Our aim was to test the direction of causation between self-report parental monitoring (PM) and the liability to illicit drug initiation (DI) as indicated by cannabis, cocaine, and stimulants. We fitted a multiple indicator model to test causal and non-causal models based on a large, genetically informative cross-sectional sample of male twins. The sample comprised 1,778 males aged 24–62 years from the Virginia Adult Twin Study of Psychiatric and Substance Use Disorders. Data came from self-report measures of lifetime cannabis, stimulants, and cocaine initiation, and retrospective assessment of PM between ages 8–17 years. Multivariate modeling showed that familial aggregation in PM and DI were both explained by a combination of additive genetic and shared environmental effects. Moreover, the significant association between PM and DI was best explained by a correlated liability model versus causal models. PM has typically been assumed to be an environmental, causal risk factor for drug use and has been shown to be among the more salient environmental risk factors for illicit DI. Our data were not consistent with this causal hypothesis. Instead, a correlated liability model in which PM and risk of DI share common genetic and environmental risks provided a better fit to the data.

Studies have suggested both adverse and protective associations of obesity with depressive symptoms. We examined the contribution of environmental and heritable factors in this association. Participants were same-sex twin pairs from two population-based twin cohort studies, the Older Finnish Twin Cohort (n = 8,215; mean age = 44.1) and the US Midlife Development in the United States (MIDUS; n = 1,105; mean age = 45.1). Body mass index (BMI) was calculated from self-reported height and weight. Depressive symptoms were assessed using Beck's Depression Inventory (BDI; Finnish Twin Cohort), and by negative and positive affect scales (MIDUS). In the Finnish Twin Cohort, higher BMI was associated with higher depressive symptoms in monozygotic (MZ) twins (B = 2.01, 95% CI = 1.0, 3.0) and dizygotic (DZ) twins (B = 1.17, 0.5, 1.9) with BMI >22. This association was observed in within-pair analysis in DZ twins (B = 1.47, CI = 0.4, 2.6) but not in within-pair analysis of MZ twins (B = 0.03, CI = -1.9, 2.0). Consistent with the latter result, a bivariate genetic model indicated that the association between higher BMI and higher depressive symptoms was largely mediated by genetic factors. The results of twin-pair analysis and bivariate genetic model were replicated in the MIDUS sample. These findings suggest an association between obesity and higher depressive symptoms, which is largely explained by shared heritable biological mechanisms.

Objectives: This research examined the familial aggregation of migraine, depression, and their co-occurrence.

Methods: Diagnoses of migraine and depression were determined in a sample of 5,319 Australian twins. Migraine was diagnosed by either self-report, the ID migraine™ Screener, or International Headache Society (IHS) criteria. Depression was defined by fulfilling either major depressive disorder (MDD) or minor depressive disorder (MiDD) based on the Diagnostic and Statistical Manual of Mental Disorders (DSM) criteria. The relative risks (RR) for migraine and depression were estimated in co-twins of twin probands reporting migraine or depression to evaluate their familial aggregation and co-occurrence.

Results: An increased RR of both migraine and depression in co-twins of probands with the same trait was observed, with significantly higher estimates within monozygotic (MZ) twin pairs compared to dizygotic (DZ) twin pairs. For cross-trait analysis, the RR for migraine in co-twins of probands reporting depression was 1.36 (95% CI: 1.24–1.48) in MZ pairs and 1.04 (95% CI: 0.95–1.14) in DZ pairs; and the RR for depression in co-twins of probands reporting migraine was 1.26 (95% CI: 1.14–1.38) in MZ pairs and 1.02 (95% CI: 0.94–1.11) in DZ pairs. The RR for strict IHS migraine in co-twins of probands reporting MDD was 2.23 (95% CI: 1.81–2.75) in MZ pairs and 1.55 (95% CI: 1.34–1.79) in DZ pairs; and the RR for MDD in co-twins of probands reporting IHS migraine was 1.35 (95% CI: 1.13–1.62) in MZ pairs and 1.06 (95% CI: 0.93–1.22) in DZ pairs.

Conclusions: We observed significant evidence for a genetic contribution to familial aggregation of migraine and depression. Our findings suggest a bi-directional association between migraine and depression, with an increased risk for depression in relatives of probands reporting migraine, and vice versa. However, the observed risk for migraine in relatives of probands reporting depression was considerably higher than the reverse. These results add further support to previous studies suggesting that patients with comorbid migraine and depression are genetically more similar to patients with only depression than patients with only migraine.

We investigated genetic and environmental correlations and gene by environment interactions (GxE) between depressive symptoms measured by the Beck Depression Inventory (BDI) and quantity smoked measured by number of cigarettes smoked per day (CPD) using quantitative genetic modeling. The population-based sample consisted of 12,063 twin individuals from the Finnish Twin Cohort Study. Bivariate Cholesky decomposition revealed that the phenotypic correlation (r = 0.09) between BDI and CPD was explained by shared genetic (r g = 0.18) and environmental (r e = 0.08) factors. GxE models incorporating moderator effects were built by using CPD as trait and BDI as moderator and vice versa. The importance of the genetic variance component increased with increasing moderator value in both models. Thus, the influence of genetic effects on variance of smoking quantity was enhanced in individuals with elevated depression score and vice versa; the genetic effects on depression variance were potentiated among heavy smokers. In conclusion, shared genetic and environmental factors as well as GxE underlie the association of smoking with depression.

Although cross-sectional twin studies have assessed the genetic and environmental etiologies of substance use during adolescence and early adulthood, comparisons of results across different samples, measures, and cohorts are problematic. While several longitudinal twin studies have investigated these issues, few corroborating adoption studies have been conducted. The current study is the first to estimate the magnitude of genetic, shared environmental, and non-shared environmental influences on substance use (cigarettes, alcohol, and marijuana) from ages 14 to 18 years, using a prospective longitudinal adoption design. Adoptive and control sibling correlations provided substantial evidence for early genetic effects on cigarette, alcohol, and marijuana use/no use. Shared environmental effects were relatively modest, except for alcohol use, which showed increases in late adolescence (age 17 to 18 years). Sibling similarity for quantity/frequency of use also support additive genetic influences across adolescence, with some shared environmental influences for all three substances. To test the stability of these influences across time, a series of independent pathway models were run to explore common and age-specific influences. For all substances, there were minimal age-specific additive genetic and shared environmental influences on quantity/frequency of use. Further, there was a trend toward increasing genetic influences on cigarette and alcohol use across ages. Genetic influences on marijuana were important early, but did not contribute substantially at age 17 and 18 years. Overall, the findings indicate that genetic influences make important contributions to the frequency/quantity of substance use in adolescence, and suggest that new genetic influences may emerge in late adolescence for cigarette and alcohol use.

Migraine frequently co-occurs with depression. Using a large sample of Australian twin pairs, we aimed to characterize the extent to which shared genetic factors underlie these two disorders. Migraine was classified using three diagnostic measures, including self-reported migraine, the ID migraine™ screening tool, or migraine without aura (MO) and migraine with aura (MA) based on International Headache Society (IHS) diagnostic criteria. Major depressive disorder (MDD) and minor depressive disorder (MiDD) were classified using the Diagnostic and Statistical Manual of Mental Disorders (DSM) criteria. Univariate and bivariate twin models, with and without sex-limitation, were constructed to estimate the univariate and bivariate variance components and genetic correlation for migraine and depression. The univariate heritability of broad migraine (self-reported, ID migraine, or IHS MO/MA) and broad depression (MiDD or MDD) was estimated at 56% (95% confidence interval [CI]: 53–60%) and 42% (95% CI: 37–46%), respectively. A significant additive genetic correlation (rG = 0.36, 95% CI: 0.29–0.43) and bivariate heritability (h2 = 5.5%, 95% CI: 3.6–7.8%) was observed between broad migraine and depression using the bivariate Cholesky model. Notably, both the bivariate h2 (13.3%, 95% CI: 7.0–24.5%) and rG (0.51, 95% CI: 0.37–0.69) estimates significantly increased when analyzing the more narrow clinically accepted diagnoses of IHS MO/MA and MDD. Our results indicate that for both broad and narrow definitions, the observed comorbidity between migraine and depression can be explained almost entirely by shared underlying genetically determined disease mechanisms.

Hair diameter and curvature are two characteristics of human scalp hair used in forensic contexts. While previous data show that subjective categorization of hair curvature is highly heritable, the heritability of objectively measured curvature and diameter, and variability of hair characteristics within each individual have not yet been studied. The present study measured hair diameter and curvature using an optical fiber diameter analyzer in a sample of 2,332 twins and siblings. Heritability was estimated using maximum likelihood structural equation modeling. Results show sex differences in the magnitude of genetic influence for mean diameter and curvature, with the vast majority of the variance accounted for by genetic effects in males (diameter = 86%, curvature = 53%) and females (diameter = 77%, curvature = 61%). The consistency of diameter (variance within an individual) was also highly heritable, but did not show sex limitation, with 68% of the variance accounted for by genetic factors. Moderate phenotypic correlations were seen between diameter and consistency (r = 0.3) but there was little correlation between diameter and curvature (r = -0.13). A bivariate Cholesky analysis was used to estimate the genetic and environmental correlations between hair diameter and consistency, yielding genetic correlations of r gF = 0.27 for females and r gM = 0.25 for males.

Strong geographical variations have been noted in the twinning rate (TWR). In general, the rate is high among people of African origin, intermediate among Europeans, and low among most Asiatic populations. In Europe, there tends to be a south–north cline, with a progressive increase in the TWR from south to north and a minimum around the Basque provinces. The highest TWRs in Europe have been found among the Nordic populations. Furthermore, within larger populations, small isolated subpopulations have been identified to have extreme, mainly high, TWRs. In the study of the temporal variation of the TWR in Norway, we consider the period from 1900 to 2014. The regional variation of the TWR in Norway is analyzed for the different counties for two periods, 1916–1926 and 1960–1988. Heterogeneity between the regional TWRs in Norway during 1916–1926 was found, but the goodness of fit for the alternative spatial models was only slight. The optimal regression model for the TWR in Norway has the longitude and its square as regressors. According to this model, the spatial variation is distributed in a west–east direction. For 1960–1988, no significant regional variation was observed. One may expect that the environmental and genetic differences between the counties in Norway have disappeared and that the regional TWRs have converged towards a common low level.

Gestational weight gain (GWG) has in numerous studies been associated with offspring birth weight (BW) and childhood weight. However, these associations might be explained by genetic confounding as offspring inherit their mother's genetic potential to gain weight. Furthermore, little is known about whether particular periods of pregnancy could influence offspring body weight differently. We therefore aimed to explore total and trimester-specific effects of GWG in monozygotic (MZ) twin mother-pairs on their offspring's BW, weight at 1 year and body mass index (BMI) at 5 and 10 years. MZ twin mothers born 1962–1975 were identified in national Swedish registers, and data on exposure and outcome variables was collected from medical records. We analyzed associations within and between twin pairs. We had complete data on the mothers’ GWG and offspring BW for 82 pairs. The results indicated that total, and possibly also second and third trimester GWG were associated with offspring BW within the twin pairs in the fully adjusted model (β = 0.08 z-score units, 95% CI: 0.001, 0.17; β = 1.32 z-score units, 95% CI: -0.29, 2.95; and β = 1.02 z-score units, 95% CI: -0.50, 2.54, respectively). Our findings, although statistically weak, suggested no associations between GWG and offspring weight or BMI during infancy or childhood. Our study suggests that total, and possibly also second and third trimester, GWG are associated with offspring BW when taking shared genetic and environmental factors within twin pairs into account. Larger family-based studies with long follow-up are needed to confirm our findings.

Twin gestation is known to be a risk factor for hypertensive disorders of pregnancy. However, the relationship between hypertensive disorders (pre-eclampsia (PE) and gestational hypertension (GH)) and chorionicity of twin pregnancy is unclear, and published data is conflicting. We decided to analyze the relationship between placentation and prevalence of hypertensive disorders. It was a retrospective cohort study. 312 twin pregnancies delivered between 2009 and 2014 were analyzed, 79 of which were monochorionic and 233 dichorionic. The occurrence of PE and GH was established according to American College of Obstetricians and Gynecologists’ (ACOG) guidelines. Hypertensive disorders were diagnosed significantly more often in dichorionic than in monochorionic twin pregnancies (19.7% vs. 8.9%; OR = 2.53 95% CI 1.04–6.45; p = .03). PE occurred more frequently in DCP (13.3% vs. 3.8%; OR = 3.88 95% CI 1.09–16.46; p = .02). There were no differences between those two groups in the prevalence of GH (6.4% vs. 5.1%; p = .79). The logistic regression model for the occurrence of PE included chorionicity, mother's age lower than 18 or higher than 40, pre-gestational obesity, in vitro fertilization, primiparity, gestational age at delivery, gestational diabetes, and active smoking. It showed that dichorionicity remained an independent risk factor for PE (adjusted OR = 4.97.0 95% CI 1.06–23.38; p = .04). Dichorionicity seems to be a risk factor for PE but not for GH development.

Hypoxia is the primary stimulus for the production of erythropoietin (EPO) in both fetal and adult life. Here, we investigated fetal plasma EPO concentrations in monochorionic (MC) twin pregnancies with selective intrauterine growth restriction (sIUGR) and abnormal umbilical artery (UA) Doppler. We diagnosed sIUGR in presence of (1) birth-weight discordance >20% and (2) either twin with a birth weight <10th percentile. An abnormal UA Doppler was defined as a persistent absent-reverse end diastolic flow (AREDF). The intertwin EPO ratio was calculated as the plasma EPO level of the smaller (or small-for-gestational-age) twin divided by the EPO concentration of the larger (or appropriate-for-gestational-age (AGA)) twin. Thirty-two MC twin pairs were included. Of these, 17 pairs were normal twins (Group 1), seven pairs were twins with sIUGR without UA Doppler abnormalities (Group 2), and eight pairs were twins with sIUGR and UA Doppler abnormalities (Group 3). The highest EPO ratio was identified in Group 3 (p < .001) but no significant differences were observed between Groups 1 and 2. Fetal hemoglobin levels did not differ significantly in the three groups, and fetal EPO concentration did not correlate with gestational age at birth. We conclude that fetal plasma EPO concentrations are selectively increased in MC twin pregnancies with sIUGR and abnormal UA Doppler, possibly as a result of uncompensated hypoxia.

A dramatic increase in twin pregnancies has been observed in the past few decades, primarily related to assisted reproductive techniques (ART) and increased average maternal age during pregnancy. Multiple pregnancies, compared to singleton pregnancies, are associated with greater perinatal morbidity and mortality. The present study evaluated the perinatal outcomes of pregnancies with discordant anomalous twins in a tertiary maternity ward in a developing country. Data were retrospectively collected from the Instituto Fernandes Figueira/FIOCRUZ, Brazil between January 2002 and December 2014. We identified 74 twin pregnancies with discordant anomalous twins. Final data analysis was based on 40 pregnancies. Congenital defects were classified according to the International Classification of Diseases: ICD-10: the digestive system was responsible in 27 (34%) cases; the central nervous system was responsible in 18 (22%) cases; the urinary tract was responsible in 14 (17%) cases; and the circulatory system was responsible in 14 (17%) cases. A total of 19 deaths occurred during the study period, and delivery before 30.4 weeks was a significant prediction of fetal death (p = .01). The presence of hydrops in the affected fetus was related to a higher number of deaths in healthy fetuses and contributed to a worse prognosis. The presence of this condition was the cause of 12 (55.6%) deaths in healthy fetuses. A 10 times higher risk of death of a normal co-twin was observed in cases of death of the anomalous twin (p = .002, OR 10.55, 95% CI: 1.9–58.52).

Twins can help researchers disentangle the roles of genes from those of the environment on human traits, health, and diseases. To realize this potential, the Australian Twin Registry (ATR), University of Melbourne, and the Charles Perkins Centre (CPC), University of Sydney, established a collaboration to form the Twins Research Node, a highly interconnected research facility dedicated specifically to research involving twins. This collaboration aims to foster the adoption of twin designs as important tools for research in a range of health-related domains. The CPC hosted their Twins Research Node's launch seminar entitled ‘Double the power of your research with twin studies’, in which experienced twin researchers described how twin studies are supporting scientific discoveries and careers. The launch also featured twin pairs who have actively participated in research through the ATR. Researchers at the CPC were surveyed before the event to gauge their level of understanding and interest in utilizing twin research. This article describes the new Twins Research Node, discusses the survey's main results and reports on the launch seminar.

The interrelatedness between twin research and the arts is explored via a new play about a famous case. In the 1960s, identical twin David Bruce Reimer was accidentally castrated as an infant during circumcision to correct a urinary problem. The decision to raise him as a girl, and the consequences of that decision, are explored in the new theatrical production of Boy. Other examples of the arts mirroring science, and vice versa, are described. Next, brief reviews and summaries of twin research on sexual orientation, 1860s’ knowledge of placental arrangements and twinning mechanisms, and genes underlying multiple birth conception and fertility related measures are provided. This article concludes with a look at twins on college campuses and the identification of individuals by their brain waves. A correction and clarification regarding my article on the Brazilian Twin Registry in the last issue of THG (Segal, 2016) is also provided.

E. M. Nicholls (1927–2011) was a humanist, medical practitioner, human biologist, geneticist and, above all, a teacher, as well as a husband and father. He believed that he had made a fundamental contribution to the two-hit model of cancer formation. This hypothesis is associated with retinoblastoma, in particular. Nicholls presented it through his observations on neurofibromatosis. He received little credit for what he believed was his most original contribution to medical science. This note attempts to redress the balance in his favor.