Genetic and environmental risk factors for depression assessed by subject-rated Symptom Check List versus Structured Clinical Interview

2001 ◽  
Vol 31 (8) ◽  
pp. 1413-1423 ◽  
Author(s):  
D. L. FOLEY ◽  
M. C. NEALE ◽  
K. S. KENDLER
Keyword(s):  
Risk Factors ◽  
Major Depression ◽  
Environmental Risk ◽  
Genetic Risk ◽  
Genetic Risk Factors ◽  
Depression Symptoms ◽  
Check List ◽  
Lifetime History ◽  
History Of ◽  
Symptom Check List

Background. It is not known if a subject's characteristic level of self-rated depression symptoms index their genetic or environmental liability to major depressive disorder when measurement error and other occasion-specific influences are taken into account.Method. Monozygotic (N = 408) and dizygotic (N = 295) adult female twin pairs from a population-based registry were surveyed twice with an average follow-up interval of 61 months. At each occasion subjects completed a structured clinical interview (SCID) to assess lifetime history of major depression and the subject-rated Symptom Check List (SCL) to assess current level of depressive symptomatology. A bivariate measurement model was used to estimate the genetic and environmental correlations between liability to reliably diagnosed lifetime history of major depression and the characteristic or temporally stable SCL depression score.Results. The genetic and non-familial environmental correlation between liability to reliably diagnosed major depression and the characteristic level of SCL depression symptoms (and the proportion of variance shared between measures) is +0·70 and +0·24 respectively.Conclusions. When allowance is made for diagnostic unreliability and temporal fluctuations in the level of subject-rated symptoms, 70% of the variance in genetic risk factors and 24% of the variance in environmental risk factors is shared by a diagnosis of lifetime major depression and total SCL depression symptom score. SCL depression scores may therefore be a useful screening measure for many of the genetic risk factors which influence liability to major depression.

scholarly journals A Swedish national adoption study of criminality

2013 ◽  
Vol 44 (9) ◽  
pp. 1913-1925 ◽  
Author(s):  
K. S. Kendler ◽  
S. Larsson Lönn ◽  
N. A. Morris ◽  
J. Sundquist ◽  
N. Långström ◽  
...  
Keyword(s):  
Risk Factors ◽  
Environmental Risk ◽  
Genetic Risk ◽  
Criminal Behavior ◽  
Risk Index ◽  
Genetic Risk Factors ◽  
Medical Illness ◽  
Adoption Study ◽  
Biological Parents ◽  
History Of

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.

scholarly journals Common Genetic Risk of Major Depression and Nicotine Dependence: The Contribution of Antisocial Traits in a United States Veteran Male Twin Cohort

2007 ◽  
Vol 10 (3) ◽  
pp. 470-478 ◽  
Author(s):  
Qiang Fu ◽  
Andrew C. Heath ◽  
Kathleen K. Bucholz ◽  
Michael J. Lyons ◽  
Ming T. Tsuang ◽  
...  
Keyword(s):  
Risk Factors ◽  
Major Depression ◽  
Predominantly White ◽  
Nicotine Dependence ◽  
Genetic Risk ◽  
Genetic Risk Factors ◽  
Diagnostic Interview ◽  
Genetic Influences ◽  
Vietnam Era ◽  
Shared Genetic

AbstractMany studies that found associations between depression and nicotine dependence have ignored possible shared genetic influences associated with antisocial traits. The present study examined the contribution of genetic and environmental effects associated with conduct disorder (CD) and antisocial personality disorder (ASPD) to the comorbidity of major depression (MD) and nicotine dependence (ND). A telephone diagnostic interview, the Diagnostic Interview Schedule-III-R, was administered to eligible twins from the Vietnam Era Twin (VET) Registry in 1992. Multivariate genetic models were fitted to 3360 middle-aged and predominantly white twin pairs (1868 monozygotic, 1492 dizygotic pairs) of which both members completed the pertinent diagnostic interview sections. Genetic influences on CD accounted for 100%, 68%, and 50% of the total genetic variance in risk for ASPD, MD and ND, respectively. After controlling for genetic influences on CD, the partial genetic correlation between MD and ND was no longer statistically significant. Nonshared environmental contributions to the comorbidity among these disorders were not significant. This study not only demonstrates that the comorbidity between ND and MD is influenced by common genetic risk factors, but also further suggests that the common genetic risk factors overlapped with those for antisocial traits such as CD and ASPD in men.

scholarly journals Factores de riesgo genético y diagnóstico prenatal

2021 ◽  
Vol 81 (03) ◽  
pp. 209-225
Author(s):  
Alisandra Morales de Machín ◽  
Karelis Urdaneta ◽  
Lisbeth Borjas ◽  
Karile Méndez ◽  
Enrique Machín ◽  
...  
Keyword(s):  
Risk Factors ◽  
Risk Factor ◽  
Genetic Counseling ◽  
Genetic Risk ◽  
Diagnostic Procedures ◽  
Genetic Risk Factors ◽  
Genetic Risk Factor ◽  
Congenital Defects ◽  
Prenatal Diagnostic ◽  
History Of

Objective: To identify genetic risk factors and frequency and to describe congenital defects of the fetus. Methods: The research was conducted at the Genetic Research Institute of the Faculty of Medicine. University of Zulia. Maracaibo. We studied patients who attend to the prenatal genetic clinic. According to the Genetic risk factors Identified, it indicated different prenatal diagnostic procedures: fetal echography, fetal echocardiography, triple maternal serum marker, amniocentesis for fetal karyotype and molecular analysis. Results: We included 568 patients. 79.05% of the total showed only one genetic risk factor and the 20.95% two or more. The advanced maternal age was the most frequent genetic risk factor found (40.85%), followed by first-degree family history with a congenital defect (35.21%), abnormal fetal echography (13.73%), exposure to teratogenic agents (10.39%), history of recurrent abortion (7.04%), history of fetal death (4.22%), consanguinity (1.93%), and history of neonatal death (1.76%). They were diagnosed 101 fetuses with congenital defects, one balanced translocation, two fetal deaths and 26 spontaneous abortions. Conclusion: The genetic risk factors identification, served as a starting point to indicate prenatal diagnostic procedures allowed a health evaluation of the fetus and adequate genetic counseling. Key words: Prenatal diagnosis, Risk factors, Genetic counseling.

Multivariate genetic analysis of the causes of temperance board registrations

1998 ◽  
Vol 172 (3) ◽  
pp. 268-272 ◽  
Author(s):  
Kenneth S. Kendler ◽  
Laura M. Karkowski ◽  
Carol A. Prescott ◽  
Michael C. Neale ◽  
Nancy L. Pedersen
Keyword(s):  
Risk Factors ◽  
Environmental Risk ◽  
Genetic Risk ◽  
Genetic Risk Factors ◽  
Environmental Risk Factors ◽  
Driving Under The Influence ◽  
Multivariate Genetic Analysis ◽  
Best Fitting ◽  
Alcohol Related Problems ◽  
Fitting Model

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.

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
Keyword(s):  
Risk Factors ◽  
Environmental Risk ◽  
Genetic Risk ◽  
Genetic Risk Factors ◽  
Environmental Risk Factors ◽  
Mental Wellbeing ◽  
Negatively Associated ◽  
Externalizing Psychopathology ◽  
Internalizing Psychopathology ◽  
The Relationship

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.

scholarly journals Evidence for HTR1A and LHPP as interacting genetic risk factors in major depression

2008 ◽  
Vol 14 (6) ◽  
pp. 621-630 ◽  
Author(s):  
C D Neff ◽  
V Abkevich ◽  
J C L Packer ◽  
Y Chen ◽  
J Potter ◽  
...  
Keyword(s):  
Risk Factors ◽  
Major Depression ◽  
Genetic Risk ◽  
Genetic Risk Factors

scholarly journals Shared and specific genetic risk factors for lifetime major depression, depressive symptoms and neuroticism in three population-based twin samples

2018 ◽  
Vol 49 (16) ◽  
pp. 2745-2753 ◽  
Author(s):  
Kenneth S. Kendler ◽  
Charles O. Gardner ◽  
Michael C. Neale ◽  
Steve Aggen ◽  
Andrew Heath ◽  
...  
Keyword(s):  
Risk Factors ◽  
Depressive Symptoms ◽  
Major Depression ◽  
Genetic Risk ◽  
Structural Equation ◽  
Common Factor ◽  
Genetic Risk Factors ◽  
Population Based ◽  
Self Report ◽  
Equation Modeling

AbstractBackgroundVulnerability to depression can be measured in different ways. We here examine how genetic risk factors are inter-related for lifetime major depression (MD), self-report current depressive symptoms and the personality trait Neuroticism.MethodWe obtained data from three population-based adult twin samples (Virginia n = 4672, Australia #1 n = 3598 and Australia #2 n = 1878) to which we fitted a common factor model where risk for ‘broadly defined depression’ was indexed by (i) lifetime MD assessed at personal interview, (ii) depressive symptoms, and (iii) neuroticism. We examined the proportion of genetic risk for MD deriving from the common factor v. specific to MD in each sample and then analyzed them jointly. Structural equation modeling was conducted in Mx.ResultsThe best fit models in all samples included additive genetic and unique environmental effects. The proportion of genetic effects unique to lifetime MD and not shared with the broad depression common factor in the three samples were estimated as 77, 61, and 65%, respectively. A cross-sample mega-analysis model fit well and estimated that 65% of the genetic risk for MD was unique.ConclusionA large proportion of genetic risk factors for lifetime MD was not, in the samples studied, captured by a common factor for broadly defined depression utilizing MD and self-report measures of current depressive symptoms and Neuroticism. The genetic substrate for MD may reflect neurobiological processes underlying the episodic nature of its cognitive, motor and neurovegetative manifestations, which are not well indexed by current depressive symptom and neuroticism.

scholarly journals Suicide and genes: Commentary on Hawton and van Heeringen (Lancet 2009; 373: 1372-81)

2021 ◽  
Author(s):  
Martin Voracek
Keyword(s):  
Risk Factors ◽  
Genetic Risk ◽  
Mental Health Literacy ◽  
Current Knowledge ◽  
Genetic Risk Factors ◽  
Research Designs ◽  
Familial Clustering ◽  
History Of ◽  
Genetic Loading ◽  
Health Agenda

Hawton’s and van Heeringen’s seminar on suicide is a rich source of current knowledge on the topic and highly useful for generalists. However, genetic risk factors for suicide are underappreciated in the seminar. Although family history of suicide is mentioned as important and genetic loading is listed under distal risk factors, their close connection is not emphasised: familial clustering of suicide is partly due to genetic risk factors. Convergent evidence towards this end has emerged from distinctly different genetically informative research designs. Appropriate consideration of these insights is an important public health agenda and matters for mental health literacy, as international surveys suggest disbelief in the genetics of suicide is widespread among medical and psychology undergraduates and in the general population.

scholarly journals Environmental Risk Factors for Schizophrenia and Bipolar Disorder and Their Relationship to Genetic Risk: Current Knowledge and Future Directions

2021 ◽  
Vol 12 ◽  
Author(s):  
Natassia Robinson ◽  
Sarah E. Bergen
Keyword(s):  
Risk Factors ◽  
Bipolar Disorder ◽  
Environmental Factors ◽  
Environmental Risk ◽  
Genetic Risk ◽  
Childhood Adversity ◽  
Environmental Exposures ◽  
Genetic Risk Factors ◽  
Environmental Risk Factors ◽  
Early Gene

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.

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