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Adipose co-expression networks across Finns and Mexicans identify novel triglyceride-associated genes.

https://arctichealth.org/en/permalink/ahliterature118360
Source
BMC Med Genomics. 2012;5:61
Publication Type
Article
Date
2012
Author
Blake E Haas
Steve Horvath
Kirsi H Pietiläinen
Rita M Cantor
Elina Nikkola
Daphna Weissglas-Volkov
Aila Rissanen
Mete Civelek
Ivette Cruz-Bautista
Laura Riba
Johanna Kuusisto
Jaakko Kaprio
Teresa Tusie-Luna
Markku Laakso
Carlos A Aguilar-Salinas
Päivi Pajukanta
Author Affiliation
Department of Human Genetics, Gonda Center, Los Angeles, California, 90095-7088, USA.
Source
BMC Med Genomics. 2012;5:61
Date
2012
Language
English
Publication Type
Article
Keywords
Adipose Tissue - metabolism
Case-Control Studies
Finland
Gene Expression Profiling
Gene Expression Regulation
Gene Regulatory Networks - genetics
Genetic Loci - genetics
Genome-Wide Association Study
Humans
Immunity - genetics
Inflammation - blood - genetics
Mexico
Polymorphism, Single Nucleotide - genetics
Triglycerides - blood - genetics
Twins - genetics
Abstract
High serum triglyceride (TG) levels is an established risk factor for coronary heart disease (CHD). Fat is stored in the form of TGs in human adipose tissue. We hypothesized that gene co-expression networks in human adipose tissue may be correlated with serum TG levels and help reveal novel genes involved in TG regulation.
Gene co-expression networks were constructed from two Finnish and one Mexican study sample using the blockwiseModules R function in Weighted Gene Co-expression Network Analysis (WGCNA). Overlap between TG-associated networks from each of the three study samples were calculated using a Fisher's Exact test. Gene ontology was used to determine known pathways enriched in each TG-associated network.
We measured gene expression in adipose samples from two Finnish and one Mexican study sample. In each study sample, we observed a gene co-expression network that was significantly associated with serum TG levels. The TG modules observed in Finns and Mexicans significantly overlapped and shared 34 genes. Seven of the 34 genes (ARHGAP30, CCR1, CXCL16, FERMT3, HCST, RNASET2, SELPG) were identified as the key hub genes of all three TG modules. Furthermore, two of the 34 genes (ARHGAP9, LST1) reside in previous TG GWAS regions, suggesting them as the regional candidates underlying the GWAS signals.
This study presents a novel adipose gene co-expression network with 34 genes significantly correlated with serum TG across populations.
Notes
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PubMed ID
23217153 View in PubMed
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Adolescent age moderates genetic and environmental influences on parent-adolescent positivity and negativity: Implications for genotype-environment correlation.

https://arctichealth.org/en/permalink/ahliterature275825
Source
Dev Psychopathol. 2016 Feb;28(1):149-66
Publication Type
Article
Date
Feb-2016
Author
Kristine Marceau
Valerie S Knopik
Jenae M Neiderhiser
Paul Lichtenstein
Erica L Spotts
Jody M Ganiban
David Reiss
Source
Dev Psychopathol. 2016 Feb;28(1):149-66
Date
Feb-2016
Language
English
Publication Type
Article
Keywords
Adolescent
Age Factors
Child
Environment
Family Relations
Female
Gene-Environment Interaction
Genotype
Humans
Male
Mothers
Parent-Child Relations
Parents
Social Environment
Sweden
Twins - genetics - psychology
Abstract
We examined how genotype-environment correlation processes differ as a function of adolescent age. We tested whether adolescent age moderates genetic and environmental influences on positivity and negativity in mother-adolescent and father-adolescent relationships using parallel samples of twin parents from the Twin and Offspring Study in Sweden and twin/sibling adolescents from the Nonshared Environment in Adolescent Development Study. We inferred differences in the role of passive and nonpassive genotype-environment correlation based on biometric moderation findings. The findings indicated that nonpassive gene-environment correlation played a stronger role for positivity in mother- and father-adolescent relationships in families with older adolescents than in families with younger adolescents, and that passive gene-environment correlation played a stronger role for positivity in the mother-adolescent relationship in families with younger adolescents than in families with older adolescents. Implications of these findings for the timing and targeting of interventions on family relationships are discussed.
Notes
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PubMed ID
25924807 View in PubMed
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Adolescent alcohol abuse and adverse adult outcomes: evaluating confounds with drinking-discordant twins.

https://arctichealth.org/en/permalink/ahliterature262747
Source
Alcohol Clin Exp Res. 2014 Aug;38(8):2314-21
Publication Type
Article
Date
Aug-2014
Author
Richard J Rose
Torsten Winter
Richard J Viken
Jaakko Kaprio
Source
Alcohol Clin Exp Res. 2014 Aug;38(8):2314-21
Date
Aug-2014
Language
English
Publication Type
Article
Keywords
Adolescent
Adolescent Behavior - psychology
Adult
Alcoholism - genetics - psychology
Diseases in Twins - genetics - psychology
Educational Status
Female
Finland - epidemiology
Health status
Humans
Income
Longitudinal Studies
Male
Sexual Behavior - psychology
Substance-Related Disorders - complications - epidemiology
Twins, Dizygotic - psychology
Twins, Monozygotic - psychology
Abstract
Adolescent alcohol abuse is associated with adverse outcomes in early adulthood, but differences in familial status and structure and household and community environments correlate with both adolescent drinking and adverse adult outcomes and may explain their association. We studied drinking-discordant twin pairs to evaluate such confounds to ask: Will between-family associations replicate in within-family comparisons?
With longitudinal data from >3,000 Finnish twins, we associated drinking problems at age 18½ with 13 outcomes assessed at age 25; included were sustained substance abuse, poor health, physical symptoms, early coital debut, multiple sexual partners, life dissatisfaction, truncated education, and financial problems. We assessed associations among twins as individuals with linear regression adjusted for correlated observations; within-family analyses of discordant twin pairs followed, comparing paired means for adult outcomes among co-twins discordant for adolescent problem drinking. Defining discordance by extreme scores on self-reported problem drinking at age 18½ permitted parallel analyses of twins as individuals and discordant twin pairs. Alternate definitions of pair-wise discordance and difference score correlations across the entire twin sample yielded supplementary analyses.
All individual associations were highly significant for all definitions of discordance we employed. Depending on definitions of discordance, 11 to 13 comparisons of all drinking-discordant twin pairs and 3 to 6 comparisons of discordant monozygotic (MZ) twin pairs replicated between-family associations. For most outcomes, effect size attenuated from individual-level analysis to that within discordant MZ twin pairs providing evidence of partial confounding in associations reported in earlier research. The exception was the General Health Questionnaire (GHQ); at age 25, GHQ-12 had equivalent associations with age 18½ Rutgers Alcohol Problem Index across all comparisons.
Our analyses control for shared family background, and, partly or fully, for shared genes, to yield within-family replications and more compelling evidence than previously available that adolescent alcohol abuse disrupts transitions into early adulthood.
Notes
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PubMed ID
25040879 View in PubMed
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Aetiology of teenage childbearing: reasons for familial effects.

https://arctichealth.org/en/permalink/ahliterature63962
Source
Twin Res. 2000 Mar;3(1):23-7
Publication Type
Article
Date
Mar-2000
Author
P O Olausson
P. Lichtenstein
S. Cnattingius
Author Affiliation
Department of Medical Epidemiology, Karolinska Institute, Stockholm, Sweden. petra.otterblad@mep.ki.se
Source
Twin Res. 2000 Mar;3(1):23-7
Date
Mar-2000
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Chi-Square Distribution
Environment
Female
Humans
Life Style
Logistic Models
Personality
Pregnancy
Pregnancy in adolescence
Questionnaires
Registries
Research Support, Non-U.S. Gov't
Risk factors
Socioeconomic Factors
Sweden
Twins - genetics - psychology
Abstract
The aims of the present study were to evaluate the contribution of the genetic and environmental factors to the risk of teenage childbearing, and to study whether life style, socio-economic conditions, and personality traits could explain possible familial effects. We linked two population-based registers: the Swedish Twin Register and the Swedish Medical Birth Register. The study covers female twin pairs born between 1953 and 1958, having their first infant before the age of 30 years (n = 1885). In order to separate familial effects from other environmental influences, and genetic effects from shared environmental effects, only complete twin pairs with known zygosity were included, in all 260 monozygotic and 370 dizygotic twin pairs. We used quantitative genetic analyses to evaluate the importance of genetic and environmental effects for liability to teenage childbearing. Logistic regression analyses were used to estimate the effects of life style, socio-economic situation, and personality on the probability of teenage childbearing, and to study whether psychosocial factors could explain possible familial effects. Fifty-nine percent (0-76%) of the variance in being a teenage mother was attributable to heritable factors; 0% (0-49%) was due to shared environmental factors; and 41% (23-67%) was explained by non-shared environmental factors. Thus, the data were consistent with the hypothesis that the familial aggregation of teenage childbearing is completely explained by genetic factors, although the alternative hypothesis that familial aggregation is entirely explained by shared environmental factors cannot be ruled out. Significant effects of smoking habits, housing conditions, and educational level were found in relation to liability to teenage childbearing. However, the familial effects on risk of teenage childbearing were not mediated through similarities in life style and socio-economic factors. When studying risk factors for teenage childbearing, it is recommended to include life style and socio-economic variables as well as information about family history of teenage childbearing. Twin Research (2000) 3, 23-27.
PubMed ID
10808237 View in PubMed
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Age of onset in concordant twins and other relative pairs with multiple sclerosis.

https://arctichealth.org/en/permalink/ahliterature150146
Source
Am J Epidemiol. 2009 Aug 1;170(3):289-96
Publication Type
Article
Date
Aug-1-2009
Author
A Dessa Sadovnick
Irene M Yee
Colleen Guimond
Jacques Reis
David A Dyment
George C Ebers
Author Affiliation
Department of Medical Genetics, Vancouver Coastal Health Authority-University of British Columbia Hospital, G-920 Detwiller Pavilion, Vancouver, British Columbia, Canada. sadovnik@infinet.net
Source
Am J Epidemiol. 2009 Aug 1;170(3):289-96
Date
Aug-1-2009
Language
English
Publication Type
Article
Keywords
Adult
Age of Onset
British Columbia - epidemiology
Diseases in Twins - diagnosis - epidemiology - genetics
Family
Female
Genetic Predisposition to Disease
Humans
Male
Multiple Sclerosis - diagnosis - epidemiology - genetics
Parents
Pedigree
Risk factors
Siblings
Time Factors
Twins - genetics
Twins, Dizygotic - genetics
Twins, Monozygotic - genetics
Abstract
The ages of onset in multiple sclerosis cases span more than 7 decades. Data are presented for affected relative pairs from a Canadian population base of 30,000 multiple sclerosis index cases (1993-2008). The effects of genetic sharing, parent of origin, intergenerational versus collinear differences, and gender on the ages of onset were evaluated in the following concordant pairs: monozygotic twins (n = 29), dizygotic twins (n = 10), siblings (n = 614), first cousins (n = 405), half siblings (n = 29), parent/child (n = 285), and aunt/uncle/niece/nephew (avunculars) (n = 289). Fisher's z test assessed intraclass correlation (r) for ages of onset. Correlations for monozygotic twins, dizygotic twins, full siblings, and first cousins were 0.60, 0.54, 0.20, and 0.10, respectively. Dizygotic twins resembled monozygotic twins more than siblings. The age-of-onset correlation for maternal half siblings (r = 0.37) was higher than that for paternal half siblings (r = 0.26), consistent with other observations suggesting an intrauterine environmental effect on multiple sclerosis risk. Intergenerational comparisons are complicated by substantial increases of multiple sclerosis incidence over time. Genetic loading (familial vs. sporadic cases) did not generally influence the age of onset, but correlation of age of onset in multiple sclerosis relative pairs was proportional to genetic sharing. A maternal parent-of-origin effect on the age of onset in collinear generations was suggested.
Notes
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PubMed ID
19546151 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
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PubMed ID
27097014 View in PubMed
Less detail
Source
Twin Res Hum Genet. 2015 Oct;18(5):619-20
Publication Type
Article
Date
Oct-2015
Author
Johan Fellman
Paolo Parisi
Source
Twin Res Hum Genet. 2015 Oct;18(5):619-20
Date
Oct-2015
Language
English
Publication Type
Article
Keywords
Finland
Genetics, Medical - history
History, 20th Century
History, 21st Century
Humans
Twins - genetics - history
PubMed ID
26271158 View in PubMed
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[An (inter)national resource. The Swedish registry on twins informs on the role of environment and heredity in diseases]

https://arctichealth.org/en/permalink/ahliterature34866
Source
Lakartidningen. 1996 Mar 20;93(12):1127-30
Publication Type
Article
Date
Mar-20-1996

An MHC (HLA-A, -B, C2, BF, HLA-DR, GLO1) haplotype study of 497 Danish normal families with 1970 children including 97 twin pairs.

https://arctichealth.org/en/permalink/ahliterature37544
Source
Tissue Antigens. 1990 Oct;36(4):141-8
Publication Type
Article
Date
Oct-1990
Author
L S Nielsen
H. Eiberg
K. Fenger
J. Mohr
Author Affiliation
Institute of Medical Genetics, University of Copenhagen, Denmark.
Source
Tissue Antigens. 1990 Oct;36(4):141-8
Date
Oct-1990
Language
English
Publication Type
Article
Keywords
Denmark
Female
Genetic Screening
HLA-A Antigens - genetics
HLA-B Antigens - genetics
HLA-C Antigens - genetics
HLA-DR Antigens - genetics
Haplotypes - genetics
Histocompatibility testing
Humans
Major Histocompatibility Complex - genetics
Male
Recombination, Genetic
Research Support, Non-U.S. Gov't
Twins - genetics
Twins, Dizygotic - genetics
Abstract
Extended MHC haplotypes comprising HLA-A, -B, -DR, C2, BF and GLO1 loci observed in the parents of 497 Danish normal families are presented, with particular regard to the haplotypes that include BF variants or the C2*2 allele. The known association of HLA-B35, -DR1 with both -A3 and -A11 appeared to depend upon the BF type: HLA-B35, BF*S, -DR1 is strongly associated with -A11, whereas -B35,BF*F,-DR1 is strongly associated with -A3. Further, in the present material DZ twins of the same sex shared HLA-haplotypes more often than did twin pairs of different sex.
PubMed ID
2077670 View in PubMed
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Anorexia and bulimia nervosa in same-sex and opposite-sex twins: lack of association with twin type in a nationwide study of Finnish twins.

https://arctichealth.org/en/permalink/ahliterature154434
Source
Am J Psychiatry. 2008 Dec;165(12):1604-10
Publication Type
Article
Date
Dec-2008
Author
Anu Raevuori
Jaakko Kaprio
Hans W Hoek
Elina Sihvola
Aila Rissanen
Anna Keski-Rahkonen
Author Affiliation
Columbia University, New York State Psychiatric Institute, 1051 Riverside Dr., Unit 23, New York, NY 10032, USA. anu.raevuori@helsinki.fi
Source
Am J Psychiatry. 2008 Dec;165(12):1604-10
Date
Dec-2008
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Anorexia Nervosa - diagnosis - epidemiology - genetics
Bulimia Nervosa - diagnosis - epidemiology - genetics
Diagnostic and Statistical Manual of Mental Disorders
Female
Finland - epidemiology
Humans
Incidence
Male
Phenotype
Prevalence
Questionnaires
Twins - genetics
Abstract
The authors tested the hypothesis that either prenatal feminization or masculinization hormone influences in utero or later socialization affects the risk for anorexia and bulimia nervosa and disordered eating in members of opposite-sex twin pairs.
Finnish twins (N=2,426 women, N=1,962 men with known zygosity) from birth cohorts born 1974-1979 were assessed at age 22 to 28 years with a questionnaire for eating disorder symptoms. Based on the questionnaire screen, women (N=292), men (N=53), and their cotwins were interviewed to assess diagnoses of anorexia nervosa and bulimia nervosa (per DSM-IV and broad criteria).
In women from opposite-sex twin pairs, the prevalence of DSM-IV or broad anorexia nervosa was not significantly different than that of women from monozygotic pairs or same-sex dizygotic pairs. Of the five male anorexia nervosa probands, only one was from an opposite-sex twin pair. Bulimia nervosa in men was too rare to be assessed by zygosity; the prevalence of DSM-IV or broad bulimia nervosa did not differ in women from opposite- versus same-sex twin pairs. In both sexes, the overall profile of indicators on eating disorders was rather similar between individuals from opposite- and same-sex pairs.
The authors found little evidence that the risk for anorexia nervosa, bulimia nervosa, or disordered eating was associated with zygosity or sex composition of twin pairs, thus making it unlikely that in utero femininization or masculinization or socialization effects of growing up with an opposite-sex twin have a major influence on the later development of eating disorders.
PubMed ID
18981064 View in PubMed
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