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Advancing paternal age and risk of autism: new evidence from a population-based study and a meta-analysis of epidemiological studies.

https://arctichealth.org/en/permalink/ahliterature138993
Source
Mol Psychiatry. 2011 Dec;16(12):1203-12
Publication Type
Article
Date
Dec-2011
Author
C M Hultman
S. Sandin
S Z Levine
P. Lichtenstein
A. Reichenberg
Author Affiliation
Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
Source
Mol Psychiatry. 2011 Dec;16(12):1203-12
Date
Dec-2011
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Autistic Disorder - epidemiology - genetics - psychology
Cohort Studies
Databases, Factual - statistics & numerical data
Family Health - statistics & numerical data
Female
Humans
Male
Maternal Age
Middle Aged
Paternal Age
Risk factors
Siblings - psychology
Sweden - epidemiology
Abstract
Advanced paternal age has been suggested as a risk factor for autism, but empirical evidence is mixed. This study examines whether the association between paternal age and autism in the offspring (1) persists controlling for documented autism risk factors, including family psychiatric history, perinatal conditions, infant characteristics and demographic variables; (2) may be explained by familial traits associated with the autism phenotype, or confounding by parity; and (3) is consistent across epidemiological studies. Multiple study methods were adopted. First, a Swedish 10-year birth cohort (N=1?075?588) was established. Linkage to the National Patient Register ascertained all autism cases (N=883). Second, 660 families identified within the birth cohort had siblings discordant for autism. Finally, meta-analysis included population-based epidemiological studies. In the birth cohort, autism risk increased monotonically with increasing paternal age. Offspring of men aged =50 years were 2.2 times (95% confidence interval: 1.26-3.88: P=0.006) more likely to have autism than offspring of men aged =29 years, after controlling for maternal age and documented risk factors for autism. Within-family analysis of discordant siblings showed that affected siblings had older paternal age, adjusting for maternal age and parity (P
PubMed ID
21116277 View in PubMed
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An assessment of the developmental, reproductive, and neurotoxicity of endosulfan.

https://arctichealth.org/en/permalink/ahliterature89883
Source
Birth Defects Res B Dev Reprod Toxicol. 2009 Feb;86(1):1-28
Publication Type
Article
Date
Feb-2009
Author
Silva Marilyn H
Gammon Derek
Author Affiliation
Department of Pesticide Regulation, California Environmental Protection Agency, 1001 I Street, Sacramento, CA 95812, USA. msilva@cdpr.ca.gov
Source
Birth Defects Res B Dev Reprod Toxicol. 2009 Feb;86(1):1-28
Date
Feb-2009
Language
English
Publication Type
Article
Keywords
Adult
Animals
Autistic Disorder - epidemiology - etiology
Databases, Factual
Dose-Response Relationship, Drug
Embryo, Mammalian - embryology
Endocrine Disruptors - classification - toxicity
Endosulfan - classification - toxicity
Female
Fetal Development - drug effects
Humans
Infertility, Male - epidemiology - etiology
Inhalation Exposure
Insecticides - classification - toxicity
Male
Nervous System Diseases - chemically induced - epidemiology
No-Observed-Adverse-Effect Level
Pesticide Residues - toxicity
Pregnancy
Rabbits
Rats
Reproduction - drug effects
Risk assessment
Spermatozoa - drug effects
Teratogens - classification - toxicity
Young Adult
Abstract
BACKGROUND: Endosulfan has been used for over 50 years. Although most analogs have been discontinued, endosulfan has less environmental persistence. Nevertheless, pressure groups are lobbying for a worldwide ban. The reasons are: possible rodent male reproductive toxicity, other endocrine effects and cancer; human epidemiology, and exposure studies; residues appearing in remote areas of the world, e.g., the Arctic. METHODS: The endosulfan toxicology database is described and risks of its use assessed. RESULTS: Endosulfan is an antagonist at the GABA(A) receptor Cl(-) ionophore in mammalian CNS. Rat acute toxicity is moderate, LD(50)=48 (M) or 10 mg/kg/d (F), oral gavage; 130 (M), 70 mg/kg/d (F) dermal; LC(50)=34.5 microg/L (M), 12.6 microg/L (F), inhalation. Critical NOELs for risk assessment: acute oral (gavage)=0.7 mg/kg/d (rabbit developmental); Subchronic oral (diet)=1.2 mg/kg/d (rat reproduction); Chronic oral (diet)=0.6 mg/kg/d. There were no acceptable dermal toxicity studies. The critical acute and subchronic inhalation NOELs=0.001 mg/L, chronic inhalation=0.0001 mg/L (estimated). Toxicity to rat sperm occurred at doses causing neurotoxicity. Endocrine effects, resulting from P450 oxygenase(s) induction, were reversible. Increased cancer, genotoxicity, or histopathology in rodents was not observed in any organ. Possible effects on brain biogenic amine levels were probably secondary. CONCLUSIONS: Epidemiology and rodent studies suggesting autism and male reproductive toxicity are open to other interpretations. Developmental/ reproductive toxicity or endocrine disruption occurs only at doses causing neurotoxicity. Toxicity to the fetus or young animals is not more severe than that shown by adults.
PubMed ID
19243027 View in PubMed
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Asperger syndrome--some epidemiological considerations: a research note.

https://arctichealth.org/en/permalink/ahliterature38104
Source
J Child Psychol Psychiatry. 1989 Jul;30(4):631-8
Publication Type
Article
Date
Jul-1989
Author
I C Gillberg
C. Gillberg
Author Affiliation
Department of Child and Adolescent Psychiatry, University of Göteborg, Sweden.
Source
J Child Psychol Psychiatry. 1989 Jul;30(4):631-8
Date
Jul-1989
Language
English
Publication Type
Article
Keywords
Adolescent
Autistic Disorder - epidemiology
Child
Cross-Sectional Studies
Humans
London
Sweden
Syndrome
Abstract
Asperger syndrome has so far been the subject of very little systematic empirical inquiry. This paper reviews those few studies in the literature and some data from a new Swedish study which has reported findings pertinent to estimations of Asperger syndrome prevalence. It is concluded that among children with normal intelligence, rates of 10-26 per 10,000 children are minimum figures. Another 0.4 per 10,000 Swedish teenagers showed the combination of Asperger syndrome and mild mental retardation.
PubMed ID
2670981 View in PubMed
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The association between congenital anomalies and autism spectrum disorders in a Finnish national birth cohort.

https://arctichealth.org/en/permalink/ahliterature260640
Source
Dev Med Child Neurol. 2015 Jan;57(1):75-80
Publication Type
Article
Date
Jan-2015
Author
Laura Timonen-Soivio
Raija Vanhala
Heli Malm
Susanna Leivonen
Elina Jokiranta
Susanna Hinkka-Yli-Salomäki
Mika Gissler
Alan S Brown
Andre Sourander
Source
Dev Med Child Neurol. 2015 Jan;57(1):75-80
Date
Jan-2015
Language
English
Publication Type
Article
Keywords
Autistic Disorder - epidemiology
Child
Child Development Disorders, Pervasive - epidemiology
Cohort Studies
Comorbidity
Congenital Abnormalities - epidemiology
Female
Finland - epidemiology
Humans
Intellectual Disability - epidemiology
Male
Registries - statistics & numerical data
Abstract
The first aim of this study was to evaluate the association between different subgroups of autism spectrum disorders (ASDs) (childhood autism, Asperger syndrome, and pervasive developmental disorder/pervasive developmental disorder - not otherwise specified [PDD/PDD-NOS]) and congenital anomalies. Second, we assessed the association among intellectually disabled children with ASDs in the subgroups of childhood autism and PDD/PDD-NOS.
Nationwide population-based register data for children with a diagnosis of ASD (n=4449; 3548 males, 901 females) were collected during years 1987-2000 from the Finnish Hospital Discharge Register. Data on congenital anomalies were derived from the National Register of Congenital Malformations. Conditional logistic regression models were used as a statistical method. The association between ASD subgroups and congenital anomalies was stratified by the presence or absence of intellectual disability.
Congenital anomalies occurred more frequently in all subgroups of ASD than in comparison participants (adjusted odds ratio [OR] for major congenital anomalies 1.8, 95% confidence interval [CI] 1.5-2.2, p
Notes
Comment In: Dev Med Child Neurol. 2015 Jan;57(1):10-125312764
PubMed ID
25200584 View in PubMed
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Association of family history of autoimmune diseases and autism spectrum disorders.

https://arctichealth.org/en/permalink/ahliterature88485
Source
Pediatrics. 2009 Aug;124(2):687-94
Publication Type
Article
Date
Aug-2009
Author
Atladóttir Hjördís O
Pedersen Marianne G
Thorsen Poul
Mortensen Preben Bo
Deleuran Bent
Eaton William W
Parner Erik T
Author Affiliation
Nanea, Department of Epidemiology, Institute of Public Health, bNational Centre for Register-Based Research, and eInstitute of Medical Microbiology and Immunology, University of Aarhus, Aarhus, Denmark. hoa@soci.au.dk
Source
Pediatrics. 2009 Aug;124(2):687-94
Date
Aug-2009
Language
English
Publication Type
Article
Keywords
Arthritis, Rheumatoid - epidemiology - genetics
Autistic Disorder - epidemiology - genetics
Autoimmune Diseases - epidemiology - genetics
Celiac Disease - epidemiology - genetics
Child
Child, Preschool
Cohort Studies
Denmark
Diabetes Mellitus, Type 1 - epidemiology - genetics
Factor Analysis, Statistical
Female
Genetic Predisposition to Disease - genetics
Health Surveys
Humans
Infant
Male
Registries
Abstract
OBJECTIVES: Recent studies suggest that familial autoimmunity plays a part in the pathogenesis of ASDs. In this study we investigated the association between family history of autoimmune diseases (ADs) and ASDs/infantile autism. We perform confirmatory analyses based on results from previous studies, as well as various explorative analyses. METHODS: The study cohort consisted of all of the children born in Denmark from 1993 through 2004 (689 196 children). Outcome data consisted of both inpatient and outpatient diagnoses reported to the Danish National Psychiatric Registry. Information on ADs in parents and siblings of the cohort members was obtained from the Danish National Hospital Register. The incidence rate ratio of autism was estimated by using log-linear Poisson regression. RESULTS: A total of 3325 children were diagnosed with ASDs, of which 1089 had an infantile autism diagnosis. Increased risk of ASDs was observed for children with a maternal history of rheumatoid arthritis and celiac disease. Also, increased risk of infantile autism was observed for children with a family history of type 1 diabetes. CONCLUSIONS: Associations regarding family history of type 1 diabetes and infantile autism and maternal history of rheumatoid arthritis and ASDs were confirmed from previous studies. A significant association between maternal history of celiac disease and ASDs was observed for the first time. The observed associations between familial autoimmunity and ASDs/infantile autism are probably attributable to a combination of a common genetic background and a possible prenatal antibody exposure or alteration in fetal environment during pregnancy.
PubMed ID
19581261 View in PubMed
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Association of Genetic and Environmental Factors With Autism in a 5-Country Cohort.

https://arctichealth.org/en/permalink/ahliterature310272
Source
JAMA Psychiatry. 2019 10 01; 76(10):1035-1043
Publication Type
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Date
10-01-2019
Author
Dan Bai
Benjamin Hon Kei Yip
Gayle C Windham
Andre Sourander
Richard Francis
Rinat Yoffe
Emma Glasson
Behrang Mahjani
Auli Suominen
Helen Leonard
Mika Gissler
Joseph D Buxbaum
Kingsley Wong
Diana Schendel
Arad Kodesh
Michaeline Breshnahan
Stephen Z Levine
Erik T Parner
Stefan N Hansen
Christina Hultman
Abraham Reichenberg
Sven Sandin
Author Affiliation
Jockey Club School of Public Health and Primary Care, The Chinese University of Hong Kong, Hong Kong SAR.
Source
JAMA Psychiatry. 2019 10 01; 76(10):1035-1043
Date
10-01-2019
Language
English
Publication Type
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Keywords
Adolescent
Autism Spectrum Disorder - epidemiology - etiology - genetics
Autistic Disorder - epidemiology - etiology
Child
Cohort Studies
Denmark - epidemiology
Environment
Family
Female
Finland - epidemiology
Genetic Association Studies - methods - standards
Genetic Predisposition to Disease - epidemiology - genetics
Humans
Inheritance Patterns - genetics
Israel - epidemiology
Male
Maternal Inheritance - genetics
Sensitivity and specificity
Sweden - epidemiology
Western Australia - epidemiology
Abstract
The origins and development of autism spectrum disorder (ASD) remain unresolved. No individual-level study has provided estimates of additive genetic, maternal, and environmental effects in ASD across several countries.
To estimate the additive genetic, maternal, and environmental effects in ASD.
Population-based, multinational cohort study including full birth cohorts of children from Denmark, Finland, Sweden, Israel, and Western Australia born between January 1, 1998, and December 31, 2011, and followed up to age 16 years. Data were analyzed from September 23, 2016 through February 4, 2018.
Across 5 countries, models were fitted to estimate variance components describing the total variance in risk for ASD occurrence owing to additive genetics, maternal, and shared and nonshared environmental effects.
The analytic sample included 2?001?631 individuals, of whom 1?027?546 (51.3%) were male. Among the entire sample, 22?156 were diagnosed with ASD. The median (95% CI) ASD heritability was 80.8% (73.2%-85.5%) for country-specific point estimates, ranging from 50.9% (25.1%-75.6%) (Finland) to 86.8% (69.8%-100.0%) (Israel). For the Nordic countries combined, heritability estimates ranged from 81.2% (73.9%-85.3%) to 82.7% (79.1%-86.0%). Maternal effect was estimated to range from 0.4% to 1.6%. Estimates of genetic, maternal, and environmental effects for autistic disorder were similar with ASD.
Based on population data from 5 countries, the heritability of ASD was estimated to be approximately 80%, indicating that the variation in ASD occurrence in the population is mostly owing to inherited genetic influences, with no support for contribution from maternal effects. The results suggest possible modest differences in the sources of ASD risk between countries.
Notes
CommentIn: JAMA Psychiatry. 2019 Oct 1;76(10):1005-1006 PMID 31314055
PubMed ID
31314057 View in PubMed
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Association of hospitalization for infection in childhood with diagnosis of autism spectrum disorders: a Danish cohort study.

https://arctichealth.org/en/permalink/ahliterature97108
Source
Arch Pediatr Adolesc Med. 2010 May;164(5):470-7
Publication Type
Article
Date
May-2010
Author
Hjördís Osk Atladóttir
Poul Thorsen
Diana E Schendel
Lars Østergaard
Saane Lemcke
Erik T Parner
Author Affiliation
Department of Epidemiology, Institute of Public Health, University of Arhus, Bartholin Allé 2, Arhus C, Denmark. hoa@soci.au.dk
Source
Arch Pediatr Adolesc Med. 2010 May;164(5):470-7
Date
May-2010
Language
English
Publication Type
Article
Keywords
Autistic Disorder - epidemiology
Birth weight
Child
Child, Hospitalized - statistics & numerical data
Child, Preschool
Denmark - epidemiology
Female
Gestational Age
Hospitalization - statistics & numerical data
Humans
Incidence
Infant
Infant, Newborn
Infant, Premature
Infection - epidemiology
Male
Proportional Hazards Models
Registries
Risk factors
Sex Factors
Abstract
OBJECTIVE: To investigate the association between hospitalization for infection in the perinatal/neonatal period or childhood and the diagnosis of autism spectrum disorders (ASDs). DESIGN: A population-based cohort study. SETTING: Denmark. PARTICIPANTS: All children born in Denmark from January 1, 1980, through December 31, 2002, comprising a total of 1 418 152 children. EXPOSURE: Infection requiring hospitalization. MAIN OUTCOME MEASURE: The adjusted hazard ratio (HR) for ASDs among children hospitalized for infection compared with other children. RESULTS: A total of 7379 children were diagnosed as having ASDs. Children admitted to the hospital for any infectious disease displayed an increased rate of ASD diagnoses (HR, 1.38 [95% confidence interval, 1.31-1.45]). This association was found to be similar for infectious diseases of bacterial and viral origin. Furthermore, children admitted to the hospital for noninfectious disease also displayed an increased rate of ASD diagnoses (HR, 1.76 [95% confidence interval, 1.68-1.86]), and admissions for infection increased the rate of mental retardation (2.18 [2.06-2.31]). CONCLUSIONS: The association between hospitalization for infection and ASDs observed in this study does not suggest causality because a general association is observed across different infection groups. Also, the association is not specific for infection or for ASDs. We discuss a number of noncausal explanatory models.
PubMed ID
20439799 View in PubMed
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Attention deficit/hyperactivity disorder and childhood autism in association with prenatal exposure to perfluoroalkyl substances: a nested case-control study in the Danish National Birth Cohort.

https://arctichealth.org/en/permalink/ahliterature269614
Source
Environ Health Perspect. 2015 Apr;123(4):367-73
Publication Type
Article
Date
Apr-2015
Author
Zeyan Liew
Beate Ritz
Ondine S von Ehrenstein
Bodil Hammer Bech
Ellen Aagaard Nohr
Chunyuan Fei
Rossana Bossi
Tine Brink Henriksen
Eva Cecilie Bonefeld-Jørgensen
Jørn Olsen
Source
Environ Health Perspect. 2015 Apr;123(4):367-73
Date
Apr-2015
Language
English
Publication Type
Article
Keywords
Adult
Alkanesulfonic Acids - blood - toxicity
Attention Deficit Disorder with Hyperactivity - epidemiology - etiology
Autistic Disorder - epidemiology - etiology
Caprylates - blood - toxicity
Case-Control Studies
Child
Cohort Studies
Denmark - epidemiology
Environmental Pollutants - toxicity
Female
Fluorocarbons - blood - toxicity
Humans
Male
Maternal Exposure - adverse effects
Pregnancy
Prenatal Exposure Delayed Effects - epidemiology - etiology
Abstract
Perfluoroalkyl substances (PFASs) are persistent pollutants found to be endocrine disruptive and neurotoxic in animals. Positive correlations between PFASs and neurobehavioral problems in children were reported in cross-sectional data, but findings from prospective studies are limited.
We investigated whether prenatal exposure to PFASs is associated with attention deficit/hyperactivity disorder (ADHD) or childhood autism in children.
Among 83,389 mother-child pairs enrolled in the Danish National Birth Cohort during 1996-2002, we identified 890 ADHD cases and 301 childhood autism cases from the Danish National Hospital Registry and the Danish Psychiatric Central Registry. From this cohort, we randomly selected 220 cases each of ADHD and autism, and we also randomly selected 550 controls frequency matched by child's sex. Sixteen PFASs were measured in maternal plasma collected in early or mid-pregnancy. We calculated risk ratios (RRs) using generalized linear models, taking into account sampling weights.
Perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA) were detected in all samples; four other PFASs were quantified in = 90% of the samples. We did not find consistent evidence of associations between mother's PFAS plasma levels and ADHD [per natural log nanograms per milliliter increase: PFOS RR = 0.87 (95% CI: 0.74, 1.02); PFOA RR = 0.98 (95% CI: 0.82, 1.16)] or autism [per natural log nanograms per milliliter increase: PFOS RR = 0.92 (95% CI: 0.69, 1.22); PFOA RR = 0.98 (95% CI: 0.73, 1.31)]. We found positive as well as negative associations between higher PFAS quartiles and ADHD in models that simultaneously adjusted for all PFASs, but these estimates were imprecise.
In this study we found no consistent evidence to suggest that prenatal PFAS exposure increases the risk of ADHD or childhood autism in children.
Notes
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PubMed ID
25616253 View in PubMed
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Autism and attention-deficit/hyperactivity disorder among individuals with a family history of alcohol use disorders.

https://arctichealth.org/en/permalink/ahliterature262712
Source
Elife. 2014;3:e02917
Publication Type
Article
Date
2014
Author
Jan Sundquist
Kristina Sundquist
Jianguang Ji
Source
Elife. 2014;3:e02917
Date
2014
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Alcoholism - complications - epidemiology - physiopathology
Attention Deficit Disorder with Hyperactivity - epidemiology - etiology - physiopathology
Autistic Disorder - epidemiology - etiology - physiopathology
Child
Confidence Intervals
Epidemiological Monitoring
Female
Humans
Incidence
Longitudinal Studies
Male
Parents
Registries
Risk factors
Sweden - epidemiology
Abstract
Recent studies suggest de novo mutations may involve the pathogenesis of autism and attention-deficit/hyperactivity disorder (ADHD). Based on the evidence that excessive alcohol consumption may be associated with an increased rate of de novo mutations in germ cells (sperms or eggs), we examine here whether the risks of autism and ADHD are increased among individuals with a family history of alcohol use disorders (AUDs). The standardized incidence ratios (SIRs) of autism and ADHD among individuals with a biological parental history of AUDs were 1.39 (95% CI 1.34-1.44) and 2.19 (95% CI 2.15-2.23), respectively, compared to individuals without an affected parent. Among offspring whose parents were diagnosed with AUDs before their birth, the corresponding risks were 1.46 (95% CI 1.36-1.58) and 2.70 (95% CI 2.59-2.81), respectively. Our study calls for extra surveillance for children with a family history of AUDs, and further studies examining the underlying mechanisms are needed.
Notes
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PubMed ID
25139954 View in PubMed
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Autism and autistic-like conditions in Swedish rural and urban areas: a population study.

https://arctichealth.org/en/permalink/ahliterature39173
Source
Br J Psychiatry. 1986 Jul;149:81-7
Publication Type
Article
Date
Jul-1986
Author
S. Steffenburg
C. Gillberg
Source
Br J Psychiatry. 1986 Jul;149:81-7
Date
Jul-1986
Language
English
Publication Type
Article
Keywords
Autistic Disorder - epidemiology
Central Nervous System Diseases - complications
Child
Female
Humans
Intelligence
Male
Research Support, Non-U.S. Gov't
Rural Health
Social Class
Sweden
Urban health
Abstract
The total population of children under 10 years in one Swedish urban area and one rural area was screened for infantile autism (IA) and autistic-like conditions (AC). A total prevalence of 6.6 per 10 000 was found, which is somewhat higher than in previous similar studies of the same region. Infantile autism accounted for two-thirds of the cases. Boys far outnumbered girls, but this was entirely accounted for by the IA group. The preponderance of autistic boys was less pronounced among the severely mentally retarded children. Mental retardation was seen in almost 90% of cases and only one child had an IQ exceeding 100; clinical and laboratory signs of brain dysfunction were also found in a majority of cases. Distribution by social class was no different in either patient group from the general population.
PubMed ID
3779317 View in PubMed
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99 records – page 1 of 10.