Temporal relationship between body mass index and uric acid and their joint impact on blood pressure in children and adults: the Bogalusa Heart Study.
Ontology highlight
ABSTRACT: Objective
This study aimed to examine the temporal relationship between body mass index (BMI) and uric acid (UA), and their joint effect on blood pressure (BP) in children and adults.Methods
The longitudinal cohorts for temporal relationship analyses consisted of 564 and 911 subjects examined twice 5-14 years apart from childhood to adulthood. The cross-sectional cohorts for mediation analyses consisted of 3102 children and 3402 nondiabetic adults. Cross-lagged panel analysis models were used to examine the temporal relationship between BMI and UA, and mediation analysis models the mediation effect of UA on the BMI-BP association.Results
After adjusting for age, race, sex and follow-up years in children, and additionally smoking and alcohol drinking in adults, the path coefficients (standardized regression coefficients) from baseline BMI to follow-up UA (0.145 in children and 0.068 in adults) were significant, but the path coefficients from baseline UA to follow-up BMI (0.011 in children and 0.016 in adults) were not. In mediation analyses, indirect effects through UA on the BMI-systolic BP association were estimated at 0.028 (mediation effect = 8.8%) in children and 0.033 (mediation effect = 13.5%) in adults (P < 0.001 for both). Direct effects of BMI on systolic BP (0.289 in children and 0.212 in adults) were significant. The mediation effect parameters did not differ significantly between Blacks and Whites.Conclusions
Changes in BMI precede alterations in UA, and the BMI-BP association is in part mediated through BMI-related increase in UA both in children and in adults. These findings have implications for addressing mechanisms of obesity hypertension beginning in early life.
SUBMITTER: Yun M
PROVIDER: S-EPMC8236402 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:Although obesity and insulin resistance are closely correlated, their temporal sequences in early life and influence on adult hypertension are largely unknown. This study aims to delineate the temporal relationship patterns between body mass index (BMI) and insulin in childhood and their impact on adult hypertension. The longitudinal cohort consisted of 990 adults (630 whites and 360 blacks) who had BMI and fasting insulin measured twice 5.4 years apart in childhood (mean age, 10.5 years at baseline and 15.9 years at follow-up) and blood pressure measured 14.7 years later in adulthood (mean age, 30.5 years). Cross-lagged panel and mediation analysis models were used to examine the temporal relationship between childhood BMI and insulin and its impact on adult hypertension. After adjusting for age, race, sex, and follow-up years, the cross-lagged path coefficient (?=0.33; P<0.001) from baseline BMI to follow-up insulin was significantly greater than the path coefficient (?=-0.02; P>0.05) from baseline insulin to follow-up BMI in childhood with P<0.001 for the difference in ?s. Blacks and whites showed similar patterns of the temporal relationship. The path coefficient (?=0.59; P<0.001) from BMI to insulin in the hypertensive group was significantly greater than that (?=0.24; P<0.001) in normotensive group, with P<0.001 for the difference in ?s between these 2 groups. The mediation effect of childhood insulin on the childhood BMI-adult hypertension association was estimated at 21.1% (P<0.001). These findings provide evidence that higher BMI levels precede hyperinsulinemia during childhood, and this 1-directional relation plays a role in the development of hypertension.
| S-EPMC4982798 | biostudies-literature
Project description:OBJECTIVES:Despite the inverse association between cigarette smoking and body mass index (BMI), it is unknown whether the effect of smoking on insulin is mediated through decreased BMI. This study aims to examine the temporal relationship between BMI and insulin, the impact of smoking on this relationship and the mediation effect of BMI on the association between smoking and insulin levels. METHODS:The longitudinal cohort consisted of 1121 adults (807 white and 314 black participants, mean age, 42.0 years at follow-up) for whom BMI and fasting insulin were measured twice, with an average follow-up period of 17.1 years. Cross-lagged panel and mediation analysis models were used to examine the temporal relationship between BMI and insulin, and the mediation effect of BMI on the smoking-insulin association. RESULTS:Smoking was inversely associated with insulin (regression coefficient, -0.073; P = .015 at baseline and -0.121; P < .001 at follow-up), adjusting for age, race and gender. After additional adjustment for follow-up periods, the cross-lagged path coefficient from BMI to insulin (?, 0.226; P < .001) was significantly greater than that from insulin to BMI (?, -0.029; P = .208), with P < .001 for the difference. The path coefficient from BMI to insulin was significantly greater in non-smokers (?, 0.273; P < .001) than in smokers (?, 0.122; P = .046), with P = .013 for the difference. The mediation effect of BMI on the smoking-insulin association was estimated at 53.4% (P = .030) at baseline and 58.7% (P < .001) at follow-up. CONCLUSIONS:These findings suggest that cigarette smoking has a significant impact on the one-directional relationship from BMI to insulin. The insulin-lowering effect of smoking is predominantly mediated through decreased BMI as the result of smoking.
| S-EPMC5999532 | biostudies-literature
Project description:BackgroundInflammation and insulin resistance play crucial roles in the development of type 2 diabetes mellitus (T2DM). We aim to examine the temporal relationship between high-sensitivity C-reactive protein (hsCRP) and insulin resistance in non-diabetic adults and their joint effect on the development of hyperglycemia.MethodsThe longitudinal cohort from the Bogalusa Heart Study consisted of 509 non-diabetic adults (360 whites and 149 blacks, mean age = 42.8 years at follow-up) who had hsCRP, fasting glucose and insulin measured twice at baseline and follow-up over 6.8 years. Cross-lagged panel model was used to examine the temporal relationship between hsCRP and homeostasis model assessment for insulin resistance (HOMA-IR). Information on incident T2DM was collected in a survey in 6.1 years after the follow-up survey.ResultsAfter adjusting for race, sex, age, body mass index, smoking, alcohol drinking and follow-up years, the path coefficient from baseline hsCRP to follow-up HOMA-IR (β2 = 0.105, p = 0.009) was significant and greater than the path from baseline HOMA-IR to follow-up hsCRP (β1 = 0.005, p = 0.903), with p = 0.011 for the difference between β1 and β2. This one-directional path from baseline hsCRP to follow-up HOMA-IR was significant in the hyperglycemia group but not in the normoglycemia group. In addition, participants with high levels of baseline hsCRP and follow-up HOMA-IR had greater risks of T2DM (odds ratio, OR = 2.38, p = 0.035), pre-T2DM (OR = 2.27, p = 0.006) and hyperglycemia (OR = 2.18, p = 0.003) than those with low-low levels.ConclusionsThese findings suggest that elevated hsCRP is associated with future insulin resistance in non-diabetic adults, and their joint effect is predictive of the development of T2DM.
| S-EPMC6706925 | biostudies-literature
Project description:RationaleData are limited regarding the influence of life-course cumulative burden of increased body mass index (BMI) and elevated blood pressure (BP) on the progression of left ventricular (LV) geometric remodeling in midlife.ObjectiveTo investigate the dynamic changes in LV mass and LV geometry over 6.4 years during midlife and to examine whether the adverse progression of LV geometric remodeling is influenced by the cumulative burden of BMI and BP from childhood to adulthood.Methods and resultsThe study consisted of 877 adults (604 whites and 273 blacks; 355 males; mean age=41.4 years at follow-up) who had 5 to 15 examinations of BMI and BP from childhood and 2 examinations of LV dimensions at baseline and follow-up 6.4 years apart during adulthood. The area under the curve (AUC) was calculated as a measure of long-term burden (total AUC) and trends (incremental AUC) of BMI and systolic BP (SBP). After adjusting for age, race, sex, smoking, alcohol drinking, and baseline LV mass index, the annual increase rate of LV mass index was associated with all BMI measures (β=0.16-0.36, P<0.05 for all), adult SBP (β=0.07, P=0.04), and total AUC of SBP (β=0.09, P=0.01) but not with childhood and incremental AUC values of SBP. All BMI and SBP measures (except childhood SBP) were significantly associated with increased risk of incident LV hypertrophy, with odds ratios of BMI (odds ratio=1.85-2.74, P<0.05 for all) being significantly greater than those of SBP (odds ratio=1.09-1.34, P<0.05 for all except childhood SBP). In addition, all BMI measures were significantly and positively associated with incident eccentric and concentric LV hypertrophy.ConclusionsLife-course cumulative burden of BMI and BP is associated with the development of LV hypertrophy in midlife, with BMI showing stronger associations than BP. Visual Overview: An online visual overview is available for this article.
| S-EPMC7047524 | 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:BackgroundLower leisure-time physical activity (LTPA) and higher body mass index (BMI) are independently associated with risk of heart failure (HF). However, it is unclear if this relationship is consistent for both heart failure with preserved ejection fraction (HFpEF) and heart failure with reduced ejection fraction (HFrEF).ObjectivesThis study sought to quantify dose-response associations between LTPA, BMI, and the risk of different HF subtypes.MethodsIndividual-level data from 3 cohort studies (WHI [Women's Health Initiative], MESA [Multi-Ethnic Study of Atherosclerosis], and CHS [Cardiovascular Health Study]) were pooled and participants were stratified into guideline-recommended categories of LTPA and BMI. Associations between LTPA, BMI, and risk of overall HF, HFpEF (ejection fraction ≥45%), and HFrEF (ejection fraction <45%) were assessed by using multivariable adjusted Cox models and restricted cubic splines.ResultsThe study included 51,451 participants with 3,180 HF events (1,252 HFpEF, 914 HFrEF, and 1,014 unclassified HF). In the adjusted analysis, there was a dose-dependent association between higher LTPA levels, lower BMI, and overall HF risk. Among HF subtypes, LTPA in any dose range was not associated with HFrEF risk. In contrast, lower levels of LTPA (<500 MET-min/week) were not associated with HFpEF risk, and dose-dependent associations with lower HFpEF risk were observed at higher levels. Compared with no LTPA, higher than twice the guideline-recommended minimum LTPA levels (>1,000 MET-min/week) were associated with an 19% lower risk of HFpEF (hazard ratio: 0.81; 95% confidence interval: 0.68 to 0.97). The dose-response relationship for BMI with HFpEF risk was also more consistent than with HFrEF risk, such that increasing BMI above the normal range (≥25 kg/m2) was associated with a greater increase in risk of HFpEF than HFrEF.ConclusionsOur study findings show strong, dose-dependent associations between LTPA levels, BMI, and risk of overall HF. Among HF subtypes, higher LTPA levels and lower BMI were more consistently associated with lower risk of HFpEF compared with HFrEF.
| S-EPMC5848099 | biostudies-literature
Project description:BackgroundElevated cardiovascular disease risk factor burden is a recognized contributor to poorer cognitive function; however, the physiological mechanisms underlying this association are not well understood. We sought to assess the potential mediation effect of left ventricular (LV) remodeling on the association between lifetime systolic blood pressure and cognitive function in a community-based cohort of middle-aged adults.MethodsNine hundred sixty participants of the Bogalusa Heart Study (59.2% women, 33.8% black, aged 48.4±5.1 years) received 2-dimensional echocardiography to quantify relative wall thickness, LV mass, and diastolic and systolic LV function; and a standardized neurocognitive battery to assess memory, executive functioning, and language processing. Multivariable linear regression assessed the association of cardiac structure and function with a global composite cognitive function score, adjusting for traditional cardiovascular disease risk factors. Mediation analysis assessed the effect of LV mass index on the association between lifetime systolic blood pressure burden and cognitive function.ResultsThere were 233 (24.3%) and 136 (14.2%) individuals with concentric LV remodeling and concentric LV hypertrophy, respectively. Each g/m2.7 increment in LV mass index was associated with a 0.03 standardized unit decrement in global cognitive function (P=0.03). Individuals with concentric LV remodeling and isolated diastolic dysfunction had the poorest cognitive function, and a greater ratio between early mitral inflow velocity and early diastolic mitral annular velocity (E/e') was associated with poorer cognitive function, even after adjustment for LV mass index (B=-0.12; P=0.03). A total of 18.8% of the association between lifetime systolic blood pressure burden and midlife cognitive function was accounted for by LV mass index.ConclusionsCardiac remodeling partially mediates the association between lifespan systolic blood pressure burden and adult cognition in individuals without dementia or clinical cardiovascular disease. Slowing or reversing the progression of cardiac remodeling in middle-age may be a novel therapeutic approach to prevent cognitive decline.
| S-EPMC7428065 | biostudies-literature
Project description:BackgroundCardiopulmonary exercise testing (CPX) in patients with systolic heart failure (HF) is important for determining HF prognosis and helping guide timing of heart transplantation. Although approximately 20% to 30% of patients with HF are obese (body mass index [BMI] >30 kg/m(2)), the impact of BMI on CPX results is not well established. The objective of this study was to assess the relationship between BMI and CPX variables, including peak oxygen uptake (VO(2)) at ventilatory threshold, oxygen pulse, and ventilation-carbon dioxide production ratio.MethodsConsecutive patients with systolic HF (n = 2,324) enrolled in the Heart Failure and A Controlled Trial Investigating Outcomes of Exercise Training trial who had baseline BMI recorded were included in this study. Subjects were divided into strata based on BMI: underweight (BMI <18.5 kg/m(2)), normal weight (BMI 18.5-24.9 kg/m(2)), overweight (BMI 25.0-29.9 kg/m(2)), obese I (BMI 30-34.9 kg/m(2)), obese II (BMI 35-39.9 kg/m(2)), and obese III (BMI > or = 40 kg/m(2)).ResultsObese III, but not overweight; obese I; or obese II was associated with decreased peak VO(2) (mL kg(-1) min(-1)) compared to normal weight status. Increasing BMI category was inversely related to ventilation/carbon dioxide production (V(E)/V(CO2)) ratio (P < .0001). On multivariable analysis, BMI was a significant independent predictor of peak VO(2) (partial R(2) = 0.07, P < .0001) and V(E)/V(CO2) slope (partial R(2) = 0.03, P < .0001) in patients with chronic systolic HF.ConclusionsBody mass index is significantly associated with key CPX fitness variables in patients with HF. The influence of BMI on the prognostic value of CPX in HF requires further evaluation in longitudinal studies.
| S-EPMC2762950 | biostudies-literature
Project description:BackgroundElevated pulse pressure (PP) is a robust independent predictor of cardiovascular diseases. The relationship between PP and body mass index (BMI) was presented in a few studies. However, the findings were inconsistent. Therefore, the aim of the present study is to identify the association between elevated PP and BMI using a large sample of active-duty Royal Thai Army (RTA) personnel.MethodsA cross-sectional study was conducted through the use of the dataset obtained from the annual health examination database of RTA personnel in Thailand in 2022. BMI 25.0-29.9 kg/m2 was classified as obesity I, whereas BMI ≥ 30.0 kg/m2 was classified as obesity II. Elevated PP was defined as PP ≥ 50 mmHg. Multivariable linear regression and log-binomial regression models were utilized for determining the association between elevated PP and BMI.ResultsA total of 62,113 active-duty RTA personnel were included in the study. The average BMI was 25.4 ± 3.8 kg/m2, while the average PP was 50.1 ± 11.2 mmHg. Compared to individuals with normal weight, the [Formula: see text] coefficients of PP and BMI were 1.38 (95% CI: 1.15-1.60) and 2.57 (95% CI: 2.25-2.88) in individuals with obesity I and obesity II, respectively. Effect modification by high blood pressure (BP) on the association between elevated PP and BMI was observed. Among participants with normal BP, in comparison with BMI of 18.5-22.9 kg/m2, the adjusted prevalence ratio (PR) for elevated PP was 1.23 (95% CI: 1.19-1.28) and 1.41 (95% CI: 1.35-1.48) in those with obesity I and obesity II, respectively. Meanwhile, among individuals with high BP, the adjusted PR for elevated PP was 1.05 (95% CI: 1.01-1.08) and 1.09 (95% CI: 1.06-1.13) in those with obesity I and obesity II, respectively.ConclusionPP was positively associated with BMI in active-duty RTA personnel. High BP was the modifier of the association between PP and BMI. A weaker association between elevated PP and BMI was observed among RTA personnel with high BP.
| S-EPMC10355046 | biostudies-literature
Project description:BackgroundCandidate gene and twin studies suggest that interactions between body mass index (BMI) and genes contribute to the variability of blood pressure (BP). To determine whether there is evidence for gene-BMI interactions, we investigated the modulation of BP heritability by BMI using 4,153 blacks, 1,538 Asians, 4,013 whites, and 2,199 Hispanic Americans from the Family Blood Pressure Program.MethodsTo capture the BP heritability dependence on BMI, we employed a generalized variance components model incorporating linear and Gaussian interactions between BMI and the genetic component. Within each race and network subgroup, we used the Akaike information criterion and likelihood ratio test to select the appropriate interaction function for each BP trait (systolic BP (SBP), diastolic BP (DBP), mean arterial pressure (MAP), and pulse pressure (PP)) and determine interaction significance, respectively.ResultsBP heritabilities were significantly modified by BMI in the GenNet and SAPPHIRe Networks, which contained the youngest and least-obese participants, respectively. GenNet Whites had unimodal SBP, MAP, and PP heritabilities that peaked between BMI values of 33 and 37kg/m(2). The SBP and MAP heritabilities in GenNet Hispanic Americans, as well as the PP heritability in GenNet blacks, were increasing functions of BMI. The DBP and SBP heritabilities in the SAPPHIRe Chinese and Japanese, respectively, were decreasing functions of BMI.ConclusionsBP heritability differed by BMI in the youngest and least-obese networks, although the shape of this dependence differed by race. Use of nonlinear gene-BMI interactions may enhance BP gene discovery efforts in individuals of European ancestry.
| S-EPMC3958601 | biostudies-literature