The choice of where to live would appear to be determined by a combination of economic constraints and personal preferences. We have tested how far this choice is affected by the continuing effects of the environment shared within families, and genetic variation between people, using data from twin studies conducted in Australia. The addresses provided by study participants were categorized as urban, suburban and nonurban, and data were analyzed in three adult age groups. There were significant effects of both shared environment and genes, and the balance between them was affected by both sex and age. Shared environment accounted for some 50% of variation in the youngest group, but only about 10% in the oldest. As shared environmental effects decreased, additive genetic effects increased. These results have implications for internal migration of people within countries and, over the long term, for gene flow within and between populations. They may also be pertinent to the different prevalences of certain psychiatric diseases between city and country locations. Comparisons between countries with different demography are needed to confirm and further characterize these effects.

Incorporation of sex-limitation (genotype-sex interaction) effects into a model of quantitative trait loci (QTL) analysis has been shown to increase the power to detect linkage when analyzing traits in which sex limitation is present (Towne et al., 1997). The present note provides a parameterization of the nonscalar sex-limitation ACE model incorporating autosomal sex-limited QTL effects for use with the Mx matrix algebra program (Neale et al., 2002). An example script designed for use with extended sib- ships that takes advantage of the versatile treatment of covariates within Mx is included.

Behavior genetics has convincingly shown the importance of genetic factors in objective tests of memory function. However, self-report memory tests have received little attention. This study used items from the Multifactorial Memory Questionnaire (MMQ) to estimate the heritability of self-reported memory contentment and ability in 909 monozygotic (MZ) and 1034 dizygotic (DZ) twin pairs aged between 20 and 84 years from the St Thomas' Adult UK Twin Register. Heritability estimates ranged between 37% and 64% for contentment (e.g., reporting to worry about one's memory) and approximately 45% for ability (e.g., reporting a tendency to forget keys). Shared family environmental influences (between 32% and 33%) were found for some abilities (e.g., learning to use a new gadget). Given their clinical significance and ease of administration, these tests could prove to be useful in examining memory functioning in large-scale population studies.

The main aim of this paper was to resolve the correlation between intelligence test scores and standing height into genetic and environmental components. Data on 1181 identical and 1412 fraternal twin pairs (all males) were retrieved by matching files from the Norwegian Army with twin registries. The data were analyzed by means of a structural equation model comprising latent genetic, shared environmental and nonshared environmental factors and correlations between them. A major part of the height–intelligence correlation was due to correlated shared environments (59% of the phenotypic height–intelligence correlation), but statistically significant effects of correlated genes and nonshared environments were also found (respectively 35% and 6% of the phenotypic correlation).

Twins are sometimes used as proxy informants but little is known about reliability and validity of the information thus obtained. The present study asks: (1) to what extent do twin pairs agree with each other on comparative ratings of health, psychosocial traits, and environmental exposures?; and (2) how well do comparative ratings agree with usual self-reported information about the exposures? Using 55 monozygotic (MZ) and 71 dizygotic (DZ) same-sex pairs reared together, percentage agreement was calculated for 44 comparative ratings. Pairs agreed on average about half of the time. Agreement was higher for more discrete exposures, such as smoking, but lower for more subjective variables, such as the degree to which life is experienced as stressful. Signed rank tests were used to contrast comparative ratings to differences in self- reports. Differences between twin partners in their self-report indices, where available, were in the direction suggested by the comparative rating. Comparative ratings appear most accurate for smoking and alcohol use, and less consistent for mental health symptoms and self-rated health.

Twin studies that examine the effect of specific environmental risk factors on psychiatric disorders assume that there are no differences in prevalences of these risk factors between twins and singletons. Violation of this assumption signifies that the results from twin studies might not generalize to singletons. Another assumption, not only often underlying twin studies but also epidemiological research, is that life- events are not influenced by familial factors. We tested differences in prevalences of experienced life events in a Dutch sample of 2086 monozygotic (MZ) twins, 2090 dizygotic (DZ) twins and 1307 of their siblings. Self-reported data on life events (illness of self, illness of a significant other, spouse/romantic relationship, divorce/break-up of a relationship, death of a significant other, traffic accident, robbery, violent assault, sexual assault) were available from a survey- study. We further investigated whether familial resemblance was present for the exposure to these life events and, if so, whether this resemblance was due to genetic or common environmental factors. No differences were found in the prevalences of life events between MZ twins, DZ twins and their siblings. There was evidence for familial aggregation of all life events, except for traffic accidents in women. Results indicated genetic control on the presence of a spouse or involvement in a relationship. Familial resemblance of illness and death of a significant other was mainly due to common environment. For the other life events, it was not possible to distinguish between genetic and common environmental effects.

Alcohol abuse and dependence are among the most common psychiatric conditions identified in epidemiological surveys of the general population. The aim of this article is to examine the psychometric properties of Diagnostic and Statistical Manual of Mental Disorders, (4th ed.; DSM-IV; American Psychiatric Association, 1994) criteria for alcohol abuse and dependence using latent class analysis (LCA). Six thousand two hundred and sixty-five young Australian twins (median age 30 years) were interviewed by telephone between 1996 and 2000 using a modified version of the Semi-Structured Assessment for the Genetics of Alcoholism (SSAGA). DSM-IV symptoms of alcohol abuse and dependence were collected by structured diagnostic interview and analyzed using methods of LCA. LCA revealed a 4-class solution for women that classified individuals according to the severity of their alcohol- related problems: no/few problems (66.5%), heavy drinking (23.9%), moderate dependence (7.6%) and severe dependence (2.0%). Among men the preferred solution included 5 classes corresponding to no/few problems (46.4%), heavy drinking (34.3%), moderate dependence (12.2%), severe dependence (3.0%) and abuse (4.0%). Evidence of a male-specific class of alcohol-related problems corresponding to abuse partially supports the DSM conceptualization of alcohol use disorders but suggests that this conceptualization — and measurement — may need to be refined for women. Identification of a male- specific abuse class also has important implications for interventions and treatment as these individuals experienced significant alcohol-related problems and comprised approximately 21% of all men classified with an alcohol use disorder.

The prevalence and frequency of comorbidity of possible bipolar disorder was examined with attention-deficit hyperactivity disorder (ADHD) in a nonreferred population of twins. Children and adolescents aged 7 to 18 years with a history of manic symptoms were identified from a population-based twin sample obtained from state birth records (n = 1610). The sample was enriched for ADHD; however, there was also a random control sample (n = 466), which allowed a look at the population prevalence of the disorder. Juveniles with threshold or below threshold manic episodes were further assessed for comorbidity with Diagnostic and Statistical Manual of Mental Disorders (4th ed.; DSM-IV; American Psychiatric Association, 1994) and population-defined ADHD subtypes (from latent class analysis) using Fisher's exact test. Nine juveniles who exhibited DSM-IV manic (n = 1), hypomanic (n = 2) or below threshold episodes (n = 6) were identified. The population prevalence of broadly defined mania in the random sample was 0.2%. The possible manic episodes showed significant comorbidity with population-defined severe combined and talkative ADHD subtypes. It can be concluded that there is a significant association of bipolar symptoms with two population-defined subtypes of ADHD. Episodes of possible bipolar disorders as defined by DSM-IV are uncommon in this nonreferred sample. Children and adolescents with ADHD appear to be only modestly at increased risk for bipolar disorders.

The heritability of the degree of residential area urbanization in twins and their siblings in the Dutch population was examined. The postal code was known for 6879 twins and 2724 siblings registered with the Netherlands Twin Register and born between 1940 and 1983. Using data from Statistics Netherlands (Centraal Bureau voor de Statistiek, 2001), these postal codes could be related to residential area characteristics, including urbanization level. The degree of urbanization was assessed on a 5-point scale: very heavy, heavy, moderate, low and not urbanized. Genetic model-fitting was carried out in three age cohorts: young adults (born 1975 to 1983), adults (born 1965 to 1974) and older adults (born 1940 to1964). Twin and sibling resemblance in urbanization level was expressed in polychoric correlations. These correlations decreased from the youngest cohort (.66 to .86) to the oldest cohort (.20 to .58). In all 3 age cohorts, genetic factors did not contribute to familial resemblance. The influence of common environment decreased in importance from the young cohort (70% to 83%) to the old cohort (46% to 47%) and was lower in women than in men in all but the oldest age cohort. This study did not replicate Australian findings of a genetic contribution in the older cohorts; common environmental factors and, increasingly with age, unique environmental factors determine where the Dutch live. Future studies in European and other populations will reveal whether these results are specific to the Dutch population.

This study reports on genetic and environmental influences on the frequency of orgasm in women during sexual intercourse, during other sexual contact with a partner, and during masturbation. Participants were drawn from the Australian Twin Registry, and recruited from a large, partly longitudinal twin-family study. Three thousand and eighty women responded to the anonymous self-report questionnaire, including 667 complete monozygotic (MZ) pairs and 377 complete dizygotic (DZ) same-sex pairs, 366 women from complete DZ opposite-sex pairs, and 626 women whose co-twins did not participate. Significant twin correlations were found for both MZ and DZ twin pairs for all three items of interest. Age effects were statistically significant for some items. Models incorporating additive genetic, shared and nonshared environmental influences provided the best fit for Items 1 and 3, while a model with additive and nonadditive genetic influences along with nonshared envir-onment fitted the data from Item 2. While an independent pathway model fits the data most par-simoniously, a common pathway model incorporating additive genetic (A), shared environment (C), and unique environment (E) effects cannot be ruled out. Overall, genetic influences account for approximately 31% of the variance of frequency of orgasm during sexual intercourse, 37% of the variance of frequency of orgasm during sexual contact other than during intercourse, and 51% of the variance of frequency of orgasm during masturbation. Following Baker (1996), we speculate that this additive genetic variance might arise from frequency-dependent selection for a variety of female sexual strategies.

Not only are alcoholism and externalizing disorders frequently comorbid, they often co-occur in families across generations; for example, paternal alcoholism predicts offspring conduct disorder just as it does offspring alcoholism. To clarify this relationship, the current study examined the ‘common genes’ hypothesis utilizing a children-of-twins research design. Participants were male monozygotic (MZ) and dizygotic (DZ) twins from the Vietnam Era Twin Registry who were concordant or discordant for alcohol dependence together with their offspring and the mothers of those offspring. All participants were conducted through a structured psychiatric interview. Offspring risk of conduct disorder was examined as a function of alcoholism genetic risk (due to paternal and co-twin alcohol dependence) and alcoholism environmental risk (due to being reared by a father with an alcohol dependence diagnosis). After controlling for potentially confounding variables, the offspring of alcohol- dependent fathers were significantly more likely to exhibit conduct disorder diagnoses than were off- spring of nonalcohol-dependent fathers, thus indicating diagnostic crossover in generational family transmission. Comparing offspring at high genetic and high environmental risk with offspring at high genetic and low environmental risk indicated that genetic factors were most likely responsible for the alcoholism–conduct disorder association. The observed diagnostic crossover (from paternal alcoholism to offspring conduct disorder) across generations in the context of both high and low environmental risk (while genetic risk remained high) supported the common genes hypothesis.

Previous longevity studies of related individuals such as twins or siblings based on the major gene model have shown that the frequency and the relative risk of mortality of a beneficial allele in the population could be estimated. If, in addition to survival data for related individuals, the genetic markers data are available, one could try to locate the longevity allele in the genome. In the case where the phenotypic trait is life span or age at onset of disease, a two-step procedure can be used. First, the parameters of bivariate survival functions must be estimated from bivariate survival data for twins without markers. The second step is focused on determining the position of longevity genes between respective markers. To calculate the joint distribution of inheritance vector and genetic markers, the hidden Markov chain technique is used. This approach is illustrated with a simulation example for one longevity gene.

The genetic etiology of mathematical and reading (dis)ability has been studied in a number of distinct samples, but the true nature of the relationship between the two remains unclear. Data from the Netherlands Twin Register was used to determine the etiology of the relationship between mathematical and reading (dis)ability in adolescent twins. Ratings of mathematical and reading problems were obtained from parents of over 1500 twin pairs. Results of bivariate structural equation modeling showed a genetic correlation around .60, which explained over 90% of the phenotypic correlation between mathematical and reading ability. The genetic model was the same for males and females.

Substantial effort has been put into the exploration of the biological background of eating disorders, through family, twin and molecular genetic studies. Family studies have shown that anorexia (AN) and bulimia nervosa (BN) are strongly familial, and that familial etiologic factors appear to be shared by both disorders. Twin studies often focus on broader phenotypes or subthreshold eating disorders. These studies consistently yielded moderate to substantial heritabilities. In addition, there has been a proliferation of molecular genetic studies that focused on Diagnostic and Statistical Manual of Mental Disorders (4th ed.; DSM-IV; American Psychiatric Association, 1994) AN and BN. Seven linkage regions have been identified in genome-wide screens. Many genetic association studies have been performed, but no consistent association between a candidate gene and AN or BN has been reported. Larger genetic association studies and collaborations are needed to examine the involvement of several candidate genes and biological pathways in eating disorders. In addition, twin studies should be designed to assist the molecular work by further exploring genetic determinants of endophenotypes, evaluating the magnitude of contribution to liability of measured genotypes as well as environmental risk factors related to eating disorders. In this manner twin and molecular studies can move the field forward in a mutually informative way.

The 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.

Although it has been suggested that genetic influences on reading difficulties may differ in boys and girls, results obtained from previous analyses of data from same-sex twin pairs have failed to provide evidence for a differential genetic etiology of reading disability (RD) as a function of gender. However, results of a recent study in which data from both same-sex and opposite-sex twin pairs were analyzed indicated a higher heritability for reading difficulties in boys (Harlaar et al., 2005). Because the current sample of twin pairs tested in the Colorado Learning Disabilities Research Center is substantially larger than that analyzed for our previous report (Wadsworth et al., 2000), this hypothesis was tested more rigorously using data from both same-sex and opposite-sex twin pairs in our current augmented sample. Composite reading scores from 634 twin pairs were subjected to DeFries–Fulker sex-limitation analysis using the model-fitting approach of Purcell and Sham (2003). Analysis of data from the combined sample of male and female twins indicated that genetic influences account for more than half the proband reading deficit (h2g = .58). When this model was extended to test for gender differences in the magnitude of genetic influences on RD, h2g estimates were somewhat higher for females than for males (.63 and .53, respectively), but the difference was nonsignificant (p > .3). A test for qualitative gender differences was also nonsignificant. Thus, these results provide little evidence for a differential genetic etiology of RD in boys and girls.

We investigated the genetic component of noise sensitivity using a twin-study design. The study sample consisted of 573 same-sexed twin pairs from the Finnish Twin Cohort. The 131 monozygotic (MZ) and 442 dizygotic (DZ) twin pairs with an age range of 31 to 88 years replied to a questionnaire on noise and health-related items in 1988. The noise sensitivity of respondents was defined as high, quite high, quite low or low. MZ pairs were more similar with regards noise sensitivity than DZ pairs, and quantitative genetic modeling indicated significant familiality. The best z-fitting genetic model provided an estimate of heritability of 36% (95% CI = .20–.50) and when hearing impaired subjects were excluded this rose to 40% (95% CI = .24–.54). In conclusion, noise sensitivity does aggregate in families and probably has a genetic component.

Monozygotic (MZ) twins may be discordant for complex traits due to differential environmental exposure in utero, epigenetic variability in imprinting, X chromosome inactivation, or stochastic effects. Occasionally MZ twins may be discordant for chromosomal and single gene disorders due to somatic mosaicism. For complex traits, which are due to the interactive effects of multiple genes and environmental factors, the affected twin of a discordant MZ pair offers the possibility for identifying somatic mutations in candidate genes. DNA sequencing of candidate genes in discordant MZ twins can identify those rare etiologic mutational events responsible for the different phenotypes since the confounding effects of common single nucleotide polymorphisms are eliminated, as DNA sequences should be identical in MZ pairs. In this report we describe the extensive DNA sequencing of 18 candidate genes in a sample of MZ and dizygotic (DZ) twins with nonsyndromic cleft lip with or without cleft palate. We were unable to identify any somatic differences in approximately 34 Kb of DNA sequenced in 13 MZ pairs, for a total of approximately 900 Kb of sequence comparisons, supporting the hypothesis that nonetiologic posttwinning mutations are rare. While no etiologic variants were identified in this study, sequence comparisons of discordant MZ twins can serve as a tool for identifying etiologic mutations in clefting and other complex traits.

Boys and girls may display different styles of aggression. The aim of this study was to identify subtypes of aggression within the Child Behavior Checklist (CBCL) aggression scale, and determine their characteristics for both sexes. Maternal CBCL ratings of 7449 7-year-old twin pairs were analyzed using principal components analyses to identify sub- types of aggression, and structural equation modeling to carry out genetic analyses. Two aggression subtypes were identified: relational and direct aggression. The correlation between these subtypes was .58 for boys and .47 for girls. Boys had higher mean scores for both subtypes of aggression, but sex differences were largest for direct aggression. For relational aggression, 66% of the variance was due to additive genetic influences, 16% to shared environment and 18% to nonshared environment. For direct aggression, additive genetic effects accounted for 53% of the variance in males and 60% in females, shared environment explained 23% of the variance in males and 13% in females, and nonshared environmental effects explained 24% of the variance in males and 27% in females. Covariance between the aggression subtypes was mostly accounted for by additive genetic (55% for boys, 58% for girls) and shared environmental influences (33% for boys, 30% for girls). Direct and relational aggression were both influenced by one underlying set of shared environmental factors, but only partly by the same genes (the genetic correlation was .54 for boys and .43 for girls). These findings may have implications for how aggressive behavior should be assessed in boys and girls.