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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.

Background: Despite an increasing number of studies investigating the links between increased BMI and a better prognosis of cardiovascular disease, which has been termed the "obesity paradox," few of them take the lean mass into consideration., Objectives: This study aimed to explore the associations of body composition compartments, especially the lean mass, with cardiometabolic abnormalities in children and adolescents., Methods: In a nationwide cross-sectional study of 6- to 18-y-old children (n = 8967, 50.1% boys), we measured body composition using DXA scan, and calculated BMI, fat mass index (FMI), and lean mass index (LMI). The exploratory outcomes were cardiometabolic abnormalities, including hypertension, dyslipidemia, hyperglycemia, and insulin resistance. Adjusted linear regression coefficients and ORs were calculated to assess the associations between body composition indicators and cardiometabolic abnormalities., Results: Unlike BMI and FMI, LMI was inversely associated with homeostasis model assessment of insulin resistance (β: -0.06; 95% CI: -0.09, -0.03; P < 0.001), fasting plasma glucose (β: -0.08; 95% CI: -0.11, -0.05; P < 0.001), non-HDL cholesterol (β: -0.10; 95% CI: -0.13, -0.08; P < 0.001), LDL cholesterol (β: -0.12; 95% CI: -0.14, -0.09; P < 0.001), and total cholesterol (TC) (β: -0.16; 95% CI: -0.19, -0.14; P < 0.001). After multivariable adjustment, all the odds of cardiometabolic abnormalities were increased from the lowest quartile to the highest quartile of BMI and FMI (P-trend < 0.05); however, the odds of high TC, high LDL cholesterol, hyperglycemia, and insulin resistance were decreased with LMI (P-trend < 0.05). Obese children with high LMI did not have significantly increased odds of high TC, high LDL cholesterol, and high non-HDL cholesterol compared with normal-weight children without high LMI., Conclusions: Greater lean mass may have a protective impact on high TC, high LDL cholesterol, hyperglycemia, and insulin resistance in children and adolescents. This finding suggests that the "obesity paradox" may be partly explained by high lean mass., (© The Author(s) 2020. Published by Oxford University Press on behalf of the American Society for Nutrition.)

Background: It has been controversial whether to adjust for current body weight while examining the relationship between birthweight and blood pressure (BP)., Objective: The present study aims to partition the total effect of birthweight on BP into its direct effect and indirect effect through current body mass index (BMI)., Methods: The study cohort consisted of 6251 participants who had birthweight information with 13 443 observations on BMI and BP in pre-adolescence (4-11 years), adolescence (12-19 years), young adulthood (20-30 years) and mid-adulthood (31-58 years). General third-variable models were used to distinguish the mediation and suppression effects of current BMI on the birthweight-BP association at different ages., Results: The total effect of birthweight on systolic BP measured as standardized regression coefficient (β) without current BMI included in the model was 0.003 (P = .810) in pre-adolescents, -0.032 (P = .029) in adolescents, -0.066 (P = .002) in young adults and -0.051 (P = .023) in midlife adults. With additional adjustment for BMI, the direct effect of birthweight on systolic BP was strengthened to β = -0.066 (P = .013), β = -0.058 (P = .014), β = -0.094 (P = .020), β = -0.066 (P = .023); the suppression effects of BMI were calculated at 0.070, 0.027, 0.028 and 0.015 in the respective age groups. The decreasing trend of suppression effects with increasing age mimicked the trends of birthweight-BMI and BMI-BP correlations., Conclusions: Current body weight has a suppression effect, not a mediation effect, on the birthweight-BP association, with pre-adolescents having the greatest suppression effect. The suppression effect is predominantly determined by birthweight-BMI and BMI-BP correlations., (© 2020 World Obesity Federation.)

Background Data are limited regarding the relationship between the life-course burden of risk factors and adult cardiac function. This study sought to examine the impact of long-term burden of body mass index (BMI) and blood pressure (BP) levels on changes in adult left ventricular (LV) structure and function in a community-based cohort. Methods and Results The longitudinal study cohort consisted of 1108 adult patients (726 White; 41.9% men; mean age, 48.2 years in the last survey) who had been examined 4 to 16 times for BMI and BP and echocardiographic LV structure and function in adulthood, with a mean follow-up period of 38.8 years. The area under the curve was used as a measure of long-term burden of BMI and BP. Adult LV mass index was significantly associated with childhood and adulthood BMI and systolic BP (SBP), and their area under the curve values (β=0.07-0.37; P <0.05 for all). Adult LV ejection fraction was negatively associated with childhood BMI (β=-0.08), adult BMI (β=-0.07) and BMI area under the curve (β=-0.07) ( P <0.05 for all); the effects of SBP measures were not significant. Adult E/A ratio was negatively associated with adulthood SBP (β=-0.13; P <0.01) and total area under the curve of SBP (β=-0.13; P <0.01). E/e' ratio was positively associated with BMI and SBP measures. The effects of diastolic BP measures were substantially similar to those of SBP measures. Participants with LV hypertrophy, eccentric hypertrophy, and concentric hypertrophy had significantly lower LV ejection fraction and higher E/e' ratio. Conclusions These observations provide strong evidence that early-life adiposity and BP levels and their life-course cumulative burdens are associated with subclinical changes in adult LV structure and function in the general population.

Rationale: Data 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., Objective: To 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 Results: The 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., Conclusions: Life-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.

Objective: To investigate the association of abdominal visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) with cardiometabolic risk factors in children and adolescents., Research Design and Methods: This cross-sectional study consisted of 8460 children and adolescents aged 6-18 years from Chinese urban areas who underwent dual-energy X-ray absorptiometry scan and had metabolic risk factors measured., Results: In multivariate analysis adjusted for region, family income, age, puberty development, physical activity, and smoking, VAT and SAT were significantly associated with all metabolic risk factors for both sexes (all p<0.01). After additional adjustment for fat mass index, most of these associations remain significantly positive. In boys, SAT had greater ORs for all risk factors compared with VAT; in girls, however, SAT had greater odds for high triglycerides, smaller odds for high low-density lipid cholesterol, and similar odds for other risk factors compared with VAT. In addition, boys had greater magnitude of associations of SAT with high total cholesterol, high low-density lipid cholesterol, and low high-density lipid cholesterol compared with girls; no sex differences for VAT were observed., Conclusions: Both abdominal VAT and SAT have adverse impacts on most of the cardiometabolic risk factors in youth. However, their relative contributions differ between sexes., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2019. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

Background: BMI as a body weight indicator, may inadequately represent the biological effect of body fat on lipid profiles. This study aims to assess whether body fat indicators were superior to BMI for recognizing children with dyslipidemia., Methods: A nationwide cross-sectional study involving 8944 pediatric participants aged 6-18 years. Measures of fat mass index (FMI), fat mass percentage (FMP), BMI, and four lipid profiles were obtained., Results: Among boys, the standard multi-linear regression coefficients of FMI for TC, LDL-C, and TG were higher than those of BMI (P < 0.01), but not for HDL-C. Also, the prevalence ratios and area under curves (AUCs) of excess fat classified by FMI for specific abnormal lipid profiles (except for HDL-C) were greater than overweight classified by BMI. The AUCs for detecting children with abnormal TC, LDL-C, and TG of FMI-based excess fat were 3.9%, 5.6%, and 2.8% higher than those of BMI-based overweight, respectively, all P < 0.01. Among girls, the associations of BMI with lipid profiles were substantially similar to FMI. All these results were almost identical when FMP was used instead of FMI., Conclusions: DXA measured body fat performs better than BMI in identifying abnormal lipid profiles in boys but not in girls.

Objective: Atherosclerosis and arterial stiffness predict cardiovascular morbidity and mortality. We aimed to investigate the influence of BMI and blood pressure (BP) in childhood, and change in BMI and BP, on the development of subclinical atherosclerosis and arterial stiffness in adulthood., Methods: The study consisted of 1252 individuals aged 27-42 years who had 2-10 measurements of BMI and BP from childhood. In the final survey (2010-2011), subclinical markers of vascular damage, including carotid intima-media thickness (cIMT), carotid-femoral pulse wave velocity (cfPWV), and brachial-ankle pulse wave velocity (baPWV), were measured., Results: Pearson correlation analyses showed that BMI and BP in childhood and adulthood, and also cumulative and incremental values from childhood to adulthood, were all significantly associated with adult cIMT, cfPWV, and baPWV in males and in females (all P < 0.05). In the multivariate logistical analyses, for both sexes, childhood BMI and systolic BP (SBP) predicted high cIMT in adulthood, and childhood SBP predicted high cfPWV and high baPWV in adulthood. However, these associations were largely attenuated and became nonsignificant after additional adjustment for adult BMI and SBP, except that childhood SBP showed a borderline significant association with high cfPWV in adulthood for males. In addition, for both sexes, incremental BMI and SBP from childhood to adulthood predicted high cIMT in adulthood, and incremental SBP predicted high cfPWV and high baPWV in adulthood, independent of childhood values., Conclusion: The adverse influence of high BMI and high BP on subclinical vascular damage begins in childhood. This study enhances the importance of early prevention and lifelong treatment of excessive weight and elevated BP.

We aimed to examine the association between serum cotinine and leukocyte telomere length (LTL) and the intermediate effects of body mass index (BMI) and C-reactive protein (CRP) on modulating the association. This study included 4,047 adults from the 1999 to 2002 National Health and Nutrition Examination Survey. In the combined sample, after adjusting for age, race, sex, physical activity, and alcohol use, the total effect of serum cotinine on LTL was significant (standardized regression coefficient, β = −0.049, p = 0.001) without BMI and CRP included in the model. With inclusion of BMI but without CRP in the model, the direct effect of cotinine on LTL in its absolute value increased to β = −0.053 (p < 0.001), and the suppression effect of BMI was estimated at 8.8%. With inclusion of CRP but without BMI in the model, the direct effect of cotinine on LTL in its absolute value decreased to β = −0.040 (p = 0.008), and the mediation effect of CRP was estimated at 16.9%. With inclusion of both BMI and CRP in the model, BMI and CRP still had significant suppression and mediation effects, respectively, on the cotinine-LTL association. These findings suggest that weight and inflammation have different roles in the inverse association between serum cotinine and LTL. [ABSTRACT FROM AUTHOR]

Context: Both obesity and inflammation are related to accelerated aging. It is not yet known whether inflammation mediates the effects of obesity on aging.Objective: This work aims to dissect the direct effect of body mass index (BMI) and its indirect effect through C-reactive protein (CRP) on leukocyte telomere length (LTL) to determine the mediation effect of CRP on the BMI-LTL association.Methods: The study cohort included 5451 adults (1404 Mexican American, 3114 White, and 933 Black individuals; 53.5% male; mean age = 49.2 years) from the 1999 to 2002 National Health and Nutrition Examination Survey. General mediation models were used to examine the mediation effect of CRP on the BMI-LTL association.Results: After adjusting for age, race, sex, physical activity, alcohol use, and serum cotinine, the total effect of BMI on LTL was significant (standardized regression coefficient, β = -.054, P < .001) without CRP included in the model. With inclusion of CRP in the model, the indirect effect of BMI on LTL through CRP was estimated at β equal to -.023 (P < .001), and the direct effect of BMI on LTL in its absolute value decreased to β equal to -.031 (P = .025). The mediation effect of CRP was estimated at 42.6%. The mediation model parameters did not differ significantly between race and sex groups.Conclusion: These results suggest that the inverse BMI-LTL association is partly mediated by obesity-induced inflammation. The significant direct effect of BMI on LTL with removal of the mediation effect through CRP indicates that obesity is associated with LTL attrition also through other noninflammatory mechanisms. [ABSTRACT FROM AUTHOR]

Importance: The impact of long‐term burden of excessive body weight, beginning in childhood, on inflammatory status in adulthood has been poorly described. Objective: To characterize the longitudinal body mass index (BMI) trajectory from childhood and examine its relationship with inflammatory status in adulthood. Methods: We included 1285 adults who had 4–15 repeat measurements of BMI from childhood to adulthood. The area under the curve (AUC) of growth curves was calculated to characterize long‐term burden (total AUC) and trends (incremental AUC) of BMI. Results: After adjusting for covariates, higher values of BMI in terms of childhood and adulthood, as well as total and incremental AUC, were strongly associated with elevated levels of adult C‐reactive protein (CRP) in the four race‐sex groups. There were significant differences in linear and nonlinear curve parameters between the normal and high CRP groups for all race‐sex groups (P < 0.01). Compared with participants who had consistently low BMI in both childhood and adulthood, participants with high BMI in adulthood had higher CRP levels (P < 0.001), irrespective of their childhood BMI status; participants with high BMI in childhood but low BMI in adulthood had similar adult CRP levels. Interpretation: The impact of excessive body weight on inflammation is cumulative and exacerbated over time. The influence of childhood overweight/obesity on inflammatory status in adulthood can be alleviated by reducing adiposity in adulthood. [ABSTRACT FROM AUTHOR]

Obesity and hypertension are important risk factors of arterial stiffness. However, the complex relationship between increased body mass index (BMI), elevated blood pressure (BP), and arterial stiffness is largely unknown. We aim to examine the mediation effect of elevated BP on the association of early life BMI, long-term burden, and trend of BMI with arterial stiffness in midlife. The longitudinal study cohort consisted of 1190 participants (829 whites and 361 blacks, 518 males, mean age=40.0 years at follow-up) who had been examined for BMI and BP 4 to 15 times from childhood and aortic-femoral pulse wave velocity (afPWV) in adulthood, with a mean follow-up period of 30.3 years. Total area under the curve (AUCt) and incremental AUC (AUCi) were calculated in random-effects models and used as long-term measures of BMI and BP. Total effects of BMI measures on adult afPWV, adjusted for covariates were all significant without adult BMI and systolic BP (SBP) measures included in the models. The mediation effects of adult SBP (20.2%) and SBP AUCi (16.9%) were significant on the childhood BMI-afPWV association. Adult SBP showed significant mediation effects of 36.7% on the BMI AUCi-afPWV association and 36.4% on the BMI AUCt-afPWV association. The mediation effect of SBP AUCi was estimated at 63.3% ( P<0.01) on the BMI AUCi-afPWV association. Diastolic BP had similar total and mediation effects. These findings suggest that the association of increased childhood BMI and its cumulative burden with adult arterial stiffness measured as afPWV is predominantly mediated through the long-term and increasing trend of BP. [ABSTRACT FROM AUTHOR]

Background Obesity and hypertension are two risk factors of left ventricular hypertrophy (LVH) in adults. We aimed to examine the impacts of body weight and blood pressure (BP) from childhood on adult LV geometric remodeling. Methods The study cohort consisted of 1256 adults aged 27–42 years who had 2–10 measurements of body mass index (BMI) and BP from childhood in 1987 to adulthood in 2010. We calculated the cumulative and incremental values of BMI and BP from childhood to adulthood. In adulthood, four LV geometric patterns were defined based on the values of left ventricular mass index (g/m 2.7 ) and relative wall thickness: normal geometry, concentric remodeling (CR), eccentric hypertrophy (EH) and concentric hypertrophy (CH). Results The prevalence of abnormal LV geometric patterns in adults was 26.4% for CR, 2.0% for EH and 2.5% for CH. For childhood values, systolic BP (Odds Ratio [OR] = 1.26, 95% confidence interval [CI] = 1.08–1.47) but not BMI (OR = 1.06, 95%CI = 0.93-1.18) was associated with adult CR, whereas BMI (OR = 3.53, 95%CI = 2.09–5.98) but not systolic BP (OR = 1.04, 95%CI = 0.65–1.66) was associated with adult EH. Both childhood BMI (OR = 2.69, 95%CI = 1.77–4.09) and systolic BP (OR = 1.64, 95%CI = 1.07–2.51) were independently associated with adult CH. For adulthood, cumulative and incremental values, BMI and systolic BP were independently associated with adult CR, EH and CH. Conclusion Excessive body weight and elevated BP from childhood have independent influences on the development of adult LV geometric remodeling. [ABSTRACT FROM AUTHOR]

Background: Data are limited regarding the association of cumulative burden and trajectory of body mass index (BMI) from early life with adult lipid disorders. Methods: The study cohort consisted of 5195 adults who had BMI repeatedly measured 4 to 21 times from childhood and had blood lipid measurements of low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and triglycerides (TG) and information on lipid-lowering medications in the last adult survey. The area under the curve (AUC) was calculated as a measure of long-term burden (total AUC) and trends (incremental AUC) of BMI. Results: Participants with dyslipidemia, high LDL-C, low HDL-C and high TG had consistently and significantly higher BMI levels from childhood to adulthood compared to those with normal lipid levels. After adjusting for age, race, sex, and cohort, increased risk of adult dyslipidemia was significantly associated with higher values of childhood BMI, adulthood BMI, total AUC and incremental AUC, with odds ratio (95% confidence interval) = 1.22 (1.15–1.29), 1.85 (1.74–1.97), 1.61 (1.52–1.71), and 1.59 (1.50–1.69), respectively, and p < 0.001 for all. The association patterns were similar in most race–sex subgroups. Conclusions: Adults with dyslipidemia versus normal lipid levels have consistently higher levels and distinct life-course trajectories of BMI, suggesting that the impact of excessive body weight on dyslipidemia originates in early life. [ABSTRACT FROM AUTHOR]

Background: Inflammation 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. Methods: The 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. Results: After 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. Conclusions: These 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. [ABSTRACT FROM AUTHOR]

Abstract Body mass plays a crucial role in the bone growth and development, but few studies have examined the association of long-term cumulative impact and trajectory patterns of childhood body mass index (BMI) with adult bone mass, and the mediation effect of adult BMI and body composition on these associations. A total of 397 Chinese adults (54.4%) who had been examined for BMI 4–8 times during childhood (6–19 years) and bone mass in adulthood (29–37 years), were included for analysis. Adult bone mineral content (BMC), areal bone mineral density (aBMD) and body composition were assessed via dual-energy x-ray absorptiometry. Childhood BMI growth curves were constructed using a random-effects mixed model. The area under the curve (AUC) was calculated to represent the long-term impact of childhood BMI. At baseline, 24.4%, 66.2%, 7.6% and 1.8% of the participants were underweight, normal weight, overweight and obese, respectively. Quadratic curve parameters of childhood BMI differed significantly between groups of adult whole body (WB) BMC, lumbar spine (LS) aBMD and femoral neck (FN) aBMD, with low BMC/aBMD groups having lower childhood BMI than the normal groups. AUC of childhood BMI was significantly and positively related to adult WB BMC and aBMD at each site, irrespective of sex. Significant mediation effects of adult BMI were shown on the association of childhood BMI AUC with adult WB BMC in males (52.0%) and FN aBMD in both sexes (males: 65.4%; females: 64.3%). Additionally, mediation effect of fat mass index was only noted on the association of childhood BMI AUC with adult WB BMC (41.3%), with a positive total indirect effect estimated at 0.118. The adult lean mass index, by contrast, mediated the childhood BMI-adult BMC/aBMD association positively at all sites in males (71.5%~89.2%) and at WB BMC in females (45.0%). These findings suggest that the impact of body weight on adult bones originates from childhood, which is mediated by concurrent BMI and body composition. Highlights • Childhood cumulative BMI was positively associated with adult bone mass at multiple skeletal sites. • The childhood BMI-adult bone mass associations were mediated by concurrent BMI and body composition. • Mediation effects of adult BMI and body composition were stronger at femoral neck (FN) than at other sites. • The dominant mediator for childhood BMI-adult FN aBMD association was lean mass in males, but fat mass in females. [ABSTRACT FROM AUTHOR]