Swedish Twin Study Research Articles

Exploring the genetic etiology across the continuum of the general psychopathology factor: a Swedish population-based family and twin study

Psychiatric comorbidity can be accounted for by a latent general psychopathology factor (p factor), which quantifies the variance that is shared to varying degrees by every dimension of psychopathology. It is unclear whether the entire continuum of the p factor shares the same genetic origin. We investigated whether mild, moderate, and extreme elevations on the p factor shared the same genetic etiology by, first, examining the linearity of the association between p factors across siblings (N = 580,891 pairs). Second, we estimated the group heritability in a twin sample (N = 17,170 pairs), which involves testing whether the same genetic variants influence both extreme and normal variations in the p factor. In both samples, the p factor was based on 10 register-based psychiatric diagnoses. Results showed that the association between siblings’ p factors appeared linear, even into the extreme range. Likewise, the twin group heritabilities ranged from 0.42 to 0.45 (95% CI: 0.33–0.57) depending on the thresholds defining the probands (2–3.33 SD beyond the mean; >2 SD beyond the mean; >4.33 SD beyond the mean; and >5.33 SD beyond the mean), and these estimates were highly similar to the estimated individual differences heritability (0.41, 95% CI: 0.39–0.43), indicating that scores above and below these thresholds shared a common genetic origin. Together, these results suggest that the entire continuum of the p factor shares the same genetic origin, with common genetic variants likely playing an important role. This implies, first, genetic risk factors for the aspect that is shared between all forms of psychopathology (i.e., genetic risk factors for the p factor) might be generalizable between population-based cohorts with a higher prevalence of milder cases, and clinical samples with a preponderance of more severe cases. Second, prioritizing low-cost genome-wide association studies capable of identifying common genetic variants, rather than expensive whole genome sequencing that can identify rare variants, may increase the efficiency when studying the genetic architecture of the p factor.

Preliminary Validation of a General Factor Model of Chronic Overlapping Pain Conditions

Chronic overlapping pain conditions (COPCs) by definition, frequently co-occur, perhaps reflecting their shared etiologies. Their overlapping nature presents a methodological challenge, possibly masking associations between COPCs and health outcomes attributable to either general or specific processes. To address this challenge, we used population-based cohort data to evaluate the predictive validity of a bifactor model of 9 self-reported COPCs by assessing its association with incident pain-related clinical diagnoses; pain-relevant pharmacotherapy; and other health outcomes. We obtained data from a 2005 to 2006 study of Swedish adult twins linked with health data from nationwide registers through 2016 (N = 25,418). We then fit a bifactor model comprising a general COPC factor and 2 independent specific factors measuring pain-related somatic symptoms and neck and shoulder pain. Accounting for age, biological sex, and cancer, the general factor was associated with increased risk of all pain-related outcomes (eg, COPC diagnosis adjusted odds ratio [aOR], 1.71; 95% confidence interval [1.62, 1.81]), most mental health-related outcomes (eg, depression aOR, 1.72 [1.60, 1.85]), and overdose and mortality (eg, all-cause mortality aOR, 1.25 [1.09, 1.43]). The somatic symptoms specific factor was associated with pain-relevant pharmacotherapy (eg, prescribed opioids aOR, 1.25 [1.15, 1.36]), most mental health-related outcomes (eg, depression aOR, 1.95 [1.70, 2.23]), and overdose (eg, nonfatal overdose aOR, 1.66 [1.31, 2.10]). The neck and shoulder pain-specific factor was weakly and inconsistently associated with the outcomes. Findings provide initial support for the validity and utility of a general-factor model of COPCs as a tool to strengthen understanding of co-occurrence, etiology, and consequences of chronic pain. PerspectiveThis article presents associations between a novel measurement model of COPCs and various health outcomes. Findings provide support for measuring pain across multiple domains rather than only measuring pain specific to one physical location in both research and clinical contexts.

The association between change and stability in subjective health ratings and dementia risk: a multi‐cohort study in Swedish and Danish twins

AbstractBackgroundPoorer self‐rated health (SRH) is associated with increased dementia risk (Stephan et al., 2021). However, it is unclear whether genetic and/or environmental variance accounts for this risk. Although SRH declines with age (Finkel et al. 2020), it is unknown whether rates of change in SRH are independently associated with dementia outcomes. Using a validated latent dementia index (LDI) (Beam et al., 2022), we tested whether stability and change components of SRH predicted LDI via genetic and environmental pathways in two international cohorts of twins.MethodOur data consisted of two samples of monozygotic (MZ) and dizygotic (DZ) twins. We used data from the Swedish Adoption Twin Study of Aging (SATSA; Ntwins = 548, Npairs = 339) and the Longitudinal Study of Aging Danish Twins (LSADT; Ntwins = 3238, Npairs = 2561). Bivariate Cholesky decompositions and three‐level growth‐curve models with predictive intercepts and slopes were used for our cross‐sectional and longitudinal analyses respectively. All models were estimated in Mplus (Muthen & Muthen, 2017) using maximum likelihood with robust standard errors.ResultsCross‐sectional model results indicate that those with poorer SRH have lower LDI scores (b = ‐0.01, p = .008), even after adjusting for shared genetic covariance, age, sex, education, and depressive symptoms. Predictive growth models indicate that rates of change in SRH are negatively associated with LDI after adjusting for age, sex, education, and depressive symptoms (b = ‐0.17, p = .032). The degree of genetic confounding in the association between rates of change and LDI was inconclusive.ConclusionOur study provides novel insights into the relationship between individual ratings of health and dementia risk. SRH predicted dementia likelihood after controlling for genetic confounding, opening up the possibility that subjective ratings of health account for unique variance in dementia risk. Additionally, changes in SRH also predicted dementia likelihood beyond their mean score. Taken together these results highlight the importance of subjective health measures in understanding dementia risk.

A permutation-based approach using a rank-based statistic to identify sex differences in epigenetics

Epigenetic sex differences and their resulting implications for human health have been studied for about a decade. The objective of this paper is to use permutation-based inference and a new ranked-based test statistic to identify sex-based epigenetic differences in the human DNA methylome. In particular, we examine whether we could identify separations between the female and male distributions of DNA methylation across hundred of thousands CpG sites in two independent cohorts, the Swedish Adoption Twin study and the Lamarck study. Based on Fisherian p-values, we set a threshold for methylation differences “worth further scrutiny”. At this threshold, we were able to confirm previously-found CpG sites that stratify with respect to sex. These CpG sites with sex differences in DNA methylation should be further investigated for their possible contribution to various physiological and pathological functions in the human body. We followed-up our statistical analyses with a literature review in order to inform the proposed disease implications for the loci we uncovered.

Associations of Internalizing and Externalizing Problems in Childhood and Adolescence With Adult Labor Market Marginalization

Mental health problems in early life are associated with labor market marginalization, especially in youths with persistent internalizing and externalizing problems. However, previous research has not adjusted for familial (genetic and shared environmental) factors. To examine associations of early-life internalizing and externalizing problems with adulthood unemployment and work disability, adjusting for familial factors. This population-based prospective cohort study included Swedish twins who were born in 1985-1986 and surveyed at 4 consecutive waves across childhood and adolescence until 2005. Through linkage to nationwide registries, participants were followed up from 2006 to 2018. Data analyses were conducted between September 2022 and April 2023. Internalizing and externalizing problems, assessed with the Child Behavior Checklist. Participants were differentiated regarding duration of internalizing and externalizing problems (persistent, episodic, and noncases). Unemployment (180 days or more of being unemployed) and work disability (60 days or more of being sickness absent or disability pensioned) during follow-up. Cox proportional hazards regression models were calculated to obtain cause-specific hazard ratios (HRs) with 95% CIs in the whole cohort and exposure-discordant twin pairs. Of 2845 participants, 1464 (51.5%) were female. Incident unemployment was experienced by 944 (33.2%) and incident work disability by 522 (18.3%) participants. Compared with noncases, persistent internalizing problems were associated with unemployment (HR, 1.56; 95% CI, 1.27-1.92) and work disability (HR, 2.32; 95% CI, 1.80-2.99). Similarly, compared with noncases, persistent externalizing problems were associated with unemployment (HR, 1.87; 95% CI, 1.55-2.26) and work disability (HR, 2.38; 95% CI, 1.87-3.03). Persistent cases had overall higher risks of adverse outcomes than episodic cases. After adjustment for familial factors, associations with unemployment were no longer statistically significant, whereas associations with work disability remained or were only slightly reduced. In this cohort study of young Swedish twins, familial factors explained the associations between early-life persistent internalizing and externalizing problems and unemployment; such factors were comparatively less important for the association with work disability. This suggests nonshared environmental factors may be important for the risk of future work disability among young individuals with persistent internalizing and externalizing problems.

Family-Related Life Events as Predictors of Labor Market Marginalization Trajectories: A Cohort Study of Swedish Twins.

The aims of the study are to investigate trajectories of labor market marginalization (LMM) and to examine the associations between family-related life events and LMM trajectories while accounting for familial factors. This is a prospective cohort study of 37,867 Swedish twins. Data were analyzed by group-based trajectory modeling. Associations of family-related life events with trajectory groups were estimated by multinomial logistic regression. Most participants had no or low levels of LMM. Individuals who stayed married over time or changed from single without children to married with children had a decreased risk of LMM. The risk of LMM over time was higher among individuals who changed from married to being single. Being or getting married as well as having children decreases the risk of LMM while divorce is a risk factor for LMM.

Etiology of the Broad Avoidant Restrictive Food Intake Disorder Phenotype in Swedish Twins Aged 6 to 12 Years

Avoidant restrictive food intake disorder (ARFID) is characterized by an extremely limited range and/or amount of food eaten, resulting in the persistent failure to meet nutritional and/or energy needs. Its etiology is poorly understood, and knowledge of genetic and environmental contributions to ARFID is needed to guide future research. To estimate the extent to which genetic and environmental factors contribute to the liability to the broad ARFID phenotype. This nationwide Swedish twin study includes 16 951 twin pairs born between 1992 and 2010 whose parents participated in the Child and Adolescent Twin Study in Sweden (CATSS) at twin age 9 or 12 years. CATSS was linked to the National Patient Register (NPR) and the Prescribed Drug Register (PDR). Data were collected from July 2004 to April 2020, and data were analyzed from October 2021 to October 2022. From CATSS, NPR, and PDR, all parent reports, diagnoses, procedures, and prescribed drugs that were relevant to the DSM-5 ARFID criteria were extracted when twin pairs were aged 6 to 12 years and integrated into a composite measure for the ARFID phenotype (ie, avoidant/restrictive eating with clinically significant impact, such as low weight or nutritional deficiency, and with fear of weight gain as an exclusion). In sensitivity analyses, autism and medical conditions that could account for the eating disturbance were controlled for. Univariate liability threshold models were fitted to estimate the relative contribution of genetic and environmental variation to the liability to the ARFID phenotype. Of 33 902 included children, 17 151 (50.6%) were male. A total of 682 children (2.0%) with the ARFID phenotype were identified. The heritability of ARFID was 0.79 (95% CI, 0.70-0.85), with significant contributions from nonshared environmental factors (0.21; 95% CI, 0.15-0.30). Heritability was very similar when excluding children with autism (0.77; 95% CI, 0.67-0.84) or medical illnesses that could account for the eating disturbance (0.79; 95% CI, 0.70-0.86). Prevalence and sex distribution of the broad ARFID phenotype were similar to previous studies, supporting the use of existing epidemiological data to identify children with ARFID. This study of the estimated genetic and environmental etiology of ARFID suggests that ARFID is highly heritable, encouraging future twin and molecular genetic studies.

Does lower educational attainment increase the risk of osteoarthritis surgery? a Swedish twin study

BackgroundPrevious studies have reported an inverse association between educational attainment and different osteoarthritis (OA) outcomes. However, none of the previous studies have accounted for potential confounding by early-life environment and genetics. Thus, we aimed to examine the association between educational attainment and knee and hip OA surgery using twin data.MethodsFrom the Swedish Twin Registry (STR), we identified dizygotic (DZ) and monozygotic (MZ) twins. All twins in the STR aged 35 to 64 years were followed from January the 1st 1987 or the date they turned 35 years until OA surgery, relocation outside Sweden, death or the end of 2016 (18,784 DZ and 8,657 MZ complete twin pairs). Associations between educational attainment and knee and hip OA surgery were estimated in models matched on twin pairs, using Weibull within-between (WB) shared frailty model.ResultsFor knee OA surgery, the analysis matched on MZ twins yielded a within-estimate hazard ratio (HR) per 3 years of education, of 1.06 (95% CI: 0.81, 1.32), suggesting no association between the outcome and the individual´s education. Rather, there seemed to be a so called familial effect of education, with a between-pair estimate of HR = 0.71 (95% CI: 0.41, 1.01). For hip OA surgery, the within- and between-pair estimates for MZ twins were 0.92 (95% CI: 0.69, 1.14) and 1.15 (95% CI: 0.87, 1.42), respectively.ConclusionsOur results suggest that the inverse associations between education and knee/hip OA surgery observed in cohort studies are potentially confounded by unobserved familial factors like genetics and/or early life exposures.

Chronic pain conditions and risk of suicidal behavior: a 10-year longitudinal co-twin control study

BackgroundUnderstanding the relationship between chronic pain conditions and suicidal behavior—suicide attempt, other intentional self-harm, and death by suicide—is imperative for suicide prevention efforts. Although chronic pain conditions are associated with suicidal behaviors, these associations might be attributed to unmeasured confounding or mediated via pain comorbidity.MethodsWe linked a population-based Swedish twin study (N=17,148 twins) with 10 years of longitudinal, nationwide records of suicidal behavior from health and mortality registers through 2016. To investigate whether pain comorbidity versus specific pain conditions were more important for later suicidal behavior, we modeled a general factor of pain and two independent specific pain factors (measuring pain-related somatic symptoms and neck-shoulder pain, respectively) based on 9 self-reported chronic pain conditions. To examine whether the pain-suicidal behavior associations were attributable to familial confounding, we applied a co-twin control model.ResultsIndividuals scoring one standard deviation above the mean on the general pain factor had a 51% higher risk of experiencing suicidal behavior (odds ratio (OR), 1.51; 95% confidence interval (CI), 1.34–1.72). The specific factor of somatic pain was also associated with increased risk for suicidal behavior (OR, 1.80; 95% CI, 1.45–2.22]). However, after adjustment for familial confounding, the associations were greatly attenuated and not statistically significant within monozygotic twin pairs (general pain factor OR, 0.89; 95% CI, 0.59–1.33; somatic pain factor OR, 1.02; 95% CI, 0.49–2.11)ConclusionClinicians might benefit from measuring not only specific types of pain, but also pain comorbidity; however, treating pain might not necessarily reduce future suicidal behavior, as the associations appeared attributable to familial confounding.

Gene-Environment Interactions in Attention-Deficit/Hyperactivity Disorder Symptom Dimensions: The Role of Unhealthy Food Habits.

Background: Dietary habits were investigated as environmental risk factors for Attention-Deficit/Hyperactivity Disorder (ADHD). However, no previous studies explored the effects of dietary factors on modifying the role of genetic factors on ADHD. Methods: Based on a Swedish population-based twin study with 1518 twin pairs aged 20–47 years, we tested whether the importance of genetic and environmental effects on ADHD varied as a function of dietary habits. Self-reported dietary habits and ADHD symptoms were collected. Twin methods were used to test the degree to which high-sugar and unhealthy food intake moderated the genetic and environmental influences on ADHD symptoms. Results: In middle-aged adults, genetic influences on inattention symptoms were statistically significantly higher among individuals with higher levels of high-sugar (45%, 95%CI: 25–54%) and unhealthy food intake (51%, 95%CI: 31–60%), compared with those with lower levels of consumption of high-sugar (36%, 95%CI: 25–47%) and unhealthy foods (30%, 95%CI: 20–41%). Similar patterns were also found for the associations between hyperactivity/impulsivity and high-sugar/unhealthy food intake, even though the moderation effects were not statistically significant. Conclusion The present study suggests that genetic factors play a more prominent role in individual differences of ADHD symptoms in the presence of the high consumption of sugar and unhealthy foods. Future longitudinal studies with multiple assessments of ADHD and dietary habits are needed to replicate our findings.

What Matters and What Matters Most for Survival After age 80? A Multidisciplinary Exploration Based on Twin Data.

Given research and public interest for conditions related to an extended lifespan, we addressed the questions of what matters and what matters most for subsequent survival past age 80. The data was drawn from the population-based and multidisciplinary Swedish OCTO Twin Study, in which a sample (N = 699) consisting of identical and same-sex fraternal twin pairs, followed from age 80 until death, provided detailed data on health, physical functioning, life style, personality, and sociodemographic conditions. Information concerning date of birth and death were obtained from population census register. We estimated heritability using an ACE model and evaluated the role of multiple predictors for the mortality-related hazard rate using Cox regression. Our findings confirmed a low heritability of 12%. As expected, longer survival was associated with being a female, an apolipoprotein E (APOE) e4 allele non-carrier, and a non-smoker. Several diseases were found to be associated with shorter survival (cerebrovascular, dementia, Parkinson’s, and diabetes) as well as certain health conditions (high diastolic blood pressure, low body mass index, and hip fracture). Stronger grip and better lung function, as well as better vision (but not hearing), and better cognitive function (self-evaluated and measured) was related to longer survival. Social embeddedness, better self-evaluated health, and life-satisfaction were also significantly associated with longer survival. After controlling for the impact of comorbidity, functional markers, and personality-related predictors, we found that sex, cerebrovascular diseases, compromised cognitive functioning, self-related health, and life-satisfaction remained as strong predictors. Cancer was only associated with the mortality hazard when accounting for other co-morbidities. The survival estimates were mostly in anticipated directions and contained effect sizes within the expected range. Noteworthy, we found that some of the so-called “soft-markers” remained strong predictors, despite a control for other factors. For example, self-evaluation of health and ratings of life-satisfaction provide additional and valuable information.

Preterm birth reduces the risk of IgE sensitization up to early adulthood: A population-based birth cohort study.

Immunoglobulin E (IgE) sensitization is associated with asthma and allergic diseases. Gestational age influences early immune system development, thereby potentially affecting the process of tolerance induction to allergens. To study IgE sensitization to common allergens by gestational age from childhood up to early adulthood. Population-based birth cohort, data from the Swedish BAMSE study were used. Allergen-specific IgE antibodies to a mix of common food (fx5) and inhalant (Phadiatop) allergens were analysed at 4, 8, 16 and 24years. Sensitization was defined as allergen-specific IgE ≥0.35kUA /L to fx5 and/or Phadiatop at each time point.Using logistic regression and generalized estimated equations, adjusted odds ratios (aORs) for sensitization in relation to gestational age were calculated. Replication was sought within the Swedish twin study STOPPA. In BAMSE, 3522 participants were screened for IgE antibodies during follow-up; of these, 197 (5.6%) were born preterm (<37gestational weeks) and 330 (9.4%) post-term (≥42weeks). Preterm birth reduced the risk of sensitization to common food and/or inhalant allergens up to early adulthood by 29% (overall aOR=0.71; 95% CI: 0.52-0.98), and to food allergens specifically by 40% (overall aOR=0.60; 95% CI: 0.38-0.93). No relation was found between post-term birth and IgE sensitization at any time point. Replication analyses in STOPPA (N=675) showed similar risk estimates for sensitization to food and/or inhalant allergens (aOR=0.72; 95% CI: 0.42-1.21), which resulted in a combined meta-analysis aOR=0.71 (95% CI: 0.54-0.94). Our study suggests an inverse association between preterm birth and long-term IgE sensitization.

The epigenetic etiology of cardiovascular disease in a longitudinal Swedish twin study

BackgroundStudies on DNA methylation have the potential to discover mechanisms of cardiovascular disease (CVD) risk. However, the role of DNA methylation in CVD etiology remains unclear.ResultsWe performed an epigenome-wide association study (EWAS) on CVD in a longitudinal sample of Swedish twins (535 individuals). We selected CpGs reaching the Bonferroni-corrected significance level (2 times 10–7) or the top-ranked 20 CpGs with the lowest P values if they did not reach this significance level in EWAS analysis associated with non-stroke CVD, overall stroke, and ischemic stroke, respectively. We further applied a bivariate autoregressive latent trajectory model with structured residuals (ALT-SR) to evaluate the cross-lagged effect between DNA methylation of these CpGs and cardiometabolic traits (blood lipids, blood pressure, and body mass index). Furthermore, mediation analysis was performed to evaluate whether the cross-lagged effects had causal impacts on CVD. In the EWAS models, none of the CpGs we selected reached the Bonferroni-corrected significance level. The ALT-SR model showed that DNA methylation levels were more likely to predict the subsequent level of cardiometabolic traits rather than the other way around (numbers of significant cross-lagged paths of methylation → trait/trait → methylation were 84/4, 45/6, 66/1 for the identified three CpG sets, respectively). Finally, we demonstrated significant indirect effects from DNA methylation on CVD mediated by cardiometabolic traits.ConclusionsWe present evidence for a directional association from DNA methylation on cardiometabolic traits and CVD, rather than the opposite, highlighting the role of epigenetics in CVD development.

Gestational diabetes mellitus and risks of gynecologic cancers: Results from a nationwide Swedish twin study

BackgroundType 2 diabetes has been associated with increased risk of gynecologic cancers, yet the effect of gestational diabetes mellitus (GDM) on gynecologic cancers is unclear. ObjectivesTo examine associations between GDM history and subsequent gynecologic cancers in parous women, and to explore whether gestational hypertension (GH) plays a role in the associations. Study designThe population-based cohort study included 15,941 individuals from the Swedish Twin Registry. The history of GDM and GH was ascertained based on self-reports. Incident cases of gynecologic cancers (including cancers of the cervix, uterus, ovaries and other female genitalia) were obtained from the National Patients Registry and the Swedish Cancer Registry. Generalized estimating equation models were applied to analyze associations between GDM and gynecologic cancers. Stratified analysis was used to explore whether associations between GDM and gynecologic cancers differed by GH. Additive and multiplicative interactions were calculated between GDM and GH. ResultsOf all participants, 350 (2.2%) had GDM, and 1762 (11.1%) had incident gynecologic cancers. No statistically significant associations were found between GDM and risks of any gynecologic cancers. However, GDM was associated with an increased risk of ovarian cancer (OR = 5.29, 95% CI: 1.63–17.19) in women with GH. Interactions between GDM and GH were observed on the additive scale (Attributable proportion due to interaction: 0.86, 95% CI 0.42–1.30, P < 0.001). ConclusionsThe associations between GDM and risks of gynecologic cancers were not evident, but the effect of GDM on the risk of ovarian cancer was modified by GH. Further validation in larger cohorts is warranted.

Gene-Environment Covariance as a Mechanism of Declines in Openness in Late Adulthood

We previously demonstrated that openness to experience declines with age and these declines correlate with mortality risk. We posited that decline in openness was related to change in behavior in relation to a change in future time perspective, defined here as dynamic changes in scope of time that influence persons’ behavior. This idea, based on Baltes’ selection, optimization, and compensation theory of lifespan development, suggests that with foreshortened time horizons individuals adapt their behavior leading to lesser engagement in novel experiences and relationships. The current study examined the genetically informed mechanisms underpinning the relationship between openness and mortality. Using identical and fraternal twins from the Swedish Adoption Twin Study of Aging (SATSA), we examined whether twins further from death nonrandomly select environments that maintain their openness scores while their co-twins nearer to death nonrandomly select environments that contribute to declines in openness. Using a sample of 822 twin pairs, we estimated a genetically-informed longitudinal model that quantified time-varying effects of twins’ openness scores at time t-1 on latent nonshared environmental scores at time t. The model generates within-family gene-environment correlation, a statistical coefficient that quantifies the genetic basis for nonrandom exposure to environments. Results suggest significant time-varying correlations between twins’ openness scores and their unique environments as well as increasing gene-environment correlation over time. Findings are consistent with the view that environments can support and reinforce maintenance of or declines in openness depending on the length of persons’ time horizons.

Mania symptoms in a Swedish longitudinal population study: The roles of childhood trauma and neurodevelopmental disorders

BackgroundAdult psychiatric disorders are associated with both childhood traumatic experiences (CTEs) and neurodevelopmental disorders (NDDs). CTEs and NDDs frequently co-occur in childhood, but their combined risk effect on the emergence of juvenile mania symptoms has not yet been examined. MethodsIn a population-representative Swedish twin study, CTEs and NDDs were assessed in 3,348 nine-year old twins born between 1998 and 2001, and treated as dichotomous predictors (any CTEs, any NDDs). Follow-up data were gathered at age 15 through parental reports of mania symptoms, yielding a symptom count score. ResultsBoth CTEs and NDDs at age 9 contributed uniquely to an increase in mania symptoms at age 15. Children with both risk factors had 1.6 times the rate of mania symptoms as children with CTEs-only (Incidence rate ratio [IRR] 1.63, 95% CI 1.37-1.93), and 1.3 times the rate of mania symptoms as children with NDDs-only (IRR 1.26, 95% CI 1.06-1.50). There was no evidence for an interactive effect of CTEs and NDDs. NDDs showed a trend towards having a larger effect on mania symptoms than CTEs (NDDs-only vs. CTEs-only: IRR 1.29, 95% CI 0.99-1.68). LimitationsAlthough it is a strength of the study that the data on exposures and outcome were collected prospectively, parental recall of CTEs was required and CTEs may be under-reported. ConclusionsNDDs are at least as important as CTEs in the development of mania symptoms, and their risk is additive. Those with a history of both CTEs and NDDs should be monitored closely for the development of more severe psychiatric presentations.

Do I lose cognitive function as fast as my twin partner? Analyses based on classes of MMSE trajectories of twins aged 80 and older.

Aging is associated with an increasing risk of decline in cognitive abilities. The decline is, however, not a homogeneous process. There are substantial differences across individuals although previous investigations have identified individuals with distinct cognitive trajectories. Evidence is accumulating that lifestyle contributes significantly to the classification of individuals into various clusters. How and whether genetically related individuals, like twins, change in a more similar manner is yet not fully understood. In this study, we fitted growth mixture models to Mini Mental State Exam (MMSE) scores from participants of the Swedish OCTO twin study of oldest-old monozygotic and same-sex dizygotic twins with the purpose of investigating whether twin pairs can be assigned to the same class of cognitive change. We identified four distinct groups (latent classes) whose MMSE trajectories followed different patterns of change over time: two classes of high performing individuals who remained stable and declined slowly, respectively, a group of mildly impaired individuals with a fast decline and a small group of impaired individuals who declined more rapidly. Notably, our analyses show no association between zygosity and class assignment. Our study provides evidence for a more substantial impact of environmental, rather than genetic, influences on cognitive change trajectories in later life.

Attention-deficit/hyperactivity disorder symptoms and dietary habits in adulthood: A large population-based twin study in Sweden.

Associations between adult attention‐deficit/hyperactivity disorder (ADHD) symptoms and dietary habits have not been well established and the underlying mechanisms remain unclear. We explored these associations using a Swedish population‐based twin study with 17,999 individuals aged 20–47 years. We estimated correlations between inattention and hyperactivity/impulsivity with dietary habits and fitted twin models to determine the genetic and environmental contributions. Dietary habits were defined as (a) consumption of food groups, (b) consumption of food items rich in particular macronutrients, and (c) healthy and unhealthy dietary patterns. At the phenotypic level, inattention was positively correlated with seafood, high‐fat, high‐sugar, high‐protein food consumptions, and unhealthy dietary pattern, with correlation coefficients ranging from 0.03 (95%CI: 0.01, 0.05) to 0.13 (95% CI: 0.11, 0.15). Inattention was negatively correlated with fruits, vegetables consumptions and healthy dietary pattern, with correlation coefficients ranging from −0.06 (95%CI: −0.08, −0.04) to −0.07 (95%CI: −0.09, −0.05). Hyperactivity/impulsivity and dietary habits showed similar but weaker patterns compared to inattention. All associations remained stable across age, sex and socioeconomic status. Nonshared environmental effects contributed substantially to the correlations of inattention (56–60%) and hyperactivity/impulsivity (63–80%) with dietary habits. The highest and lowest genetic correlations were between inattention and high‐sugar food (r A = .16, 95% CI: 0.07, 0.25), and between hyperactivity/impulsivity and unhealthy dietary pattern (r A = .05, 95% CI: −0.05, 0.14), respectively. We found phenotypic and etiological overlap between ADHD and dietary habits, although these associations were weak. Our findings contribute to a better understanding of common etiological pathways between ADHD symptoms and various dietary habits.

Gestational Diabetes Mellitus and Risk of Gynecologic Cancers: Results from a Nationwide Swedish Twin Study

Gestational Diabetes Mellitus and Risk of Gynecologic Cancers: Results from a Nationwide Swedish Twin Study

Low prevalence of risk drinking in adolescents and young adults with autism spectrum problems

Individuals with Autism Spectrum Disorder (ASD) have high rates of “comorbidity”. Research on concurrent substance use (disorder) in ASD, however, is scarce and findings have been inconsistent. This study aims at assessing the prevalence of risk drinking in adolescent and young adult twins with and without autism spectrum problems.Data from a Swedish longitudinal nationwide twin study were analyzed. Across three age groups of 15- (N = 10,050), 18- (N = 7,931) and 24-year-olds (N = 2,882) prevalence rates of risk drinking were compared between twins with and without an ASD proxy diagnosis and between different ASD subgroups based on comorbid proxies for attention-deficit/hyperactivity disorder (ADHD) and/or Learning Disorder (LD). ASD, ADHD, and LD were assessed using the Autism-Tics, ADHD, and other Comorbidities inventory (A-TAC), and risk drinking was captured by the Alcohol Use Disorders Identification Test (AUDIT; age 18 and 24) and another set of self-report questions (age 15).In each age group, the prevalence of risk drinking in ASD was lower than in individuals without ASD, yet increasing continuously with age. Exploratory subgroup ASD analyses showed a trend towards risk drinking being more common among individuals with co-existing ADHD or LD problems than among those without “comorbidity”, although sample sizes were too small to draw any certain conclusions.This study indicates low prevalence of risk drinking in adolescents and young adults with autism spectrum problems and highlights the need for further research on alcohol use in individuals with ASD and comorbid disorders.