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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
Less detail

Age, Sex, and Genetic and Environmental Effects on Unintentional Injuries in Young and Adult Twins.

https://arctichealth.org/en/permalink/ahliterature298559
Source
Twin Res Hum Genet. 2018 12; 21(6):502-506
Publication Type
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Twin Study
Date
12-2018
Author
Simo Salminen
Eero Vuoksimaa
Richard J Rose
Jaakko Kaprio
Author Affiliation
Department of Social Psychology,University of Helsinki,Helsinki,Finland.
Source
Twin Res Hum Genet. 2018 12; 21(6):502-506
Date
12-2018
Language
English
Publication Type
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Twin Study
Keywords
Adolescent
Adult
Age Factors
Diseases in Twins - epidemiology - genetics
Environment
Female
Finland - epidemiology
Humans
Longitudinal Studies
Male
Middle Aged
Registries
Risk factors
Sex Factors
Twins, Dizygotic - genetics
Twins, Monozygotic - genetics
Wounds and Injuries - epidemiology - genetics
Young Adult
Abstract
The aim of this study was to examine the effects of genetic and environment influences and sex on injury involvement using two sets of Finnish twin data. The younger participants were 955 twins born between 1983 and 1987, aged 20 to 24 years. The older participants were 12,428 twins born between 1930 and 1957, aged 33 to 60 years. Within-twin correlations in monozygotic and dizygotic twins suggested that genetic effects play no role in injury involvement among young twins, but do have some effect at older ages. The results indicated that environmental factors have greater importance in injury involvement than genetic factors in the younger twin data set (FT12), whereas in a middle-aged (33-60 years) twin data set, genetic effects explained about quarter of the variance in injury involvement. Sex was a strong contributing factor, with males being generally more prone to injuries than females.
PubMed ID
30428952 View in PubMed
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Aggression as a mediator of genetic contributions to the association between negative parent-child relationships and adolescent antisocial behavior.

https://arctichealth.org/en/permalink/ahliterature79587
Source
Eur Child Adolesc Psychiatry. 2007 Mar;16(2):128-37
Publication Type
Article
Date
Mar-2007
Author
Narusyte Jurgita
Andershed Anna-Karin
Neiderhiser Jenae M
Lichtenstein Paul
Author Affiliation
Dept. of Medical Epidemiology and Biostatistics, Karolinska Institutet, Box 281, 171 77 Stockholm, Sweden. jurgita.narusyte@ki.se
Source
Eur Child Adolesc Psychiatry. 2007 Mar;16(2):128-37
Date
Mar-2007
Language
English
Publication Type
Article
Keywords
Adolescent
Aggression
Antisocial Personality Disorder - epidemiology - genetics
Female
Humans
Longitudinal Studies
Male
Models, Genetic
Parent-Child Relations
Risk factors
Sweden - epidemiology
Twins, Dizygotic - genetics
Twins, Monozygotic - genetics
Abstract
Previous research suggests that the association between conflictual parent-child relationships and maladjustment among adolescents is influenced by genetic effects emanating from the adolescents. In this study, we examined whether these effects are mediated by childhood aggression. The data come from the Twin study of CHild and Adolescent Development (TCHAD), a Swedish longitudinal study including 1,314 twin pairs followed from age 13-14 to 16-17. Early adolescent aggression, parental criticism, and delinquency in later adolescence were rated by parents and children at different time points. Multivariate genetic structural equation models were used to estimate genetic and environmental influences on these constructs and on their covariation. The results showed that approximately half of the genetic contribution to the association between parental criticism and delinquency was explained by early adolescent aggression. It suggests that aggression in children evokes negative parenting, which in turn influences adolescent antisocial behavior. The mechanism proposed by these findings is consistent with evocative gene-environment correlation.
PubMed ID
17136502 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
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PubMed ID
27981669 View in PubMed
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Analyzing the etiology of benign rolandic epilepsy: a multicenter twin collaboration.

https://arctichealth.org/en/permalink/ahliterature76297
Source
Epilepsia. 2006 Mar;47(3):550-5
Publication Type
Article
Date
Mar-2006
Author
Lata Vadlamudi
Marianne J Kjeldsen
Linda A Corey
Marit H Solaas
Mogen L Friis
John M Pellock
Karl O Nakken
Roger L Milne
Ingrid E Scheffer
A Simon Harvey
John L Hopper
Samuel F Berkovic
Author Affiliation
Epilepsy Research Centre, Department of Medicine (Neurology), University of Melbourne, Austin Health, Heidelberg, Victoria, Australia.
Source
Epilepsia. 2006 Mar;47(3):550-5
Date
Mar-2006
Language
English
Publication Type
Article
Keywords
Adult
Age of Onset
Australia - epidemiology
Comparative Study
Denmark - epidemiology
Diseases in Twins - diagnosis - epidemiology - genetics
Electroencephalography - statistics & numerical data
Epilepsy, Rolandic - diagnosis - epidemiology - genetics
Family
Female
Genetic Heterogeneity
Genotype
Humans
Male
Models, Genetic
Norway - epidemiology
Pedigree
Prevalence
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Twins, Dizygotic - genetics
Twins, Monozygotic - genetics
United States - epidemiology
Variation (Genetics)
Abstract
PURPOSE: Benign rolandic epilepsy (BRE) is considered a genetically determined idiopathic partial epilepsy. We analyzed a large sample of twins from four international twin registers to probe the genetics of BRE. We also aim to synthesize the apparently conflicting family and twin data into a model of BRE etiology. METHODS: Large population-based twin registries of epilepsies from Odense (Denmark), Richmond, Virginia (United States), and Oslo (Norway) were reviewed for BRE cases and added to our Australian twin data. Diagnosis of classic BRE was based on electroclinical criteria with normal neurologic development. Cases with a compatible electroclinical picture but abnormal neurologic development were termed non-classic BRE. RESULTS: Eighteen twin pairs were identified (10 monozygous; eight dizygous) of whom at least one twin was diagnosed with classic BRE among a total sample of 1,952 twin pairs validated for seizures, and all were discordant for BRE. The estimated monozygous pairwise concordance for BRE in this sample was 0.0 [95% confidence interval (CI), 0.0-0.3). Four twin pairs (one monozygous, three dizygous) had non-classic BRE, and all co-twins had seizures. CONCLUSIONS: The twin data showing an absence of any concordant twin pairs with classic BRE suggest that noninherited factors are of major importance in BRE. Modelling the data shows that the familial occurrence of centrotemporal spikes makes only a minor contribution to the familial aggregation of BRE. Genetic factors are probably more important in non-classic BRE. The etiology and mode(s) of inheritance of BRE are much more complicated than initially conceptualized.
PubMed ID
16529620 View in PubMed
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Ankylosing spondylitis in Danish and Norwegian twins: occurrence and the relative importance of genetic vs. environmental effectors in disease causation.

https://arctichealth.org/en/permalink/ahliterature93296
Source
Scand J Rheumatol. 2008 Mar-Apr;37(2):120-6
Publication Type
Article
Author
Pedersen O B
Svendsen A J
Ejstrup L.
Skytthe A.
Harris J R
Junker P.
Author Affiliation
Department of Internal Medicine C, Section of Rheumatology, Odense University Hospital, Odense, Denmark. obpedersen@health.sdu.dk
Source
Scand J Rheumatol. 2008 Mar-Apr;37(2):120-6
Language
English
Publication Type
Article
Keywords
Adult
Aged
Denmark - epidemiology
Female
Humans
Male
Middle Aged
Norway - epidemiology
Prevalence
Registries
Reproducibility of Results
Spondylitis, Ankylosing - diagnosis - epidemiology - genetics
Twins, Dizygotic - genetics
Twins, Monozygotic - genetics
Abstract
OBJECTIVE: To estimate the influence of genetic effects in the aetiology and pathogenesis of ankylosing spondylitis (AS). METHODS: The study comprised one Norwegian and two Danish nationwide twin surveys. In 1994 and 2002, respectively, 37,388 and 46,331 Danish twin individuals were asked by questionnaire if they had AS. Similarly, in 1998, 12,718 Norwegian twins were asked if they had AS using a questionnaire phrased according to the Danish survey. Twins reporting AS were categorized according to the modified New York criteria. RESULTS: A total of 113 twin individuals reported AS, of whom 81 (72.3%) participated in validation of the diagnosis. After validation, 39 probands were diagnosed with AS. Subsequent invitation of co-twins resulted in 27 complete pairs. The point prevalence and the annual incidence of AS was 0.1% and 3/100,000 person-years (pyr) among the Danish twins. The positive predictive value of self-reported AS was 49.3%. Probandwise concordance rates on AS were (2/5) 40% in monozygotic (MZ) and (1/23) 4% in dizygotic (DZ) twins [difference 35% (95% CI 2.9-72.8), p = 0.26]. Heredity analysis including previously published and the present HLA-B27-positive twin pairs indicated that additive genetic effects account for 94% (95% CI 0.56-0.99) of the variance in the causation of AS. CONCLUSION: Self-reported AS needs careful validation. The occurrence of AS in a Danish twin population was 0.1% and accords well with previous studies on singletons in hospital settings. The present study adds to previous evidence of a major genetic effect in the pathogenesis of AS.
Notes
Erratum In: Scand J Rheumatol. 2008 Sep-Oct;37(5):400
PubMed ID
18415769 View in PubMed
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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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An Underlying Common Factor, Influenced by Genetics and Unique Environment, Explains the Covariation Between Major Depressive Disorder, Generalized Anxiety Disorder, and Burnout: A Swedish Twin Study.

https://arctichealth.org/en/permalink/ahliterature286745
Source
Twin Res Hum Genet. 2016 Dec;19(6):619-627
Publication Type
Article
Date
Dec-2016
Author
Lisa Mather
Victoria Blom
Gunnar Bergström
Pia Svedberg
Source
Twin Res Hum Genet. 2016 Dec;19(6):619-627
Date
Dec-2016
Language
English
Publication Type
Article
Keywords
Adult
Aged
Anxiety Disorders - epidemiology - genetics - pathology
Burnout, Professional - epidemiology - genetics - pathology
Depressive Disorder, Major - epidemiology - genetics - pathology
Diseases in Twins - epidemiology - genetics - pathology
Environment
Female
Humans
Male
Middle Aged
Risk factors
Sweden
Twins, Dizygotic - genetics
Twins, Monozygotic - genetics
Young Adult
Abstract
Depression and anxiety are highly comorbid due to shared genetic risk factors, but less is known about whether burnout shares these risk factors. We aimed to examine whether the covariation between major depressive disorder (MDD), generalized anxiety disorder (GAD), and burnout is explained by common genetic and/or environmental factors. This cross-sectional study included 25,378 Swedish twins responding to a survey in 2005-2006. Structural equation models were used to analyze whether the trait variances and covariances were due to additive genetics, non-additive genetics, shared environment, and unique environment. Univariate analyses tested sex limitation models and multivariate analysis tested Cholesky, independent pathway, and common pathway models. The phenotypic correlations were 0.71 (0.69-0.74) between MDD and GAD, 0.58 (0.56-0.60) between MDD and burnout, and 0.53 (0.50-0.56) between GAD and burnout. Heritabilities were 45% for MDD, 49% for GAD, and 38% for burnout; no statistically significant sex differences were found. A common pathway model was chosen as the final model. The common factor was influenced by genetics (58%) and unique environment (42%), and explained 77% of the variation in MDD, 69% in GAD, and 44% in burnout. GAD and burnout had additive genetic factors unique to the phenotypes (11% each), while MDD did not. Unique environment explained 23% of the variability in MDD, 20% in GAD, and 45% in burnout. In conclusion, the covariation was explained by an underlying common factor, largely influenced by genetics. Burnout was to a large degree influenced by unique environmental factors not shared with MDD and GAD.
PubMed ID
27620693 View in PubMed
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Assessing the heritability of anorexia nervosa symptoms using a marginal maximal likelihood approach.

https://arctichealth.org/en/permalink/ahliterature93166
Source
Psychol Med. 2009 Mar;39(3):463-73
Publication Type
Article
Date
Mar-2009
Author
Mazzeo S E
Mitchell K S
Bulik C M
Reichborn-Kjennerud T.
Kendler K S
Neale M C
Author Affiliation
Department of Psychology, Virginia Commonwealth University, Richmond, VA 23284-2018, USA. semazzeo@vcu.edu
Source
Psychol Med. 2009 Mar;39(3):463-73
Date
Mar-2009
Language
English
Publication Type
Article
Keywords
Adult
Amenorrhea - diagnosis - epidemiology - genetics
Anorexia Nervosa - diagnosis - epidemiology - genetics
Body mass index
Body Weight - genetics
Diagnostic and Statistical Manual of Mental Disorders
Diseases in Twins - diagnosis - genetics
Female
Genetic Predisposition to Disease
Humans
International Classification of Diseases
Models, Genetic
Norway - epidemiology
Phenotype
Psychiatric Status Rating Scales
Questionnaires
Social Environment
Twins, Dizygotic - genetics
Twins, Monozygotic - genetics
Weight Loss - genetics
Abstract
BACKGROUND: Assessment of eating disorders at the symptom level can facilitate the refinement of phenotypes. We examined genetic and environmental contributions to liability to anorexia nervosa (AN) symptoms in a population-based twin sample using a genetic common pathway model. METHOD: Participants were from the Norwegian Institute of Public Health Twin Panel (NIPHTP) and included all female monozygotic (MZ; 448 complete pairs and four singletons) and dizygotic (DZ; 263 complete pairs and four singletons) twins who completed the Composite International Diagnostic Interview (CIDI) assessing DSM-IV Axis I and ICD-10 criteria. Responses to items assessing AN symptoms were included in a model fitted using the marginal maximum likelihood (MML) approach. RESULTS: Heritability of the overall AN diagnosis was moderate [a2=0.22, 95% confidence interval (CI) 0.0-0.50] whereas heritabilities of the specific items varied. Heritability estimates for weight loss items were moderate (a2=0.31-0.34) and items assessing weight concern when at a low weight were smaller (0.18-0.29). Additive genetic factors contributed little to the variance of amenorrhea, which was most strongly influenced by unshared environment (a2=0.16, e2=0.71). CONCLUSIONS: AN symptoms are differentially heritable. Specific criteria such as those related to body weight and weight loss history represent more biologically driven potential endophenotypes or liability indices. The results regarding weight concern differ somewhat from those of previous studies, highlighting the importance of assessing genetic and environmental influences on variance of traits within specific subgroups of interest.
PubMed ID
18485259 View in PubMed
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The association between low birth weight and type 2 diabetes: contribution of genetic factors.

https://arctichealth.org/en/permalink/ahliterature92433
Source
Epidemiology. 2008 Sep;19(5):659-65
Publication Type
Article
Date
Sep-2008
Author
Johansson Stefan
Iliadou Anastasia
Bergvall Niklas
dé Fairé Ulf
Kramer Michael S
Pawitan Yudi
Pedersen Nancy L
Norman Mikael
Lichtenstein Paul
Cnattingius Sven
Author Affiliation
Departments of Medical Epidemiology, and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
Source
Epidemiology. 2008 Sep;19(5):659-65
Date
Sep-2008
Language
English
Publication Type
Article
Keywords
Birth Certificates
Diabetes Mellitus, Type 2 - epidemiology - etiology - genetics
Female
Humans
Infant, Low Birth Weight
Infant, Newborn
Logistic Models
Male
Maternal Age
Middle Aged
Questionnaires
Social Class
Sweden - epidemiology
Twins, Dizygotic - genetics
Twins, Monozygotic - genetics
Abstract
BACKGROUND: Low birth weight has been associated with an increased risk of type 2 diabetes in adulthood. Poor fetal nutrition has been suggested to explain this association. Our objective was to determine whether genetic factors contribute to the association between low birth weight and subsequent risk of type 2 diabetes. METHODS: We retrieved information from original birth records on same-sex Swedish twins with known zygosity, born from 1926 to 1958. We used regression models to investigate whether birth weight was associated with risk of type 2 diabetes in the cohort of twins overall, and in case-control analyses within disease-discordant dizygotic and monozygotic twin pairs. RESULTS: Of 18,230 twins, 592 (3.2%) had type 2 diabetes. The rate of type 2 diabetes consistently increased with decreasing birth weight, from 2.4% among twins with birth weights of 3500 g or more to 5.3% among those with birth weights less than 2000 g. In the cohort analysis, in which twins are analyzed as independent individuals, the adjusted odds ratio (95% confidence interval) of type 2 diabetes per 500-g decrease in birth weight was 1.44 (1.28-1.63). When we compared the diseased twin with the healthy cotwin, the corresponding odds ratios were 1.38 (1.02-1.85), among dizygotic twins, and 1.02 (0.63-1.64), among monozygotic twins. CONCLUSIONS: Low birth weight is associated with type 2 diabetes in adulthood. The difference in this association between monozygotic and dizygotic twin pairs suggests that genetic mechanisms play an important role in this association.
PubMed ID
18714437 View in PubMed
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