National Trends in Beverage Consumption in Children from Birth to 5 Years: Analysis of NHANES Across Three Decades

Abstract

The association of obesity with noncommunicable diseases, such as cardiovascular complications and diabetes, is considered a major threat to the management of health care worldwide. Epidemiological findings show that childhood obesity is rapidly rising in Western society, as well as in developing countries. This pandemic is not without consequences and can affect the risk of future cardiovascular disease in these children. Childhood obesity is associated with endothelial dysfunction, the first yet still reversible step towards atherosclerosis. Advanced research techniques have added further insight on how childhood obesity and associated comorbidities lead to endothelial dysfunction. Techniques used to measure endothelial function were further brought to perfection, and novel biomarkers, including endothelial progenitor cells, were discovered. The aim of this paper is to provide a critical overview on both in vivo as well as in vitro markers for endothelial integrity. Additionally, an in-depth description of the mechanisms that disrupt the delicate balance between endothelial damage and repair will be given. Finally, the effects of lifestyle interventions and pharmacotherapy on endothelial dysfunction will be reviewed.

Diet, Exercise, and Endothelial Function in Obese Adolescents

“…Endothelial function is negatively affected by both traditional cardiovascular risk factors, such as hypertension and sedentary lifestyle, and novel cardiovascular risk factors, including inflammatory (eg, high C-reactive protein) and antiinflammatory markers (eg, low adiponectin). 5 Macrovascular endothelial function in obese adolescents, assessed using flow-mediated dilation, can be improved by exercise training 6 and diet, 7 and combining both induces the greatest improvements. 8 However, whether lifestyle interventions are also capable of reversing endothelial dysfunction at the microvascular level is currently not clear.…”

Childhood obesity–related endothelial dysfunction: an update on pathophysiological mechanisms and diagnostic advancements

“…Elevated LDL cholesterol is often seen in obese adults but is rarely observed in obese children (19). Therefore, the focus of attention has recently shifted toward HDL cholesterol.…”

“…Risk factors in obese children include not only classical cardiovascular risk factors such as hypertension (19) but also newly discovered cytokines and signaling molecules including micro RNA (miRNAs). The impact of these factors has been demonstrated in clinical and fundamental studies, and below we discuss the latest data in this field.…”

Cardiovascular Risk in Patients with Non-alcoholic Fatty Liver Disease

“…The Korean Journal of Gastroenterology 34,35 Portal hypertension affecting the systemic vascular resistance Metalloproteinase 38 Decreased elastic fiber and increased collagen in media of the large arteries increased arterial stiffness VEGF [39][40][41][42] Instability of atheroma 43,44 HMGB-1 45 Involving in Systemic inflammation and angiogenesis Dysfunction of endothelial cells ADMA 47 Increased arterial wall stiffness EMPs 48,49 Increased EMPs which are products of endothelial destruction Endothelial progenitor cell 48,49 Decreased endothelial progenitor cells which indicating endothelial repair function Inflammation and cytokine IL-1b 50 , IL-6 51,52 hs-CRP, TNF-a, CCL3, sICAM-1 51,53 Inflammation markers increased in NAFLD Homocysteine and inflammation Hyperhomocysteinemia [58][59][60] Oxidative stress, Decreased NO synthesis, Involving hepatic fibrosis Hepatokine and insulin resistance FetA 65 Increased inflammatory cytokine and insulin resistance and decreased adiponectin 65 Decreased vascular calcification by inhibiting TGF-β1signal pathway 65 FGF-21 [66][67][68] Increased level of FGF-21 for compensating insulin resistance in NAFLD SeP 69,70 Involving in Insulin resistance, hs-CRP, increased intimal thickness of carotid artery Lipid profiles TG, LDL, small dense LDL particles (LDL3, LDL4) 73 Increased in NAFLD, contributing to atherogenesis HDL 72 A defending factor of atherogenesis, but decrease in NAFLD. oxLDL 77 Contributing to oxidative stress in NASH and hepatic fibrosis Coagulation factors Factor 8, 9, 10, 12 78 Increased in NAFLD PAI-1 79,80 Increa...…”