Nutrition
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Oxidation of plasma cysteine/cystine (Cys/CySS) redox potential (E(h)CySS) has been associated with risk factors for cardiovascular disease in humans. Cys and CySS are derived from dietary sulfur amino acids (SAA), but the specific effects of SAA depletion and repletion on Cys/CySS redox indices are unknown. The present study examined the effect of dietary SAA intake level on free Cys, free CySS, and E(h)CySS in human plasma under fasting conditions. ⋯ These results show that free Cys and Cys/CySS redox potential (E(h)CySS) in fasting plasma are affected by dietary SAA intake level in humans. Significant changes occur slowly over 4 d with insufficient SAA intake, but rapidly (after 1 d) with repletion.
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We investigated the availability of healthier food choices and whether a healthier diet costs more than a diet commonly eaten by low-income families in South Africa. ⋯ Healthier food choices are, in general, considerably more expensive than commonly consumed foods. As a result, a healthy diet is unaffordable for the large majority of the population.
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To estimate the efficacy of iron supplementation in anemic pregnant women on the basis of occurrence of pregnancy complications and birth outcomes. ⋯ A higher rate of preterm birth was found in anemic pregnant women without iron treatment but this adverse birth outcome was prevented with iron supplementation. There was no higher rate of congenital abnormalities in the offspring of anemic pregnant women supplemented with iron and/or folic acid supplements.
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Clinical Trial
Outcome of a hospital based multidisciplinary weight loss program in obese Filipino children.
Childhood obesity is becoming a problem for Filipino children with an increasing national prevalence of pediatric overweight and obesity. A multidisciplinary approach combining behavioral therapy with diet and exercise is often advocated as having the greatest impact in pediatric weight management. ⋯ The use of a multidisciplinary 3-mo staged program resulted in an effective weight loss in obese Filipino children, which was directly related to the frequency of sessions attended.
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Lower brain glucose metabolism is present before the onset of clinically measurable cognitive decline in two groups of people at risk of Alzheimer's disease--carriers of apolipoprotein E4, and in those with a maternal family history of AD. Supported by emerging evidence from in vitro and animal studies, these reports suggest that brain hypometabolism may precede and therefore contribute to the neuropathologic cascade leading to cognitive decline in AD. The reason brain hypometabolism develops is unclear but may include defects in brain glucose transport, disrupted glycolysis, and/or impaired mitochondrial function. ⋯ Nevertheless, aging appears to increase the risk of deteriorating systemic control of glucose utilization, which, in turn, may increase the risk of declining brain glucose uptake, at least in some brain regions. A contributing role of deteriorating glucose availability to or metabolism by the brain in AD does not exclude the opposite effect, i.e., that neurodegenerative processes in AD further decrease brain glucose metabolism because of reduced synaptic functionality and hence reduced energy needs, thereby completing a vicious cycle. Strategies to reduce the risk of AD by breaking this cycle should aim to (1) improve insulin sensitivity by improving systemic glucose utilization, or (2) bypass deteriorating brain glucose metabolism using approaches that safely induce mild, sustainable ketonemia.