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Alcohol use disorder and divorce: evidence for a genetic correlation in a population-based Swedish sample.

https://arctichealth.org/en/permalink/ahliterature290102
Source
Addiction. 2017 Apr; 112(4):586-593
Publication Type
Journal Article
Twin Study
Date
Apr-2017
Author
Jessica E Salvatore
Sara Larsson Lönn
Jan Sundquist
Paul Lichtenstein
Kristina Sundquist
Kenneth S Kendler
Author Affiliation
Department of Psychology, Virginia Commonwealth University, Richmond, VA, USA.
Source
Addiction. 2017 Apr; 112(4):586-593
Date
Apr-2017
Language
English
Publication Type
Journal Article
Twin Study
Keywords
Aged
Alcoholism - epidemiology - genetics
Divorce - statistics & numerical data
Environment
European Continental Ancestry Group - genetics
Female
Gene-Environment Interaction
Genetic Predisposition to Disease
Humans
Male
Middle Aged
Registries
Risk factors
Siblings
Sweden - epidemiology
Twins, Dizygotic - genetics
Twins, Monozygotic - genetics
Abstract
We tested the association between alcohol use disorder (AUD) and divorce; estimated the genetic and environmental influences on divorce; estimated how much genetic and environmental influences accounted for covariance between AUD and divorce; and estimated latent genetic and environmental correlations between AUD and divorce. We tested sex differences in these effects.
We identified twin and sibling pairs with AUD and divorce information in Swedish national registers. We described the association between AUD and divorce using tetrachorics and used twin and sibling models to estimate genetic and environmental influences on divorce, on the covariance between AUD and divorce and the latent genetic and environmental correlations between AUD and divorce.
Sweden.
A total of 670?836 individuals (53% male) born 1940-1965.
Life-time measures of AUD and divorce.
AUD and divorce were related strongly (males: rtet  = +0.44, 95% CI = 0.43, 0.45; females rtet  = +0.37, 95% CI = 0.36, 0.38). Genetic factors accounted for a modest proportion of the variance in divorce (males: 21.3%, 95% CI = 7.6, 28.5; females: 31.0%, 95% CI = 18.8, 37.1). Genetic factors accounted for most of the covariance between AUD and divorce (males: 52.0%, 95% CI = 48.8, 67.9; females: 53.74%, 95% CI = 17.6, 54.5), followed by non-shared environmental factors (males: 45.0%, 95% CI = 37.5, 54.9; females: 41.6%, 95% CI = 40.3, 60.2). Shared environmental factors accounted for a negligible proportion of the covariance (males: 3.0%, 95% CI = -3.0, 13.5; females: 4.75%, 95% CI = 0.0, 6.6). The AUD-divorce genetic correlations were high (males: rA = +0.76, 95% CI = 0.53, 0.90; females +0.52, 95% CI = 0.24, 0.67). The non-shared environmental correlations were modest (males: rE = +0.32, 95% CI = 0.31, 0.40; females: +0.27, 95% CI = 0.27, 0.36).
Divorce and alcohol use disorder are correlated strongly in the Swedish population, and the heritability of divorce is consistent with previous studies. Covariation between AUD and divorce results from overlapping genetic and non-shared environmental factors. Latent genetic and non-shared environmental correlations for alcohol use disorder and divorce are high and moderate.
Notes
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PubMed ID
27981669 View in PubMed
Less detail

Association between major depression and type 2 diabetes in midlife: findings from the Screening Across the Lifespan Twin Study.

https://arctichealth.org/en/permalink/ahliterature271541
Source
Psychosom Med. 2015 Jun;77(5):559-66
Publication Type
Article
Date
Jun-2015
Author
Briana Mezuk
Victor Heh
Elizabeth Prom-Wormley
Kenneth S Kendler
Nancy L Pedersen
Source
Psychosom Med. 2015 Jun;77(5):559-66
Date
Jun-2015
Language
English
Publication Type
Article
Keywords
Adult
Comorbidity
Depressive Disorder, Major - epidemiology - etiology
Diabetes Mellitus, Type 2 - epidemiology - etiology
Female
Humans
Male
Middle Aged
Registries
Sweden - epidemiology
Abstract
Cohort studies suggest that the relationship between major depression (MD) and Type 2 diabetes (T2DM) is bidirectional. However, this association may be confounded by shared genetic or environmental factors. The objective of this study was to use a twin design to investigate the association between MD and T2DM.
Data come from the Screening Across the Lifespan Twin Study, a sample of monozygotic and dizygotic twins 40 years or older sampled from the Swedish Twin Registry (n = 37,043). MD was assessed by using the Composite International Diagnostic Inventory. Structural equation twin modeling and Cox proportional hazards modeling were used to assess the relationship between MD and T2DM.
Approximately 19% of respondents had a history of MD and 5% had a history of T2DM. MD was associated with 32% increased likelihood of T2DM (95% confidence interval = 1.00-1.80) among twins aged 40 to 55 years, even after accounting for genetic risk, but was not associated with T2DM among twins older than 55 years. T2DM was associated with 33% increased likelihood of MD (95% confidence interval = 1.02-1.72) among younger, but not older twins. Cholesky decomposition twin modeling indicated that common unique environmental factors contribute to the association between MD and T2DM.
Environmental factors that are unique to individuals (i.e., not shared within families) but common to both MD and T2DM contribute to their co-occurrence in midlife. However, we cannot exclude the possibility of bidirectional causation as an alternate explanation. It is likely that multiple processes are operating to effect the relation between psychiatric and medical conditions in midlife.
Notes
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PubMed ID
25967355 View in PubMed
Less detail

A Bivariate Genetic Analysis of Drug Abuse Ascertained Through Medical and Criminal Registries in Swedish Twins, Siblings and Half-Siblings.

https://arctichealth.org/en/permalink/ahliterature282467
Source
Behav Genet. 2016 Nov;46(6):735-741
Publication Type
Article
Date
Nov-2016
Author
Hermine H Maes
Michael C Neale
Henrik Ohlsson
Mahsa Zahery
Paul Lichtenstein
Kristina Sundquist
Jan Sundquist
Kenneth S Kendler
Source
Behav Genet. 2016 Nov;46(6):735-741
Date
Nov-2016
Language
English
Publication Type
Article
Keywords
Criminals
Female
Genetic Heterogeneity
Humans
Male
Registries
Siblings
Substance-Related Disorders - epidemiology - genetics
Sweden - epidemiology
Twins - genetics
Abstract
Using Swedish nationwide registry data, the authors investigated the correlation of genetic and environmental risk factors in the etiology of drug abuse as ascertained from medical and criminal registries by modeling twin and sibling data. Medical drug abuse was defined using public inpatient and outpatient records, while criminal drug abuse was ascertained through legal records. Twin, full and half sibling pairs were obtained from the national twin and genealogical registers. Information about sibling pair residence within the same household was obtained from Statistics Sweden. Standard bivariate genetic structural equation modeling was applied to the population-based data on drug abuse ascertained through medical and crime registries, using OpenMx. Analyses of all possible pairs of twins (MZ: N = 4482; DZ: N = 9838 pairs), full- (N = 1,278,086) and half-siblings (paternal: N = 7767; maternal N = 70,553) who grew up together suggested that factors explaining familial resemblance for drug abuse as defined through medical or criminal registries were mostly the same. Results showed substantial heritability and moderate contributions of shared environmental factors to drug abuse; both were higher in males versus females, and higher for drug abuse ascertained through criminal than medical records. Because of the low prevalence of both assessments of drug abuse, having access to population data was crucial to obtain stable estimates. Using objective registry data, the authors found that drug abuse-whether ascertained through medical versus criminal records-was highly heritable. Furthermore, shared environmental factors contributed significantly to the liability of drug abuse. Genetic and shared environmental risk factors for these two forms of drug abuse were highly correlated.
Notes
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PubMed ID
27480873 View in PubMed
Less detail

The Decomposition of Shared Environmental Influences on Externalizing Syndromes in the Swedish Population: A Multivariate Study.

https://arctichealth.org/en/permalink/ahliterature289628
Source
Twin Res Hum Genet. 2017 08; 20(4):298-309
Publication Type
Clinical Trial
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Date
08-2017
Author
Henrik Ohlsson
Kenneth S Kendler
Paul Lichtenstein
Jan Sundquist
Kristina Sundquist
Author Affiliation
Center for Primary Health Care Research,Lund University,Malmö,Sweden.
Source
Twin Res Hum Genet. 2017 08; 20(4):298-309
Date
08-2017
Language
English
Publication Type
Clinical Trial
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Keywords
Adult
Alcoholism - genetics
Criminal Behavior
Environment
Family
Female
Humans
Male
Middle Aged
Models, Genetic
Registries
Substance-Related Disorders - genetics
Sweden
Syndrome
Abstract
Using information from Swedish population registries, we attempt to decompose the shared environment (C) into four subcomponents: close family, family, household, and community. Among pairs differing in their genetic and geographical/household relationships, we examine three externalizing syndromes: drug abuse (DA), criminal behavior (CB), and alcohol use disorders (AUD). The best-fitting common pathway model suggested that total estimates for C were higher for DA (21% for males and 18% for females) than for AUD (16% and 14%) and CB (17% and 10%). Concerning syndrome-specific influences in males, close family effects were stronger for CB and AUD, while community effects were stronger for DA. The two C components in between community experiences and close family experiences (family and household) were estimated to almost entirely derive from the common latent factor. In females, among the four components of C, the community experiences were just slightly above zero, while the C components referred to as the household effect were almost zero. The total close family experiences were similar and most important across syndromes were also divided into common and specific components. For all syndromes, for both males and females, the effects of additive genetic factors were 2-4 times the size of the total effect of the shared environment. Applying standard methods to novel relationships, we expand our understanding of how the shared environment contributes to individual differences in three externalizing syndromes.
Notes
Cites: Psychol Med. 2015 Aug;45(11):2253-62 PMID 25936380
Cites: Psychol Bull. 2009 Jul;135(4):608-37 PMID 19586164
Cites: Behav Genet. 2016 Mar;46(2):183-92 PMID 26494460
Cites: Psychol Med. 2015 Apr;45(5):1061-72 PMID 25171596
Cites: Am J Psychiatry. 2014 Feb;171(2):209-17 PMID 24077613
Cites: Psychol Med. 2014 Jul;44(9):1913-25 PMID 24180693
Cites: Soc Psychiatry Psychiatr Epidemiol. 2015 Aug;50(8):1277-84 PMID 25708193
Cites: Nat Genet. 2012 Feb 19;44(3):247-50 PMID 22344220
Cites: Psychol Med. 2014 Nov;44(15):3181-7 PMID 24766797
Cites: Psychol Med. 2015 Oct;45(13):2897-907 PMID 26040779
Cites: J Abnorm Psychol. 1992 Feb;101(1):3-17 PMID 1537970
Cites: J Adolesc. 2012 Aug;35(4):823-31 PMID 22240325
Cites: J Subst Abuse. 2001;13(4):391-424 PMID 11775073
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Cites: Behav Genet. 2002 May;32(3):221-7 PMID 12141783
Cites: Psychol Bull. 2002 May;128(3):490-529 PMID 12002699
Cites: JAMA Psychiatry. 2015 Mar;72(3):211-8 PMID 25565339
Cites: Arch Gen Psychiatry. 2012 Jul;69(7):690-7 PMID 22393206
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PubMed ID
28578747 View in PubMed
Less detail

The Decomposition of Shared Environmental Influences on Externalizing Syndromes in the Swedish Population: A Multivariate Study.

https://arctichealth.org/en/permalink/ahliterature289470
Source
Twin Res Hum Genet. 2017 08; 20(4):298-309
Publication Type
Clinical Trial
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Date
08-2017
Author
Henrik Ohlsson
Kenneth S Kendler
Paul Lichtenstein
Jan Sundquist
Kristina Sundquist
Author Affiliation
Center for Primary Health Care Research,Lund University,Malmö,Sweden.
Source
Twin Res Hum Genet. 2017 08; 20(4):298-309
Date
08-2017
Language
English
Publication Type
Clinical Trial
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Keywords
Adult
Alcoholism - genetics
Criminal Behavior
Environment
Family
Female
Humans
Male
Middle Aged
Models, Genetic
Registries
Substance-Related Disorders - genetics
Sweden
Syndrome
Abstract
Using information from Swedish population registries, we attempt to decompose the shared environment (C) into four subcomponents: close family, family, household, and community. Among pairs differing in their genetic and geographical/household relationships, we examine three externalizing syndromes: drug abuse (DA), criminal behavior (CB), and alcohol use disorders (AUD). The best-fitting common pathway model suggested that total estimates for C were higher for DA (21% for males and 18% for females) than for AUD (16% and 14%) and CB (17% and 10%). Concerning syndrome-specific influences in males, close family effects were stronger for CB and AUD, while community effects were stronger for DA. The two C components in between community experiences and close family experiences (family and household) were estimated to almost entirely derive from the common latent factor. In females, among the four components of C, the community experiences were just slightly above zero, while the C components referred to as the household effect were almost zero. The total close family experiences were similar and most important across syndromes were also divided into common and specific components. For all syndromes, for both males and females, the effects of additive genetic factors were 2-4 times the size of the total effect of the shared environment. Applying standard methods to novel relationships, we expand our understanding of how the shared environment contributes to individual differences in three externalizing syndromes.
Notes
Cites: Psychol Med. 2015 Aug;45(11):2253-62 PMID 25936380
Cites: Psychol Bull. 2009 Jul;135(4):608-37 PMID 19586164
Cites: Behav Genet. 2016 Mar;46(2):183-92 PMID 26494460
Cites: Psychol Med. 2015 Apr;45(5):1061-72 PMID 25171596
Cites: Am J Psychiatry. 2014 Feb;171(2):209-17 PMID 24077613
Cites: Psychol Med. 2014 Jul;44(9):1913-25 PMID 24180693
Cites: Soc Psychiatry Psychiatr Epidemiol. 2015 Aug;50(8):1277-84 PMID 25708193
Cites: Nat Genet. 2012 Feb 19;44(3):247-50 PMID 22344220
Cites: Psychol Med. 2014 Nov;44(15):3181-7 PMID 24766797
Cites: Psychol Med. 2015 Oct;45(13):2897-907 PMID 26040779
Cites: J Abnorm Psychol. 1992 Feb;101(1):3-17 PMID 1537970
Cites: J Adolesc. 2012 Aug;35(4):823-31 PMID 22240325
Cites: J Subst Abuse. 2001;13(4):391-424 PMID 11775073
Cites: Psychol Sci. 2003 May;14(3):273-7 PMID 12741753
Cites: J Child Psychol Psychiatry. 2014 Apr;55(4):304-12 PMID 24261560
Cites: Am J Psychiatry. 2003 Apr;160(4):687-95 PMID 12668357
Cites: Psychometrika. 2016 Jun;81(2):535-49 PMID 25622929
Cites: Behav Genet. 2002 May;32(3):221-7 PMID 12141783
Cites: Psychol Bull. 2002 May;128(3):490-529 PMID 12002699
Cites: JAMA Psychiatry. 2015 Mar;72(3):211-8 PMID 25565339
Cites: Arch Gen Psychiatry. 2012 Jul;69(7):690-7 PMID 22393206
Cites: Soc Psychiatry Psychiatr Epidemiol. 2013 Nov;48(11):1841-9 PMID 23344783
Cites: Psychol Med. 2000 Mar;30(2):281-94 PMID 10824649
Cites: JAMA Psychiatry. 2013 Feb;70(2):235-42 PMID 23229904
Cites: Psychol Med. 2016 Jun;46(8):1639-50 PMID 26996079
Cites: Nature. 2014 Feb 13;506(7487):185-90 PMID 24463508
Cites: Arch Gen Psychiatry. 1997 Feb;54(2):178-84 PMID 9040286
Cites: Nature. 2009 Aug 6;460(7256):748-52 PMID 19571811
Cites: Behav Genet. 1994 Jan;24(1):35-49 PMID 8192619
PubMed ID
28578747 View in PubMed
Less detail

Does low alcohol use increase the risk of sickness absence? A discordant twin study.

https://arctichealth.org/en/permalink/ahliterature284782
Source
BMC Public Health. 2016 Aug 18;16(1):825
Publication Type
Article
Date
Aug-18-2016
Author
Kristian Amundsen Østby
Nikolai Czajkowski
Gun Peggy Knudsen
Eivind Ystrøm
Line C Gjerde
Kenneth S Kendler
Ragnhild E Ørstavik
Ted Reichborn-Kjennerud
Source
BMC Public Health. 2016 Aug 18;16(1):825
Date
Aug-18-2016
Language
English
Publication Type
Article
Keywords
Adult
Alcohol Drinking - adverse effects
Alcoholism - complications
Female
Humans
Male
Middle Aged
Norway
Occupational Diseases - etiology
Risk factors
Sick Leave - statistics & numerical data
Twins - statistics & numerical data
Young Adult
Abstract
Results from observational studies suggest that people who drink little or no alcohol are less healthy than medium drinkers. This has been demonstrated for many different measures of health, including sick leave. However, whether these associations are causal or due to confounding remains to be clarified. The aim of this study was to use a discordant twin design to determine whether the increased level of sick leave associated with a low level of alcohol consumption, as compared to those with a medium level of consumption, reflects a causal mechanism or is due to genetic or environmental confounding.
Six thousand seven hundred thirty-four young adult twins from the Norwegian Institute of Public Health's twin panel were in 1998 assessed for frequency of alcohol use and binge drinking. Data were linked to the Norwegian National Insurance Administration's recordings of sick leave over a 10 year period. The associations between alcohol consumption and sick leave were first estimated in the total study population, and then within di- and monozygotic twin pairs discordant for alcohol use.
Compared to medium consumption, both low and high alcohol consumption was associated with increased risk of sick leave. When low level drinkers were compared to medium level drinkers in a discordant twin design, the results were consistent with the association being due to genetic confounding rather than a causal effect.
The increased level of sick leave observed with low level drinkers seems to be mainly explained by confounding from genetic factors. In all observational studies of the relationship between alcohol consumption and health, one should be aware that important genetic confounders are likely to influence the results.
Notes
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PubMed ID
27538396 View in PubMed
Less detail

Effect of Marriage on Risk for Onset of Alcohol Use Disorder: A Longitudinal and Co-Relative Analysis in a Swedish National Sample.

https://arctichealth.org/en/permalink/ahliterature282325
Source
Am J Psychiatry. 2016 Sep 01;173(9):911-8
Publication Type
Article
Date
Sep-01-2016
Author
Kenneth S Kendler
Sara Larsson Lönn
Jessica Salvatore
Jan Sundquist
Kristina Sundquist
Source
Am J Psychiatry. 2016 Sep 01;173(9):911-8
Date
Sep-01-2016
Language
English
Publication Type
Article
Keywords
Adult
Alcoholism - epidemiology - genetics - psychology
Cohort Studies
Female
Genetic Predisposition to Disease
Humans
Male
Marriage - psychology
Middle Aged
Registries
Risk assessment
Risk factors
Sex Factors
Statistics as Topic
Survival Analysis
Sweden
Abstract
The authors sought to clarify the relationship between marriage and risk for alcohol use disorder.
The association between marital status and risk for first registration for alcohol use disorder in medical, criminal, and pharmacy registries was assessed in a population-based Swedish cohort (N=3,220,628) using longitudinal time-dependent survival and co-relative designs.
First marriage was associated with a substantial decline in risk for onset of alcohol use disorder in men (hazard ratio=0.41, 95% CI=0.40-0.42) and women (hazard ratio=0.27, 95% CI=0.26-0.28). This association was slightly stronger when the spouse had no lifetime alcohol use disorder, while marriage to a spouse with lifetime alcohol use disorder increased risk for subsequent alcohol use disorder registration in both men (hazard ratio=1.29, 95% CI=1.16-1.43) and women (hazard ratio=1.18, 95% CI=1.06-1.30). In both sexes, the protective effect of marriage was significantly stronger in those with than those without a family history of alcohol use disorder. In both men and women, the associations between marriage and risk for alcohol use disorder in cousins, half siblings, full siblings, and monozygotic twins discordant for marital status were as strong as that seen in the general population.
First marriage to a spouse with no lifetime alcohol use disorder is associated with a large reduction in risk for alcohol use disorder. This association cannot be explained by standard covariates or, as indicated by co-relative analyses, familial genetic or shared environmental confounders. These results are consistent with the hypothesis that the psychological and social aspects of marriage, and in particular health-monitoring spousal interactions, strongly protect against the development of alcohol use disorder. The protective effects of marriage on risk for alcohol use disorder are increased in those at high familial risk for alcoholism.
Notes
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PubMed ID
27180900 View in PubMed
Less detail

Evidence for distinct genetic effects associated with response to 35% CO2.

https://arctichealth.org/en/permalink/ahliterature116916
Source
Depress Anxiety. 2013 Mar;30(3):259-66
Publication Type
Article
Date
Mar-2013
Author
Roxann Roberson-Nay
Sara Moruzzi
Anna Ogliari
Elettra Pezzica
Kristian Tambs
Kenneth S Kendler
Marco Battaglia
Author Affiliation
Department of Psychiatry, Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University, Richmond, VA 23298, USA. rrobersonnay@vcu.edu
Source
Depress Anxiety. 2013 Mar;30(3):259-66
Date
Mar-2013
Language
English
Publication Type
Article
Keywords
Adult
Anxiety Disorders - chemically induced - epidemiology - genetics
Biological Markers
Carbon Dioxide - administration & dosage - adverse effects
Diseases in Twins - genetics
Female
Gene-Environment Interaction
Health Surveys
Humans
Inhalation - genetics
Male
Middle Aged
Norway - epidemiology
Respiratory Hypersensitivity - chemically induced - epidemiology - genetics
Risk factors
Abstract
Carbon dioxide (CO2 ) hypersensitivity represents an individual difference response to breathing CO2 enriched air. People with a history of panic attacks or panic disorder are particularly prone to anxious response, suggesting that CO2 hypersensitivity is a robust risk marker of panic spectrum vulnerability.
Twin pairs (n = 346) from the general population-based Norwegian NIPH Mental Health Study completed a measure of anxiety before and after vital capacity inhalation of 35% CO2 air and before and after inhalation of regular air. Three hypotheses regarding genetic factors for CO2 hypersensitivity were examined: (1) a single set of genetic risk factors impacts anxiety before exposure to CO2 and these same genes constitute the only genetic influences on anxiety in response to CO2 , (2) the genetic effects on pre-CO2 anxiety are entirely different from the genetic effects on anxiety in response to exposure to CO2 (i.e., new genetic effects), and (3) pre-CO2 anxiety influences anxiety in response to CO2 as well as unique genetic factors that become activated by respiratory stimulation.
Our results support the latter hypothesis for response to 35% CO2 , with additive genetic and unique environmental factors best fitting the data. Evidence of new genetic effects was observed, accounting for 20% unique variance in post 35% CO2 anxiety response. New genetic effects were not observed for anxiety ratings made post regular air where only preregular air anxiety ratings explained significant variance in this outcome.
These data suggest that there are distinct genetic factors associated with responsivity to respiratory stimulation via 35% CO2 .
Notes
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PubMed ID
23349098 View in PubMed
Less detail

Familial and neighborhood effects on psychiatric disorders in childhood and adolescence.

https://arctichealth.org/en/permalink/ahliterature270483
Source
J Psychiatr Res. 2015 Jul-Aug;66-67:7-15
Publication Type
Article
Author
Jan Sundquist
Xinjun Li
Henrik Ohlsson
Maria Råstam
Marilyn Winkleby
Kristina Sundquist
Kenneth S Kendler
Casey Crump
Source
J Psychiatr Res. 2015 Jul-Aug;66-67:7-15
Language
English
Publication Type
Article
Keywords
Adolescent
Anxiety Disorders - epidemiology
Attention Deficit Disorder with Hyperactivity - epidemiology
Child
Child, Preschool
Cohort Studies
Conduct Disorder - epidemiology
Family
Follow-Up Studies
Humans
Individuality
Logistic Models
Mood Disorders - epidemiology
Registries
Social Environment
Socioeconomic Factors
Sweden - epidemiology
Abstract
More knowledge is needed on potential associations between individual-, family-, and neighborhood-level factors and psychiatric disorders in children and adolescents.
To examine associations between, individual-, family-, and neighborhood-level factors and incident internalizing (anxiety and mood) disorders and externalizing (ADHD and conduct) disorders in children and adolescents, and to estimate the relative contributions of family and neighborhood to individual variation in these disorders.
We performed a three-level logistic regression on all 542,195 children born in Sweden in 1992-1996, nested in 427,954 families, which in turn were nested in 8475 neighborhoods. The children were followed from 2000 to 2010 for incident internalizing and externalizing psychiatric disorders, assessed from medical records.
26,514 children (4.8%) were diagnosed with internalizing or externalizing psychiatric disorders. Approximately 29% of the total individual variance in internalizing disorders could be attributed to the family level, which includes both genetic and family environmental effects, and 5% to the neighborhood level. The corresponding figures for externalizing disorders were 43.5% and 5.5%, respectively. After adjustment for individual-level sociodemographic factors, high neighborhood deprivation was associated with increased risks of externalizing and internalizing psychiatric disorders (odds ratio [OR] = 1.37, 95% credible interval [CI] = 1.25-1.50 and OR = 1.34, 95% CI = 1.25-1.45, respectively), including conduct disorder (OR = 2.01, 95% CI = 1.58-2.55), anxiety disorders (OR = 1.40, 95% CI = 1.29-1.52), and mood disorders (OR = 1.21, 95% CI, 1.09-1.35). The strongest association between neighborhood deprivation and ADHD was observed in moderately deprived neighborhoods (OR = 1.31, 95% CI = 1.19-1.44).
These findings call for policies to promote mental health that consider potential influences from children's family and neighborhood environments.conclusion
Not applicable.
Notes
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PubMed ID
25953099 View in PubMed
Less detail

Genetic and environmental contributions to long-term sick leave and disability pension: a population-based study of young adult Norwegian twins.

https://arctichealth.org/en/permalink/ahliterature113302
Source
Twin Res Hum Genet. 2013 Aug;16(4):759-66
Publication Type
Article
Date
Aug-2013
Author
Line C Gjerde
Gun Peggy Knudsen
Nikolai Czajkowski
Nathan Gillespie
Steven H Aggen
Espen Røysamb
Ted Reichborn-Kjennerud
Kristian Tambs
Kenneth S Kendler
Ragnhild E Orstavik
Author Affiliation
Department of Mental Health, Norwegian Institute of Public Health, Oslo, Norway. line.gjerde@fhi.no
Source
Twin Res Hum Genet. 2013 Aug;16(4):759-66
Date
Aug-2013
Language
English
Publication Type
Article
Keywords
Adult
Disabled persons - statistics & numerical data
Female
Gene-Environment Interaction
Genetic Predisposition to Disease
Genetics, Population
Humans
Insurance, Disability - statistics & numerical data - trends
Male
Models, Theoretical
Norway - epidemiology
Pensions - statistics & numerical data
Risk factors
Sick Leave - statistics & numerical data - trends
Twins - genetics
Young Adult
Abstract
Although exclusion from the workforce due to long-term sick leave (LTSL) and disability pension (DP) is a major problem in many Western countries, the etiology of LTSL and DP is not well understood. These phenomena have a strong association as most patients receiving DP have first been on LTSL. However, only a few of those on LTSL end up with DP. The present study aimed to investigate the common and specific genetic and environmental risk factors for LTSL and DP. The present study utilizes a population-based sample of 7,710 young adult twins from the Norwegian Institute of Public Health Twin Panel, which has been linked to the Historical-Event Database (FD-Trygd; 1998-2008). Univariate and bivariate twin models were fitted to determine to what degree genetic and environmental factors contribute to variation in LTSL and DP. The estimated heritabilities of LTSL and DP were 0.49 and 0.66, respectively. There was no evidence for shared environmental or sex-specific factors. The phenotypic-, genetic-, and non-familial environmental correlations between the variables were 0.86, 0.82, and 0.94, respectively. Our results indicate that familial transmission of LTSL and DP is due to genetic and not environmental factors. The risk factors contributing to LTSL and DP were mainly shared, suggesting that what increases risk for LTSL also increases risk for DP. However, a non-negligible part of the genetic variance was not shared between the variables, which may contribute to explaining why some progress from LTSL to DP, whereas others return to work.
Notes
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PubMed ID
23743022 View in PubMed
Less detail

Genetic and Environmental Structure of DSM-IV Criteria for Antisocial Personality Disorder: A Twin Study.

https://arctichealth.org/en/permalink/ahliterature288056
Source
Behav Genet. 2017 May;47(3):265-277
Publication Type
Article
Date
May-2017
Author
Tom Rosenström
Eivind Ystrom
Fartein Ask Torvik
Nikolai Olavi Czajkowski
Nathan A Gillespie
Steven H Aggen
Robert F Krueger
Kenneth S Kendler
Ted Reichborn-Kjennerud
Source
Behav Genet. 2017 May;47(3):265-277
Date
May-2017
Language
English
Publication Type
Article
Keywords
Adult
Antisocial Personality Disorder - genetics
Diagnostic and Statistical Manual of Mental Disorders
Diseases in Twins - genetics
Environment
Female
Genotype
Humans
Male
Norway
Phenotype
Twins, Dizygotic - genetics
Twins, Monozygotic - genetics
Young Adult
Abstract
Results from previous studies on DSM-IV and DSM-5 Antisocial Personality Disorder (ASPD) have suggested that the construct is etiologically multidimensional. To our knowledge, however, the structure of genetic and environmental influences in ASPD has not been examined using an appropriate range of biometric models and diagnostic interviews. The 7 ASPD criteria (section A) were assessed in a population-based sample of 2794 Norwegian twins by a structured interview for DSM-IV personality disorders. Exploratory analyses were conducted at the phenotypic level. Multivariate biometric models, including both independent and common pathways, were compared. A single phenotypic factor was found, and the best-fitting biometric model was a single-factor common pathway model, with common-factor heritability of 51% (95% CI 40-67%). In other words, both genetic and environmental correlations between the ASPD criteria could be accounted for by a single common latent variable. The findings support the validity of ASPD as a unidimensional diagnostic construct.
Notes
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PubMed ID
28108863 View in PubMed
Less detail

Genetic and family and community environmental effects on drug abuse in adolescence: a Swedish national twin and sibling study.

https://arctichealth.org/en/permalink/ahliterature106984
Source
Am J Psychiatry. 2014 Feb 1;171(2):209-17
Publication Type
Article
Date
Feb-1-2014
Author
Kenneth S Kendler
Hermine H Maes
Kristina Sundquist
Henrik Ohlsson
Jan Sundquist
Source
Am J Psychiatry. 2014 Feb 1;171(2):209-17
Date
Feb-1-2014
Language
English
Publication Type
Article
Keywords
Age Factors
Diseases in Twins - epidemiology - genetics
Family Health
Female
Humans
Male
Prevalence
Registries
Risk factors
Siblings - psychology
Social Environment
Substance-Related Disorders - epidemiology - genetics
Sweden - epidemiology
Twins - genetics - psychology
Abstract
Using Swedish nationwide registry data, the authors investigated genetic and environmental risk factors in the etiology of drug abuse by twin sibling modeling. The authors followed up with epidemiological analyses to identify shared environmental influences on drug abuse.
Drug abuse was defined using public medical, legal, or pharmacy records. Twin and sibling pairs were obtained from the national twin and genealogical registers. Information about sibling pair residence within the same household, small residential area, or municipality was obtained from Statistics Sweden. The authors predicted concordance for drug abuse by years of co-residence until the older sibling turned 21 and risk for future drug abuse in adolescents living with parental figures as a function of family-level socioeconomic status and neighborhood social deprivation.
The best twin sibling fit model predicted substantial heritability for drug abuse in males (55%) and females (73%), with environmental factors shared by siblings operating only in males and accounting for 23% of the variance in liability. For each year of living in the same household, the probability of sibling concordance for drug abuse increased 2%-5%. When not residing in the same household, concordance was predicted from residence in the same small residential area or municipality. Risk for drug abuse was predicted both by family socioeconomic status and neighborhood social deprivation. Controlling for family socioeconomic status, each year of living in a high social deprivation neighborhood increased the risk for drug abuse by 2%.
Using objective registry data, the authors found that drug abuse is highly heritable. A substantial proportion of the shared environmental effect on drug abuse comes from community-wide rather than household-level influences. Genetic effects demonstrated in twin studies have led to molecular analyses to elucidate biological pathways. In a parallel manner, environmental effects can be followed up by epidemiological studies to clarify social mechanisms.
Notes
Comment In: Am J Psychiatry. 2014 Feb 1;171(2):140-124500456
PubMed ID
24077613 View in PubMed
Less detail

Genetic variance of body mass index from childhood to early adulthood.

https://arctichealth.org/en/permalink/ahliterature132425
Source
Behav Genet. 2012 Jan;42(1):86-95
Publication Type
Article
Date
Jan-2012
Author
Jocilyn E Dellava
Paul Lichtenstein
Kenneth S Kendler
Author Affiliation
Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University, PO Box 980126 MCV, Richmond, VA 23298, USA. jdellava@vcu.edu
Source
Behav Genet. 2012 Jan;42(1):86-95
Date
Jan-2012
Language
English
Publication Type
Article
Keywords
Adolescent
Body Composition - genetics
Body mass index
Body Weight
Child
Environment
Genetic Variation
Humans
Models, Genetic
Models, Statistical
Phenotype
Puberty - genetics
Registries
Sweden
Young Adult
Abstract
Research has been conducted to determine genetic and environmental components of body mass index (BMI). The portion of phenotypic correlation attributed to genetic, and environmental effects, the effects of puberty stage on BMI means and variances, and consistency of parent/twin report remain largely unknown. The current study seeks to address these questions using four waves of data from 1480 twin pairs in the Swedish Twin Registry: Swedish Twin Study of Child and Adolescent Development. Two Cholesky decomposition models were fit (parental and twin report). For wave 2, a univariate model was fit allowing puberty stage moderation. Parent/twin concordance of reported BMI is high. Genetic factors are largely responsible for phenotypic correlation: puberty stage has a significant effect on BMI variance, with higher genetic variance at more advanced puberty stages. Results provide additional information about this phenotype and suggest early adolescent and parental reports for BMI are roughly equivalent.
Notes
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PubMed ID
21818663 View in PubMed
Less detail

Illicit psychoactive substance use, abuse and dependence in a population-based sample of Norwegian twins.

https://arctichealth.org/en/permalink/ahliterature76222
Source
Psychol Med. 2006 May 2;:1-8
Publication Type
Article
Date
May-2-2006
Author
Kenneth S Kendler
Steven H Aggen
Kristian Tambs
Ted Reichborn-Kjennerud
Author Affiliation
Department of Psychiatry, Medical College of Virginia of Virginia Commonwealth University, Richmond, VA, USADepartment of Human Genetics, Medical College of Virginia of Virginia Commonwealth University, Richmond, VA, USA.
Source
Psychol Med. 2006 May 2;:1-8
Date
May-2-2006
Language
English
Publication Type
Article
Abstract
Background. Prior population-based twin studies from two Anglophonic countries with relatively high rates of drug use - the USA and Australia - suggest that genetic factors contribute substantially to individual differences in the use, abuse and dependence of illicit psychoactive substances. Would these results replicate in Norway, a Nordic country with a low prevalence of illicit drug use?Method. Lifetime use, abuse and dependence of five illicit drug categories (cannabis, stimulants, opiates, cocaine and psychedelics) were assessed at personal interview in 1386 complete young adult twin pairs ascertained from the Norwegian Institute of Public Health Twin Panel. Twin model fitting was performed using the Mx statistical package on three phenotypes: any lifetime use, endorsement of at least one DSM-IV symptom of abuse or dependence, and meeting DSM-IV criteria for abuse or dependence.Results. Significant lifetime use of illicit substances (defined as use 10 or more times) was reported by only 6.4% of the sample. Meaningful analyses were possible for use of any substance and each of the five substances individually, but for symptoms or a diagnosis of abuse/dependence meaningful analyses were possible only for any substance and cannabis. Full twin models uniformly found twin resemblance to be due largely or entirely to genetic factors. Best-fit models for all analyses included only genetic and individual-specific environmental effects with heritability estimates ranging from 58% to 81%.Conclusion. In accord with prior results from the USA and Australia, genetic factors appear to play an important role in the etiology of use and abuse/dependence of illicit drugs in Norway.
PubMed ID
16650346 View in PubMed
Less detail

Personality disorders and long-term sick leave: a population-based study of young adult Norwegian twins.

https://arctichealth.org/en/permalink/ahliterature105329
Source
Twin Res Hum Genet. 2014 Feb;17(1):1-9
Publication Type
Article
Date
Feb-2014
Author
Line C Gjerde
Espen Røysamb
Nikolai Czajkowski
Gun Peggy Knudsen
Kristian Ostby
Kristian Tambs
Kenneth S Kendler
Ted Reichborn-Kjennerud
Ragnhild E Orstavik
Author Affiliation
Department of Mental Health, Norwegian Institute of Public Health, Oslo, Norway.
Source
Twin Res Hum Genet. 2014 Feb;17(1):1-9
Date
Feb-2014
Language
English
Publication Type
Article
Keywords
Adult
Diagnostic and Statistical Manual of Mental Disorders
Diseases in Twins - diagnosis - genetics
Female
Humans
Interview, Psychological
Male
Norway
Personality Disorders - diagnosis - genetics - psychology
Population - genetics
Questionnaires
Sick Leave
Twins - genetics - psychology
Abstract
Personality disorders (PDs) reduce global functioning, are associated with high levels of work disability, and are thus also likely to influence long-term sick leave (LTSL). Previous research has indicated significant genetic influence on both DSM-IV PDs and LTSL. To what degree genes contributing to PDs also influence LTSL has not been investigated. The aims of the current study were to investigate which PDs were significantly associated with LTSL, to what extent the genetic contributions to these PDs account for the heritability of LTSL, and to explore the hypothesis of a causal association between PDs and LTSL. The sample consisted of 2,771 young, adult Norwegian twins, born 1967-1979. PDs were assessed using the Structured Interview for DSM-IV Personality (SIDP-IV). The age range for the interview was 20-32. The data were subsequently linked to public records of LTSL (sick leave >16 days) up to 11 years later. The odds ratio for being in the highest LTSL category (>15% sick leave) when fulfilling the DSM-IV criteria for any PD diagnosis was 2.6 (1.8-3.8, 95% CI). Dimensional representations of schizotypal, paranoid, and borderline PD were independently and significantly associated with LTSL. The heritability of LTSL was 0.50. Genetic factors shared with the PDs accounted for 20% of this. The association between PDs and LTSL was due to shared genetic and not environmental influences, and was mainly explained by one common genetic factor. The hypothesis of a causal association was not supported, indicating that the association is explained by overlapping genetic liability between PDs and LTSL.
PubMed ID
24417773 View in PubMed
Less detail

A population-based study of familial and individual-specific environmental contributions to traumatic event exposure and posttraumatic stress disorder symptoms in a Norwegian twin sample.

https://arctichealth.org/en/permalink/ahliterature121792
Source
Twin Res Hum Genet. 2012 Oct;15(5):656-62
Publication Type
Article
Date
Oct-2012
Author
Ananda B Amstadter
Steven H Aggen
Gun Peggy Knudsen
Ted Reichborn-Kjennerud
Kenneth S Kendler
Author Affiliation
Department of Psychiatry, Virginia Institute of Psychiatric and Behavioral Genetics, Virginia Commonwealth University, Richmond, VA, USA. abamstadter@vcu.edu
Source
Twin Res Hum Genet. 2012 Oct;15(5):656-62
Date
Oct-2012
Language
English
Publication Type
Article
Keywords
Adult
Diseases in Twins - etiology
Environment
Female
Genetic Predisposition to Disease
Humans
Male
Models, Theoretical
Norway
Pedigree
Stress Disorders, Post-Traumatic - etiology
Twins, Dizygotic
Twins, Monozygotic
Abstract
Posttraumatic stress disorder (PTSD) is one of the only disorders in the Diagnostic and Statistical Manual of Mental Disorders that requires an environmental exposure. The relationship between liability factors for trauma exposure and those for PTSD symptoms following exposure are unclear.
Exposure to a trauma and resulting PTSD symptoms were assessed in a sample of 2,794 members of the Norwegian Institute of Public Health Twin Panel.
In the full sample, 737 twins experienced a trauma. A modified causal, contingent, common pathway model was used to examine trauma exposure and liability for PTSD. Genetic and common environmental factors could not be distinguished, so a model that included only familial and individual specific components was fit. The best-fitting model suggested that familial factors played an important role in liability for trauma exposure and for resulting PTSD symptoms, and that there was a modest transmission between trauma exposure and subsequent PTSD symptoms.
One third of the variance in liability of PTSD symptoms is due to familial factors, and of this, approximately one fifth overlaps with the familial liability for trauma exposure while the other four fifths of the variance is specific to the risk of PTSD symptoms following exposure. The hypothesis that PTSD is etiologically similar to exposures to a traumatic event is not supported, suggesting that the factors that confer risk for trauma do not overlap completely with those that confer risk for PTSD.
Notes
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PubMed ID
22877512 View in PubMed
Less detail

Prediction of alcohol use disorder using personality disorder traits: a twin study.

https://arctichealth.org/en/permalink/ahliterature294336
Source
Addiction. 2018 Jan; 113(1):15-24
Publication Type
Journal Article
Observational Study
Twin Study
Date
Jan-2018
Author
Tom Rosenström
Fartein Ask Torvik
Eivind Ystrom
Nikolai Olavi Czajkowski
Nathan A Gillespie
Steven H Aggen
Robert F Krueger
Kenneth S Kendler
Ted Reichborn-Kjennerud
Author Affiliation
Department of Mental Disorders, Norwegian Institute of Public Health, Oslo, Norway.
Source
Addiction. 2018 Jan; 113(1):15-24
Date
Jan-2018
Language
English
Publication Type
Journal Article
Observational Study
Twin Study
Keywords
Adult
Alcoholism - epidemiology - genetics - psychology
Antisocial Personality Disorder - epidemiology - genetics - psychology
Borderline Personality Disorder - epidemiology - genetics - psychology
Comorbidity
Conduct Disorder - epidemiology - genetics - psychology
Female
Humans
Impulsive Behavior
Male
Middle Aged
Norway - epidemiology
Odds Ratio
Personality
Personality Disorders - epidemiology - genetics - psychology
Prospective Studies
Risk assessment
Twins, Dizygotic
Twins, Monozygotic
Young Adult
Abstract
The DSM-IV personality disorders (PDs) are comorbid with alcohol use disorder (AUD) and with each other. It remains unclear which PD criteria are most likely to drive onset and recurrence of AUD and which are merely confounded with those criteria. We determine which individual PD criteria predict AUD and the degree of underlying genetic and/or environmental aetiology.
A prospective observational twin study.
Norway 1999-2011.
A total of 2528 and 2275 Norwegian adult twins in waves 1 and 2 variable-selection analyses, and 2785 in biometric analyses.
DSM-IV PDs and their 80 criteria were assessed using a structured personal interview, and AUD using the World Health Organization's Composite International Diagnostic Interview.
In a variable-selection analysis, two PD criteria were associated with AUD even after taking all the other criteria into account: criterion 8 of antisocial PD (childhood conduct disorder) and criterion 4 of borderline PD (self-damaging impulsive behaviours). Adjusting for each other, their respective odds ratios were 3.4 [confidence interval (CI) = 2.1-5.4] and 5.0 (CI = 3.3-7.7). Endorsement strength of the criteria was associated with AUD in a dose-response manner and they explained 5.5% of variation in AUD risk-more than the full diagnoses of antisocial and borderline PDs together (0.5%). The association between borderline criterion 4 and AUD 10 years later derived mainly from their overlapping genetic factors, whereas the association between antisocial criterion 8 and AUD 10 years later was due to both genetic and non-genetic factors.
Conduct disorder and self-harming impulsivity are the foremost risk traits for alcohol use disorder among the 80 personality disorder criteria of DSM-IV, predicting alcohol use disorder more effectively than personality disorder diagnoses. The twin-study analysis suggested that conduct disorder represents a joint genetic and developmental risk for alcohol use disorder and that impulsivity is a genetic risk.
Notes
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PubMed ID
28734091 View in PubMed
Less detail

Resilience and Risk for Alcohol Use Disorders: A Swedish Twin Study.

https://arctichealth.org/en/permalink/ahliterature287835
Source
Alcohol Clin Exp Res. 2017 Jan;41(1):149-155
Publication Type
Article
Date
Jan-2017
Author
Elizabeth C Long
Sara L Lönn
Jianguang Ji
Paul Lichtenstein
Jan Sundquist
Kristina Sundquist
Kenneth S Kendler
Source
Alcohol Clin Exp Res. 2017 Jan;41(1):149-155
Date
Jan-2017
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Alcohol-Related Disorders - diagnosis - epidemiology - psychology
Humans
Male
Registries
Resilience, Psychological
Risk factors
Social Environment
Sweden - epidemiology
Twins - psychology
Young Adult
Abstract
Resilience has been shown to be protective against alcohol use disorders (AUDs), but the magnitude and nature of the relationship between these 2 phenotypes are not clear. The aim of this study was to examine the strength of this relationship and the degree to which it results from common genetic or common environmental influences.
Resilience was assessed on a 9-point scale during a personal interview in 1,653,721 Swedish men aged 17 to 25 years. AUD was identified based on Swedish medical, legal, and pharmacy registries. The magnitude of the relationship between resilience and AUD was examined using logistic regression. The extent to which the relationship arises from common genetic or common environmental factors was examined using a bivariate Cholesky decomposition model.
The 5 single items that comprised the resilience assessment (social maturity, interest, psychological energy, home environment, and emotional control) all reduced risk for subsequent AUD, with social maturity showing the strongest effect. The linear effect by logistic regression showed that a 1-point increase on the resilience scale was associated with a 29% decrease in odds of AUD. The Cholesky decomposition model demonstrated that the resilience-AUD relationship was largely attributable to overlapping genetic and shared environmental factors (57 and 36%, respectively).
Resilience is strongly associated with a reduction in risk for AUD. This relationship appears to be the result of overlapping genetic and shared environmental influences that impact resilience and risk of AUD, rather than a directly causal relationship.
Notes
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PubMed ID
27918840 View in PubMed
Less detail

Stability and change in etiological factors for alcohol use disorder and major depression.

https://arctichealth.org/en/permalink/ahliterature289801
Source
J Abnorm Psychol. 2017 Aug; 126(6):812-822
Publication Type
Journal Article
Twin Study
Date
Aug-2017
Author
Fartein Ask Torvik
Tom Henrik Rosenström
Eivind Ystrom
Kristian Tambs
Espen Røysamb
Nikolai Czajkowski
Nathan Gillespie
Gun Peggy Knudsen
Kenneth S Kendler
Ted Reichborn-Kjennerud
Author Affiliation
Department of Mental Disorders, Norwegian Institute of Public Health.
Source
J Abnorm Psychol. 2017 Aug; 126(6):812-822
Date
Aug-2017
Language
English
Publication Type
Journal Article
Twin Study
Keywords
Adult
Age Factors
Alcoholism - genetics
Depressive Disorder, Major - genetics
Female
Gene-Environment Interaction
Genomic Instability - genetics
Humans
Male
Norway
Phenotype
Registries
Risk factors
Twins, Dizygotic
Twins, Monozygotic
Young Adult
Abstract
Alcohol use disorder (AUD) and major depressive disorder (MDD) are often comorbid. It is not understood how genetic risk factors for these disorders relate to each other over time and to what degree they are stable. Age-dependent characteristics of the disorders indicate that different genetic factors could be relevant at different stages of life, and MDD may become increasingly correlated with AUD over time. DSM-IV diagnoses of AUD and MDD were assessed by interviews of 2,801 young adult twins between 1999 and 2004 (T1) and 2,284 of the same twins between 2010 and 2011 (T2). Stability, change, and covariation were investigated in longitudinal biometric models. New genetic factors explained 56.4% of the genetic variance in AUD at T2. For MDD, there was full overlap between genetic influences at T1 and T2. Genetic risk factors for MDD were related to AUD, but their association with AUD did not increase over time. Thus, genetic risk factors for AUD, but not MDD, vary with age, suggesting that AUD has age-dependent heritable etiologies. Molecular genetic studies of AUD may therefore benefit from stratifying by age. The new genetic factors in AUD were not related to MDD. Environmental influences on the 2 disorders were correlated in middle, but not in young adulthood. The environmental components for AUD correlated over time (r = .27), but not for MDD. Environmental influences on AUD can have long-lasting effects, and the effects of preventive efforts may be enduring. Environment influences seem to be largely transient. (PsycINFO Database Record
Notes
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PubMed ID
28541064 View in PubMed
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Strong genetic correlation between interview-assessed internalizing disorders and a brief self-report symptom scale.

https://arctichealth.org/en/permalink/ahliterature137124
Source
Twin Res Hum Genet. 2011 Feb;14(1):64-72
Publication Type
Article
Date
Feb-2011
Author
Line C Gjerde
Espen Røysamb
Nikolai Czajkowski
Ted Reichborn-Kjennerud
Ragnhild E Orstavik
Kenneth S Kendler
Kristian Tambs
Author Affiliation
Department of Psychology, University of Oslo, Norway; Norwegian Institute of Public Health, Division of Mental Health, Norway. linecgj@student.sv.uio.no
Source
Twin Res Hum Genet. 2011 Feb;14(1):64-72
Date
Feb-2011
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Anxiety Disorders - diagnosis - genetics - psychology
Depressive Disorder - diagnosis - genetics - psychology
Environment
Female
Genetic Variation
Humans
Interviews as Topic
Male
Norway
Phenotype
Regression Analysis
Risk factors
Self Report
Social Environment
Twins, Dizygotic - genetics - psychology
Twins, Monozygotic - genetics - psychology
Young Adult
Abstract
Self-report scales for symptoms of anxiety and depression are frequently used for screening and research purposes. A moderate phenotypic association between disorders measured by diagnostic interviews and symptoms of anxiety and depression measured by self-report scales has been shown, but little is known about the overlap in these phenotypes' genetic and environmental variance. In the present study, we used twin modeling to identify common genetic and environmental liabilities underlying the phenotypic association between the self-report Symptom Checklist-5 (SCL-5) and lifetime internalizing disorders derived from the Composite International Diagnostic Interview (CIDI). The sample consisted of 7,992 young adult twins from the Norwegian Institute of Public Health Twin Panel (NIPHT), who all responded to a questionnaire. A subset of 2,793 individuals later underwent structured interviews. The best fitting model showed a strong genetic correlation of 0.82 (95% confidence interval; 0.61-1.0) between current self-report symptoms of anxiety and depression, and lifetime internalizing disorders, which suggests an almost complete overlap in genetic liability. The correlation between environmental factors was much lower: 0.16 (0.00-0.34, 95% CI). This implies that brief self-report scales capture genetic variance that is highly overlapping with the genetic variance common to internalizing disorder diagnoses. It thus follows that SCL-5 and similar instruments may be used as screening instruments for genetic risk factors that influence liability to internalizing disorders. In addition, existing data on self-report symptoms of anxiety and depression can be used with increased confidence to specify models including effects from genes coding for internalizing disorders.
Notes
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PubMed ID
21314257 View in PubMed
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