General Genetic Factor Research Articles

The latent structure of emerging cognitive abilities: An infant twin study

It is well known that genetic factors account for up to 70% of variability in cognition from childhood to adulthood. However, less is known about the first year of life. This study investigated the etiological factors influencing individual variability in different domains of emerging cognitive and motor abilities in early infancy, and to what extent genetic and environmental influences are unique or shared across different domains. We compared multivariate twin models built on scores from the five scales of the Mullen Scales of Early Learning (MSEL) in a community sample of monozygotic and dizygotic twins at 5 months of age (n=567). The results indicated a hierarchical etiological structure whereby a general genetic latent factor accounted for 54% of variance underlying the different domains of emerging cognitive and motor abilities (A=0.54, confidence interval CI=[0; 0.82]). We also found additional genetic influences that were specific to early motor and language development. Unlike previous findings on older children, we did not find significant influences of shared environment on the shared factor (C=0, CI=[0, 0.57]), or any specific scale. Furthermore, influences of unique environment, which include measurement error, were moderate and statistically significant (E=0.46, CI=0.18; 0.81]). This study provides strong evidence for a unitary hierarchical structure across different domains of emerging cognition. Evidence that a single common etiological factor, which we term infant g, contributes to a range of different abilities supports the view that in young infants, intrinsic and general neurodevelopmental processes are key drivers of observable behavioural differences in specific domains.

Association of polygenic risk scores and hair cortisol with mental health trajectories during COVID lockdown

The COVID-19 pandemic is a global stressor with inter-individually differing influences on mental health trajectories. Polygenic Risk Scores (PRSs) for psychiatric phenotypes are associated with individual mental health predispositions. Elevated hair cortisol concentrations (HCC) and high PRSs are related to negative mental health outcomes. We analyzed whether PRSs and HCC are related to different mental health trajectories during the first COVID lockdown in Germany. Among 523 participants selected from the longitudinal resilience assessment study (LORA), we previously reported three subgroups (acute dysfunction, delayed dysfunction, resilient) based on weekly mental health (GHQ-28) assessment during COVID lockdown. DNA from blood was collected at the baseline of the original LORA study (n = 364) and used to calculate the PRSs of 12 different psychopathological phenotypes. An explorative bifactor model with Schmid-Leiman transformation was calculated to extract a general genetic factor for psychiatric disorders. Hair samples were collected quarterly prior to the pandemic for determining HCC (n = 192). Bivariate logistic regressions were performed to test the associations of HCC and the PRS factors with the reported trajectories. The bifactor model revealed 1 general factor and 4 sub-factors. Results indicate a significant association between increased values on the general risk factor and the allocation to the acute dysfunction class. The same was found for elevated HCC and the exploratorily tested sub-factor “childhood-onset neurodevelopmental disorders”. Genetic risk and long-term cortisol secretion as a potential indicator of stress, indicated by PRSs and HCC, respectively, predicted different mental health trajectories. Results indicate a potential for future studies on risk prediction.

Latent, genetic, and molecular genetic structure of the Wisconsin Card Sorting Test.

The main goal of this study was to explore the latent structure and genetic basis of cognitive processes involved in the Wisconsin Card Sorting Task (WCST) within phenotypic, behavioral genetic, and molecular genetic research paradigms. The sample used in phenotypic and behavioral genetic analyses comprised 468 twins (154 monozygotic and 80 dizygotic twin pairs), while molecular genetic analyses were performed on 404 twins from the same sample. The zygosity of most twin pairs (96.8%) was determined via deoxyribonucleic acid (DNA) analysis of buccal swabs. Trained researchers administered the Wisconsin Card Sorting Test (WCST; Heaton et al., 1993) to the entire sample. A phenotypic factor analysis of WCST variables suggested a single-factor solution. Overall heritability ranged from 0.19 to 0.23 across different measures of the WCST. The presence of a single general genetic factor, which could be identified from different measures of the WCST, indicated the unity of various WCST indicators and the existence of a common basic ability. Performance on the WCST did not reveal significant differences between the three genotypes on catechol-O-methyltransferase (COMT) and dopamine receptor D2 (DRD2). Carriers of the brain-derived neurotrophic factor (BDNF) Met + genotype exhibited better performance in cognitive functions in comparison to the BDNF Met- genotype. This study highlighted similarities in the phenotypic and genetic structures of the WCST, suggesting one general factor underlying different cognitive functions. The BDNF Met + genotype showed significant main effects on different WCST measures. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

Novel variants in helicase for meiosis 1 lead to male infertility due to non-obstructive azoospermia

BackgroundNon-obstructive azoospermia (NOA) is the most severe form of male infertility; more than half of the NOA patients are idiopathic. Although many NOA risk genes have been detected, the genetic factors for NOA in majority of the patients are unknown. In addition, it is difficult to retrieve sperm from these patients despite using the microsurgical testicular sperm extraction (microTESE) method. Therefore, we conducted this genetic study to identify the potential genetic factors responsible for NOA and investigate the sperm retrieval rate of microTESE for genetically deficient NOA patients.MethodsSemen analyses, sex hormone testing, and testicular biopsy were performed to categorize the patients with NOA. The chromosome karyotypes and Y chromosome microdeletion analyses were used to exclude general genetic factors. Whole exome sequencing and Sanger sequencing were performed to identify potential genetic variants in 51 patients with NOA. Hematoxylin and eosin staining (H&E) and anti-phosphorylated H2AX were used to assess the histopathology of spermatogenesis. Quantitative real time-polymerase chain reaction, western blotting, and immunofluorescence were performed to verify the effects of gene variation on expression.ResultsWe performed whole exome sequencing in 51 NOA patients and identified homozygous helicase for meiosis 1(HFM1) variants (NM_001017975: c.3490C > T: p.Q1164X; c.3470G > A: p.C1157Y) in two patients (3.9%, 2/51). Histopathology of the testis showed that spermatogenesis was completely blocked at metaphase in these two patients carrying the HFM1 homozygous variants. In comparison with unaffected controls, we found a significant reduction in the levels of HFM1 mRNA and protein expression in the testicular tissues from these two patients. The patients were also subjected to microTESE treatment, but the sperms could not be retrieved.ConclusionsThis study identified novel homozygous variants of HFM1 that are responsible for spermatogenic failure and NOA, and microTESE did not aid in retrieving sperms from these patients.

Executive functions and intelligence- are there genetic difference?

The first aim of this study was to explore the aetiology of phenotypic relationships between different measures of executive functions. The second objective was to examine sources of the covariation between different measures of executive functions and the measure of general cognitive ability. The study sample consisted of 468 twins (154 pairs of monozygotic twins and 80 pairs of dizygotic twins) of the same and different gender who grew up together. Executive functions were evaluated by the Wisconsin Card Sorting Test, the Trail Making Test – form B, and verbal fluency tests. Raven's Advanced Progressive Matrices were used as a measure of general cognitive ability. The study results suggest a primarily genetic origin of the mutual covariation of different executive measures and their covariation with the general cognitive ability construct. While the shared genetic variance primarily lies in the bases of similarity/unity of the used cognitive measures, their particularity/difference is determined by a specific unshared environment. The obtained result on the presence of a single general genetic factor, which can be singled out in the case of different executive measures, at least partially speaks in favor of the thesis about the unity of various executive measures and the existence of a common basic ability. Together with the specific unshared environment, the specific genetic influence speaks in favor of a difference between each of the individual measures.

Associations Between Attention-Deficit/Hyperactivity Disorder and Various Eating Disorders: A Swedish Nationwide Population Study Using Multiple Genetically Informative Approaches

BackgroundAlthough attention-deficit/hyperactivity disorder (ADHD) and eating disorders (EDs) frequently co-occur, little is known about the shared etiology. In this study, we comprehensively investigated the genetic association between ADHD and various EDs, including anorexia nervosa (AN) and other EDs such as bulimia nervosa. MethodsWe applied different genetically informative designs to register-based information of a Swedish nationwide population (N = 3,550,118). We first examined the familial coaggregation of clinically diagnosed ADHD and EDs across multiple types of relatives. We then applied quantitative genetic modeling in full-sisters and maternal half-sisters to estimate the genetic correlations between ADHD and EDs. We further tested the associations between ADHD polygenic risk scores and ED symptoms, and between AN polygenic risk scores and ADHD symptoms, in a genotyped population-based sample (N = 13,472). ResultsIncreased risk of all types of EDs was found in individuals with ADHD (any ED: odds ratio [OR] = 3.97, 95% confidence interval [CI] = 3.81, 4.14; AN: OR = 2.68, 95% CI = 2.15, 2.86; other EDs: OR = 4.66, 95% CI = 4.47, 4.87; bulimia nervosa: OR = 5.01, 95% CI = 4.63, 5.41) and their relatives compared with individuals without ADHD and their relatives. The magnitude of the associations decreased as the degree of relatedness decreased, suggesting shared familial liability between ADHD and EDs. Quantitative genetic models revealed stronger genetic correlation of ADHD with other EDs (.37, 95% CI = .31, .42) than with AN (.14, 95% CI = .05, .22). ADHD polygenic risk scores correlated positively with ED symptom measures overall and with the subscales Drive for Thinness and Body Dissatisfaction despite small effect sizes. ConclusionsWe observed stronger genetic association with ADHD for non-AN EDs than for AN, highlighting specific genetic correlation beyond a general genetic factor across psychiatric disorders.

Genetic Structure of IQ, Phonemic Decoding Skill, and Academic Achievement.

The aim of this study was to examine whether phonemic decoding skill (deficits of which characterize dyslexia) shares genetic and/or environmental covariance with scholastic abilities independent of general intelligence. Non-word reading ability, verbal and non-verbal IQ, and standardized academic achievement (Queensland Core Skills Test; QCST) were measured in Australian twins (up to 876 twin pairs and 80 singleton twins). Multivariate genetic analysis showed the presence of a general genetic factor, likely reflecting crystallized ability, which accounted for 45–76% of phenotypic variance in QCST scores, 62% of variance in Verbal IQ, 23% of variance in Performance IQ, and 19% of variance in phonological reading ability. The phonemic decoding genetic factor (explaining 48% of variance in phonemic decoding) was negatively associated with mathematical achievement scores (0.4%). Shared effects of common environment did not explain the relationship between reading ability and academic achievement beyond those also influencing IQ. The unique environmental reading factor (accounting for 26% of variance) influenced academic abilities related to written expression. Future research will need to address whether these reading-specific genetic and unique environment relationships arise from causal effects of reading on scholastic abilities, or whether both share a common influence, such as pleiotropic genes/environmental factors.

GENETIC AND ENVIRONMENTAL FACTORS IN EMOTION REGULATION AND LIFE SATISFACTION: A TWIN STUDY

An expansion of the mental health research at the end of the 20th century largely places well-being in the focus of interest of contemporary psychological science. However, the state of the art results of behavioral-genetic studies provide a complete framework of the factors that influence the indicators of subjective well-being through the specification of etiology of their relationship. The main aim of this study is to evaluate genetic and environmental factors that contribute to connections among life satisfaction measures and emotional regulation. The study included 182 pairs of twins of both sexes (121 monozygotic and 61 dizygotic twin pairs), aged 18-48. The proportion of individual sources of covariance between the examined phenotypes was tested with a multivariate biometric method. Genetic factors explained a slightly higher variance of life satisfaction (53%), while the environmental factors had a significant role in explaining different types of emotional regulation. General genetic factors were potentially important only in the explanation of the cognitive reappraisal of negative emotions. In other cases, the environmental factors were of the greater importance. An insight into the phenotypic correlations suggests these constructs have low to moderate intercorrelations; likewise genetic factors have a potential significance (45%) merely in the case of two types of cognitive reappraisal of emotions.

The quantitative genetics of disgust sensitivity.

[Correction Notice: An Erratum for this article was reported in Vol 16(1) of Emotion (see record 2015-57029-001). In the article, the name of author Joshua M. Tybur was misspelled as Joshua M. Tyber. All versions of this article have been corrected.] Response sensitivity to common disgust elicitors varies considerably among individuals. The sources of these individual differences are largely unknown. In the current study, we use a large sample of female identical and nonidentical twins (N = 1,041 individuals) and their siblings (N = 170) to estimate the proportion of variation due to genetic effects, the shared environment, and other (residual) sources across multiple domains of disgust sensitivity. We also investigate the genetic and environmental influences on the covariation between the different disgust domains. Twin modeling revealed that approximately half of the variation in pathogen, sexual, and moral disgust is due to genetic effects. An independent pathways twin model also revealed that sexual and pathogen disgust sensitivity were influenced by unique sources of genetic variation, while also being significantly affected by a general genetic factor underlying all 3 disgust domains. Moral disgust sensitivity, in contrast, did not exhibit domain-specific genetic variation. These findings are discussed in light of contemporary evolutionary approaches to disgust sensitivity.

Common psychiatric disorders share the same genetic origin: a multivariate sibling study of the Swedish population

Recent studies have shown that different mental-health problems appear to be partly influenced by the same set of genes, which can be summarized by a general genetic factor. To date, such studies have relied on surveys of community-based samples, which could introduce potential biases. The goal of this study was to examine whether a general genetic factor would still emerge when based on a different ascertainment method with different biases from previous studies. We targeted all adults in Sweden (n=3 475 112) using national registers and identified those who had received one or more psychiatric diagnoses after seeking or being forced into mental health care. In order to examine the genetic versus environmental etiology of the general factor, we examined whether participants' full- or half-siblings had also received diagnoses. We focused on eight major psychiatric disorders based on the International Classification of Diseases, including schizophrenia, schizoaffective disorder, bipolar disorder, depression, anxiety, attention-deficit/hyperactivity disorder, alcohol use disorder and drug abuse. In addition, we included convictions of violent crimes. Multivariate analyses demonstrated that a general genetic factor influenced all disorders and convictions of violent crimes, accounting for between 10% (attention-deficit/hyperactivity disorder) and 36% (drug abuse) of the variance of the conditions. Thus, a general genetic factor of psychopathology emerges when based on both surveys as well as national registers, indicating that a set of pleiotropic genes influence a variety of psychiatric disorders.

Intelligence GWAS hits: Selection signal or population structure? A test of the null hypothesis

An index of population structure (Fst) is used to test the null hypothesis that the genetic factor extracted from GWAS hits represents differences between populations due to migrations and drift. Employing the 1000 Genomes data, a regression of average IQ distances on the general intelligence genetic factor and Fst distances shows that the former is the only significant predictor of IQ distances(Beta= 0.82), whereas the population structure has no independent predictive power (Beta=-0.05). This result suggests that the null hypothesis can be rejected.

Etiological distinction of working memory components in relation to mathematics

Working memory has been consistently associated with mathematics achievement, although the etiology of these relations remains poorly understood. The present study examined the genetic and environmental underpinnings of math story problem solving, timed calculation, and untimed calculation alongside working memory components in 12-year-old monozygotic (n=105) and same-sex dizygotic (n=143) twin pairs. Results indicated significant phenotypic correlation between each working memory component and all mathematics outcomes (r=0.18–0.33). Additive genetic influences shared between the visuo-spatial sketchpad and mathematics achievement were significant, accounting for roughly 89% of the observed correlation. In addition, genetic covariance was found between the phonological loop and math story problem solving. In contrast, despite there being a significant observed relationship between phonological loop and timed and untimed calculations, there was no significant genetic or environmental covariance between the phonological loop and timed or untimed calculation skills. Further analyses indicated that genetic overlap between the visuo-spatial sketchpad and math story problem solving and math fluency was distinct from general genetic factors, whereas g, phonological loop, and mathematics shared generalist genes. Thus, although each working memory component was related to mathematics, the etiology of their relationships may be distinct.

INTELIGENCIJA I ŠKOLSKO POSTIGNUĆE U SVETLU NASLEDNIH I SREDINSKIH ČINILACA

Inteligencija i školsko postignuće, kao tesno vezani, ispitivani su zajedno od najranijih empirijskih istraživanja ovih konstrukata. Međutim, tek rezultati bihejvioralno-genetičkih studija pružaju potpunu sliku o faktorima koji utiču na inteligenciju i školski uspeh, specifikujući etiologiju njihovog odnosa. Osnovni cilj ovog istraživanja usmeren je na procenu genetskih i sredinskih faktora koji utiču na kovariranje među merom opšte intelektualne sposobnosti i osnovnoškolskog i srednjoškolskog uspeha. Istraživanje je obuhvatilo 340 parova blizanaca oba pola, od toga 168 monozigotnih i 172 dizigotna blizanca, u starosnoj dobi 18–44 godine. Udeo pojedinih izvora kovariranja između ispitivanih fenotipa testiran je multivarijantnim biometrijskim metodom. Uvid u fenotipske korelacije opšte intelektualne sposobnosti, uspeha u osnovnoj školi i uspeha u srednjoj, ukazuje da je reč o konstruktima koji međusobno umereno koreliraju (.33–.53). Opšti/zajednički genetski uticaj objašnjava najveći deo kovarijanse školskog uspeha (kako u osnovnoj, tako i u srednjoj školi) i opšte intelektualne sposobnosti, što govori u prilog pretpostavci da isti set gena određuje etiologiju individualnih razlika na ispitivanim varijablama. Objašnjenju korelacije između uspeha u osnovnoj i uspeha u srednjoj školi umereno doprinose i mere opšte/zajedničke deljene sredine. Pored nedeljenih sredinskih uticaja, ono što razlikuje ispitivane konstrukte jesu uticaji specifičnih genetskih faktora, koji su jedinstveni za svaki konstrukt.

Comment on: Current initiatives to improve prudent antibiotic use amongst school-aged children

Sir, With great interest, we read the recent leading article by Lecky and McNulty, describing an overview of some initiatives aimed at limiting the extent of inappropriate antibiotic use in children. In the case of e-Bug, educating parents through children is novel and interesting. Even though children and their parents increased their awareness of hygiene, the spread of infection, vaccination uptake and prudent antibiotic use, this ‘antibiotic awareness’ programme could be unsuccessful if prescribers have inadequate knowledge about antibiotics. For education through e-Bug to be highly effective, there is an additional point according to our recent report, as follows. Prudent antibiotic use depends on educating clinicians about their everyday treatment decisions. It is noteworthy that while only specialists in oncology can prescribe and administer anticancer drugs, any clinician can prescribe antibiotics, irrespective of their level of training. To optimize antimicrobial prescribing, the prescribers should have appropriate knowledge of general medicine, microbial virulence, immunological and genetic host factors and pharmacokinetic and pharmacodynamic properties of drugs as well as basic knowledge of epidemiology. When prescribing antibiotics, clinicians face a dilemma not encountered with other drugs. On the one hand, they need to provide optimal therapy for their patients, which may result in overuse of broadspectrum antibiotics. On the other hand, they have a responsibility to future patients and to public health in sustaining the efficiency of antibiotics and minimizing antibiotic resistance. Achieving this balance may pose a significant challenge. There have been reports that 50% of antibiotic prescriptions, both in the community and in hospitals, can be considered inappropriate (inadequate dosing and/or wrong duration). As most antibiotics are used in primary care, education on antibiotic prescribing in primary care is important. Some reports demonstrate that, notwithstanding the advice to decrease antibiotic prescribing in primary healthcare, misuse or overuse of antibiotics continues. In France, only 21% of the surveyed primary care physicians followed the guidelines in prescribing antibiotic treatment for urinary tract infection. About 50% of primary care prescriptions for nephritis were wrong and 70% of asymptomatic bacteriuria was treated with antibiotics. Similar results were reported from Greece, where only 55% of community physicians restricted antibiotic use for sore throat and only 26% utilized a strep test to guide antibiotic use. Eighty-nine percent of the surveyed physicians prescribed antibiotics for chronic obstructive pulmonary disease exacerbations and only 17% of them followed the widely accepted Anthonisen criteria. Lack of knowledge in microbial virulence and antibiotics may significantly affect the quality of prescribing. Physicians with inadequate knowledge may prefer prescribing maximal broadspectrum treatment. Therefore, educating physicians is certainly required. Recent reports emphasize that undergraduate training courses would be successful if the students are imparted with adequate knowledge and trained in developing the right attitude and behaviour. As is the practice in some countries, including the UK, education on prudent antibiotic prescribing should be included as a component of the undergraduate curriculum. Teaching postgraduate students, particularly those who will prescribe in community settings, requires internship/foundation training or close collaboration between local healthcare providers and academics. Antibiotic treatment guideline teachers must be trained regarding the available educational strategies as well as current information on antimicrobial stewardship. As has been the practice in some countries, nurses, clinical pharmacists and midwives may also be allowed to prescribe some antibiotics in special clinical situations; all healthcare professionals who have to deal with patients must be educated about prudent antibiotic treatment and the management of patients demanding an overuse of antibiotics. Antibiotic management requires effective teamwork between all healthcare professionals. If patients receive inconsistent messages from healthcare professionals when taking antibiotics, all efforts of prudent antibiotic prescribing may become unsuccessful. Therefore, all healthcare professionals must receive continual education on prudent antibiotic prescribing, the benefits and limitations of antibiotics, and antibiotic resistance. In conclusion, it is necessary to educate prescribers as well as school-aged children. If e-Bug resources can be extended for prescribers (or undergraduate and postgraduate students who will be prescribers) by close collaboration between healthcare providers and academics, education through e-Bug should be very successful.

Common low-penetrance risk variants associated with breast cancer in Polish women

BackgroundBreast cancer is the most common type of cancer and the second leading cause of cancer-death among women in Poland. The known high-risk mutations account for 25% of familial aggregation cases and 5% of total breast cancer predisposition. Genome-wide association studies have identified a number of common low-penetrance genetic variants, but their contribution to disease risk differs between populations.MethodsTo verify selected associations with breast cancer susceptibility among Polish women, the replication study was performed, included 1424 women with breast cancer and 1788 healthy persons. Sixteen single-nucleotide polymorphisms (SNPs) were analyzed using TaqMan SNP Genotyping Assays. Allele frequency differences were tested using chi2-test implemented in PLINK v1.07 and Cochran-Armitage trend test was performed using R software.ResultsSignificant differences (Bonferroni corrected p-valuecor ≤ 0.0197) in the frequency of alleles distribution between all cancer and control subjects were observed for four (rs2736098, rs13281615, rs1219648, rs2981582) out of 16 SNPs. The same result was obtained for group of patients without high-risk BRCA1/2 mutations. The rs1219648 (p-valuecor ≤ 6.73E-03) and rs2981582 (p-valuecor ≤ 6.48E-03) SNPs showed significant association with both familial and sporadic cancers. Additionally, rs2736098 (p-valuecor ≤ 0.0234) was associated with only sporadic cancers; also in group without carriers of high-risk mutation. All these associations revealed their significance also in Cochran-Armitage trend test. Opposite to other SNPs, rs2736098 was associated with a decreased risk of breast cancer.ConclusionThe association of four known susceptibility SNPs, representing three individual loci, with breast cancer risk in Polish women was confirmed. One of them (rs2736098) seems to be specific for the Polish population. Due to the population differences in allele frequencies, identification of general genetic risk factors requires sets of association studies conducted on different populations.

Different neurodevelopmental symptoms have a common genetic etiology

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

Genetic Influences on Psychological Well‐Being: A Nationally Representative Twin Study

Psychological well-being, or eudaimonia, features strongly in theories of human development and thriving. However, the factors of eudaimonia are debated, and their genetic architecture has not been studied in detail. A classical twin design was used to decompose behavioral variance into genetic and environmental components implemented in a multigroup, multivariate structural equation modeling framework. Subjects were 837 pairs of adult U.S. twins from the nationally representative MIDUS II sample. Psychological well-being was measured using the 42-item Ryff Psychological Well-Being Scale, which assesses autonomy, environmental mastery, personal growth, positive relations with others, purpose in life, and self-acceptance. Substantial genetic influences were observed on all components of well-being. Attempts to model these six factors as reflecting a single common psychological mechanism gave a poor fit to the data. The best-fitting model supported the existence of five distinct genetic effects. Effects of shared environment were weak and nonsignificant. Unique environmental effects for all measures were mostly trait specific. These results indicate that psychological well-being is underpinned by a general genetic factor influencing self-control, and four underlying biological mechanisms enabling the psychological capabilities of purpose, agency, growth, and positive social relations.

Etiology of obsessions and compulsions: A behavioral-genetic analysis.

It is unknown whether various types of obsessive-compulsive (OC) symptoms have a common genetic or environmental etiology. For example, it is unknown whether hoarding is etiologically associated with prototypic OC symptoms, such as washing, checking, and obsessing. Also unknown is whether particular OC-related symptoms are etiologically linked to the general tendency to experience emotional distress (negative emotionality). To investigate these and other issues, a community sample of 307 pairs of monozygotic and dizygotic adult twins provided scores on 6 OC-related symptoms (obsessing, neutralizing, checking, washing, ordering, and hoarding) and 2 markers of negative emotionality (trait anxiety and affective lability). Genetic factors accounted for 40%-56% of variance in the 8 phenotypic scores (M = 49% of variance for OC-related symptoms). Remaining variance was due to nonshared (person-specific) environment. More detailed analyses revealed a complex etiologic architecture, where OC-related symptoms arise from a mix of common and symptom-specific genetic and environmental factors. A general genetic factor was identified, which influenced all symptoms and negative emotionality. An environmental factor was identified that influenced all symptoms but did not influence negative emotionality. Each of the 6 types of symptoms was also shaped by its own set of symptom-specific genetic and environmental factors. The importance of genetic factors did not vary as a function of age or sex, and the architecture of general and specific etiologic factors was replicated for participants having relatively more severe OC symptoms. Gene-environment interactions were identified. Implications for an etiology-based classification system are discussed.

Exploring How Symptoms of Attention-Deficit/Hyperactivity Disorder Are Related to Reading and Mathematics Performance

Children with attention-deficit/hyperactivity disorder (ADHD) tend to perform more poorly on tests of reading and mathematical performance than their typical peers. Quantitative genetic analyses allow for a better understanding of the etiology of ADHD and reading and mathematics outcomes, by examining their common and unique genetic and environmental influences. Analyses were conducted on a sample 271 pairs of 10-year-old monozygotic and dizygotic twins drawn from the Western Reserve Reading and Mathematics Project. In general, the results suggested that the associations among ADHD symptoms, reading outcomes, and math outcomes were influenced by both general genetic and general shared-environment factors. The analyses also suggested significant independent genetic effects for ADHD symptoms. The results imply that differing etiological factors underlie the relationships among ADHD and reading and mathematics performance. It appears that both genetic and common family or school environments link ADHD with academic performance.

Decomposing group differences of latent means of ordered categorical variables within a genetic factor model.

A genetic factor model is introduced for decomposition of group differences of the means of phenotypic behavior as well as individual differences when the research variables under consideration are ordered categorical. The model employs the general Genetic Factor Model proposed by Neale and Cardon (Methodology for genetic studies of twins and families, 1992) and, more specifically, the extension proposed by Dolan et al. (Behav Genet 22: 319-335, 1992) which enables decomposition of group differences of the means associated with genetic and environmental factors. Using a latent response variable (LRV) formulation (Muthén and Asparouhov, Latent variable analysis with categorical outcomes: multiple-group and growth modeling in Mplus. Mplus web notes: No. 4, Version 5, 2002), proportional differences of response categories between groups are modeled within the genetic factor model in terms of the distributional differences of latent response variables assumed to underlie the observed ordered categorical variables. Use of the proposed model is illustrated using a measure of conservatism in the data collected from the Australian Twin Registry.