Clinically significant anxiety symptoms are prevalent among the elderly, yet knowledge about the longitudinal course of anxiety symptoms in later life remains scarce. The goals of this study were to (a) characterize age trajectories of state anxiety symptoms in the second half of life, and (b) estimate genetic and environmental contributions to individual differences in the age trajectory of state anxiety. This study was based on data from 1,482 participants in the Swedish Adoption/Twin Study of Aging who were aged 50 and older at their first occasion (512 complete twin pairs, 458 singletons) and had up to 6 measurement occasions spanning 11 years. Consistent with life span developmental theories of age-related emotional change, anxiety symptom levels declined during the transition from midlife to the mid-60s, followed by a mild increase that gradually plateaued in the 80s. There were substantial individual differences in the age trajectory of anxiety. After accounting for effects of sex, cohort, mode of testing, and proximity to death, this longitudinal variation was partitioned into biometric sources. Nonshared environmental variance was highest in the late 60s and declined thereafter, whereas genetic variance increased at an accelerated pace from approximately age 60 onward. There was no evidence for effects of rearing or other shared environment on anxiety symptoms in later life. These findings highlight how the etiology of anxiety symptoms changes from midlife to old age.
Notes
Cites: Twin Res Hum Genet. 2007 Jun;10(3):423-3317564500
Cites: Acta Genet Med Gemellol (Roma). 1991;40(1):7-201950353
To investigate whether diagnostic data from structured interviews, primary care and specialist care registries on major depressive disorder (MDD), anxiety disorders (AD) and alcohol use disorder (AUD) identify the same individuals, yield comparable comorbidity estimates and reflect the same genetic influences.
Registry data from primary and specialist care were available for 11 727 twins and diagnostic interview data for 2271 of these. We used logistic regression analyses and biometric modelling to investigate the overlap between the data sources.
Most individuals meeting diagnostic criteria at interview were not registered with a corresponding diagnosis. The rates of registration were higher for MDD (36% in primary care and 15% in specialist care) and AD (21% and 18%) than for AUD (3% and 7%). Comorbidity estimated as odds ratios, but not as polychoric correlations, was higher in the registries than in the interviews. Genetic influences on the disorders were highly correlated across data sources (median r = 0.81), bordering unity for MDD and AD.
Prevalence and comorbidity estimates differ between registries and population-based assessment. Nevertheless, diagnoses from health registries reflect the same genetic influences as common mental disorders assessed in the general population, indicating generalizability of aetiological factors across data sources.
Early age of alcohol initiation is not the cause of alcohol use disorders in adulthood, but is a major indicator of genetic risk. A population-based twin study.
An early age of alcohol initiation (AAI) is associated with and has been hypothesized to be a cause of alcohol use disorders (AUD) in adulthood. Results from twin studies, however, indicate that AAI is an indicator of risk for AUD. We aimed to test a causal hypothesis versus a risk indicator hypothesis for the relationship between early AAI and AUD.
A population-based twin study using biometric twin modelling.
Norway.
A population-based sample of 1336 Norwegian twins.
Life-time DSM-IV AUDs were assessed by structured clinical interview and AAI by questionnaire.
The risk indicator model in which the association between AAI and AUD was explained by common vulnerability was the best fitted to the data. The heritability was 37% [95% confidence interval (CI)?=?21%, 53%] for AAI and 62% (95% CI?=?51%, 73%) for AUD. Genetic risk for AAI accounted for 44% (95% CI?=?17%, 71%) of the total genetic risk for AUD and the correlation between genetic factors for AAI and AUD was -0.66 (95%CI -0.87, -0.46). Individual-specific environmental risk for AAI explained only 1% (95% CI?=?0%, 3%) of the risk for AUD. Shared environmental factors did not influence AUD, but accounted for 25% (95% CI?=?7%, 35%) of the variance in AAI.
The association between early age of alcohol initiation and alcohol use disorders in later life does not reflect a causal relationship, but is due almost entirely to common genetic risk factors.
Notes
Cites: Twin Res. 2002 Oct;5(5):415-2312613498
Cites: Psychol Med. 1997 Nov;27(6):1381-969403910
Cites: Arch Gen Psychiatry. 2003 Sep;60(9):929-3712963675
Cites: Subst Use Misuse. 2003 Dec;38(14):1983-201614677779
The purpose of this review is to provide a detailed and updated description of the FinnTwin16 (FT16) study and its future directions. The Finnish Twin Cohort comprises three different cohorts: the Older Twin Cohort established in the 1970s and the FinnTwin12 and FT16 initiated in the 1990s. FT16 was initiated in 1991 to identify the genetic and environmental precursors of alcoholism, but later the scope of the project expanded to studying the determinants of various health-related behaviors and diseases in different stages of life. The main areas addressed are alcohol use and its consequences, smoking, physical activity, overall physical health, eating behaviors and eating disorders, weight development, obesity, life satisfaction and personality. To date, five waves of data collection have been completed and the sixth is now planned. Data from the FT16 cohort have contributed to several hundred studies and many substudies, with more detailed phenotyping and collection of omics data completed or underway. FT16 has also contributed to many national and international collaborations.
Virginia Institute of Psychiatric and Behavioral Genetics, Medical College of Virginia/Virginia Commonwealth University, Richmond, VA 23298-012, USA. kendler@vcu.edu
Externalizing traits or behaviors are typically assessed by self-report scales or criminal records. Few genetically informative studies have used both methods to determine whether they assess the same genetic or environmental risk factors.
We examined 442 male Swedish twin pairs with self-reported externalizing behaviors at age 16–17 years [externalizing traits (EXT), self-reported delinquency (SRD), impulsivity (IMP), grandiosity (GRD) and callousness (CLS)] and criminal behavior (CB) from the National Suspect Registry from age 13 to 25 years. Multivariate structural equation modeling was conducted with Mx.
The best-fit model contained one genetic, one shared environmental and two non-shared environmental common factors, and variable specific genetic and non-shared environmental factors. The risk for CB was influenced substantially by both genetic (a2=0.48) and familial–environmental factors (c2=0.22). About one-third of the genetic risk for CB but all of the shared environmental risk was indexed by the self-report measures. The degree to which the individual measures reflected genetic versus familial–environmental risks for CB varied widely. GRD and CLS were correlated with CB mainly through common genetic risk factors. SRD and CB covaried largely because of shared familial–environmental factors. For EXT and IMP, observed correlations with CB resulted in about equal parts from shared genetic and shared familial–environmental factors.
In adolescence, measures of grandiose and callous temperament best tap the genetic liability to CB.Measures of antisocial behaviors better index familial–environmental risks for CB. A substantial proportion of the genetic risk to CB was not well reflected in any of the self-report measures.
BACKGROUND. Twin registers provide a valuable source for research into disease causation. The existing population-based registers comprise mostly old twins. In order to be able to study diseases which occur in childhood and youth a new Danish twin register has been established. METHODS. The register is based on the Danish Civil Registration, with information on number of twin births from the Danish Vital Statistics Office as the source of validation. All twins resident in Denmark at 1 March 1991 were sent a one-side questionnaire asking about diabetes, willingness to participate in other research projects and similarity in the twins. RESULTS. The register, comprising 20,888 twin pairs, covers 74.4% of all twin pairs born 1953-1967 (incl.) and 97.4% of those born 1968-1982 (incl.). The response rate to the questionnaire study was 92.3%. The responders represented 19,180 twin pairs distributed as 5304 monozygotic pairs, 6861 same-sex dizygotic pairs, 6244 opposite-sex dizygotic pairs and 771 pairs of unknown zygosity. Of the respondent twins, 96% declared their willingness to participate in additional studies. An analysis of trends in the twinning rates for the years 1968-1982 showed that the rate of monozygotic twinning is increasing and the twinning rate of opposite-sex twin pairs is decreasing. CONCLUSIONS. Earlier estimated trends in twinning rates have been confirmed. Due to the high response rate and opportunities for linkage with other Danish registers, the present material provides a valuable resource for twin studies in diseases and human traits.
The Norwegian Institute of Public Health in Oslo has an ongoing program of twin research using population-based cohorts of twins. The current database includes information on twins identified through the Medical Birth Registry of Norway and born from 1967-1979, altogether 15,370 twins. This is a longitudinal study with a cohort sequential design whereby new cohorts are recruited into the study at 5-6 year intervals. Sub-samples of these twins have participated in questionnaire studies and clinical assessment sub-projects. These projects include national and international collaborations. Our primary areas of interest include mental health and psychological well-being, obesity, asthma and allergies, health behaviors and health perceptions, comorbidity, and perinatal influences on health outcomes. This paper provides a brief overview of the data, sample, and the various research projects associated with this twin program of research.
The Norwegian Twin Registers include several sets of population-based sub-registers, and covers twin pairs born between 1895 and today. Except for the missing birth years 1960 to 1967, the register is almost complete. Most of the register contains information about both same-sexed and opposite-sexed twin pairs, except for twin pairs born between 1946 and 1960, where only same-sexed twins are registered. In a substantial part of the register, information about zygosity is obtained, mainly by a mailed questionnaire and in some cases supported by DNA testing. These are the birth years 1915 to 1960 and the birth years 1967 to 1979. Zygosity information is further obtained in the different twin studies derived from the twin register. In 1990 the whole register was made available in a computerized form. Several twin studies have been derived from the different parts of the register. In this article, studies from the two earliest parts of the register are reviewed and grouped by recruitment specifics. Finally, future plans for the register and twin studies are discussed.
The Swedish Adoption/Twin Study of Aging (SATSA) is a longitudinal program of research in gerontological genetics which is currently in its fifth year. The base population is comprised of 351 pairs of twins reared apart and 407 matched control pairs of twins reared together who responded to a questionnaire (Q1) in 1984. Two additional stages of SATSA have recently been completed: a longitudinal follow-up questionnaire mailed out in 1987 (Q2) and extensive in-person testing (IPT1) which included a health examination and cognitive battery. A second wave of IPT was started in January 1989. A summary of some of the major findings from Q1 and a description of IPT1 are reported.
Since the Swedish Twin Registry was first established in the late 1950s to study the importance of smoking and alcohol consumption on cancer and cardiovascular diseases, it has been expanded and updated on several occasions. The focus has similarly broadened to most common complex diseases. The content of the database is described, ongoing projects based on the registry are summarized, and we review some of the principal findings on aging, cancer and cardiovascular disease that have come from the registry. Ongoing efforts and future plans for the STR are discussed. Among others, we plan blood collection and genotyping to study the genetic bases of complex diseases, a first contact ever with the cohorts born after 1958, and in-depth studies of selected diseases, such as Parkinson's disease and chronic fatigue syndrome.
