Huijie Zhang

Long-term Impact of Childhood Adiposity on Adult Metabolic Syndrome Is Modified by Insulin Resistance: The Bogalusa Heart Study.

Childhood adiposity and insulin resistance are well-known risk factors for adult metabolic syndrome (MetS). This study aims to examine whether the association between childhood adiposity and adult MetS is modified by insulin resistance. The cohort consisted of 1,593 black and white subjects, aged 19–50 years at follow-up, who were examined 19 years apart on average as children and adults for MetS variables. The prevalence of adult MetS was compared between the insulin-sensitive obesity and insulin-resistant obesity groups in childhood. Adult MetS prevalence was higher in the insulin-resistant obesity group than in the insulin-sensitive obesity group (34.9% vs. 24.3%, p = 0.008). In multivariable logistic regression analyses adjusted for age, race, gender, and follow-up years, individuals with insulin-resistant obesity in childhood were 1.7 times (p = 0.011) more likely to have MetS 19 years later on average than those with insulin-sensitive obesity in childhood. Odds ratio did not differ significantly between blacks and whites (p = 0.724). ORs for the association of childhood BMI with adult MetS significantly increased with increasing tertiles of childhood HOMA (p < 0.001 for trend). These findings suggest that insulin resistance amplifies the association between childhood adiposity and adult MetS and underscore the importance of preventing both adiposity and insulin resistance in early life.

Impact of Adiposity on Incident Hypertension Is Modified by Insulin Resistance in Adults: Longitudinal Observation From the Bogalusa Heart Study

Adiposity and insulin resistance are closely associated with hypertension. This study aims to investigate whether the association between adiposity and hypertension is modified by insulin resistance. The cohort consisted of 1624 middle-aged normotensive black and white adults aged 18 to 43 years at baseline who followed for 16 years on average. Overweight/obesity at baseline was defined as body mass index (BMI) ≥25, and insulin resistance was measured using homeostasis model assessment of insulin resistance. Prevalence of incident hypertension was compared between the insulin-sensitive adiposity and insulin-resistant adiposity groups. The prevalence of incident hypertension was higher in the insulin-resistant adiposity than in the insulin-sensitive adiposity group (32.1% versus 22.1%, P<0.001). In multivariable logistic analyses, adjusted for baseline age, race, sex, follow-up years, and smoking, baseline insulin-resistant obesity was associated with incident hypertension (odds ratio, 1.9; P=0.008). Odds ratios did not differ between blacks and whites (P=0.238). Of note, the odds ratios of BMI associated with hypertension significantly increased with increasing quartiles of baseline homeostasis model assessment (odds ratio, 1.3, 1.1, 1.5, and 2.5 in quartiles I, II, III, and IV, respectively; P=0.006 for trend). Slopes of increasing follow-up blood pressure with baseline BMI, measured as regression coefficients (&bgr;), were significantly greater in insulin-resistant than in insulin-sensitive individuals (&bgr;=0.74 versus &bgr;=0.35 for systolic blood pressure, P=0.004 for difference; &bgr;=0.51 versus &bgr;=0.23 for diastolic blood pressure, P=0.001 for difference). These findings suggest that insulin resistance has a synergistic effect on the obesity–hypertension association in young adults, indicating that the role of adiposity in the development of hypertension is modified by insulin resistance.Adiposity and insulin resistance are closely associated with hypertension. This study aims to investigate whether the association between adiposity and hypertension is modified by insulin resistance. The cohort consisted of 1624 middle-aged normotensive black and white adults aged 18 to 43 years at baseline who followed for 16 years on average. Overweight/obesity at baseline was defined as body mass index (BMI) ≥25, and insulin resistance was measured using homeostasis model assessment of insulin resistance. Prevalence of incident hypertension was compared between the insulin-sensitive adiposity and insulin-resistant adiposity groups. The prevalence of incident hypertension was higher in the insulin-resistant adiposity than in the insulin-sensitive adiposity group (32.1% versus 22.1%, P <0.001). In multivariable logistic analyses, adjusted for baseline age, race, sex, follow-up years, and smoking, baseline insulin-resistant obesity was associated with incident hypertension (odds ratio, 1.9; P =0.008). Odds ratios did not differ between blacks and whites ( P =0.238). Of note, the odds ratios of BMI associated with hypertension significantly increased with increasing quartiles of baseline homeostasis model assessment (odds ratio, 1.3, 1.1, 1.5, and 2.5 in quartiles I, II, III, and IV, respectively; P =0.006 for trend). Slopes of increasing follow-up blood pressure with baseline BMI, measured as regression coefficients (β), were significantly greater in insulin-resistant than in insulin-sensitive individuals (β=0.74 versus β=0.35 for systolic blood pressure, P =0.004 for difference; β=0.51 versus β=0.23 for diastolic blood pressure, P =0.001 for difference). These findings suggest that insulin resistance has a synergistic effect on the obesity–hypertension association in young adults, indicating that the role of adiposity in the development of hypertension is modified by insulin resistance. # Novelty and Significance {#article-title-47}

Long-term Impact of Temporal Sequence from Childhood Obesity to Hyperinsulinemia on Adult Metabolic Syndrome and Diabetes: The Bogalusa Heart Study

This study aims to delineate the temporal relations between body mass index (BMI) and insulin in childhood and their impact on adult metabolic syndrome (MetS) and type 2 diabetes mellitus (T2DM).The longitudinal cohort consisted of 609 whites and 339 blacks who had BMI and fasting insulin measured twice in childhood (mean age = 10.5 years at baseline and 15.9 years at follow-up). Incident MetS and T2DM were identified in adulthood (mean age = 30.5 years). Cross-lagged panel and mediation analysis models were used. After adjusting for age, race, gender, and follow-up years, the cross-lagged path coefficient of BMI → insulin (β = 0.326, p < 0.001) was significantly greater than that of insulin → BMI (β = −0.023, p = 0.207) in childhood, with p < 0.001 for the difference in βs. The path coefficient for BMI → insulin was significantly greater in MetS than in non-MetS groups (0.510 vs 0.190, p < 0.001), and greater in hyperglycemia than in normoglycemia groups (0.503 vs 0.285, p = 0.026). The mediation effect of childhood insulin on the BMI-MetS and BMI-hyperglycemia associations was estimated at 19.2% (p < 0.001) and 18.3% (p < 0.001), respectively. These findings provide evidence that higher BMI levels precede hyperinsulinemia during childhood, and this one-directional relation plays a significant role in the development of MetS and T2DM in adult life.

Temporal Relationship Between Childhood Body Mass Index and Insulin and Its Impact on Adult Hypertension: The Bogalusa Heart Study

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 (&bgr;=0.33; P<0.001) from baseline BMI to follow-up insulin was significantly greater than the path coefficient (&bgr;=−0.02; P>0.05) from baseline insulin to follow-up BMI in childhood with P<0.001 for the difference in &bgr;s. Blacks and whites showed similar patterns of the temporal relationship. The path coefficient (&bgr;=0.59; P<0.001) from BMI to insulin in the hypertensive group was significantly greater than that (&bgr;=0.24; P<0.001) in normotensive group, with P<0.001 for the difference in &bgr;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.

Race and Sex Differences of Long-Term Blood Pressure Profiles From Childhood and Adult Hypertension

This study aims to characterize longitudinal blood pressure (BP) trajectories from childhood in black–white and sex groups and examine the association between childhood level–independent trajectories of BP and adult hypertension. The longitudinal cohort consisted of 2732 adults who had body mass index and BP measured 4 to 15 times from childhood (4–19 years) to adulthood (20–51 years). Model-estimated levels and linear slopes of BP and body mass index at childhood age points were calculated at 1-year intervals using the growth curve parameters and their first derivatives, respectively. Linear and nonlinear curve parameters differed significantly between race–sex groups; BP levels showed race and sex differences 15 years of age onward. Hypertensives had higher long-term BP levels than normotensives in race–sex groups. Although linear and nonlinear slope parameters of BP were race and sex specific, they differed consistently, significantly between hypertension and normotension groups. BP trajectories during young adulthood (20–35 years) were significantly greater in hypertensives than in normotensives; however, the trajectories during middle-aged adulthood (36–51 years) were significantly smaller in hypertensives than in normotensives. Level-independent linear slopes of systolic BP showed significantly negative associations (odds ratio=0.50≈0.76; P<0.001) during prepuberty period (4–11 years) but significantly positive associations (odd ratio=1.44≈2.80, P<0.001) during the puberty period (13–19 years) with adult hypertension, adjusting for covariates. These associations were consistent across race–sex groups. These observations indicate that adult hypertension originates in childhood, with different longitudinal BP trajectory profiles during young and middle-aged adulthood in black–white and sex groups. Puberty is a crucial period for the development of hypertension in later life.

Long-term Excessive Body Weight and Adult Left Ventricular Hypertrophy Are Linked Through Later Life Body Size and Blood Pressure: The Bogalusa Heart Study

Rationale: Childhood adiposity is associated with cardiac structure in later life, but little is known regarding to what extent childhood body weight affects adult left ventricular geometric patterns through adult body size and blood pressure (BP). Objective: Determine quantitatively the mediation effect of adult body weight and BP on the association of childhood body mass index (BMI) with adult left ventricular (LV) hypertrophy. Methods and Results: This longitudinal study consisted of 710 adults, aged 26 to 48 years, who had been examined for BMI and BP measured ≥4× during childhood and ≥2× during adulthood, with a mean follow-up period of 28.0 years. After adjusting for age, race, and sex, adult BMI had a significant mediation effect (76.4%; P<0.01) on the childhood BMI–adult LV mass index association. The mediation effects of adult systolic BP (15.2%), long-term burden (12.1%), and increasing trends of systolic BP (7.9%) were all significant (P<0.01). Furthermore, these mediators also had significant mediation effects on the association of childhood BMI with adult LV hypertrophy, eccentric hypertrophy, and concentric hypertrophy. Importantly, the mediation effects of adult BMI were all significantly stronger than those of adult systolic BP on LV mass index, LV hypertrophy, and LV remodeling patterns (P<0.01). Additionally, the mediation effect of systolic BP on concentric hypertrophy was significantly stronger than that on eccentric hypertrophy (P<0.01). Conclusions: These findings suggest that increased childhood BMI has long-term adverse impact on subclinical changes in adult cardiac structure, and early life excessive body weight and adult LV hypertrophy are linked through later life excessive body weight and elevated BP.

Relationship Between Birth Weight and the Double Product in Childhood, Adolescence, and Adulthood (from the Bogalusa Heart Study)

Low birth weight is associated with cardiovascular disease and its risk factors, including heart rate and blood pressure. Therefore, we examined the hypothesis that birth weight is related to blood pressure-heart rate product (double product, DP), an index of oxygen consumption and workload of the heart, at different ages. Heart rate at rest, blood pressure at rest, and birth weight data were available in 2,340 children (4 to 11 years), 1,621 adolescents (12 to 19 years), and 2,315 adults (20 to 52 years) from the Bogalusa Heart Study (total n = 6,276). After adjustment for age, sex, race, and body mass index, gestational age-adjusted birth weight was inversely associated with DP, with per 100-g decrease in birth weight associated with an increase of 12.8, 22.9, and 23.2 beats/min × mmHg in DP in children (p = 0.016), adolescents (p = 0.0007), and adults (p = 0.0006), respectively. An amplifying trend of the association with age was observed in the total sample (p = 0.002). In conclusion, birth weight is associated with increased DP beginning in childhood, which may partly mediate the association between low birth weight and increased cardiovascular risk later in life.

Long-Term Excessive Body Weight and Adult Left Ventricular Hypertrophy Are Linked Through Later-Life Body Size and Blood PressureNovelty and Significance

Rationale: Childhood adiposity is associated with cardiac structure in later life, but little is known regarding to what extent childhood body weight affects adult left ventricular geometric patterns through adult body size and blood pressure (BP). Objective: Determine quantitatively the mediation effect of adult body weight and BP on the association of childhood body mass index (BMI) with adult left ventricular (LV) hypertrophy. Methods and Results: This longitudinal study consisted of 710 adults, aged 26 to 48 years, who had been examined for BMI and BP measured ≥4× during childhood and ≥2× during adulthood, with a mean follow-up period of 28.0 years. After adjusting for age, race, and sex, adult BMI had a significant mediation effect (76.4%; P<0.01) on the childhood BMI–adult LV mass index association. The mediation effects of adult systolic BP (15.2%), long-term burden (12.1%), and increasing trends of systolic BP (7.9%) were all significant (P<0.01). Furthermore, these mediators also had significant mediation effects on the association of childhood BMI with adult LV hypertrophy, eccentric hypertrophy, and concentric hypertrophy. Importantly, the mediation effects of adult BMI were all significantly stronger than those of adult systolic BP on LV mass index, LV hypertrophy, and LV remodeling patterns (P<0.01). Additionally, the mediation effect of systolic BP on concentric hypertrophy was significantly stronger than that on eccentric hypertrophy (P<0.01). Conclusions: These findings suggest that increased childhood BMI has long-term adverse impact on subclinical changes in adult cardiac structure, and early life excessive body weight and adult LV hypertrophy are linked through later life excessive body weight and elevated BP.

Long-Term Excessive Body Weight and Adult Left Ventricular Hypertrophy Are Linked Through Later-Life Body Size and Blood PressureNovelty and Significance: The Bogalusa Heart Study

Rationale: Childhood adiposity is associated with cardiac structure in later life, but little is known regarding to what extent childhood body weight affects adult left ventricular geometric patterns through adult body size and blood pressure (BP). Objective: Determine quantitatively the mediation effect of adult body weight and BP on the association of childhood body mass index (BMI) with adult left ventricular (LV) hypertrophy. Methods and Results: This longitudinal study consisted of 710 adults, aged 26 to 48 years, who had been examined for BMI and BP measured ≥4× during childhood and ≥2× during adulthood, with a mean follow-up period of 28.0 years. After adjusting for age, race, and sex, adult BMI had a significant mediation effect (76.4%; P<0.01) on the childhood BMI–adult LV mass index association. The mediation effects of adult systolic BP (15.2%), long-term burden (12.1%), and increasing trends of systolic BP (7.9%) were all significant (P<0.01). Furthermore, these mediators also had significant mediation effects on the association of childhood BMI with adult LV hypertrophy, eccentric hypertrophy, and concentric hypertrophy. Importantly, the mediation effects of adult BMI were all significantly stronger than those of adult systolic BP on LV mass index, LV hypertrophy, and LV remodeling patterns (P<0.01). Additionally, the mediation effect of systolic BP on concentric hypertrophy was significantly stronger than that on eccentric hypertrophy (P<0.01). Conclusions: These findings suggest that increased childhood BMI has long-term adverse impact on subclinical changes in adult cardiac structure, and early life excessive body weight and adult LV hypertrophy are linked through later life excessive body weight and elevated BP.

Long-Term Excessive Body Weight and Adult Left Ventricular Hypertrophy Are Linked Through Later-Life Body Size and Blood Pressure

Rationale: Childhood adiposity is associated with cardiac structure in later life, but little is known regarding to what extent childhood body weight affects adult left ventricular geometric patterns through adult body size and blood pressure (BP). Objective: Determine quantitatively the mediation effect of adult body weight and BP on the association of childhood body mass index (BMI) with adult left ventricular (LV) hypertrophy. Methods and Results: This longitudinal study consisted of 710 adults, aged 26 to 48 years, who had been examined for BMI and BP measured ≥4× during childhood and ≥2× during adulthood, with a mean follow-up period of 28.0 years. After adjusting for age, race, and sex, adult BMI had a significant mediation effect (76.4%; P<0.01) on the childhood BMI–adult LV mass index association. The mediation effects of adult systolic BP (15.2%), long-term burden (12.1%), and increasing trends of systolic BP (7.9%) were all significant (P<0.01). Furthermore, these mediators also had significant mediation effects on the association of childhood BMI with adult LV hypertrophy, eccentric hypertrophy, and concentric hypertrophy. Importantly, the mediation effects of adult BMI were all significantly stronger than those of adult systolic BP on LV mass index, LV hypertrophy, and LV remodeling patterns (P<0.01). Additionally, the mediation effect of systolic BP on concentric hypertrophy was significantly stronger than that on eccentric hypertrophy (P<0.01). Conclusions: These findings suggest that increased childhood BMI has long-term adverse impact on subclinical changes in adult cardiac structure, and early life excessive body weight and adult LV hypertrophy are linked through later life excessive body weight and elevated BP.