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- Chen, Shuyun, et al.
(författare)
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Correlations of Subjective and Social Well-Being With Sedentary Behavior and Physical Activity in Older Adults—A Population-Based Study
- 2021
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Ingår i: The journals of gerontology. Series A, Biological sciences and medical sciences. - : Oxford University Press (OUP). - 1079-5006 .- 1758-535X. ; 76:10, s. 1789-1795
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Tidskriftsartikel (refereegranskat)abstract
- Background: Subjective and social well-being, avoiding sedentary behavior (SB), and engaging in physical activity (PA) are important factors for health in older adults, but the extent to which they are related to each other remains unclear. We aimed to investigate these correlations, and whether they differ by age.Method: A cross-sectional study was carried out in 595 people aged 66 years and older, from the Swedish National study on Aging and Care in Kungsholmen. Subjective and social well-being (life satisfaction, positive and negative affect, social connections, social support, and social participation) were assessed through validated questionnaires and activPAL3 accelerometers provided information on SB and PA. Data were analyzed using multi-adjusted quantile regression models.Results: Higher positive affect was significantly associated with less daily sitting time (β = −27.08, 95% confidence interval [CI]: −47.77, −6.39) and higher levels of light PA (LPA) (β = 40.67, 95% CI: 21.06, 60.28). Higher levels of social support and social participation were associated with less daily sitting time (β = −22.79, 95% CI: −39.97, −5.62; and β = −21.22, 95% CI: −39.99, −2.44) and more time in LPA (β = 23.86, 95% CI: 4.91, 42.81; and β = 25.37, 95% CI: 6.27, 44.47). Stratified analyses suggested that the associations of positive affect and social participation were strongest for individuals aged 80 years and older.Conclusions: Our results suggest that older adults with higher levels of subjective and social well-being spend less time sitting and engage more in PA. This was especially evident among the oldest-old individuals. Future research should longitudinally investigate the directionality of these correlations.
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| 2. |
- Chen, Shuyun
(författare)
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Maternal metabolic health and neurodevelopmental conditions in offspring
- 2023
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Background Observational studies published in the last decade have indicated relationships between maternal “overnutrition” states and offspring neurodevelopmental conditions (NDCs), such as autism, attention deficit/hyperactivity disorder (ADHD), and intellectual disability (ID). “Maternal overnutrition” states have been characterized by a series of metabolic conditions before pregnancy (i.e., overweight/obesity, Type I [T1DM] and II [T2DM] diabetes) and during pregnancy (i.e., gestational diabetes mellitus [GDM] and excessive gestational weight gain [GWG]). NDCs often co-occur and have multifactorial etiologies, shaped by both genetic and environmental factors. However, previous studies have not thoroughly considered these complex etiologies when examining associations. For instance, they did not explore whether the relationships between maternal diabetes and offspring NDCs could differ based on the cooccurrence of NDCs or be influenced by genetic predispositions. Moreover, as the fetal brain evolves dramatically and sequentially during pregnancy, it accentuates the need for epidemiological studies to account for the timing and intensity of perturbations during this period. Prior research hasn’t determined whether relationships between maternal conditions such as excessive GWG or hyperglycemia and offspring NDCs could differ based on the GWG rate and glucose concentrations at different pregnancy phases. Maternal overweight/obesity and diabetes might be associated with offspring NDCs due to complications encountered during pregnancy, childbirth, and the neonatal period. Research has suggested that these complications lie at the intersection of, and relate to, maternal metabolic conditions and offspring NDCs. Grasping the mediation of these complications can offer deeper insights into preventative measures during these stages; however, no studies have yet quantified these complications’ mediating impact on the associations. Lastly, the causal influence of BMI, including maternal BMI, on offspring autism and ADHD has seldom been thoroughly explored. In the absence of compelling evidence, the question remains as to whether better weight management among obese women before conception could help reduce the potential risks of offspring NDCs. Methods We used two databases, “Psychiatry Sweden (PS), 1987-2016” and “Developmental Origins of Health And Disease (DOHAD), 1997-2021”, which are register linkages across Swedish nationwide registers using the unique identification number assigned to each Swedish resident. Offspring were linked to their biological mothers, fathers, and maternal grandparents using the Total Population Register (Study I, IV, V). We also used a series of maternal weight and capillary glucose records across pregnancy from the Stockholm Obstetrix system, an electronic medical journal of antenatal care, which was nested within the “Stockholm Youth Cohort (SYC)”. The SYC is a part of PS that also includes regional health and administrative registers (Study II, III). In Studies I, IV, and V, we used the National Patient Register to identify offspring NDCs (i.e., autism, ADHD, and ID), which was supplemented by regional register information in Studies II and III as well as the National Prescribed Drug Register (for ADHD). Finally, we utilized genetic data and information from mothers and children in the “Avon Longitudinal Study of Parents and Children (ALSPAC)” cohort (Study V). In Study I, we utilized a generalized estimating equation (GEE)/population average model with a logit link. This model was clustered based on pseudonymized maternal identification numbers and employed robust standard errors for the computation of odds ratios (ORs) and 95% confidence intervals (CIs) regarding neurodevelopmental conditions (NDCs) in offspring. In Study II, we used Cox regression models, again clustered on maternal numbers and with robust standard errors, to determine hazard ratios (HRs) and 95% CIs for offspring NDCs. In Study III, we employed group-based trajectory modeling (GBTM) to ascertain the varying patterns of glucose alteration throughout pregnancy. GEE models were utilized to evaluate the associations with both obstetric and neonatal outcomes and offspring NDCs. In Study IV, we used a parametric regression approach within a counterfactual framework to conduct both single and multiple mediation analyses. This study aimed to quantify the total effect (TE), natural indirect effects (NIE), and natural direct effects (NDE) in the associations of maternal diabetes (both pregestational diabetes mellitus [PGDM] and GDM) and overweight/obesity with NDCs through individual components of mediators. We employed a paternal negative control comparison analysis in Study I to examine if the associations of maternal T1DM and T2DM with offspring NDCs could be confounded by genetic predispositions to diabetes and NDCs. In Study V, we applied a “triangulation” approach. Analyses were performed using maternal cousin and full sibling comparisons to address unobserved, shared genetic and environmental factors in the associations between maternal BMI and offspring autism and ADHD. In addition, we explored the genetic correlation through Linkage Disequilibrium Score Regression (LDSC). Moreover, we examined the association between the genetic predisposition to both maternal and children’s BMI and various traits of children’s autism and ADHD using Polygenic Risk Score (PRS) analysis. Lastly, we employed a two-sample Mendelian randomization analysis (MR) in Study V to evaluate the causal impacts of BMI on NDCs, including autism and ADHD. Results Maternal T1DM, T2DM, and GDM were all associated with offspring autism, ADHD, and ID, with greater risks linked to comorbid diagnoses involving ID. Stronger associations with GDM were observed when diagnosed between 27-30 wkGA. Paternal T1DM and T2DM were also associated with offspring NDCs, though the strength of these associations was less than those observed with maternal diabetes (Study I). Lower rates of GWG in the second trimester and higher rates of GWG in the third trimester were associated with increased risks for offspring NDCs (Study II). Among those without PGDM, persistently high glucose levels throughout pregnancy demonstrated the strongest association with adverse obstetric/neonatal complications. Transient hyperglycemic states followed by periods of potential glycemic control were also associated with these complications but to a lesser extent. Notably, subclinical states of hyperglycemia, which were less likely to receive a GDM diagnosis, remained associated with these complications, albeit to a lesser degree. A similar pattern of associations was observed for offspring NDCs. Persistently high glucose levels showed stronger associations with offspring NDCs (i.e., ADHD only), while weaker associations were identified with transient hyperglycemic states followed by improved glucose control. Notably, we found that hyperglycemia in early pregnancy, but not in mid-pregnancy, was associated with offspring NDCs when followed by improved glucose control. However, none of these associations regarding NDC outcomes survived the false discovery rate correction using the Benjamini- Hochberg approach (Study III). The joint mediating effects of all obstetric and neonatal complications were more pronounced in the associations between PGDM and offspring NDCs (accounting for 30-50% of the association) than in those concerning maternal GDM and overweight/obesity. Although the mediating effects of obstetric and neonatal complications were generally insignificant for GDM and minor for maternal overweight/obesity, we observed direct associations between GDM (10-30% increased risks compared to non-diabetes) and maternal overweight/obesity (30-60% increased risks compared to normal weight) with the risks of offspring NDCs. However, these associations might still contain residual confounding due to unobserved factors. The combined mediating effects of these complications, especially those emerging during the neonatal period, were particularly strong in the relationship between maternal PGDM and offspring NDCs. For individual mediators, the effects were generally minimal, except for complications such as pregnancy hypertensive diseases, preterm birth, neonatal asphyxia, and hematological comorbidities in the association between PGDM and offspring NDCs (with proportions mediated exceeding 10%) (Study IV). Maternal obesity was linked to increased risks of autism and ADHD in both the full cohort analysis and family designs (i.e., maternal cousin comparisons and full sibling analyses). It is worth noting that when accounting for shared familial factors in family designs, the associations were attenuated but modest associations remained. For instance, among full siblings, children exposed to maternal obesity had a 0.87% higher risk of autism and a 2.13% higher risk of ADHD at age 16, compared to those exposed to mothers of normal weight. The LDSC analysis showed a genetic correlation between BMI and ADHD, but not with autism. The PRS analysis provided less evidence suggesting a relationship between maternal and children’s genetic liability to BMI and various autism and ADHD traits. Specifically, a one-unit increase in BMI was associated with a 12% higher risk for autism and a 77% increased risk for ADHD (Study V). Conclusions In conclusion, my research has reaffirmed known associations between maternal metabolic conditions and offspring NDCs while providing new insights into the underlying mechanisms and causal relationships. Greater associations between maternal diabetes and NDCs involving ID suggested distinct pathophysiological mechanisms. The associations involving PGDM and offspring NDCs might be partially confounded by a genetic predisposition to both the exposure and outcomes; however, its intrauterine effects cannot be completely discounted. Further i
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| 3. |
- Chen, Shuyun, et al.
(författare)
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Random capillary glucose levels throughout pregnancy, obstetric and neonatal outcomes, and long-term neurodevelopmental conditions in children : a group-based trajectory analysis.
- 2023
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Ingår i: BMC Medicine. - : BioMed Central (BMC). - 1741-7015. ; 21:1
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Gestational diabetes mellitus (GDM) is associated with both short- and long-term risks, although it is unknown if risks vary by severity, timing, and duration of gestational hyperglycemia. We aimed to identify trajectories of random capillary glucose (RCG) levels throughout pregnancy and assess their associations with both obstetric/neonatal outcomes and children's risk of neurodevelopmental conditions (NDCs) (i.e., autism, intellectual disability, and attention-deficit/hyperactivity disorders [ADHD]).METHODS: A population-based cohort study was conducted involving 76,228 children born to 68,768 mothers without pregestational diabetes. Group-based trajectory modeling was utilized to identify distinct glucose trajectories across RCG values throughout the course of pregnancy. The associations between these trajectory groups and obstetric/neonatal outcomes as well as children's NDCs were then assessed using generalized estimating equation models with a logit link. The Benjamini-Hochberg (BH) procedure was employed to adjust P-values for multiple comparisons, controlling the false discovery rate (FDR).RESULTS: Five distinct glucose trajectory groups were identified, each with varying percentages diagnosed with GDM. Their associations with obstetric/neonatal outcomes as well as children's NDCs varied. For example, when compared to the "Persistently Low" group, other groups exhibited varying degrees of increased risk for large-for-gestational-age babies, with the exception of the "High in Early Pregnancy" group. Compared to the "Persistently Low" group, all other trajectory groups were associated with NDC outcomes, except the "High in Mid-Pregnancy" group. However, none of the associations with offspring NDCs remained significant after accounting for the FDR correction.CONCLUSIONS: Persistent high glucose levels or moderately elevated glucose levels throughout pregnancy, as well as transient states of hyperglycemia in early or mid-pregnancy, were found to be associated with increased risks of specific obstetric and neonatal complications, and potentially offspring NDCs. These risks varied depending on the severity, timing, duration, and management of hyperglycemia. The findings underscore the need for continuous surveillance and individualized management strategies for women displaying different glucose trajectories during pregnancy. Limitations such as potential residual confounding, the role of mediators, and small sample size should be addressed in future studies.
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