A longitudinal study of personality and major depression in a population-based sample of male twins

2007 ◽  
Vol 37 (8) ◽  
pp. 1163-1172 ◽  
Author(s):  
AYMAN H. FANOUS ◽  
MICHAEL C. NEALE ◽  
STEVEN H. AGGEN ◽  
KENNETH S. KENDLER

ABSTRACTBackgroundThe relationship between personality and psychiatric illness is complex. It is not clear whether one directly causes the other.MethodIn a population-based sample of male twins (n=3030), we attempted to predict major depression (MD) from neuroticism (N) and extraversion (E) and vice versa, to evaluate the causal, scar, state, and prodromal hypotheses. In a longitudinal, structural equation twin model, we decomposed the covariation between N and MD into (a) genetic and environmental factors that are common to both traits, as well as specific to each one and (b) direct causal effects of N at time 1 on subsequent MD, as well as between MD and subsequent N.ResultsE was negatively correlated with lifetime and one-year prevalence of MD. N predicted the new onset of MD, and was predicted by both current and past MD. It did not predict the time to onset of MD. All of the covariation between N and MD was due to additive genetic and individual-specific environmental factors shared by both traits and a direct causal path between MD and N assessed later. No genetic factors were unique to either trait.ConclusionsIn men, N may be a vulnerability factor for MD but does not cause it directly. However, MD may have a direct causal effect on N. The genetic overlap between N and MD in men may be greater than in women.

2011 ◽  
Vol 41 (9) ◽  
pp. 1987-1995 ◽  
Author(s):  
N. Czajkowski ◽  
K. S. Kendler ◽  
K. Tambs ◽  
E. Røysamb ◽  
T. Reichborn-Kjennerud

BackgroundTo explore the genetic and environmental factors underlying the co-occurrence of lifetime diagnoses of DSM-IV phobia.MethodFemale 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.ResultsPhenotypic 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.ConclusionsPhobias 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.


1992 ◽  
Vol 22 (3) ◽  
pp. 617-622 ◽  
Author(s):  
Ellen E. Walters ◽  
Michael C. Neale ◽  
Lindon J. Eaves ◽  
Andrew C. Heath ◽  
Ronald C. Kessler ◽  
...  

SynopsisA genetic analysis of the co-occurrence of bulimia and major depression (MD) was performed on 1033 female twin pairs obtained from a population based register. Personal interviews were conducted and clinical diagnoses made according to DSM-III-R criteria.Additive genes, but not family environment, are found to play an important aetiological role in both bulimia and MD. The genetic liabilities of the two disorders are correlated 0·456. While unique environmental factors account for around half of the variation in liability to both bulimia and MD, these risk factors appear to be unrelated, i.e., each disorder has its own set of unique environmental risk factors. Thus, the genetic liability of bulimia and MD is neither highly specific nor entirely nonspecific. There is some genetic correlation between the two disorders as well as some genetic and environmental risk factors unique to each disorder. Limitations and directions for future research are discussed.


2003 ◽  
Vol 33 (5) ◽  
pp. 817-825 ◽  
Author(s):  
K. S. KENDLER ◽  
S. H. AGGEN ◽  
K. C. JACOBSON ◽  
M. C. NEALE

Background. While the family environment can directly influence later risk for psychopathology, dysfunction in the family of origin may also moderate the impact of genetic factors on liability for psychiatric disorders. Can a similar pattern be seen for the personality trait of Neuroticism (N) – which is a risk factor for many psychiatric conditions?Method. Our sample of 957 complete female–female twin pairs from a population-based register had measures of self-reported N and multiple reporters (twin, co-twin, mother, father) for family dysfunction (FD). Statistical analysis was conducted by traditional regression analysis and a moderator structural equation twin model operationalized in the computer program Mx.Results. Dividing the sample into quartiles based on increasing levels of FD, the mean of N increased substantially while correlations of N in monozygotic (MZ) and dizygotic (DZ) twins were relatively constant. Regression analyses did not suggest greater twin resemblance for N with increasing levels of FD. The best-fit structural equation model was the standard un-moderated model in which the proportion of variance in N due to genetic (39%) and unique environmental effects (61%) remained constant across values of FD.Conclusions. Although a false-negative result due to limited power cannot be excluded, these analyses do not support the hypothesis that FD moderates the impact of genetic factors on levels of N.


2020 ◽  
Vol 14 (12) ◽  
pp. 1662-1671
Author(s):  
Kimberley W J van der Sloot ◽  
Rinse K Weersma ◽  
Behrooz Z Alizadeh ◽  
Gerard Dijkstra

Abstract Background and Aims Multiple genetic and environmental factors are involved in the aetiology of inflammatory bowel disease [IBD] including Crohn’s disease [CD] and ulcerative colitis [UC], but data on these exposome factors are difficult to identify. Several exposome factors such as smoking have been shown to be involved; as for other environmental factors, eg stress, results have been conflicting. Methods We performed a case-control study including 674 IBD patients of the 1000IBD cohort, frequency-matched based on sex and age with 1348 controls from the population-based Lifelines Cohort Study. Exposome data were obtained using the validated Groningen IBD Environmental Questionnaire [GIEQ], capturing exposome factors through different stages of life using 844 items, of which 454 were applicable to study the role of 93 exposome factors in disease aetiology. Logistic regression [LR] modelling with Bonferroni correction for multiple testing was applied to estimate the multivariable-adjusted effect of each exposome factor. Results For IBD, we identified four novel factors: stressful life events (CD odds ratio [OR] 2.61/UC OR 2.92), high perceived stress [2.29/2.67], alcohol use [0.40/0.43], and bronchial hyper-reactivity [3.04/2.36]. Four novel factors were associated with only CD: prenatal smoke exposure [1.89], having a bed partner [0.53], allergies [2.66], and cow’s milk hypersensitivity [5.87]; and two solely with UC: carpet flooring [0.57] and neuroticism [1.32]. Nine factors were replicated. Conclusions In this study we identified 10 novel, and replicated nine previously reported, exposome factors associated with IBD. Identifying these factors is important for both understanding disease aetiology and future prevention strategies to decrease the development of IBD in genetically susceptible persons.


Author(s):  
Eunjung Kim ◽  
Ho-jang Kwon ◽  
Mina Ha ◽  
Ji-Ae Lim ◽  
Myung Lim ◽  
...  

Although studies have shown that a low socioeconomic status (SES) is associated with high blood lead levels (BLLs) in children, the mechanism underlying this observation is not well known. To determine how SES influences BLLs via environmental factors in Korean children, we conducted a population-based cross-sectional study of 4744 children aged 5–13 years. Questionnaires on sociodemographic information, environmental factors, and food consumption were administered to the children’s parents. BLLs in the study subjects were measured.The complete set of hypothesized associations was assessed using regression analysis and structural equation modeling. SES was associated with high BLLs. The total effects of nutritional factors, lead in the air and total length of nearby roads, and agriculture on BLLs were −0.062 (p < 0.001), 0.068 (p = 0.005), and 0.038 (p = 0.035), respectively. The direct effects of playing outdoors and SES on BLLs were 0.113 (p < 0.001) and −0.111 (p < 0.001), respectively. Although playing outdoors had a greater direct effect on BLLs than did SES, the total effect of SES (standardized β = −0.132, p < 0.001) was greater than that of other sources owing to indirect effects (β = −0.020, p = 0.004). A low SES was a major risk factor for elevated BLLs via environmental factors.


2006 ◽  
Vol 9 (3) ◽  
pp. 431-437 ◽  
Author(s):  
Anu Raevuori ◽  
Anna Keski-Rahkonen ◽  
Richard J. Rose ◽  
Aila Rissanen ◽  
Jaakko Kaprio

AbstractIn the population-based FinnTwin16 study, proportions of genetic and environmental factors contributing to muscle dissatisfaction and muscle-enhancing substance use were assessed in 319 pairs of twin brothers: 141 monozygotic (MZ) and 178 dizygotic (DZ) pairs. In addition there were 86 twin individuals from pairs in which only one co-twin responded. Of all respondents, 30% experienced high muscle dissatisfaction. The corresponding proportion of muscle-enhancing substance use was 10%. The subjects were similar in age (23.8 years, 95% confidence interval [CI] 23.76–23.84), body mass index (23.7, 95% CI 23.5–23.9), and waist circumference (84.5 cm, 95% CI 83.7–85.2), independent of their muscle dissatisfaction or muscle-enhancing substance use status and independent of their zygosity. The MZ polychoric correlation for muscle dissatisfaction was .39 (95% CI .17–.58) and .27 for DZ pairs (95% CI .07–.46). The MZ tetrachoric correlation for muscle-enhancing substance use was .65 (95% CI .28–.87) and .56 for DZ pairs (95% CI .26–.78). The AE model, where additive genetic factors (A) accounted for 42% (95% CI .23–.59) and unique environmental factors (E) 58% (95% CI .41–.77) of the liability, provided the best fit for muscle dissatisfaction. The CE model, where common environmental factors (C) accounted for 60% (95% CI .37–.77) and unique environmental factors (E) 40% (95% CI .23–.63) of the liability, provided the best fit for muscle-enhancing substance use. Both genetic and unique (nonfamilial) environmental factors are involved in muscle dissatisfaction in the population. Nongenetic factors (both familial and non-familial) appear to best explain the use of muscle-enhancing substances.


2004 ◽  
Vol 34 (7) ◽  
pp. 1263-1269 ◽  
Author(s):  
KENNETH S. KENDLER ◽  
STEVEN H. AGGEN ◽  
CAROL A. PRESCOTT ◽  
KRISTEN C. JACOBSON ◽  
MICHAEL C. NEALE

Background. An adoption study of alcoholism suggests that in women, the impact of genetic risk factors become greater in the presence of conflict in the family of origin. Is the same true for cigarette smoking (CS)?Method. We obtained, in a sample of 1676 twins from female–female twin pairs from a population-based register, a measure of maximum lifetime CS (divided into six ordinal categories) and family dysfunction (FD) assessed as the mean report of up to four informants (twin, co-twin, mother, father). Statistical analysis was conducted by traditional regression analysis and a moderator structural equation twin model using the computer program Mx.Results. With increasing levels of FD, maximum CS increased substantially while correlations for CS in monozygotic (MZ) and dizygotic (DZ) twins decreased modestly. Regression analyses demonstrated reduced twin-pair resemblance for CS with increasing levels of FD. The best-fit structural equation model found high levels of heritability for CS and no evidence for a role of shared environment. With increasing levels of FD, the proportion of variance in CS due to genetic factors (i.e. heritability) decreased while that due to unique environmental effects increased.Conclusions. Several different statistical methods suggested that, contrary to prediction, heritability of CS decreased rather than increased with higher levels of dysfunction in the family of origin. The hypothesis that genetic effects for psychiatric and drug-use disorders become stronger in more adverse environments is not universally true.


2000 ◽  
Vol 6 (2) ◽  
pp. 115-120 ◽  
Author(s):  
Scott B Patten ◽  
Luanne M Metz ◽  
Marlene A Reimer

The objective of this paper was to evaluate the lifetime and point prevalence of major depression in a population-based Multiple Sclerosis (MS) clinic sample, and to describe associations between selected biopsychosocial variables and the prevalence of lifetime major depression in this sample. Subjects who had participated in an earlier study were re-contacted for additional data collection. Eighty-three per cent (n=136) of those eligible consented to participate. Each subject completed the Composite International Diagnostic Interview (CIDI) and an interviewer-administered questionnaire evaluating a series of biopsychosocial variables. The lifetime prevalence of major depression in this sample was 22.8%, somewhat lower than previous estimates in MS clinic populations. Women, those under 35, and those with a family history of major depression had a higher prevalence. Also, subject reporting high levels of stress and heavy ingestion of caffeine (>400 mg) had a higher prevalence of major depression. As this was a cross-sectional analysis, the direction of causal effect for the observed associations could not be determined. By identifying variables that are associated with lifetime major depression, these data generate hypotheses for future prospective studies. Such studies will be needed to further understand the etiology of depressive disorders in MS.


1992 ◽  
Vol 22 (1) ◽  
pp. 85-100 ◽  
Author(s):  
K. S. Kendler ◽  
J. L. Silberg ◽  
M. C. Neale ◽  
R. C. Kessler ◽  
A. C. Heath ◽  
...  

SYNOPSISSymptoms during the premenstrual and menstrual phases of the female reproductive cycle were assessed in 827 pairs of female same-sex twins from a population-based registry. By conventional factor analysis, premenstrual and menstrual symptoms were relatively independent of one another and of baseline ‘neurotic’ symptoms (i.e. anxiety, depression and somatization). Familial resemblance for menstrual and premenstrual symptoms was due solely to genetic factors with heritability estimates of 39·2% and 35·1%, respectively. Multivariate genetic analysis revealed distinct genetic and environmental factors for menstrual, premenstrual and neurotic symptoms. The genes and individual-specific experiences that predispose to premenstrual symptoms appear to be largely distinct from those which predispose either to menstrual or to neurotic symptoms. The generalizability of these results may be limited because only a modest number of premenstrual and menstrual symptoms were assessed, all by retrospective self-report.


2001 ◽  
Vol 44 (2-3) ◽  
pp. 167-178 ◽  
Author(s):  
Marianne Juel Kjeldsen ◽  
Kirsten Ohm Kyvik ◽  
Kaare Christensen ◽  
Mogens Laue Friis

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