A Twin study of Individuals with both Schizophrenia and Alcoholism

1985 ◽  
Vol 147 (1) ◽  
pp. 48-53 ◽  
Author(s):  
Kenneth S. Kendler

SummarySubstantial evidence suggests that genetic factors contribute to the aetiology of both schizophrenia and alcoholism, when they occur alone. To examine the role of genetic factors in schizophrenia and alcoholism when they occur together in the same individual, the frequency of both conditions was investigated in the co-twins of 34 monozygotic (MZ) and 47 dizygotic (DZ) index twins with a diagnosis of both schizophrenia and alcoholism. Both disorders alone were significantly more common in the MZ than in the DZ co-twins, suggesting that individuals suffering from schizophrenia and alcoholism have a genetic predisposition to both disorders, which is of the same nature as that which causes the two when they occur alone. In the co-twins of the MZ index twins, the diagnoses of schizophrenia and alcoholism were uncorrelated, indicating that the specific environmental factors of causal importance in the two disorders are not closely related.

2015 ◽  
Vol 70 (5) ◽  
pp. 647-653 ◽  
Author(s):  
Renata Bogo ◽  
Ahmed Farah ◽  
Ann-Christin Johnson ◽  
Kjell K. Karlsson ◽  
Nancy L. Pedersen ◽  
...  
Keyword(s):  

1979 ◽  
Vol 134 (4) ◽  
pp. 343-351 ◽  
Author(s):  
Svenn Torgersen

SummaryBy means of a twin study an attempt was made to throw light upon the aetiology and nosology of phobic fears. Factor analyses revealed five factors, namely separation fears, animal fears, mutilation fears, social fears and nature fears. The study demonstrated that, apart from separation fears, genetic factors play a part in the strength as well as content of phobic fears. Environmental factors, affecting the development of dependence, reserve and neurotic traits generally, seemed also to be of some importance. It was further demonstrated that phobic fears were related to emotional and social adjustment and this was true to an even greater extent for separation fears.


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.


2009 ◽  
Vol 41 (3) ◽  
pp. 142-147 ◽  
Author(s):  
M. Dirani ◽  
M. Chamberlain ◽  
T.A. Couper ◽  
R.H. Guymer ◽  
P.N. Baird

2008 ◽  
Vol 22 (2) ◽  
pp. 143-153 ◽  
Author(s):  
Steven Taylor ◽  
Kerry L. Jang ◽  
Murray B. Stein ◽  
Gordon J. G. Asmundson

The leading contemporary cognitive-behavioral model of excessive health anxiety (HA) emphasizes the importance of environmental factors, such as learning experiences. The model has little to say about the role of genetic factors and, by ignoring these factors, seems to imply that they are unimportant. In contrast, results from the University of British Columbia Twin Study, using a sample of 88 monozygotic and 65 dizygotic twin pairs, indicated that various facets of HA, such as excessive disease fear, unrealistic beliefs that one has a serious disease, and HA-related interference in functioning, are moderately heritable. The present study extended the analyses of this data set by investigating the extent to which the various facets of HA are due to genetic or environmental factors that are common to all facets versus specific to each facet. Results indicated that all facets of HA are influenced by a common set of genes—there was very little evidence of facet-specific genetic influences. There was considerably stronger evidence for facet-specific environmental influences, where each facet is strongly influenced by environmental experiences that are specific to that facet. However, there was also evidence that particular environmental influences—especially those that shape disease conviction—also influence some of the other HA facets (fear and interference). The importance of environmental factors is consistent with the cognitive-behavioral model of HA, although the model needs to be refined to account for the role of genetic factors. Possibilities for refining the model are discussed, along with promising research directions to better understand the role of genes and the environment in HA.


2017 ◽  
Vol 2017 ◽  
pp. 1-7 ◽  
Author(s):  
Cheng Hu ◽  
Li Wen ◽  
Lihui Deng ◽  
Chenlong Zhang ◽  
Aurelia Lugea ◽  
...  

Background. Environmental factors and genetic mutations have been increasingly recognized as risk factors for chronic pancreatitis (CP). ThePRSS1p.R122H mutation was the first discovered to affect hereditary CP, with 80% penetrance. We performed here a systematic review and meta-analysis to evaluate the associations ofPRSS1p.R122H mutation with CP of diverse etiology.Methods. The PubMed, EMBASE, and MEDLINE database were reviewed. The pooled odds ratio (OR) with 95% confidence intervals was used to evaluate the association of p.R122H mutation with CP. Initial analysis was conducted with all etiologies of CP, followed by a subgroup analysis for hereditary and nonhereditary CP, including alcoholic or idiopathic CP.Results. A total of eight case-control studies (1733 cases and 2415 controls) were identified and included. Overall,PRSS1p.R122H mutation was significantly associated with an increased risk of CP (OR = 4.78[1.13–20.20]). Further analysis showed p.R122H mutation strongly associated with the increased risk of hereditary CP (OR = 65.52[9.09–472.48]) but not with nonhereditary CP, both alcoholic and idiopathic CP.Conclusions. Our study showing the differential role of p.R122H mutation in various etiologies of CP indicates that this complex disorder is likely influenced by multiple genetic factors as well as environmental factors.


Author(s):  
Nick Archer ◽  
Nicky Manning

Introduction 18Environmental factors 20Genetic factors 26Risk of associated non-cardiac anomalies 32Prevention of congential heart disease 34• The incidence of congenital heart disease (CHD) is approximately 8:1000 lives births but is higher in the prenatal population.• The aetiology of CHD has been considered to be multifactorial—a combination of environmental factors and a genetic predisposition but increasing numbers of specific genetic causes are being identified....


2020 ◽  
Vol 32 (4) ◽  
pp. 711-730
Author(s):  
Aleksander Ksiazkiewicz ◽  
Robert Klemmensen ◽  
Christopher T Dawes ◽  
Kaare Christensen ◽  
Matt McGue ◽  
...  

Abstract Existing research shows that ideological orientations are stable after young adulthood. Extending research on the sources of ideological stability, we examine social and economic ideology over a 3- to 4-year period in two twin panels (one Danish and one American). We find evidence for the importance of genetic influences and individual life experiences on the stability of social ideology in both contexts; shared environmental factors play an important role in the younger, Danish sample only. For economic ideology, genetic factors contribute to stability in the American sample only. Our findings show that the role of genetic and environmental factors in the stability of ideological orientations varies by type of ideology, national context, and, possibly, age cohort.


2014 ◽  
Vol 17 (6) ◽  
pp. 563-573 ◽  
Author(s):  
Sevgi Yurt Öncel ◽  
Danielle M. Dick ◽  
Hermine H. Maes ◽  
Fazil Alıev

Aim: In this study, we introduce the first twin study in Turkey, focusing on smoking behavior, and laying the foundation to register all twins born in Turkey for research purposes. Using Turkish twins will contribute to our understanding of health problems in the context of cultural differences. Materials and methods: We assessed 309 twin pairs (339 males and 279 females) aged between 15 and 45 years living in the Kırıkkale and Ankara regions of Turkey, and administered a health and lifestyle interview that included questions about smoking status and smoking history. We analyzed the data using descriptive statistics, t-tests, chi-square tests, and bivariate and multivariate clustered logistic regression. In addition, we fit bivariate Structural Equation Models (SEM) to determine contributions of latent genetic and environmental factors to smoking outcomes in this sample. Results: One hundred seventy-eight participants (28.8%) were identified as smokers, smoking every day for a month or longer, of whom 79.2% were males and 20.8% were females. Mean values for number of cigarettes per day and the Fagerstrom Test of Nicotine Dependence (FTND; Fagerstrom, 1978) score were higher in males than in females, and age of onset was earlier in males. There was a significant positive correlation between the FTND score and number of cigarettes smoked per day, and a significant negative correlation between both variables and age at onset of smoking. Our study showed that gender, presence of a smoking twin in the family, age, alcohol use, marital status, daily sports activities, and feeling moody all played a significant role in smoking behavior among twins. The twin analysis suggested that 79.5% of the liability to FTND was influenced by genetic factors and 20.5% by unique environment, while familial resemblance for smoking initiation was best explained by common environmental factors. Conclusions: Marked differences in the prevalence of smoking behavior in men versus women were observed for the Turkish population. Genetic analyses showed that common environmental factors primarily contributed to smoking initiation, while genetic factors explained a greater proportion of variance in liability to nicotine dependence. Our study shows higher heritability estimate of the FTND scores and higher shared environmental influence on smoking initiation for both males and females than reported in previous studies.


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