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Age, period and cohort trends in drug abuse hospitalizations within the total Swedish population (1975-2010).

https://arctichealth.org/en/permalink/ahliterature105832
Source
Drug Alcohol Depend. 2014 Jan 1;134:355-61
Publication Type
Article
Date
Jan-1-2014
Author
Giuseppe N Giordano
Henrik Ohlsson
Kenneth S Kendler
Marilyn A Winkleby
Kristina Sundquist
Jan Sundquist
Author Affiliation
Center for Primary Health Care Research, Lund University, Jan Waldenströmsgata 35, CRC, building 28, floor 11, entrance 72, Malmö University Hospital, Malmö, S-205 02, Sweden. Electronic address: giuseppe_nicola.giordano@med.lu.se.
Source
Drug Alcohol Depend. 2014 Jan 1;134:355-61
Date
Jan-1-2014
Language
English
Publication Type
Article
Keywords
Adult
Age Factors
Cohort Studies
Female
Hospitalization - trends
Humans
Male
Middle Aged
Population Surveillance - methods
Substance-Related Disorders - diagnosis - epidemiology - therapy
Sweden - epidemiology
Time Factors
Young Adult
Abstract
The societal consequences of drug abuse (DA) are severe and well documented, the World Health Organization recommending tracking of population trends for effective policy responses in treatment of DA and delivery of health care services. However, to correctly identify possible sources of DA change, one must first disentangle three different time-related influences on the need for treatment due to DA: age effects, period effects and cohort effects.
We constructed our main Swedish national DA database (spanning four decades) by linking healthcare data from the Swedish Hospital Discharge Register to individuals, which included hospitalisations in Sweden for 1975-2010. All hospitalized DA cases were identified by ICD codes. Our Swedish national sample consisted of 3078,129 men and 2921,816 women. We employed a cross-classified multilevel logistic regression model to disentangle any net age, period and cohort effects on DA hospitalization rates.
We found distinct net age, period and cohort effects, each influencing the predicted probability of hospitalisation for DA in men and women. Peak age for DA in both sexes was 33-35 years; net period effects showed an increase in hospitalisation for DA from 1996 to 2001; and in birth cohorts 1968-1974, we saw a considerable reduction (around 75%) in predicted probability of hospitalisation for DA.
The use of hospital admissions could be regarded as a proxy of the population's health service use for DA. Our results may thus constitute a basis for effective prevention planning, treatment and other appropriate policy responses.
PubMed ID
24300899 View in PubMed
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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
Cites: Psychol Med. 2015 Aug;45(11):2353-64 PMID 25782712
Cites: J Stud Alcohol Drugs. 2015 Sep;76(5):773-80 PMID 26402358
Cites: Am J Public Health. 1991 Mar;81(3):305-18 PMID 1994739
Cites: Psychol Addict Behav. 2008 Mar;22(1):25-35 PMID 18298228
Cites: Psychol Med. 2015 Apr;45(5):1061-72 PMID 25171596
Cites: J Pers Soc Psychol. 1996 Aug;71(2):288-99 PMID 8765483
Cites: J Consult Clin Psychol. 2015 Jun;83(3):617-29 PMID 25664643
Cites: J Stud Alcohol Drugs. 2014 May;75(3):520-9 PMID 24766764
Cites: Psychometrika. 2011 Apr 1;76(2):306-317 PMID 23258944
Cites: Behav Genet. 2006 Mar;36(2):201-15 PMID 16645902
Cites: J Abnorm Psychol. 2002 Feb;111(1):124-33 PMID 11871377
Cites: Am J Psychiatry. 1998 Aug;155(8):1092-6 PMID 9699699
Cites: J Clin Psychol. 2012 May;68(5):514-25 PMID 22504611
Cites: Psychol Addict Behav. 2004 Dec;18(4):340-9 PMID 15631606
Cites: Alcohol Clin Exp Res. 2008 Sep;32(9):1615-22 PMID 18616689
Cites: Alcohol Clin Exp Res. 1999 Jan;23(1):101-7 PMID 10029209
Cites: Arch Gen Psychiatry. 2003 Sep;60(9):929-37 PMID 12963675
Cites: Psychol Bull. 2000 Jan;126(1):78-108 PMID 10668351
Cites: J Abnorm Psychol. 2005 Nov;114(4):570-86 PMID 16351381
Cites: Drug Alcohol Depend. 2006 Jun 28;83(2):137-46 PMID 16364565
Cites: JAMA Psychiatry. 2015 Aug;72(8):757-66 PMID 26039070
Cites: Twin Res Hum Genet. 2006 Aug;9(4):481-9 PMID 16899154
Cites: Addiction. 1999 Oct;94(10 ):1477-87 PMID 10790900
Cites: Br J Addict. 1991 Oct;86(10):1269-81 PMID 1836409
Cites: J Intern Med. 2002 Sep;252(3):184-205 PMID 12270000
Cites: Behav Genet. 2002 May;32(3):221-7 PMID 12141783
Cites: Pers Individ Dif. 2010 Oct 1;49(5):473-478 PMID 20729979
Cites: Soc Sci Med. 2005 Dec;61(11):2304-16 PMID 16139939
Cites: Am J Med Genet. 2000 Oct 9;96(5):684-95 PMID 11054778
Cites: JAMA Psychiatry. 2015 Mar;72(3):211-8 PMID 25565339
Cites: Psychol Addict Behav. 2014 Sep;28(3):780-9 PMID 24128287
Cites: Addiction. 2016 Aug;111(8):1323-5 PMID 26929107
Cites: J Stud Alcohol. 1999 Sep;60(5):647-52 PMID 10487734
Cites: J Pers Soc Psychol. 1993 Jul;65(1):56-68 PMID 8355143
Cites: Alcohol Clin Exp Res. 2011 Apr;35(4):632-42 PMID 21244438
Cites: Scand J Soc Med. 1992 Sep;20(3):134-42 PMID 1485149
Cites: J Abnorm Psychol. 2002 Aug;111(3):411-24 PMID 12150417
Cites: Am J Psychiatry. 2001 Jul;158(7):1091-8 PMID 11431231
Cites: J Abnorm Psychol. 2011 Feb;120(1):210-22 PMID 21133510
PubMed ID
27981669 View in PubMed
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Alcohol Use Disorder and Mortality Across the Lifespan: A Longitudinal Cohort and Co-relative Analysis.

https://arctichealth.org/en/permalink/ahliterature282515
Source
JAMA Psychiatry. 2016 Jun 01;73(6):575-81
Publication Type
Article
Date
Jun-01-2016
Author
Kenneth S Kendler
Henrik Ohlsson
Jan Sundquist
Kristina Sundquist
Source
JAMA Psychiatry. 2016 Jun 01;73(6):575-81
Date
Jun-01-2016
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Age Factors
Age of Onset
Aged
Alcoholism - genetics - mortality
Cause of Death
Cohort Studies
Diseases in Twins - genetics - mortality
Female
Genetic Predisposition to Disease - genetics
Humans
Longitudinal Studies
Male
Middle Aged
Proportional Hazards Models
Registries
Risk factors
Statistics as Topic
Sweden
Young Adult
Abstract
Excess alcohol consumption and alcohol use disorders (AUDs) are associated with substantially increased mortality. Efforts to reduce this toll require an understanding of their causes.
To clarify the degree to which the excess mortality associated with AUDs arises (1) from the predispositions of the person who develops AUD (and which would likely be shared by close relatives) and (2) as a direct result of AUD itself.
A prospective cohort and co-relative design study involving all individuals born in Sweden from 1940 to 1965 who had neither died nor migrated prior to 1973 or age 15 years (N?=?2?821?036). They were followed up from January 1, 1973, until December 31, 2010. Alcohol use disorder was assessed from medical, criminal, and pharmacy registries. Half-siblings, full-siblings, and monozygotic twin pairs discordant for AUD were obtained from the Multi-Generation and Twin Register.
Death obtained from the Swedish Death registry.
Our cohort (1?447?887 males and 1?373?149 females) included 131?895 males and 42?163 females registered with AUD. The mean (SD) age at first AUD registration was 39 (13.4) years. We ascertained 127?347 and 76?325 deaths in the male and female subsamples, respectively. Controlling for sex, educational status, and year of birth, the mortality hazard ratio associated with AUD was 5.83 (95% CI, 5.76-5.90) and varied-with an inverted U-shaped function-by age. Examining the AUD-mortality association in the general population and in relative pairs discordant for AUD exposure demonstrated substantial familial confounding in early to mid-adulthood: the AUD-associated mortality hazard ratio was much lower in discordant close relatives than in the general population. In middle to late adulthood, evidence for familial confounding decreased with increasing evidence for a direct effect of AUD on elevated mortality. In the oldest age group (65-70 years), the mortality hazard ratios were similar across the population and all relative pairs, suggesting that the excess mortality was largely a result of having AUD. Adding years since onset of AUD to the model showed that both increasing age and increasing years of duration of AUD contributed to the reduction of familial confounding in the association between AUD and elevated mortality.
Excess mortality associated with AUD arises both from the predispositions of the person who develops AUD and the direct result of having AUD. The effect of predisposition is more prominent early in the life course and in the early years of AUD. The direct effect of AUD becomes progressively more important later in life and with longer duration of AUD. These results have implications for interventions seeking to reduce the elevated AUD-associated mortality.
Notes
Cites: Acta Psychiatr Scand. 2015 Apr;131(4):297-30625243359
Cites: Nat Genet. 2015 Jul;47(7):702-925985137
Cites: JAMA Psychiatry. 2015 Aug;72(8):757-6626039070
Cites: EBioMedicine. 2015 Oct;2(10):1394-40426629534
Cites: J Gerontol A Biol Sci Med Sci. 1998 Nov;53(6):M441-69823748
Cites: Lancet. 1997 Aug 9;350(9075):383-89259651
Cites: J Abnorm Psychol. 1994 Feb;103(1):92-1028040486
Cites: Proc Natl Acad Sci U S A. 2015 Dec 8;112(49):15078-8326575631
Cites: Arch Gen Psychiatry. 1994 Jan;51(1):8-198279933
Cites: Br J Addict. 1988 Oct;83(10):1193-2003191267
Cites: Br Med J (Clin Res Ed). 1988 Apr 9;296(6628):1021-53130122
Cites: J Occup Med. 1973 Feb;15(2):120-54685423
Cites: Twin Res. 2004 Feb;7(1):72-8115053856
Cites: JAMA. 2004 Mar 10;291(10):1238-4515010446
Cites: Am J Psychiatry. 2001 Jul;158(7):1091-811431231
Cites: Alcohol Alcohol. 2000 Nov-Dec;35(6):601-1111093968
Cites: JAMA Psychiatry. 2015 Mar;72(3):211-825565339
Cites: Int J Epidemiol. 2014 Jun;43(3):906-1924513684
Cites: Addiction. 2013 Sep;108(9):1562-7823627868
Cites: Addiction. 1994 Jan;89(1):87-938148748
Cites: Lancet. 2012 Dec 15;380(9859):2095-12823245604
Cites: J Stud Alcohol Drugs. 2012 Nov;73(6):938-5023036212
Cites: Drug Alcohol Depend. 2011 Oct 1;118(1):56-6121440382
Cites: Addiction. 2009 Mar;104(3):413-919207349
Cites: Arch Gen Psychiatry. 2007 Nov;64(11):1313-2017984400
Cites: Nat Rev Genet. 2006 Jun;7(6):436-4816708071
Cites: Hum Genet. 2006 Apr;119(3):312-2116463022
Cites: Twin Res. 1998 Dec;1(4):196-20510100811
Cites: Alcohol Alcohol. 2013 Jul-Aug;48(4):509-1323531718
PubMed ID
27097014 View in PubMed
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An extended Swedish national adoption study of alcohol use disorder.

https://arctichealth.org/en/permalink/ahliterature263536
Source
JAMA Psychiatry. 2015 Mar;72(3):211-8
Publication Type
Article
Date
Mar-2015
Author
Kenneth S Kendler
Jianguang Ji
Alexis C Edwards
Henrik Ohlsson
Jan Sundquist
Kristina Sundquist
Source
JAMA Psychiatry. 2015 Mar;72(3):211-8
Date
Mar-2015
Language
English
Publication Type
Article
Keywords
Adoption
Adult
Alcohol-Related Disorders - epidemiology - etiology - genetics
Child
Environment
Female
Genetic Predisposition to Disease - epidemiology
Humans
Male
Middle Aged
Parents
Registries - statistics & numerical data
Risk factors
Siblings
Sweden - epidemiology
Young Adult
Abstract
Alcohol use disorder (AUD) runs strongly in families. It is unclear to what extent the cross-generational transmission of AUD results from genetic vs environmental factors.
To determine to what extent genetic and environmental factors contribute to the risk for AUD.
Follow-up in 8 public data registers of adoptees, their biological and adoptive relatives, and offspring and parents from stepfamilies and not-lived-with families in Sweden. In this cohort study, subtypes of AUD were assessed by latent class analysis. A total of 18,115 adoptees (born 1950-1993) and 171,989 and 107,696 offspring of not-lived-with parents and stepparents, respectively (born 1960-1993).
Alcohol use disorder recorded in medical, legal, or pharmacy registry records.
Alcohol use disorder in adoptees was significantly predicted by AUD in biological parents (odds ratio, 1.46; 95% CI, 1.29-1.66) and siblings (odds ratio, 1.94; 95% CI, 1.55-2.44) as well as adoptive parents (odds ratio, 1.40; 95% CI, 1.09-1.80). Genetic and environmental risk indices created from biological and adoptive relatives acted additively on adoptee AUD liability. Results from biological and adoptive relatives were replicated and extended from examinations of, respectively, not-lived-with parents and stepparents. Multivariate models in these families showed that AUD in offspring was significantly predicted by AUD, drug abuse, psychiatric illness, and crime in not-lived-with parents and by AUD, drug abuse, crime, and premature death in stepparents. Latent class analyses of adoptees and offspring of not-lived-with parents with AUDs revealed 3 AUD classes characterized by (1) female preponderance and high rates of psychiatric illness, (2) mild nonrecurrent symptoms, and (3) early-onset recurrence, drug abuse, and crime. These classes had distinct genetic signatures in the patterns of risk for various disorders in their not-lived-with parents and striking differences in the rates of recorded mood disorders.
Parent-offspring transmission of AUD results from both genetic and environmental factors. Genetic risk for AUD reflects both a specific liability to AUD and to other externalizing disorders. Environmental risk reflects features of both parental psychopathology and other aspects of the rearing environment. Alcohol use disorder is a heterogeneous syndrome and meaningful subtypes emerged from latent class analysis, which were validated by patterns of disorders in biological parents and specific psychiatric comorbidities. The general population contains informative family constellations that can complement more traditional adoption designs in clarifying the sources of parent-offspring resemblance.
Notes
Cites: Arch Gen Psychiatry. 1992 Aug;49(8):599-6081637250
Cites: Arch Gen Psychiatry. 1994 Jan;51(1):8-198279933
Cites: Compr Psychiatry. 1994 May-Jun;35(3):171-98045106
Cites: Psychol Med. 1996 Jan;26(1):79-958643766
Cites: Arch Gen Psychiatry. 1996 Aug;53(8):681-78694681
Cites: Alcohol Clin Exp Res. 1996 Dec;20(9):1528-338986199
Cites: Arch Gen Psychiatry. 1997 Feb;54(2):178-849040286
Cites: Psychol Med. 1997 Nov;27(6):1381-969403910
Cites: Am J Psychiatry. 1999 Jan;156(1):34-409892295
Cites: Br J Psychiatry. 2010 Sep;197(3):170-120807958
Cites: Am J Psychiatry. 2011 Jan;168(1):29-3920952461
Cites: Arch Gen Psychiatry. 1977 Sep;34(9):1005-9901132
Cites: Arch Gen Psychiatry. 2004 Sep;61(9):922-815351771
Cites: Arch Gen Psychiatry. 2003 Sep;60(9):929-3712963675
Cites: Am J Psychiatry. 2001 Jul;158(7):1091-811431231
Cites: Acta Psychiatr Scand. 1991 Jan;83(1):12-52011949
Cites: Arch Gen Psychiatry. 1985 Feb;42(2):161-73977542
Cites: J Stud Alcohol. 1987 Jan;48(1):1-83821113
Cites: Arch Gen Psychiatry. 1991 Jan;48(1):19-281984758
Cites: Arch Gen Psychiatry. 1981 Sep;38(9):965-97283667
Cites: J Stud Alcohol. 1979;40(1):89-116376949
Cites: Arch Gen Psychiatry. 1981 Aug;38(8):861-87259422
PubMed ID
25565339 View in PubMed
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Association between co-twin sex and eating disorders in opposite sex twin pairs: evaluations in North American, Norwegian, and Swedish samples.

https://arctichealth.org/en/permalink/ahliterature128481
Source
J Psychosom Res. 2012 Jan;72(1):73-7
Publication Type
Article
Date
Jan-2012
Author
Janet A Lydecker
Emily M Pisetsky
Karen S Mitchell
Laura M Thornton
Kenneth S Kendler
Ted Reichborn-Kjennerud
Paul Lichtenstein
Cynthia M Bulik
Suzanne E Mazzeo
Author Affiliation
Department of Psychology, Virginia Commonwealth University, Richmond, VA, USA.
Source
J Psychosom Res. 2012 Jan;72(1):73-7
Date
Jan-2012
Language
English
Publication Type
Article
Keywords
Adult
Diseases in Twins - diagnosis - genetics
Eating Disorders - diagnosis - genetics
Female
Humans
Male
North America
Norway
Sex Factors
Sweden
Twins
Abstract
These three studies examined the hypothesis that prenatal exposure to sex hormones influences twins' risk for eating disorders based on co-twin sex, such that individuals with a female co-twin would be more likely than individuals with a male co-twin to meet diagnostic criteria for an eating disorder.
Male and female twins from the United States (N=2607), Norway (N=2796) and Sweden (N=16,458) with known co-twin sex and zygosity were assessed for eating disorders.
In the U.S. and Swedish samples, sex was significantly associated with eating disorder diagnoses, and although co-twin sex was not associated with eating disorders overall, it was associated with broadly defined bulimia nervosa in the Swedish sample. The effects for bulimia were not sustained when monozygotic twins were excluded, suggesting that the effects of prenatal sex hormones play a minor role in influencing eating disorders. Sex and co-twin sex were not associated with eating disorders in the Norwegian sample.
The prenatal sex hormone hypothesis, which proposes that prenatal hormone exposure is associated with later eating disorder symptomatology, was not supported in these three population-based twin samples.
Notes
Cites: Arch Gen Psychiatry. 2008 Mar;65(3):329-3618316679
Cites: Psychol Med. 2008 Dec;38(12):1749-5718307829
Cites: Int J Eat Disord. 2008 Dec;41(8):673-8018537168
Cites: Am J Psychiatry. 2008 Dec;165(12):1604-1018981064
Cites: J Sch Psychol. 2008 Jun;46(3):343-6619083363
Cites: Br J Psychiatry. 2009 Apr;194(4):375-619336794
Cites: Twin Res Hum Genet. 2009 Apr;12(2):158-6819335186
Cites: Biol Psychiatry. 2010 Jan 1;67(1):71-719828139
Cites: Psychol Med. 2010 Oct;40(10):1745-5320059800
Cites: Int J Eat Disord. 2010 Sep;43(6):543-819718667
Cites: J Abnorm Psychol. 2000 May;109(2):239-5110895562
Cites: Mol Psychiatry. 2002;7(1):86-911803451
Cites: J Intern Med. 2002 Sep;252(3):184-20512270000
Cites: Twin Res. 2002 Oct;5(5):427-3212537870
Cites: Int J Eat Disord. 2003 Dec;34(4):383-9614566926
Cites: Physiol Behav. 2003 Nov;80(2-3):273-914637226
Cites: Mol Psychiatry. 2004 Jan;9(1):28-3414699439
Cites: Psychoneuroendocrinology. 2004 Aug;29(7):911-615177706
Cites: Physiol Behav. 2004 Aug;82(1):35-4115234587
Cites: Horm Behav. 1978 Feb;10(1):40-53658890
Cites: J Consult Clin Psychol. 1987 Oct;55(5):635-443331627
Cites: Physiol Behav. 1993 Feb;53(2):329-358446694
Cites: Int J Eat Disord. 1994 Dec;16(4):363-707866415
Cites: Arch Gen Psychiatry. 1999 Jan;56(1):39-449892254
Cites: Science. 1964 Jan 17;143(3603):212-814077548
Cites: Endocrinology. 1959 Sep;65:369-8214432658
Cites: Horm Behav. 2005 Feb;47(2):230-715664027
Cites: Neurosci Biobehav Rev. 2005 Apr;29(2):353-8415811504
Cites: Psychol Med. 2006 Apr;36(4):539-4616336745
Cites: Int J Eat Disord. 2006 Apr;39(3):202-1116498586
Cites: Psychol Med. 2007 Jan;37(1):131-4117038206
Cites: Biol Psychiatry. 2007 Feb 1;61(3):348-5816815322
Cites: Twin Res Hum Genet. 2006 Dec;9(6):875-8217254424
PubMed ID
22200526 View in PubMed
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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
Cites: Am J Public Health. 2010 May;100(5):933-919846689
Cites: Psychosom Med. 2010 May;72(4):370-520190130
Cites: Psychosom Med. 2011 Feb-Mar;73(2):114-2621257974
Cites: Diabetes Care. 2011 Mar;34(3):752-6221357362
Cites: Twin Res Hum Genet. 2011 Apr;14(2):169-7221425899
Cites: Diabetologia. 2011 Nov;54(11):2811-921826484
Cites: Diabetologia. 2012 Jan;55(1):63-7221811871
Cites: Diabetes Care. 2012 Dec;35(12):2479-8422923665
Cites: Diabetes Care. 2013 Jan;36 Suppl 1:S67-7423264425
Cites: Health Psychol. 2013 Mar;32(3):254-6323437855
Cites: PLoS One. 2013;8(3):e5705823472075
Cites: Diabetes Metab Res Rev. 2013 May;29(4):273-8423390036
Cites: Mol Psychiatry. 2013 Jun;18(6):692-923089630
Cites: Diabet Med. 2013 Jul;30(7):767-7723711019
Cites: Psychosomatics. 2013 Sep-Oct;54(5):428-3623756124
Cites: Diabetes Care. 2013 Oct;36(10):3337-4524065841
Cites: Brain Behav Immun. 2014 Feb;36:46-5324095894
Cites: JAMA Psychiatry. 2014 Mar;71(3):273-8024402003
Cites: Psychosom Med. 2014 Sep;76(7):555-6125077428
Cites: J Intern Med. 2000 Feb;247(2):188-9710692081
Cites: Br J Psychiatry. 2001 Nov;179:450-511689404
Cites: J Intern Med. 2002 Sep;252(3):184-20512270000
Cites: Twin Res. 2002 Oct;5(5):427-3212537870
Cites: Psychosom Med. 2003 May-Jun;65(3):490-712764224
Cites: Lancet. 2004 Sep 11-17;364(9438):953-6215364186
Cites: Behav Genet. 1993 Jan;23(1):29-508476389
Cites: Am J Hum Genet. 1995 Oct;57(4):935-537573055
Cites: Annu Rev Psychol. 1997;48:191-2149046559
Cites: Diabetologia. 1999 Feb;42(2):139-4510064092
Cites: Am J Epidemiol. 2005 Apr 1;161(7):652-6015781954
Cites: Lancet. 2005 Mar 19-25;365(9464):1099-10415781105
Cites: Psychol Med. 2005 Nov;35(11):1573-916219115
Cites: Am J Psychiatry. 2006 Jan;163(1):109-1416390897
Cites: Int Rev Psychiatry. 2007 Oct;19(5):497-50717896230
Cites: Ann Clin Psychiatry. 2007 Oct-Dec;19(4):289-30318058286
Cites: Diabetes Care. 2008 Mar;31(3):420-618071002
Cites: JAMA. 2008 Jun 18;299(23):2751-918560002
Cites: Am J Public Health. 2008 Aug;98(8):1480-518556604
Cites: Diabetologia. 2008 Dec;51(12):2168-7818806995
Cites: Diabetes Care. 2008 Dec;31(12):2383-9019033418
Cites: Psychosom Med. 2009 Jan;71(1):57-6219073750
Cites: Annu Rev Clin Psychol. 2009;5:363-8919327033
Cites: Arch Gen Psychiatry. 2009 Aug;66(8):857-6319652125
Cites: Trends Endocrinol Metab. 2010 Mar;21(3):159-6519926299
Cites: Ann N Y Acad Sci. 2010 Feb;1186:190-22220201874
PubMed ID
25967355 View in PubMed
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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
Cites: Proc Assoc Am Physicians. 1999 Mar-Apr;111(2):109-1810220805
Cites: Am J Psychiatry. 2014 Feb;171(2):209-1724077613
Cites: Psychometrika. 2011 Apr 1;76(2):306-31723258944
Cites: Arch Gen Psychiatry. 2007 May;64(5):566-7617485608
Cites: Am J Med Genet. 1996 Sep 20;67(5):473-78886164
Cites: Dev Psychol. 2013 May;49(5):887-9922799581
Cites: Behav Genet. 2014 Jul;44(4):337-4624647834
Cites: Am J Psychiatry. 2015 Jun;172(6):553-6025698436
Cites: Psychometrika. 2016 Jun;81(2):535-4925622929
Cites: Twin Res Hum Genet. 2006 Aug;9(4):481-916899154
Cites: Twin Res Hum Genet. 2006 Dec;9(6):875-8217254424
Cites: Addict Behav. 2006 Jun;31(6):1010-3416723188
Cites: Arch Gen Psychiatry. 2012 Jul;69(7):690-722393206
Cites: Bull World Health Organ. 2013 Feb 1;91(2):102-2323554523
Cites: Am J Psychiatry. 2001 Jul;158(7):1091-811431231
Cites: JAMA Psychiatry. 2014 Apr;71(4):439-4524576925
PubMed ID
27480873 View in PubMed
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Childhood trauma and personality disorder criterion counts: a co-twin control analysis.

https://arctichealth.org/en/permalink/ahliterature105514
Source
J Abnorm Psychol. 2013 Nov;122(4):1070-6
Publication Type
Article
Date
Nov-2013
Author
Erin C Berenz
Ananda B Amstadter
Steven H Aggen
Gun Peggy Knudsen
Ted Reichborn-Kjennerud
Charles O Gardner
Kenneth S Kendler
Author Affiliation
Department of Psychiatry, Virginia Institute for Psychiatric and Behavioral Genetics.
Source
J Abnorm Psychol. 2013 Nov;122(4):1070-6
Date
Nov-2013
Language
English
Publication Type
Article
Keywords
Adult
Case-Control Studies
Child
Child Abuse - psychology
Diseases in Twins
Educational Status
Female
Humans
Life Change Events
Male
Norway
Personality Disorders - etiology
Regression Analysis
Sex Factors
Wounds and Injuries - psychology
Young Adult
Abstract
Correlational studies consistently report relationships between childhood trauma (CT) and most personality disorder (PD) criteria and diagnoses. However, it is not clear whether CT is directly related to PDs or whether common familial factors (i.e., shared environment and/or genetic factors) better account for that relationship. The current study used a cotwin control design to examine support for a direct effect of CT on PD criterion counts. Participants were from the Norwegian Twin Registry (N = 2,780), including a subset (n = 898) of twin pairs (449 pairs, 45% monozygotic [MZ]) discordant for CT meeting DSM-IV Posttraumatic Stress Disorder Criterion A. All participants completed the Norwegian version of the Structured Interview for DSM-IV Personality. Significant associations between CT and all PD criterion counts were detected in the general sample; however, the magnitude of observed effects was small, with CT accounting for no more than approximately 1% of variance in PD criterion counts. A significant, yet modest, interactive effect was detected for sex and CT on Schizoid and Schizotypal PD criterion counts, with CT being related to these disorders among women but not men. After common familial factors were accounted for in the discordant twin sample, CT was significantly related to Borderline and Antisocial PD criterion counts, but no other disorders; however, the magnitude of observed effects was quite modest (r2 = .006 for both outcomes), indicating that the small effect observed in the full sample is likely better accounted for by common genetic and/or environmental factors. CT does not appear to be a key factor in PD etiology.
PubMed ID
24364608 View in PubMed
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Clinical features of registry-ascertained alcohol use disorders that reflect familial risk.

https://arctichealth.org/en/permalink/ahliterature286578
Source
Drug Alcohol Depend. 2016 Jul 01;164:135-42
Publication Type
Article
Date
Jul-01-2016
Author
Kenneth S Kendler
Henrik Ohlsson
Alexis C Edwards
Katherine J Karriker-Jaffe
Jan Sundquist
Kristina Sundquist
Source
Drug Alcohol Depend. 2016 Jul 01;164:135-42
Date
Jul-01-2016
Language
English
Publication Type
Article
Keywords
Adult
Age of Onset
Alcohol-Related Disorders - diagnosis - epidemiology - genetics
Cross-Sectional Studies
Diseases in Twins - diagnosis - epidemiology - genetics
Female
Genotype
Humans
Male
Middle Aged
Registries
Risk
Sweden
Twins, Monozygotic - genetics - statistics & numerical data
Abstract
Alcohol Use Disorder (AUD) is clinically heterogeneous. Using a large epidemiological sample ascertained via public registries, is it possible to identify clinical and historical features of AUD that reflect familial risk?
Using registration in national medical, legal or pharmacy registries, we identified four kinds of relative pairs (n=683,223) starting with a proband with AUD: cousins, half-siblings, full-siblings and monozygotic cotwins. Using linear hazard regression, we examined the interaction between five clinical/historical features of AUD in the proband and risk for AUD in these relatives.
Increased risk for AUD in relatives was predicted by the proband's early age at first registration, total number of registrations, recurrence, history of drug abuse and ascertainment in the medical versus the legal or pharmacy registry. In multivariate models, age at first registration, number of registrations, recurrence and history of drug abuse remained significant and in aggregate strongly predicted the risk for AUD in relatives. The risk for AUD in siblings of AUD probands in the highest decile of genetic risk predicted by these four indices was more than twice as great as that predicted in siblings of probands in the lowest risk decile.
In an epidemiological sample, familial risk for AUD can be assessed by simple clinical and historical variables.
Notes
Cites: J Stud Alcohol. 1979;40(1):89-116376949
Cites: Behav Genet. 2016 Mar;46(2):183-9226494460
Cites: Arch Gen Psychiatry. 2007 Nov;64(11):1313-2017984400
Cites: Methods Mol Biol. 2011;675:215-2020949391
Cites: N Engl J Med. 1994 Apr 14;330(15):1041-68127331
Cites: Psychol Med. 2015 Apr;45(5):1061-7225171596
Cites: Br J Psychiatry. 2010 Sep;197(3):170-120807958
Cites: J Stat Softw. 2011 Jan;38(2):null22707920
Cites: Arch Gen Psychiatry. 1996 Aug;53(8):681-78694681
Cites: J Abnorm Psychol. 1992 Feb;101(1):3-171537970
Cites: Alcohol Clin Exp Res. 1999 Jan;23(1):101-710029209
Cites: Twin Res Hum Genet. 2006 Dec;9(6):875-8217254424
Cites: Addiction. 2012 Apr;107(4):748-5522008293
Cites: J Stud Alcohol. 1999 Jan;60(1):7-1710096304
Cites: Arch Gen Psychiatry. 1981 Oct;38(10):1085-906457579
Cites: JAMA Psychiatry. 2015 Mar;72(3):211-825565339
Cites: Arch Gen Psychiatry. 2012 Jul;69(7):690-722393206
Cites: Psychol Med. 2014 Sep;44(12):2547-5624461082
Cites: Biol Psychiatry. 2000 Aug 15;48(4):265-7510960157
Cites: Am J Psychiatry. 2000 Oct;157(10):1552-6211007705
Cites: Acta Psychiatr Scand. 2007 Mar;115(3):214-2017302621
Cites: Am J Psychiatry. 2011 Jan;168(1):29-3920952461
Cites: Blood. 2001 Feb 15;97(4):858-6211159508
Cites: Am J Psychiatry. 2001 Jul;158(7):1091-811431231
Cites: Arch Gen Psychiatry. 1989 Mar;46(3):225-302919951
PubMed ID
27234657 View in PubMed
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