frequent social contact with one another reported greater similarity in their use of alcohol, but heritable variance remained after the effects of age and social contact were removed from both mean levels and co-twin resemblance. Reported frequency of passouts yielded significant, but equivalent, correlations in both MZ and DZ twins and no evidence of genetic influence.
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.