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Acetaminophen use during pregnancy, behavioral problems, and hyperkinetic disorders.

https://arctichealth.org/en/permalink/ahliterature104902
Source
JAMA Pediatr. 2014 Apr;168(4):313-20
Publication Type
Article
Date
Apr-2014
Author
Zeyan Liew
Beate Ritz
Cristina Rebordosa
Pei-Chen Lee
Jørn Olsen
Author Affiliation
Department of Epidemiology, Fielding School of Public Health, University of California, Los Angeles.
Source
JAMA Pediatr. 2014 Apr;168(4):313-20
Date
Apr-2014
Language
English
Publication Type
Article
Keywords
Acetaminophen - adverse effects
Adult
Attention Deficit Disorder with Hyperactivity - chemically induced - diagnosis - epidemiology
Child
Child, Preschool
Denmark
Female
Humans
Hyperkinesis - chemically induced - diagnosis
Infant
Male
Mental Disorders - chemically induced - epidemiology
Mothers
Pregnancy
Prenatal Exposure Delayed Effects - chemically induced - diagnosis - epidemiology
Proportional Hazards Models
Prospective Studies
Questionnaires
Risk assessment
Risk factors
Abstract
Acetaminophen (paracetamol) is the most commonly used medication for pain and fever during pregnancy in many countries. Research data suggest that acetaminophen is a hormone disruptor, and abnormal hormonal exposures in pregnancy may influence fetal brain development.
To evaluate whether prenatal exposure to acetaminophen increases the risk for developing attention-deficit/hyperactivity disorder (ADHD)-like behavioral problems or hyperkinetic disorders (HKDs) in children.
We studied 64,322 live-born children and mothers enrolled in the Danish National Birth Cohort during 1996-2002.
Acetaminophen use during pregnancy was assessed prospectively via 3 computer-assisted telephone interviews during pregnancy and 6 months after child birth.
To ascertain outcome information we used (1) parental reports of behavioral problems in children 7 years of age using the Strengths and Difficulties Questionnaire; (2) retrieved HKD diagnoses from the Danish National Hospital Registry or the Danish Psychiatric Central Registry prior to 2011; and (3) identified ADHD prescriptions (mainly Ritalin) for children from the Danish Prescription Registry. We estimated hazard ratios for receiving an HKD diagnosis or using ADHD medications and risk ratios for behavioral problems in children after prenatal exposure to acetaminophen.
More than half of all mothers reported acetaminophen use while pregnant. Children whose mothers used acetaminophen during pregnancy were at higher risk for receiving a hospital diagnosis of HKD (hazard ratio?=?1.37; 95% CI, 1.19-1.59), use of ADHD medications (hazard ratio?=?1.29; 95% CI, 1.15-1.44), or having ADHD-like behaviors at age 7 years (risk ratio?=?1.13; 95% CI, 1.01-1.27). Stronger associations were observed with use in more than 1 trimester during pregnancy, and exposure response trends were found with increasing frequency of acetaminophen use during gestation for all outcomes (ie, HKD diagnosis, ADHD medication use, and ADHD-like behaviors; P trend
Notes
Comment In: JAMA Pediatr. 2014 Apr;168(4):306-724566519
PubMed ID
24566677 View in PubMed
Less detail

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
Less detail

Bias from conditioning on live birth in pregnancy cohorts: an illustration based on neurodevelopment in children after prenatal exposure to organic pollutants.

https://arctichealth.org/en/permalink/ahliterature268382
Source
Int J Epidemiol. 2015 Feb;44(1):345-54
Publication Type
Article
Date
Feb-2015
Author
Zeyan Liew
Jørn Olsen
Xin Cui
Beate Ritz
Onyebuchi A Arah
Source
Int J Epidemiol. 2015 Feb;44(1):345-54
Date
Feb-2015
Language
English
Publication Type
Article
Keywords
Attention Deficit Disorder with Hyperactivity - epidemiology
Bias (epidemiology)
Denmark
Environmental Pollutants - toxicity
Female
Fetal Death
Fluorocarbons - toxicity
Humans
Live Birth
Monte Carlo Method
Pregnancy
Pregnancy Outcome - epidemiology
Prenatal Exposure Delayed Effects - epidemiology
Abstract
Only 60-70% of fertilized eggs may result in a live birth, and very early fetal loss mainly goes unnoticed. Outcomes that can only be ascertained in live-born children will be missing for those who do not survive till birth. In this article, we illustrate a common bias structure (leading to 'live-birth bias') that arises from studying the effects of prenatal exposure to environmental factors on long-term health outcomes among live births only in pregnancy cohorts. To illustrate this we used prenatal exposure to perfluoroalkyl substances (PFAS) and attention-deficit/hyperactivity disorder (ADHD) in school-aged children as an example. PFAS are persistent organic pollutants that may impact human fecundity and be toxic for neurodevelopment. We simulated several hypothetical scenarios based on characteristics from the Danish National Birth Cohort and found that a weak inverse association may appear even if PFAS do not cause ADHD but have a considerable effect on fetal survival. The magnitude of the negative bias was generally small, and adjusting for common causes of the outcome and fetal loss can reduce the bias. Our example highlights the need to identify the determinants of pregnancy loss and the importance of quantifying bias arising from conditioning on live birth in observational studies.
Notes
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Comment In: Int J Epidemiol. 2015 Jun;44(3):1079-8026163686
Comment In: Int J Epidemiol. 2015 Jun;44(3):1080-126163685
PubMed ID
25604449 View in PubMed
Less detail

Carnitine levels and mutations in the SLC22A5 gene in Faroes patients with Parkinson's disease.

https://arctichealth.org/en/permalink/ahliterature290945
Source
Neurosci Lett. 2018 May 14; 675:116-119
Publication Type
Journal Article
Date
May-14-2018
Author
Súsanna A Crooks
Sára Bech
Jónrit Halling
Debes H Christiansen
Beate Ritz
Maria Skaalum Petersen
Author Affiliation
Department of Occupational Medicine and Public Health, The Faroese Hospital System, Tórshavn, Faroe Islands.
Source
Neurosci Lett. 2018 May 14; 675:116-119
Date
May-14-2018
Language
English
Publication Type
Journal Article
Abstract
Mitochondrial dysfunction, oxidative stress and energy production have been implicated in the etiology of Parkinson's disease (PD). Several agents are under investigation for potential neuroprotective effects including acetyl-l-carnitine (ALC).
To investigate whether low carnitine levels and mutations in the SLC22A5 gene encoding the carnitine transporter are associates with PD risk in the Faroe Islands where the prevalence of both PD and carnitine transporter deficiency (CTD) is high.
We conducted a case-control study with 121 cases and 235 randomly selected controls, matched by gender and age. Blood spots were analyzed for free and total carnitine levels by QUATTRO LC triple quadrupole mass spectrometry (MS/MS) and sequencing performed for five genetic mutations in the SLC22A5 gene with ABI PRISM 3130.
PD cases had significantly lower levels of free and total carnitine levels compared with controls (P??G mutation frequency in the SLC22A5 gene among cases and controls (p?=?.70).
Low carnitine levels seem to be associated with PD, but only in individuals without the c.95A?>?G mutation rendering the carnitine transporter less efficient. Thus, the difference in carnitine levels is not caused by a higher frequency of c.95A?>?G mutation carriers in cases. The cause may be dietary or due to different gut microbiota among cases.
PubMed ID
29614331 View in PubMed
Less detail

Carnitine levels and mutations in the SLC22A5 gene in Faroes patients with Parkinson's disease.

https://arctichealth.org/en/permalink/ahliterature298366
Source
Neurosci Lett. 2018 05 14; 675:116-119
Publication Type
Journal Article
Research Support, Non-U.S. Gov't
Date
05-14-2018
Author
Súsanna A Crooks
Sára Bech
Jónrit Halling
Debes H Christiansen
Beate Ritz
Maria Skaalum Petersen
Author Affiliation
Department of Occupational Medicine and Public Health, The Faroese Hospital System, Tórshavn, Faroe Islands.
Source
Neurosci Lett. 2018 05 14; 675:116-119
Date
05-14-2018
Language
English
Publication Type
Journal Article
Research Support, Non-U.S. Gov't
Keywords
Adult
Aged
Aged, 80 and over
Cardiomyopathies - complications
Carnitine - deficiency - metabolism
Case-Control Studies
Denmark - epidemiology
Female
Humans
Hyperammonemia - complications
Male
Middle Aged
Muscular Diseases - complications
Mutation
Parkinson Disease - complications - epidemiology - genetics - metabolism
Solute Carrier Family 22 Member 5 - genetics
Abstract
Mitochondrial dysfunction, oxidative stress and energy production have been implicated in the etiology of Parkinson's disease (PD). Several agents are under investigation for potential neuroprotective effects including acetyl-l-carnitine (ALC).
To investigate whether low carnitine levels and mutations in the SLC22A5 gene encoding the carnitine transporter are associates with PD risk in the Faroe Islands where the prevalence of both PD and carnitine transporter deficiency (CTD) is high.
We conducted a case-control study with 121 cases and 235 randomly selected controls, matched by gender and age. Blood spots were analyzed for free and total carnitine levels by QUATTRO LC triple quadrupole mass spectrometry (MS/MS) and sequencing performed for five genetic mutations in the SLC22A5 gene with ABI PRISM 3130.
PD cases had significantly lower levels of free and total carnitine levels compared with controls (P??G mutation frequency in the SLC22A5 gene among cases and controls (p?=?.70).
Low carnitine levels seem to be associated with PD, but only in individuals without the c.95A?>?G mutation rendering the carnitine transporter less efficient. Thus, the difference in carnitine levels is not caused by a higher frequency of c.95A?>?G mutation carriers in cases. The cause may be dietary or due to different gut microbiota among cases.
PubMed ID
29614331 View in PubMed
Less detail

Cause-specific mortality among spouses of Parkinson disease patients.

https://arctichealth.org/en/permalink/ahliterature257409
Source
Epidemiology. 2014 Mar;25(2):225-32
Publication Type
Article
Date
Mar-2014
Author
Malene Nielsen
Johnni Hansen
Beate Ritz
Helene Nordahl
Eva Schernhammer
Lene Wermuth
Naja Hulvej Rod
Author Affiliation
From the aDepartment of Public Health, Section of Social Medicine, University of Copenhagen, Copenhagen, Denmark; bDanish Cancer Society, Institute of Cancer Epidemiology, Copenhagen, Denmark; cSchool of Public Health, UCLA, Los Angeles, CA; dHarvard School of Public Health, Department of Epidemiology, Boston, MA; eDepartment of Neurology, Odense University Hospital, Odense, Denmark; and fThe Copenhagen Stress Research Center, Copenhagen, Denmark.
Source
Epidemiology. 2014 Mar;25(2):225-32
Date
Mar-2014
Language
English
Publication Type
Article
Keywords
Adult
Aged
Aged, 80 and over
Caregivers
Cause of Death
Denmark - epidemiology
Female
Follow-Up Studies
Humans
Male
Middle Aged
Parkinson Disease
Proportional Hazards Models
Registries
Sex Factors
Spouses
Abstract
Caring for a chronically ill spouse is stressful, but the health effects of caregiving are not fully understood. We studied the effect on mortality of being married to a person with Parkinson disease.
All patients in Denmark with a first-time hospitalization for Parkinson disease between 1986 and 2009 were identified, and each case was matched to five population controls. We further identified all spouses of those with Parkinson disease (n = 8,515) and also the spouses of controls (n = 43,432). All spouses were followed in nationwide registries until 2011.
Among men, being married to a Parkinson disease patient was associated with a slightly higher risk of all-cause mortality (hazard ratio = 1.06 [95% confidence interval = 1.00-1.11]). Mortality was particularly high for death due to external causes (1.42 [1.09-1.84]) including suicide (1.89 [1.05-3.42]) and death from undefined symptoms/abnormal findings (1.25 [1.07-1.47]). Censoring at the time of death of the patient attenuated the findings for all-cause mortality in husbands (1.02 [0.95-1.09]), indicating that part of the association is with bereavement. Still, living with a person with Parkinson disease 5 years after first Parkinson hospitalization was associated with higher risk of all-cause mortality for both husbands (1.15 [1.07-1.23]) and wives (1.11 [1.04-1.17]).
Caring for a spouse with a serious chronic illness is associated with a slight but consistent elevation in mortality risk.
PubMed ID
24378369 View in PubMed
Less detail

Childhood Bereavement and Type 1 Diabetes: a Danish National Register Study.

https://arctichealth.org/en/permalink/ahliterature276807
Source
Paediatr Perinat Epidemiol. 2016 Jan;30(1):86-92
Publication Type
Article
Date
Jan-2016
Author
Jasveer Virk
Beate Ritz
Jiong Li
Carsten Obel
Jørn Olsen
Source
Paediatr Perinat Epidemiol. 2016 Jan;30(1):86-92
Date
Jan-2016
Language
English
Publication Type
Article
Keywords
Affect
Bereavement
Child
Denmark - epidemiology
Diabetes Mellitus, Type 1 - physiopathology - psychology
Fathers
Female
Follow-Up Studies
Humans
Life Change Events
Longitudinal Studies
Male
Mothers
Parent-Child Relations
Registries
Risk factors
Siblings
Stress, Psychological - complications - physiopathology - psychology
Abstract
Death of a close family member such as a parent or a sibling can cause prolonged stress and changes in the family structure that may have extensive social and health effects on a young child. The aim of this paper is to examine the rate of type 1 diabetes following bereavement due to death of a first-degree family member in early life.
We used data from the Danish Civil Registration System (CRS) to identify singleton births in Denmark born 1 January 1980 through 31 December 2005, n?=?1?740?245 and their next of kin. We categorised children as exposed to bereavement if they lost a mother, father or sibling from age 5 years onwards, the remaining children were considered unexposed. Children were followed until first diagnosis of diabetes, death, emigration, or 31 December 2010. We estimated incidence rate ratios (IRRs) from birth using log-linear Poisson regression models with person-years as an offset variable. Exposed children were followed up for an average of 9.1 years [standard deviation (SD) 6.7] and unexposed children were followed up for an average of 12.3 years (SD 7.3).
In our sample 94?943 children were exposed to bereavement, and 6110 cases of type 1 diabetes were identified. Bereavement was associated with an increased rate of type 1 diabetes when exposure onset began after 11 years of age (adjusted IRR 1.28, 95% confidence interval 1.08, 1.51).
We found some evidence to indicate an increase in the rate of type 1 diabetes among children exposed to bereavement when exposure occurred after 11 years of age.
PubMed ID
26444317 View in PubMed
Less detail

Diabetes and the risk of developing Parkinson's disease in Denmark.

https://arctichealth.org/en/permalink/ahliterature136125
Source
Diabetes Care. 2011 May;34(5):1102-8
Publication Type
Article
Date
May-2011
Author
Eva Schernhammer
Johnni Hansen
Kathrine Rugbjerg
Lene Wermuth
Beate Ritz
Author Affiliation
Channing Laboratory, Department of Medicine, Harvard Medical School, Boston, Massachusetts, USA. eva.schernhammer@channing.harvard.edu
Source
Diabetes Care. 2011 May;34(5):1102-8
Date
May-2011
Language
English
Publication Type
Article
Keywords
Aged
Aged, 80 and over
Denmark - epidemiology
Diabetes Mellitus - epidemiology - physiopathology
Female
Humans
Logistic Models
Male
Middle Aged
Odds Ratio
Parkinson Disease - epidemiology - etiology
Risk factors
Abstract
Insulin contributes to normal brain function. Previous studies have suggested associations between midlife diabetes and neurodegenerative diseases, including Parkinson's disease. Using Danish population registers, we investigated whether a history of diabetes or the use of antidiabetes drugs was associated with Parkinson's disease.
From the nationwide Danish Hospital Register hospital records, we identified 1,931 patients with a first-time diagnosis of Parkinson's disease between 2001 and 2006. We randomly selected 9,651 population control subjects from the Central Population Registry and density matched them by birth year and sex. Pharmacy records comprising all antidiabetes and anti-Parkinson drug prescriptions in Denmark were available. Odds ratios (ORs) were estimated by logistic regression models.
Having diabetes, as defined by one or more hospitalizations and/or outpatient visits for the condition, was associated with a 36% increased risk of developing Parkinson's disease (OR 1.36 [95% CI 1.08-1.71]). Similarly, diabetes defined by the use of any antidiabetes medications was associated with a 35% increased Parkinson's disease risk (1.35 [1.10-1.65]). When diabetes was defined as the use of oral antidiabetes medications, effect estimates were stronger in women (2.92 [1.34-6.36]), whereas when diabetes was defined as any antidiabetes drug prescription, patients with early-onset Parkinson's disease were at highest risk (i.e., Parkinson's disease diagnosed before the age of 60 years; 3.07 [1.65-5.70]).
We found that a diagnosis of, or treatment received for, diabetes was significantly associated with an increased risk of developing Parkinson's disease, especially younger-onset Parkinson's disease. Our results suggest a common pathophysiologic pathway between the two diseases. Future studies should take age at Parkinson's disease onset into account.
Notes
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PubMed ID
21411503 View in PubMed
Less detail

Fetal growth and air pollution - A study on ultrasound and birth measures.

https://arctichealth.org/en/permalink/ahliterature282471
Source
Environ Res. 2017 Jan;152:73-80
Publication Type
Article
Date
Jan-2017
Author
Ebba Malmqvist
Zeyan Liew
Karin Källén
Anna Rignell-Hydbom
Ralf Rittner
Lars Rylander
Beate Ritz
Source
Environ Res. 2017 Jan;152:73-80
Date
Jan-2017
Language
English
Publication Type
Article
Keywords
Air Pollutants - analysis
Biomarkers - analysis
Cohort Studies
Environmental Exposure
Environmental monitoring
Female
Fetal Development
Fetus - diagnostic imaging
Humans
Male
Maternal Exposure
Nitrogen Oxides - analysis
Pregnancy
Sweden
Ultrasonography
Vehicle Emissions - analysis
Abstract
Air pollution has been suggested to affect fetal growth, but more data is needed to assess the timing of exposure effects by using ultrasound measures. It is also important to study effects in low exposure areas to assess eventual thresholds of effects. The MAPSS (Maternal Air Pollution in Southern Sweden) cohort consists of linked registry data for around 48,000 pregnancies from an ultrasound database, birth registry and exposure data based on residential addresses. Measures of air pollution exposure were obtained through dispersion modelling with input data from an emissions database (NOx) with high resolution (100-500m grids). Air pollution effects were assessed with linear regressions for the following endpoints; biparietal diameter, femur length, abdominal diameter and estimated fetal weight measured in late pregnancy and birth weight and head circumference measured at birth. We estimated negative effects for NOx; in the adjusted analyses the decrease of abdominal diameter and femur length were -0.10 (-0.17, -0.03) and -0.13 (-0.17, -0.01)mm, respectively, per 10µg/m(3) increment of NOx. We also estimated an effect of NOx-exposures on birth weight by reducing birth weight by 9g per 10µg/m(3) increment of NOx. We estimated small but statistically significant effects of air pollution on late fetal and birth size and reduced fetal growth late in pregnancy in a geographic area with levels below current WHO air quality guidelines.
PubMed ID
27741452 View in PubMed
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Gout and the risk of Parkinson's disease in Denmark.

https://arctichealth.org/en/permalink/ahliterature115892
Source
Eur J Epidemiol. 2013 Apr;28(4):359-60
Publication Type
Article
Date
Apr-2013
Author
Eva Schernhammer
Jiaheng Qiu
Lene Wermuth
Christina Funch Lassen
Soren Friis
Beate Ritz
Source
Eur J Epidemiol. 2013 Apr;28(4):359-60
Date
Apr-2013
Language
English
Publication Type
Article
Keywords
Adult
Aged
Aged, 80 and over
Case-Control Studies
Denmark - epidemiology
Drug Prescriptions - statistics & numerical data
Female
Gout - drug therapy - epidemiology - metabolism
Gout Suppressants - adverse effects - therapeutic use
Humans
Logistic Models
Male
Middle Aged
Parkinson Disease - diagnosis - epidemiology
Population Surveillance
Registries
Risk factors
Uric Acid - metabolism
Notes
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Cites: Eur J Epidemiol. 2013 Jan;28(1):67-7723377703
PubMed ID
23456139 View in PubMed
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