Adv Nutr Research Articles

Retraction notice to “Fructooligosaccharides: From Breast Milk Components to Potential Supplements. A Systematic Review” [Adv Nutr 13 (2022) 318–327

Retraction notice to “Fructooligosaccharides: From Breast Milk Components to Potential Supplements. A Systematic Review” [Adv Nutr 13 (2022) 318–327

Bidirectionality between Cardiometabolic Diseases and COVID-19: Role of Humoral Immunity.

Cardiometabolic diseases and abnormalities have recently emerged as independent risk factors of coronavirus disease 2019 (COVID-19) severity, including hospitalizations, invasive mechanical ventilation, and mortality. Determining whether and how this observation translates to more effective long-term pandemic mitigation strategies remains a challenge due to key research gaps. Specific pathways by which cardiometabolic pathophysiology affects humoral immunity against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and vice versa, remain unclear. This review summarizes current evidence of the bidirectional influences between cardiometabolic diseases (diabetes, adiposity, hypertension, CVDs) and SARS-CoV-2 antibodies induced from infection and vaccination based on human studies. Ninety-two studies among >408,000 participants in 37 countries on 5 continents (Europe, Asia, Africa, and North and South America) were included in this review. Obesity was associated with higher neutralizing antibody titers following SARS-CoV-2 infection. Most studies conducted prior to vaccinations found positive or null associations between binding antibodies (levels, seropositivity) and diabetes; after vaccinations, antibody responses did not differ by diabetes. Hypertension and CVDs were not associated with SARS-CoV-2 antibodies. Findings underscore the importance of elucidating the extent that tailored recommendations for COVID-19 prevention, vaccination effectiveness, screening, and diagnoses among people with obesity could reduce disease burden caused by SARS-CoV-2.

Are Lipid-Lowering and Antihypertensive Medications Used as Complements to Heart-Healthy Diets? A Scoping Review.

In cardiovascular disease (CVD) prevention, whether antihypertensive and lipid-lowering medications are used as complements to heart-healthy diets has not been thoroughly assessed. This scoping review aimed to 1) analyze observational studies that assessed the relationship between diet and antihypertensive/lipid-lowering medication use and 2) evaluate whether medication was used as a complement to heart-healthy dietary intakes. We searched MEDLINE, Embase, Web of Science, and CINAHL through 14 January, 2023, for studies that assessed either 1) intraindividual changes in diet associated with lipid-lowering/antihypertensive medication initiation or use or 2) interindividual differences in diet between users and nonusers of these medications. A total of 17 studies were included. Of those, 3 prospectively assessed the intraindividual changes in diet associated with medication initiation or use, but none documented potential changes in diet prior to medication initiation. The 14 other studies compared dietary intakes of medication users and nonusers, most of which also relied on an incomplete assessment of the temporal dynamics between diet and medication use as they employed cross-sectional (n = 12) or repeated cross-sectional (n = 2) designs. Data from 8 studies, including 4 of the 5 studies from Europe, suggested that medication was used as a complement to heart-healthy diets, whereas data from the 9 other studies, including the 4 conducted in the United States, provided no such evidence, indicating potential between-country differences in this relationship. Finally, no studies investigated how the dynamics between diet and medication use influenced the long-term CVD risk. This scoping review suggests that the current literature on the relationship between lipid-lowering/antihypertensive medication use and diet provides an incomplete perspective on how medication may influence diet in CVD prevention. Prospective studies assessing intraindividual changes in diet associated with medication initiation and use and how these dynamics influence the CVD risk are thus needed. Adv Nutr 2023;x:xx.

Kidney Stone Prevention

Kidney stone disease (KSD) (alternatively nephrolithiasis or urolithiasis) is a global health care problem that affects people in almost all of developed and developing countries. Its prevalence has been continuously increasing with a high recurrence rate after stone removal. Although effective therapeutic modalities are available, preventive strategies for both new and recurrent stones are required to reduce physical and financial burdens of KSD. To prevent kidney stone formation, its etiology and risk factors should be first considered. Low urine output and dehydration are the common risks of all stone types, whereas hypercalciuria, hyperoxaluria, and hypocitraturia are the major risks of calcium stones. In this article, up-to-date knowledge on strategies (nutrition-based mainly) to prevent KSD is provided. Important roles of fluid intake (2.5-3.0 L/d), diuresis (>2.0-2.5 L/d), lifestyle and habit modifications (for example, maintain normal body mass index, fluid compensation for working in high-temperature environment, and avoid cigarette smoking), and dietary management [for example, sufficient calcium at 1000-1200 mg/d, limit sodium at 2 or 3-5 g/d of sodium chloride (NaCl), limit oxalate-rich foods, avoid vitamin C and vitamin D supplements, limit animal proteins to 0.8-1.0 g/kg body weight/d but increase plant proteins in patients with calcium and uric acid stone and those with hyperuricosuria, increase proportion of citrus fruits, and consider lime powder supplementation] are summarized. Moreover, uses of natural bioactive products (for example, caffeine, epigallocatechin gallate, and diosmin), medications (for example, thiazides, alkaline citrate, other alkalinizing agents, and allopurinol), bacterial eradication, and probiotics are also discussed.

Effect of FADS1 rs174556 Genotype on Polyunsaturated Fatty Acid Status: A Systematic Review and Meta-Analysis.

PUFA status is highly implicated in cognitive development and metabolic disorder-related diseases. Genetic variants of FADS genes encoding enzymes that catalyze the rate-limiting steps of PUFA biosynthesis appear to be associated with n-3 and n-6 PUFA contents. Therefore, we conducted the first systematic review and meta-analysis to explore the association of the A-allele carriers of the FADS1 rs174556 with PUFA status. The PRISMA guidelines were followed. The literature search was conducted up to November 2022 in PubMed, Web of Science, Embase, Cochrane Library, Airiti Library, and CINAHL. The Joanna Briggs Institute checklists were used to assess the methodological quality. The correlation with 95% CIs was determined by a random-effect meta-analysis. Eleven studies that met the inclusion criteria and acceptable quality were included in this systematic review. The data on PUFA contents were collected when they were mainly analyzed using blood samples and breast milk. Results of the meta-analysis on eight studies (one randomized controlled trial, one cohort study, and six cross-sectional studies) showed that the A-allele carriers of rs174556 were significantly negatively correlated with the concentrations of AA (P = 0.001), EPA (P = 0.004), and DHA (P = 0.025). However, ALA and LA were not associated with the A-allele carriers. To clarify the discrepancy, we further divided the studies into blood samples and breast milk subgroups. The subgroup analysis revealed that the A-allele carriers of rs174556 were significantly positively correlated with LA (P = 0.031) and negatively correlated with AA (P = 0.001), EPA (P = 0.036), and DHA (P < 0.001) in the blood sample group, but not in the breast milk group. The current meta-analysis proved that the A-allele carriers of the FADS1 rs174556 appeared to be highly associated with lower concentrations of AA, EPA, and DHA but higher LA in the blood samples. The study has been registered on the International Prospective Register of Systematic Reviews (PROSPERO:CRD42022363978). Adv Nutr 2023;x:xx-xx.

Measuring Adherence to Sustainable Healthy Diets: A Scoping Review of Dietary Metrics.

Comprehensive metrics that provide a measure of dietary patterns at global and national levels are needed to inform and assess the effectiveness of policy actions that promote sustainable healthy diets. In 2019, the Food and Agriculture Organization of the United Nations and the World Health Organization reported 16 guiding principles of sustainable healthy diets, but it is still unknown how these principles are considered in dietary metrics. This scoping review aimed to explore how principles of sustainable healthy diets are considered in dietary metrics used worldwide. Forty-eight food-based, investigator-defined dietary pattern metrics assessing diet quality in free-living, healthy populations at the individual or household level were assessed against the 16 guiding principles of sustainable healthy diets, which was used as a theoretical framework. A strong adherence of the metrics to health-related guiding principles was found. Metrics had a weak adherence to principles related to environmental and sociocultural aspects of diets, except for the principle related to diets being culturally appropriate. No existing dietary metric captures all principles of sustainable healthy diets. Notably, the significance food processing, environmental, and sociocultural aspects of diets are generally understated. This likely reflects the lack of focus on these aspects in current dietary guidelines, which highlights the importance of including these emerging topics in future dietary recommendations. The absence of quantitative metrics that comprehensively measure sustainable healthy diets limits the body of evidence that would otherwise inform national and international guideline developments. Our findings can help grow the quantity and quality of the body of evidence available to inform policy activities to realize 2030 Sustainable Development Goals of multiple United Nations. Adv Nutr 2022;x:xx.

Nutrition and Supplement Use Characteristics in the Myeloproliferative Neoplasms: Results from the Nutrient Survey

Background: Some complementary and alternative medicine interventions, namely diets and supplements, have demonstrated antioxidant and anti-inflammatory pharmacological properties such as decreased inflammatory markers and reactive oxygen species (Biofactors 2013, J Am Coll Cardiol. 2004, Adv Nutr. 2015). Myeloproliferative neoplasm (MPN) patients have increased inflammatory cytokines (e.g., IL-1, IL-6, IL-8, and TNF-a) that contribute to symptom burden (e.g., fatigue, pruritus, night sweats, bone pain) and nutritional deficiencies (e,g., hypocholesterolemia, hypoalbuminemia, weight loss). To date no studies have evaluated the habits, needs, and preferences of these specific interventions among an MPN population.Methods: An internet-based survey was hosted by the Mayo Clinic Survey Research Center and promoted on multiple MPN-focused Internet websites and communities during February of 2017. The survey included data on demographics, MPN characteristics, nutritional habits, supplement use, and symptom burden using the MPN-10 (JCO 2012). T tests and chi square tests compared group means and frequencies, respectively. Statistical significance was defined as P values < 0.05.Results: Demographics : 1329 international MPN patients responded to the online survey of which 24% were diagnosed with MF, 37% with PV, and 38% with ET. 1131 respondents consented to the survey, completed >10 multiple choice questions, and were age 18 years or older. Respondents represented individuals with an MPN diagnosis from 37 countries. Average MPN-SAF TSS score was 31 (SD=17).Nutritional Education Preferences : Overall, 34% of respondents endorsed using diet to help control their symptoms or MPN disease. 23% of respondents endorsed having food allergies or intolerances. 31% of individuals followed a specific diet or had dietary restrictions. The vast majority (96%) of MPN respondents endorsed being willing to eat only certain foods if it helped to control symptom burden and or could help their MPN to stabilize or reduce the risk of their MPN getting worse (98%).Supplement Use : 72% of MPN respondents reported use of over the counter supplements. MPN-10 symptom scores were compared for specific supplements between users and non-users (Table 1). Supplement use was significantly more common among females (74%) than among males (66%, p=0.01). Supplement users were significantly more likely to be older (mean age 59 versus(vs) 56 years old, P <0.001) with lower self-reported body mass index (mean 25.7 vs 26.6, P=0.02), and higher frequency of engaging in at least 30 minutes of physical activity (mean of 4 days vs 3 days per week, P=0.04).Symptom Burden Associations : Intake of alcohol (<0.0001), baked foods (0.02), dairy (0.02), and pasta (0.02) was associated with significantly lower TSS when analyzed as a continuous variable based on frequency of intake over an average week. Fast food (0.0007), pre-made snacks (0.03), soda (<0.0001), refined sugar (0.01), and taco (0.03) intake was associated with worsened symptom score. Symptom burden was significantly lower among individuals using amino acid supplements (2.8 vs 3.4, P=0.02) and N-Acetylcysteine (2.4 vs 3.4, P=0.02) and significantly higher in individuals taking Bach flowers (5.2 vs 3.4, P=0.008).Conclusions: Few low risk interventions are available which improve symptom burden among MPN patients with indolent disease. Supplement use and nutritional alteration have the potential to be paired with standard therapy to allow MPN patients to self-manage symptom burden and possibly reduce disease-related inflammation. The results of this analysis will be used to inform the further investigation of diet and supplement use among MPN patients. [Display omitted] DisclosuresMesa:Ariad: Consultancy; Galena Biopharma, Inc.: Consultancy; Novartis Pharmaceuticals Corporation: Consultancy; Gilead Sciences, Inc.: Research Funding; Promedico: Research Funding; Celgene Corporation: Research Funding; Incyte Corporation: Research Funding; CTI BioPharma Corp.: Research Funding.

Milk microbiome: evaluation study on the differences among cows with a different health status classified by leukocyte pattern

Milk microbiome: evaluation study on the differences among cows with a different health status classified by leukocyte pattern

Corrigendum for Webb et al. Micronutrient status: potential modifiers-drugs and chronic disease. Adv Nutr 2018;9(Suppl):509S-10S.

[This corrects the article DOI: 10.1093/advances/nmy028.].

Erratum for Farebrother J et al. Effects of iodized salt and iodine supplements on prenatal and postnatal growth: a systematic review. Adv Nutr 2018;9(3):219-37.

Erratum for Farebrother J et al. Effects of iodized salt and iodine supplements on prenatal and postnatal growth: a systematic review. Adv Nutr 2018;9(3):219-37.

Effects of Initial Selenium Status on Apparent Dietary Selenium Requirements in Rodents

Robust biomarkers – that are specific for the nutrient, fall dramatically in deficiency, and reach well‐defined plateaus – are essential for the careful determination of dietary nutrient requirements (Adv Nutr 2016;7:1129). A second key component of dietary nutrient requirement studies is initial status at the start of an experiment. Se‐adequate male weanling rats fed Se‐deficient diets supplemented with graded levels of Se (as selenite) for 4 wk result in sigmoidal Se response curves with well‐defined plateaus for glutathione peroxidase (Gpx) activity, and with plateau breakpoints indicating minimum Se requirements of 0.06, 0.06, and 0.09 μg Se/g diet based on liver Gpx4, plasma Gpx3 and liver Gpx1 activity, respectively. Underlying these requirements, the Se requirement for liver Gpx1 mRNA is 0.06 μg Se/g diet. When second‐generation Se‐deficient weanling male rats were fed graded Se levels for 4 wk, apparent dietary Se requirements increased to 0.08, 0.1 and 0.14 μg Se/g for liver Gpx4, plasma Gpx3, and liver Gpx1 activities, respectively. The Se requirement for liver Gpx1 mRNA was 0.08 μg Se/g diet, which is 25% higher than when starting with Se‐adequate pups (Biol Trace Elem Res 2016, in press). Clearly, repleting Se‐deficient rats using an identical paradigm increased apparent dietary Se requirements by 33–67%, showing that limited dietary Se was being diverted to replete deeper body pools of Se. The higher dietary Se required to protect liver Gpx1 mRNA from nonsense mediated decay further substantiates this shift of Se from liver to other tissues. To explore in a preliminary study the role of Gpx1 mRNA and selenoprotein expression on restoration of Se status, Gpx1 wildtype (Gpx1+/+), heterozygote (Gpx1+/−), and knockout (Gpx1−/−) mice were fed Se‐deficient diets for 16 wk, then re‐supplemented with graded levels of dietary Se (0–0.3 μg Se/g) for 7 days to partially replete Gpx activities. Liver Gpx1 activity in Gpx1+/+ mice reached a plateau with 0.15 μg Se/g, whereas in Gpx1+/− mice, liver Gpx1 activity increased linearly over the full dietary range from 0 to 0.3 μg Se/g, showing the effect of limited Gpx1 mRNA as well as Se availability; there was no increase in Gpx1 activity in Gpx1−/− mice, as expected. In contrast, red blood cell (RBC) Gpx1 activity was little altered by 0 to 0.15 μg Se/g in both Gpx1+/+ and Gpx1+/− mice, but then reached a similar level for both genotypes at 0.3 μg Se/g, suggesting that Se availability but not mRNA was controlling level of RBC Gpx1. The plasma Gpx3 activity Se response curve for Gpx1+/+ mice was similar to the Se response curve for RBC Gpx1 activity for Gpx1+/+ mice, only reaching a maximum at 0.3 μg Se/g. Surprisingly, the Se response curve for plasma Gpx3 activity in Gpx1−/− mice overlay the response curve for Gpx1+/+ mice, indicating that similar quantities of Se were transported to kidney for Gpx3 synthesis, whereas Gpx1+/− mice fed 0.3 μg Se/g had considerable less Gpx3 activity than Gpx1+/+ or Gpx1−/− mice, again suggesting that Se was diverted to other tissues. Collectively, these studies illustrate that diversion of nutrient to depleted stores can result in higher apparent nutrient requirements when starting with initially depleted animals.Support or Funding InformationWisconsin Alumni Foundation Selenium Nutrition Research Fund (No. 2046295)

Sickeningly Sweet: Does Sugar Cause Chronic Disease? No.

Sugars have emerged as 1 of the most important public health concerns. Special attention has focused on the fructose moiety of sugars owing to its unique metabolic and endocrinologic responses. Low-quality ecologic studies ( 1 Bray G.A. Nielsen S.J. Popkin B.M. Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity. Am J Clin Nutr. 2004; 794 (Erratum in Am J Clin Nutr 2004;804:1090): 537-543 Google Scholar , 2 Basu S. Yoffe P. Hills N. Lustig R.H. The relationship of sugar to population-level diabetes prevalence: An econometric analysis of repeated cross-sectional data. PLoS ONE. 2013; 82: e57873 Crossref Scopus (256) Google Scholar , 3 Goran M.I. Ulijaszek S.J. Ventura E.E. High fructose corn syrup and diabetes prevalence: A global perspective. Glob Pub Health. 2013; 81: 55-64 Crossref Scopus (144) Google Scholar ), animal models of overfeeding at levels of exposure far beyond mean population levels of intake ( 4 Sievenpiper J.L. de Souza R.J. Kendall C.W. Jenkins D.J. Is fructose a story of mice but not men?. J Am Diet Assoc. 2011; 1112: 219-220 Abstract Full Text Full Text PDF Scopus (38) Google Scholar ) and select human interventions lacking control for energy ( 5 Lustig R.H. Mulligan K. Noworolski S.M. et al. Isocaloric fructose restriction and metabolic improvement in children with obesity and metabolic syndrome. Obesity (Silver Spring). 2016; 242: 453-460 Crossref Scopus (119) Google Scholar ) have been used to implicate fructose-containing sugars in the epidemics of obesity and diabetes. Although experimental models have been invoked to offer plausible biochemical mechanisms to support these positions, whereby fructose acts as an unregulated substrate for de novo lipogenesis, depletes intracellular adenosine triphosphate and impairs satiety signalling through insulin, leptin and ghrelin ( 6 Lustig R.H. Schmidt L.A. Brindis C.D. Public health: The toxic truth about sugar. Nature. 2012; 482: 27-29 Crossref PubMed Scopus (535) Google Scholar , 7 Lustig R.H. Fructose: It's “alcohol without the buzz.”. Adv Nutr. 2013; 42: 226-235 Crossref Scopus (137) Google Scholar , 8 Johnson R.J. Perez-Pozo S.E. Sautin Y.Y. et al. Hypothesis: Could excessive fructose intake and uric acid cause type 2 diabetes?. Endocr Rev. 2009; 301: 96-116 Crossref Scopus (381) Google Scholar , 9 Johnson R.J. Nakagawa T. Sanchez-Lozada L.G. et al. Sugar, uric acid, and the etiology of diabetes and obesity. Diabetes. 2013; 62: 3307-3315 Crossref PubMed Scopus (480) Google Scholar ), the clinical translation of these mechanisms remains in question. Erratum to ‘Sickeningly Sweet: Does Sugar Cause Chronic Disease? No’ (Canadian Journal of Diabetes, Volume 40 [2016] Pages 287–295)Canadian Journal of DiabetesVol. 40Issue 6PreviewThe publisher regrets that the declaration of interest for this article was not included. The acknowledgment should have read: Full-Text PDF

Correction to: Rejuvenation Res 2016;19:90-93.

It has come to our attention that our recent publication Thymus Maintenance and Regeneration by Specific Molecular Factors contains errors. The following sentence from the article was misattributed to Reis et al. Immun Ageing. 2015;12:18]: This FGF21 resistance was due to epigenomic changes at the FGF21 gene, specifically increased DNA methylation. Moreover, the sentence is inaccurate. For clarity, this sentence should be modified: This FGF21 resistance, which is associated with metabolic syndrome and non-alcoholic fatty liver disease (NAFLD) may be due to epigenomic changes in DNA and/or histone methylation due to altered methionine metabolism affecting FGF21 expression ( (Inagaki, Front Endocrinol (Lausanne). 2015 6:147). One possible mechanism is that diet-related DNA methylation changes at the PPARalpha locus in the liver (Contreras et al Adv Nutr, 2013; 4: 439-452) may alter FGF21 expression, because PPARalpha is a key regulator of FGF21 expression involved in insulin resistance, dyslipidemia (...

Spotlight on infant formula: coordinated global action needed

Breastfeeding has often been described as cost free. 1 Rippeyoung PL Noonan MC Is breastfeeding truly cost free? Income consequences of breastfeeding for women. Am Sociol Rev. 2012; 77: 244-267 Crossref Scopus (63) Google Scholar It is not free. Breastfeeding requires investment to overcome the sociopolitical barriers that exist in many countries 2 WHOUNICEFGlobal strategy for infant and young child feeding. World Health Organization, Geneva2003 Google Scholar , 3 Pérez-Escamilla R Curry L Minhas D Taylor L Bradley E Scaling up of breastfeeding promotion programs in low-and middle-income countries: the “breastfeeding gear” model. Adv Nutr. 2012; 3: 790-800 Crossref PubMed Scopus (156) Google Scholar through the effective approaches and practices described in the second paper of the Lancet Breastfeeding Series. 4 Rollins NC Bhandari N Hajeebhoy N et al. on behalf of The Lancet Breastfeeding Series GroupWhy invest, and what it will take to improve breastfeeding practices?. Lancet. 2016; 387: 491-504 Summary Full Text Full Text PDF PubMed Scopus (1075) Google Scholar As shown in the first Series paper, infants, children, and mothers who do not breastfeed experience an increased risk of mortality and morbidity. 5 Victora CG Bahl R Barros AJD et al. for The Lancet Breastfeeding Series GroupBreastfeeding in the 21st century: epidemiology, mechanisms, and lifelong effect. Lancet. 2016; 387: 475-490 Summary Full Text Full Text PDF PubMed Scopus (3313) Google Scholar Breastfeeding is nutritionally, immunologically, neurologically, endocrinologically, economically and ecologically superior to breastmilk substitutes (BMS), and does not require quality control of manufacture, transport, storage, and feeding mechanisms. 4 Rollins NC Bhandari N Hajeebhoy N et al. on behalf of The Lancet Breastfeeding Series GroupWhy invest, and what it will take to improve breastfeeding practices?. Lancet. 2016; 387: 491-504 Summary Full Text Full Text PDF PubMed Scopus (1075) Google Scholar , 5 Victora CG Bahl R Barros AJD et al. for The Lancet Breastfeeding Series GroupBreastfeeding in the 21st century: epidemiology, mechanisms, and lifelong effect. Lancet. 2016; 387: 475-490 Summary Full Text Full Text PDF PubMed Scopus (3313) Google Scholar Breastfeeding: achieving the new normalBreastmilk makes the world healthier, smarter, and more equal: these are the conclusions of a new Lancet Series on breastfeeding. The deaths of 823 000 children and 20 000 mothers each year could be averted through universal breastfeeding, along with economic savings of US$300 billion. The Series confirms the benefits of breastfeeding in fewer infections, increased intelligence, probable protection against overweight and diabetes, and cancer prevention for mothers. The Series represents the most in-depth analysis done so far into the health and economic benefits that breastfeeding can produce. Full-Text PDF Breastfeeding in the 21st century: epidemiology, mechanisms, and lifelong effectThe importance of breastfeeding in low-income and middle-income countries is well recognised, but less consensus exists about its importance in high-income countries. In low-income and middle-income countries, only 37% of children younger than 6 months of age are exclusively breastfed. With few exceptions, breastfeeding duration is shorter in high-income countries than in those that are resource-poor. Our meta-analyses indicate protection against child infections and malocclusion, increases in intelligence, and probable reductions in overweight and diabetes. Full-Text PDF Why invest, and what it will take to improve breastfeeding practices?Despite its established benefits, breastfeeding is no longer a norm in many communities. Multifactorial determinants of breastfeeding need supportive measures at many levels, from legal and policy directives to social attitudes and values, women's work and employment conditions, and health-care services to enable women to breastfeed. When relevant interventions are delivered adequately, breastfeeding practices are responsive and can improve rapidly. The best outcomes are achieved when interventions are implemented concurrently through several channels. Full-Text PDF

Vitamin D influences asthmatic pathology through its action on diverse immunological pathways.

The prevalence of vitamin D insufficiency and deficiency has increased markedly in recent decades to current epidemic levels (Hyppönen E, et al. Am J Clin Nutr 2007;85:860-868). In parallel, there has been an increase in the incidence of a range of immune-mediated conditions ranging from cancer to autoimmune and respiratory diseases, including chronic obstructive pulmonary disease and asthma (Holick MF. N Engl J Med 2007;357:266-281; Finklea et al. Adv Nutr 2011;2:244-253). There is also an association with increased respiratory infections, which are the most common cause of asthma exacerbations (Finklea et al. Adv Nutr 2011;2:244-253). Together, this has resulted in considerable interest in the therapeutic potential of vitamin D to prevent and improve treatment of asthma and other respiratory diseases. To this end, data from clinical trials involving supplementation with active vitamin D, or more commonly a precursor, are starting to emerge. This review considers mechanisms by which vitamin D may act on the immune system to dampen inappropriate inflammatory responses in the airway while also promoting tolerance and antimicrobial defense mechanisms that collectively maintain respiratory health.

Is Plasma Pentadecanoic Acid a Reasonable Biomarker of Dairy Consumption?

Despite advances in biomedical research and clinical medicine, the burden of cardiovascular disease (CVD) remains extremely high.[1][1] This underscores the importance of primary prevention and the search for novel therapeutic strategies. Modifiable lifestyle factors, including dietary habits, play

An epigenetic perspective on pharmacologic ascorbate in colon cancer

AimThere is growing interest in pharmacologic ascorbate (Asc) and its therapeutic properties (Levine et al. Adv Nutr 2011;2:78). We examined cell viability, histone deacetylase (HDAC) expression, and related protein modifications in cancer versus noncancer colon epithelial cells following exposure to Asc.MethodsMTT assays were conducted in HCT116 colon cancer and CCD841 non‐transformed colonic epithelial cells treated with 0.25 to 16 mM Asc or ascorbate‐2‐phosphate (AAp), in the presence and absence of catalase (CAT, 280 U/mg), or with 5 to 160 μM H2O2. Cell lysates obtained 6 h and 24 h post‐treatment were immunoblotted as reported by Rajendran et al. Mol Cancer 2011;10:68.ResultsIn MTT assays, IC50 data were as follows: 8 mM Asc (CCD841); 3 mM Asc (HCT116), &gt;;50mM AAp (HCT116), and 65 μM H2O2 (HCT116). CAT protected against both Asc‐ and H2O2‐ induced cytotoxicity. At 6 h, Asc and H2O2 altered the expression of HDACs (HDAC4, HDAC6, SIRT3) and enhanced the acetylation of histone (H3, H4) and non‐histone proteins (tubulin, p53).ConclusionsAsc was more cytotoxic to colon cancer cells than non‐cancer cells. Findings with the non‐H2O2 producing compound AAp, and with CAT, implicated H2O2 in Asc‐induced cytotoxicity. Asc was shown, for the first time, to alter epigenetic end‐points related to HDAC changes in colon cancer cells.Grant Funding Source: CA090890, CA090890, AT002034