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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: 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]

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]

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 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 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]

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]

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]

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]

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]