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Background: Attention‐deficit/hyperactivity disorder (ADHD) is an increasingly commonly diagnosed neurodevelopmental condition. One possibility is that this reflects a genuine increase in the prevalence of ADHD due to secular environmental changes, yet this hypothesis remains untested. We therefore investigated whether the genetic and environmental variance underlying ADHD, and traits of ADHD, has changed over time. Methods: We identified twins born from 1982 to 2008 from the Swedish Twin Registry (STR). We linked the STR with the Swedish National Patient Register and Prescribed Drug Register to identify diagnoses of ADHD and prescriptions of ADHD medication for these twins. We also utilized data collected from participants in the Child and Adolescent Twin Study in Sweden (CATSS), born from 1992 to 2008. Their parents completed a structured ADHD screening tool, which was used to measure traits of ADHD and assign broad screening diagnoses of ADHD. We used the classical twin design to test whether the degree to which variation in these measures was influenced by genetic and environmental variation changed over time. Results: We included 22,678 twin pairs from the STR and 15,036 pairs from CATSS. The heritability of ADHD in the STR ranged from 66% to 86% over time, although these fluctuations were not statistically significant. We observed a modest increase in variance in ADHD traits, from 0.98 to 1.09. This was driven by small increases in the underlying genetic and environmental variance, with heritability estimated as 64%–65%. No statistically significant changes in variance in screening diagnoses were observed. Conclusions: The relative contribution of genetic and environmental factors to ADHD has remained stable over time, despite its increasing prevalence. Thus, changes in the underlying etiology of ADHD over time are unlikely to explain the increase in ADHD diagnoses. [ABSTRACT FROM AUTHOR]

Background: Twin studies have demonstrated shared genetic and environmental effects between eating disorders and alcohol involvement in adults and middle adolescents. However, fewer studies have focused on late adolescents or investigated a wide range of eating disorder dimensions and alcohol involvement subscales in both sexes. We examined genetic and environmental correlations among three eating disorder dimensions and two alcohol involvement subscale scores in late adolescent twins using bivariate twin models. Methods: Participants were 3568 female and 2526 male same‐sex twins aged 18 years old from the Child and Adolescent Twin Study in Sweden. The Eating Disorder Inventory‐2 (EDI) assessed the drive for thinness, bulimia, and body dissatisfaction. Alcohol involvement was assessed with the Alcohol Use Disorder Identification Test consumption (AUDIT‐C) and problem (AUDIT‐P) subscales. Results: Only phenotypic and twin correlations in female twins met our threshold for twin modeling. The proportion of total variance for each trait accounted for by additive genetic factors ranged from 0.50 to 0.64 in female twins, with the rest explained by nonshared environmental factors and measurement error. Shared environmental factors played a minimal role in the variance of each trait. The strongest genetic correlation (ra) emerged between EDI bulimia and AUDIT‐P (ra = 0.46, 95% confidence interval: 0.37, 0.55), indicating that the proportion of genetic variance of one trait that was shared with the other trait was 0.21. Nonshared environmental correlations between eating disorder dimensions and alcohol involvement ranged from 0.03 to 0.13. Conclusions: We observed distinct patterns of genetic and environmental effects for co‐occurring eating disorder dimensions and alcohol involvement in female vs. male twins, supporting sex‐specific treatment strategies for late adolescents with comorbid eating disorders and alcohol use disorder. Our findings emphasize the importance of assessing family history of multiple eating disorder dimensions while treating late adolescents with problematic alcohol use, and vice versa, to improve detection and treatment. [ABSTRACT FROM AUTHOR]

Background: From birth, infants orient preferentially to faces, and when looking at the face, they attend primarily to eyes and mouth. These areas convey different types of information, and earlier research suggests that genetic factors influence the preference for one or the other in young children. Methods: In a sample of 535 5‐month‐old infant twins, we assessed eye (relative to mouth) preference in early infancy, i.e., before neural systems for social communication and language are fully developed. We investigated the contribution of genetic and environmental factors to the preference for looking at eyes, and the association with concurrent traits and follow‐up measures. Results: Eye preference was independent from all other concurrent traits measured, and had a moderate‐to‐high contribution from genetic influences (A = 0.57; 95% CI: 0.45, 0.66). Preference for eyes at 5 months was associated with higher parent ratings of receptive vocabulary at 14 months. No statistically significant association with later autistic traits was found. Preference for eyes was strikingly stable across different stimulus types (e.g., dynamic vs. still), suggesting that infants' preference at this age does not reflect sensitivity to low‐level visual cues. Conclusions: These results suggest that individual differences in infants' preferential looking to eyes versus mouth to a substantial degree reflect genetic variation. The findings provide new leads on both the perceptual basis and the developmental consequences of these attentional biases. [ABSTRACT FROM AUTHOR]

Background: Intellectual disability (ID) aggregates in families, but factors affecting individual risk and heritability estimates remain unknown. Methods: A population‐based family cohort study of 4,165,785 individuals born 1973–2013 in Sweden, including 37,787 ID individuals and their relatives. The relative risks (RR) of ID with 95% confidence intervals (95% CI) were obtained from stratified Cox proportional‐hazards models. Relatives of ID individuals were compared to relatives of unaffected individuals. Structural equation modeling was used to estimate heritability. Results: Relatives of ID individuals were at increased risk of ID compared to individuals with unaffected relatives. The RR of ID among relatives increased proportionally to the degree of genetic relatedness with ID probands; 256.70(95% CI 161.30–408.53) for monozygotic twins, 16.47(13.32–20.38) for parents, 14.88(12.19–18.16) for children, 7.04(4.67–10.61) for dizygotic twins, 8.38(7.97–8.83) for full siblings, 4.56(4.02–5.16) for maternal, 2.90(2.49–3.37) for paternal half‐siblings, 3.03(2.61–3.50) for nephews/nieces, 2.84(2.45–3.29) for uncles/aunts, and 2.04(1.91–2.20) for cousins. Lower RRs were observed for siblings of probands with chromosomal abnormalities (RR 5.53, 4.74–6.46) and more severe ID (mild RR 9.15, 8.55–9.78, moderate RR 8.13, 7.28–9.08, severe RR 6.80, 5.74–8.07, and profound RR 5.88, 4.52–7.65). Male sex of relative and maternal line of relationship with proband was related to higher risk (RR 1.33, 1.25–1.41 for brothers vs. sisters and RR 1.49, 1.34–1.68 for maternal vs. paternal half‐siblings). ID was substantially heritable with 0.95(95% CI 0.93–0.98) of the variance in liability attributed to genetic influences. Conclusions: The risk estimates will benefit researchers, clinicians, families in understanding the risk of ID in the family and the whole population. The higher risk of ID related to male sex and maternal linage will be of value for planning and interpreting etiological studies in ID. [ABSTRACT FROM AUTHOR]

The article explores the role of genetic risk in the association between psychedelic use and manic symptoms in adolescents. Topics discussed include a study of adolescent twins, the impact of genetic vulnerability to schizophrenia or bipolar disorder on manic symptoms, and the limitations of the study regarding the recreational use of psychedelics.

Despite the importance and prevalence of intellectual disability (ID), its origins have not been well understood until now. Lichtenstein et al. report in this issue findings from a population‐based sample four times larger than all previous family studies of ID put together (Lichtenstein et al., 2022). From more than four million people, 37,787 individuals were identified with ID. Relative risks (RRs) are reported for relatives of ID probands (55,000 first‐degree, 55,000 second‐degree, and 170,000 third‐degree) as compared with matched relatives of individuals without ID. These relatives plus 400 pairs of twins in which at least one twin was diagnosed with ID yield an astonishing estimate of 95% heritability with no evidence for shared environmental influence in their model. Another important finding is that maternal half‐siblings of ID individuals were at greater risk than paternal half‐siblings, a maternal effect that could indicate X‐chromosome linkage. Finally, profound and severe ID is etiologically distinct from the normal distribution, due in part to noninherited (de novo) genetic mutations and chromosomal abnormalities. However, 90% of individuals with ID are moderate or mild, and these represent the low end of the normal distribution of genetic influence on cognitive ability, which has important implications for DNA research on ID. [ABSTRACT FROM AUTHOR]

Background: Research has demonstrated that individuals who identify as a sexual minority (e.g., gay/lesbian, bisexual) are at increased risk for suicidality‐related outcomes. However, previous research is primarily limited by the lack of adjustment for unmeasured (i.e., genetic and environmental) confounding factors and previous psychopathology. Methods: Using the Child and Adolescent Twin Study in Sweden, we employed a co‐twin control design to examine the extent to which the association between sexual orientation and adolescent suicide attempt and self‐harm (SA/SH) was independent of genetic and environmental factors shared by twins, as well as measured symptoms of childhood psychopathology. Results: Adolescents who identified as a sexual minority (i.e., gay/lesbian, bisexual, or other sexual orientation) were at two‐fold increased odds for SA/SH (OR, 2.01 [95% confidence interval, 1.63–2.49) compared to heterosexual adolescents. When adjusting for all genetic and shared environmental factors that make twins similar and for measured childhood psychopathology, the association remained positive but attenuated to OR, 1.55 (1.11–2.16). Conclusions: Identifying as a sexual minority was associated with approximately 50% increased odds of SA/SH in adolescence after adjusting for unmeasured genetic and environmental factors shared by twins and for childhood psychopathology. The results support that environmental factors specifically associated with identifying as a sexual minority likely increase risk for SA/SH. Our findings highlight the need to monitor suicidality risk among this group. [ABSTRACT FROM AUTHOR]

Abstract: Objective: Understanding the role of premorbid body mass index (BMI) in the emergence of eating disorders may be key to identifying effective prevention strategies. We explore relations between BMI and eating disorders traits in young twins. Method: The effect of BMI at age 9/12 and 15 on eating disorder traits measured using the Eating Disorders Inventory‐2 (EDI) at ages 15 and 18 was examined using bivariate modelling in a longitudinal population sample of Swedish twins. Results: The correlation between BMI and EDI within individuals was stable across all ages and remained significant after adjusting for later BMI. Bivariate analysis indicated significant positive genetic correlations between BMI ages 9/12 and 15 and subsequent EDI scores. The relationship remained significant for BMI age 9/12 and EDI age 15 in the adjusted model, indicating a longitudinal association. Conclusion: Our results have implications for conceptualizing the interrelation of BMI and eating disorders across childhood and adolescence. [ABSTRACT FROM AUTHOR]

Background: Autism spectrum disorder (ASD), Attention‐deficit/Hyperactivity disorder (ADHD), and other related neurodevelopmental disorders (NDDs) have, in some previous studies, been shown to increase the risk of being sexually victimized. However, no studies have examined whether the association is driven by a general NDD phenotype versus specific diagnoses, nor the etiology of the association. Method: Using a genetically informative, prospective design, we examined the association between ASD and ADHD in childhood and coercive sexual victimization up to age 18. A total of 4,500 children participating in the Child and Adolescent Twin Study in Sweden (CATSS) were rated by their parents on NDDs at age 9 or 12 years, and self‐reported at age 18 on lifetime experiences of coercive sexual touching and/or coercive sex. First, we regressed sexual victimization on the NDDs. Second, we regressed sexual victimization on general and specific NDD symptoms identified via a bifactor model. Third, we decomposed the observed associations into genetic and environmental parts. Results: In females, ASD was associated with an almost threefolded increased risk of coercive sexual victimization, and ADHD with a doubled risk. In males, the risk associated with ASD and ADHD was of the same magnitude but not significant. When controlling for overall NDD symptom load ASD or ADHD, no longer uniquely predicted coercive sexual victimization. The association between the NDD general factor and coercive sexual victimization was due to shared genetics. Conclusions: General NDD symptom load, rather than specific ASD or ADHD symptoms, seems to be a moderate vulnerability factor for coercive sexual victimization. We speculate that an evocative gene–environment correlation might account for this observation, such that sexual perpetrators actively target NDD individuals. [ABSTRACT FROM AUTHOR]

Background Childhood maltreatment ( CM) is strongly associated with psychiatric disorders in childhood and adulthood. Previous findings suggest that the association between CM and psychiatric disorders is partly causal and partly due to familial confounding, but few studies have investigated the mechanisms behind the association between CM and neurodevelopmental disorders ( NDDs). Our objective was to determine whether maltreated children have an elevated number of NDDs and whether CM is a risk factor for an increased NDD 'load' and increased NDD symptoms when controlling for familial effects. Methods We used a cross-sectional sample from a population-representative Swedish twin study, comprising 8,192 nine-year-old twins born in Sweden between 1997 and 2005. CM was defined as parent-reported exposure to emotional abuse/neglect, physical neglect, physical abuse, and/or sexual abuse. Four NDDs were measured with the Autism-Tics, AD/ HD, and other comorbidities inventory. Results Maltreated children had a greater mean number of NDDs than nonmaltreated children. In a co-twin control design, CM-discordant monozygotic twins did not differ significantly for their number of NDDs, suggesting that CM is not associated with an increased load of NDDs when genetic and shared environmental factors are taken into account. However, CM was associated with a small increase in symptoms of attention-deficit/hyperactivity disorder and autism spectrum disorder in CM-discordant MZ twins, although most of the covariance of CM with NDD symptoms was explained by common genetic effects. Conclusions Maltreated children are at higher risk of having multiple NDDs. Our findings are, however, not consistent with the notion that CM causes the increased NDD load in maltreated children. Maltreated children should receive a full neurodevelopmental assessment, and clinicians should be aware that children with multiple NDDs are at higher risk of maltreatment. [ABSTRACT FROM AUTHOR]

Background Resilience has been shown to be protective against alcohol use disorders (AUDs), but the magnitude and nature of the relationship between these 2 phenotypes are not clear. The aim of this study was to examine the strength of this relationship and the degree to which it results from common genetic or common environmental influences. Methods Resilience was assessed on a 9-point scale during a personal interview in 1,653,721 Swedish men aged 17 to 25 years. AUD was identified based on Swedish medical, legal, and pharmacy registries. The magnitude of the relationship between resilience and AUD was examined using logistic regression. The extent to which the relationship arises from common genetic or common environmental factors was examined using a bivariate Cholesky decomposition model. Results The 5 single items that comprised the resilience assessment (social maturity, interest, psychological energy, home environment, and emotional control) all reduced risk for subsequent AUD, with social maturity showing the strongest effect. The linear effect by logistic regression showed that a 1-point increase on the resilience scale was associated with a 29% decrease in odds of AUD. The Cholesky decomposition model demonstrated that the resilience-AUD relationship was largely attributable to overlapping genetic and shared environmental factors (57 and 36%, respectively). Conclusions Resilience is strongly associated with a reduction in risk for AUD. This relationship appears to be the result of overlapping genetic and shared environmental influences that impact resilience and risk of AUD, rather than a directly causal relationship. [ABSTRACT FROM AUTHOR]

Background: Low self-worth during adolescence predicts a range of emotional and behavioural problems. As such, identifying potential sources of influence on self-worth is important. Aspects of the parent-child relationship are often associated with adolescent self-worth but to date it is unclear whether such associations may be attributable to familial confounding (e.g. genetic relatedness). We set out to clarify the nature of relationships between parental expressed affection and adolescent self-worth, and parent-child closeness and adolescent self-worth. Methods: We used data from the Twin and Offspring Study in Sweden, a children-of-twins sample comprising 909 adult twin pairs with adolescent children. Using these data we were able to apply structural equation models with which we could examine whether associations remained after accounting for genetic transmission. Results: Results demonstrated that parent-child closeness and parental-expressed affection were both phenotypically associated with adolescent self-worth. Associations could not be attributed to genetic relatedness between parent and child. Conclusions: Parent-child closeness and parental affection are associated with adolescent self-worth above and beyond effects attributable to genetic relatedness. Data were cross-sectional, so the direction of effects cannot be confirmed but findings support the notion that positive parent-child relationships increase adolescent self-worth. [ABSTRACT FROM AUTHOR]

In the self-worth model, burnout is considered to be a syndrome of performance-based self-esteem (PBSE) and experiences of exhaustion. Studies have shown that PBSE and burnout indices such as Pines' Burnout Measure (BM) are associated. Whether these variables have overlapping etiologies has however not been studied before. Genetic and environmental components of covariation between PBSE and exhaustion measured with Pines' BM were examined in a bivariate Cholesky model using data from 14,875 monozygotic and dizygotic Swedish twins. Fifty-two per cent of the phenotypic correlation (r = 0.41) between PBSE and Pines' BM was explained by genetics and 48% by environmental factors. The findings of the present study strengthen the assumption that PBSE should be considered in the burnout process as proposed by the self-worth conception of burnout. The present results extend our understanding of the link between this contingent self-esteem construct and exhaustion and provide additional information about the underlying mechanisms in terms of genetics and environment. This finding corroborates the assumed syndrome view on burnout, while it also suggests an altered view of how the syndrome emerges and how it can be alleviated. [ABSTRACT FROM AUTHOR]

Objective: Cognitive performance shows a marked deterioration in close proximity to death, as postulated by the terminal decline hypothesis. The effect of education on the rate of terminal decline in the oldest people (i.e. persons 85+ years) has been controversial and not entirely understood. In the current study, we investigated the rate of decline prior to death with a special focus on the role of education and socioeconomic position, in two European longitudinal studies of ageing: the Origins of Variance in the Old-Old: Octogenarian Twins (OCTO-Twin) and the Newcastle 85+ study.Methods: A process-based approach was used in which individuals' cognitive scores were aligned according to distance to death. In a coordinated analysis, multilevel models were employed to examine associations between different markers of cognitive reserve (education and socioeconomic position) and terminal decline using the mini-mental state examination (MMSE), controlling for age at baseline, sex, dementia incidence and time to death from the study entry to the time of death within each cohort.Results: The current findings suggest that education was positively associated with higher MMSE scores prior to death in the OCTO-Twin, but not in the Newcastle 85+ study, independent of socioeconomic position and other factors such as baseline age, sex and time to death from the study entry. However, education was not associated with the rate of terminal decline in both of these studies.Conclusions: Our results offer only partial support to the cognitive reserve hypothesis and cognitive performance prior to death. [ABSTRACT FROM AUTHOR]

ABSTRACT Objective We examined the association between the genetic and environmental factors contributing to the liability to having ever engaged in self-induced vomiting (SIV initiation) and the genetic and environmental factors contributing to regular SIV behaviors (weekly or daily) for weight control. Method SIV was assessed in 3,942 women from monozygotic twin pairs and 2,790 women from same-sex dizygotic twin pairs, aged 20-47, from the Swedish Twin study of Adults: Genes and Environment. A causal-contingent-common pathway model assessed the extent to which genetic and environmental factors that influence initiation of SIV also influence regular SIV behaviors. Results In the best-fit model, genetic and individual-specific environmental factors influenced liability to SIV initiation. The genetic factors influencing regular SIV behaviors were the same as the genetic factors influencing SIV initiation. Additional individual-specific environmental factors that were unrelated to SIV initiation influenced regular SIV behaviors. Discussion Our findings provide evidence that the underlying liabilities for SIV initiation and regular SIV lie on the same continuum given the degree of overlap in risk between SIV initiation and regular SIV behaviors. Further, the lack of specific genetic factors and the importance of individual-specific environmental factors for regular SIV behaviors highlight the significance of environmental factors in the etiology of eating disorder symptomatology and the non-deterministic nature of genetic factors. Finally, our results suggest that when it comes to preventing individuals from developing regular SIV behavior, intervening at an environmental level is warranted. © 2015 Wiley Periodicals, Inc. (Int J Eat Disord 2016; 49:421-427) [ABSTRACT FROM AUTHOR]

ABSTRACT Objective This study explored the cross-sectional and predictive effect of drive for thinness and/or negative affect scores on the development of self-reported anorexia nervosa (AN) and bulimia nervosa (BN). Method K-means were used to cluster the Eating Disorder Inventory-Drive for Thinness (DT) and Child Behavior Checklist Anxious/Depressed (A/D) scores from 615 unrelated female twins at age 16-17. Logistic regressions were used to assess the effect of these clusters on self-reported eating disorder diagnosis at ages 16-17 ( n = 565) and 19-20 ( n = 451). Results DT and A/D scores were grouped into four clusters: Mild (scores lower than 90th percentile on both scales), DT (higher scores only on DT), A/D (higher scores only on A/D), and DT-A/D (higher scores on both the DT and A/D scales). DT and DT-A/D clusters at age 16-17 were associated cross-sectionally with AN and both cross-sectionally and longitudinally with BN. The DT-A/D cluster had the highest prevalence of AN at follow-up compared with all other clusters. Similarly, an interaction was observed between DT and A/D that predicted risk for AN. Discussion Having elevated DT and A/D scores may increase risk for eating disorder symptomatology above and beyond a high score on either alone. Findings suggest that cluster modeling based on DT and A/D may be useful to inform novel and useful intervention strategies for AN and BN in adolescents. © 2015 Wiley Periodicals, Inc. (Int J Eat Disord 2015; 48:692-699) [ABSTRACT FROM AUTHOR]

Background Evidence from twin and molecular genetic studies is accumulating that Autism Spectrum Disorder ( ASD) shares substantial etiological factors with other disorders. This is mirrored in clinical practice where ASD without coexisting disorders is rare. The present study aims to examine the range of coexisting disorders in ASD in a genetically informative cohort. Methods Parents of all Swedish 9-year-old twins born between 1992 and 2001 ( n = 19,130) underwent a telephone interview designed to screen for child psychiatric disorders, including ASD. To ensure full coverage of child psychiatric disorders, data were also retrieved from population-based health registers. We investigated the coexistence of eight psychiatric disorders known to coexist with ASDs in probands and their co-twins. Results Half of the individuals with ASDs (50.3%) had four or more coexisting disorders and only 4% did not have any concomitant disorder. The 'healthy co-twin' in ASD discordant monozygotic twin pairs was very often (79% of boys and 50% of girls) affected by at least one non- ASD disorder. The corresponding figures for ASD discordant dizygotic twin pairs were significantly lower (46% of males and 30% of females). Conclusions Detailed phenotypic descriptions including symptoms of problems associated with a wide range of child psychiatric disorders may aid in unraveling the genetic architecture of ASD and should guide the development of intervention strategies addressing each problem type specifically. [ABSTRACT FROM AUTHOR]

Background Attention-Deficit/Hyperactivity Disorder ( ADHD) frequently co-occurs with externalizing disorders, but a clear understanding of the etiologic underpinnings is hampered by the limited understanding of the codevelopment of the traits from childhood into early adulthood. Methods Using a birth cohort of 2600 twins, the Swedish Twin study of Child and Adolescent Development study, assessed at ages 8-9, 13-14, 16-17, and 19-20, we investigated the codevelopment of ADHD and externalizing behavior from childhood to adulthood. The analyses examined ADHD-like and externalizing traits, as rated by twins and their parents using the Attention Problems scale and Externalizing scale of the Child Behavior Checklist, and estimated cross-lagged effects (one trait at one time-point predicting the other at the next). The covariation between the traits were decomposed into stable (effects carried over from the prior time-points) and innovative (new effects for each time-point) sources; each source was further decomposed into additive genetics, shared and nonshared environment. Results The analysis suggested that externalizing traits in middle childhood (age 8-9) predicted ADHD-like traits in early adolescence (age 13-14), whereas the reverse association was nonsignificant. In contrast, ADHD-like traits in lateadolescence (age 16-17) predicted externalizing traits in early adulthood (age 19-20). The correlation between ADHD-like and externalizing traits increased over time. At all time-points, innovative sources contributed substantially to maintained comorbidity. Genetic effects explained 67% of the covariation at each time-point; importantly, nearly 50% of these effects were innovative. Conclusions This study challenges the belief that ADHD generally precedes externalizing behaviors; rather, change in the etiologic factors across the development is the rule. The effects were due to both new genetic and environmental factors emerging up to young adulthood. Clinicians and researchers needs to consider complex etiologic and developmental models for the comorbidity between ADHD and externalizing behaviors. [ABSTRACT FROM AUTHOR]

Background Studies have found an association between low birth weight and ADHD, but the nature of this relation is unclear. First, it is uncertain whether birth weight is associated with both of the ADHD dimensions, inattentiveness and hyperactivity-impulsivity. Second, it remains uncertain whether the association between birth weight and ADHD symptom severity is confounded by familial factors. Method Parents of all Swedish 9- and 12-year-old twins born between 1992 and 2000 were interviewed for DSM- IV inattentive and hyperactive-impulsive ADHD symptoms by the Autism - Tics, AD/ HD and other Comorbidities (A- TAC) inventory ( N = 21,775 twins). Birth weight was collected prospectively through the Medical Birth Registry. We used a within-twin pair design to control for genetic and shared environmental factors. Results Reduced birth weight was significantly associated with a mean increase in total ADHD (β = −.42; 95% CI: −.53, −.30), inattentive (β = −.26; 95% CI: −.33, −.19), and hyperactive-impulsive (β = −.16; 95% CI: −.22, −.10) symptom severity. These results imply that a change of one kilogram of birth weight corresponded to parents rating their child nearly one unit higher (going from 'no' to 'yes, to some extent' on a given symptom) on the total ADHD scale. These associations remained within pairs of MZ and DZ twins, and were also present when restricting the analyses to full term births. Conclusions There is an independent association between low birth weight and all forms of ADHD symptoms, even after controlling for all environmental and genetic confounds shared within twin pairs. These results indicate that fetal growth restriction (as reflected in birth weight differences within twin pairs) and/or the environmental factors which influence it is in the casual pathway leading to ADHD. [ABSTRACT FROM AUTHOR]

Background There is evidence both that parental monitoring is an environmental influence serving to diminish adolescent externalizing problems and that this association may be driven by adolescents' characteristics via genetic and/or environmental mechanisms, such that adolescents with fewer problems tell their parents more, and therefore appear to be better monitored. Without information on how parents' and children's genes and environments influence correlated parent and child behaviors, it is impossible to clarify the mechanisms underlying this association. Method The present study used the Extended Children of Twins model to distinguish types of gene-environment correlation and direct environmental effects underlying associations between parental knowledge and adolescent (age 11-22 years) externalizing behavior with a Swedish sample of 909 twin parents and their adolescent offspring and a US-based sample of 405 White adolescent siblings and their parents. Results Results suggest that more parental knowledge is associated with less adolescent externalizing via a direct environmental influence independent of any genetic influences. There was no evidence of a child-driven explanation of the association between parental knowledge and adolescent externalizing problems. Conclusions In this sample of adolescents, parental knowledge exerted an environmental influence on adolescent externalizing after accounting for genetic influences of parents and adolescents. Because the association between parenting and child development originates in the parent, treatment for adolescent externalizing must not only include parents but should also focus on altering their parental style. Thus, findings suggest that teaching parents better knowledge-related monitoring strategies is likely to help reduce externalizing problems in adolescents. [ABSTRACT FROM AUTHOR]

Background and Aims Anabolic androgenic steroid ( AAS) use is associated with aggressive and violent behaviour, but it remains uncertain if this relationship is causal in humans. We examined the link between AAS use and violent crime while controlling for polysubstance abuse and additional suggested risk factors for violence. Design Cross-sectional study of a population-based sample. Setting In 2005, all Swedish-born male twins aged 20-47 years were invited to participate in the Swedish Twin Adults: Genes and Environment ( STAGE) survey of the Swedish Twin Register (response rate = 60%). Participants A total of 10 365 male survey participants with information on AAS use. Measurement Data on self-reported use of AAS, alcohol and other substances, attention deficit hyperactivity disorder ( ADHD) and personality disorder symptoms were linked to nation-wide, longitudinal register information on criminal convictions, IQ, psychological functioning and childhood socio-economic status ( SES) covariates. Findings Any life-time use of AAS was associated strongly with conviction for a violent crime [2.7 versus 0.6% in convicted and non-convicted men, respectively; odds ratio ( OR) = 5.0, 95% confidence interval ( CI) = 2.7-9.3]. However, this link was substantially reduced and no longer significant when controlling for other substance abuse ( OR = 1.6, 95% CI = 0.8-3.3). Controlling for IQ, psychological functioning, ADHD, personality disorder symptoms and childhood SES did not reduce the risk further. Conclusion In the general population, co-occurring polysubstance abuse, but not IQ, other neuropsychological risks or socio-economic status, explains most of the relatively strong association between any anabolic androgenic steroid use and conviction for a violent crime. [ABSTRACT FROM AUTHOR]

Background: We addressed if immaturity relative to peers reflected in birth month increases the likelihood of ADHD diagnosis and treatment. Methods: We linked nationwide Patient and Prescribed Drug Registers and used prospective cohort and nested case-control designs to study 6-69 year-old individuals in Sweden from July 2005 to December 2009 (Cohort 1). Cohort 1 included 56,263 individuals diagnosed with ADHD or ever used prescribed ADHD-specific medication. Complementary population-representative cohorts provided DSM-IV ADHD symptom ratings; parent-reported for 10,760 9-year-old twins born 1995-2000 from the CATSS study (Cohort 2) and self-reported for 6,970 adult twins age 20-47 years born 1959-1970 from the STAGE study (Cohort 3). We calculated odds ratios (OR:s) for ADHD across age for individuals born in November/December compared to January/February (Cohort 1). ADHD symptoms in Cohorts 2 and 3 were studied as a function of calendar birth month. Results: ADHD diagnoses and medication treatment were both significantly more common in individuals born in November/December versus January/February; peaking at ages 6 (OR: 1.8; 95% CI: 1.5-2.2) and 7 years (OR: 1.6; 95% CI: 1.3- 1.8) in the Patient and Prescribed Drug Registers, respectively. We found no corresponding differences in parent- or self-reported ADHD symptoms by calendar birth month. Conclusion: Relative immaturity compared to class mates might contribute to ADHD diagnosis and pharmacotherapy despite absence of parallel findings in reported ADHD symptom loads by relative immaturity. Increased clinical awareness of this phenomenon may be warranted to decrease risk for imprecise diagnostics and treatment. We speculate that flexibility regarding age at school start according to individual maturity could reduce developmentally inappropriate demands on children and improve the precision of ADHD diagnostic practice and pharmacological treatment. [ABSTRACT FROM AUTHOR]

Background Although neurodevelopmental disorders are demarcated as discrete entities in the Diagnostic Statistical Manual of mental disorders, empirical evidence indicates that there is a high degree of overlap among them. The first aim of this investigation was to explore if a single general factor could account for the large degree of observed overlap among neurodevelopmental problems, and explore whether this potential factor was primarily genetic or environmental in origin. The second aim was to explore whether there was systematic covariation, either genetic or environmental, over and above that contributed by the potential general factor, unique to each syndrome. Method Parents of all Swedish 9- and 12-year-old twin pairs born between 1992 and 2002 were targeted for interview regarding problems typical of autism spectrum disorders, ADHD and other neurodevelopmental conditions (response rate: 80 percent). Structural equation modeling was conducted on 6,595 pairs to examine the genetic and environmental structure of 53 neurodevelopmental problems. Results One general genetic factor accounted for a large proportion of the phenotypic covariation among the 53 symptoms. Three specific genetic subfactors identified 'impulsivity,' 'learning problems,' and 'tics and autism,' respectively. Three unique environment factors identified 'autism,' 'hyperactivity and impulsivity,' and 'inattention and learning problems,' respectively. Conclusion One general genetic factor was responsible for the wide-spread phenotypic overlap among all neurodevelopmental symptoms, highlighting the importance of addressing broad patient needs rather than specific diagnoses. The unique genetic factors may help guide diagnostic nomenclature, whereas the unique environmental factors may highlight that neurodevelopmental symptoms are responsive to change at the individual level and may provide clues into different mechanisms and treatments. Future research would benefit from assessing the general factor separately from specific factors to better understand observed overlap among neurodevelopmental problems. [ABSTRACT FROM AUTHOR]

Background Twins and triplets fall behind singletons in cognitive and physical development. We analysed whether these differences are modified by family social position. Methods IQ, height, body mass index ( BMI) and elbow flexion, handgrip and knee extension strength were measured in Swedish men born between 1951 and 1976 during the conscription examination at 17 to 20 years of age. Information from Swedish registers on all siblings and parental socio-economic position were linked to these measures. Together, the measures were available for 1 140 329 singletons, 19 755 twins and 207 triplets. The data were analysed using regression analyses and fixed-effect models which compare twins and triplets with their singleton brothers. Results Twins and triplets had slightly lower IQ, height, BMI and muscle strength than did singletons both at the population level as well as when compared with their singleton brothers. Although the differences between twins and triplets were small, they were largest in families with lower socio-economic position. We also found larger differences in IQ among the sons of mothers born before 1940. Conclusions Twins and triplets fall slightly behind singletons in cognitive and physical development, even in early adulthood, but twins and triplets show no major differences. These differences are largest in families in a low socio-economic position. Our results underscore the importance of the postnatal environment in the development of twins and triplets and suggest that their parents, especially those in a low socio-economic position, need special support. [ABSTRACT FROM AUTHOR]

Objectives To examine how body mass index ( BMI) and change in BMI are associated with mortality in old (70-79) and very old (≥80) individuals. Design Pooled data from three multidisciplinary prospective population-based studies: OCTO-twin, Gender, and NONA. Setting Sweden. Participants Eight hundred eighty-two individuals aged 70 to 95. Measurements BMI was calculated from measured height and weight as kg/m2. Information about survival status and time of death was obtained from the Swedish Civil Registration System. Results Mortality hazard was 20% lower for the overweight group than the normal-underweight group (relative risk ( RR) = 0.80, P = .011), and the mortality hazard for the obese group did not differ significantly from that of the normal-underweight group ( RR = 0.93, P = .603), independent of age, education, and multimorbidity. Furthermore, mortality hazard was 65% higher for the BMI loss group than for the BMI stable group ( RR = 1.65, P < .001) and 53% higher for the BMI gain group than for the BMI stable group ( RR = 1.53, P = .001). Age moderated the BMI change differences. That is, the higher mortality risks associated with BMI loss and gain were less severe in very old age. Conclusion Old persons who were overweight had a lower mortality risk than old persons who were of normal weight, even after controlling for weight change and multimorbidity. Persons who increased or decreased in BMI had a greater mortality risk than those who had a stable BMI, particularly those aged 70 to 79. This study lends further support to the belief that the World Health Organization guidelines for BMI are overly restrictive in old age. [ABSTRACT FROM AUTHOR]

Objective: Early maturing girls are at increased risk for disordered eating. However, it is unclear if the association between puberty and disordered eating continues throughout pubertal development and if a similar association is exhibited in boys. Method: Participants included 1340 same- and 624 opposite-sex twins from the Swedish Twin Study of Child and Adolescent Development. Pubertal development was assessed at age 13-14 with the pubertal development scale. General disordered eating, measured with the eating disorder inventory-2 (EDI) was assessed at age 16-17, and dieting and purging behaviors were assessed at both ages 16-17 and 19-20. We applied analysis of variance and logistic regression analyses to determine whether pubertal development in early-to-mid adolescence predicted eating disorder-related behaviors in late adolescence and young adulthood. Results: Pubertal development in early-to-mid adolescence was significantly associated with EDI scores and dieting in late adolescence. No significant association was observed between pubertal development and dieting and purging in young adulthood. Discussion: Complex combinations of cultural and biological influences likely converge during pubertal development increasing vulnerability to disordered eating. The impact of pubertal development on disordered eating appears to be limited to the adolescent period. © 2012 by Wiley Periodicals, Inc. (Int J Eat Disord 2012;45:819-826) [ABSTRACT FROM AUTHOR]

Objective: We examined the association among current self-reported sleep problems, lifetime binge eating (BE), and current obesity in women from the Swedish Twin study of Adults: Genes and Environment. Method: Logistic regression analyses were used to evaluate these associations in 3,790 women aged 20-47 years. Results: BE was reported by 244 (6.4%) women and was positively associated with not getting enough sleep ( p < .015), sleeping poorly ( p < .001), problems falling asleep ( p < .001), feeling sleepy during work or free time ( p < .001), and disturbed sleep ( p < .001). These same sleep variables, as well as napping and being a night person, were also significantly associated with obesity. The associations between BE and sleep remained after accounting for obesity. Discussion: This investigation offers empirical support for an independent association between sleep problems and BE, which is likely due to complex psychological, biological, neuroendocrine, and metabolic factors. © 2012 by Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Objective: We assessed the impact of reducing the binge eating frequency and duration thresholds on the diagnostic criteria for bulimia nervosa (BN) and binge eating disorder (BED). Method: We estimated the lifetime population prevalence of BN and BED in 13,295 female twins from the Swedish Twin study of Adults: Genes and Environment employing a range of frequency and duration thresholds. External validation (risk to cotwin) was used to investigate empirical evidence for an optimal binge eating frequency threshold. Results: The lifetime prevalence estimates of BN and BED increased linearly as the frequency criterion decreased. As the required duration increased, the prevalence of BED decreased slightly. Discontinuity in cotwin risk was observed in BN between at least four times per month and at least five times per month. This model could not be fit for BED. Discussion: The proposed changes to the DSM-5 binge eating frequency and duration criteria would allow for better detection of binge eating pathology without resulting in a markedly higher lifetime prevalence of BN or BED. © 2011 by Wiley Periodicals, Inc. (Int J Eat Disord 2012) [ABSTRACT FROM AUTHOR]

Objectives To examine job control, job demands, social support at work, and job strain (ratio of demands to control) in relation to risk of any dementia, Alzheimer's disease ( AD), and vascular dementia ( VaD). Design Cohort study. Setting The population-based Study of Dementia in Swedish Twins. Participants Two hundred fifty-seven people with dementia (167 AD, 46 VaD) and 9,849 without. Measurements Dementia diagnoses were based on telephone screening for cognitive impairment followed by in-person clinical examination. An established job exposure matrix was matched to main occupation categories to measure work characteristics. Results In generalized estimating equations (adjusted for the inclusion of complete twin pairs), lower job control was associated with greater risk of any dementia (odds ratio ( OR) = 1.17, 95% confidence interval ( CI) = 1.04-1.31) and VaD specifically ( OR = 1.39, 95% CI = 1.07-1.81). Lower social support at work was associated with greater risk of dementia ( OR = 1.15, 95% CI = 1.03-1.28), AD ( OR = 1.14, 95% CI = 1.00-1.31), and VaD ( OR = 1.28, 95% CI = 1.02-1.60). Greater job strain was associated with greater risk of VaD only ( OR = 1.28, 95% CI = 1.02-1.60), especially in combination with low social support ( OR = 1.35, 95% CI = 1.11-1.64). Age, sex, and education were controlled for. Work complexity, manual work, and vascular disease did not explain the results. No differences in work-related stress scores were observed in the 54 twin pairs discordant for dementia, although only two pairs included a twin with VaD. Conclusion Work-related stress, including low job control and low social support at work, may increase the risk of dementia, particularly VaD. Modification to work environment, including attention to social context and provision of meaningful roles for employees, may contribute to efforts to promote cognitive health. [ABSTRACT FROM AUTHOR]

Background: Although the clinical utility of categorically defined attention-deficit hyperactivity disorder (ADHD) is well established, there is also strong evidence supporting the notion of ADHD as an extreme of a continuous trait. Nevertheless, the question of whether the etiology is the same for different levels of DSM-IV ADHD symptoms remains to be investigated. The aim of this study was to assess genetic links between the extreme and the subthreshold range of ADHD symptoms. Method: Parents of all Swedish 9- and 12-year-old twins born between 1992 and 2000 were interviewed for DSM-IV ADHD symptoms and associated conditions. Two validated cutoff values were used for screening and assigning research diagnoses. Response rate was 80%. Twin methods were applied to investigate the extent to which ADHD is etiologically distinct from subthreshold variations in ADHD symptoms. Results: Extremes analyses indicated a strong genetic link between the extreme and the subthreshold variation, with almost identical group heritability estimates around .60 for the diagnostic (prevalence 1.78%) and screening (prevalence 9.75%) criteria of ADHD. Conclusion: A strong genetic link between the extreme and the subthreshold variation of DSM-IV based assessments of ADHD symptoms was found. The data suggest that ADHD is best viewed as the quantitative extreme of genetic and environmental factors operating dimensionally throughout the distribution of ADHD symptoms, indicating that the same etiologic factors are involved in the full range of symptoms of inattention, hyperactivity and impulsivity. [ABSTRACT FROM AUTHOR]

Previous studies have found inverse associations between intelligence quotient (IQ) and cigarette smoking, but the causal pathways linking IQ with smoking status and nicotine dependence (ND) are not well understood. The aim of this study was to explore the associations between IQ and ND using a genetically informative twin design to detect whether any association is because of shared genetic or environmental factors. A population-based twin cohort with IQ measured in adolescence and ND later in life, analysed by classical twin modeling based on linear structural equations. Swedish national registry data. A total of 5040 male twins born 1951-84. IQ was measured at military conscription at a mean age of 18 years. ND was self-reported at the ages of 22-57 years using the Fagerström Test for ND scale (FTND). Both cigarette smoking and Swedish snus use were analysed. Both IQ and ND showed moderate heritability (0.58 and 0.39, respectively). The heritability of ND was similar for cigarette smoking and snus use. The phenotypic correlation between IQ and ND was weak: −0.11 (−0.16, −0.06) for total ND. Bivariate analysis revealed that this correlation was mainly because of genetic factors, but still the genetic correlation between IQ and ND from cigarette smoking was only −0.24. Nicotine dependence, as measured by the Fagerström Test for Nicotine Dependence, shows moderate heritability in both smokers and snus users but is only weakly associated with intelligence quotient; common genetic factors underlying nicotine dependence and intelligence quotient probably account for little of the observed association between smoking and intelligence quotient. [ABSTRACT FROM AUTHOR]

Scand J Caring Sci; 2010; 24; 541–547 High sense of coherence in adolescence is a protective factor in the longitudinal development of ADHD symptoms The key feature of salutogenesis is that good health can be directly sustained by positive factors. The Sense of Coherence (SOC) scale was developed by Antonovsky as a measure related to the concept of salutogenesis including aspects of comprehensibility, manageability and meaningfulness. Aim: The aim was to investigate whether Sense of Coherence can serve as a salutogenetic factor modifying the long-term development of Attention Deficit Hyperactivity Disorder (ADHD) Symptoms. Subjects and methods: Twin study of Child and Adolescent Development (TCHAD) is a longitudinal study of all twin pairs born in Sweden between May 1985 and December 1986. The present project is a sub-sample of 312 individuals (135 boys and 177 girls). At 16 years of age, the young persons and their parents were interviewed with K-SADS especially symptoms of ADHD. The young person also completed the SOC questionnaire. At 21 years of age, the young person completed a questionnaire about symptoms of ADHD. Findings: Higher (worse) ADHD scores at 16 years of age were associated with higher (worse) ADHD scores at 21 years of age. However, this relationship was stronger for lower (worse) SOC. A higher (better) SOC at 16 years was associated with lower (better) ADHD at 21 years and this relationship was stronger for higher (worse) ADHD at 16 years. Conclusion: A high Sense of Coherence in adolescence was a protective factor for the long-term development of ADHD. [ABSTRACT FROM AUTHOR]

Background: Despite extensive efforts, the causes of autism remain unknown. Advancing paternal age has been associated with various neurodevelopmental disorders. We aim to investigate three unresolved questions: (a) What is the association between paternal age and autism spectrum disorders (ASD)?; (b) Does paternal age moderate the genetic and environmental etiological factors for ASD? (c) Does paternal age affect normal variation in autistic-like traits? Methods: Two nationally representative twin studies from Sweden ( n = 11, 122, assessed at age 9 or 12) and the UK ( n = 13, 524, assessed at age 9) were used. Categorical and continuous measures of ASD, autistic-like traits and autistic similarity were calculated and compared over paternal age categories. Results: Both cohorts showed a strong association between paternal age and the risk for ASD. A U-shaped risk association could be discerned since the offspring of both the youngest and oldest fathers showed an elevation in the risk for ASD. Autistic similarity increased with advancing paternal age in both monozygotic and dizygotic twins. Both cohorts showed significantly higher autistic-like traits in the offspring of the youngest and oldest fathers. Conclusions: Phenomena associated with paternal age are clearly involved in the trajectories leading to autistic-like traits and ASD. Mechanisms influencing the trajectories might differ between older and younger fathers. Molecular genetic studies are now needed in order to further understand the association between paternal age and ASD, as well as normal variation in social, language, and repetitive behaviors in the general population. [ABSTRACT FROM AUTHOR]

Background. Study of migrants offers a natural model to assess environmental risk of coronary heart disease (CHD) in countries differing in CHD occurrence. In Sweden, CHD risk has been markedly lower than in Finland from where a large migration occurred in the 1970s. Objectives. To study the structural and functional markers of subclinical atherosclerosis in twin pairs discordant for migration with the main focus on age at migration, length of residence and integration into Swedish society after migration from a high to a lower CHD risk country. Methods. Carotid intima-media thickness (IMT) and brachial artery endothelial function (EF) were assessed with high-resolution ultrasound and a set of cardiovascular, socio-economic and psychosocial risk factors were estimated in 76 middle-aged male twin pairs discordant for migration from Finland to Sweden. Results. Men who had migrated in adolescence had lower IMT values compared with their co-twins living in Finland (0.665 ± 0.114 vs. 0.802 ± 0.167 mm, P = 0.009). Also men who integrated well to Swedish society had lower (0.720 ± 0.154 vs. 0.799 ± 0.207 mm, P = 0.013) IMT values than their twin brothers living in Finland. Associations between IMT and migration age and between IMT and integration remained significant in multivariate analyses of several CHD risk factors. The intrapair difference in IMT was significantly associated with immigration age and integration (anova, P = 0.0082), the difference being greatest among pairs where the brother living in Sweden had migrated at early age and integrated well to Swedish society. EF was better in men who had migrated to Sweden before the age of 21 years, but not later, compared with their co-twins in Finland (6.4 ± 4.6% vs. 3.8 ± 3.6%, P = 0.025). Conclusions. Migration at an early age and good integration are beneficial to vascular health associated with moving from a high to a lower CHD risk country, suggesting that an environment-sensitive period influences atherogenesis before adulthood. [ABSTRACT FROM AUTHOR]

The article analyzes the effect of genetic and environmental factors on growth in a longitudinal Swedish cohort of 231 monozygotic and 144 dizygotic twin pairs born from 1973 to 1979 with length or height measured annually from birth to age 18. The results indicate that genetic regulation of growth is rather uniform, which is encouraging for further efforts to identify genes affected growth.

Aims To investigate the prevalence and patterns of transitions between cigarette and snus use. Design Cross-sectional study within the population-based Swedish Twin Registry. Setting and participants A total of 31 213 male and female twins 42–64 years old. Measurements Age-adjusted prevalence odds ratios (POR) and 95% confidence intervals (CIs) described the association between gender and tobacco use, while Kaplan–Meier survival methods produced cumulative incidence curves of age at onset of tobacco use. Life-time tobacco use histories were constructed using ages at onset of tobacco use and current tobacco use status. Findings Although more males reported ever smoking (64.4%) than females (61.7%), more males were former smokers (POR: 1.33, 95% CI: 1.27–1.39). Males were far more likely to use snus than females (POR: 18.0, 95% CI: 16.17–20.04). Age at onset of cigarette smoking occurred almost entirely before age 25, while the age at onset of snus use among males occurred over a longer time period. Most men began using cigarettes first, nearly one-third of whom switched to using cigarettes and snus in combination. While 30.6% of these combined users quit tobacco completely, only 7.4% quit snus and currently use cigarettes, while 47.7% quit cigarettes and currently use snus. Conclusions Current cigarette smoking is more prevalent among Swedish women than men, while snus use is more prevalent among men. Among men who reported using both cigarettes and snus during their life-time, it was more common to quit cigarettes and currently use snus than to quit snus and currently use cigarettes. Once snus use was initiated, more men continued using snus rather than quit tobacco completely. [ABSTRACT FROM AUTHOR]

Aim: To study the long-term relationship between symptoms of Attention Deficit Hyperactivity Disorder and the developing self-esteem in a population-based sample of twins. Methods: The cohort is all twin pair families born in Sweden between May 1985 and December 1986 (n = 1.480). Wave 1 took place in 1994 when the twins were 8 years old and wave 2 in 1999 when the children were 13 years old. In wave 1 and 2 the parents completed questionnaires regarding ADHD-symptoms about their children. In wave 2 the twins completed a questionnaire about self-esteem and Youth Self Report (YSR). ADHD-symptoms and self-esteem were analyzed in the total study group. Results: There was a long-term relationship between high scores of parental-reported ADHD-symptoms at 8 and 13 years of age and low scores in measures of self-reported self-esteem at 13 years of age. In the cotwin control method controlling for YSR internalizing problem, paired comparisons within the twin pairs revealed that a high score of ADHD-symptoms at age 8 was related to significantly lower scores at age 13 in the self-esteem. Conclusions: The long-term relationships between ADHD-symptoms and a low self-esteem in a population-based sample were confirmed by the co-twin analyses. [ABSTRACT FROM AUTHOR]

Objective: The aim of the present study was to evaluate and distinguish between environmental and genetic effects for death from coronary heart disease (CHD) as well as to determine whether the importance of genetic influences is changing with age.Design: A cohort study with a follow-up time of 36 years.Subjects: The cohort drawn for the present study includes 20 966 twins born in Sweden between 1886 and 1925 where both twins within a pair still lived within the country in 1961.Methods: Concordances and correlated gamma-frailty model were used to assess and distinguish between genetic and environmental influences as well as to evaluate age-related changes in genetic influences.Results: A total number of 4007 CHD-deaths (2208 males, and 1799 females) was observed. The probability of dying from CHD given that one's twin partner already has died from CHD decreased with increasing age, particularly amongst males. The genetic variation in susceptibility to death from CHD was moderately large, and decreased slightly across time, particularly amongst males. The heritability was 0.57 (95% CI, 0.45-0.69) amongst male twins, and 0.38 (0.26-0.50) amongst female twins.Conclusions: The genetic contribution to the variation in CHD-mortality was moderate both in females and males. Furthermore, although genetic effects appeared to be greater at younger ages of death, our findings clearly suggest that genetic factors are in operation throughout the entire life span. [ABSTRACT FROM AUTHOR]

Objective.—To examine the lifetime prevalence and other characteristics of recurrent primary headaches in twins. Background.—The twin model may provide insights into the role of genetic and environmental influences in headache disorders. However, assumptions as to whether twins are representative of the general population, and whether monozygotic and dizygotic twins are similar have rarely been addressed. Methods.—The study population consisted of a random sample of 17- to 82-year-old twins from the Swedish Twin Registry (n = 1329). Structured interviews on the telephone by lay personnel and the International Headache Society criteria were used for assessment and diagnosis of recurrent primary headaches. Prevalence data of the general population for migraine and tension-type headache was obtained from various published reports. Results.—A total of 372 subjects (29%) had ever had recurrent headaches. In total, 241 recurrent headache sufferers fulfilled the criteria for migraine or tension-type headache, and the lifetime prevalence was 7.1% for migraine without aura, 1.4% for migraine always with aura, 1.9% for migraine occasionally with aura, 9.4% for episodic tension-type headache, and 1.3% for chronic tension-type headache. The lifetime prevalence of all migraine and all tension-type headache, including another 84 subjects fulfilling all but one of the criteria for migraine or tension-type headache, was 13.8% and 13.5%, respectively. The corresponding prevalence risk for women was 2.4 (95% confidence interval [CI] 1.7, 3.4) and 1.5 (95% CI 1.1, 2.1), respectively. Zygosity was not a significant predictor for migraine. In tension-type headache, the prevalence risk for dizygotic twins and unlike-sexed twins as compared with monozygotic twins was 1.9 (95% CI: 1.2, 3.1) and 1.8 (95% CI: 1.1, 2.9), respectively. Conclusion.—There is no twin-singleton or monozygotic-dizygotic difference for the risk of migraine. In tension-type... [ABSTRACT FROM AUTHOR]

The issue of factors predisposing for inhibitor development in haemophilia patients is still largely unresolved. In an attempt to address this problem, we initiated a registry in 1996 of siblings with haemophilia and with or without a history of inhibitors. Four hundred and sixty families have accrued, of whom 388 suffer from haemophilia A and 72 haemophilia B. Twenty-five of the brother pairs are twins. The inhibitor incidence in all families with severe haemophilia A was 31.7%. The corresponding figure in the caucasian patients was 27.4%, whereas a higher incidence of inhibitors was reported in the black subjects (55.6%). Twins were reported in six of the 100 inhibitor families, for whom monozygocity was confirmed in three cases. In 32 families (32%), at least two brothers had a history of inhibitors. In 22 (69%) of these families, the inhibitor was also of the same type, i.e. either high- or low-responding. The overall concordance within the severe haemophilia A families was found to be 78.3% (195/249) compared to an expected figure of 68.0% and 58.0% using an inhibitor incidence of 20 and 30%, respectively (P < 0.0001). The corresponding figure for the twins was 88.2% (15/17). Moreover, the risk for inhibitor development in families with a previous inhibitor history was found to be 48% (95% confidence interval [CI] 35–62%), whereas the risk in families with no previous known inhibitor was only 15% (95% CI 11–21%) corresponding to a relative risk of 3.2 (95% CI 2.1–4.9). Immune-tolerance induction was reported in 24 families, of whom 13 siblings were successfully treated. Our data clearly support the concept that a genetic predisposition for inhibitor development exists. However, the markers of this predisposition remain to be elucidated and we believe that the MIBS registry will be useful for this purpose. [ABSTRACT FROM AUTHOR]

The article reports on a Swedish study which examines the factors that contribute to individuals' use of drugs. Findings reveal that heritability accounted for 55% of drug abuse in males and 73% in females, while environmental factors, such as social deprivation and family socioeconomic status, accounted for 23%. The study also found a higher risk of drug dependence in fraternal twins than in non-twin siblings.