The Genetic and Environmental Structure of the Covariation Among the Symptoms of Insomnia, Fatigue, and Depression in Adult Females

2012 ◽  
Vol 15 (6) ◽  
pp. 720-726 ◽  
Author(s):  
Yoon-Mi Hur ◽  
Andrea Burri ◽  
Tim D. Spector

Although the co-occurrence among symptoms of insomnia, fatigue, and depression has been frequently reported, the etiology of this co-occurrence remains poorly understood. A total of 3,758 adult female twins in the United Kingdom completed a mail-out survey including six questions concerning frequency and severity of symptoms of insomnia, fatigue, and depression. Correlations among the scores of the three symptoms ranged from 0.35 to 0.44. Among various multivariate models we tested, the common-pathway model explained the data best. In the best-fitting model, the common factor was explained approximately equally by genetic and unique environmental factors (49% and 51%, respectively). In addition to the common variance, there was a significant specific variance in each symptom, where unique environmental factors were much larger than genetic factors. These results imply that although there are shared genetic liabilities for the development of symptoms of depression, fatigue, and insomnia, it is environmental experiences that make etiological distinctions among three symptoms.

Twin Research ◽  
2000 ◽  
Vol 3 (4) ◽  
pp. 266-276 ◽  
Author(s):  
F Sluyter ◽  
JN Keijser ◽  
DI Boomsma ◽  
LJP van Doornen ◽  
EJCG van den Oord ◽  
...  

AbstractThe aim of this study was to determine the genetic contribution to the variation in testosterone and the aggression-hostility-anger (AHA) syndrome in middle-aged twins. Moreover, the relation between testosterone and this syndrome, and possible common genetic mechanisms were investigated. Towards this end, blood samples were collected at two time points; the AHA syndrome was measured using three questionnaires: the Buss-Durkee Hostility Inventory with seven subscales, the Jenkins Activity Survey and the Spielberger State-Trait Anger Scale. The results showed substantial heritabilities for testosterone (approximately 60%) and moderate to fair heritabilities for the nine measures of the AHA syndrome (23–53%). The best fitting model for testosterone at two time points included a small age component and additive genetic and unique environmental factors, while a multivariate analysis of the nine AHA subscales resulted in an independent pathway model with two common additive genetic and two common unique environmental factors. No correlation between the common genetic factor influencing testosterone and the AHA subscales was found. We did, however, detect a negative correlation between the common environmental factor underlying testosterone and both common environmental factors influencing the nine AHA subscales, which may reflect a tendency for testosterone levels to rise and hostility to drop (or vice versa) after repeatedly experiencing success (or failure). Twin Research (2000) 3, 266–276.


2015 ◽  
Vol 18 (5) ◽  
pp. 545-556 ◽  
Author(s):  
Tetsuya Kawamoto ◽  
Toshihiko Endo

We examined developmental trends and sources of stability and change in adolescent personality by using twin data collected from 1981 to 2010 (273 monozygotic (MZ) and 48 dizygotic (DZ) twin pairs) from a secondary school affiliated with the University of Tokyo. Phenotypic analyses showed high rank-order stability and substantial mean-level increases in neuroticism and declines in extraversion over the adolescent years. Longitudinal bivariate genetic analyses revealed that the best-fitting model for adolescent personality includes additive genetic and non-shared environmental influences. Heritability estimates ranged approximately from 0.30 to 0.60. Additionally, three-year stability in adolescent personality was influenced mainly by genetic factors, and there were both genetic and environmental innovations in mid-adolescence. Our findings suggest that both genetic and environmental effects have significant roles in the etiology of personality development across adolescence.


2012 ◽  
Vol 15 (4) ◽  
pp. 473-482 ◽  
Author(s):  
Jocilyn E. Bergin ◽  
Kenneth S. Kendler

Background: Previous studies examined caffeine use and caffeine dependence and risk for the symptoms, or diagnosis, of psychiatric disorders. The current study aimed to determine if generalized anxiety disorder (GAD), panic disorder, phobias, major depressive disorder (MDD), anorexia nervosa (AN), or bulimia nervosa (BN) shared common genetic or environmental factors with caffeine use, caffeine tolerance, or caffeine withdrawal. Method: Using 2,270 women from the Virginia Adult Twin Study of Psychiatric and Substance Use Disorders, bivariate Cholesky decomposition models were used to determine if any of the psychiatric disorders shared genetic or environmental factors with caffeine use phenotypes. Results: GAD, phobias, and MDD shared genetic factors with caffeine use, with genetic correlations estimated to be 0.48, 0.25, and 0.38, respectively. Removal of the shared genetic and environmental parameter for phobias and caffeine use resulted in a significantly worse fitting model. MDD shared unique environmental factors (environmental correlation = 0.23) with caffeine tolerance; the genetic correlation between AN and caffeine tolerance and BN and caffeine tolerance were 0.64 and 0.49, respectively. Removal of the genetic and environmental correlation parameters resulted in significantly worse fitting models for GAD, phobias, MDD, AN, and BN, which suggested that there was significant shared liability between each of these phenotypes and caffeine tolerance. GAD had modest genetic correlations with caffeine tolerance, 0.24, and caffeine withdrawal, 0.35. Conclusions: There was suggestive evidence of shared genetic and environmental liability between psychiatric disorders and caffeine phenotypes. This might inform us about the etiology of the comorbidity between these phenotypes.


2008 ◽  
Vol 11 (3) ◽  
pp. 266-274 ◽  
Author(s):  
Sarah E. Bergen ◽  
Charles O. Gardner ◽  
Steven H. Aggen ◽  
Kenneth S. Kendler

AbstractThe negative social attributes associated with drug use and abuse/dependence may arise as a result of shared genetic or environmental factors rather than through causal pathways. To evaluate this possibility, structured interviews were conducted for 3969 male and female twins from the Mid-Atlantic Twin Registry and evaluations of their socioeconomic status (SES), social interactions, and use of drugs were obtained. Drug involvement was categorized as never used, tried, or met criteria for abuse or dependence. A co-twin control design was implemented using hierarchical linear modeling to assess whether twins who used drugs experienced lower SES and social support than non-using co-twins. Poorer social functioning in the drug-exposed twin is consistent with a causal relationship, while similar functioning in the drug exposed versus naive twins imply shared genetic or common environmental factors. Use of drugs was not significantly related to any SES measures. However, education and job status appear to share genetic influences with drug abuse/dependence. Lower income was not related to abuse/dependence of drugs. Negative interactions with friends and relatives share genetic factors with use of drugs, but the escalation from trying drugs to abusing them appears to generate discord between the abuser and friends and relatives in a causal fashion. These results indicate that presumptive causal influences of drug abuse/dependence on low SES may actually be mediated by shared genes. Drug use and social discord also appear to have shared genetic factors, but increased levels of drug involvement seem to causally influence social interactions.


2004 ◽  
Vol 34 (7) ◽  
pp. 1271-1277 ◽  
Author(s):  
TED REICHBORN-KJENNERUD ◽  
ESPEN RØYSAMB ◽  
KRISTIAN TAMBS ◽  
SVENN TORGERSEN ◽  
EINAR KRINGLEN ◽  
...  

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.


2019 ◽  
Vol 27 (1) ◽  
pp. 113-139
Author(s):  
Min A Lee ◽  
Kook Hyun Chang

This paper tries to estimate the dynamic linear latent factor model (DLLFM) with jump in order to find jump risk, heteroscedasticity and time varying correlations in Global REITs Markets. Using five major Global Reits rates such as the United States, Japan, the United Kingdom, Australia and Hong Kong form January 4, 2000 to June 29, 2018, this study finds the evidence of common factor and time-varying correlations in addition to the country-specific idiosyncratic risk. According to the main estimated results of this paper, approximately 60% of the common factors of global REITs market risk. Can be explained by global stock markets. Second, REITs market integration among five countries seems to have been increasing gradually since Global Financial Crisis.


2005 ◽  
Vol 8 (1) ◽  
pp. 53-59 ◽  
Author(s):  
Andreas Wienke ◽  
Anne M. Herskind ◽  
Kaare Christensen ◽  
Axel Skytthe ◽  
Anatoli I. Yashin

AbstractCause-specific mortality data on Danish monozygotic and dizygotic twins are used to analyze heritability estimates of susceptibility to coronary heart disease (CHD) after controlling for smoking and Body Mass Index (BMI). The sample includes 1209 like-sexed twin pairs born between 1890 and 1920, where both individuals were still alive in 1966. The participants completed a questionnaire in 1966 which included questions on smoking, height and weight. The analysis was conducted with both sexes pooled due to the relatively small number of twin pairs. Follow-up was conducted from January 1, 1966 to December 31, 1993. The correlated gammafrailty model with observed covariates was used for the genetic analysis of frailty to account for censoring and truncation in the lifetime data. During the follow-up, 1437 deaths occurred, including 435 deaths due to CHD. Proportions of variance of frailty attributable to genetic and environmental factors were analyzed using the structural equation model approach. Different standard biometric models are fitted to the data to evaluate the magnitude and nature of genetic and environmental factors on mortality. Using the best-fitting model without covariates, heritability of frailty to CHD was found to be 0.45 (0.11). This result changes only slightly to 0.55 (0.13) in a DE model after controlling for smoking and BMI. This analysis underlines the existence of a substantial genetic influence on individual frailty associated with mortality caused by CHD.


2009 ◽  
Vol 19 (1) ◽  
pp. 32-38 ◽  
Author(s):  
Wing Chi Choy ◽  
Sandra López-León ◽  
Yurii S. Aulchenko ◽  
Johan P. Mackenbach ◽  
Ben A. Oostra ◽  
...  

2013 ◽  
Vol 16 (2) ◽  
pp. 575-580 ◽  
Author(s):  
Lucia Colodro-Conde ◽  
Juan F. Sánchez-Romera ◽  
Juan R. Ordoñana

Breastfeeding is considered the best and most natural way of feeding infants during the first months of life. Breastfeeding has multiple short- and long-term benefits for the health of the mother and babies, and from an evolutionist standpoint, it would be a behavior worth preserving throughout time. The aim of the present study was to explore the relative influence of genetic and environmental factors in this behavior. Three hundred and ninety pairs of adult female twins provided information about whether they breastfed their children and for how long. Three variables were analyzed: initiation and duration for the first baby, and mean duration for the complete offspring. Polychoric correlations were consistently higher for monozygotic twins, supporting a role for genetic factors (0.49 vs. 0.22 for initiation; 0.44 vs. 0.22 for duration in the first newborn; and 0.52 vs. 0.31 for duration on average). Model-fitting analyses found that in the best-fitting model, variance was explained by additive genetic and non-shared environmental factors, with estimated heritabilities ranging from 0.39 to 0.52 in the measures studied. The rest of the variance would be due to unique environmental factors. We conclude that genetic factors have a significant impact on the complex behavior of breastfeeding.


2008 ◽  
Vol 11 (1) ◽  
pp. 44-47 ◽  
Author(s):  
Philip A. Vernon ◽  
Rod A. Martin ◽  
Julie Aitken Schermer ◽  
Lynn F. Cherkas ◽  
Tim D. Spector

AbstractOne thousand and seventy three pairs of adult monozygotic (MZ) twins and 895 pairs of same sex adult dizygotic (DZ) twins from the United Kingdom (UK) completed the Humor Styles Questionnaire: a 32-item measure which assesses two positive and two negative styles of humor. MZ correlations were approximately twice as large as DZ correlations for all four humor styles, and univariate behavioral genetic model fitting indicated that individual differences in all of them can be accounted for entirely by genetic and nonshared environmental factors, with heritabilities ranging from .34 to .49. These results, while perhaps not surprising, are somewhat at odds with a previous study that we conducted in North America (Vernon et al., in press) in which genetic factors contributed significantly to individual differences in the two positive humor styles, but contributed far less to the two negative styles, variance in which was instead largely due to shared and nonshared environmental factors. We suggest that differences between North American and UK citizens in their appreciation of different kinds of humor may be responsible for the different results obtained in these two studies.


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