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Background: Evidence suggests that asthma and obesity may share a common pathway, possibly through an increase in inflammation. Sedentary time is thought to promote both inflammation and obesity and previous studies have found a relationship between self-reported sedentary and asthma. However, the relationship between objectively measured sedentary time and asthma is not well described. We hypothesized that the association between asthma and sedentary time would not be present when physical activity was measured objectively, nor would objectively-measured sedentary time play an important role in the relationship between asthma and obesity., Objective: To determine if there is an association between asthma and objectively measured sedentary time in a large, nationally representative sample of the United States youth., Methods: Using the National Health and Nutrition Examination Survey 2003-2006, we assessed the relationship between asthma and sedentary time using objectively measured and self-reported measures of sedentary time, in 6-19 years-old subjects with available accelerometry data. We used multivariate logistic regression analysis to determine associations between the risk of asthma and sedentary time controlling for accelerometer wear time, gender, age, race/ethnicity, body mass index percentile, and moderate-to-vigorous physical activity (MVPA)., Results: In this cohort, youth with asthma self-reported more time in sedentary behavior, specifically computer time, than those without asthma (p = 0.01). However, when sedentary time was measured objectively by accelerometry, sedentary time did not differ between youth with and without asthma (421 min [standard deviation 4.2] versus. 414 min [standard deviation 7.8] [p = 0.38]). Controlling for measures of activity, such as MVPA, or time spent in long versus short bouts of sedentary time did not modify our results., Conclusions: Differences in sedentary time by self-report between those with and without asthma were not born out by examining sedentary time using objective measures. Further work is necessary to examine the complex interaction among inactivity, obesity, and asthma over time, specifically focusing on whether the type of sedentary activity (e.g., computer vs. television time) is important., (© 2023 Wiley Periodicals LLC.)

Objective: This study aimed to determine the relation of maternal prepregnancy weight with offspring BMI across adulthood from almost 40 years of follow-up., Methods: BMI was measured in Framingham Heart Study Offspring cohort participants between 1971 and 2008. The association of maternal prepregnancy weight category (ascertained via direct measure and questionnaire) with serial offspring BMI, overweight, obesity, and change in BMI over time was tested, adjusted for age, sex, and a BMI genetic risk score; secondary models additionally adjusted for physical activity, dietary factors, smoking, education, and familial relatedness., Results: Among 863 participants at initial assessment (83 exposed and 780 controls), mean (SD) age was 33 (10) years, 53% were female, and mean BMI was 24.5 (4.1) kg/m 2 . Exposed offspring BMI was higher at every examination cycle, ranging from 1.5 (0.5) to 3.0 (0.5) kg/m 2 (P < 0.001), with larger differences at later assessments. The rate of increase in offspring BMI over time was higher in exposed offspring before the age of 50 years (β [SE] = 0.07 [0.02] kg/m 2 per year; P = 0.004) but not after the age of 50 years (-0.05 [0.04] kg/m 2 per year; P = 0.2)., Conclusions: Maternal prepregnancy weight is associated with greater offspring BMI throughout adulthood, with more rapid weight acceleration in early and midadulthood., (© 2018 The Obesity Society.)

Background: Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a key regulator of low-density lipoprotein cholesterol and cardiovascular disease risk, and is an emerging therapeutic target., Objective: We compared serum PCSK9 levels in young adults, with and without type 2 diabetes., Subjects and Methods: Cross-sectional analysis was conducted in a cohort, aged 15 to 26 years, in Cincinnati, OH, from 2005 to 2010. Serum PCSK9 levels were measured in 94 youth with type 2 diabetes, 93 obese control subjects, and 99 lean control subjects. Correlative analyses were conducted to determine significant covariates of PCSK9 by group and sex, and multivariate linear regression models were used to study the independent determinants of PCSK9., Results: In females, PCSK9 levels were significantly increased in the obese and type 2 diabetes subjects relative to the lean controls (P < .01). Moreover, PCSK9 was positively correlated with multiple metabolic parameters in females: body mass index, systolic blood pressure, fasting glucose, fasting insulin, and C-reactive protein levels (P ≤ .02). In males, PCSK9 levels were decreased overall compared with females (P = .03), and did not differ between the lean, obese, or type 2 diabetes groups., Conclusions: Obesity and type 2 diabetes were associated with significantly higher levels of PCSK9 in young women, but not in young men. These data suggest that sex could modify the effects of obesity and diabetes on PCSK9 in young adults., (© 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Leptin treatment has beneficial effects on plasma lipids in patients with lipodystrophy, but the underlying mechanism is unknown. Proprotein convertase subtilisin/kexin type 9 (PCSK9) decreases low-density lipoprotein (LDL) clearance, promotes hypercholesterolemia, and has recently emerged as a novel therapeutic target. To determine the effect of leptin on PCSK9, we treated male and female ob/ob mice with leptin for 4 days via sc osmotic pumps (∼24 μg/d). Leptin reduced body weight and food intake in all mice, but the effects of leptin on plasma PCSK9 and lipids differed markedly between the sexes. In male mice, leptin suppressed PCSK9 but had no effect on plasma triglycerides or cholesterol. In female mice, leptin suppressed plasma triglycerides and cholesterol but had no effect on plasma PCSK9. In parallel, we treated female lipodystrophic patients (8 females, ages 5-23 y) with sc metreleptin injections (∼4.4 mg/d) for 4-6 months. In this case, leptin reduced plasma PCSK9 by 26% (298 ± 109 vs 221 ± 102 ng/mL; n = 8; P = .008), and the change in PCSK9 was correlated with a decrease in LDL cholesterol (r(2) = 0.564, P = .03). In summary, in leptin-deficient ob/ob mice, the effects of leptin on PCSK9 and plasma lipids appeared to be independent of one another and strongly modified by sex. On the other hand, in lipodystrophic females, leptin treatment reduced plasma PCSK9 in parallel with LDL cholesterol.

Background: Somatic growth in childhood is accompanied by substantial remodeling of the aorta. Obesity is associated with increased aortic stiffness and flow and may interfere with aortic remodeling during growth. Wide pulse pressure (PP) indicates mismatch between aortic impedance and pulsatile flow and increases risk for future systolic hypertension and cardiovascular disease (CVD). We hypothesized that the rise of pediatric obesity would be associated with a temporal trend to higher PP., Methods and Results: We analyzed demographic, anthropometric, and blood pressure (BP) data for 8- to 17-year-old children (N=16 457) from the cross-sectional National Health and Nutrition Examination Surveys (NHANES) for 1976 through 2008. Multivariable adjusted survey regression was used to examine temporal trends in PP and mean arterial pressure (MAP) and the relation to obesity. Across this period, unadjusted PP was higher (0.29 mm Hg/y, 95% CI 0.26 to 0.33 mm Hg/y; P<0.0001), while MAP was lower (-0.24 mm Hg/y, 95% CI -0.27 to -0.20 mm Hg/y; P<0.0001) across examinations. Adjusting for body mass index partially attenuated the temporal trend for PP by 32% (P<0.0001). Obesity amplified the relation between taller height and higher PP (from 0.23 [95% CI 0.19 to 0.28] to 0.27 [95% CI 0.21 to 0.34] mm Hg/cm height in boys and from 0.08 [95% CI 0.04 to 0.13] to 0.22 [95% CI 0.13 to 0.31] mm Hg/cm height in girls; P<0.01 for both)., Conclusions: PP has increased during the rise of pediatric obesity. Higher PP may indicate mismatch between aortic diameter, wall stiffness, and flow in obese children during a period of rapid somatic growth when the aorta is already under considerable remodeling stress.

Background: As the prevalence of adiposity soars in both developed and developing nations, appreciation of the close links between obesity and disease increases. The strong relationships between excess adipose tissue and poor health outcomes, including cardiovascular disease, diabetes, and cancer, mandate elucidation of the complex cellular, hormonal, and molecular pathophysiology whereby adiposity initiates and maintains adverse health effects., Content: In this report we review adipocyte metabolism and function in the context of energy imbalance and postprandial nutrient excess, including adipocyte hypertrophy and hyperplasia, adipocyte dysfunction, and other systemic consequences. We also discuss implications for laboratory evaluation and clinical care, including the role of lifestyle modifications. Chronic energy imbalance produces adipocyte hypertrophy and hyperplasia, endoplasmic reticulum stress, and mitochondrial dysfunction. These processes lead to increased intracellular and systemic release of adipokines, free fatty acids, and inflammatory mediators that cause adipocyte dysfunction and induce adverse effects in the liver, pancreatic beta-cells, and skeletal muscle as well as the heart and vascular beds. Several specialized laboratory tests can quantify these processes and predict clinical risk, but translation to the clinical setting is premature. Current and future pharmacologic interventions may target these pathways; modest changes in diet, physical activity, weight, and smoking are likely to have the greatest impact., Summary: Adipocyte endoplasmic reticulum and mitochondrial stress, and associated changes in circulating adipokines, free fatty acids, and inflammatory mediators, are central to adverse health effects of adiposity. Future investigation should focus on these pathways and on reversing the adverse lifestyle behaviors that are the fundamental causes of adiposity.

Objectives: Obesity may pose additional cardiovascular risk to children with acquired and congenital heart disease. Many children with heart disease are sedentary as a result of physician-, parent-, and/or self-imposed restrictions. The aim of this study was to evaluate the impact of the epidemic of obesity on children with heart disease., Patients and Methods: A cross-sectional review was performed of children evaluated in 2004 at 2 cardiology outpatient clinics. Differences in the prevalence of obese (BMI > or = 95%) and overweight (BMI 85%-95%) children were compared with national data and healthy control subjects. Dictated letters were reviewed to determine whether obesity was discussed with referring practitioners., Results: Of 2921 patients assessed, 1523 had heart disease. Diagnostic subgroups included "mild" heart disease (n = 401), arrhythmia (n = 447), biventricular repair (n = 511), univentricular palliation (Fontan; n = 108), and heart transplantation (n = 56). More than 25% of the patients with heart disease were obese or overweight; the prevalence of obese and overweight children was significantly lower only in the Fontan group (15.9%). Pediatric cardiologists failed to document obesity or weight counseling in the majority of clinic letters., Conclusions: Obesity is common in children with congenital and acquired heart disease. Pediatric cardiologists demonstrate inadequate communication regarding this problem to referring practitioners. Healthy-lifestyle counseling and routine exercise in children with heart disease may be underemphasized.

Childhood and adolescence provide a unique window of opportunity to prevent atherosclerotic cardiovascular disease later in life, especially for pediatric groups at risk. The growing list of pediatric groups at risk includes individuals with chronic inflammatory disorders, organ transplants, familial hypercholesterolemia, endocrine disorders, childhood cancer, chronic kidney diseases, congenital heart diseases, and premature birth, as well as increasing numbers of children and adolescents with traditional risk factors such as obesity, hypertension, hyperlipidemia, and hyperglycemia. Here, we focus on recent advances in cardiovascular risk assessment and management and their implications for pediatric practice. First, hyperlipidemia and hyperglycemia are highly prevalent in the young, with hyperlipidemia occurring in 14.6% and hyperglycemia in 16.4% of children and adolescents with a normal weight. Implementation of nonfasting lipid and glycated hemoglobin screening in youth at risk is emerging as a promising avenue to improve testing compliance and lipid and glucose management. Second, blood pressure, lipid, and glucose management in youth at risk are reviewed in depth. Third, multisite and multimodal assessment of early atherosclerosis is discussed as a way to capture the complexity of atherosclerosis as a systemic disease. In addition to conventional carotid intima-media thickness measurements, the measurement of aortic pulse wave velocity and peripheral arterial tonometry can advance the assessment of early atherosclerosis in pediatrics. Finally, we make a plea for lifetime atherosclerotic cardiovascular disease risk stratification that integrates disease-associated risk factors and traditional risk factors and could facilitate tailored cardiovascular risk management in growing numbers of children and adolescents at risk. [ABSTRACT FROM AUTHOR]

Objective: Insulin resistance (IR) is a hallmark of obesity and metabolic disease. Circulating extracellular RNAs (ex-RNAs), stable RNA molecules in plasma, may play a role in IR, though most studies on ex-RNAs in IR are small. We sought to characterize the relationship between ex-RNAs and metabolic phenotypes in a large community-based human cohort.Research Design and Methods: We measured circulating plasma ex-RNAs in 2,317 participants without diabetes in the Framingham Heart Study (FHS) Offspring Cohort at cycle 8 and defined associations between ex-RNAs and IR (measured by circulating insulin level). We measured association between candidate ex-RNAs and markers of adiposity. Sensitivity analyses included individuals with diabetes. In a separate cohort of 90 overweight/obese youth, we measured selected ex-RNAs and metabolites. Biology of candidate microRNAs was investigated in silico.Results: The mean age of FHS participants was 65.8 years (56% female), with average BMI 27.7 kg/m2; participants in the youth cohort had a mean age of 15.5 years (60% female), with mean BMI 33.8 kg/m2. In age-, sex-, and BMI-adjusted models across 391 ex-RNAs in FHS, 18 ex-RNAs were associated with IR (of which 16 were microRNAs). miR-122 was associated with IR and regional adiposity in adults and IR in children (independent of metabolites). Pathway analysis revealed metabolic regulatory roles for miR-122, including regulation of IR pathways (AMPK, target of rapamycin signaling, and mitogen-activated protein kinase).Conclusions: These results provide translational evidence in support of an important role of ex-RNAs as novel circulating factors implicated in IR. [ABSTRACT FROM AUTHOR]

Background: Lower socioeconomic status has been associated with adverse lipid levels in adult populations. Childhood dyslipidemia is a risk factor for future cardiovascular disease. However, studies examining relationships between socioeconomic indicators and lipid levels in children are limited. To examine the relationship between income level and lipid levels in childhood. Methods: We conducted a retrospective chart review of primary care patients, ages 2 to 18 years, who had lipid levels drawn at two large pediatric practices in Boston, MA between August 01, 2008 and August 31, 2010. Income level was determined using geocoding census tract data. Analysis was performed using t-test, Anova and Spearman correlation coefficients. BMI percentile, age, sex, race/ethnicity, and site were adjusted for on multivariate analyses. Results: Reviewing 930 charts of patients with measured lipid levels, 730 had a valid address, no previously diagnosed lipid disorder and met other study eligibility criteria. Mean total cholesterol level did not vary by income level (low 155. 5 mg/dl ±26.9, moderate 153.5 mg/dl ±30.4, middle 155.3 mg/dl ±26.6 and high income 155.5 mg/dl ±27.9; p =.87)on multivariate analysis. Income level was not related to LDL, HDL, or triglycerides. Conclusions: In this analysis of children cared for in two urban pediatric primary practices, there was no association between income level determined by census tract and lipid levels in childhood. If confirmed in prospective investigations in other geographical locations, income level may not be a key driver of childhood lipid levels. [ABSTRACT FROM AUTHOR]

The rapid increase in the prevalence and severity of obesity in children is likely to lower the age of onset and increase the incidence of cardiovascular disease worldwide. Understanding the pathophysiology and improving the clinical management of cardiovascular disease involve a knowledge of novel risk factors and biomarkers. The clinical and mechanistic roles of these novel biological factors during childhood are currently being investigated. The goals of this scientific statement are to present the existing knowledge and theoretical framework of nontraditional risk factors for cardiovascular disease as they relate to children and adolescents, to describe the relevance and weight of available experimental and clinical evidence and the therapeutic implications pertaining to nontraditional risk factors in the pediatric population, and to stimulate further research with a goal of developing valid and reliable approaches to identify and validate novel risk factors that will aid in the clinical evaluation and perhaps prediction of cardiovascular disease in the pediatric population. Although several biomarkers are promising, substantial research is required before nontraditional risk factors can be used to identify and reduce cardiovascular disease risk in children and adolescents. [ABSTRACT FROM AUTHOR]

The epidemic in childhood obesity is a driving force behind the increase in paediatric metabolic syndrome, a collection of abnormalities that is associated in adults with increased risk for cardiovascular disease and type 2 diabetes mellitus. Although there is no clear consensus about the paediatric definition for metabolic syndrome, the prevalence of this syndrome is clearly rising. Children with metabolic syndrome are at increased risk for metabolic syndrome in adulthood. A late consequence of metabolic syndrome is type 2 diabetes, which increasingly affects adolescents. The rise in metabolic syndrome and type 2 diabetes in children is almost sure to lead to an increase in associated complications in young adulthood, including early cardiovascular disease. This epidemic will bear fruit in forthcoming decades, putting further stress on the healthcare system and probably leading to increased morbidity and a shorter lifespan for future generations. [ABSTRACT FROM PUBLISHER]

Background: Childhood obesity is a significant risk factor for cardiovascular disease in adulthood. Although ventricular remodeling has been reported in obese youth, early tissue‐level markers within the myocardium that precede organ‐level alterations have not been described. Methods and Results: We studied 21 obese adolescents (mean age, 17.7±2.6 years; mean body mass index [BMI], 41.9±9.5 kg/m2, including 11 patients with type 2 diabetes [T2D]) and 12 healthy volunteers (age, 15.1±4.5 years; BMI, 20.1±3.5 kg/m2) using biomarkers of cardiometabolic risk and cardiac magnetic resonance imaging (CMR) to phenotype cardiac structure, function, and interstitial matrix remodeling by standard techniques. Although left ventricular ejection fraction and left atrial volumes were similar in healthy volunteers and obese patients (and within normal body size‐adjusted limits), interstitial matrix expansion by CMR extracellular volume fraction (ECV) was significantly different between healthy volunteers (median, 0.264; interquartile range [IQR], 0.253 to 0.271), obese adolescents without T2D (median, 0.328; IQR, 0.278 to 0.345), and obese adolescents with T2D (median, 0.376; IQR, 0.336 to 0.407; P=0.0001). ECV was associated with BMI for the entire population (r=0.58, P<0.001) and with high‐sensitivity C‐reactive protein (r=0.47, P<0.05), serum triglycerides (r=0.51, P<0.05), and hemoglobin A1c (r=0.76, P<0.0001) in the obese stratum. Conclusions: Obese adolescents (particularly those with T2D) have subclinical alterations in myocardial tissue architecture associated with inflammation and insulin resistance. These alterations precede significant left ventricular hypertrophy or decreased cardiac function.

Background: Payer-type (government-sponsored health coverage versus private health insurance) has been shown to influence a variety of cardiovascular disease outcomes in adults. However, it is unclear if the payer-type impacts the response to a lifestyle intervention in children with dyslipidemia.Methods: We analyzed data prospectively collected from patients under the age of 25 years who were referred to a large regional preventive cardiology clinic from 2010 to 2016 in Massachusetts. We compared baseline high density lipoprotein cholesterol (HDL-C), triglycerides (TG), non-HDL-C, and low density lipoprotein cholesterol (LDL-C) by payer-type. Further, we analyzed the change in lipid values in response to a clinic-based multidisciplinary intervention over a nearly six-year period by payer-type with multi-variable adjusted linear regression models. We also tested for effect modifications by age, sex, race, and body mass index (BMI) category.Results: Of the 1739 eligible patients (mean age 13 years, 52% female, 60% overweight and obese, 59% White), we found that patients with government-sponsored coverage (n = 354, 20%) presented to referral lipid clinic with lower HDL-C (- 3.5 mg/dL [1.0], p < 0.001) and higher natural log-transformed TG (+ 0.14 [0.04], p < 0.001) as compared to those with private insurance; however, the association was attenuated to the null after additionally adjusting for BMI category (- 1.1 [0.9], p = 0.13, and + 0.05 [0.04], p = 0.2 for HDL-C and natural log-transformed TG, respectively). We found no difference in baseline LDL-C between payer-types (+ 3.4 mg/dL [3.0], p = 0.3). However, longitudinally, we found patients with private insurance and a self-reported race of White to have a clinically meaningful additional improvement in LDL-C, decreasing 12.8 (5.5) mg/dL (p = 0.02) between baseline and first follow-up, as compared to White patients with government-sponsored health coverage, after adjusting for age, sex, time between visits, and baseline LDL-C.Conclusions: Our results suggest that youth with government-sponsored coverage are referred with poorer lipid profiles than those with private insurance, although this is largely explained by higher rates of overweight and obesity in the government-sponsored health coverage group. White patients with private insurance had substantially better improvement in LDL-C longitudinally, suggesting that higher socioeconomic status facilitates improvement in LDL-C, but is less beneficial for HDL-C and triglyceride levels. [ABSTRACT FROM AUTHOR]

The article presents the authors' comments on the study, titled "Impact of lipid measurements in youth in addition to conventional clinic-based risk factors on predicting preclinical atherosclerosis in adulthood: International Childhood Cardiovascular Cohort Consortium," by J. Koskinen and colleagues, in the current issue. The authors comment that the findings underscore obesity, hypertension, and dyslipidemia as key risk factors in childhood of high carotid intima media thickness (cIMT).

The article presents a summary of the updates made to the Heart Disease and Stroke Statistical Update in 2016 outlined by the nonprofit organization American Heart Association (AHA). Updates include the cardiovascular health behaviors of the U.S. children and adults, the development of effective approaches towards the improvement of cardiovascular health and health behaviors including tobacco use, physical inactivity and obesity.

Background: Excess adipose tissue is associated with abnormal lipids, glucose, blood pressure, and inflammatory factors. In children, body mass index percentiles (BMI%) are commonly used to define adiposity. Although waist circumference percentiles (WC%) have not been universally accepted, they may better reflect visceral fat. The objective of this study was to determine the relationship between BMI% and WC% in identifying risk factor patterns in children at risk for developing cardiovascular disease. Methods: Children (8-19y free of major disorders and medications) with obesity, hypertension, lipid disorders, and/or a family history of premature cardiovascular disease (< 55 years in male and <65 years in female first-degree relatives) were recruited from the Preventive Cardiology clinic at Boston Children's Hospital (n=150). Lifestyle (physical activity, screen time, tobacco exposure), anthropomorphic (height, weight, WC) and blood pressure (SBP, DBP) measures were made, as well as fasting lipids (total cholesterol, HDL, triglycerides (TG), LDL, VLDL) and inflammatory markers (hs-CRP, ICAM-1, P-selectin, and TNFaR2) from a serum sample. Principal component analysis (PCA) with varimax rotation was used to identify independent patterns explaining risk factor variance. Quintiles of pattern scores were associated with BMI% and WC% using multiple linear regression. Results: PCA identified 4 patterns: lipid (low HDL, high TG and LDL), inflammatory (high ICAM and TNFaR2), blood pressure (high SBP and DBP) and Lp(a) [high Lp(a)]. BMI% was significantly associated with higher levels of the lipid and blood pressure patterns (p<0.03), explaining 15.8% and 4.7% of variance (partial r2) respectively. A higher WC% was associated with significantly higher levels of the lipid pattern (p<0.001), explaining 16.2% of variance. When both BMI% and WC% were used together, neither BMI% nor WC% remained associated with the lipid pattern;, however, BMI% was inversely associated (p=0.02) and WC% positively associated (p=0.01) with the inflammatory pattern. The combined use of BMI and WC explained 12.2% of variance in the inflammatory pattern. Conclusion: In a sample of high-risk children, BMI% or WC% explained similar variance in lipid levels; however, the combined use of BMI% (representing lean body mass) and WC% (representing abdominal fat) together explained greater variance in elevated inflammatory factors than either alone. This suggests that using WC% along with BMI% may contribute to cardiovascular risk assessments of high-risk children. [ABSTRACT FROM AUTHOR]