Evaluation of ethnic differences in cardiometabolic risk in children.

PURPOSE: In adults, cardiometabolic conditions manifest differently by ethnicity with South Asians particularly predisposed. Whether these differences arise in childhood remains narrowly explored. To address this evidence gap, we examined whether children of different ethnicities display differences in cardiometabolic risk (CMR). METHODS: A cross-sectional analysis was conducted among 5557 children (3-11 years). Multivariable linear regression models adjusted for age, sex, z-body mass index, and demographic factors were used to estimate differences in CMR outcomes between children with parents that self-reported European ancestry (reference group) and one of 13 other ethnicities (African, Arab, East Asian, Latin American, South Asian, Southeast Asian, Mixed Ethnicities, and Other). The primary outcome was a CMR score, calculated as the sum of age- and sex-standardized waist circumference, systolic blood pressure (SBP), glucose, log-triglycerides, and inverse high-density lipoprotein cholesterol (HDL-C), divided by √5. RESULTS: Lower mean CMR scores were observed among children with African (ß = -0.62, 95% CI: -0.92; -0.32) and East Asian (ß = -0.41, 95% CI: -0.68, -0.15) ancestry compared to children with European ancestry. Children with South Asian ancestry had higher SBP (ß = 2.25, 95% CI: 1.27, 3.22) and non-HDL-C (ß = 0.17, 95% CI: 0.07, 0.26) than children with European ancestry. CONCLUSIONS: Ethnic differences in CMR were observed in early and middle childhood.

Sugar-sweetened beverage consumption and weight gain in children and adults: a systematic review and meta-analysis of prospective cohort studies and randomized controlled trials.

BACKGROUND: Sugar-sweetened beverages (SSBs) have been implicated in fueling the obesity epidemic. OBJECTIVES: This study aimed to update a synthesis of the evidence on SSBs and weight gain in children and adults. METHODS: MEDLINE, Embase, and Cochrane databases were searched through September 8, 2022, for prospective cohort studies and randomized controlled trials (RCTs) that evaluated intake of SSBs in relation to BMI and body weight in children and adults, respectively. Eligible interventions were compared against a noncaloric control. Study-level estimates were pooled using random-effects meta-analysis and presented as ß-coefficients with 95% CIs for cohorts and weighted mean differences (MDs) with 95% CIs for RCTs. RESULTS: We identified 85 articles including 48 in children (40 cohorts, n = 91,713; 8 RCTs, n = 2783) and 37 in adults (21 cohorts, n = 448,661; 16 RCTs, n = 1343). Among cohort studies, each serving/day increase in SSB intake was associated with a 0.07-kg/m2 (95% CI: 0.04 kg/m2, 0.10 kg/m2) higher BMI in children and a 0.42-kg (95% CI: 0.26 kg, 0.58 kg) higher body weight in adults. RCTs in children indicated less BMI gain with SSB reduction interventions compared with control (MD: -0.21 kg/m2; 95% CI: -0.40 kg/m2, -0.01 kg/m2). In adults, randomization to addition of SSBs to the diet led to greater body weight gain (MD: 0.83 kg; 95% CI: 0.47 kg, 1.19 kg), and subtraction of SSBs led to weight loss (MD: -0.49 kg; 95% CI: -0.66 kg, -0.32 kg) compared with the control groups. A positive linear dose-response association between SSB consumption and weight gain was found in all outcomes assessed. CONCLUSIONS: Our updated systematic review and meta-analysis expands on prior evidence to confirm that SSB consumption promotes higher BMI and body weight in both children and adults, underscoring the importance of dietary guidance and public policy strategies to limit intake. This meta-analysis was registered at the International Prospective Register of Systematic Reviews as CRD42020209915.

An Update on the Epidemiology of Type 2 Diabetes: A Global Perspective.

Type 2 diabetes (T2D) is a public health burden associated with immense health care and societal costs, early death, and morbidity. Largely because of epidemiologic changes, including nutrition transitions, urbanization, and sedentary lifestyles, T2D is increasing in every region of the world, particularly in low-income and middle-income countries. This article highlights global trends in T2D and discusses the role of genes, early-life exposures, and lifestyle risk factors in the cause of T2D, with an emphasis on populations in current hotspots of the epidemic. It also considers potential impacts of the coronavirus disease 2019 pandemic and T2D prevention policies and action.

Recent Developments in Vascular Adventitial Pathobiology: The Dynamic Adventitia as a Complex Regulator of Vascular Disease.

The adventitia, the outer layer of the blood vessel wall, may be the most complex layer of the wall and may be the master regulator of wall physiology and pathobiology. This review proposes a major shift in thinking to apply a functional lens to the adventitia rather than only a structural lens. Human and experimental in vivo and in vitro studies show that the adventitia is a dynamic microenvironment in which adventitial and perivascular adipose tissue cells initiate and regulate important vascular functions in disease, especially intimal hyperplasia and atherosclerosis. Although well away from the blood-wall interface, where much pathology has been identified, the adventitia has a profound influence on the population of intimal and medial endothelial, macrophage, and smooth muscle cell function. Vascular injury and dysfunction of the perivascular adipose tissue promote expansion of the vasa vasorum, activation of fibroblasts, and differentiation of myofibroblasts. This regulates further biologic processes, including fibroblast and myofibroblast migration and proliferation, inflammation, immunity, stem cell activation and regulation, extracellular matrix remodeling, and angiogenesis. A debate exists as to whether the adventitia initiates disease or is just an important participant. We describe a mechanistic model of adventitial function that brings together current knowledge and guides the design of future investigations to test specific hypotheses on adventitial pathobiology.