The interplay between cognitive ability, alcohol consumption, and health characteristics.

BACKGROUND: Higher cognitive ability is associated with favourable health characteristics. The relation between ability and alcohol consumption, and their interplay with other health characteristics, is unclear. We aimed to assess the relationship between cognitive ability and alcohol consumption and to assess whether alcohol consumption relates differently to health characteristics across strata of ability. METHODS: For 63 120 Norwegian males, data on cognitive ability in early adulthood were linked to midlife data on alcohol consumption frequency (times per month, 0-30) and other health characteristics, including cardiovascular risk factors and mental distress. Relations were assessed using linear regression and reported as unstandardised beta coefficients [95% confidence interval (CI)]. RESULTS: The mean ± s.d. frequency of total alcohol consumption in the sample was 4.0 ± 3.8 times per month. In the low, medium, and high group of ability, the frequencies were 3.0 ± 3.3, 3.7 ± 3.5, and 4.7 ± 4.1, respectively. In the full sample, alcohol consumption was associated with physical activity, heart rate, fat mass, smoking, and mental distress. Most notably, each additional day of consumption was associated with a 0.54% (0.44-0.64) and 0.14% (0.09-0.18) increase in the probability of current smoking and mental distress, respectively. In each strata of ability (low, medium, high), estimates were 0.87% (0.57-1.17), 0.48% (0.31-0.66) and 0.49% (0.36-0.62) for current smoking, and 0.44% (0.28-0.60), 0.10% (0.02-0.18), and 0.09% (0.03-0.15) for mental distress, respectively. CONCLUSIONS: Participants with low cognitive ability drink less frequently, but in this group, more frequent alcohol consumption is more strongly associated with adverse health characteristics.

The relationship between anxiety disorders and dimensional representations of DSM-IV personality disorders: A co-twin control study.

BACKGROUND: There is substantial comorbidity between personality disorders (PDs) and anxiety disorders (ADs). Sharing of familial risk factors possibly explains the co-occurrence, but direct causal relationships between the disorders may also exist. METHODS: 2801 persons from 1391 twin pairs from the Norwegian Institute of Public Health Twin Panel were assessed for all DSM-IV PDs and ADs. Bivariate Poisson-regression analyses were performed to assess whether PDs predicted ADs at three different levels: All PDs combined, PDs combined within DSM-IV-clusters and each individual PD separately. Next, bivariate co-twin control analyses were executed within monozygotic (MZ) and dizygotic (DZ) twin pairs. A similar analytic strategy was employed in multivariate models including PDs as independent variables. RESULTS: PDs predicted ADs at all levels of analysis in bivariate regression models. Bivariate co-twin control analyses demonstrated an increased risk of ADs in all PDs combined, all PD-clusters and in schizotypal, paranoid, borderline, antisocial, avoidant and dependent PD. In the multivariate regression model, all PD-clusters and schizotypal, borderline, avoidant and obsessive-compulsive PD predicted ADs. Only borderline and avoidant PD predicted ADs in the multivariate co-twin control analysis. LIMITATIONS: Over-adjustment may explain the results from the multivariate analyses. The cross-sectional study design hampers causal inference. CONCLUSIONS: Comorbidity between ADs and PDs can be largely accounted for by shared familial risk factors. However, the results are also consistent with a direct causal relationship partly explaining the co-occurrence. Our results indicate specific environmental factors for comorbidity of ADs and borderline and avoidant PDs that are not shared with other PDs.

A longitudinal, population-based twin study of avoidant and obsessive-compulsive personality disorder traits from early to middle adulthood.

BACKGROUND: The phenotypic stability of avoidant personality disorder (AVPD) and obsessive-compulsive personality disorder (OCPD) has previously been found to be moderate. However, little is known about the longitudinal structure of genetic and environmental factors for these disorders separately and jointly, and to what extent genetic and environmental factors contribute to their stability. METHOD: AVPD and OCPD criteria were assessed using the Structured Interview for DSM-IV Personality in 2793 young adult twins (1385 pairs, 23 singletons) from the Norwegian Institute of Public Health Twin Panel at wave 1 and 2282 (986 pairs, 310 singletons) of these on average 10 years later at wave 2. Longitudinal biometric models were fitted to AVPD and OCPD traits. RESULTS: For twins who participated at both time-points, the number of endorsed sub-threshold criteria for both personality disorders (PDs) decreased 31% from wave 1 to wave 2. Phenotypic correlations between waves were 0.54 and 0.37 for AVPD and OCPD, respectively. The heritability estimates of the stable PD liabilities were 0.67 for AVPD and 0.53 for OCPD. The genetic correlations were 1.00 for AVPD and 0.72 for OCPD, while the unique environmental influences correlated 0.26 and 0.23, respectively. The correlation between the stable AVPD and OCPD liabilities was 0.39 of which 63% was attributable to genetic influences. Shared environmental factors did not significantly contribute to PD variance at either waves 1 or 2. CONCLUSION: Phenotypic stability was moderate for AVPD and OCPD traits, and genetic factors contributed more than unique environmental factors to the stability both within and across phenotypes.

A longitudinal twin study of borderline and antisocial personality disorder traits in early to middle adulthood.

BACKGROUND: Antisocial personality disorder (ASPD) and borderline personality disorder (BPD) share genetic and environmental risk factors. Little is known about the temporal stability of these etiological factors in adulthood. METHOD: DSM-IV criteria for ASPD and BPD were assessed using structured interviews in 2282 Norwegian twins in early adulthood and again approximately 10 years later. Longitudinal biometric models were used to analyze the number of endorsed criteria. RESULTS: The mean criterion count for ASPD and BPD decreased 40% and 28%, respectively, from early to middle adulthood. Rank-order stability was 0.58 for ASPD and 0.45 for BPD. The best-fitting longitudinal twin model included only genetic and individual-specific environmental factors. Genetic effects, both those shared by ASPD and BPD, and those specific to each disorder remained completely stable. The unique environmental effects, however, changed substantially, with a correlation across time of 0.19 for the shared effects, and 0.39 and 0.15, respectively, for those specific to ASPD and BPD. Genetic effects accounted for 71% and 72% of the stability over time for ASPD and BPD, respectively. The genetic and environmental correlations between ASPD and BPD were 0.73, and 0.43, respectively, at both time points. CONCLUSION: ASPD and BPD traits were moderately stable from early to middle adulthood, mostly due to genetic risk factors which did not change over the 10-year assessment period. Environmental risk factors were mostly transient, and appear to be the main source of phenotypic change. Genetic liability factors were, to a large extent, shared by ASPD and BPD.

A longitudinal twin study of cluster A personality disorders.

BACKGROUND: While cluster A personality disorders (PDs) have been shown to be moderately heritable, we know little about the temporal stability of these genetic risk factors. METHOD: Paranoid PD (PPD) and schizotypal PD (STPD) were assessed using the Structured Interview for DSM-IV Personality in 2793 young adult twins from the Norwegian Institute of Public Health Twin Panel at wave 1 and 2282 twins on average 10 years later at wave 2. Using the program Mx, we fitted a longitudinal latent factor model using the number of endorsed criteria for PPD and STPD. RESULTS: The stability over time of the criteria counts for PPD and STPD, estimated as polychoric correlations, were +0.34 and +0.40, respectively. The best-fit longitudinal model included only additive genetic and individual-specific environmental factors with parameter estimates constrained to equality across the two waves. The cross-wave genetic and individual-specific environmental correlations for a latent cluster A factor were estimated to equal +1.00 and +0.13, respectively. The cross-time correlations for genetic and environmental effects specific to the individual PDs were estimated at +1.00 and +0.16-0.20, respectively. We found that 68% and 71% of the temporal stability of PPD and STPD derived, respectively, from the effect of genetic factors. CONCLUSION: Shared genetic risk factors for two of the cluster A PDs are highly stable in adults over a 10-year period while environmental risk factors are relatively transient. Over two-thirds of the long-term stability of the common cluster A PD liability can be attributed to genetic influences.

Hearing status among Norwegian train drivers and train conductors.

BACKGROUND: There is a general perception that train drivers and conductors may be at increased risk of developing noise-induced hearing loss. AIMS: To study job-related hearing loss among train drivers and train conductors. METHODS: Audiograms from train drivers and train conductors were obtained from the medical records of the occupational health service of the major Norwegian railway company. The results were compared with audiograms from an internal control group of railway workers and an external reference group of people not occupationally exposed to noise. The monaural hearing threshold level at 4kHz, the mean binaural value at 3, 4 and 6kHz and the prevalence of audiometric notches (≥25 dB at 4kHz) were used for comparison. RESULTS: Audiograms were available for 1567 drivers, 1565 conductors, 4029 railway worker controls and 15 012 people not occupationally exposed to noise. No difference in hearing level or prevalence of audiometric notches was found between study groups after adjusting for age and gender. CONCLUSIONS: Norwegian train drivers and conductors have normal hearing threshold levels comparable with those in non-exposed groups.

Genetic and environmental contributions to the relationship between education and anxiety disorders - a twin study.

OBJECTIVE: To examine the negative statistical relationship between educational level and risk of anxiety disorders, and to estimate to what extent this relationship may be explained by genes or environmental factors influencing both phenotypes. METHOD: Registry data on educational level for 3339 young adult Norwegian twin pairs and diagnostic data on anxiety disorders for 1385 of these pairs were analysed, specifying structural equations models using MX software. RESULTS: In the best-fitting model, genes accounted for 59% of the variance in education. 18% of the variance was due to environmental factors shared by co-twins, and the remaining 23% due to non-shared environment; 46% of the variance in liability to anxiety disorders was genetic, the remaining variance was due to non-shared environment. A phenotypic polychoric correlation of -0.30 between educational level and 'any anxiety disorder' was estimated to be primarily (83% in the best-fitting model) caused by genes common to the two traits. CONCLUSION: The relationship between low education and risk of anxiety disorders appears to be primarily determined by genetic effect common to educational level and anxiety disorders.

The structure of genetic and environmental risk factors for phobias in women.

BACKGROUND: To explore the genetic and environmental factors underlying the co-occurrence of lifetime diagnoses of DSM-IV phobia. METHOD: Female twins (n=1430) from the population-based Norwegian Institute of Public Health Twin Panel were assessed at personal interview for DSM-IV lifetime specific phobia, social phobia and agoraphobia. Comorbidity between the phobias were assessed by odds ratios (ORs) and polychoric correlations and multivariate twin models were fitted in Mx. RESULTS: Phenotypic correlations of lifetime phobia diagnoses ranged from 0.55 (agoraphobia and social phobia, OR 10.95) to 0.06 (animal phobia and social phobia, OR 1.21). In the best fitting twin model, which did not include shared environmental factors, heritability estimates for the phobias ranged from 0.43 to 0.63. Comorbidity between the phobias was accounted for by two common liability factors. The first loaded principally on animal phobia and did not influence the complex phobias (agoraphobia and social phobia). The second liability factor strongly influenced the complex phobias, but also loaded weak to moderate on all the other phobias. Blood phobia was mainly influenced by a specific genetic factor, which accounted for 51% of the total and 81% of the genetic variance. CONCLUSIONS: Phobias are highly co-morbid and heritable. Our results suggest that the co-morbidity between phobias is best explained by two distinct liability factors rather than a single factor, as has been assumed in most previous multivariate twin analyses. One of these factors was specific to the simple phobias, while the other was more general. Blood phobia was mainly influenced by disorder specific genetic factors.

Family matters: happiness in nuclear families and twins.

Biometric studies have shown that happiness is strongly affected by genes. The findings are mainly based on twin data, however, and the full validity of the results has been debated. To overcome some limitations in classical twin research, we examined aetiological sources of subjective well-being (SWB), using two independent population-based samples, one including nuclear families (N = 54,540) and one including twins (N = 6,620). Biometric modelling using R was conducted to test for a data structure implying either non-additive genetic effects or higher environmental co-twin correlation in MZ than DZ pairs (violation of the EEA). We also estimated non-random mating, cultural transmission and shared environments specific for regular siblings and twins. Two sets of nested models were fitted and compared. The best explanatory model shows that family matters for happiness predominantly due to quantitative sex-specific genetic effects, a moderate spousal correlation and a shared twin environment. Upper limits for broad-sense heritability were estimated to be 0.33 (females) and 0.36 (males). Our study constitutes the most elaborate biometric study of SWB to date and illustrates the utility of including responses from multiple types of relatives in quantitative genetic analyses.

Does a higher educational level protect against anxiety and depression? The HUNT study.

The relationship of education to the experience of anxiety and depression throughout adult life is unclear. Our knowledge of this relationship is limited and inconclusive. The aim of this study was to examine (1) whether higher educational level protects against anxiety and/or depression, (2) whether this protection accumulates or attenuates with age or time, and (3) whether such a relationship appears to be mediated by other variables. In a sample from the Nord-Trøndelag Health Study 1995--1997 (HUNT 2) (N=50,918) of adults, the cross-sectional associations between educational level and symptom levels of anxiety and depression were examined, stratified by age. The long-term effects of educational level on anxiety/depression were studied in a cohort followed up from HUNT 1 (1984--1986) to HUNT 2 (N=33,774). Low educational levels were significantly associated with both anxiety and depression. The coefficients decreased with increasing age, except for the age group 65-74 years. In the longitudinal analysis, however, the protective effect of education accumulated somewhat with time. The discrepancy between these two analyses may be due to a cohort effect in the cross-sectional analysis. Among the mediators, somatic health exerted the strongest influence, followed by health behaviors and socio-demographic factors. Higher educational level seems to have a protective effect against anxiety and depression, which accumulates throughout life.

A short matrix-version of the Edinburgh Depression Scale.

OBJECTIVE: Given the importance of depression as a world health problem, depression assessment should be standard practice in large-scale health surveys. The aim of the study was to construct a short matrix-version of the Edinburgh Depression Scale (EDS) that can be used in questionnaire studies. METHOD: On the basis of the complete EDS scale of ten items, answered by 2730 women, stepwise multiple regression analysis was used to find the combination of items that explains the maximum proportion of the variance of the full scale sum score. The selected EDS items were thereafter correlated with the Hopkins Symptom Check List (SCL-25) for external validation. RESULTS: The sum of five selected items from the EDS correlated at r = 0.96 with the full version. The EDS-5 scores correlated strongly with the SCL-25 (r = 0.75). CONCLUSION: The EDS-5 version shows good psychometric properties and may, for some scientific purposes, substitute the full EDS scale.

Subjective well-being: genetic and environmental contributions to stability and change.

BACKGROUND: Previous cross-sectional studies have found substantial genetic influences on individual variation in subjective well-being (SWB), and evidence for sex-specific genetic effects has been reported. However, the genetic and environmental influences on stability and change in SWB over time are largely unexplored. METHOD: Questionnaire data on SWB from a population-based sample of Norwegian twins born 1967 to 1979, initially surveyed in 1992 (T1) and re-surveyed in 1998 (T2), were analysed using structural equation modelling to explore the relative effects of genetic and environmental influences on phenotypic stability and change. RESULTS: The phenotypic cross-time correlations for SWB were 0.51 and 0.49 for males and females respectively. The best-fitting longitudinal model specified only additive genetic and individual environmental effects with qualitative and quantitative sex-specific genetic influences. For both males and females, the additive genetic factors influencing SWB were largely stable, although some time-specific genetic contributions were indicated. Cross-time correlations for genetic effects were 0.85 and 0.78 for males and females respectively. The individual environmental influences were primarily time-specific. Additive genetic effects explained approximately 80% of the phenotypic cross-time correlation. For females, the magnitude of the additive genetic effects decreased significantly from T1 to T2, whereas for males, the estimates generally remained unchanged. CONCLUSIONS: For both males and females, long-term stability of SWB was mainly attributable to stable additive genetic factors, whereas susceptibility to change was mostly related to individual environmental factors. However, both stable environmental contributions and emerging genetic influences were indicated.

Psoriasis in Norway as observed in a population-based Norwegian twin panel.

BACKGROUND: Psoriasis is a chronic T-cell-mediated immunological skin disease. The occurrence of the disease appears to differ with geography and ethnicity. There is a need for epidemiological data obtained from defined population-based studies, and the sex-specific differences observed in the natural history of the disease require more attention. OBJECTIVES: To describe the occurrence and risk of psoriasis in Norway by age and sex. PATIENTS/METHODS: A population-based health survey was conducted in 1998 in Norwegian twins aged 19-31 years. The present study is based upon the self-reported history of psoriasis among the 8045 questionnaire responders. RESULTS: Altogether, 334 (4.2%) reported a positive history of psoriasis. There were no sex differences in the overall prevalence rates, but significantly higher point-prevalences emerged in females in the teenage-year intervals. A fairly linear increase in incidence rates by every 4-year age-interval peaked at a lower age in females. The mean age at onset was also significantly lower in females (14.8 years) than in males (17.3 years). The absolute risk of developing psoriasis appeared higher for females across the entire age range. However, by the age of 31 the cumulative risks were similar in females and males (0.056 and 0.053, respectively). CONCLUSIONS: In this historical cohort of Norwegian twins, we find a high prevalence of psoriasis in congruence with previously reported data among whites in north-western Europe. We have found sex-specific characteristics in point-prevalences and incidence rates which may contribute to the understanding of the earlier age at onset of the disease in females.

The Nord-Trøndelag Norway Audiometric Survey 1996-98: unscreened thresholds and prevalence of hearing impairment for adults > 20 years.

As supplement to a general health screening examination (HUNT-II), we conducted a puretone audiometry study in 1996-98 on adults (>20 years) in 17 of 23 municipalities in Nord-Trøndelag, Norway, including questionnaires on occupational and leisure noise exposure, medical history, and symptoms of hearing impairment. The study aims to contribute to updated normative hearing thresholds for age and gender, while evaluating the effects of noise exposure, medical history, and familial or genetic influences on hearing. This paper presents the unscreened hearing threshold data and prevalence of hearing impairment for different age groups and by gender. Valid audiometric data were collected from 62% (n=50,723) of 82,141 unscreened invited subjects (age-range 20-101 years, mean=50.2 years, SD=17.0 years). Two ambulant audiometric teams each conducted 5 parallel self-administered, pure-tone hearing threshold examinations with the standard test frequencies 0.25-0.5-1-2-3-4-6-8 kHz (manual procedure when needed). Tracking audiometers were used in dismountable booths with in-booth noise levels well within ISO criteria, except being at the criterion around 200 Hz. The data were electronically transferred to a personal computer. Test-retest correlations for 99 randomly drawn subjects examined twice were high. The mean thresholds recorded were some dB elevated from "audiometric zero" even for age group 20-24 years. As also found in other studies, this might indicate too restrictive audiometric reference thresholds. Males had slightly better hearing < or =0.5 kHz for all age groups. Mean thresholds were poorer in males > or = 30 years from > or =2 kHz, with maximal gender differences of approximately 20 dB at 3-4 kHz for subjects aged 55-74 years. Weighted prevalence data averaged over 0.5-1-2-4 kHz showed hearing impairment >25 dB hearing threshold level of 18.8% (better ear) and 27.2% (worse ear) for the total population--for males 22.2% and 32.0%, for females 15.9% and 23.0%, respectively. Mean hearing loss > or =10 dB at 6 kHz registered for both genders even in age groups 20-24 years may be partly due to calibration artefacts, but might possibly also reflect noise-related socio-acusis.

Depression during pregnancy and after delivery: a repeated measurement study.

The aim of this study was to examine the risk of depression in the postpartum period (first four months after delivery) as compared to the remaining postnatal year and the pregnancy period. All postpartum women from two municipalities in Norway were included in a questionnaire study of mental health (n = 416). Over 50% of the women (n = 259) answered an identical questionnaire at an additional time either before or after the postpartum period. The level of depression was measured by the Edinburgh Postnatal Depression Scale (EPDS) and the Hopkins Symptom Check List-25 items (SCL-25). The point prevalence of depression (EPDS> or =10) in the first four months postpartum did not differ significantly as compared to other time periods during pregnancy and the postnatal year. This finding remained also after controlling for other risk factors of depression; high score on the life event scale, prior depression and poor partner relationship. There was a non-significant trend of lower prevalence of depression during early pregnancy and after the first eight postnatal months. In conclusion, our findings suggest that the first four months postpartum were not distinguished by higher depression prevalence as compared to other time periods during pregnancy and the first postnatal year.

Gender differences in binge-eating: a population-based twin study.

OBJECTIVE: To assess whether genetic and environmental effects on liability to binge-eating (BE) are of equal importance for males and females and whether the same genetic risk factors predispose to BE in the two sexes. METHOD: Questionnaire data on 8045 same sex and opposite sex twins, aged 19-31 years, from a population-based Norwegian registry, was used to estimate the relative contribution of genetic and environmental factors to liability for BE utilizing structural equation modeling. RESULTS: In the best-fitting model, the magnitude of genetic and environmental effects on BE was the same for males and females. Heritability was 51%. The correlation between genetic risk factors in men and women was estimated to be +0.57. CONCLUSION: Binge-eating appears to be equally heritable in males and females. Although the majority of the genetic risk factors are shared between the sexes, there may exist gender-specific genetic effects on liability.

Depression in postpartum and non-postpartum women: prevalence and risk factors.

OBJECTIVE: The aim of the study was to assess the prevalence of depression in postpartum women as compared with non-postpartum women, and to identify risk factors of depression in both groups. METHOD: A population based questionnaire study was performed among women 18-40 years in two municipalities in Norway in 1998-1999. A total of 2,730 women were included, of whom 416 were in the postpartum period. RESULTS: The prevalence of depression was higher in non-postpartum as compared with postpartum women. High scores on the life event scale, a history of depression and a poor relationship to the partner were associated with depression in both postpartum and non-postpartum women. When controlling for the identified risk factors of depression the odds-ratio for depression in the postpartum period was 1.6 (95% CI: 1.0-2.6). CONCLUSION: The risk for depression was increased in the postpartum period, when controlling for the uneven distribution of risk factors.

Back-neck pain and symptoms of anxiety and depression: a population-based twin study.

BACKGROUND: Clinical and epidemiological studies have shown an association between anxiety and depression and pain in the back and neck. The nature of this relationship is not clear. This study aimed to investigate the extent to which common genetic and environmental aetiological factors contribute to the covariance between symptoms of anxiety and depression and back-neck pain. METHODS: Measures of back-neck pain and symptoms of anxiety and depression were part of a self-report questionnaire sent in 1992 to twins born in Norway between 1967 and 1974 (3996 pairs). Structural equation modelling was applied to determine to what extent back-neck pain and symptoms of anxiety and depression share genetic and environmental liability factors. RESULTS: The phenotypic correlation between symptoms of anxiety and depression and back-neck pain was 0.31. Individual differences in both anxiety and depression and back-neck pain were best accounted for by additive genetic and individual environmental factors. Heritability estimates were 0.53 and 0.30 respectively. For back-neck pain, however, a model specifying only shared- and individual environmental effects could not be rejected. Bivariate analyses revealed that the correlation between back-neck pain and symptoms of anxiety and depression was best explained by additive genetic and individual environmental factors. Genetic factors affecting both phenotypes accounted for 60% of the covariation. There were no significant sex differences. CONCLUSION: The results support previous findings of a moderate association between back-neck pain and symptoms of anxiety and depression, and suggest that this association is primarily due to common genetic effects.

Child related strain and maternal mental health: a longitudinal study.

OBJECTIVE: To explore how normal age-related behaviour patterns and medical status affect maternal mental health in children aged 1.5-4 years. METHOD: Data were collected via questionnaires from a population-based sample. Outcome variable was the Hopkins Symptom Checklist (HSCL-25). Multiple regression analyses were used to assess the extent to which changes in the predictors (sociodemographic variables, chronic strains, negative life events, maternal somatic health and social support) explained changes in maternal distress. RESULTS: Changes in strain related to children and child care-taking predicted changes in maternal mental distress stronger than the other explanatory variables. Only effects of changes in child care-taking were significant for both time periods. CONCLUSION: Changes in maternal symptoms of anxiety and depression appear to be influenced by changes associated with children's behaviour, their medical status and child care-taking arrangements.

Review of validation studies of the Edinburgh Postnatal Depression Scale.

OBJECTIVE: To review validation studies of the Edinburgh Postnatal Depression Scale (EPDS). METHOD: A systematic search was performed in Medline and the Science Citation Index Expanded (ISI) from the period 1987-2000. For sensitivity and specificity of the EPDS presented in each study, 95% confidence intervals were estimated. Positive and negative predictive values were estimated assuming prevalences of postpartum depression ranging from 5% to 20%. RESULTS: Eighteen validation studies were identified. The study design varied between studies. The sensitivity and specificity estimates also varied: 65-100% and 49-100%, respectively. The confidence intervals were estimated to be wide. Our estimates suggest a lower positive predictive value in a normal population than in the validation study samples. CONCLUSION: Most studies show a high sensitivity of the EPDS. Because of the differences in study design and large confidence intervals, uncertainty remains regarding the comparability between the sensitivity and specificity estimates of the different EPDS versions.