Assessment of a causal relationship between body mass index and atopic dermatitis.
Ontology highlight
ABSTRACT:
SUBMITTER: Budu-Aggrey A
PROVIDER: S-EPMC7794861 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:Population studies suggest that atopic dermatitis (AD) is associated with an increased risk of obesity, however a causal relationship between these two conditions remains to be established. We therefore use Mendelian randomization (MR) to evaluate whether obesity and AD are causally interlinked. We used summary statistics extracted from genome wide association studies of Body Mass Index (BMI) and AD. MR analysis was performed in both directions to establish the direction of causality between BMI and AD. We find that genetically determined increase in adiposity is associated with increased risk of AD (odds ratio of AD 1.08 [95% CI 1.01 to 1.14; p = 0.015] per unit increase in BMI). Conversely, genetically determined increased risk of AD is not associated with a higher BMI (change in BMI attributable to AD based on genetic information: 0.00; 95% CI - 0.02 to 0.02; p = 0.862). There was no evidence for confounding of these genetic analyses by horizontal pleiotropy. Our results indicate that the association of AD with obesity is likely to reflect a causal role for adiposity in the development of AD. Our findings enhance understanding of the etiology of AD, and the basis for experimental studies to evaluate the mechanistic pathways by which adiposity promotes AD.
| S-EPMC7498603 | biostudies-literature
Project description:ObjectiveThe study aimed to explore the causal effect of body mass index (BMI) on osteoarthritis.MethodsThe genome-wide association data of BMI and osteoarthritis were obtained via the Mendelian randomization (MR)-base platform. Single nucleotide polymorphisms (SNPs) significantly associated with BMI were identified and used as instrumental variables, and the causal relationship between BMI and osteoarthritis was examined using the two-sample MR research method. Three statistical methods including inverse-variance weighted (IVW) method, weighted median estimator, and MR-Egger regression were employed.ResultsA total of 79 SNPs significantly associated with BMI were identified in the study (P<5×10-8; linkage disequilibrium r2 <0.1). Consistent association between BMI and osteoarthritis was observed when evaluated by different methods (IVW: odds ratio (OR) 1.028, 95% confidence interval (CI) 1.021-1.036; weighted median estimator: OR 1.028, 95% CI 1.019-1.037; MR-Egger regression: OR 1.028, 95% CI 1.009-1.046), which suggests that BMI is positively associated with increased risk of osteoarthritis. There was no evidence that the observed causal effect between BMI and the risk of osteoarthritis was affected by genetic pleiotropy (MR-Egger intercept 1.3×10-5, P=0.959).ConclusionThe MR analysis provided the strong evidence to indicate that BMI might be causally associated with the risk of osteoarthritis.
| S-EPMC8180293 | biostudies-literature
Project description:BackgroundPsoriasis is a common inflammatory skin disease that has been reported to be associated with obesity. We aimed to investigate a possible causal relationship between body mass index (BMI) and psoriasis.Methods and findingsFollowing a review of published epidemiological evidence of the association between obesity and psoriasis, mendelian randomization (MR) was used to test for a causal relationship with BMI. We used a genetic instrument comprising 97 single-nucleotide polymorphisms (SNPs) associated with BMI as a proxy for BMI (expected to be much less confounded than measured BMI). One-sample MR was conducted using individual-level data (396,495 individuals) from the UK Biobank and the Nord-Trøndelag Health Study (HUNT), Norway. Two-sample MR was performed with summary-level data (356,926 individuals) from published BMI and psoriasis genome-wide association studies (GWASs). The one-sample and two-sample MR estimates were meta-analysed using a fixed-effect model. To test for a potential reverse causal effect, MR analysis with genetic instruments comprising variants from recent genome-wide analyses for psoriasis were used to test whether genetic risk for this skin disease has a causal effect on BMI. Published observational data showed an association of higher BMI with psoriasis. A mean difference in BMI of 1.26 kg/m2 (95% CI 1.02-1.51) between psoriasis cases and controls was observed in adults, while a 1.55 kg/m2 mean difference (95% CI 1.13-1.98) was observed in children. The observational association was confirmed in UK Biobank and HUNT data sets. Overall, a 1 kg/m2 increase in BMI was associated with 4% higher odds of psoriasis (meta-analysis odds ratio [OR] = 1.04; 95% CI 1.03-1.04; P = 1.73 × 10(-60)). MR analyses provided evidence that higher BMI causally increases the odds of psoriasis (by 9% per 1 unit increase in BMI; OR = 1.09 (1.06-1.12) per 1 kg/m2; P = 4.67 × 10(-9)). In contrast, MR estimates gave little support to a possible causal effect of psoriasis genetic risk on BMI (0.004 kg/m2 change in BMI per doubling odds of psoriasis (-0.003 to 0.011). Limitations of our study include possible misreporting of psoriasis by patients, as well as potential misdiagnosis by clinicians. In addition, there is also limited ethnic variation in the cohorts studied.ConclusionsOur study, using genetic variants as instrumental variables for BMI, provides evidence that higher BMI leads to a higher risk of psoriasis. This supports the prioritization of therapies and lifestyle interventions aimed at controlling weight for the prevention or treatment of this common skin disease. Mechanistic studies are required to improve understanding of this relationship.
| S-EPMC6354959 | biostudies-literature
Project description:BackgroundIt is unclear whether the relationship between cigarette smoking and atopy is mediated by body fat mass, such as the Body Mass Index (BMI). We assessed the mediating role of BMI on the relationship between smoking and atopy in Chinese adults.MethodsA hospital-based case-control study of 786 atopic cases and 2771 controls was conducted in adults aged 18 years or older from March 2010 to September 2014 in Harbin, China. Mediation models were used to estimate the indirect effects of smoking on atopic sensitization through BMI.ResultsCompared to non-smokers, light smokers and moderate smokers had a lower risk of inhalant allergen sensitization. The indirect effect of smoking and sensitization to aeroallergens were only observed in light smokers (point estimate, -0.026; 95% CI, -0.062 to -0.004). The mediating roles of BMI on the relationships between smoking and other types of allergic sensitization were not statistically significant.ConclusionBMI appeared to partially mediate the effect of light smoking on sensitization to aeroallergens. However, considering the other harmful health effects of cigarette smoking, the effective method to lower the incidence of atopy would be to decrease body fat mass by physical exercise and employing other more healthy ways of living rather than smoking.
| S-EPMC4377972 | biostudies-literature
Project description:BackgroundThe relationship between obesity and asthma is an area of debate.ObjectiveTo investigate the association of elevated body mass index (BMI) at a young age and young adult asthma.MethodsBMI, questionnaires, and serologic tests results were analyzed in participants of a predominantly white, middle-class, population-based birth cohort from Detroit, Michigan at 6 to 8 and 18 years of age. Asthma diagnosis was based on medical record data. Allergen specific IgE was analyzed using UniCAP, with atopy defined as 1 or more allergen specific IgE levels of 0.35 kU/L or higher. Overweight was defined as a BMI in 85th percentile or higher.ResultsA total of 10.6% of overweight males at 6 to 8 years of age had current asthma at 18 to 20 years of age compared with 3.2% of males who were normal or underweight (relative risk [RR], 3.3; 95% confidence interval [CI], 1.0-11.0; P=.048). A total of 19.6% of females who were overweight at 6 to 8 years of age had asthma compared with 10.3% of females who were normal or underweight (RR, 1.9; 95% CI, 0.9-3.9; P=.09). After adjustment for atopy at 6 to 8 years of age, overweight males had an adjusted RR of 4.7 (95% CI, 1.4-16.2; P=.01), and overweight females had an adjusted RR of 1.7 (95% CI, 0.8-3.3; P=.15). Change in BMI between 6 to 8 years of age and 18 to 20 years of age was also examined. Patients with persistently elevated BMI exhibited increased risk of asthma as young adults (RR, 2.4; 95% CI, 1.2-4.7) but not with an increasing BMI (RR, 0.8; 95% CI, 0.3-2.2) or a decreasing BMI (RR, 0.8; 95% CI, 0.3-2.2).ConclusionOverweight males 6 to 8 years of age have increased risk of asthma as young adults. Being overweight remains a predictor of asthma after adjustment for early atopy. A similar but not statistically significant trend was also seen among overweight females. Overweight body habitus throughout childhood is a risk factor for young adult asthma.
| S-EPMC3769639 | biostudies-literature
Project description:OBJECTIVE:Sleep duration is associated with obesity and cardiometabolic disease. It is unclear, though, how these relationship differs across age groups. METHODS:Data from 2007 to 2008 National Health and Nutrition Examination Survey (NHANES) were used, including respondents aged 16+ with complete data (N?=?5,607). Sleep duration and age were evaluated by self-report, and body mass index (BMI) was assessed objectively. Sleep duration was evaluated continuously and categorically [very short (?4 h), short (5-6 h), and long (?9 h) versus average (7-8 h)]. Age was also evaluated continuously and categorically [adolescent (16-17 years), young adult (18-29 years), early middle age (30-49 years), late middle age (50-64 years), and older adult (?65 years)]. RESULTS:There was a significant interaction with age for both continuous (Pinteraction ?=?0.014) and categorical (Pinteraction ?=?0.035) sleep duration. A pseudo-linear relationship was seen among the youngest respondents, with the highest BMI associated with the shortest sleepers and the lowest BMI associated with the longest sleepers. This relationship became U-shaped in middle-age, and less of a relationship was seen among the oldest respondents. CONCLUSIONS:These findings may provide insights for clinical recommendations and could help to guide mechanistic research regarding the sleep-obesity relationship.
| S-EPMC4700549 | biostudies-literature
Project description:BACKGROUND:While restrictive and compensatory eating disorders (e.g. anorexia and bulimia) are associated with elevated risk of suicide, less is known about binge eating disorder (BED). There is suggestive evidence of a U-shaped relationship between body mass index (BMI) and completed suicide, but fewer studies on suicidal ideation or attempts. This study examined the association between BED, BMI, and suicidality, and assessed whether these relationships varied by gender. METHODS:Data come from the Collaborative Psychiatric Epidemiologic Surveys (N =?14,497). Binge episodes and BED were assessed using the Composite International Diagnostic Inventory (CIDI). BMI was calculated from self-reported height and weight. Suicidal ideation/attempts were assessed using the CIDI. Weighted logistic regression was used to assess the association between binging/BED, BMI and suicidality. Interaction terms were used to assess whether the relationship between BMI and suicidality was moderated by binging/BED, and whether the relationships between binging/BED and BMI differed by gender. RESULTS:One-third of adults with BED had a history of suicidality, compared to 19% of those without. Both binging (OR: 1.95, 95% CI: 1.50-2.53) and BED (OR: 2.01, 95% CI: 1.41-2.86) were associated with suicidality in fully-adjusted models. BMI was associated with suicidality in a curvilinear manner, and this relationship was exacerbated by binging/BED (ORBinge eating x BMI: 1.04, 95% CI: 1.01-1.09, p <?0.05). The relationship between BMI and suicidality did not differ by gender (ORgender x BMI: 1.00, p <?0.770). However, the relationship between binge eating and suicidality was stronger for women relative to men (ORgender X binge: 1.87, p <?0.012). CONCLUSIONS:Binge eating, even below the threshold for BED, is associated with suicidality. BMI is associated with suicidality in a curvilinear manner, and the BMI-suicidality relationship is potentiated by binge eating/BED. Findings support the thoughtful integration of psychiatric care into weight loss programs for adults with a history of binging behavior.
| S-EPMC6003111 | biostudies-literature
Project description:Over the past few decades, overweight and obesity have become a growing health problem of particular concern for women of reproductive age as obesity in pregnancy has been associated with increased risk of obstetric and neonatal complications. The objective of this study is to describe the incidence of obstetric and perinatal complications in relation to maternal body mass index (BMI) at the time prior to delivery within the Spanish Health System. For this purpose, a cross-sectional observational study was conducted aimed at women who have been mothers between 2013 and 2018 in Spain. Data were collected through an online survey of 42 items that was distributed through lactation associations and postpartum support groups. A total of 5871 women answered the survey, with a mean age of 33.9 years (SD = 4.26 years). In the data analysis, crude odds ratios (OR) and adjusted odds ratios (AOR) were calculated through a multivariate analysis. A linear relationship was observed between the highest BMI figures and the highest risk of cephalopelvic disproportion (AOR of 1.79 for obesity type III (95% CI: 1.06-3.02)), preeclampsia (AOR of 6.86 for obesity type III (3.01-15.40)), labor induction (AOR of 1.78 for obesity type III (95% CI: 1.16-2.74)), emergency C-section (AOR of 2.92 for obesity type III (95% CI: 1.68-5.08)), morbidity composite in childbirth (AOR of 3.64 for obesity type III (95% CI: 2.13-6.24)), and macrosomia (AOR of 6.06 for obesity type III (95% CI: 3.17-11.60)), as compared with women with normoweight. Women with a higher BMI are more likely to develop complications during childbirth and macrosomia.
| S-EPMC7141254 | biostudies-literature
Project description:AimsThere are limited data examining whether body mass index (BMI) influences the association between cardiovascular biomarkers and incident heart failure (HF).Methods and resultsThirteen biomarkers representing key HF domains were measured: N-terminal pro-B-type natriuretic peptide (NT-proBNP), mid-regional pro-A-type natriuretic peptide (MR-proANP), cardiac troponin T (cTnT), C-reactive protein, procalcitonin, galectin-3, C-terminal pro-endothelin-1 (CT-proET-1), mid-regional pro-adrenomedullin, plasminogen activator inhibitor-1, copeptin, renin, aldosterone, and cystatin-C. Associations of biomarkers with BMI were examined using linear regression models, and with incident HF using Cox regression models. We selected biomarkers significantly associated with incident HF, and evaluated whether BMI modified these associations. Among 8202 individuals, 41% were overweight (BMI 25-30 kg/m2 ), and 16% were obese (BMI ≥30 kg/m2 ). Mean age of the cohort was 49 years (range 28-75), and 50% were women. All biomarkers except renin were associated with BMI: inverse associations were observed with NT-proBNP, MR-proANP, CT-proET-1 and aldosterone whereas positive associations were observed with the remaining biomarkers (all P ≤ 0.001). During 11.3 ± 3.1 years of follow-up, 357 HF events were recorded. Only NT-proBNP, MR-proANP and cTnT remained associated with incident HF (P < 0.001), and a significant biomarker*BMI interaction was not observed (interaction P > 0.1). Combined NT-proBNP and cTnT measurements modestly improved performance metrics of the clinical HF model in overweight (ΔC-statistic = 0.024; likelihood ratio χ2 = 38; P < 0.001) and obese (ΔC-statistic = 0.020; likelihood ratio χ2 = 32; P < 0.001) individuals.ConclusionsPlasma concentrations of several cardiovascular biomarkers are influenced by obesity. Only NT-proBNP, MR-proANP and cTnT were associated with incident HF, and BMI did not modify these associations. A combination of NT-proBNP and cTnT improves HF risk prediction in overweight and obese individuals.
| S-EPMC8247970 | biostudies-literature
Project description:BackgroundRecent studies have reported associations between body mass index (BMI) and various autoimmune disorders. However, it is still uncertain whether there exists a direct cause-and-effect relationship between BMI and autoimmune thyroiditis (AIT). The aim of our study is to investigate the causal association between BMI and AIT.MethodsWe conducted a two-sample summary data Mendelian randomization (MR) analysis using genome-wide association studies (GWAS) summary statistics data related to BMI as exposure, and GWAS summary statistic data sets for AIT as the outcome. Robustly associated single-nucleotide polymorphisms (SNPs) for BMI were selected as instrumental variables (IVs). We used the inverse variance weighted (IVW) method as the primary method and performed other MR methods such as MR-Egger regression, weighted median, simple mode, and weighted mode analyses for further validation. The slope of MR-Egger regression was used to correct for pleiotropy and provide estimates of causality. The p-value for the intercept in MR-Egger was utilized to detect any directional pleiotropic effects. Heterogeneity and sensitivity analyses were performed to assess the robustness of our findings.ResultsSeventy-eight SNPs were selected from GWAS on BMI as the IVs. Our MR analysis using the IVW method showed a potential causal association between BMI and AIT (OR = 3.071, 95% CI 1.324-7.118). Findings from other MR methods are non-significant, although the direction of effect is consistent. There was no evidence that the result was affected by genetic pleiotropy (MR-Egger regression intercept = 0.01, SE = 0.00025, p = 0.719). Heterogeneity and sensitivity analyses revealed no significant heterogeneity among SNPs, and no single SNP drove the observed associations.ConclusionOur findings suggest a potential causal association between BMI and AIT, which may provide a basis for further investigation into the relationship between BMI and AIT. Further studies are required as only the IVW method shows significant results, and the case sample size is small.
| S-EPMC10652572 | biostudies-literature