We localised three important enzymes histochemically in placental trophoblasts from women who gave birth to dichorionic discordant twins, in which the co-twin was affected by foetal growth restriction (FGR). The enzymes studied were adenosine diphosphate-degrading enzyme (ADPdegrading enzyme, plasma membrane enzyme), cytochrome c oxidase (mitochondrial enzyme), and glucose-6-phosphatase (endoplasmic reticular enzyme). We compared these enzyme activities and their distribution patterns among placentas of the smaller (FGR) co-twin, larger co-twin, preeclamptic singleton with FGR, and normal singletons with birth weight of appropriate for their gestational ages. In FGR co-twin placentas, the intensity and localisation pattern of these three enzymes did not differ from those seen in the larger co-twin and normal singleton placentas. Decreased ADP-degrading activity and cytochrome c oxidase negative mitochondria, which were characteristic features of pre-eclamptic trophoblasts, were not observed in FGR co-twin placentas. These observations indicated that, in the FGR co-twin, enzyme-histochemically detectable trophoblastic cell dysfunction may be absent, or if present, less prominent, compared with preeclamptic FGR. We previously reported that placental trophoblasts from singleton idiopathic FGR also showed no reduction in these enzyme activities. In mechanism and pathophysiology, FGR in dichorionic discordant twins may be quite different from pre-eclamptic FGR, but somewhat resembles idiopathic FGR, though all three disorders lead to placental insufficiency, resulting in limited foetal growth. Twin Research (2000) 3, 123–128.

A parental report questionnaire posted to a population sample of 18-month-old twins correctly assigned zygosity in 95%of cases when validated against zygosity determined by identity of polymorphic DNA markers. The questionnaire was as accurate when readministered at 3 years of age, with 96% of children being assigned the same zygosity on both occasions. The results validate the use of parental report questionnaire data to determine zygosity in infancy. Twin Research (2000) 3, 129–133.

This study reports on zygosity determination in twins of childhood age. Parents responded to questionnaire items dealing with twin similarity in physical characteristics and frequency of mistaking one twin for another by parents, relatives and strangers. The accuracy of zygosity diagnosis was evaluated across twins aged 6, 8, and 10 and across parents. In addition, it was examined whether the use of multiple raters and the use of longitudinal data lead to an improvement of zygosity assignment. Complete data on zygosity questions and on genetic markers or blood profiles were available for 618 twin pairs at the age of 6 years. The method used was predictive discriminant analyses. Agreement between zygosity assigned by the replies to the questions and zygosity determined by DNA markers/blood typing was around 93%. The accuracy of assignment remained constant across age and parents. Analyses of data provided by both parents and collected over multiple ages did not result in better prediction of zygosity. Details on the discriminant function are provided. Twin Research (2000) 3, 134–141.

In both traditional and modern societies, twinship, as an unusual mode of reproduction, involves difficulties for social systems in maintaining consistent classification systems. It is proposed that the most prevalent response to twinship involves various ‘strategies of normalisation’ to defuse and contain the potential disruption. This proposition is illustrated and analysed in relation to ethnographic maternal drawn mainly (but not exclusively) from African communities in the twentieth century. Following a discussion of twin infanticide as the most extreme of the normalising strategies, the article concludes by identifying a number of paradoxes in the social construction of twinship. Twin Research (2000) 3, 142–147.

Homeostasis model assessment (HOMA) provides indices of insulin secretion (β) and insulin resistance (R) derived from fasting plasma glucose (FPG) and fasting plasma insulin (FPI) levels. However, these indices could not account for a significant heritability of fasting plasma glucose (FPG) (h2 = 0.75, P < 0.01) in a group of 214 female twins. This result is consistent with a misclassification between effects due to insulin secretion and resistance in the HOMA indices. We report here evidence of such misclassification in the HOMA indices and describe a minor modification to the model which corrects it. Direct measures of insulin resistance (euglycaemic clamp) and secretion (i.v. glucose bolus) were obtained in 43 non-diabetic subjects. Heritability was estimated by statistical modelling of genetic and environmental influences in data from 214 non-diabetic female subjects. Modified HOMA (HOMA′) indices were obtained from β′ = (Ln(FPI)–c)/FPG and R′ = (Ln(FPI)–c)* FPG where c is a constant derived from regression analysis of Ln(FPI) vs FPG. Indices from both models correlated with the direct measures similarly (r = 0.63 (R), 0.49 (R′), 0.45 (β), 0.39 (β′), all P < 0.01). Directly measured insulin resistance and secretion were not significantly correlated (r = 0.13, P = 0.21). However, unmodified HOMA- and R were strongly related (r = 0.78, P < 0.0001 vs 0.13) demonstrating substantial misclassification. The relationship between β′ and R′ (r = 0.13) was not different from that between the two direct measures and significant heritability of β′ (h2 = 0.68, P < 0.01) and R′ (h2 = 0.59, P < 0.05) was evident in the twin data. The proposed modification to HOMA significantly reduces misclassification and reveals separate components of insulin resistance and insulin secretion in the heritability of FPG. Twin Research (2000) 3, 148–151.

The effects of apolipoprotein (a), apolipoprotein-E, and apolipoprotein-A4 isoforms on quantitative lipoprotein(a) [Lp(a)] levels were assessed in a sample of 142 Dutch families consisting of two parents and their adolescent twin offspring. A total heritability of 95% was estimated for plasma Lp(a) concentrations. The largest part of this heritability was due to the apo(a) locus which explained 61% of the total variance in Lp(a) levels. The pattern of familial correlations for the residual part of the Lp(a) variance that could not be attributed to the apo(a) isoforms, suggested genetic influences on the residual variance. We addressed the question whether this residual genetic variance could be ascribed to the apoE or the apoA4 locus. A simultaneous analysis of all three loci showed that both the apoE and the apoA4 polymorphism did not contribute significantly to Lp(a) variation. Twin Research (2000) 3, 152–158.

In studies that employ matched pair analysis to identify environmental exposures important for a disorder, criteria for discordant pairs are seldom discussed. Yet several assumptions concerning the definition of discordancy may have considerable influence over what results are found. Problems are exacerbated when age of onset for a disorder is late in life. We propose a new set of criteria for defining discordant pairs in studies of dementia, taking into account duration of discordance and competing causes of mortality, and evaluate the consequences of choosing alternative definitions of discordancy. Twin Research (2000) 3, 159–164.

We describe methods to fit structured latent growth curves to data from MZ and DZ twins. The well-known Gompertz, logistic and exponential curves may be written as a function of three components – asymptote, initial value, and rate of change. These components are allowed to vary and covary within individuals in a structured latent growth model. Such models are highly economical, requiring a small number of parameters to describe covariation across many occasions of measurement. We extend these methods to analyse longitudinal data from MZ and DZ twins and focus on the estimation of genetic and environmental variation and covariation in each of the asymptote, initial and rate of growth factors. For illustration, the models are fitted to longitudinal Bayley Infant Mental Development Scale data published by McArdle (1986). In these data, all three components of growth appear strongly familial with the majority of variance associated with the shared environment; differences between the models were not great. Occasion-specific residual factors not associated with the curve components account for approximately 40% of variance of which a significant proportion is additive genetic. Though the growth curve model fit less well than some others, they make restrictive, falsifiable predictions about the mean, variance and twin covariance of other (not yet measured) occasions of measurement. Twin Research (2000) 3, 165–177.