Birth statistics for the Johannesburg Metropolitan Region were collected for 757 151 confinements from 1969 to 1989 (467 513 Black, 194 375 White, 67 250 Coloured and 28 013 Indian confinements). From 1969 to 1978 data on the sexes of twins were also collected for 375 203 of the confinements (203 504 Black, 129 631 White, 28 253 Coloured and 13 815 Indian confinements). A twin confinement was defined as two deliveries during one confinement. Twinning rates (TRs), defined as the number of twin confinements per 1000 total confinements, were calculated per year for each population group and from 1969–1978 estimates of the relative proportions of dizygotic (DZ) and monozygotic (MZ) twins were calculated and thus the relative DZTRs and MZTRs. A significant decline in Black and Coloured TRs was observed between 1969 and 1989. A significant decline in Black DZTR but not Black MZTR was observed between 1969 and 1978, the Coloured twin sample was too small to show significant trends over this period. It is probable that the overall decline in Black twinning may be explained by a decline in the DZTR. An analysis of birth statistics for 159 748 confinements (134 504 Black and 25 244 White confinements) collected as part of a prospective study of TRs in the Johannesburg Metropolitan Region from 1988 to 1990, indicated that the Black TR continued to decline at least until the end of 1990. TRs in the Johannesburg Metropolitan Region calculated from City Health Department birth statistics collected from 1988 to 1990 were: 13.8 and 10.77 for the Black and White populations, respectively. TRs for this period calculated from the combined birth statistics of 14 hospitals, nursing homes and maternity clinics across the region were: 12.4 and 10.88 for the Black and White populations, respectively.

The East Flanders Prospective Twin Survey (EFPTS), started in 1964, is unique among the 17 major European twin registers because it is population based, the twins (and higher order births) are ascertained at birth, basic perinatal data are collected, chorion type is established and, when appropriate, genetic markers including DNA fingerprints, are determined. The total number of sets is 5089 twin, 158 triplet and 14 of higher order. Zygosity has been diagnosed on the basis of sex, placental structure and genetic markers in more than 95% of pairs. The EFPTS is the only large register that includes placental data and allows differentiation of three subtypes of monozygotic twins based on the time of the initial zygotic division: the dichorionic—diamnionic pairs (early), the monochorionic—diamnionic pairs (intermediate), and the monochorionic—monoamnionic pairs (late). Methodology and basic results in twins are considered in this article; detailed studies will be reported later. The sex proportion in dizygotic (DZ) twins is the same as in singletons, whereas monozygotic (MZ) twins number more girls than boys. The difference in perinatal mortality between DZ and MZ twins is limited to the monochorionic MZ subgroup. Birth weight is highest in DZ twins and diminishes stepwise in MZ dichorionic and MZ monochorionic twins. Duration of pregnancy follows the same trend but is limited to a few days. Iatrogenic pregnancies are increasing to the point of representing almost 50% of the twin births in 1997.

Depression scores (DSSI) were available for 1232 MZ and 751 DZ female twin pairs who completed a mailed questionnaire. Pairs were divided into those concordant for being in a marriage-like state, concordant for having no partners, and those discordant. The pattern of twin correlations differed according to marital status. Our results suggest that having a marriage-like relationship acts as a protective factor in reducing the impact of inherited liability to symptoms of depression in the general population.

Birth weight is in large extent influenced by gestational age. In addition genetic and environmental factors determine intrauterine growth and birth weight. The contributions of these factors may be influenced by maternal smoking during pregnancy. We examined birth weight and maternal smoking in a sample of 2930 twin pairs from the Netherlands Twin Register using structural equation modelling. Gestational age accounted for 27–44% of the variance in birth weight. A lower variability of birth weight and a lower association of birth weight with gestational age was found in twins whose mothers smoked during pregnancy. The variance not associated with gestational age was independent of maternal smoking during pregnancy. A systematic smaller part of the variability in birth weight was associated with variability in gestational age in second born twins compared to first born twins. The heritability of interindividual differences in birth weight was modest (10% for twins with non-smoking mothers and 11% for twins with smoking mothers). Common environmental influences other than gestational age accounted for a slightly larger part of the variance not associated with gestational age (17–20%).

Models are presented for the analysis of longitudinal data from same-age twins which permit the exploration of a remarkably diverse array of alternative explanations for continuity and change during development. Data of this type permit the detection of new sources of genetic or environmental covariation during development that are not expressed at earlier ages and, because they include the effects of age-specific genes, the resulting heritability estimates are more reliable than those obtained from relatives who differ in age. The proposed models were applied to measurements of HDL cholesterol obtained on 81 pairs of monozygotic (MZ) twins and 69 dizygotic (DZ) pairs at 11, 12.5 and 14 years of age. All three MZ co-twin correlations were substantially higher than the self correlations across occasions, suggesting that new sources of genetic or environmental covariation must be expressed during early adolescence. This interpretation was confirmed by analysis of the full covariance matrices which showed that only models which assumed the expression of new or age-specific genes could explain the observed pattern of covariation. Because they include the effects of age-specific genes, the resulting heritabilities (0.80–0.83) were substantially higher than many previous estimates.

The predictive relation between neonatal reactivity and 12-, 18-, and 24-month temperament was assessed for 22 appropriate-for-gestational-age (AGA)/small-for-gestational-age (SGA) twin pairs. Neonatal reactivity included ratings of visual and auditory orienting responses to a bull's-eye, rattle, bell, voice, and face plus voice combined, as well as alertness. Infant temperament ratings were made of emotional tone, activity, attentiveness, and social orientation to staff during ageappropriate activities in the laboratory. There were no group differences in the neonatal or infant ratings. For AGA twins, a pattern of predictive correlations was obtained between neonatal reactivity and temperament at each age. A similar predictive pattern was not observed for the SGA twins. Group differences in rates of maturation related to stresses associated with intrauterine growth retardation influenced the significance of the neonatal variables for later temperament development.

The effects on sleep pattern (‘short-sleep’ versus ‘long-sleep’) and subjective sleep disturbance of genotype, personality, symptoms of anxiety and depression, and lifestyle, were examined using survey data on a clinically unselected sample of adult Australian twin pairs, aged 17–88 years. When the effects of genotype, personality and symptoms were ignored, lifestyle variables appeared to account for roughly 4% of the variance in sleep disturbance, and 9% of the variance in sleep pattern. Significant genetic effects on sleep disturbance and sleep pattern were found, which were only partly explained by the effects of personality and symptoms of anxiety and depression. Much of the association between sleep disturbance and lifestyle appeared to be explained by separate effects of personality and symptoms of anxiety and depression on sleep and lifestyle (‘genotype – risk-factor correlation’). There was little evidence for genetically determined differences in sensitivity to the lifestyle variables (‘genotype × risk-factor interaction’).

We examined the cumulative prevalences of 22 symptoms thought to reflect immune system function reported in a questionnaire mailed to 7616 Australian twins. The associations between symptoms and demographic variables were expressed in terms of polychoric or polyserial correlations, and a principal components analysis performed. Factors representing underlying propensities respectively to allergic disease, various minor infections, diseases associated with aging such as arthritis, skin disease, and respiratory tract infection were extracted. Possible processes underlying these symptom clusters and the relative strengths and weaknesses of this type of analysis are discussed.

New large-sample data show that non-additive genetic effects, probably epistatic interactions between loci, and sex-limited gene expression are significant features of the genetic architecture of human personality as measured by questionnaire scales of extraversion and neuroticism. Three large data sets – new data on large samples (n = 20 554) of US twins, their spouses, parents, siblings and children, correlations for Australian twins (n = 7 532), and previously published twin data from Finland (n = 14 288) – are subjected to an integrated analysis to test alternative hypotheses about the genetic causes of family resemblance in personality. When allowance is made for differences in reliability of the scales, the combined data are consistent with the same model for variation. There are significant amounts of genetic non-additivity for both dimensions of personality. The evidence favours additive × additive epistatic interactions rather than dominance. In the case of neuroticism, there is especially strong evidence of sex differences in genetic architecture favouring a greater relative contribution of non-additive genetic effects in males. The data confirm previous claims to find no major contribution of the shared environment of twins and siblings to these dimensions of personality. Correlations between spouses are zero, and the correlations for very large samples of siblings and non-identical twins do not differ significantly.

The dynamics of perinatal mortality rates (PNMR) and causes of death in twin pregnancies over 13 years in the Northern Region of the National Health Service in England is described. All twin perinatal deaths occurring between 1982–1994 were identified from the Northern Region Perinatal Mortality Survey. The twinning rate increased from 9.9 per 1000 maternities in 1982 to 12.0 in 1994. There was a total of 10734 twin pregnancies and of these 421 resulted in 530 perinatal deaths. The perinatal mortality rate in twins significantly decreased over time (1982–87, 55.4 per 1000; 1988–94, 44.4 per 1000; P = 0.01). The PNMR was significantly higher for twins from like-sexed than from unlike-sexed pairs (53.5 and 34.4 per 1000 respectively, P < 0.001). Despite no improvement in birthweight distribution in the twin population, birthweight-specific perinatal mortality rates for both like and unlike-sexed twins decreased for each birthweight category in 1988–94 compared with 1982–87. Twins with very low birthweight ( < 1500 g) comprised 69%, and preterm twins ( < 37 completed weeks of gestation) 74.9% of all twin perinatal deaths. The major immediate cause of early neonatal death was pulmonary immaturity (63%); antepartum anoxia caused 76.9% of antenatal deaths. Unexplained preterm labour and intrauterine death were the leading obstetric factors underlying death in twins. Despite a decrease over the 13 years, the perinatal mortality rate in twins in the Northern Region remains high. Continued monitoring of trends in twinning and mortality rates is needed to inform health care planning.

A retrospective longitudinal study was performed to quantify foetal growth velocities in twin pregnancies and to determine the effect of variables specific to twin pregnancies on growth velocity. Foetal growth velocity standard deviation (Z) scores were calculated from serial ultrasound data using published singleton reference data for 131 consecutive sets of twins from 30 to 37 weeks' gestation. Compared with low-risk pregnancies, the twin foetal abdominal area growth velocity Z scores were significantly reduced from 30 to 37 weeks and biparietal diameter growth velocity Z scores were also significantly lower, from 30 to 33 weeks. Amongst the twin pairs there were no significant differences in Z scores with respect to chorionicity, foetal sex, birth order to whether delivery was premature or term. This retrospective study has demonstrated that twin foetal growth velocity is reduced when compared to singletons from at least as early as 30 weeks' gestation. Twin specific variables such as chorionicity, sex, birth order and subsequent premature birth do not need to be accounted for in the interpretation of growth velocities in twins. The clinical importance of determining foetal growth velocity in twin pregnancies awaits further prospective study.

Molecular epidemiological studies confirm a substantial contribution of individual genes to variability in susceptibility to disease and death for humans. To evaluate the contribution of all genes to susceptibility and to estimate individual survival characteristics, survival data on related individuals (eg twins or other relatives) are needed. Correlated gamma-frailty models of bivariate survival are used in a joint analysis of survival data on more than 31 000 pairs of Danish, Swedish and Finnish male and female twins using the maximum likelihood method. Additive decomposition of frailty into genetic and environmental components is used to estimate heritability in frailty. The estimate of the standard deviation of frailty from the pooled data is about 1.5. The hypothesis that variance in frailty and correlations of frailty for twins are similar in the data from all three countries is accepted. The estimate of narrow-sense heritability in frailty is about 0.5. The age trajectories of individual hazards are evaluated for all three populations of twins and both sexes. The results of our analysis confirm the presence of genetic infiuences on individual frailty and longevity. They also suggest that the mechanism of these genetic infiuences may be similar for the three Scandinavian countries. Furthermore, results indicate that the increase in individual hazard with age is more rapid than predicted by traditional demographic life tables.

We studied the influence of mental stress on the contributions of genes and environment to individual variation in systolic (SBP) and diastolic (DBP) blood pressure by structural equation modelling in 320 adolescent male and female twins. Blood pressure data were collected during rest and during a reaction time and a mental arithmetic task. Univariate analyses of SBP and DBP showed familial aggregation for blood pressure. A genetic explanation for this resemblance was most likely, although during rest conditions a model that attributed familial resemblance to shared environmental factors, also fitted the data. There was no evidence for sex differences in heritabilities. Multivariate analyses showed significant heterogeneity between sexes for the intercorrelations of the blood pressure data measured under different rest and task conditions. Multivariate genetic analyses were therefore carried out separately in males and females. For SBP and DBP in females and for SBP in males an increase in heritabilities was seen for blood pressure measured during stress, as compared to rest measurements. The influence of shared environ-mental factors decreased during stress. For DBP in males no significant contributions of shared environment were found. The multivariate analyses indicated that the same genetic and environmental influences are expressed during rest and stress conditions.

A fear of interlocking twins is one factor that has led to a high Cesarean section (C/S) rate in breech (A)/vertex (B) (Bra/Vtxb) twins. We sought to estimate the frequency of occurrence of twin entanglement, and of interlocking Bra/Vtxb twins in vaginal deliveries. 541 twins and 48 195 deliveries were retrospectively studied for the period 1987–1995. The incidence of Bra/Vtxb deliveries was noted, and the number of deliveries marked by interlocking and collision of fetuses. The mode of delivery, reason for C/S, and sources of perinatal mortality were noted. Only 43 deliveries were Bra/Vtxb (7.9% of all twins) and of these only 14 (32.6%) were delivered vaginally. One case of interlocking (2.3% of all Bra/Vtxb pairs) and five cases of collision of twins (ie competition for entry into the pelvic inlet with obstruction) were noted. All cases mentioned were delivered by C/S. No perinatal mortality resulted from these cases. In recent years the trend has been for greater use of C/S and ultrasound in managing twin deliveries. In this study 67.4% of Bra/Vtxb twins were delivered by C/S. Although there are fewer vaginal deliveries of these twins and the rate for interlocking (2.3%; 95% CI: 0.06–12.3%) for the whole group has remained about the same, we found the rate in those twins allowed vaginal delivery was 6.7% (95% CI: 0.2–31.9%). The presentation at greatest risk for entanglement was found to be Bra/Vtxb.

In order to investigate a possible association between maternal smoking during pregnancy and twinning, information on 1 096 330 single births and 12 342 twin births in 1983–95 was obtained from the Swedish Medical Birth Registry (MBR). All odds ratios (OR) were estimated after stratification for year of birth and maternal age, parity, and educational level. Smoking women, compared with non-smoking women, were at increased risk of having dizygotic (DZ) twins, but the risk increase was only evident among multiparas. A strong association between previous involuntary childlessness and dizygotic (DZ) twinning (especially in primiparas) was found. The strongest association between maternal smoking and DZ twinning was found among multiparas without any history of involuntary childlessness (OR: 1.35, 95%CI:1.22–1.49), whereas among women who had experienced involuntary childlessness, the opposite was seen (OR: 0.82, 95%CI:0.66–1.00, no difference between parity strata). Weinberg's differential method was used to estimate the number of monozygotic (MZ) twins, and a method of estimating stratified ORs among mothers of MZ twins was presented. No association was found between MZ twinning and maternal smoking (OR: 0.96, 95%CI:0.86–1.07), and no confounding by parity or previous involuntary childlessness was indicated. Several non-causal explanations to the positive association between DZ twinning and maternal smoking among multiparas were discussed, but homogeneity over strata indicated that maternal smoking may be a true risk factor for double ovulation.

In this study, expectant parents of twins were questioned about their feelings and need for information and counselling on the parenting of twins. Data were obtained from self-rating questionnaires and an interview with the expectant mother. From the results it is argued that expectant parents of twins need specific information and counselling about the medical, emotional and parenting issues of having twins. Guidelines for organising this counselling are proposed.

For a quantitative genetic study of pre-school problem behaviours, we have collected data with the Child Behavior Checklist for 2 and 3-year-old children (CBCL 2/3). Questionnaires were completed by mothers of 3620 twin pairs: 633 monozygotic males, 581 dizygotic males, 695 monozygotic females, 519 dizygotic females and 1192 dizygotic opposite sex twin pairs. The genetic and environmental influences on the Externalising and Internalising Problem scales were estimated, simultaneously with sex differences and sibling interaction effects. Genetic factors explained most of the observed variance for both Externalising and Internalising Problems. Cooperative sibling interactions were found for Externalising Problems, indicating that twins reinforce each other's behaviour. Sex differences in genetic architecture were found for Externalising Problems. Genetic factors explained 75% of the variance in girls and 50% in boys. Shared environmental influences were only of importance in boys. For both problem scales, non-shared environmental factors accounted for 25 to 32% of the variance. The observed variances of Internalising Problems could be adequately explained by genetic and nonshared environmental factors, with genetic factors accounting for 68% of the variance.