Human chromosomes terminate in a number of repeats of the sequence TTAGGG. At birth, each chromosome end is equipped with approximately 15 kb of telomere sequence, but this sequence is shortened during each cell division. In cell cultures telomere shortening is associated with senescence, a phenomenon that has also been observed in normal adult tissues, indicating that telomere loss is associated with organismal ageing. Previous work has established that the rate of telomere loss in humans is age dependent, and recent work shows a sex-specific difference in telomere length and shortening in individuals over the age span of 20 to 75 years. Here, terminal restriction fragment lengths on DNA purified from whole blood were measured to examine the mean telomere length in a cross-sectional cohort of 816 Danish individuals of age 73 to 101 years. In this age group, females show a linear correlation between telomere length and age, whereas the pattern tends to be nonlinear (quadratic in age) for males. This difference in telomere length dynamics between the 2 sexes may be caused by several different mechanisms, including differences in selection by mortality, differences in leukocyte population or different telomerase expression pattern.

A tight link exists between telomere length and both population doublings of a cell culture and age of a given organism. The more population doublings of the cell culture or the higher the age of the organism, the shorter the telomeres. The proposed model for telomere shortening, called the end replication problem, explains why the telomere erodes at each cellular turnover. Telomere length is regulated by a number of associated proteins through a number of different signaling pathways. The determinants of telomere length were studied using whole blood samples from 287 twin pairs aged 73 to 95 years. Structural equation models revealed that a model including additive genetic effects and non- shared environment was the best fitting model and that telomere length was moderately heritable, with an estimate that was sensitive to the telomere length standardization procedure. Sex-specific analyses showed lower heritability in males, although not statistically significant, which is in line with our earlier finding of a sex difference in telomere dynamics among the elderly and oldest-old.

The relationship between subjective wellbeing (SWB) and self-reported sleep problems was investigated in a cohort of Norwegian twins aged 18 to 31 years. Questionnaire data from 8045 same- and opposite-sex twins were analyzed using structural equation modeling to explore the relative effects of genetic and environmental influences on phenotypic variance and covariance. Special attention was paid to sex-specific effects. The correlation between the phenotypes was estimated to be −.43. Univariate analyses indicated considerable genetic influences for both SWB and sleep problems, for male and female twins alike. The best fitting bivariate model specified additive genetic and individual environmental factors for both phenotypes, and nonadditive genetic effects for sleep problems, with no sex-specific effects. Genetic and environmental effects accounted for 60% and 40% of the phenotypic correlation, respectively. Additive genetic factors affecting the two phenotypes were correlated (−.85), suggesting that part of the genetic effects that positively influence SWB also protect against sleep problems. In conclusion, the results indicate considerable overlap in genetic etiology for SWB and sleep problems, for males and females alike.

Genetic factors have historically been thought of as important in the development of obsessive–compulsive disorder (OCD). For the estimation of the relative importance of genetic and environmental factors, twin studies are an obvious approach. Twin studies of OCD have a long history, starting in 1929. In this review, over 70 years of twin research of OCD is presented, using four different approaches that represent the steps in the twin research of OCD from past to present. These steps include (1) case-studies of twins with OCD from the old literature; (2) twin studies of OCD using Diagnostic and Statistical Manual of Mental Disorders (DSM) criteria; (3) twin studies of OCD using a dimensional approach, comparing resemblances in monozygotic and dizygotic twins; and (4) twin studies of OCD using a dimensional approach, analyzing the data with Structural Equation Modeling. It is concluded that only the studies using the last method have convincingly shown that, in children, obsessive–compulsive (OC) symptoms are heritable, with genetic influences in the range of 45% to 65%. In adults, studies are suggestive for a genetic influence on OC symptoms, ranging from 27% to 47%, but a large twin study using a bio- metrical approach with continuous data is still needed to provide conclusive evidence. Strategies for future twin studies of OCD are discussed.

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.

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.

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.

Twin studies of lipids have almost exclusively involved Caucasians. People of African descent are known to show a healthier lipid profile, but relatively little is known about ethnic differences in genetic and environmental influences on lipids. One hundred and six African American (AA) and 106 European American (EA) twins (30 singletons and 91 complete pairs: 49 monozygotic, 21 dizygotic and 21 opposite-sex) from the south-eastern United States were studied (mean age 17.9 ± 3.2 years; 79% fasting). Lipids were assayed with the Cholestech LDX system. Analyses were adjusted for fasting status. Generalized estimating equations were used to test for the effects of sex and ethnicity on means, controlling for the dependence within twin pairs. Structural equation modeling was used to estimate genetic and environmental effects on each lipid variable. Females showed higher high-density lipoprotein (HDL) values than males (p < .001) and AAs showed higher HDL values than EAs (p < .001). EA males had higher triglyceride values than other groups (p = .02). All parameter estimates could be set equal across sex. Parameter estimates for total cholesterol, triglycerides and HDL could be set equal across ethnicity. The best fitting model for low- density lipoprotein (LDL) showed higher heritability in AAs (.92) than EAs (.69). Heritabilities ranged from 69% to 92%, with remaining variation explained by nonshared environmental effects. Adjustment for body mass index had virtually no effect on the heritability estimates. In this first twin study on lipids to include AAs, no ethnic differences in heritability were found except for LDL, where AAs exhibited higher estimates.

We examined the contribution of genetic and environmental influences to variation in resting systolic (SBP) and diastolic (DBP) blood pressure in participants from 4 twin studies carried out between 1986 and 2003. A total of 1577 subjects (682 males, 895 females) participated. There were 580 monozygotic twins, 664 dizygotic twins and 333 of their siblings. The 4 studies sampled subjects in different age groups (average age 17, 32, 37, 44 years), allowing for comparison of the relative contribution of genetic and environmental factors across the first part of the life span. Blood pressure was assessed under laboratory conditions in 3 studies and by ambulatory monitoring in 1 study. Univariate analyses of SBP and DBP showed significant heritability of blood pressure in all studies (SBP h2 48% to 60%, DBP h2 34% to 67%). Overall, there was little evidence for sex differences in blood pressure heritability, and no evidence for differences in heritability due to measurement strategy (laboratory vs. ambulatory). For 431 subjects there were data from 2 or more occasions that allowed us to assess the tracking of blood pressure over time and to estimate the genetic and environmental contributions to blood pressure tracking. Correlations over time across an average period of 7.1 years (tracking) were between .41 and .70. Multivariate genetic analyses showed that blood pressure tracking was entirely explained by the same genetic factors being expressed across time. It was concluded that whole genome scans for resting blood pressure can safely pool data from males and females, laboratory and ambulatory recordings, and different age cohorts.

A few twin studies on cancer have addressed questions on the possible carcinogenic or protective effects of twining by comparing the occurrence of cancer in twins and singletons. The nationwide Swedish Family-Cancer Database of 10.2 million individuals and 69,654 0- to 70-year-old twin pairs were used to calculate standardized incidence ratios (SIRs) and 95% confidence intervals (CIs) for all main cancers compared to singletons. The overall risk of cancer in same- or different-sex twins was at the same level as the risk for singletons. Testicular cancer, particularly seminoma, was increased among same-sex twins (1.54) and all twins to an SIR of 1.38. Among other tumors, neurinomas and nonthyroid endocrine gland tumors were increased. Colorectal cancers and leukemia were decreased among all twins. Melanoma and squamous cell skin cancer were decreased in male same-sex twins. The data on this unselected population of twins suggest that twinning per se is not a risk factor of cancer. In utero hormonal exposures or postnatal growth stimulation may be related to the risk of testicular cancer and pituitary tumors. Protective effects against colorectal cancer may be related to a beneficial diet, and in melanoma and skin cancer, to socioeconomic factors. The study involved multiple comparisons, and internal consistency between the results was one of the main factors considered for their plausibility. The results should encourage others working on twin and singleton populations to examine the specific associations and emerging hypotheses.

Maternal age is the most important nongenetic factor influencing the twinning rate. Every study of the effect of other factors should consider the age distribution of the mothers. Besides standardizing techniques, the age-specific twinning rates are analyzed. Especially, the slope of the regression line is considered when the age-specific twinning rates are regressed against maternal age. How well the maximum age-specific twinning rate measures the variation in the maternal age effect is also studied. The two measures, which are strongly correlated, give consistent results. The proposed methods are applied to data from Finland (1866 to 2003) and Denmark (1855 to 2000). Comparisons with Sweden (1861 to 2000) and Norway (1855 to 2003) are also made. In general, marked decreasing trends in the twinning rates are discernible up to the middle of the 20th century. In Sweden the decline starts around the beginning of the 20th century and is stronger than in Denmark and Norway. The decrease in the twinning rate for Finland, which up to World War II was rather isolated, sets in around the middle of the 20th century and is not as strong as in other Nordic countries. After the minima around 1980, strong increasing trends are noted. This is mainly caused by the influence of the artificial reproduction technologies and particularly the use of fertility-enhancing drugs on the commonly noted dependence between maternal age and the twinning rate. Similar temporal trends can be observed in the slopes of the regression line and in the maximum age-specific twinning rates.

While preterm birth and restricted fetal growth are strongly associated with infant mortality, the extent to which these associations are modified by placental abruption remains unknown. A retrospective cohort study was carried out to examine the risk of infant mortality among twins in relation to abruption, and explore the independent contributions of preterm birth and restricted fetal growth to these associations. The study was restricted to women who had delivered twins at 22 weeks' gestation or more and fetuses weighing 500 grams or more in the United States (1989–2000). Risks of preterm birth (less than 37 weeks' gestation), fetal growth restriction and infant mortality, in relation to placental abruption, were evaluated. All analyses were adjusted for potential sociodemographic confounding factors. The association between restricted twin fetal growth and abruption was the strongest among the most severely growth-restricted babies (i.e., less than 1 centile), with the strength of association diminishing with increasing birthweight centiles. The risk of preterm birth among pregnancies with and without abruption were 80.1% and 51.9%, respectively (relative risk [RR] 1.5, 95% confidence interval [CI] 1.4–1.6). The risk of small-for-gestational-age (SGA; birthweight of less than the 10th centile for gestational age) among abruption and nonabruption births was 11.7% and 9.2%, respectively (RR 1.3, 95% CI 1.2–1.4). Compared with twins of the appropriate growth delivered at term, the relative risks for infant mortality in the presence of abruption were 9.9 (95% CI 5.4–18.2) for term-SGA, 25.0 (95% CI 22.3–28.1) for preterm-non-SGA, and 36.2 (95% CI 28.4–46.1) for preterm-SGA births. The association between infant mortality and abruption among twins appears largely mediated through preterm birth, and to a lesser extent, through SGA. The association between fetal growth and abruption is strongest among the severely growth-restricted babies, suggesting that the origins of placental abruption may develop in early pregnancy.

The objective of this study was to compare length of gestation, fetal growth, and birthweight by race/ethnicity and pregravid weight groups in twin pregnancies. Three thousand and thirty-six twin pregnancies of 28 weeks or more gestation were divided by race/ethnicity (White, Black and Hispanic), and pregravid body mass index (BMI) groups (less than 25.0 vs. 25.0 or more). Outcomes were modeled using multiple regression, controlling for confounders, with White non-Hispanic women as the reference group. Hispanic women had the highest average birthweight and the longest gestation, as well as the lowest proportions of low birthweight, very low birthweight, preterm and early preterm births of the 3 race/ethnicity groups. In the multivariate analyses, Hispanic women had significantly longer gestations (by 7.8 days) and faster rates of fetal growth midgestation (20 to 28 weeks, by 17.4 g/week) and late gestation (after 28 weeks, by 5.3 g/week), whereas Black women had significantly slower rates of fetal growth (by 5.7 g/week and by 4.5 g/week, respectively). These findings in twins reflect the racial and ethnic disparities previously shown in singletons, including the Hispanic paradox of longer gestations and higher rates of fetal growth.

An overview of the nature and success of organ transplantation in monozygotic (MZ) twins is presented. Recent timely examples demonstrate the unique donor–recipient relationship shared by MZ co-twins. Next, a recent analysis of MZ co-twin differences in the epigenetic profile and associations with differences in life history factors is presented. This work has been the focus of considerable attention by scientists and the media. The final section of this column summarizes information and events concerning twins' longevity, screen careers, older parenting of twins and the origin of the word ‘twin’.