Division of Pediatric Endocrinology, Department of Pediatrics, University of Virginia, Charlottesville, Virginia, USA Institute of Biomedicine, Federal University of Ceará, Fortaleza, Ceará, Brazil Division of Developmental & Behavioral Pediatrics, Department of Pediatrics, University of Virginia, Charlottesville, Virginia, USA, and the Center for Global Health, University of Virginia, Charlottesville, Virginia, USA Division of Pediatric Gastroenterology, Hepatology & Nutrition, Department of Pediatrics, Cincinnati Children's Hospital Medical Center, University of Cincinnati, Cincinnati, Ohio, USA Division of Cardiovascular Medicine, Department of Medicine, University of Virginia, Charlottesville, Virginia, USA.
Hypotheses regarding the developmental origins of health and disease postulate that developing fetuses - and potentially young children - undergo adaptive epigenetic changes that have longstanding effects on metabolism and other processes. Ongoing research explores whether these adaptations occur during early life following early childhood malnutrition. In the developing world, there remains a high degree of nutritional stunting, defined as linear growth failure caused by inadequate caloric intake, which may be exacerbated by inflammation from ongoing infections. In areas with poor sanitation, children experience vicious cycles of enteric infections and malnutrition, resulting in poor nutrient absorption as a result of changes in the intestinal mucosa, now termed "environmental enteropathy." Emerging evidence links early childhood diarrhea and/or growth failure with an increased occurrence of risk factors for cardiovascular disease in later life, including dyslipidemia, hypertension, and glucose intolerance. The mechanisms for these associations remain poorly understood and may relate to epigenetic responses to poor nutrition, increased inflammation, or both. Given the increased incidence of cardiovascular disease in developing areas of the world, associations between childhood malnutrition, early-life infections, and the increased occurrence of risk factors for cardiovascular disease underscore further reasons to improve nutrition and infection-related outcomes for young children worldwide.
"American Journal of Human Biology b-cells, resulting in decreased insulin production. Alternatively , pro-inflammatory consequences (e.g., increase in tumor necrosis factor) of repeated infections and/or chronic stress during childhood might lead to insulin resistance and thereby increase risk for type 2 diabetes (DeBoer et al., 2012). The Dutch Famine Study demonstrated that even a short period of moderate or severe undernutrition during the postnatal period can increase risk for diabetes (van Abeelen et al., 2012). "
"We hypothesize that exposure to environmental pathogens, measured through household sanitation and individual illness history, will be associated with acute elevations in CRP. Further, we would expect to see this pattern more strongly in children and adolescents with higher exposures in rural areas, since children tend to be more vulnerable to environmental pathogens (DeBoer et al. 2012). Second, we hypothesize that moderate elevations in CRP will be associated with obesogenic exposures, such as high BMI and waist circumference, that are increasingly common among adults living in urban areas. "
[Show abstract][Hide abstract] ABSTRACT: Malnutrition below 5 years remains a global health issue. Severe acute malnutrition (SAM) presents in childhood as oedematous (kwashiorkor) or nonoedematous (marasmic) forms, with unknown long-term cardiovascular consequences. We hypothesized that cardiovascular structure and function would be poorer in SAM survivors than unexposed controls. We studied 116 adult SAM survivors, 54 after marasmus, 62 kwashiorkor, and 45 age/sex/body mass index-matched community controls who had standardized anthropometry, blood pressure, echocardiography, and arterial tonometry performed. Left ventricular indices and outflow tract diameter, carotid parameters, and pulse wave velocity were measured, with systemic vascular resistance calculated. All were expressed as SD scores. Mean (SD) age was 28.8±7.8 years (55% men). Adjusting for age, sex, height, and weight, SAM survivors had mean (SE) reductions for left ventricular outflow tract diameter of 0.67 (0.16; P<0.001), stroke volume 0.44 (0.17; P=0.009), cardiac output 0.5 (0.16; P=0.001), and pulse wave velocity 0.32 (0.15; P=0.03) compared with controls but higher diastolic blood pressures (by 4.3; 1.2-7.3 mm Hg; P=0.007). Systemic vascular resistance was higher in marasmus and kwashiorkor survivors (30.2 [1.2] and 30.8 [1.1], respectively) than controls 25.3 (0.8), overall difference 5.5 (95% confidence interval, 2.8-8.4 mm Hg min/L; P<0.0001). No evidence of large vessel or cardiac remodeling was found, except closer relationships between these indices in former marasmic survivors. Other parameters did not differ between SAM survivor groups. We conclude that adult SAM survivors had smaller outflow tracts and cardiac output when compared with controls, yet markedly elevated peripheral resistance. Malnutrition survivors are thus likely to develop excess hypertension in later life, especially when exposed to obesity.
Artery Research 12/2012; 6(4):144. DOI:10.1016/j.artres.2012.09.016
Seok Hui Kang, Da Jung Jung, Kyu Yup Lee, Eun Woo Choi, Jun Young Do,
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.