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ADHD treatment and diagnosis in relation to children's birth month: Nationwide cohort study from Norway.

https://arctichealth.org/en/permalink/ahliterature283440
Source
Scand J Public Health. 2017 Jun;45(4):343-349
Publication Type
Article
Date
Jun-2017
Author
Øystein Karlstad
Kari Furu
Camilla Stoltenberg
Siri E Håberg
Inger Johanne Bakken
Source
Scand J Public Health. 2017 Jun;45(4):343-349
Date
Jun-2017
Language
English
Publication Type
Article
Keywords
Adolescent
Age Distribution
Attention Deficit Disorder with Hyperactivity - diagnosis - drug therapy - epidemiology
Child
Cohort Studies
Cross-Sectional Studies
Female
Humans
Male
Norway - epidemiology
Proportional Hazards Models
Risk
Siblings
Abstract
Studies from several countries have reported that children youngest in grade are at higher risk of attention-deficit/hyperactivity disorder (ADHD) diagnosis and treatment. Norwegian children start school the year they turn six, making children born in December youngest in their grade. We used data on medication, specialist healthcare diagnoses, and primary healthcare diagnoses from national registers to investigate associations between birth month and ADHD.
All children born in Norway between 1998 and 2006 ( N=509,827) were followed from age six until 31 December 2014. We estimated hazard ratios for ADHD medication and diagnoses by birth month in Cox proportional-hazards models. We compared risk among siblings to control for potentially confounding socioeconomic factors, and assessed risk of receiving ADHD medication by birth month while attending different grades in cross-sectional time-series analyses.
At end of follow-up, 5.3% of boys born in October-December had received ADHD medication, compared with 3.7% of boys born in January-March. Corresponding numbers for girls were 2.2% and 1.3%, respectively. The adjusted hazard ratio for ADHD medication for children born in October-December (reference: January-March) was 1.4 (95% confidence interval: 1.4-1.5) for boys and 1.8 (1.7-2.0) for girls. Analyses with diagnoses as outcome showed consistent results, and analyses restricted to siblings within the study population also supported the findings. Analysis by grade revealed an increased risk for children born late in the year from grade 3 onwards, with most marked differences in higher grades.
Children youngest in grade had the highest risk of receiving ADHD treatment. Differences were most marked among older children.
PubMed ID
28482754 View in PubMed
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Analysis of self-selection bias in a population-based cohort study of autism spectrum disorders.

https://arctichealth.org/en/permalink/ahliterature108216
Source
Paediatr Perinat Epidemiol. 2013 Nov;27(6):553-63
Publication Type
Article
Date
Nov-2013
Author
Roy M Nilsen
Pål Surén
Nina Gunnes
Elin R Alsaker
Michaeline Bresnahan
Deborah Hirtz
Mady Hornig
Kari Kveim Lie
W Ian Lipkin
Ted Reichborn-Kjennerud
Christine Roth
Synnve Schjølberg
George Davey Smith
Ezra Susser
Stein Emil Vollset
Anne-Siri Øyen
Per Magnus
Camilla Stoltenberg
Source
Paediatr Perinat Epidemiol. 2013 Nov;27(6):553-63
Date
Nov-2013
Language
English
Publication Type
Article
Keywords
Adult
Child
Child Development Disorders, Pervasive - epidemiology - etiology
Cohort Studies
Female
Humans
Incidence
Infant, Newborn
Male
Middle Aged
Norway - epidemiology
Odds Ratio
Pregnancy
Prenatal Exposure Delayed Effects - epidemiology
Prospective Studies
Registries
Risk factors
Selection Bias
Young Adult
Abstract
This study examined potential self-selection bias in a large pregnancy cohort by comparing exposure-outcome associations from the cohort to similar associations obtained from nationwide registry data. The outcome under study was specialist-confirmed diagnosis of autism spectrum disorders (ASDs).
The cohort sample (n = 89 836) was derived from the population-based prospective Norwegian Mother and Child Cohort Study and its substudy of ASDs, the Autism Birth Cohort (ABC) study. The nationwide registry data were derived from the Medical Birth Registry of Norway (n = 507 856). The children were born in 1999–2007, and seven prenatal and perinatal exposures were selected for analyses.
ASDs were reported for 234 (0.26%) children in the cohort and 2072 (0.41%) in the nationwide population. Compared with the nationwide population, the cohort had an under-representation of the youngest women (
Notes
Comment In: Paediatr Perinat Epidemiol. 2014 Mar;28(2):17824494985
Comment In: Paediatr Perinat Epidemiol. 2014 Mar;28(2):17724494984
PubMed ID
23919580 View in PubMed
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Association between maternal use of folic acid supplements and risk of autism spectrum disorders in children.

https://arctichealth.org/en/permalink/ahliterature116379
Source
JAMA. 2013 Feb 13;309(6):570-7
Publication Type
Article
Date
Feb-13-2013
Author
Pål Surén
Christine Roth
Michaeline Bresnahan
Margaretha Haugen
Mady Hornig
Deborah Hirtz
Kari Kveim Lie
W Ian Lipkin
Per Magnus
Ted Reichborn-Kjennerud
Synnve Schjølberg
George Davey Smith
Anne-Siri Øyen
Ezra Susser
Camilla Stoltenberg
Author Affiliation
Norwegian Institute of Public Health, PO Box 4404, Nydalen, N-0403 Oslo, Norway. pal.suren@fhi.no
Source
JAMA. 2013 Feb 13;309(6):570-7
Date
Feb-13-2013
Language
English
Publication Type
Article
Keywords
Adolescent
Child
Child Development Disorders, Pervasive - epidemiology - prevention & control
Child, Preschool
Cohort Studies
Dietary Supplements
Female
Folic Acid - therapeutic use
Humans
Male
Norway - epidemiology
Odds Ratio
Pregnancy
Pregnancy Trimester, First
Prenatal Care
Prenatal Exposure Delayed Effects
Regression Analysis
Risk
Vitamin B Complex - therapeutic use
Young Adult
Abstract
Prenatal folic acid supplements reduce the risk of neural tube defects in children, but it has not been determined whether they protect against other neurodevelopmental disorders.
To examine the association between maternal use of prenatal folic acid supplements and subsequent risk of autism spectrum disorders (ASDs) (autistic disorder, Asperger syndrome, pervasive developmental disorder-not otherwise specified [PDD-NOS]) in children.
The study sample of 85,176 children was derived from the population-based, prospective Norwegian Mother and Child Cohort Study (MoBa). The children were born in 2002-2008; by the end of follow-up on March 31, 2012, the age range was 3.3 through 10.2 years (mean, 6.4 years). The exposure of primary interest was use of folic acid from 4 weeks before to 8 weeks after the start of pregnancy, defined as the first day of the last menstrual period before conception. Relative risks of ASDs were estimated by odds ratios (ORs) with 95% CIs in a logistic regression analysis. Analyses were adjusted for maternal education level, year of birth, and parity.
Specialist-confirmed diagnosis of ASDs.
At the end of follow-up, 270 children in the study sample had been diagnosed with ASDs: 114 with autistic disorder, 56 with Asperger syndrome, and 100 with PDD-NOS. In children whose mothers took folic acid, 0.10% (64/61,042) had autistic disorder, compared with 0.21% (50/24,134) in those unexposed to folic acid. The adjusted OR for autistic disorder in children of folic acid users was 0.61 (95% CI, 0.41-0.90). No association was found with Asperger syndrome or PDD-NOS, but power was limited. Similar analyses for prenatal fish oil supplements showed no such association with autistic disorder, even though fish oil use was associated with the same maternal characteristics as folic acid use.
Use of prenatal folic acid supplements around the time of conception was associated with a lower risk of autistic disorder in the MoBa cohort. Although these findings cannot establish causality, they do support prenatal folic acid supplementation.
Notes
Cites: Mol Psychiatry. 2010 Jul;15(7):676-8020571529
Cites: Lancet. 2006 Jul 15;368(9531):210-516844490
Cites: Matern Child Nutr. 2008 Jan;4(1):28-4318171405
Cites: Matern Child Nutr. 2008 Jan;4(1):14-2718171404
Cites: Int J Epidemiol. 2006 Oct;35(5):1146-5016926217
Cites: MMWR Morb Mortal Wkly Rep. 2010 Aug 13;59(31):980-420703205
Cites: Epidemiology. 2011 Jul;22(4):476-8521610500
Cites: JAMA. 2011 Oct 12;306(14):1566-7321990300
Cites: Arch Gen Psychiatry. 2012 Mar;69(3):306-1322065253
Cites: MMWR Surveill Summ. 2012 Mar 30;61(3):1-1922456193
Cites: Am J Clin Nutr. 2012 Jul;96(1):80-922648721
Cites: Pediatrics. 2012 Jul;130(1):e152-822711729
Cites: Basic Clin Pharmacol Toxicol. 2008 Feb;102(2):245-5618226080
Cites: N Engl J Med. 1999 Nov 11;341(20):1485-9010559448
Cites: J Autism Dev Disord. 2000 Jun;30(3):205-2311055457
Cites: JAMA. 1989 Nov 24;262(20):2847-522478730
Cites: Lancet. 1991 Jul 20;338(8760):131-71677062
Cites: N Engl J Med. 1992 Dec 24;327(26):1832-51307234
Cites: JAMA. 1993 Mar 10;269(10):1257-618437302
Cites: J Autism Dev Disord. 1994 Oct;24(5):659-857814313
Cites: Epidemiology. 1995 May;6(3):219-267619926
Cites: JAMA. 1995 Dec 6;274(21):1698-7027474275
Cites: Paediatr Perinat Epidemiol. 2009 Nov;23(6):597-60819840297
Comment In: JAMA. 2013 Jun 5;309(21):220823736720
Comment In: JAMA. 2013 Jun 5;309(21):220823736721
Comment In: JAMA. 2013 Feb 13;309(6):611-323403688
Comment In: Evid Based Med. 2013 Dec;18(6):e5323635843
Comment In: J Pediatr. 2013 Jul;163(1):303-423796343
Comment In: J Midwifery Womens Health. 2013 Jul-Aug;58(4):471-223837678
PubMed ID
23403681 View in PubMed
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Association of maternal report of infant and toddler gastrointestinal symptoms with autism: evidence from a prospective birth cohort.

https://arctichealth.org/en/permalink/ahliterature265147
Source
JAMA Psychiatry. 2015 May;72(5):466-74
Publication Type
Article
Date
May-2015
Author
Michaeline Bresnahan
Mady Hornig
Andrew F Schultz
Nina Gunnes
Deborah Hirtz
Kari Kveim Lie
Per Magnus
Ted Reichborn-Kjennerud
Christine Roth
Synnve Schjølberg
Camilla Stoltenberg
Pål Surén
Ezra Susser
W Ian Lipkin
Source
JAMA Psychiatry. 2015 May;72(5):466-74
Date
May-2015
Language
English
Publication Type
Article
Keywords
Adult
Child Development
Child Development Disorders, Pervasive - complications - epidemiology - psychology
Child, Preschool
Constipation - epidemiology - psychology
Developmental Disabilities - complications - epidemiology - psychology
Diarrhea - epidemiology - psychology
Evidence-Based Medicine
Female
Food Hypersensitivity - epidemiology - psychology
Humans
Infant
Male
Mothers
Norway - epidemiology
Prevalence
Prospective Studies
Questionnaires
Abstract
Gastrointestinal (GI) comorbidities are frequently described in association with autism spectrum disorder (ASD). However, the prevalence of GI disturbances and the age at which such problems first appear are unclear, and their specificity for ASD compared with other neurodevelopmental disorders is uncertain.
To compare maternal report of GI symptoms during the first 3 years of life in children with ASD, developmental delay (DD), and typical development (TD).
This large prospective cohort study consists of participants in the Norwegian Mother and Child Cohort Study. During a 10-year period (January 1, 1999, through December 31, 2008), women throughout Norway were recruited at the first prenatal ultrasonographic visit (approximately 18 weeks' gestation). The study enrolled 95,278 mothers, 75,248 fathers, and 114,516 children. Our analyses are based on MoBa data released through October 1, 2013, and NPR diagnoses registered through December 31, 2012, and include children born from January 1, 2002, through December 31, 2008, with completed age 18- and 36-month questionnaires.
We defined 3 groups of children: children with ASD (n = 195), children with DD and delayed language and/or motor development (n = 4636), and children with TD (n = 40?,95).
The GI symptoms were based on maternal report of constipation, diarrhea, and food allergy/intolerance.
Children with ASD were at significantly increased odds of maternally reported constipation (adjusted odds ratio [aOR], 2.7; 95% CI, 1.9-3.8; P
PubMed ID
25806498 View in PubMed
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Autism spectrum disorder, ADHD, epilepsy, and cerebral palsy in Norwegian children.

https://arctichealth.org/en/permalink/ahliterature123313
Source
Pediatrics. 2012 Jul;130(1):e152-8
Publication Type
Article
Date
Jul-2012
Author
Pål Surén
Inger Johanne Bakken
Heidi Aase
Richard Chin
Nina Gunnes
Kari Kveim Lie
Per Magnus
Ted Reichborn-Kjennerud
Synnve Schjølberg
Anne-Siri Øyen
Camilla Stoltenberg
Author Affiliation
Centre for Paediatric Epidemiology and Biostatistics, University College London Institute of Child Health, London, United Kingdom. pal.suren@fhi.no
Source
Pediatrics. 2012 Jul;130(1):e152-8
Date
Jul-2012
Language
English
Publication Type
Article
Keywords
Age Distribution
Attention Deficit Disorder with Hyperactivity - epidemiology
Cerebral Palsy - epidemiology
Child
Child Development Disorders, Pervasive - epidemiology
Child, Preschool
Comorbidity
Epilepsy - epidemiology
Female
Follow-Up Studies
Humans
Incidence
Infant
Infant, Newborn
Male
Norway - epidemiology
Registries
Sex Distribution
Abstract
Numerous studies have investigated the prevalence of neurologic and neurodevelopmental disorders individually, but few have examined them collectively, and there is uncertainty as to what extent they overlap.
The study has determined the proportions of children aged 0 to 11 years with diagnoses of autism spectrum disorder (ASD), attention-deficit/hyperactivity disorder (ADHD), epilepsy, and cerebral palsy (CP) in Norway. The data were obtained from the Norwegian Patient Register, which is nationwide and contains diagnoses assigned by Norwegian specialist health services (hospitals and outpatient clinics). The Norwegian Patient Register started collecting individual-level data in 2008, and the follow-up period for the study is years 2008 through 2010.
For ASD, ADHD, and epilepsy, the proportions were highest in the oldest children. At age 11 years, the incidence was 0.7% for ASD, 2.9% for ADHD, and 0.9% for epilepsy. The cumulative incidence is likely to be higher because some cases diagnosed before 2008 were probably missed. For CP, the proportions were ~0.3% for age = 5 years. There was considerable overlap between diagnoses. For all disorders, boys had a significantly increased risk. In school-age children (aged 6-11 years) the male/female ratio was 4.3 for ASD, 2.9 for ADHD, 1.2 for epilepsy, and 1.3 for CP.
The findings demonstrate the significant burden of disease associated with neurologic and neurodevelopmental disorders in children and that this burden is disproportionately skewed toward boys.
Notes
Cites: J Child Neurol. 2002 Jan;17 Suppl 1:S4-1711918462
Cites: J Autism Dev Disord. 2000 Jun;30(3):205-2311055457
Cites: J Autism Dev Disord. 1994 Oct;24(5):659-857814313
Cites: Disabil Rehabil. 2006 Feb 28;28(4):183-9116467053
Cites: Lancet. 2006 Jul 15;368(9531):210-516844490
Cites: Int J Epidemiol. 2006 Oct;35(5):1146-5016926217
Cites: Arch Pediatr Adolesc Med. 2007 Feb;161(2):193-817283306
Cites: Am J Psychiatry. 2007 Jun;164(6):942-817541055
Cites: Eur J Paediatr Neurol. 2008 Jan;12(1):4-1317574886
Cites: Arch Pediatr Adolesc Med. 2009 Jan;163(1):19-2619124699
Cites: Pediatr Res. 2009 Jun;65(6):591-819218885
Cites: Pediatr Res. 2009 Jun;65(6):599-60619454962
Cites: MMWR Surveill Summ. 2009 Dec 18;58(10):1-2020023608
Cites: Eur Child Adolesc Psychiatry. 2010 Mar;19(3):281-9520148275
Cites: Mol Psychiatry. 2010 Jul;15(7):676-8020571529
Cites: Orthop Clin North Am. 2010 Oct;41(4):441-5520868877
Cites: Pediatrics. 2011 Jun;127(6):1034-4221606152
Cites: Pediatrics. 1994 Mar;93(3):399-4037509480
PubMed ID
22711729 View in PubMed
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Birthweight and Childhood Cancer: Preliminary Findings from the International Childhood Cancer Cohort Consortium (I4C).

https://arctichealth.org/en/permalink/ahliterature273002
Source
Paediatr Perinat Epidemiol. 2015 Jul;29(4):335-45
Publication Type
Article
Date
Jul-2015
Author
Ora Paltiel
Gabriella Tikellis
Martha Linet
Jean Golding
Stanley Lemeshow
Gary Phillips
Karen Lamb
Camilla Stoltenberg
Siri E Håberg
Marin Strøm
Charlotta Granstrøm
Kate Northstone
Mark Klebanoff
Anne-Louise Ponsonby
Elizabeth Milne
Marie Pedersen
Manolis Kogevinas
Eunhee Ha
Terence Dwyer
Source
Paediatr Perinat Epidemiol. 2015 Jul;29(4):335-45
Date
Jul-2015
Language
English
Publication Type
Article
Keywords
Adolescent
Age of Onset
Australia - epidemiology
Birth weight
Child
Child, Preschool
Denmark - epidemiology
Female
Great Britain - epidemiology
Humans
Infant
Infant, Newborn
Israel - epidemiology
Male
Neoplasms - epidemiology - etiology
Norway - epidemiology
Odds Ratio
Risk factors
United States - epidemiology
Abstract
Evidence relating childhood cancer to high birthweight is derived primarily from registry and case-control studies. We aimed to investigate this association, exploring the potential modifying roles of age at diagnosis and maternal anthropometrics, using prospectively collected data from the International Childhood Cancer Cohort Consortium.
We pooled data on infant and parental characteristics and cancer incidence from six geographically and temporally diverse member cohorts [the Avon Longitudinal Study of Parents and Children (UK), the Collaborative Perinatal Project (USA), the Danish National Birth Cohort (Denmark), the Jerusalem Perinatal Study (Israel), the Norwegian Mother and Child Cohort Study (Norway), and the Tasmanian Infant Health Survey (Australia)]. Birthweight metrics included a continuous measure, deciles, and categories (= 4.0 vs.
Notes
Cites: Cancer Causes Control. 2012 Sep;23(9):1577-8522878902
Cites: Circulation. 2012 Mar 20;125(11):1381-922344037
Cites: Eur J Cancer. 2013 Apr;49(6):1437-4723266048
Cites: Pediatrics. 2013 Nov;132(5):e1265-7524167169
Cites: Int J Cancer. 2013 Dec 15;133(12):2968-7923754574
Cites: Mol Genet Metab. 2012 Sep;107(1-2):25-3022867885
Cites: Int J Epidemiol. 2015 Feb;44(1):153-6825626438
Cites: PLoS One. 2013;8(8):e7054923936446
Cites: Am J Obstet Gynecol. 2001 Oct;185(4):845-911641663
Cites: Arch Dis Child Fetal Neonatal Ed. 2002 Jan;86(1):F2-311815536
Cites: Int J Cancer. 2004 Jun 20;110(3):465-715095317
Cites: J Natl Cancer Inst. 2004 Oct 20;96(20):1549-5615494605
Cites: Acta Paediatr Scand. 1966;:Suppl 167:1+5940749
Cites: Cancer. 1969 Apr;23(4):913-95775981
Cites: Am J Epidemiol. 1984 May;119(5):788-956720675
Cites: Arch Dis Child. 1987 Mar;62(3):279-873646026
Cites: Obstet Gynecol. 1994 Mar;83(3):342-528127523
Cites: J Natl Cancer Inst. 1997 Jul 2;89(13):939-479214673
Cites: J Natl Cancer Inst. 1962 Jan;28:231-4414468028
Cites: Br J Cancer. 2006 Jun 5;94(11):1738-4416736025
Cites: Pediatr Int. 2006 Oct;48(5):470-816970785
Cites: Cancer Causes Control. 2007 Aug;18(6):655-6317503007
Cites: Am J Epidemiol. 2007 Jul 15;166(2):151-917443021
Cites: BMC Public Health. 2007;7:16817650297
Cites: Int J Epidemiol. 2007 Aug;36(4):724-3017255350
Cites: Am J Clin Nutr. 2008 Jun;87(6):1750-918541565
Cites: Int J Cancer. 2009 Jun 1;124(11):2658-7019173295
Cites: Epidemiology. 2009 Jul;20(4):484-719525684
Cites: Am J Epidemiol. 2009 Aug 1;170(3):379-8719498073
Cites: Pediatr Blood Cancer. 2010 Feb;54(2):242-919813253
Cites: Curr Opin Obstet Gynecol. 2009 Dec;21(6):521-619809317
Cites: Cancer Epidemiol Biomarkers Prev. 2010 Apr;19(4):1042-5220332267
Cites: Eur J Pediatr. 2010 Jul;169(7):875-8120101509
Cites: Paediatr Perinat Epidemiol. 2010 Sep;24(5):449-6920670226
Cites: Stat Med. 2011 Feb 20;30(4):377-9921225900
Cites: Leuk Lymphoma. 2011 Apr;52(4):709-1221438834
Erratum In: Paediatr Perinat Epidemiol. 2015 Nov;29(6):58926443988
PubMed ID
25989709 View in PubMed
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Caesarean section by immigrants' length of residence in Norway: a population-based study.

https://arctichealth.org/en/permalink/ahliterature267430
Source
Eur J Public Health. 2015 Feb;25(1):78-84
Publication Type
Article
Date
Feb-2015
Author
Ingvil K Sørbye
Anne K Daltveit
Johanne Sundby
Camilla Stoltenberg
Siri Vangen
Source
Eur J Public Health. 2015 Feb;25(1):78-84
Date
Feb-2015
Language
English
Publication Type
Article
Keywords
Adult
Analysis of Variance
Cesarean Section - statistics & numerical data
Emigrants and Immigrants - statistics & numerical data
Female
Humans
Norway
Registries - statistics & numerical data
Time Factors
Abstract
Immigrants to Europe account for a significant proportion of births in a context of rising caesarean rates. We examined the risk of planned and emergency caesarean section (CS) by immigrants' length of residence in Norway, and compared the results with those of non-immigrants.
We linked population-based birth registry data to immigration data for first deliveries among 23 147 immigrants from 10 countries and 385 306 non-immigrants between 1990-2009. Countries were grouped as having low CS levels (22%; the Philippines, Somalia, Sri Lanka, Thailand). Associations between length of residence and planned/emergency CS were estimated as relative risks (RR) with 95% confidence intervals (CI) in multivariable models.
In the immigrant group with low CS levels, planned, but not emergency, CS was independently associated with longer length of residence. Compared with recent immigrants (2 years had greater risk of emergency CS. In the high group, the risk of planned CS was similar to non-immigrants, while emergency CS was 51-75% higher irrespective of length of residency.
Efforts to improve immigrants' labour outcomes should target subgroups with sustained high emergency caesarean risk.
PubMed ID
25192708 View in PubMed
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Cardiovascular mortality in relation to birth weight of children and grandchildren in 500,000 Norwegian families.

https://arctichealth.org/en/permalink/ahliterature257690
Source
Eur Heart J. 2013 Nov;34(44):3427-36
Publication Type
Article
Date
Nov-2013
Author
Oyvind Naess
Camilla Stoltenberg
Dominic A Hoff
Wenche Nystad
Per Magnus
Aage Tverdal
George Davey Smith
Author Affiliation
Division of Epidemiology, National Institute of Public Health, Oslo, Norway.
Source
Eur Heart J. 2013 Nov;34(44):3427-36
Date
Nov-2013
Language
English
Publication Type
Article
Keywords
Adult
Aged
Aged, 80 and over
Birth Weight - physiology
Cardiovascular Diseases - mortality
Child
Fathers - statistics & numerical data
Female
Follow-Up Studies
Humans
Male
Maternal Age
Maternal Exposure - statistics & numerical data
Mothers - statistics & numerical data
Norway - epidemiology
Paternal Age
Pregnancy
Prenatal Exposure Delayed Effects - mortality
Smoking - mortality
Abstract
Cardiovascular diseases (CVDs) have been related to low birth weight, suggesting the foetal environment may program future risk. Alternatively, common genetic factors for both low birth weight and CVD could explain such associations. We investigated associations between offspring birth weight and paternal and maternal cardiovascular mortality and offspring birth weight and cardiovascular mortality among all four grandparents, and further assessed the mediating role of maternal smoking during pregnancy.
All births from 1967 to 2008 that could be linked to parents and grandparents comprised the population (n = 1,004,255). The mortality follow-up among parents was from 1970 to 2008 and among grandparents from 1960 to 2008. The association of grandparental mortality with maternal smoking during pregnancy was analysed in a subpopulation of those born after 1997 (n = 345,624). Per quintile higher in birth weight was related to 0.82 (0.75-0.89) hazard ratio from coronary heart disease in mothers and 0.94 (0.92-0.97) in fathers. For stroke, these were 0.85 (0.78-0.92) and 0.94 (0.89-1.00), respectively. In grandparents for cardiovascular causes, the effects were 0.95 (0.93-0.96) (maternal grandmother), 0.97 (0.96-0.98) (maternal grandfather), 0.96 (0.94-0.98) (paternal grandmother), and 0.98 (0.98-1.00) (paternal grandfather). Adjusting for maternal smoking in pregnancy in the subpopulation accounted for much of the effect on grandparental cardiovascular mortality in all categories of birth weight. For grandparental diabetes mortality, U-shaped associations were seen with grandchild birth weight for the maternal grandmother and inverse associations for all other grandparents.
Associations between CVD mortality in all four grandparents and grandchild birth weight exist, and while genetic and environmental factors may contribute to these, it appears that there is an important role for maternal smoking during pregnancy (and associated paternal smoking) in generating these associations. For diabetes, however, it appears that intrauterine environmental influences and genetic factors contribute to the transgenerational associations.
Notes
Comment In: Eur Heart J. 2013 Nov;34(44):3398-923103662
PubMed ID
22977224 View in PubMed
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Chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) is associated with pandemic influenza infection, but not with an adjuvanted pandemic influenza vaccine.

https://arctichealth.org/en/permalink/ahliterature275416
Source
Vaccine. 2015 Nov 17;33(46):6173-7
Publication Type
Article
Date
Nov-17-2015
Author
Per Magnus
Nina Gunnes
Kari Tveito
Inger Johanne Bakken
Sara Ghaderi
Camilla Stoltenberg
Mady Hornig
W Ian Lipkin
Lill Trogstad
Siri E Håberg
Source
Vaccine. 2015 Nov 17;33(46):6173-7
Date
Nov-17-2015
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Aged
Aged, 80 and over
Child
Child, Preschool
Cohort Studies
Drug-Related Side Effects and Adverse Reactions - epidemiology - pathology
Fatigue Syndrome, Chronic - epidemiology
Female
Humans
Incidence
Infant
Infant, Newborn
Influenza Vaccines - administration & dosage - adverse effects
Influenza, Human - complications
Male
Middle Aged
Norway - epidemiology
Risk assessment
Young Adult
Abstract
Chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) is associated to infections and it has been suggested that vaccination can trigger the disease. However, little is known about the specific association between clinically manifest influenza/influenza vaccine and CFS/ME. As part of a registry surveillance of adverse effects after mass vaccination in Norway during the 2009 influenza A (H1N1) pandemic, we had the opportunity to estimate and contrast the risk of CFS/ME after infection and vaccination.
Using the unique personal identification number assigned to everybody who is registered as resident in Norway, we followed the complete Norwegian population as of October 1, 2009, through national registries of vaccination, communicable diseases, primary health, and specialist health care until December 31, 2012. Hazard ratios (HRs) of CFS/ME, as diagnosed in the specialist health care services (diagnostic code G93.3 in the International Classification of Diseases, Version 10), after influenza infection and/or vaccination were estimated using Cox proportional-hazards regression.
The incidence rate of CFS/ME was 2.08 per 100,000 person-months at risk. The adjusted HR of CFS/ME after pandemic vaccination was 0.97 (95% confidence interval [CI]: 0.91-1.04), while it was 2.04 (95% CI: 1.78-2.33) after being diagnosed with influenza infection during the peak pandemic period.
Pandemic influenza A (H1N1) infection was associated with a more than two-fold increased risk of CFS/ME. We found no indication of increased risk of CFS/ME after vaccination. Our findings are consistent with a model whereby symptomatic infection, rather than antigenic stimulation may trigger CFS/ME.
PubMed ID
26475444 View in PubMed
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Cohort profile: cerebral palsy in the Norwegian and Danish birth cohorts (MOBAND-CP).

https://arctichealth.org/en/permalink/ahliterature287693
Source
BMJ Open. 2016 Sep 02;6(9):e012777
Publication Type
Article
Date
Sep-02-2016
Author
Mette C Tollånes
Katrine Strandberg-Larsen
Ingeborg Forthun
Tanja Gram Petersen
Dag Moster
Anne-Marie Nybo Andersen
Camilla Stoltenberg
Jørn Olsen
Allen J Wilcox
Source
BMJ Open. 2016 Sep 02;6(9):e012777
Date
Sep-02-2016
Language
English
Publication Type
Article
Keywords
Adult
Cerebral Palsy - etiology
Cohort Studies
Denmark
Female
Humans
Infant
Male
Norway
Pregnancy
Pregnancy Complications
Prospective Studies
Registries
Risk factors
Surveys and Questionnaires
Abstract
The purpose of MOthers and BAbies in Norway and Denmark cerebral palsy (MOBAND-CP) was to study CP aetiology in a prospective design.
MOBAND-CP is a cohort of more than 210 000 children, created as a collaboration between the world's two largest pregnancy cohorts-the Norwegian Mother and Child Cohort study (MoBa) and the Danish National Birth Cohort. MOBAND-CP includes maternal interview/questionnaire data collected during pregnancy and follow-up, plus linked information from national health registries.
Initial harmonisation of data from the 2 cohorts has created 140 variables for children and their mothers. In the MOBAND-CP cohort, 438 children with CP have been identified through record linkage with validated national registries, providing by far the largest such sample with prospectively collected detailed pregnancy data. Several studies investigating various hypotheses regarding CP aetiology are currently on-going.
Additional data can be harmonised as necessary to meet requirements of new projects. Biological specimens collected during pregnancy and at delivery are potentially available for assay, as are results from assays conducted on these specimens for other projects. The study size allows consideration of CP subtypes, which is rare in aetiological studies of CP. In addition, MOBAND-CP provides a platform within the context of a merged birth cohort of exceptional size that could, after appropriate permissions have been sought, be used for cohort and case-cohort studies of other relatively rare health conditions of infants and children.
Notes
Cites: Pediatrics. 2012 Jul;130(1):e152-822711729
Cites: Nat Rev Dis Primers. 2016 Jan 07;2:1508227188686
Cites: Int J Epidemiol. 2006 Oct;35(5):1146-5016926217
Cites: Epidemiology. 2006 Jul;17(4):413-816755269
Cites: Dev Med Child Neurol. 2014 Aug;56(8):779-8524621110
Cites: Acta Obstet Gynecol Scand. 2014 Nov;93(11):1131-4025250851
Cites: Dev Med Child Neurol. 2013 Jun;55(6):499-50823181910
Cites: Paediatr Perinat Epidemiol. 2015 May;29(3):172-8325808200
Cites: N Engl J Med. 2015 Sep 3;373(10):946-5326332549
Cites: Dev Med Child Neurol. 2002 Sep;44(9):633-4012227618
Cites: Dan Med Bull. 2001 Aug;48(3):161-311556266
Cites: Nat Commun. 2015 Aug 03;6:794926236009
Cites: BMJ. 2014 Jul 15;349:g429425028249
Cites: Dan Med Bull. 1998 Jun;45(3):320-39675544
Cites: Eur J Epidemiol. 2010 May;25(5):349-5520349116
Cites: Scand J Public Health. 2001 Dec;29(4):300-711775787
Cites: Scand J Work Environ Health. 2015 Jul;41(4):384-9625940455
Cites: Eur J Paediatr Neurol. 2008 Jan;12(1):4-1317574886
Cites: Dev Med Child Neurol Suppl. 2007 Feb;109:8-1417370477
Cites: Int J Epidemiol. 2016 Apr;45(2):382-827063603
Cites: Scand J Public Health. 2011 Jul;39(7 Suppl):115-2021775368
Cites: Scand J Public Health. 2011 Jul;39(7 Suppl):30-321775347
Cites: Acta Obstet Gynecol Scand. 2000 Jun;79(6):435-910857866
Cites: Mol Psychiatry. 2015 Feb;20(2):176-8225666757
Cites: Paediatr Perinat Epidemiol. 2013 Jul;27(4):393-41423772942
Cites: Dan Med Bull. 1999 Sep;46(4):357-6010514944
Cites: Paediatr Perinat Epidemiol. 2009 Nov;23(6):597-60819840297
PubMed ID
27591025 View in PubMed
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