Dizygotic Co-twins Research Articles

Depressive symptoms, cognitive functions and daily activities: An extended network analysis in monozygotic and dizygotic twins

BackgroundThe network theory posits that depression emerges as the result of individual symptoms triggering each other. Risk factors for depression can impact these between-symptoms interactions through extended networks. The study aimed to model the extended network of depressive symptoms and known depression risk factors – objective cognitive function, intellectual, physical, and social daily activities, and then, compare the observed networks between monozygotic (MZ) and dizygotic (DZ) co-twins. MethodsTwin pairs, 722 MZ and 2200 DZ, aged 40–79, were selected from the Dansh Twin Registry for having complete measures of depressive symptoms (e.g., sadness), cognitive functions (e.g., verbal memory), physical (e.g., brisk walk), intellectual (e.g., reading newspapers) and social activities (e.g., phone calls). Gaussian graphical models were used to estimate and compare the networks first between co-twins and then, between MZ to DZ twin pairs separately. ResultsSpecific intellectual, physical and social activities were central in the extended networks of depressive symptoms and, with the exception of processing speed, more central than cognition. The extended networks' structure was more homogeneous between MZ co-twins relative to DZ co-twins. Cognitive nodes were more central in MZ than DZ co-twins. LimitationsCross-sectional design, participants were middle-aged or older, mostly affective (non-somatic) depressive symptoms. ConclusionsIn depression networks, core connecting elements were intellectual, physical and social activities. The interaction between cognition and daily activities seems critical for triggering depressive symptoms. Thus, clinical interventions aimed at preventing depression and associated cognitive deficits should focus on maintenance and/or engagement in stimulating daily activities.

Developmental trends in intelligence revisited with novel kinships: Monozygotic twins reared apart v. same-age unrelated siblings reared together

Prior research has reported convergence of monozygotic (MZ) cotwins' intelligence scores over time, with divergence observed between dizygotic (DZ) cotwins. These patterns have been variously explained with reference to the increased influence of genetic factors (MZ and DZ twins) and nonshared environmental factors (DZ twins), and the reduced effects of shared environmental events (DZ twins). Studies of unrelated siblings have found modest within-pair resemblance in intelligence, with increasing divergence over time. This subject is revisited in a study using three novel kinships: young reared-apart MZ twins from China (CTA-MZ), adult reared-apart twins from Denmark (D-MZA) and findings from a previous study of same-age unrelated siblings (virtual twins or VTs). Despite modest sample sizes, the anticipated trends described above were observed, replicating extant findings. Intraclass correlations for overall IQ score at Time 1 and Time 2, respectively, were ris = 0.51, 0.81 (CTA-MZs) and ris = 0.64, 0.74 (D-MZAs). The hypothesis that VTs would show score divergence at Time 2 was confirmed. Increased genetic influence (CTA-MZ, D-MZA and VT), reduced impact of shared environments (VT), and increased effects of nonshared environments (VT) appear to best explain the findings. These results also inform parent and educator expectations regarding twins' and siblings' academic performance.

Association of cardiometabolic multimorbidity with risk of late-life depression: a nationwide twin study.

Cardiometabolic diseases (CMDs) including heart disease, stroke, and type 2 diabetes have been individually linked to depression. However, their combined impact on depression risk is unclear. We aimed to examine the association between cardiometabolic multimorbidity and depression and explore the role of genetic background in this association. Within the Swedish Twin Registry, 40,080 depression-free individuals (mean age 60years) were followed for 18years. Cardiometabolic multimorbidity was defined as having ≥2 CMDs. CMDs and depression were ascertained based on the National Patient Register. Cox regression was used to estimate the CMD-depression association in a classical cohort study design and a matched co-twin design involving 176 twin pairs. By comparing the associations between monozygotic and dizygotic co-twins, the contribution of genetic background was estimated. At baseline, 4809 (12.0%) participants had one CMD and 969 (2.4%) had ≥2 CMDs. Over the follow-up period, 1361 participants developed depression. In the classical cohort design, the multi-adjusted hazard ratios (95% confidence interval [CIs]) of depression were 1.52 (1.31-1.76) for those with one CMD and 1.83 (1.29-2.58) for those with ≥2 CMDs. CMDs had a greater risk effect on depression if they developed in mid-life (<60years) as opposed to late life (≥60years). In matched co-twin analysis, the CMD-depression association was significant among dizygotic twins (HR=1.63, 95% CI, 1.02-2.59) but not monozygotic twins (HR=0.90, 95% CI, 0.32-2.51). Cardiometabolic multimorbidity is associated with an elevated risk of depression. Genetic factors may contribute to the association between CMDs and depression.

Mental, physical, and social well-being and quality of life in healthy young adult twin pairs discordant and concordant for body mass index.

The relationship between obesity and mental health is complex and is moderated by the level of obesity, age, sex, and social and genetic factors. In the current study, we used a unique co-twin control design, with twin pairs discordant for body mass index (BMI), to control for shared genetic and environmental effects between obesity and several dimensions of mental health. We studied 74 monozygotic (MZ) twin pairs, of whom 36 were BMI-discordant (intra-pair difference in BMI ≥ 3 kg/m2), and 77 dizygotic (DZ) twin pairs (46 BMI-discordant). We assessed subjective health, especially mental health and mental well-being (depression, anxiety, self-esteem, health-related quality of life, life satisfaction, and social well-being) through questionnaires. Heavier MZ co-twins from BMI-discordant pairs had poorer general health (58.8±3.0 vs. 72.4±3.8, P = 0.001, FDR = 0.017 on a scale from 0 to 100 where higher scores indicate more positive results), physical functioning (90.3±1.1 vs. 95.5±2.2, P = 0.024, FDR = 0.122), energy levels (55.6±3.4 vs. 66.6±3.3, P = 0.013, FDR = 0.109), and emotional well-being (65.9±3.2 vs. 75.4±2.9, P = 0.031, FDR = 0.122), as well as a tendency for depressive symptoms (8.4±1.3 vs. 5.6±0.9, P = 0.071, FDR = 0.166) compared to their leaner co-twins. Heavier DZ co-twins had poorer total physical well-being (91.6±1.9 vs. 95.6±1.0, P = 0.035, FDR = 0.356) and more depressive symptoms (4.3±0.9 vs. 2.4±0.5, P = 0.016, FDR = 0.345 on a scale from 0 to 63 where lower scores indicate fewer depressive symptoms) than their leaner co-twins. Association analyses, using all twin pairs, confirmed that higher BMI within pairs linked to general health, physical functioning and depressive symptoms. No association was found between BMI and anxiety, self-esteem, life satisfaction, or social well-being. In conclusion, this study underscores the notable association between elevated BMI and physical well-being and to a lesser extent between elevated BMI and depressive symptoms, while revealing no discernible connections with anxiety, self-esteem, life satisfaction, or social well-being.

Etiological links between autism and difficulties in initiating and maintaining sleep: a familial co-aggregation and twin study.

Difficulties initiating and maintaining sleep (DIMS) are frequent features of autism, yet little is known about why these conditions co-occur. One possibility is that they share etiological factors, yet this hypothesis remains to be tested using quantitative genetic designs. We thus investigated etiological links between autism and DIMS using familial co-aggregation and twin methods. Twins, siblings, half-siblings, and cousins of 50,097 individuals with autism were identified from Swedish population registries. Their risk of DIMS, defined through diagnoses of insomnia and/or melatonin prescriptions, was then estimated. Twin analyses conducted on 15,279 child and adolescent twin pairs investigated etiological links between DIMS and ASD. 22.8% of autistic individuals had DIMS. Monozygotic co-twins of individuals with autism were most at risk of DIMS compared to the reference group (OR = 6.6 [2.5-17.4]), followed by dizygotic co-twins (OR = 2.6 [1.5-4.5]) and full siblings (OR = 2.5 [2.4-2.6]). Half-siblings and cousins of individuals with autism were least likely to have DIMS relative to the reference group (OR range = 1.3-1.5). Twin analyses estimated a correlation of 0.57 (0.53-0.61) between autism and DIMS, with a genetic correlation of 0.62 (0.60-0.68). These overlapping genetic factors explained 94% of the covariance between these conditions. Autistic traits also showed genetic overlap with DIMS. Our results suggest that shared genetic mechanisms underlie autism and DIMS, which may lead them to co-occur. Untangling the etiological overlap between these conditions has potential to assist in understanding the etiology of each condition, as well as their associated outcomes.

Genetic Influence on the Peripheral Differentiation Signature of Vδ2+ γδ and CD4+ αβ T Cells in Adults.

Adaptive as well as innate immune traits are variously affected by environmental and genetic influences, but little is known about the impact of genetics on the diversity, differentiation and functionality of γδ T cells in humans. Here, we analyzed a cohort of 95 middle-aged twins from the Danish Twin Registry. The differentiation status of peripheral αβ and γδ T cells was assessed by flow cytometry based on the surface expression of CD27, CD28 and CD45RA. Our data confirm the established associations of latent cytomegalovirus (CMV) infection with an accumulation of late differentiated memory T cells in the αβ compartment as well as in the Vδ1+ γδ T cell subset. A comparison of differentiation phenotypes of γδ and αβ T cells that were not affected by CMV seropositivity identified a significant correlation of early differentiated (ED) Vδ2+ and intermediate differentiated (ID) CD4+ T cells in monozygotic (MZ), but not in dizygotic (DZ) co-twins. Thus, our data suggest a genetic influence on the differentiation of γδ and αß T cell subsets.

Risk of Islet and Celiac Autoimmunity in Cotwins of Probands With Type 1 Diabetes

ContextConcordance for persistent islet autoimmunity (IA) and type 1 diabetes in monozygotic twins after probands are diagnosed is variable (30%-70%). Risk for development of IA in dizygotic twins is thought to be similar to nontwin siblings. Little is known in regard to the development of celiac autoimmunity (CDA) in twins of subjects with type 1 diabetes.ObjectiveOur aim was to investigate the development of IA and CDA in cotwins of probands with type 1 diabetes.MethodsSince 1995, the Twin Family Study has followed 336 twins (168 twin probands with type 1 diabetes and 168 cotwins) for a median of 14 years (interquartile range:10-18 years). Cotwins were followed for the development of IA, type 1 diabetes, and CDA.ResultsIn monozygotic cotwins, cumulative incidence by age 20 was 14% for IA and 10% for CDA. Development of IA and CDA by age 20 was 9% and 12% in dizygotic cotwins, respectively. While the numbers are small, IA by age 30 years was 26% in monozygotic and 39% in dizygotic twins. In proportional hazards models, the proband’s younger age at diagnosis, but not sex or human leukocyte antigen were associated with time to IA and CDA in cotwins.ConclusionCDA risk by age 20 in cotwins was 10% to 12%. With long-term follow-up, cumulative incidence for IA is high in dizygotic twins, similar to monozygotic twins, suggesting a role of possible early environmental factors shared by type 1 diabetes discordant cotwins.

Accuracy of self-reported anthropometric measures — Findings from the Finnish Twin Study

ObjectiveTo determine the accuracy of self-reported height, weight, body mass index (BMI) and waist circumference (WC) compared to the measured values, and to assess the similarity between self-reported and measured values within dizygotic (DZ) and monozygotic (MZ) twin pairs. MethodsThe data on self-reported and measured height, weight and WC values as well as measured hip circumference (HC) were collected from 444 twin individuals (53–67 years old, 60% women). Accuracies between self-reported and measured values were assessed by Pearson’s correlation coefficients, Cohen’s kappa coefficients and Bland-Altman 95% limits of agreement. Intra-class correlation was used in within-pair analyses. ResultsThe correlations between self-reported and measured values were high for all variables (r=0.86–0.98), although the agreement assessed by Bland-Altman 95% limits had relatively wide variation. The degree of overestimating height was similar in both sexes, whereas women tended to underestimate and men overestimate their weight. Cohen’s kappa coefficients between self-reported and measured BMI categories were high: 0.71 in men and 0.70 in women. Further, the mean self-reported WC was less than the mean measured WC (difference in men 2.5cm and women 2.6cm). The within-pair correlations indicated a tendency of MZ co-twins to report anthropometric measures more similarly than DZ co-twins. ConclusionsSelf-reported anthropometric measures are reasonably accurate indicators for obesity in large cohort studies. However, the possibility of more similar reporting among MZ pairs should be taken into account in twin studies exploring the heritability of different phenotypes.

Twins Early Development Study: A Genetically Sensitive Investigation into Behavioral and Cognitive Development from Infancy to Emerging Adulthood

The Twins Early Development Study (TEDS) is a longitudinal twin study that recruited over 16,000 twin-pairs born between 1994 and 1996 in England and Wales through national birth records. More than 10,000 of these families are still engaged in the study. TEDS was and still is a representative sample of the population in England and Wales. Rich cognitive and emotional/behavioral data have been collected from the twins from infancy to emerging adulthood, with data collection at first contact and at ages 2, 3, 4, 7, 8, 9, 10, 12, 14, 16, 18 and 21, enabling longitudinal genetically sensitive analyses. Data have been collected from the twins themselves, from their parents and teachers, and from the UK National Pupil Database. Genotyped DNA data are available for 10,346 individuals (who are unrelated except for 3320 dizygotic co-twins). TEDS data have contributed to over 400 scientific papers involving more than 140 researchers in 50 research institutions. TEDS offers an outstanding resource for investigating cognitive and behavioral development across childhood and early adulthood and actively fosters scientific collaborations.

Evidence for cerebello-thalamo-cortical hyperconnectivity as a heritable trait for schizophrenia

Our recent study has demonstrated that increased connectivity in the cerebello-thalamo-cortical (CTC) circuitry is a state-independent neural trait that can potentially predict the onset of psychosis. One possible cause of such “trait” abnormality would be genetic predisposition. Here, we tested this hypothesis using multi-paradigm functional magnetic resonance imaging (fMRI) data from two independent twin cohorts. In a sample of 85 monozygotic (MZ) and 52 dizygotic (DZ) healthy twin pairs acquired from the Human Connectome Project, we showed that the connectivity pattern of the identified CTC circuitry was more similar in the MZ twins (r = 0.54) compared with that in the DZ twins (r = 0.22). The structural equation modeling analysis revealed a heritability estimate of 0.52 for the CTC connectivity, suggesting a moderately strong genetic effect. Moreover, using an independent schizophrenia cotwin sample (10 discordant MZ cotwins, 30 discordant DZ cotwins, and 32 control cotwins), we observed a significant linear relationship between genetic distance to schizophrenia and the connectivity strength in the CTC circuitry (i.e., schizophrenia MZ cotwins > schizophrenia DZ cotwins > control twins, P = 0.045). The present data provide converging evidence that increased connectivity in the CTC circuitry is likely to be a heritable trait that is associated with the genetic risk of schizophrenia.

Nonverbal cognition across genetic and environmentally informative kinships: The case for opposite-sex twin pairs and virtual twins

The extent to which prenatal intrauterine testosterone affects cognitive development in females has been of interest. Previous twin research has, however, been limited in its attempts to disentangle prenatal and psychosocial environmental factors influencing cognitive development. The current study applied a novel approach to addressing this concern. Specifically, the nonverbal cognitive performances of female opposite-sex dizygotic co-twins (DZOSfs) and female opposite-sex virtual co-twins (same-age unrelated siblings or VTOSfs) were compared to separate the biological and environmental influences on the nonverbal IQ score and its component subtests. The DZOSf twins showed a trend toward outperforming the younger VTOSf twins on the Block Design subtest only. Using these biologically and environmentally informative kinships offers a novel approach to understanding sex differences in nonverbal cognition. Including VTOSfs as a comparison group creates an experimental design that eliminates confounds and spurious associations left unaddressed in prior twin research.

Heredity of interocular similarities in components of refraction: a population-based twin study among 66- to 79-year-old female twins.

To examine genetic influences on interocular similarities in ocular refraction and components of refraction among elderly female twins. Refraction was assessed in 94 monozygotic (MZ) and 74 dizygotic (DZ) female twins aged 66-78years. Absolute values of interocular differences (Aniso variables) in spherical refraction (SR), refractive astigmatism (AST), spherical equivalent (SE), corneal refractive power (CR), corneal astigmatism (CAST), anterior chamber depth (ACD) and axial length (AL) were calculated. The differences between sisters in each of the Aniso variables were calculated and graded into two categories, best differentiating the groups, here isometropic and anisometropic values. The cut-offs for grading as isometropic were AnisoSR<0.75 D, AnisoAST<0.5 D, AnisoSE<1.0 D, AnisoCR<0.5 D, AnisoCAST<0.50 D, AnisoACD<0.1mm and AniosAL<0.1mm. Genetic influences on these traits were investigated by comparing the prevalence of isometropic and anisometropic differences between the MZ and DZ pairs in the Aniso variables and the interrelationships between the Aniso variables. When the Aniso variables were treated as continuous, no significant differences were found between the MZ and DZ subjects. When the proportions of isometropic intratwinpair interocular differences in the Aniso variables in the MZ and DZ cotwins were compared, the prevalences (MZ/DZ) were AnisoSR: 68%/60%; AnisoAST: 66%/57%; AnisoSE: 87%/68%; AnisoCR: 83%/78%; AnisoCAST: 69%/35%; AnisoACD: 77%/63%; and AnisoAL: 76%/60%. The differences were statistically significant for Aniso SE (p=0.035, Fisher's exact test) and CAST (p=0.007). The greater homogeneity in the interocular differences between the MZ sisters supports the assumption that isometropia of different elements of refraction is genetically influenced and tending to continue up to older ages. In cases where AnisoSE was <1.0 D, higher CR in one eye was associated with shorter AL (r=-0.398, p<0.001), thereby contributing to emmetropization, irrespective of zygosity. In the cases of AnisoSE ≥1 D, no similar influence on emmetropization was observed. The difference between sisters in AnisoSE was associated with the intratwinpair difference in Aniso AL, but not with the intratwinpair differences in AnisoCR, irrespective of zygosity. The higher prevalence of similarities in isometropia of the spherical equivalent and corneal astigmatism between the MZ pairs compared to DZ pairs is consistent with the view that genetic influences on the refractive elements of the eye, tending to isometropia, continue into older age. The interrelation between CR and AL tends to maintain isometropia of SE irrespective of zygosity.

Gut Barrier Dysfunction-A Primary Defect in Twins with Crohn's Disease Predominantly Caused by Genetic Predisposition.

Background and AimsThe aetiology of Crohn’s disease is poorly understood. By investigating twin pairs discordant for Crohn’s disease, we aimed to assess whether the dysregulated barrier represents a cause or a consequence of inflammation and to evaluate the impact of genetic predisposition on barrier function.MethodsIleal biopsies from 15 twin pairs discordant for Crohn’s disease [monozygotic n = 9, dizygotic n = 6] and 10 external controls were mounted in Ussing chambers to assess paracellular permeability to 51Chromium [Cr]-EDTA and trancellular passage to non-pathogenic E. coli K-12. Experiments were performed with and without provocation with acetylsalicylic acid. Immunofluorescence and ELISA were used to quantify the expression level of tight junction proteins.ResultsHealthy co-twins and affected twins displayed increased 51Cr-EDTA permeability at 120 min, both with acetylsalicylic acid [p < 0.001] and without [p < 0.001] when compared with controls. A significant increase in 51Cr-EDTA flux was already seen at 20 min in healthy monozygotic co-twins compared with controls [p≤0.05] when stratified by zygosity, but not in healthy dizygotic co-twins. No difference in E. coli passage was observed between groups. Immunofluorescence of the tight junction proteins claudin-5 and tricellulin showed lower levels in healthy co-twins [p < 0.05] and affected twins [p < 0.05] compared with external controls, while ELISA only showed lower tricellulin in Crohn’s disease twins [p < 0.05].ConclusionOur results suggest that barrier dysfunction is a primary defect in Crohn’s disease, since changes were predominantly seen in healthy monozygotic co-twins. Passage of E. coli seems to be a consequence of inflammation, rather than representing a primary defect.

OP001 Gut barrier dysfunction: a primary defect in twins with Crohn’s disease predominantly caused by genetic predisposition

The aetiology of the dysfunctional barrier in Crohn’s disease (CD) is poorly understood. By investigating twin pairs discordant for CD we aimed to assess whether the dysregulated barrier in CD represents a cause or a consequence of the inflammation and to evaluate the impact of genetics and environmental exposure on barrier function. Ileal biopsies from 15 twin pairs discordant for CD (monozygotic n = 9, dizygotic n = 6) and 10 external controls were mounted in Ussing chambers to assess paracellular permeability to 51Cr-EDTA and transcellular passage to non-pathogenic E. coli K-12. Experiments were performed with and without provocation with acetylsalicylic acid (ASA). Immunofluorescence and ELISA were used to quantify the expression level of tight junction proteins in the biopsies. Healthy co-twins and CD twins displayed increased 51Cr-EDTA permeability at 120 min both with ASA (p < 0.001) and without ASA (p < 0.001) when compared with controls (Figure 1). The difference was observed already at 20 min with ASA, when healthy co-twins were compared with external controls (p < 0.05). Stratification by zygosity revealed an increased permeability at 20 min both with ASA (p = 0.05) and without ASA (p < 0.05) in healthy monozygotic co-twins, but no statistical difference was observed between healthy dizygotic co-twins and external controls. Consistently, healthy monozygotic displayed an increased permeability at 20 min without ASA when compared with healthy dizygotic co-twins (p < 0.05). No difference in E. coli passage could be observed between groups. Immunofluorescence of the tight junction proteins claudin-5 and tricellulin showed lower levels in healthy co-twins (p < 0.05) and CD twins (p < 0.05) compared with external controls, while ELISA only showed lower tricellulin in CD compared with controls (p < 0.05). Paracellular permeability across biopsies mounted in Ussing chambers from twin pairs (n = 15) disconcordant for Crohn’s disease and external controls (n = 10). Experiments were performed with and without provocation to ASA for 20 and 120 min. Our result indicates that barrier dysfunction is a primary defect in CD, since changes were predominantly seen in the healthy monozygotic co-twins. Moreover, passage of E. coli K-12 seems to be a consequence of inflammation rather than representing a primary defect.

Network Approach to Understanding Emotion Dynamics in Relation to Childhood Trauma and Genetic Liability to Psychopathology: Replication of a Prospective Experience Sampling Analysis.

Background: The network analysis of intensive time series data collected using the Experience Sampling Method (ESM) may provide vital information in gaining insight into the link between emotion regulation and vulnerability to psychopathology. The aim of this study was to apply the network approach to investigate whether genetic liability (GL) to psychopathology and childhood trauma (CT) are associated with the network structure of the emotions “cheerful,” “insecure,” “relaxed,” “anxious,” “irritated,” and “down”—collected using the ESM method.Methods: Using data from a population-based sample of twin pairs and siblings (704 individuals), we examined whether momentary emotion network structures differed across strata of CT and GL. GL was determined empirically using the level of psychopathology in monozygotic and dizygotic co-twins. Network models were generated using multilevel time-lagged regression analysis and were compared across three strata (low, medium, and high) of CT and GL, respectively. Permutations were utilized to calculate p values and compare regressions coefficients, density, and centrality indices. Regression coefficients were presented as connections, while variables represented the nodes in the network.Results: In comparison to the low GL stratum, the high GL stratum had significantly denser overall (p = 0.018) and negative affect network density (p < 0.001). The medium GL stratum also showed a directionally similar (in-between high and low GL strata) but statistically inconclusive association with network density. In contrast to GL, the results of the CT analysis were less conclusive, with increased positive affect density (p = 0.021) and overall density (p = 0.042) in the high CT stratum compared to the medium CT stratum but not to the low CT stratum. The individual node comparisons across strata of GL and CT yielded only very few significant results, after adjusting for multiple testing.Conclusions: The present findings demonstrate that the network approach may have some value in understanding the relation between established risk factors for mental disorders (particularly GL) and the dynamic interplay between emotions. The present finding partially replicates an earlier analysis, suggesting it may be instructive to model negative emotional dynamics as a function of genetic influence.

Familiality and Heritability of Fatigue in an Australian Twin Sample.

Familial factors have previously been implicated in the etiology of fatigue, of which a significant proportion is likely attributable to genetic influences. However, family studies have primarily focused on chronic fatigue syndrome, while univariate twin studies have investigated broader fatigue phenotypes. The results for similar fatigue phenotypes vary between studies, particularly with regard to sex-specific contributions to the heritability of the traits. Therefore, the current study aims to investigate the familiality and sex-specific effects of fatigue experienced over the past few weeks in an older Australian population of 660 monozygotic (MZ) twin pairs, 190 MZ singleton twins, 593 dizygotic (DZ) twin pairs, and 365 DZ singleton twins. Higher risks for fatigue were observed in MZ compared to DZ co-twins of probands with fatigue. Univariate heritability analyses indicated fatigue has a significant genetic component, with a heritability (h 2) estimate of 40%. Sex-specific effects did not significantly contribute to the heritability of fatigue, with similar estimates for males (h 2 = 41%, 95% CI [18, 62]) and females (h 2 = 40%, 95% CI [27, 52]). These results indicate that fatigue experienced over the past few weeks has a familial contribution, with additive genetic factors playing an important role in its etiology.

'Biracial'-Looking Twins: A New Twin Type?/Twin Research: Twins with Cystic Teratomas; Sleep Quality and Body Mass Index; Previable Membrane Rupture/Print and Online Reports: Twins Born to a Sister Surrogate; NASA Twin Study; African-Cosmopolitan Twin Fashion Inspirations; Triplet Hockey Stars.

Dizygotic (DZ) co-twins born to mothers and fathers from different racial or ethnic backgrounds often resemble one parent much more than the other. As such, these pairs comprise a unique subset of twins for investigating how others' responses to their different looks may affect their personalities and self-esteem. This article describes some of these twin pairs and some challenges of raising them, and suggests ways they may be used in research. Next, recent twin research on cystic teratomas, relations between sleep quality and body mass index, and previable membrane rupture is described. The final section concerns twins, twin studies, and related events in the media, namely: twins born to a sister surrogate, the NASA twin investigation, inspiring African-Cosmopolitan twins in fashion, and triplet Hockey Stars.

Familial risk and ADHD-specific neural activity revealed by case-control, discordant twin pair design

Individuals with ADHD, as well as their family members who do not meet clinical criteria, have shown deficits in executive function. However, it remains unclear whether underlying neural alterations are familial or ADHD-specific. To investigate this issue, neural activation underlying executive function was assessed using functional magnetic resonance imaging during performance of a Stroop task in three groups of individuals: 20 young adults who were diagnosed with ADHD in childhood, their 20 dizygotic co-twins without ADHD in childhood, and 20 unrelated controls selected from dizygotic twin pairs in which neither twin had ADHD in childhood (total n=60). Implicating the frontoparietal network as a location of effects specific to ADHD, activation in the superior frontal (Brodmann’s Area — BA 6) and parietal regions (BA 40) was significantly reduced in twins with childhood ADHD compared to both their control co-twins and unrelated control twins. Consistent with familial influences, activity in the anterior cingulate and insula was significantly reduced in both the twins with ADHD and their co-twins compared to the unrelated controls. These results show that both ADHD-specific and familial influences related to an ADHD diagnosis impact neural systems underlying executive function.

Oral bony outgrowths: Prevalence and genetic factor influence. Study of twins

ObjectiveThe aim of the study was to verify the influence of a genetic factor on the etiology of oral bony outgrowths and to determine the prevalence and type of oral bony outgrowths (tori and exostoses) among a group of Lithuanian twins. Materials and methodsIn total, 162 twins (81 twin pairs) were analyzed for the presence or absence, type, and size of oral bony outgrowths. Statistical analysis was carried out to find the prevalence of bony protuberances and the relationship between zygosity and occurrence of oral bony enlargements. Zygosity of twins was confirmed by DNA analysis. Results59.9% of the subjects had oral bony outgrowths. Mandibular tori were found in 56.8% and palatal tori in 1.8% of the sample. Palatal exostoses and mandibular exostoses were present in 1.8% and 3.1% of the sample, respectively, whereas maxillary exostoses were not found. A higher percentage of tori and exostoses were found in the group of older subjects (>18 years old, p=0.025). No significant difference was found between men and women in the prevalence of bony outgrowths. High κ and r values (0.91±0.062) showed very good concordance of oral bony outgrowths between monozygotic and moderate concordance (0.58±0.141) between dizygotic co-twins (p<0.001). The calculation of heritability estimate verifies dominant influence of genetic factor on the etiology of oral bony outgrowths (h2=0.658). ConclusionThe most common bony outgrowth was torus mandibularis. Our results show that the genetic factor is dominant in the etiology of oral bony outgrowths.

Twin and family studies reveal strong environmental and weaker genetic cues explaining heritability of eosinophilic esophagitis

Eosinophilic esophagitis (EoE) is a chronic antigen-driven allergic inflammatory disease, likely involving the interplay of genetic and environmental factors, yet their respective contributions to heritability are unknown. To quantify the risk associated with genes and environment on familial clustering of EoE. Family history was obtained from a hospital-based cohort of 914 EoE probands (n = 2192 first-degree "Nuclear-Family" relatives) and an international registry of monozygotic and dizygotic twins/triplets (n = 63 EoE "Twins" probands). Frequencies, recurrence risk ratios (RRRs), heritability, and twin concordance were estimated. Environmental exposures were preliminarily examined. Analysis of the Nuclear-Family-based cohort revealed that the rate of EoE, in first-degree relatives of a proband, was 1.8% (unadjusted) and 2.3% (sex-adjusted). RRRs ranged from 10 to 64, depending on the family relationship, and were higher in brothers (64.0; P = .04), fathers (42.9; P = .004), and males (50.7; P < .001) than in sisters, mothers, and females, respectively. The risk of EoE for other siblings was 2.4%. In the Nuclear-Family cohort, combined gene and common environment heritability was 72.0% ± 2.7% (P < .001). In the Twins cohort, genetic heritability was 14.5% ± 4.0% (P < .001), and common family environment contributed 81.0% ± 4% (P < .001) to phenotypic variance. Probandwise concordance in monozygotic co-twins was 57.9% ± 9.5% compared with 36.4% ± 9.3% in dizygotic co-twins (P = .11). Greater birth weight difference between twins (P = .01), breast-feeding (P = .15), and fall birth season (P = .02) were associated with twin discordance in disease status. EoE RRRs are increased 10- to 64-fold compared with the general population. EoE in relatives is 1.8% to 2.4%, depending on relationship and sex. Nuclear-Family heritability appeared to be high (72.0%). However, the Twins cohort analysis revealed a powerful role for common environment (81.0%) compared with additive genetic heritability (14.5%).