scholarly journals The Relationship Between the Genetic and Environmental Influences on Common Externalizing Psychopathology and Mental Wellbeing

2011 ◽  
Vol 14 (6) ◽  
pp. 516-523 ◽  
Author(s):  
Kenneth S. Kendler ◽  
John M. Myers ◽  
Corey L. M. Keyes

To determine the relationship between the genetic and environmental risk factors for externalizing psychopathology and mental wellbeing, we examined detailed measures of emotional, social and psychological wellbeing, and a history of alcohol-related problems and smoking behavior in the last year in 1,386 individual twins from same-sex pairs from the MIDUS national US sample assessed in 1995. Cholesky decomposition analyses were performed withthe Mx program. The best fit model contained one highly heritable common externalizing psychopathology factor for both substance use/abuse measures, and one strongly heritable common factor for the three wellbeing measures. Genetic and environmental risk factors for externalizing psychopathology were both negatively associated with levels of mental wellbeing and accounted for, respectively, 7% and 21% of its genetic and environmental influences. Adding internalizing psychopathology assessed in the last year to the model, genetic risk factors unique for externalizing psychopathology were now positively related to levels of mental wellbeing, although accounting for only 5% of the genetic variance. Environmental risk factors unique to externalizing psychopathology continued to be negatively associated with mental wellbeing, accounting for 26% of the environmental variance. When both internalizing psychopathology and externalizing psychopathology are associated with mental wellbeing, the strongest risk factors for low mental wellbeing are genetic factors that impact on both internalizing psychopathology and externalizing psychopathology, and environmental factors unique to externalizing psychopathology. In this model, genetic risk factors for externalizing psychopathology predict, albeit weakly, higher levels of mental wellbeing.

1998 ◽  
Vol 172 (3) ◽  
pp. 268-272 ◽  
Author(s):  
Kenneth S. Kendler ◽  
Laura M. Karkowski ◽  
Carol A. Prescott ◽  
Michael C. Neale ◽  
Nancy L. Pedersen

BackgroundThe Temperance Boards in Sweden registered individuals for three reasons: public drunkenness, driving under the influence of alcohol and committing a crime in connection with alcohol. We wanted to ascertain whether these three forms of alcohol-related problems result from similar or different genetic and environmental risk factors.MethodWe conducted a trivariate twin analysis of these three causes of registration in all male-female twin pairs of known zygosity born in Sweden, 1926–1949 (n=5177 twin pairs).ResultsPrevalences of registration for public drunkenness, drink-driving and alcohol-related crime were, respectively, 9.0, 3.6 and 4.0%. The best-fitting model had one general genetic and one general familial – environmental factor with specific genetic risk factors for drink-driving and specific familial – environmental risk factors for alcohol-related crime.ConclusionsThe three causes for alcohol registration in Sweden largely reflect the same genetic and environmental risk factors. Estimated heritabilities were similar for the three forms of registration. However, specific genetic risk factors exist for drink-driving and specific familial – environmental risk factors for alcohol-related crime. Genetic factors are somewhat less important and familial –environmental factors more important for public drunkenness than for drink-driving and alcohol related crime.


2021 ◽  
Vol 12 ◽  
Author(s):  
Natassia Robinson ◽  
Sarah E. Bergen

Schizophrenia (SZ) and bipolar disorder (BD) are severe psychiatric disorders which result from complex interplay between genetic and environmental factors. It is well-established that they are highly heritable disorders, and considerable progress has been made identifying their shared and distinct genetic risk factors. However, the 15–40% of risk that is derived from environmental sources is less definitively known. Environmental factors that have been repeatedly investigated and often associated with SZ include: obstetric complications, infections, winter or spring birth, migration, urban living, childhood adversity, and cannabis use. There is evidence that childhood adversity and some types of infections are also associated with BD. Evidence for other risk factors in BD is weaker due to fewer studies and often smaller sample sizes. Relatively few environmental exposures have ever been examined for SZ or BD, and additional ones likely remain to be discovered. A complete picture of how genetic and environmental risk factors confer risk for these disorders requires an understanding of how they interact. Early gene-by-environment interaction studies for both SZ and BD often involved candidate genes and were underpowered. Larger samples with genome-wide data and polygenic risk scores now offer enhanced prospects to reveal genetic interactions with environmental exposures that contribute to risk for these disorders. Overall, although some environmental risk factors have been identified for SZ, few have been for BD, and the extent to which these account for the total risk from environmental sources remains unknown. For both disorders, interactions between genetic and environmental risk factors are also not well understood and merit further investigation. Questions remain regarding the mechanisms by which risk factors exert their effects, and the ways in which environmental factors differ by sex. Concurrent investigations of environmental and genetic risk factors in SZ and BD are needed as we work toward a more comprehensive understanding of the ways in which these disorders arise.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Vaisakh Puthusseryppady ◽  
Ed Manley ◽  
Ellen Lowry ◽  
Martyn Patel ◽  
Michael Hornberger

Abstract Dementia-related missing incidents are a highly prevalent issue worldwide. Despite being associated with potentially life-threatening consequences, very little is still known about what environmental risk factors may potentially contribute to these missing incidents. The aim of this study was to conduct a retrospective, observational analysis using a large sample of police case records of missing individuals with dementia (n = 210). Due to the influence that road network structure has on our real world navigation, we aimed to explore the relationship between road intersection density, intersection complexity, and orientation entropy to the dementia-related missing incidents. For each missing incident location, the above three variables were computed at a 1 km radius buffer zone around these locations; these values were then compared to that of a set of random locations. The results showed that higher road intersection density, intersection complexity, and orientation entropy were all significantly associated with dementia-related missing incidents. Our results suggest that these properties of road network structure emerge as significant environmental risk factors for dementia-related missing incidents, informing future prospective studies as well as safeguarding guidelines.


2013 ◽  
Vol 16 (1) ◽  
pp. 86-90 ◽  
Author(s):  
Liming Li ◽  
Wenjing Gao ◽  
Canqing Yu ◽  
Jun Lv ◽  
Weihua Cao ◽  
...  

The Chinese National Twin Registry (CNTR), established in 2001, is the first and largest population-based twin registry in China. Based on the CNTR, a new twin cohort was recruited from 2011 to study the relationship between environmental risk factors and chronic diseases. So far, 33,874 twin pairs from nine provinces have been recruited, in which hundreds of disease-discordant twin pairs and even thousands of exposure-discordant twin pairs were found in this cohort. The updates of the CNTR will be introduced in detail in this article.


2013 ◽  
Vol 44 (9) ◽  
pp. 1913-1925 ◽  
Author(s):  
K. S. Kendler ◽  
S. Larsson Lönn ◽  
N. A. Morris ◽  
J. Sundquist ◽  
N. Långström ◽  
...  

BackgroundTo clarify the role of genetic and environmental factors in criminal behavior (CB), we examined all CB and violent and non-violent subtypes (VCB and NVCB, respectively) in a Swedish national sample of adoptees and their relatives.MethodCB was defined by a conviction in the Swedish Crime Register with standard definitions for VCB and NVCB subtypes. We examined adoptees born 1950–1991 (n = 18 070) and their biological (n = 79 206) and adoptive (n = 47 311) relatives.ResultsThe risk for all CB was significantly elevated in the adopted-away offspring of biological parents of which at least one had CB [odds ratio (OR) 1.5, 95% confidence interval (CI) 1.4–1.6] and in the biological full and half-siblings of CB adoptees (OR 1.4, 95% CI 1.2–1.6 and OR 1.3, 95% CI 1.2–1.3, respectively). A genetic risk index (including biological parental/sibling history of CB and alcohol abuse) and an environmental risk index (including adoptive parental and sibling CB and a history of adoptive parental divorce, death, and medical illness) both strongly predicted probability of CB. These genetic and environmental risk indices acted additively on adoptee risk for CB. Moderate specificity was seen in the transmission of genetic risk for VCB and NVCB between biological parents and siblings and adoptees.ConclusionsCB is etiologically complex and influenced by a range of genetic risk factors including a specific liability to CB and a vulnerability to broader externalizing behaviors, and by features of the adoptive environment including parental CB, divorce and death. Genetic risk factors for VCB and NVCB may be at least partially distinct.


2020 ◽  
Author(s):  
Xilin Jiang ◽  
Chris Holmes ◽  
Gil McVean

AbstractInherited genetic variation contributes to individual risk for many complex diseases and is increasingly being used for predictive patient stratification. Recent work has shown that genetic factors are not equally relevant to human traits across age and other contexts, though the reasons for such variation are not clear. Here, we introduce methods to infer the form of the relationship between genetic risk for disease and age and to test whether all genetic risk factors behave similarly. We use a proportional hazards model within an interval-based censoring methodology to estimate age-varying individual variant contributions to genetic risk for 24 common diseases within the British ancestry subset of UK Biobank, applying a Bayesian clustering approach to group variants by their risk profile over age and permutation tests for age dependency and multiplicity of profiles. We find evidence for age-varying risk profiles in nine diseases, including hypertension, skin cancer, atherosclerotic heart disease, hypothyroidism and calculus of gallbladder, several of which show evidence, albeit weak, for multiple distinct profiles of genetic risk. The predominant pattern shows genetic risk factors having the greatest impact on risk of early disease, with a monotonic decrease over time, at least for the majority of variants although the magnitude and form of the decrease varies among diseases. We show that these patterns cannot be explained by a simple model involving the presence of unobserved covariates such as environmental factors. We discuss possible models that can explain our observations and the implications for genetic risk prediction.Author summaryThe genes we inherit from our parents influence our risk for almost all diseases, from cancer to severe infections. With the explosion of genomic technologies, we are now able to use an individual’s genome to make useful predictions about future disease risk. However, recent work has shown that the predictive value of genetic information varies by context, including age, sex and ethnicity. In this paper we introduce, validate and apply new statistical methods for investigating the relationship between age and genetic risk. These methods allow us to ask questions such as whether risk is constant over time, precisely how risk changes over time and whether all genetic risk factors have similar age profiles. By applying the methods to data from the UK Biobank, a prospective study of 500,000 people, we show that there is a tendency for genetic risk to decline with increasing age. We consider a series of possible explanations for the observation and conclude that there must be processes acting that we are currently unaware of, such as distinct phases of life in which genetic risk manifests itself, or interactions between genes and the environment.


2014 ◽  
Vol 17 (4) ◽  
pp. 225-235 ◽  
Author(s):  
Fartein A. Torvik ◽  
Line C. Gjerde ◽  
Espen Røysamb ◽  
Kristian Tambs ◽  
Kenneth S. Kendler ◽  
...  

This study investigates the degree to which internalizing disorders (anxiety and mood disorders) are prospectively associated with sick leave granted for mental and somatic disorders, and the extent to which common genetic and environmental risk factors influence these relationships. Data include self-reported symptoms of psychological distress from 7,598 young adult twins and diagnostic interviews on a subsample of 2,766 adult twins, subsequently linked to registry data on sick leave. Regression analyses and multivariate twin models were used to investigate the relationship between internalizing disorders and sick leave. Internalizing disorders were associated with sick leave granted for both mental disorders and somatic disorders. The association between internalizing disorders and sick leave granted for mental disorders was influenced by genetic and non-shared environmental factors, while the association between internalizing disorders and sick leave granted for somatic disorders could be explained by common genetic factors alone. Monozygotic twins discordant for internalizing disorders differed significantly in rates of sick leave granted for mental but not somatic disorders. In conclusion, internalizing disorders in young adults predict sick leave granted for both mental and somatic disorders. Environmental risk factors for internalizing disorders seem to influence sick leave granted for mental disorders, but not sick leave granted for somatic disorders.


2013 ◽  
Vol 43 (10) ◽  
pp. 2161-2168 ◽  
Author(s):  
K. S. Kendler ◽  
C. J. Patrick ◽  
H. Larsson ◽  
C. O. Gardner ◽  
P. Lichtenstein

BackgroundExternalizing traits or behaviors are typically assessed by self-report scales or criminal records. Few genetically informative studies have used both methods to determine whether they assess the same genetic or environmental risk factors.MethodWe examined 442 male Swedish twin pairs with self-reported externalizing behaviors at age 16–17 years [externalizing traits (EXT), self-reported delinquency (SRD), impulsivity (IMP), grandiosity (GRD) and callousness (CLS)] and criminal behavior (CB) from the National Suspect Registry from age 13 to 25 years. Multivariate structural equation modeling was conducted with Mx.ResultsThe best-fit model contained one genetic, one shared environmental and two non-shared environmental common factors, and variable specific genetic and non-shared environmental factors. The risk for CB was influenced substantially by both genetic (a2 = 0.48) and familial–environmental factors (c2 = 0.22). About one-third of the genetic risk for CB but all of the shared environmental risk was indexed by the self-report measures. The degree to which the individual measures reflected genetic versus familial–environmental risks for CB varied widely. GRD and CLS were correlated with CB mainly through common genetic risk factors. SRD and CB covaried largely because of shared familial–environmental factors. For EXT and IMP, observed correlations with CB resulted in about equal parts from shared genetic and shared familial–environmental factors.ConclusionsIn adolescence, measures of grandiose and callous temperament best tap the genetic liability to CB. Measures of antisocial behaviors better index familial–environmental risks for CB. A substantial proportion of the genetic risk to CB was not well reflected in any of the self-report measures.


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