Association between Findings in Oral Health Screening and Body Mass Index: A Nation-Wide Longitudinal Study.
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ABSTRACT:
SUBMITTER: Chang Y
PROVIDER: S-EPMC8582665 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:To explore the association between maternal origin and birthplace, and caesarean section (CS) by pre-pregnancy body mass index (BMI) and length of residence. We linked records from 118,459 primiparous women in the Medical Birth Registry of Norway between 2013 and 2017 with data from the National Population Register. We categorized pre-pregnancy BMI (kg/m2) into underweight (<18.5), normal weight (18.5-24.9) and overweight/obese (≥25). Multinomial regression analysis estimated crude and adjusted relative risk ratios (RRR) with 95% confidence intervals (CI) for emergency and elective CS. Compared to normal weight women from Norway, women from Sub-Saharan Africa and Southeast Asia/Pacific had a decreased risk of elective CS (aRRR = 0.57, 95% CI 0.37-0.87 and aRRR = 0.56, 0.41-0.77, respectively). Overweight/obese women from Europe/Central Asia had the highest risk of elective CS (aRRR = 1.42, 1.09-1.86). Both normal weight and overweight/obese Sub-Saharan African women had the highest risks of emergency CS (aRRR = 2.61, 2.28-2.99; 2.18, 1.81-2.63, respectively). Compared to women from high-income countries, the risk of elective CS was increasing with a longer length of residence among European/Central Asian women. Newly arrived migrants from Sub-Saharan Africa had the highest risk of emergency CS. Women from Sub-Saharan Africa had more than two times the risk of emergency CS compared to women originating from Norway, regardless of pre-pregnancy BMI.
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Project description:Objective: We investigated gene interactions (epistasis) for body mass index (BMI) in a European-American adult female cohort via genome-wide interaction analyses (GWIA) and pathway association analyses. Methods: Genome-wide pairwise interaction analyses were carried out for BMI in 493 extremely obese cases (BMI > 35 kg/m2) and 537 never-overweight controls (BMI < 25 kg/m2). To further validate the results, specific SNPs were selected based on the GWIA results for haplotype-based association studies. Pathway-based association analyses were performed using a modified Gene Set Enrichment Algorithm (GSEA) (GenGen program) to further explore BMI-related pathways using our genome wide association study (GWAS) data set, GIANT, ENGAGE, and DIAGRAM Consortia. Results: The EXOC4-1q23.1 interaction was associated with BMI, with the most significant epistasis between rs7800006 and rs10797020 (P = 2.63 × 10-11). In the pathway-based association analysis, Tob1 pathway showed the most significant association with BMI (empirical P < 0.001, FDR = 0.044, FWER = 0.040). These findings were further validated in different populations. Conclusion: Genome-wide pairwise SNP-SNP interaction and pathway analyses suggest that EXOC4 and TOB1-related pathways may contribute to the development of obesity.
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Project description:ObjectiveHealth-related quality of life (HRQoL) is an important outcome in individuals with a high risk for cardiovascular diseases. We investigated the association of HRQoL and body mass index (BMI) as an indicator for obesity.DesignSecondary longitudinal analysis of the ORBITAL study, an intervention study which included high-risk cardiovascular primary care patients with hypercholesterolemia and an indication for statin therapy.MethodsHRQoL was determined with the generic Short Form (SF)-12 health status instrument. Body weight and height were assessed at baseline and at months 6, 12, 18, 24, 30, and 36. We used a linear and a linear mixed-effects regression model to investigate the association between BMI and SF-12 summary scores at baseline as well as between change in BMI and SF-12 summary scores over 3 years. We adjusted for age, sex, smoking status, and in the longitudinal analysis also for the study arm and its interaction term with time.ResultsOf the 7640 participants who completed the baseline questionnaire, 6726 participants (mean age: 61 years) were analyzed. The baseline BMI was inversely associated with physical and mental SF-12 summary scores (? [95% CI] per 1 kg/m2: -0.36 [-0.41; -0.30] and -0.05 [-0.11; -0.00], respectively). A significant association between the change in BMI and physical SF-12 summary scores over time was only present in women (-0.18 [-0.27; -0.09]) and only in obese participants (-0.19 [-0.29; -0.10]). A change in BMI was directly associated with mental SF-12 summary scores (0.12 [0.06; 0.19]) in the total population.ConclusionIncreases in BMI were associated with decreases in physical HRQoL, particularly in obese individuals and in women. In contrast, the mental HRQoL seemed to increase with increasing BMI over time. Thus, body weight management with respect to the HRQoL should be evaluated differentially by sex and body weight status.Trial registrationClinicalTrials.gov NCT00379249.
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Project description:BACKGROUND:Childhood obesity is a major health problem in Mexico. Obesity prevalence estimated by body mass index (BMI) is almost half than that estimated by percent body fat (%BF) in the Childhood Obesity pediatric cohort (COIPIS). OBJECTIVE:We performed a genome-wide association study (GWAS) of BMI and %BF in 828 children from the COIPIS to identify markers of predisposition to high values for both phenotypes used for obesity classification. METHODS:For the GWAS we used the LAT Axiom 1, Affymetrix and 2.5 million single loci from the 1000 Genomes Phase 3 imputation panel. We used a linear model, adjusted by age, sex, and Amerindian ancestry assuming an additive inheritance model. RESULTS:Genome-wide significance (p ? 5.0 × 10-8) and 80% of statistical power was reached for associations of two loci in two genes (CERS3 and CYP2E1) to BMI. Also, 11 loci in six genes (ANKS1B, ARNTL2, KCNS3, LMNB1, SRGAP3, TRPC7) reached genome-wide significance for associations to %BF, though not 80% of statistical power. DISCUSSION:None of the SNPs were previously reported as being associated to BMI or %BF. In addition, different loci were found for BMI and %BF. These results highlight the importance of gaining deeper understanding of genetic markers of predisposition to high values for the phenotypes used for obesity diagnosis.
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Project description:Background:There are few large prospective cohort studies evaluating predictors of outcomes in acute pancreatitis. Objectives:The purpose of this study was to determine the role of age and co-morbid disease in predicting major outcomes in acute pancreatitis. Methods:Data points were collected according to a predefined electronic data collection form. Acute pancreatitis and its complications were defined according to the revised Atlanta classification. Univariable and multivariable analyses were conducted using Cox proportional hazard regression and multiple logistic regression. Results:From June 2013-February 2015, 1655 adult patients were recruited from 23 centres across Spain. Co-morbid disease, obesity, open surgical necrosectomy within 30 days, and pancreatic necrosis were independently associated with both 30-day mortality and persistent organ failure (p < 0.05 for all). Age was not associated with persistent organ failure, however the extreme of age (>85 years) was associated with mortality (p < 0.05). Co-morbid disease and obesity were not independently associated with a prolonged length of stay or other markers of morbidity on adjusted analysis (p > 0.05). Conclusion:Comorbidity and obesity are important determinates of mortality and persistent organ failure in acute pancreatitis, but in the absence of organ failure they do not appear to independently contribute to morbidity. This has important implications for severity classification and predictive models of severity in acute pancreatitis.
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Project description:Outcomes related to disordered metabolism are common in alcohol dependence (AD). To investigate alterations in the regulation of body mass that occur in the context of AD, we performed a genome-wide association study (GWAS) of body mass index (BMI) in African Americans (AAs) and European Americans (EAs) with AD. Subjects were recruited for genetic studies of AD or drug dependence and evaluated using the Semi-structured Assessment for Drug Dependence and Alcoholism. We investigated a total of 2587 AAs and 2959 EAs with DSM-IV AD diagnosis. In the stage 1 sample (N?=?4137), we observed three genome-wide significant (GWS) single-nucleotide polymorphism associations, rs200889048 (P?=?8.98?*?10-12 ) and rs12490016 (P?=?1.44?*?10-8 ) in EAs and rs1630623 (P?=?5.14?*?10-9 ) in AAs and EAs meta-analyzed. In the stage 2 sample (N?=?1409), we replicated 278, 253 and 168 of the stage 1 suggestive loci (P?<?5*10-4 ) in AAs, EAs, and AAs and EAs meta-analyzed, respectively. A meta-analysis of stage 1 and stage 2 samples (N?=?5546) identified two additional GWS signals: rs28562191 in EAs (P?=?4.46?*?10-8 ) and rs56950471 in AAs (P?=?1.57?*?10-9 ). Three of the GWS loci identified (rs200889048, rs12490016 and rs1630623) were not previously reported by GWAS of BMI in the general population, and two of them raise interesting hypotheses: rs12490016-a regulatory variant located within LINC00880, where there are other GWAS-identified variants associated with birth size, adiposity in newborns and bulimia symptoms, which also interact with social stress in relation to birth size; rs1630623-a regulatory variant related to ALDH1A1, a gene involved in alcohol metabolism and adipocyte plasticity. These loci offer molecular insights regarding the regulatory mechanisms of body mass in the context of AD.
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Project description:BackgroundBody mass index (BMI) is a complex phenotype that may interact with genetic variants to influence colorectal cancer risk.MethodsWe tested multiplicative statistical interactions between BMI (per 5 kg/m2) and approximately 2.7 million single nucleotide polymorphisms with colorectal cancer risk among 14 059 colorectal cancer case (53.2% women) and 14 416 control (53.8% women) participants. All analyses were stratified by sex a priori. Statistical methods included 2-step (ie, Cocktail method) and single-step (ie, case-control logistic regression and a joint 2-degree of freedom test) procedures. All statistical tests were two-sided.ResultsEach 5 kg/m2 increase in BMI was associated with higher risks of colorectal cancer, less so for women (odds ratio [OR] = 1.14, 95% confidence intervals [CI] = 1.11 to 1.18; P = 9.75 × 10-17) than for men (OR = 1.26, 95% CI = 1.20 to 1.32; P = 2.13 × 10-24). The 2-step Cocktail method identified an interaction for women, but not men, between BMI and a SMAD7 intronic variant at 18q21.1 (rs4939827; Pobserved = .0009; Pthreshold = .005). A joint 2-degree of freedom test was consistent with this finding for women (joint P = 2.43 × 10-10). Each 5 kg/m2 increase in BMI was more strongly associated with colorectal cancer risk for women with the rs4939827-CC genotype (OR = 1.24, 95% CI = 1.16 to 1.32; P = 2.60 × 10-10) than for women with the CT (OR = 1.14, 95% CI = 1.09 to 1.19; P = 1.04 × 10-8) or TT (OR = 1.07, 95% CI = 1.01 to 1.14; P = .02) genotypes.ConclusionThese results provide novel insights on a potential mechanism through which a SMAD7 variant, previously identified as a susceptibility locus for colorectal cancer, and BMI may influence colorectal cancer risk for women.
| S-EPMC7781451 | biostudies-literature
Project description:BACKGROUND:Studies evaluating associations between body mass index (BMI) and optical coherence tomography (OCT) measures in multiple sclerosis (MS) are lacking. OBJECTIVE:To assess whether elevated BMI is associated with accelerated retinal atrophy. METHODS:In this observational study, 513 MS patients were followed with serial spectral-domain OCT for a median of 4.4?years. Participants were categorized as normal weight (BMI: 18.5-24.9?kg/m2), overweight (BMI: 25-29.9?kg/m2), and obese (BMI: ?30?kg/m2). Participants with diabetes mellitus or uncontrolled hypertension and eyes with optic neuritis (ON) ?6?months prior to baseline OCT or during follow-up were excluded. Statistical analyses were performed with mixed-effects linear regression. RESULTS:Obese patients (n?=?146) exhibited accelerated rates of ganglion cell?+?inner plexiform layer (GCIPL) atrophy relative to normal weight patients (n?=?214; -0.57%/year (95% confidence interval (CI): -0.65% to -0.48%) versus -0.42%/year (95% CI: -0.49% to -0.35%); p?=?0.012). GCIPL atrophy rate did not differ between overweight (n?=?153) and normal weight patients (-0.47%/year vs -0.42%/year; p?=?0.41). Each 1?kg/m2 higher BMI was associated with accelerated GCIPL (-0.011%/year; 95% CI: -0.019% to -0.004%; p?=?0.003) atrophy. Multivariable analyses accounting for age, sex, race, MS subtype, and ON history did not alter the above findings. CONCLUSIONS:Elevated BMI, in the absence of overt metabolic comorbidities, may be associated with accelerated GCIPL atrophy. Obesity, a modifiable risk factor, may be associated with accelerated neurodegeneration in MS.
| S-EPMC7293552 | biostudies-literature
Project description:ObjectiveTo investigate the longitudinal associations between active commuting (walking and cycling to work) and body mass index (BMI).MethodWe used self-reported data on height, weight and active commuting from the Commuting and Health in Cambridge study (2009 to 2012; n=809). We used linear regression to test the associations between: a) maintenance of active commuting over one year and BMI at the end of that year; and b) change in weekly time spent in active commuting and change in BMI over one year.ResultsAfter adjusting for sociodemographic variables, other physical activity, physical wellbeing and maintenance of walking, those who maintained cycle commuting reported a lower BMI on average at one year follow-up (1.14kg/m(2), 95% CI: 0.30 to 1.98, n=579) than those who never cycled to work. No significant association remained after adjustment for baseline BMI. No significant associations were observed for maintenance of walking. An increase in walking was associated with a reduction in BMI (0.32kg/m(2), 95% CI: 0.03 to 0.62, n=651, after adjustment for co-variates and baseline BMI) only when restricting the analysis to those who did not move. No other significant associations between changes in weekly time spent walking or cycling on the commute and changes in BMI were observed.ConclusionsThis work provides further evidence of the contribution of active commuting, particularly cycling, to preventing weight gain or facilitating weight loss. The findings may be valuable for employees choosing how to commute and engaging employers in the promotion of active travel.
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Project description:Asian women have a younger age at onset of breast cancer and a lower body mass index (BMI) than Western women. The link between obesity and risk of breast cancer in Asian women is still elusive. We aimed to investigate the effect of BMI on the risk of incident breast cancer in Taiwanese women.A total of 1,393,985 women who had been cancer-free before recruitment and attended a nation-wide Taiwanese breast cancer-screening program between 1999 and 2009 were enrolled using a prospective cohort study. Obesity and other relevant variables (such as menopause status and other biochemical markers) were collected through in-person interviews, anthropometric measurements and blood samples at first screen. Incident breast cancers during follow-up were ascertained through the linkage of the cohort with the National Cancer Registry and the National Death Certification System.A total of 6969 and 7039 incident breast cancer cases were identified among women enrolled before and after menopause, respectively. Compared with a BMI range of 18.5-23.9 kg m(-)(2), the incremental level of BMI in the enrolled women before menopause revealed a lack of statistically significant association with the risk of incident breast cancer (adjusted hazard ratio=0.94, 0.98, 1.02, 1.01 and 0.82 for BMI <18.5, 24-26.9, 27-29.9, 30-34.9 and ⩾35, respectively), but the incremental level of BMI in the enrolled women after menopause led to a statistically significant incremental increase in the risk of breast cancer (adjusted hazard ratio=0.78, 1.19, 1.31, 1.53 and 1.65 for BMI <18.5, 24-26.9, 27-29.9, 30-34.9 and ⩾35, respectively) after adjusting for other explanatory risk factors.Obesity acts mainly as an influential promoter of the development of late-onset breast cancer after menopause in Taiwanese women.
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