Biomedical subjects

Ted Reichborn-Kjennerud

Publications and source records attributed to Ted Reichborn-Kjennerud.

14 recordsLinked to original sources

PubMed2026

Family genetic designs in MoBa provide insights into health and functioning.

Genome-wide association studies using large, population-based samples of unrelated individuals have discovered thousands of genetic associations with health and disease1. These studies can help explain genetic and environmental risks. However, increasing evidence suggests that population-based estimates, while precise, can also reflect confounding that affects their use and interpretation. This confounding can be overcome using data from genotyped family members, such as nuclear mother-father-child trios2,3. However, samples of genotyped families are rare4-11. Here we illustrate some of the advantages of familial data using the Norwegian Mother, Father and Child Cohort Study (MoBa), a population-based cohort of parents and offspring with extensive genotype data (n ≈ 230,000) (ref. 3), along with broad and longitudinal phenotyping of health and functioning. We provide an overview of MoBa and describe the quality control of genotype data tailored to this extensively related sample. We then use trio data to illustrate how family-based genomic designs can identify distinct direct and indirect sources of genetic influence and structural confounding. As examples, we analyse children's height, educational achievement, depressive symptoms and sleep duration. These demonstrations highlight MoBa as a broadly valuable resource for advancing understanding of health and functioning across the lifecourse and generations.

Journal Article↗

PubMed2007

The heritability of cluster A personality disorders assessed by both personal interview and questionnaire.

BACKGROUND: Personality disorders (PDs) as assessed by questionnaires and personal interviews are heritable. However, we know neither how much unreliability of measurement impacts on heritability estimates nor whether the genetic and environmental risk factors assessed by these two methods are the same. We wish to know whether the same set of PD vulnerability factors are assessed by these two methods. METHOD: A total of 3334 young adult twin pairs from the Norwegian Institute of Public Health Twin Panel (NIPHTP) completed a questionnaire containing 91 PD items. One to 6 years later, 1386 of these pairs were interviewed with the Structured Interview for DSM-IV Personality (SIDP-IV). Self-report items predicting interview results were selected by regression. Measurement models were fitted using Mx. RESULTS: In the best-fit models, the latent liabilities to paranoid personality disorder (PPD), schizoid personality disorder (SPD) and schizotypal personality disorder (STPD) were all highly heritable with no evidence of shared environmental effects. For PPD and STPD, only unique environmental effects were specific to the interview measure whereas both environmental and genetic effects were found to be specific to the questionnaire assessment. For SPD, the best-fit model contained genetic and environmental effects specific to both forms of assessment. CONCLUSIONS: The latent liabilities to the cluster A PDs are highly heritable but are assessed by current methods with only moderate reliability. The personal interviews assessed the genetic risk for the latent trait with excellent specificity for PPD and STPD and good specificity for SPD. However, for all three PDs, the questionnaires were less specific, also indexing an independent set of genetic risk factors.

Adult↗

PubMed2006

Genetic and environmental influences on dimensional representations of DSM-IV cluster C personality disorders: a population-based multivariate twin study.

BACKGROUND: The DSM-IV cluster C Axis II disorders include avoidant (AVPD), dependent (DEPD) and obsessive-compulsive (OCPD) personality disorders. We aimed to estimate the genetic and environmental influences on dimensional representations of these disorders and examine the validity of the cluster C construct by determining to what extent common familial factors influence the individual PDs. METHOD: PDs were assessed using the Structured Interview for DSM-IV Personality (SIDP-IV) in a sample of 1386 young adult twin pairs from the Norwegian Institute of Public Health Twin Panel (NIPHTP). A single-factor independent pathway multivariate model was applied to the number of endorsed criteria for the three cluster C disorders, using the statistical modeling program Mx. RESULTS: The best-fitting model included genetic and unique environmental factors only, and equated parameters for males and females. Heritability ranged from 27% to 35%. The proportion of genetic variance explained by a common factor was 83, 48 and 15% respectively for AVPD, DEPD and OCPD. Common genetic and environmental factors accounted for 54% and 64% respectively of the variance in AVPD and DEPD but only 11% of the variance in OCPD. CONCLUSION: Cluster C PDs are moderately heritable. No evidence was found for shared environmental or sex effects. Common genetic and individual environmental factors account for a substantial proportion of the variance in AVPD and DEPD. However, OCPD appears to be largely etiologically distinct from the other two PDs. The results do not support the validity of the DSM-IV cluster C construct in its present form.

Adult↗

PubMed2006

Genetic and environmental contributions to depressive personality disorder in a population-based sample of Norwegian twins.

BACKGROUND: Depressive personality disorder (DPD) was introduced in DSM-IV as a new category requiring further study. The aim of this study was to estimate genetic and environmental contributions to DPD in a population-based twin sample, and include data on criteria performance, prevalence and diagnostic overlap. METHODS: Axis I and Axis II diagnoses were obtained by structured interviews in a population-based sample of 2794 young adult twins. Statistical analyses included correlation and factor analysis based on polychoric correlation coefficients, and diagnostic overlap applying adjusted odds ratios. Contributions from additive genetic and common and unique environmental influences to the liability to DPD were computed using structural equation modelling, applying a multiple threshold variable. RESULTS: Liability to DPD could best be explained by additive genetic and unique environmental factors, with heritability estimates of 49% (95% CI 0.41-0.57) in females and 25% (95% CI 0.12-0.40) in males. The best-fitting model indicated that some of the genes contributing to DPD differ between men and women. Chronbach's alpha was 0.87. 2.0% of participants fulfilled the criteria for DPD, and overlap was most pronounced for dysthymic disorder and avoidant personality disorder. LIMITATIONS: Low prevalence rates and subsequent inclusion of subthreshold criteria could have influenced parameter estimates, especially in males. CONCLUSIONS: DPD was almost twice as heritable in females as in males, comparable to previous studies on major depression. The proposed criteria showed good measurement properties, and DPD was not completely subsumed within any other disorder.

Adult↗

PubMed2006

Dimensional representations of DSM-IV cluster A personality disorders in a population-based sample of Norwegian twins: a multivariate study.

BACKGROUND: The 'odd' or 'Cluster A' personality disorders (PDs) - paranoid, schizoid and schizotypal PDs - were created in DSM-III with little empirical foundation. We have examined the relationship between the genetic and environmental risk factors for dimensional representations of these three personality disorders. METHOD: These personality disorders were assessed using the Structured Interview for DSM-IV Personality (SIDP-IV) in 1386 young adult twin pairs from the Norwegian Institute of Public Health Twin Panel. Using Mx, a single-factor independent pathway twin model was fitted to the number of endorsed criteria for the three disorders. RESULTS: The best-fit model included genetic and unique environmental common factors and genetic and unique environmental effects specific to each personality disorder. Total heritability was modest for these personality disorders and ranged from 21% to 28%. Loadings on the common genetic and unique environmental factors were substantially higher for schizotypal than for paranoid or schizoid PD. The proportion of genetic liability shared with all Cluster A disorders was estimated at 100, 43 and 26% respectively for schizotypal, paranoid and schizoid PDs. CONCLUSION: In support of the validity of the Cluster A construct, dimensional representations of schizotypal, paranoid and schizoid PD are all modestly heritable and share a portion of their genetic and environmental risk factors. No evidence was found for shared environmental or sex effects for these PDs. Schizotypal PD most closely reflects the genetic and environmental liability common to all three Cluster A disorders. These results should be interpreted in the context of the limited power of this sample.

Adult↗

PubMed2006

Illicit psychoactive substance use, abuse and dependence in a population-based sample of Norwegian twins.

BACKGROUND: Prior population-based twin studies from two Anglophonic countries with relatively high rates of drug use - the USA and Australia - suggest that genetic factors contribute substantially to individual differences in the use, abuse and dependence of illicit psychoactive substances. Would these results replicate in Norway, a Nordic country with a low prevalence of illicit drug use? METHOD: Lifetime use, abuse and dependence of five illicit drug categories (cannabis, stimulants, opiates, cocaine and psychedelics) were assessed at personal interview in 1386 complete young adult twin pairs ascertained from the Norwegian Institute of Public Health Twin Panel. Twin model fitting was performed using the Mx statistical package on three phenotypes: any lifetime use, endorsement of at least one DSM-IV symptom of abuse or dependence, and meeting DSM-IV criteria for abuse or dependence. RESULTS: Significant lifetime use of illicit substances (defined as use 10 or more times) was reported by only 6.4% of the sample. Meaningful analyses were possible for use of any substance and each of the five substances individually, but for symptoms or a diagnosis of abuse/dependence meaningful analyses were possible only for any substance and cannabis. Full twin models uniformly found twin resemblance to be due largely or entirely to genetic factors. Best-fit models for all analyses included only genetic and individual-specific environmental effects with heritability estimates ranging from 58% to 81%. CONCLUSION: In accord with prior results from the USA and Australia, genetic factors appear to play an important role in the etiology of use and abuse/dependence of illicit drugs in Norway.

Diseases in Twins↗

PubMed2005

Anorexia nervosa: definition, epidemiology, and cycle of risk.

Anorexia nervosa is a debilitating psychiatric disorder with profound biological, psychological, and social consequences. After an initial evaluation of the most widely used diagnostic criteria for anorexia nervosa, this paper reviews genetic and environmental risk factors for the development of anorexia with special emphasis on gene environment interplay and the impact of adverse perinatal events.

Adolescent↗

PubMed2005

Subjective wellbeing and sleep problems: a bivariate twin study.

The relationship between subjective wellbeing (SWB) and self-reported sleep problems was investigated in a cohort of Norwegian twins aged 18 to 31 years. Questionnaire data from 8045 same- and opposite-sex twins were analyzed using structural equation modeling to explore the relative effects of genetic and environmental influences on phenotypic variance and covariance. Special attention was paid to sex-specific effects. The correlation between the phenotypes was estimated to be -.43. Univariate analyses indicated considerable genetic influences for both SWB and sleep problems, for male and female twins alike. The best fitting bivariate model specified additive genetic and individual environmental factors for both phenotypes, and nonadditive genetic effects for sleep problems, with no sex-specific effects. Genetic and environmental effects accounted for 60% and 40% of the phenotypic correlation, respectively. Additive genetic factors affecting the two phenotypes were correlated (-.85), suggesting that part of the genetic effects that positively influence SWB also protect against sleep problems. In conclusion, the results indicate considerable overlap in genetic etiology for SWB and sleep problems, for males and females alike.

Adolescent↗

PubMed2004

Undue influence of weight on self-evaluation: a population-based twin study of gender differences.

OBJECTIVE: To explore the extent to which genetic and environmental factors contribute to liability to placing undue importance on weight as an indicator of self-evaluation and to determine whether differences exist across genders in the nature and magnitude of these effects. METHOD: Self-report data were collected on 8,045 same-sex and opposite-sex twins, aged 18-31 years, from a population-based registry of Norwegian twins. Structural equation modeling was utilized to estimate the relative contribution of genetic and environmental factors to liability for undue influence of weight on self-evaluation, allowing for gender-specific effects. RESULTS: Individual variation in undue influence of weight on self-evaluation was best explained by shared and individual environmental influences. No significant gender differences were found. Shared environmental factors accounted for 31% of the variance. DISCUSSION: These results raise the possibility that there may be distinct sources of familial resemblance for different symptoms of bulimia nervosa as codified in the 4th ed. of the Diagnostic and Statistical Manual of Mental Disorders (American Psychiatric Association, 1994).

Adolescent↗

PubMed2004

Genetic and environmental influences on binge eating in the absence of compensatory behaviors: a population-based twin study.

OBJECTIVE: The current study explores the extent to which genetic and environmental factors influence liability to binge eating in the absence of compensatory behaviors (BE) in a population-based sample of twins. METHOD: Questionnaire data on 8,045 same-sex and opposite-sex twins, aged 18-31 years, from a Norwegian twin registry were used to assess BE during the last 6 months. RESULTS: The best-fitting biometrical model suggested that the heritability of BE was 41% (95% confidence interval [CI]: 0.31-0.50). Individual environmental factors accounted for the rest of the variance (59%; 95% CI: 0.50-0.69). No significant sex differences were found, but the statistical power to detect such effects was low. Shared environmental influences on the liability to BE in males could not be ruled out. DISCUSSION: The findings indicate significant additive genetic influences on BE, supporting the validity of the core features of binge eating disorder as a diagnostic category.

Adaptation, Psychological↗

PubMed2004

Genetic and environmental influences on the association between smoking and panic attacks in females: a population-based twin study.

BACKGROUND: Clinical and epidemiological studies have reported an association between lifetime cigarette-smoking and panic attacks. Several explanations for this relationship have been proposed, mostly focusing on direct causal pathways. The objective of this study was to investigate a hypothesis of shared vulnerability by examining whether panic attacks and cigarette-smoking share genetic or environmental liability factors. METHOD: Questionnaire data on 3172 female-female twins (1409 complete pairs), aged 18-31 years, from a population-based Norwegian twin registry, were used to calculate the correlation between genetic factors and the correlation between environmental factors that influence lifetime measures of panic attacks and daily smoking. RESULTS: The best-fitting biometrical twin model suggested that genetic factors influencing panic and smoking were uncorrelated. Shared or familial environmental factors were perfectly correlated, and accounted for 75 % of the association between the phenotypes. The correlation between individual environmental factors influencing the phenotypes was 0.25 (0.07-0.44). In the full model, the genetic correlation was 0.17 (0.00-1.00), and genetic and shared environmental factors respectively accounted for 18 % and 61 % of the co-variance between panic and smoking. CONCLUSION: The results suggest that panic attacks and lifetime smoking have few or no genetic liability factors in common. The shared environmental factors that influence the two phenotypes are identical. Liability to panic attacks in females appears to be more influenced by shared environmental factors than previously indicated by univariate studies.

Adolescent↗

PubMed2004

Psychiatric and medical symptoms in binge eating in the absence of compensatory behaviors.

OBJECTIVE: To explore the extent to which binge eating in the absence of compensatory behaviors (BE) is associated with psychiatric and medical symptoms in men and women and to control for the independent effects of BMI. RESEARCH METHODS AND PROCEDURES: A series of regression models was applied to questionnaire data on 8045 twins, 18 to 31 years old, from a population-based Norwegian registry. RESULTS: BE was significantly associated with elevated obesity, overweight, symptoms of eating disorders, symptoms of anxiety and depression, panic attacks, depressive episodes, and reduced life satisfaction in both men and women. In women, BE was independently associated with insomnia and early menarche. In men, BE was independently associated with specific phobia, daily smoking, alcohol use, use of pain medication, impairment due to mental health, neck-shoulder, lower back, and chronic muscular pain, and impairment due to physical health. Both men and women with BE reported higher rates of psychiatric treatment. DISCUSSION: Our results indicate that there is substantial comorbidity between BE and psychiatric symptoms independently of BMI for both men and women. Medical symptoms co-occur less frequently than previously reported from treatment-seeking populations in women. Across all domains, the array of symptoms exhibited by men with BE was broader than that observed in women with BE. This observation suggests the importance of considering gender differences in future studies of psychiatric and medical morbidity, binge eating, and obesity.

Adult↗

PubMed2003

Medical morbidity in binge eating disorder.

OBJECTIVE: To explore the extent to which binge eating disorder (BED) is associated with medical morbidity. METHOD: We reviewed all existing studies on the effects of BED on physical health. RESULTS: BED may be associated with medical morbidity independent of the effects of comorbid psychopathology or comorbid obesity. DISCUSSION: Additional research specifically designed to explore the effects of BED on physical health in both clinical and community samples is required before definitive conclusions can be drawn.

Bulimia↗

PubMed2003

Happiness and health: environmental and genetic contributions to the relationship between subjective well-being, perceived health, and somatic illness.

The aim was to identify genetic and environmental influences on the covariances between subjective well-being (SWB), perceived health, and somatic illness. Analyses were based on 6576 Norwegian twins aged 18-31. Heritabilities ranged from .24 to.66. SWB correlated .50 with perceived health, -.25 with musculoskeletal pain, and -.07 with allergy. Common genetic factors accounted for 45%-60% of associations. SWB and perceived health was to a high extent influenced by the same genes (r(g)=.72 and.82 for males and females, respectively). For SWB and musculoskeletal pain, r-sub(g) =-.29 and -.42 for males and females, respectively. Effects were partly sex specific. Environmental factors shared by twins did not affect the covariances. Results support a differentiated view of SWB-health relations, and imply that both genes and environment play important roles in the associations between well-being and health.

Adolescent↗