| 1. |
- Bornehag, Carl-Gustaf, 1957-, et al.
(författare)
-
Prenatal exposure to acetaminophen and children's language development at 30 months
- 2018
-
Ingår i: European psychiatry. - : Elsevier. - 0924-9338 .- 1778-3585. ; 51, s. 98-103
-
Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: To examine prenatal APAP exposure in relation to language development in offspring at 30 months of age.METHOD: A population-based pregnancy cohort study including 754 women who enrolled in the Swedish Environmental Longitudinal, Mother and child, Asthma and allergy (SELMA) study in pregnancy week 8-13. Two exposure measures were used: (1) maternally reported number of APAP tablets taken between conception and enrollment; (2) APAP urinary concentration at enrollment. Language development at 30 months was assessed by nurse's evaluation and parental questionnaire, including the number of words the child used (<25, 25-50 and >50). Main study outcome; parental report of use of fewer than 50 words, termed language delay (LD).RESULTS: 59.2% of women enrolled in weeks 8-13 reported taking APAP between conception and enrollment. APAP was measurable in all urine samples and urinary APAP was correlated with the number of APAP taken during pregnancy (P<0.01). Language delay was more prevalent in boys (12.6%) than girls (4.1%) (8.5% in total). Both the number of APAP tablets and urinary APAP concentration were associated with greater LD in girls but not in boys. The adjusted odds ratio (OR) for LD among girls whose mothers reported >6 vs. 0 APAP tablets was 5.92 (95% confidence interval (CI) 1.10-31.94). The OR for LD in girls whose mothers' urinary APAP was in the highest compared to the lowest quartile was 10.34 (95% CI 1.37-77.86). While it cannot be ruled out, our available data do not support confounding by indication.CONCLUSIONS: Given the prevalence of prenatal APAP use and the importance of language development, these findings, if replicated, would suggest that pregnant women should limit their use of this analgesic during pregnancy.
|
|
| 2. |
- Bornehag, Carl-Gustaf, 1957-, et al.
(författare)
-
Association of Prenatal Phthalate Exposure with Language Development in Early Childhood
- 2018
-
Ingår i: JAMA pediatrics. - : American Medical Association. - 2168-6203 .- 2168-6211. ; 172:12, s. 1169-1176
-
Tidskriftsartikel (refereegranskat)abstract
- Importance: Prenatal exposure to phthalates has been associated with neurodevelopmental outcomes, but little is known about the association with language development. Objective: To examine the association of prenatal phthalate exposure with language development in children in 2 population-based pregnancy cohort studies. Design, Setting, and Participants: Data for this study were obtained from the Swedish Environmental Longitudinal Mother and Child, Asthma and Allergy (SELMA) study conducted in prenatal clinics throughout Värmland county in Sweden and The Infant Development and the Environment Study (TIDES) conducted in 4 academic centers in the United States. Participants recruited into both studies were women in their first trimester of pregnancy who had literacy in Swedish (SELMA) or English or Spanish (TIDES). This study included mothers and their children from both the SELMA study (n = 963) and TIDES (n = 370) who had complete data on prenatal urinary phthalate metabolite levels, language delay, and modeled covariables. For SELMA, the data were collected from November 1, 2007, to June 30, 2013, and data analysis was conducted from November 1, 2016, to June 30, 2018. For TIDES, data collection began January 1, 2010, and ended March 29, 2016, and data analysis was performed from September 15, 2016, to June 30, 2018. Main Outcomes and Measures: Mothers completed a language development questionnaire that asked the number of words their children could understand or use at a median of 30 months of age (SELMA) and 37 months of age (TIDES). The responses were categorized as fewer than 25, 25 to 50, and more than 50 words, with 50 words or fewer classified as language delay. Results: In the SELMA study, 963 mothers, 455 (47.2%) girls, and 508 [52.8%] boys were included. In TIDES, 370 mothers, 185 (50.0%) girls, and 185 (50.0%) boys were included in this analysis. The prevalence of language delay was 10.0% in both SELMA (96 reported) and TIDES (37 reported), with higher rates of delay in boys than girls (SELMA: 69 [13.5%] vs 27 [6.0%]; TIDES: 12 [12.4%] vs 14 [7.6%]). In crude analyses, the metabolite levels of dibutyl phthalate and butyl benzyl phthalate were statistically significantly associated with language delay in both cohorts. In adjusted analyses, a doubling of prenatal exposure of dibutyl phthalate and butyl benzyl phthalate metabolites increased the odds ratio (OR) for language delay by approximately 25% to 40%, with statistically significant results in the SELMA study (dibutyl phthalate OR, 1.29 [95% CI, 1.03-1.63; P =.03]; butyl benzyl phthalate OR, 1.26 [95% CI, 1.07-1.49; P =.003]). A doubling of prenatal monoethyl phthalate exposure was associated with an approximately 15% increase in the OR for language delay in the SELMA study (OR, 1.14; 95% CI, 1.00-1.31; P =.05), but no such association was found in TIDES (OR, 0.98; 95% CI, 0.79-1.23). Conclusions and Relevance: In findings from this study, prenatal exposure to dibutyl phthalate and butyl benzyl phthalate was statistically significantly associated with language delay in children in both the SELMA study and TIDES. These findings, along with the prevalence of prenatal exposure to phthalates, the importance of language development, and the inconsistent results from a 2017 Danish study, suggest that the association of phthalates with language delay may warrant further examination.
|
|
| 3. |
|
|
| 4. |
- Reed, Zoe E., et al.
(författare)
-
Mapping the genetic and environmental aetiology of autistic traits in Sweden and the United Kingdom
- 2021
-
Ingår i: JCPP Advances. - : John Wiley & Sons. - 2692-9384. ; 1:3
-
Tidskriftsartikel (refereegranskat)abstract
- Background: Autistic traits are influenced by both genetic and environmental factors, and are known to vary geographically in prevalence. But to what extent does their aetiology also vary from place to place?Methods: We applied a novel spatial approach to data on autistic traits from two large twin studies, the Child and Adolescent Twin Study in Sweden (CATSS; N = 16,677, including 8307 twin pairs) and the Twins Early Development Study in the UK (TEDS; N = 11,594, including 5796 twin pairs), to explore how the influence of nature and nurture on autistic traits varies from place to place.Results: We present maps of gene- and environment- by geography interactions in Sweden and the United Kingdom (UK), showing geographical variation in both genetic and environmental influences across the two countries. In Sweden genetic influences appear higher in the far south and in a band running across the centre of the country. Environmental influences appear greatest in the south and north, with reduced environmental influence across the central band. In the UK genetic influences appear greater in the south, particularly in more central southern areas and the southeast, the Midlands and the north of England. Environmental influences appear greatest in the south and east of the UK, with less influence in the north and the west.Conclusions: We hope this systematic approach to identifying aetiological interactions will inspire research to examine a wider range of previously unknown environmental influences on the aetiology of autistic traits. By doing so, we will gain greater understanding of how these environments draw out or mask genetic predisposition and interact with other environmental influences in the development of autistic traits.
|
|
| 5. |
- Shakeshaft, Nicholas G., et al.
(författare)
-
Thinking positively : The genetics of high intelligence
- 2015
-
Ingår i: Intelligence. - New York, USA : Elsevier. - 0160-2896 .- 1873-7935. ; 48, s. 123-132
-
Tidskriftsartikel (refereegranskat)abstract
- High intelligence (general cognitive ability) is fundamental to the human capital that drives societies in the information age. Understanding the origins of this intellectual capital is important for government policy, for neuroscience, and for genetics. For genetics, a key question is whether the genetic causes of high intelligence are qualitatively or quantitatively different from the normal distribution of intelligence. We report results from a sibling and twin study of high intelligence and its links with the normal distribution. We identified 360,000 sibling pairs and 9000 twin pairs from 3 million 18-year-old males with cognitive assessments administered as part of conscription to military service in Sweden between 1968 and 2010. We found that high intelligence is familial, heritable, and caused by the same genetic and environmental factors responsible for the normal distribution of intelligence. High intelligence is a good candidate for "positive genetics" - going beyond the negative effects of DNA sequence variation on disease and disorders to consider the positive end of the distribution of genetic effects.
|
|
| 6. |
- Silverman, Michael E., et al.
(författare)
-
The risk factors for postpartum depression : A population-based study
- 2017
-
Ingår i: Depression and anxiety (Print). - Hoboken, USA : John Wiley & Sons. - 1091-4269 .- 1520-6394. ; 34:2, s. 178-187
-
Tidskriftsartikel (refereegranskat)abstract
- Background: Postpartum depression (PPD) can result in negative personal and child developmental outcomes. Only a few large population-based studies of PPD have used clinical diagnoses of depression and no study has examined how a maternal depression history interacts with known risk factors. The objective of this study was to examine the impact of a depression history on PPD and pre- and perinatal risk factors.Methods: A nationwide prospective cohort study of all women with live singleton births in Sweden from 1997 through 2008 was conducted. Relative risk (RR) of clinical depression within the first year postpartum and two-sided 95% confidence intervals were estimated.Results: The RR of PPD in women with a history of depression was estimated at 21.03 (confidence interval: 19.72-22.42), compared to those without. Among all women, PPD risk increased with advanced age (1.25 (1.13-1.37)) and gestational diabetes (1.70 (1.36-2.13)). Among women with a history of depression, pregestational diabetes (1.49 (1.01-2.21)) and mild preterm delivery also increased risk (1.20 (1.06-1.36)). Among women with no depression history, young age (2.14 (1.79-2.57)), undergoing instrument-assisted (1.23 (1.09-1.38)) or cesarean (1.64(1.07-2.50)) delivery, and moderate preterm delivery increased risk (1.36 (1.05-1.75)). Rates of PPD decreased considerably after the first postpartum month (RR = 0.27).Conclusions: In the largest population-based study to date, the risk of PPD was more than 20 times higher for women with a depression history, compared to women without. Gestational diabetes was independently associated with a modestly increased PPD risk. Maternal depression history also had a modifying effect on pre- and perinatal PPD risk factors.
|
|
