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- Thompson, EJ, et al.
(författare)
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Long COVID burden and risk factors in 10 UK longitudinal studies and electronic health records
- 2022
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Ingår i: Nature communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 13:1, s. 3528-
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Tidskriftsartikel (refereegranskat)abstract
- The frequency of, and risk factors for, long COVID are unclear among community-based individuals with a history of COVID-19. To elucidate the burden and possible causes of long COVID in the community, we coordinated analyses of survey data from 6907 individuals with self-reported COVID-19 from 10 UK longitudinal study (LS) samples and 1.1 million individuals with COVID-19 diagnostic codes in electronic healthcare records (EHR) collected by spring 2021. Proportions of presumed COVID-19 cases in LS reporting any symptoms for 12+ weeks ranged from 7.8% and 17% (with 1.2 to 4.8% reporting debilitating symptoms). Increasing age, female sex, white ethnicity, poor pre-pandemic general and mental health, overweight/obesity, and asthma were associated with prolonged symptoms in both LS and EHR data, but findings for other factors, such as cardio-metabolic parameters, were inconclusive.
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- Brand, Judith, 1984-, et al.
(författare)
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Associations of maternal quitting, reducing, and continuing smoking during pregnancy with longitudinal fetal growth : Findings from Mendelian randomization and parental negative control studies
- 2019
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Ingår i: PLoS Medicine. - : Public Library of Science. - 1549-1277 .- 1549-1676. ; 16:11
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Tidskriftsartikel (refereegranskat)abstract
- Background: Maternal smoking during pregnancy is an established risk factor for low infant birth weight, but evidence on critical exposure windows and timing of fetal growth restriction is limited. Here we investigate the associations of maternal quitting, reducing, and continuing smoking during pregnancy with longitudinal fetal growth by triangulating evidence from 3 analytical approaches to strengthen causal inference.Methods and findings: We analysed data from 8,621 European liveborn singletons in 2 population-based pregnancy cohorts (the Generation R Study, the Netherlands 2002-2006 [n = 4,682]) and the Born in Bradford study, United Kingdom 2007-2010 [n = 3,939]) with fetal ultrasound and birth anthropometric measures, parental smoking during pregnancy, and maternal genetic data. Associations with trajectories of estimated fetal weight (EFW) and individual fetal parameters (head circumference, femur length [FL], and abdominal circumference [AC]) from 12-16 to 40 weeks' gestation were analysed using multilevel fractional polynomial models. We compared results from (1) confounder-adjusted multivariable analyses, (2) a Mendelian randomization (MR) analysis using maternal rs1051730 genotype as an instrument for smoking quantity and ease of quitting, and (3) a negative control analysis comparing maternal and mother's partner's smoking associations. In multivariable analyses, women who continued smoking during pregnancy had a smaller fetal size than non-smokers from early gestation (16-20 weeks) through to birth (p-value for each parameter < 0.001). Fetal size reductions in continuing smokers followed a dose-dependent pattern (compared to non-smokers, difference in mean EFW [95% CI] at 40 weeks' gestation was -144 g [-182 to -106], -215 g [-248 to -182], and -290 g [-334 to -247] for light, moderate, and heavy smoking, respectively). Overall, fetal size reductions were most pronounced for FL. The fetal growth trajectory in women who quit smoking in early pregnancy was similar to that of non-smokers, except for a shorter FL and greater AC around 36-40 weeks' gestation. In MR analyses, each genetically determined 1-cigarette-per-day increase was associated with a smaller EFW from 20 weeks' gestation to birth in smokers (p = 0.01, difference in mean EFW at 40 weeks = -45 g [95% CI -81 to -10]) and a greater EFW from 32 weeks' gestation onwards in non-smokers (p = 0.03, difference in mean EFW at 40 weeks = 26 g [95% CI 5 to 47]). There was no evidence that partner smoking was associated with fetal growth. Study limitations include measurement error due to maternal self-report of smoking and the modest sample size for MR analyses resulting in unconfounded estimates being less precise. The apparent positive association of the genetic instrument with fetal growth in non-smokers suggests that genetic pleiotropy may have masked a stronger association in smokers.Conclusions: A consistent linear dose-dependent association of maternal smoking with fetal growth was observed from the early second trimester onwards, while no major growth deficit was found in women who quit smoking early in pregnancy except for a shorter FL during late gestation. These findings reinforce the importance of smoking cessation advice in preconception and antenatal care and show that smoking reduction can lower the risk of impaired fetal growth in women who struggle to quit.Author summary:Why was this study done?Maternal smoking during pregnancy is an established risk factor for low infant birth weight. Understanding when and which parameters of fetal growth are affected by different smoking behaviours is important for strengthening and focusing clinical and public health guidelines.The importance of smoking cessation in early pregnancy and the extent to which fetal growth restriction can be prevented or minimised by lowering cigarette consumption in women who find quitting difficult is also uncertain.What did the researchers do and find?We analysed data from 8,621 white European liveborn singletons from 2 population-based pregnancy cohorts to assess the associations of maternal quitting, reducing, and continuing smoking during pregnancy with the longitudinal growth of different fetal parameters (weight, head circumference, femur length, and abdominal circumference). We compared results across 3 different analytical approaches (conventional multivariable, Mendelian randomization, and parental negative control analyses) to strengthen confidence in our findings.We found that pre-pregnancy smokers who continued smoking during pregnancy had a reduced fetal size from early gestation (12-16 weeks) onwards. Associations of maternal smoking with each fetal parameter followed a dose-dependent pattern, with fetal size reductions increasing in magnitude with the number of cigarettes smoked.While all fetal parameters were affected in women who continued smoking during pregnancy, size reductions were most pronounced for femur length. In pre-pregnancy smokers who gave up smoking early in pregnancy, no overall growth deficit was observed, except for a smaller femur length towards the end of pregnancy.The association of maternal smoking with reduced fetal growth was consistent across all 3 methods, thus providing stronger support that the association is causal, in comparison to current evidence, which relies solely on multivariable regression.What do these findings mean?Our findings reinforce existing advice promoting and supporting smoking cessation in preconception and antenatal care services; they provide strong support for these recommendations.The consistent results across methods for a linear dose-dependent association of maternal smoking with reduced fetal growth from early gestation in women who continue smoking during pregnancy provide evidence to support reducing smoking amounts in those who struggle to quit.
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- Lozano, Manuel, et al.
(författare)
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Early life exposure to mercury and relationships with telomere length and mitochondrial DNA content in European children
- 2024
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Ingår i: Science of the Total Environment. - 0048-9697 .- 1879-1026. ; 932
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Tidskriftsartikel (refereegranskat)abstract
- Background: Telomere length (TL) and mitochondrial function expressed as mitochondrial DNA copy number (mtDNAcn) are biomarkers of aging and oxidative stress and inflammation, respectively. Methylmercury (MeHg), a common pollutant in fish, induces oxidative stress. We hypothesized that elevated oxidative stress from exposure to MeHg decreases mtDNAcn and shortens TL. Methods: Study participants are 6–11-year-old children from the HELIX multi-center birth cohort study, comprising six European countries. Prenatal and postnatal total mercury (THg) concentrations were measured in blood samples, TL and mtDNAcn were determined in child DNA. Covariates and confounders were obtained by questionnaires. Robust regression models were run, considering sociodemographic and lifestyle covariates, as well as fish consumption. Sex, ethnicity, and fish consumption interaction models were also run. Results: We found longer TL with higher pre- and postnatal THg blood concentrations, even at low-level THg exposure according to the RfD proposed by the US EPA. The prenatal association showed a significant linear relationship with a 3.46 % increase in TL for each unit increased THg. The postnatal association followed an inverted U-shaped marginal non-linear relationship with 1.38 % an increase in TL for each unit increased THg until reaching a cut-point at 0.96 μg/L blood THg, from which TL attrition was observed. Higher pre- and postnatal blood THg concentrations were consistently related to longer TL among cohorts and no modification effect of fish consumption nor children's sex was observed. No association between THg exposure and mtDNAcn was found. Discussion: We found evidence that THg is associated with TL but the associations seem to be time- and concentration-dependent. Further studies are needed to clarify the mechanism behind the telomere changes of THg and related health effects.
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