Measurement Tools of Pediatric Nutrition and Health Suitable or Adaptable for Low- and Middle-Income Countries in Field Research Settings

Background: Micronutrient status, body composition, gastrointestinal (GI) functioning, and neurological functioning are important facets of pediatric nutrition and health. When studied in low- and middle-income countries (LMIC), information about these elements is usually obtained via standardized surveys and traditional anthropometry. While convenient, these evaluations offer limited information that may be prone to error and bias. However, a variety of underutilized objective measurement tools exist which can promote a more objective, comprehensive, and deeper understanding of these aspects of pediatric nutrition and health in LMIC. Objective: Identify field-friendly, relatively low-cost, and portable tools that provide objective measurements of micronutrient status, body composition, GI functioning, and neurological functioning in young children. Methods: A narrative review of the literature was conducted to assess the state-of-the-art field-friendly research tools targeting micronutrient status, body composition, GI functioning, and neurological functioning in children in LMIC. Results: A number of field-friendly tools addressing the domains of micronutrient status, GI health, body composition, and neurological functioning were identified. While many tools remain to be fully validated, these tools have yet to be used to their full potential in field-based pediatric nutrition and health research in LMICs. Conclusions: More robust, field-friendly assessment methods will help to refine knowledge on the state of pediatric health of vulnerable children in LMIC. Such awareness could contribute to the design of interventions, programs and policies, and further research

Determinants of stunting and severe stunting among under-fives : evidence from the 2011 Nepal Demographic and Health Survey

Background: Stunting remains a major public health concern in Nepal as it increases the risk of illness, irreversible body damage and mortality in children. Public health planners can reshape and redesign new interventions to reduce stunting and severe stunting among children aged less than 5 years in this country by examining their determinants. Hence, this study identifies factors associated with stunting and severe stunting among children aged less than five years in Nepal. Methods: The sample is made up of 2380 children aged 0 to 59 months with complete anthropometric measurements from the 2011 Nepal Demographic and Health Survey (NDHS). Simple and multiple logistic regression analyses were used to examine stunting and severe stunting against a set of variables. Results: The prevalences of stunting and severe stunting were 26.3% [95% confidence Interval (CI): 22.8, 30.1] and 10.2% (95%CI: 7.9, 13.1) for children aged 0–23 months, respectively, and 40.6 (95%CI: 37.3, 43.2) and 15.9% (95%CI: 13.9, 18.3) for those aged 0–59 months, respectively. After adjusting for potential confounding factors, multivariable analyses showed that the most consistent significant risk factors for stunted and severely stunted children aged 0–23 and 0–59 months were household wealth index (poorest household), perceived size of baby (small babies) and breastfeeding for more than 12 months (adjusted odds ratio (AOR) for stunted children aged 0–23 months = 2.60 [95% CI: (1.87, 4.02)]; AOR for severely stunted children aged 0–23 months = 2.87 [95% CI: (1.54, 5.34)]; AOR for stunted children aged 0–59 months = 3.54 [95% CI: (2.41, 5.19)] and AOR for severely stunted children aged 0–59 months = 4.15 [95% CI: (2.45, 6.93)]. Conclusions: This study suggests that poorest households and prolonged breastfeeding (more than 12 months) led to increased risk of stunting and severe stunting among Nepalese children. However, community-based education intervention are needed to reduce preventable deaths triggered by malnutrition in Nepal and should target children born to mothers of low socioeconomic status

Aging alters global hepatic DNA hydroxymethylation in mice, as determined by a novel LC/MS-MS method

Aging is associated with changes in global DNA methylation (mC), but changes in DNA hydroxymethylation (hmC) are not established due to a relative lack of methods available to measure hmC. Both modifications can affect gene expression and may be important in aging. We have developed a method to measure 5'-methyl-2'-deoxycytidine and 5'-hydroxymethyl-2'-deoxycytidine in DNA using liquid chromatography/tandem mass spectrometry (LC/MS-MS) and used this method to assess global hmC and mC levels in hepatic tissue from young (9 months; n=10) and old (23 months; n=6) C57BL/6 male mice. DNA was enzymatically hydrolyzed and isotopomers [15N3]-2'-deoxycytidine and (methyl-d3, ring-6-d1)-5-methyl-2'-deoxycytidine were added as internal standards. The mixture of DNA hydrolysates and internal standards were separated through LC, and nucleosides of interest were detected by MS-MS in positive ion mode using multiple reaction monitoring. Global mC and hmC levels were calculated as a percentage of total deoxycytidine residues in genomic DNA. Liver tissue from old mice had significantly higher global hmC relative to young mice (0.32\ub10.02% vs 0.24\ub10.01%; p=0.02), while mC levels did not change. Using this new method we have found that aging is associated with an increase in global DNA hmC, a finding that may be useful in understanding the physiological mechanisms behind aging

Chronic alcohol consumption has greater impact on hepatic DNA hydroxymethylation in young mice relative to old

Aging and chronic alcohol consumption affects DNA methylation, changing gene transcription. It is not yet known whether these factors also alter DNA hydroxymethylation (hmC), an epigenetic mark produced by oxidation of methylcytosine.This is the first study demonstrating the effects of chronic alcohol consumption and aging on DNA hmC levels. Chronic alcohol consumption differently affects DNA hmC in young and old mice

Hepatic DNA hydroxymethylation is site-specifically altered by chronic alcohol consumption and aging

Global DNA hydroxymethylation is markedly decreased in human cancers, including hepatocellular carcinoma, which is associated with chronic alcohol consumption and aging. Because gene-specific changes in hydroxymethylcytosine may affect gene transcription, giving rise to a carcinogenic environment, we determined genome-wide site-specific changes in hepatic hydroxymethylcytosine that are associated with chronic alcohol consumption and aging.Young (4 months) and old (18 months) male C57Bl/6 mice were fed either an ethanol-containing Lieber\u2013DeCarli liquid diet or an isocaloric control diet for 5 weeks. Genomic and gene-specific hydroxymethylcytosine patterns were determined through hydroxymethyl DNA immunoprecipitation array in hepatic DNA.Hydroxymethylcytosine patterns were more perturbed by alcohol consumption in young mice than in old mice (431 differentially hydroxymethylated regions, DhMRs, in young vs 189 DhMRs in old). A CpG island ~2.5 kb upstream of the glucocorticoid receptor gene, Nr3c1, had increased hydroxymethylation as well as increased mRNA expression (p = 0.015) in young mice fed alcohol relative to the control group. Aging alone also altered hydroxymethylcytosine patterns, with 331 DhMRs, but alcohol attenuated this effect. Aging was associated with a decrease in hydroxymethylcytosine ~1 kb upstream of the leptin receptor gene, Lepr, and decreased transcription of this gene (p = 0.029). Nr3c1 and Lepr are both involved in hepatic lipid homeostasis and hepatosteatosis, which may create a carcinogenic environment. These results suggest that the location of hydroxymethylcytosine in the genome is site specific and not random, and that changes in hydroxymethylation may play a role in the liver\u2019s response to aging and alcohol

Aging and alcohol interact to alter hepatic DNA hydroxymethylation

BACKGROUND:Aging and chronic alcohol consumption are both modifiers of DNA methylation, but it is not yet known whether chronic alcohol consumption also alters DNA hydroxymethylation, a newly discovered epigenetic mark produced by oxidation of methylcytosine. Furthermore, it has not been tested whether aging and alcohol interact to modify this epigenetic phenomenon, thereby having an independent effect on gene expression.METHODS:Old (18 months) and young (4 months) male C57BL/6 mice were pair-fed either a Lieber-DeCarli liquid diet with alcohol (18% of energy) or an isocaloric Lieber-DeCarli control diet for 5 weeks. Global DNA hydroxymethylation and DNA methylation were analyzed from hepatic DNA using a new liquid chromatography-tandem mass spectrometry method. Hepatic mRNA expression of the Tet enzymes were measured via quantitative real-time polymerase chain reaction.RESULTS:In young mice, mild chronic alcohol exposure significantly reduced global DNA hydroxymethylation compared with control mice (0.22 \ub1 0.01 vs. 0.29 \ub1 0.06%, p = 0.004). Alcohol did not significantly alter hydroxymethylcytosine levels in old mice. Old mice fed the control diet showed decreased global DNA hydroxymethylation compared with young mice fed the control diet (0.24 \ub1 0.02 vs. 0.29 \ub1 0.06%, p = 0.04). This model suggests an interaction between aging and alcohol in determining DNA hydroxymethylation (pinteraction = 0.009). Expression of Tet2 and Tet3 was decreased in the old mice relative to the young (p < 0.005).CONCLUSIONS:The observation that alcohol alters DNA hydroxymethylation indicates a new epigenetic effect of alcohol. This is the first study demonstrating the interactive effects of chronic alcohol consumption and aging on DNA hydroxymethylation

Aging alters hepatic DNA hydroxymethylation, as measured by liquid chromatography/mass spectrometry

BACKGROUND: Aging is one of the most important risk factors for cancer. It appears that aberrant epigenetic changes might be a common driver of aging and cancer. Among them are changes in DNA methylation and DNA hydroxymethylation. The 5' carbon of cytosines in CpG dinucleotides of DNA can be either methylated or hydroxymethylated. Like 5'-methylcytosine, changes in 5'-hydroxymethylcytosine may occur due to aging, potentially leading to downstream changes in transcription and cancer development. METHODS: We set up a method to measure 5'-methyl-2'-deoxycytidine and 5'-hydroxymethyl-2'-deoxycytidine in DNA using liquid chromatography/mass spectrometry (LC/MS-MS) and used this method to measure the percentage of total cytosine that was either methylated or hydroxymethylated in the liver tissues of young and old C57Bl/6 male mice. The DNA was enzymatically hydrolyzed by sequential digestion with nuclease P1, phosphodiesterase I and alkaline phosphatase. The isotopomers [(15)N3]-2'-deoxycytidine and (methyl-d 3, ring-6-d 1)-5-methyl-2'-deoxycytidine were added to the DNA hydrolysates as internal standards. DNA methylation and hydroxymethylation were calculated as a percentage of total deoxycytidine in genomic DNA. RESULTS: Within day variations for DNA methylation and hydroxymethylation were 3.45% and 8.40%, while day to day variations were 6.14% and 17.68%, respectively. Using this method it was determined that hepatic DNA of old mice had increased levels of hydroxymethylation relative to young (0.32 \ub1 0.02% vs. 0.24 \ub1 0.01%, P = 0.02), with no significant changes in 5'-methylcytosine. CONCLUSIONS: DNA hydroxymethylation measured by LC/MS-MS method can be a novel biomarker of aging. It will be useful to investigate the potential role of DNA hydroxymethylation in the development and prevention of age-associated cancer

Consumption levels of the dietary factors included in the analysis among Kuwaiti adults ≥25 years in 2009, by age and sex.

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Estimated number of cardiometabolic deaths attributable to suboptimal dietary intake in Kuwait in 2009.

Bars represent the estimated number of cardiometabolic deaths attributable to intake of individual dietary factors compared to the optimal intake (numbers in parentheses).</p