Search

The relationship between pitch-naming ability and childhood onset of music training is well established and thought to reflect both genetic predisposition and music training during a critical period. However, the importance of the amount of practice during this period has not been investigated. In a population sample of twins (N = 1447, 39% male, 367 complete twin pairs) and a sample of 290 professional musicians (51% male), we investigated the role of genes, age of onset of playing music and accumulated childhood practice on pitch-naming ability. A significant correlation between pitch-naming scores for monozygotic (r = .27, p < .001) but not dizygotic twin pairs (r = −.04, p = .63) supported the role of genetic factors. In professional musicians, the amount of practice accumulated between ages 6 and 11 predicted pitch-naming accuracy (p = .025). In twins, age of onset was no longer a significant predictor once practice was considered. Combined, these findings are in line with the notion that pitch-naming ability is associated with both genetic factors and amount of early practice, rather than just age of onset per se. This may reflect a dose–response relation between practice and pitch-naming ability in genetically predisposed individuals. Alternatively, children who excel at pitch-naming may have an increased tendency to practice.

Data from the Interplay of Genes and Environment across Multiple Studies (IGEMS) consortium were used to examine predictions of different models of gene by environment interaction to understand how genetic variance in self-rated health (SRH) varies at different levels of financial strain. A total of 11,359 individuals from 10 twin studies in Australia, Sweden and the United States contributed relevant data, including 2074 monozygotic and 2623 dizygotic twin pairs. Age ranged from 22-98 years, with a mean age of 61.05 (sd = 13.24). A factor model was used to create a harmonized measure of financial strain across studies and items. Twin analysis of genetic and environmental variance for SRH incorporating age, age(2), sex, and financial strain moderators indicated significant financial strain moderation of genetic influences on self-rated health. Moderation results did not differ across sex or country. Genetic variance for SRH increased as financial strain increased, matching the predictions of the diathesis-stress and social comparison models for components of variance. Under these models, environmental improvements would be expected to reduce genetically based health disparities.

Experts in domains such as music or sports often start training early. It has been suggested that this may reflect a sensitive period in childhood for skill acquisition. However, it could be that familial factors (e.g., genetics) contribute to the association. Here, we examined the effect of age of onset of musical training on musical aptitude and achievement in professional musicians ( n = 310) and twins ( n = 7,786). In line with previous literature, results showed that an earlier age of onset was associated with higher aptitude and achievement in both samples. After we adjusted for lifetime practice hours, age of onset was associated only with aptitude ( p < .001; achievement: p > .14). Twin analyses showed that the association with aptitude was fully explained by familial factors. Thus, these findings provide little support for a sensitive period for music but highlight that familiar factors play an important role for associations between age of onset of training and skills in adulthood.

Background As common risk factors of dementia, nine factors (low education, hearing loss, obesity, hypertension, smoking, depression, physical inactivity, diabetes and social isolation) were proposed. However, the joint impact of these factors on incident dementia is still uncertain; hence, we aimed to examine this impact. Methods We conducted a cohort study of 9017 cognitively intact individuals aged ≥ 65 years in the Swedish Twin Registry. The main exposure was the total number of reported risk factors (ranging from 0 to 9). Data on dementia diagnoses were based on clinical workup and national health registers. After estimating the adjusted hazard ratios of incident dementia, the population attributable fraction (PAF) was calculated. We then conducted additional analyses, including APOE e4 status in a genotyped subsample (n = 2810) to check the relative impact of the main exposure and discordant twin pair (n = 1158) analysis to consider confounding by familial effects (shared genetic or familial environmental factors). Results The number of dementia cases was 1950 (21.6%). A dose-response relationship between the number of risk factors and incident dementia was observed; hazard ratio (95% confidence interval) per one-unit increment in number of risk factors was 1.07 (1.03 to 1.11). The PAF for the combination of the nine risk factors was 10.4%. The PAF of all nine risk factors was smaller than that of APOE e4 genotype (20.8%) in the subsample. Discordant pair analysis suggested that the observed association was not likely explained by familial effects. Conclusion The nine risk factors may have considerable impact as modifiable factors on incident dementia.

Focus and outcomes for participants Long periods between exposures and outcomes pose a number of challenges for life course epidemiological research, including unmeasured confounding factors (e.g.; familial factors) and mediation by other covariates, which make it difficult to unequivocally establish associations let alone causality. In this symposium we will present a number of different studies based on big data utilizing a variety of methods to overcome some of the issues encountered in research across long time frames or generations. Our focus will be on the different methods, the solutions they provide as well as their limitations. The methods presented were applied in the context of life course epidemiology and include: mediation analyses; genetic epidemiology; well-established and novel family designs including twins, siblings and cousins, and a method comparable to Mendelian randomization - ICE FALCON (Inference on Causation from Examination of Familial Confounding) which is part of a more general approach called ICE CRiSTAL (Inference on Causation from Examining Changes in Regression coefficients in STatistical AnaLsyes). The intended outcomes for the audience are to increase awareness of the challenges imposed by the data frequently used in this field of research and present possible solutions to (at least partly) address those. It is our intention to generate discussion and encourage other researchers to share their experiences and solutions to increase knowledge collectively. Rationale for the symposium, including for its inclusion in the Congress The main theme of the conference is ‘Methodological Innovations in Epidemiology’. Our symposium includes six different methods to strengthen causal inferences in epidemiology. While some of the presented methods are well established in classic epidemiology research (i.e. mediation analyses), others are more commonly found in different disciplines such as the expanding genetic epidemiology field (e.g. alternative twin designs and measured genetic risk approaches). In addition, we are presenting a new method for making inference about causation developed by Prof. John Hopper and Dr Shuai Li and co-workers called ICE FALCON, which applies to twin and family data and is part of a more general approach called ICE CRiSTAL. These methods use observational data to infer or rebut causality between measured variables, similar to Mendelian randomization (without relying on genetic information or strong assumptions). All the work presented is either nearing publication or has been published in the last two years and each presenter is intimately involved with the analysis and methods they will be presenting. Beyond a range of methods and study designs we have also a diversity of researchers and research questions in our symposium by including: researchers at different stages in their career and from around the world (ranging from early Postdoctoral Fellows over Senior Research Fellows/Assistant professors to Professors); a variety of research questions and diseases; and a range of population context including Indigenous Australians, babies, children, and adults, in order to appeal to a wider audience. Presentation program 6 talks of 8 minutes each with 2 minutes for questions followed by a general discussion facilitated by the chair. Names of presenters Dr Miriam A Mosing1,2

Musicians with absolute pitch (AP) can name the pitch of a musical note in isolation. Expression of this unusual ability is thought to be influenced by heritability, early music training and current practice. However, our understanding of factors shaping its expression is hampered by testing and scoring methods that treat AP as dichotomous. These fail to capture the observed variability in pitch-naming accuracy among reported AP possessors. The aim of this study was to trial a novel explicit priming paradigm to explore phenotypic variability of AP. Thirty-five musically experienced individuals (Mage = 29 years, range 18–68; 14 males) with varying AP ability completed a standard AP task and the explicit priming AP task. Results showed: 1) phenotypic variability of AP ability, including high-accuracy AP, heterogeneous intermediate performers, and chance-level performers; 2) intermediate performance profiles that were either reliant on or independent of relative pitch strategies, as identified by the priming task; and 3) the emergence of a bimodal distribution of AP performance when adopting scoring criteria that assign credit to semitone errors. These findings show the importance of methods in studying behavioural traits, and are a key step towards identifying AP phenotypes. Replication of our results in larger samples will further establish the usefulness of this priming paradigm in AP research.

Major depression (MD) is a complex, heterogeneous neuropsychiatric disorder. An early age at onset of major depression (AAO-MD) has been associated with more severe illness, psychosis, and suicidality. However, not much is known about what contributes to individual variation in this important clinical characteristic. This study sought to investigate the genetic components underlying AAO-MD. To investigate the genetics of AAO-MD, we conducted a genome-wide association meta-analysis of AAO-MD based on self-reported age of symptoms onset and self-reported age at first diagnosis from the UK Biobank cohort (total N = 94,154). We examined the genetic relationship between AAO-MD and five other psychiatric disorders. Polygenic risk scores were derived to examine their association with five psychiatric outcomes and AAO-MD in independent sub-samples. We found a small but significant SNP-heritability (~6%) for the AAO-MD phenotype. No SNP or gene reached SNP or gene-level significance. We found evidence that AAO-MD has genetic overlap with MD risk ($$r_g$$ r g = −0.49). Similarly, we found shared genetic risks between AAO-MD and autism-spectrum disorder, schizophrenia, bipolar disorder, and anorexia nervosa ($$r_g$$ r g range: −0.3 to −0.5). Polygenic risk scores for AAO-MD were associated with MD, schizophrenia, and bipolar disorder, and AAO-MD was in turn associated with polygenic risk scores derived from these disorders. Overall, our results indicate that AAO-MD is heritable, and there is an inverse genetic relationship between AAO-MD and both major depression and other psychiatric disorders, meaning that SNPs associated with earlier age at onset tend to increase the risk for psychiatric disorders. These findings suggest that the genetics of AAO-MD contribute to the shared genetic architecture observed between psychiatric disorders.

Musical aptitude and music training are associated with language-related cognitive outcomes, even when controlling for general intelligence. However, genetic and environmental influences on these associations have not been studied, and it remains unclear whether music training can causally increase verbal ability. In a sample of 1,336 male twins, we tested the associations between verbal ability measured at time of conscription at age 18 and two music-related variables: overall musical aptitude and total amount of music training before the age of 18. We estimated the amount of specific genetic and environmental influences on the association between verbal ability and musical aptitude, over and above the factors shared with general intelligence, using classical twin modeling. Further, we tested whether music training could causally influence verbal ability using a cotwin-control analysis. Musical aptitude and music training were significantly associated with verbal ability. Controlling for general intelligence only slightly attenuated the correlations. The partial association between musical aptitude and verbal ability, corrected for general intelligence, was mostly explained by shared genetic factors (50%) and nonshared environmental influences (35%). The cotwin-control-analysis gave no support for causal effects of early music training on verbal ability at age 18. Overall, our findings in a sizable population sample converge with known associations between the music and language domains, while results from twin modeling suggested that this reflected a shared underlying etiology rather than causal transfer.

Humans are social animals that experience intense suffering when they perceive a lack of social connection. Modern societies are experiencing an epidemic of loneliness. Although the experience of loneliness is universally human, some people report experiencing greater loneliness than others. Loneliness is more strongly associated with mortality than obesity, emphasizing the need to understand the nature of the relationship between loneliness and health. Although it is intuitive that circumstantial factors such as marital status and age influence loneliness, there is also compelling evidence of a genetic predisposition toward loneliness. To better understand the genetic architecture of loneliness and its relationship with associated outcomes, we extended the genome-wide association study meta-analysis of loneliness to 511 280 subjects, and detect 19 significant genetic variants from 16 loci, including four novel loci, as well as 58 significantly associated genes. We investigated the genetic overlap with a wide range of physical and mental health traits by computing genetic correlations and by building loneliness polygenic scores in an independent sample of 18 498 individuals with EHR data to conduct a PheWAS with. A genetic predisposition toward loneliness was associated with cardiovascular, psychiatric, and metabolic disorders and triglycerides and high-density lipoproteins. Mendelian randomization analyses showed evidence of a causal, increasing, the effect of both BMI and body fat on loneliness. Our results provide a framework for future studies of the genetic basis of loneliness and its relationship to mental and physical health.

ObjectiveNeuroticism is associated with poor health outcomes, but its contribution to the accumulation of health deficits in old age, i.e. frailty, is largely unknown. We aimed to explore associations between neuroticism and frailty cross-sectionally and over up to 29 years, and to investigate the contribution of shared genetic influences.MethodData were derived from the UK Biobank (UKB, n=502,631), the Australian Over 50’s Study (AO50, n=3,011) and the Swedish Twin Registry (SALT n=23,744, SATSA n=1,637). Associations between neuroticism and the Frailty Index were investigated using regression analysis cross-sectionally in UKB, AO50 and SATSA, and longitudinally in SALT (25-29y follow-up) and SATSA (6 and 23y follow-up). The co-twin control method was applied to explore the contribution of underlying shared familial factors (SALT, SATSA, AO50). Genome-wide polygenic risk scores for neuroticism in all samples were used to further assess whether common genetic variants associated with neuroticism predict frailty.ResultsHigh neuroticism was consistently associated with greater frailty cross-sectionally (adjusted β, 95% confidence intervals in UKB= 0.32, 0.32-0.33; AO50= 0.35, 0.31-0.39; SATSA= 0.33, 0.27-0.39) and longitudinally up to 29 years (SALT= 0.24; 0.22-0.25; SATSA 6y= 0.31, 0.24-0.38; SATSA 23y= 0.16, 0.07-0.25). When controlling for underlying shared genetic and environmental factors the neuroticism-frailty association remained significant, although decreased. Polygenic risk scores for neuroticism significantly predicted frailty in the two larger samples (meta-analyzed total β= 0.06, 0.05-0.06).ConclusionHigh neuroticism is associated with the development and course of frailty. Both environmental and genetic influences, including neuroticism-associated genetic variants, contribute to this relationship.

Music listening plays an important role in the daily lives of many. It remains unclear what explains variation in how much time people spend listening to music and whether music listening improves musical auditory discrimination skills. In 10,780 Swedish twin individuals, data were available on hours of music listening, musical engagement and musical auditory discrimination. Genetic and shared environmental factors together explain half of the variation in music listening in both sexes. Hours of music listening was positively associated with musical auditory discrimination in both sexes and this effect was independent of whether individuals played a musical instrument. However, the effect disappeared when applying a co-twin control analysis to control for genetic and shared environmental confounding. These findings suggest that music listening may not causally improve musical auditory discrimination skills, but rather that the association is likely due to shared familial factors.

Though several studies show that genetic factors influence individual differences in musical engagement, aptitude, and achievement, no study to date has investigated whether specialization among musically active individuals in terms of choice of instrument and genre is heritable. Using a large twin cohort, we explored whether individual differences in instrument choice, instrument category, and the type of music individuals engage in can entirely be explained by the environment or are partly due to genetic influences. About 10,000 Swedish twins answered an extensive questionnaire about music-related traits, including information on the instrument and genre they played. Of those, 1259 same-sex twin pairs reported to either play an instrument or sing. We calculated the odds ratios (ORs) for concordance in music choices (if both twins played) comparing identical and nonidentical twin pairs, with significant ORs indicating that identical twins are more likely to engage in the same type of music-related behavior than are nonidentical twins. The results showed that for almost all music-related variables, the odds were significantly higher for identical twins to play the same musical instrument or music genre, suggesting significant genetic influences on such music specialization. Possible interpretations and implications of the findings are discussed.

Moving in synchrony to the beat is a fundamental component of musicality. Here, we conducted a genome-wide association study (GWAS) to identify common genetic variants associated with beat synchronization in 606,825 individuals. Beat synchronization exhibited a highly polygenic architecture, with sixty-nine loci reaching genome-wide significance (p−8) and SNP-based heritability (on the liability scale) of 13%-16%. Heritability was enriched for genes expressed in brain tissues, and for fetal and adult brain-specific gene regulatory elements, underscoring the role of central nervous system-expressed genes linked to the genetic basis of the trait. We performed validations of the self-report phenotype (through internet-based experiments) and of the GWAS (polygenic scores for beat synchronization were associated with patients algorithmically classified as musicians in medical records of a separate biobank). Genetic correlations with breathing function, motor function, processing speed, and chronotype suggest shared genetic architecture with beat synchronization and provide avenues for new phenotypic and genetic explorations.

The association between active musical engagement (as leisure activity or professionally) and mental health is still unclear, with earlier studies reporting contrasting findings. Here we tested whether musical engagement predicts (1) a diagnosis of depression, anxiety, schizophrenia, bipolar or stress-related disorders based on nationwide patient registers or (2) self-reported depressive, burnout and schizotypal symptoms in 10,776 Swedish twins. Information was available on the years individuals played an instrument, including their start and stop date if applicable, and their level of achievement. Survival analyses were used to test the effect of musical engagement on the incidence of psychiatric disorders. Regression analyses were applied for self-reported psychiatric symptoms. Additionally, we conducted co-twin control analyses to further explore the association while controlling for genetic and shared environmental confounding. Results showed that overall individuals playing a musical instrument (independent of their musical achievement) may have a somewhat increased risk for mental health problems, though only significant for self-reported mental health measures. When controlling for familial liability associations diminished, suggesting that the association is likely not due to a causal negative effect of playing music, but rather to shared underlying environmental or genetic factors influencing both musicianship and mental health problems.

Both genes and the environment are important for individual differences in expertise, but little is known about gene-environment interactions underlying domain-specific achievement. Here we explored this issue in a large Swedish twin cohort (N = 6,610), using moderator modeling with musical expertise as a model domain. Specifically, we tested whether musical enrichment of the childhood environment moderates adult musical achievement, as well as the magnitude of genetic and nongenetic influences on individual differences in achievement. Musical achievement was measured using the Creative Achievement Questionnaire and enrichment of the childhood environment was indexed with a principal component derived from the number of music records in the family home, number of individuals in the family environment playing an instrument, frequency of concert visits, and music education before the age of 12. As expected, we found a positive association between childhood musical enrichment and musical achievement in adulthood. Interestingly, however, the total variance in musical achievement as well as the relative importance of genetic influences increased with a higher level of musical enrichment. Estimates of genetic and environmental influences as well as the magnitude of the environmental moderation differed for men and women. These findings suggest that, in line with recent multifactorial models of expert performance, a musically enriched childhood environment amplifies individual differences, an effect which is largely driven by an increase in the importance of genetic factors. (PsycINFO Database Record (c) 2019 APA, all rights reserved).

Background Being adopted early in life, an indicator of exposure to early-life adversity, has been consistently associated with poor mental health outcomes in adulthood. Such associations have largely been attributed to stressful environments, e.g., exposure to trauma, abuse, or neglect. However, mental health is substantially heritable, and genetic influences may contribute to the exposure to childhood adversity, resulting in potential genetic confounding of such associations. Methods Here, we explored associations between childhood adoption and mental health–related outcomes in midlife in 243,797 UK Biobank participants (n adopted = 3151). We used linkage disequilibrium score regression and polygenic risk scores for depressive symptoms, schizophrenia, neuroticism, and subjective well-being to address potential genetic confounding (gene-environment correlations) and gene-environment interactions. As outcomes, we explored depressive symptoms, bipolar disorder, neuroticism, loneliness, and mental health–related socioeconomic and psychosocial measures in adoptees compared with nonadopted participants. Results Adoptees were slightly worse off on almost all mental, socioeconomic, and psychosocial measures. Each standard deviation increase in polygenic risk for depressive symptoms, schizophrenia, and neuroticism was associated with 6%, 5%, and 6% increase in the odds of being adopted, respectively. Significant genetic correlations between adoption status and depressive symptoms, major depression, and schizophrenia were observed. No evidence for gene-environment interaction between genetic risk and adoption on mental health was found. Conclusions The association between childhood adoption and mental health cannot fully be attributed to stressful environments but is partly explained by differences in genetic risk between adoptees and those who have not been adopted (i.e., gene-environment correlation).

This chapter summarizes key findings from the literature on neuroanatomical and functional correlates of expertise, concluding that expertise is related to macroanatomical properties of domain-relevant brain regions and ultrastructural properties of both the gray and the white matter. The consequence of these neural adaptations is a capacity for vastly more efficient performance of domain-specific tasks. In functional terms, this depends on multiple mechanisms that are situated at different levels of neural processing. These mechanisms include automation and alterations in functional connectivity, as well as specializations within memory systems and sensorimotor systems that optimize the processing of information that is relevant for the particular domain of expertise. Finally, the chapter discusses the neural mechanisms of expertise from the perspective of new models that emphasize a multifactorial perspective and take into account both genetic and environmental influences on expertise and its acquisition.

The Interplay of Genes and Environment across Multiple Studies (IGEMS) is a consortium of 18 twin studies from 5 different countries (Sweden, Denmark, Finland, United States, and Australia) established to explore the nature of gene–environment (GE) interplay in functioning across the adult lifespan. Fifteen of the studies are longitudinal, with follow-up as long as 59 years after baseline. The combined data from over 76,000 participants aged 14–103 at intake (including over 10,000 monozygotic and over 17,000 dizygotic twin pairs) support two primary research emphases: (1) investigation of models of GE interplay of early life adversity, and social factors at micro and macro environmental levels and with diverse outcomes, including mortality, physical functioning and psychological functioning; and (2) improved understanding of risk and protective factors for dementia by incorporating unmeasured and measured genetic factors with a wide range of exposures measured in young adulthood, midlife and later life.

Item does not contain fulltext Psychometric intelligence correlates with performance on a wide range of sensory and motor tasks that involve processing of temporal information in the millisecond-second range. For some timing tasks, e.g. reaction time and discrimination of temporal stimuli in working memory, the associations with intelligence are likely to involve top-down mechanisms such as attention. However, studies on repetitive, automatic motor timing tasks indicate that correlations between intelligence and timing also may reflect bottom-up mechanisms, i.e. basic neural properties that influence both the temporal accuracy of behavior and cognitive processes. Here, we study the genetic architecture of the associations between intelligence, perceptual timing (auditory rhythm discrimination) and motor timing (finger tapping) in a large twin cohort. Specifically, we hypothesized that the associations between these tasks on the phenotypic level involve broad pleiotropic genetic effects that influence all three tasks, as well as additional genetic effects on the covariation between perceptual and motor timing. Phenotypic associations between the variables were low to moderate, with Pearson's correlations in the range 0.17-0.32. Trivariate twin modeling showed that the associations between the three variables were essentially due to shared genetic influences. In support of the hypotheses, we found evidence for pleiotropic effects on motor timing, perceptual timing, and intelligence, as well as additional genetic covariation between the two timing tasks that was not shared with intelligence. We conclude, first, that genetic factors underlying intelligence may involve genes which influence brain properties of importance for the temporal accuracy of neural processing. We discuss possible neural substrates of such effects. Secondly, the correlation between motor and perceptual timing also partly explained by genetic influences that are unrelated to intelligence. 8 p.

Approximately half of the variation in wellbeing measures overlaps with variation in personality traits. Studies of non-human primate pedigrees and human twins suggest that this is due to common genetic influences. We tested whether personality polygenic scores for the NEO Five-Factor Inventory (NEO-FFI) domains and for item response theory (IRT) derived extraversion and neuroticism scores predict variance in wellbeing measures. Polygenic scores were based on published genome-wide association (GWA) results in over 17,000 individuals for the NEO-FFI and in over 63,000 for the IRT extraversion and neuroticism traits. The NEO-FFI polygenic scores were used to predict life satisfaction in 7 cohorts, positive affect in 12 cohorts, and general wellbeing in 1 cohort (maximalN= 46,508). Meta-analysis of these results showed no significant association between NEO-FFI personality polygenic scores and the wellbeing measures. IRT extraversion and neuroticism polygenic scores were used to predict life satisfaction and positive affect in almost 37,000 individuals from UK Biobank. Significant positive associations (effect sizes

Humans are social animals that experience intense suffering when they perceive a lack of social connection. Modern societies are experiencing an epidemic of loneliness. While the experience of loneliness is universally human, some people report experiencing greater loneliness than others. Loneliness is more strongly associated with mortality than obesity, emphasizing the need to understand the nature of the relationship between loneliness and health. While it is intuitive that circumstantial factors such as marital status and age influence loneliness, there is also compelling evidence of a genetic predisposition towards loneliness. To better understand the genetic architecture of loneliness and its relationship with associated outcomes, we conducted a genome-wide association (GWAS) meta-analysis of loneliness (N=475,661), report 12 associated loci (two novel) and significant genetic correlations with 34 other complex traits. The polygenic basis for loneliness was significantly enriched for evolutionary constrained genes and genes expressed in specific brain tissues: (frontal) cortex, cerebellum, anterior cingulate cortex, and substantia nigra. We built polygenic scores based on this GWAS meta-analysis to explore the genetic association between loneliness and health outcomes in an independent sample of 18,498 individuals for whom electronic health records were available. A genetic predisposition towards loneliness predicted cardiovascular, psychiatric, and metabolic disorders, and triglycerides and high-density lipoproteins. Mendelian randomization analyses showed evidence of a causal, increasing, effect of body fat on loneliness, and a similar weaker causal effect of BMI. Our results provide a framework for ongoing studies of the genetic basis of loneliness and its role in mental and physical health.

Background There is evidence for long-lasting effects of birth characteristics on cognitive ability in childhood and adulthood. Further, low cognitive ability throughout the lifetime has been linked to age-related cognitive decline and dementia risk. However, little is known about the effects of birth characteristics on cognitive dysfunction late in life. Here we explore potential associations between birth characteristics (weight, head circumference, length, and gestational age), adjusted and not adjusted for gestational age, and cognitive impairment and dementia late in life. Methods and findings Data from twins in the Swedish Twin Registry born 1926–1960 were merged with information from the Swedish birth, patient, and cause of death registries, resulting in a sample of 35,191 individuals. A subsample of 4,000 twins aged 65 years and older also participated in a telephone cognitive screening in 1998–2002. Associations of birth characteristics with registry-based dementia diagnoses and on telephone-assessed cognitive impairment were investigated in the full sample and subsample, respectively. The full sample contained 907 (2.6%) individuals with a dementia diagnosis (an incidence rate of 5.9% per 100,000 person-years), 803 (2.4%) individuals born small for gestational age, and 929 (2.8%) individuals born with a small head for gestational age. The subsample contained 569 (14.2%) individuals with cognitive impairment. Low birth weight for gestational age and being born with a small head for gestational age were significant risk factors for cognitive dysfunction late in life, with an up to 2-fold risk increase (p < 0.001) compared to infants with normal growth and head size, even after controlling for familial factors, childhood socioeconomic status, and education in adulthood. In line with this, each additional 100 g birth weight and each additional millimeter head circumference significantly reduced the risk for dementia (hazard ratio 0.98, 95% confidence interval 0.97 to 0.99, p = 0.004) and cognitive impairment (odds ratio 0.99, 95% confidence interval 0.99 to 1.00, p = 0.004), respectively. Within-pair analyses of identical twins, though hampered by small sample size, suggested that the observed associations between birth characteristics and dementia are likely not due to underlying shared genetic or environmental etiology. A limitation of the present study is that registry-based dementia diagnoses likely miss some of the true dementia cases in the population. Further, a more precise measure of cognitive reserve early in life as well as a date of onset for the cognitive impairment measure in the subsample would have been favorable. Conclusions In this study, we found that infants of smaller birth size (i.e., low birth weight or small head circumference adjusted and unadjusted for gestational age) have a significantly higher risk of age-related cognitive dysfunction compared to those with normal growth, highlighting the importance of closely monitoring the cognitive development of such infants and evaluating the potential of early life interventions targeted at enhancing cognitive reserve., Using data from the Swedish Birth Registry, Miriam Mosing and colleagues investigate associations between healthy prenatal growth and cognitive dysfunction in late-life., Author summary Why was this study done? There is evidence for associations between birth characteristics and cognitive ability in childhood and adulthood. Low cognitive ability throughout the lifetime has been linked to age-related cognitive decline and dementia risk. Little is known about associations between birth characteristics and cognitive dysfunction late in life, such as dementia and cognitive impairment. What did the researchers do and find? We conducted a registry-based cohort study of 35,191 individuals linking data from the Swedish birth registry to the Swedish patient, cause of death, and twin registries to explore potential associations between birth characteristics and age-related cognitive dysfunction as measured by all-cause dementia and cognitive impairment. Low birth weight and small head circumference pose a significant risk for late life cognitive dysfunction. What do these findings mean? The findings highlight the importance of healthy prenatal growth and closely monitoring the cognitive development of small infants and those with signs of poor fetal growth. Potential interventions to increase cognitive reserve could be considered for infants with low birth weight and small head circumference.

Background Genetic research on depression and burnout has focused mostly on adverse factors, although various aspects in daily life related to positive coping and well-being have been shown to potentially be protective. Using a large genetically informative sample, we aim to explore the potential relationship between flow proneness and work-related depressive symptoms and burnout. Methods About 10,000 Swedish twins filled in the Swedish Flow Proneness Questionnaire, a subscale of the Hopkins Symptom Checklist (SCL) depression scale, and the Emotional Exhaustion subscale of the Maslach Burnout Inventory-General Survey. A higher score indicated more flow, less emotional exhaustion and less depression. The classical twin design and co-twin control analyses were applied. Results Phenotypic correlations were .43 between depressive symptoms and flow proneness, .34 between burnout and flow proneness, and .62 between depressive symptoms and burnout. Broad-sense heritabilities (G) ranged between 33–35% for the three variables. Associations between the variables were due to significant genetic as well as non-shared environmental influences. Co-twin control analyses showed that associations remained significant when controlling for all genetic and shared familial factors, in line with a causal relationship. Limitations Although the co-twin control design can test for consistency of associations with a causal relationship, it cannot unequivocally establish causality. Conclusions Genetic liability has a substantial influence on associations between flow proneness and emotional problems at work (depression, burnout). However, the presence of significant environmental correlations is in line with a (partly) causal relationship between flow and work related depression and burnout, which in turn may suggest that interventions which increase flow could potentially reduce emotional problems at work.

The idea of far transfer effects in the cognitive sciences has received much attention in recent years. One domain where far transfer effects have frequently been reported is music education, with the prevailing idea that music practice entails an increase in cognitive ability (IQ). While cross-sectional studies consistently find significant associations between music practice and IQ, randomized controlled trials, however, report mixed results. An alternative to the hypothesis of cognitive transfer effects is that some underlying factors, such as shared genes, influence practice behaviour and IQ causing associations on the phenotypic level. Here we explored the hypothesis of far transfer within the framework of music practice. A co-twin control design combined with classical twin-modelling based on a sample of more than 10,500 twins was used to explore causal associations between music practice and IQ as well as underlying genetic and environmental influences. As expected, phenotypic associations were moderate (r = 0.11 and r = 0.10 for males and females, respectively). However, the relationship disappeared when controlling for genetic and shared environmental influences using the co-twin control method, indicating that a highly practiced twin did not have higher IQ than the untrained co-twin. In line with that finding, the relationship between practice and IQ was mostly due to shared genetic influences. Findings strongly suggest that associations between music practice and IQ in the general population are non-causal in nature. The implications of the present findings for research on plasticity, modularity, and transfer are discussed.

Music performance depends critically on precise processing of time. A common model behavior in studies of motor timing is isochronous serial interval production (ISIP), that is, hand/finger movements with a regular beat. ISIP accuracy is related to both music practice and intelligence. Here we present a study of these associations in a large twin cohort, demonstrating that the effects of music practice and intelligence on motor timing are additive, with no significant multiplicative (interaction) effect. Furthermore, the association between music practice and motor timing was analyzed with the use of a co-twin control design using intrapair differences. These analyses revealed that the phenotypic association disappeared when all genetic and common environmental factors were controlled. This suggests that the observed association may not reflect a causal effect of music practice on ISIP performance but rather reflect common influences (e.g., genetic effects) on both outcomes. The relevance of these findings for models of practice and expert performance is discussed.

Though several studies show that genetic factors influence individual differences in musical engagement, aptitude, and achievement, no study to date has investigated whether specialization among musically active individuals in terms of choice of instrument and genre is heritable. Using a large twin cohort, we explored whether individual differences in instrument choice, instrument category, and the type of music individuals engage in can entirely be explained by the environment or are partly due to genetic influences. About 10,000 Swedish twins answered an extensive questionnaire about music-related traits, including information on the instrument and genre they played. Of those, 1259 same-sex twin pairs reported to either play an instrument or sing. We calculated the odds ratios (ORs) for concordance in music choices (if both twins played) comparing identical and nonidentical twin pairs, with significant ORs indicating that identical twins are more likely to engage in the same type of music-related behavior than are nonidentical twins. The results showed that for almost all music-related variables, the odds were significantly higher for identical twins to play the same musical instrument or music genre, suggesting significant genetic influences on such music specialization. Possible interpretations and implications of the findings are discussed.

This chapter describes how the heritability of a trait can be estimated using data collected from pairs of twins. The principles of the classical twin design are described, followed by the assumptions, and some possible extensions of the design. In the second part of this chapter, two example scripts are presented and the basic steps for estimating heritability using the statistical program OpenMx are explained. OpenMx and the scripts used for this chapter can be downloaded so that readers can adapt and use the scripts for their own purposes.

This chapter proposes one model: The Multifactorial Gene-Environment Interaction model (the MGIM). In line with ample empirical evidence, the MGIM assumes that deliberate practice is an important predictor of expert performance, and that a main reason for this association, although not the only one, is causal effects of deliberate practice on expert performance. Long-term deliberate practice may lead to extensive anatomical and functional reorganizations of brain circuits that control performance. These plastic processes involve different brain systems and can include more efficient interactions between long-term memory and working memory (LTM-WM) and improved domain-specific sensorimotor skills. The MGIM can readily be seen to suggest a number of possible directions for future empirical research, where it and deliberate practice theory give rise to differing predictions. The MGIM represents an attempt to synthesize recent findings into a domain-general model for expert performance that takes into account both the multifactorial influences on expertise at the phenotypic level and the influence of genetic factors.

This chapter describes how the heritability of a trait can be estimated using data collected from pairs of twins. The principles of the classical twin design are described, followed by the assumptions, and some possible extensions of the design. In the second part of this chapter, two example scripts are presented and the basic steps for estimating heritability using the statistical program OpenMx are explained. OpenMx and the scripts used for this chapter can be downloaded so that readers can adapt and use the scripts for their own purposes.

We examine, in 6881 twin individuals, the psychometric properties of a new test (the Swedish Musical Discrimination Test, SMDT) that was developed to tap auditory discrimination of musical stimuli. The SMDT consists of three subtests measuring discrimination of melodies, rhythms, and single pitches, respectively. Mean test taking times for the subtests were 3.0–4.6min. Reliability and internal consistency were good with Cronbach’s alpha values and Spearman–Brown split-half reliabilities between .79 and .89. Subtests correlated positively (r values .27–.41). Criterion validity was demonstrated in three ways: individuals that had played a musical instrument scored higher than individuals that had not (Cohen’s d .38–.63); individuals that had taken music lessons scored higher than individuals that had not (Cohen’s d .35–.60); finally, total hours of musical training and SMDT scores correlated (r values .14–.28) among those participants that had played an instrument. Lastly, twin modelling revealed moderate heritability estimates for the three sub-scales. We conclude that the SMDT has good psychometric characteristics, short test taking time, and may serve as a useful complement to existing tests of musical ability.

Although music is a universal feature of human culture, little is known about its origins and functions. A prominent theory of music evolution is the sexual selection hypothesis, which proposes that music evolved as a signal of genetic quality to potential mates. The sexual selection hypothesis offers several empirically testable predictions. First, musically skilled and active individuals should have greater mating success than less-skilled individuals. Second, if musical ability functions as an indicator of genetic quality, it is expected to be associated with other traits putatively related to genetic quality. Third, associations as per the first and second predictions are expected to be at least partly due to overlapping genetic influences. We tested these predictions in a large genetically informative sample of 10,975 Swedish twin individuals aged between 27 and 54. years (M=. 40.1, SD. =. 7.7), using musical aptitude and music achievement as measures of musical ability. To assess mating success we examined number of sex-partners, age of first intercourse, sociosexuality, and number of offspring. General intelligence, simple reaction time, and height were used to investigate relationships with traits putatively related to genetic quality. Twin modeling showed moderate genetic influences on musical aptitude for both sexes (heritability estimates were 38% for males and 51% for females). Music achievement was also moderately influenced by genetic influences in males (heritability. =. 57%), but the genetic influences were low and nonsignificant for females (heritability. =. 9%). Contrary to predictions, the majority of phenotypic associations between musical ability and music achievement with mating success were nonsignificant or significant in the other direction, with those with greater musical ability scoring lower on the measures of mating success. Genetic correlations between these measures were also nonsignificant. Most correlations of musical aptitude and music achievement with genetic quality measures were significant, including correlations with general intelligence, simple reaction time, and, in females, height (but only for aptitude). However, only the correlation between musical aptitude and general intelligence in men was significantly driven by overlapping genetic influences. Our findings provide little support for a role of sexual selection in the evolution of musical ability. Alternative explanations and limitations are discussed.

We conducted genome-wide association studies of three phenotypes: subjective well-being (N = 298,420), depressive symptoms (N = 161,460), and neuroticism (N = 170,910). We identified three variants associated with subjective well-being, two with depressive symptoms, and eleven with neuroticism, including two inversion polymorphisms. The two depressive symptoms loci replicate in an independent depression sample. Joint analyses that exploit the high genetic correlations between the phenotypes (|ρ̂| ≈ 0.8) strengthen the overall credibility of the findings, and allow us to identify additional variants. Across our phenotypes, loci regulating expression in central nervous system and adrenal/pancreas tissues are strongly enriched for association.

The literature shows evidence for long-lasting effects of low birth weight (LBW) on many health outcomes, but little is known about effects on self-perceived health. Findings are mixed and studies are small, mostly focusing on LBW effects on health outcomes before adulthood. Further, as LBW and most health conditions including self-perceived health are partly heritable, associations between birth weight (BW) and adverse health outcomes may also be due to shared genetic as well as other (pre- and postnatal) unmeasured environmental influences. We explored LBW effects on self-perceived health in early and later adulthood using a very large and genetically informative sample of more than 50,000 Swedish twins. In addition, analyses within twin pairs (the co-twin control design) were used to examine potential associations between BW and the offspring's risk for poor self-perceived health independent of shared environmental or genetic factors, evidence which is critical for the understanding of underlying mechanisms. Results showed that lower BW was significantly associated with poorer self-perceived health during adulthood, although the effect size was small. Co-twin control analyses suggested that this increased risk may be due to shared underlying liability (environmental or genetic) rather than a direct effect of BW, but findings were not conclusive.

Why are some people so much more successful than other people in music, sports, games, business, and other complex domains? This question is the subject of one of psychology's oldest debates. Over 20 years ago, Ericsson, Krampe, and Tesch-Romer (1993) proposed that individual differences in performance in domains such as these largely reflect accumulated amount of “deliberate practice.” More controversially, making exceptions only for height and body size, Ericsson et al. explicitly rejected any direct role for innate factors (“talent”) in the attainment of expert performance. This view has since become the dominant theoretical account of expertise and has filtered into the popular imagination through books such as Malcolm Gladwell's (2008) Outliers. Nevertheless, as we discuss in this chapter, evidence from recent research converges on the conclusion that this view is not defensible. Recent meta-analyses have demonstrated that although deliberate practice accounts for a sizeable proportion of the variance in performance in complex domains, it consistently leaves an even larger proportion of the variance unexplained and potentially explainable by other factors. In light of this evidence, we offer a “new look” at expertise that takes into account a wide range of factors.