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The US FDA published new nutrition-labeling regulations in May 2016. For the first time since the implementation of the Nutrition Labeling and Education Act of 1990, the Daily Value (DV) for most vitamins will change, as will the units of measurement used in nutrition labeling for some vitamins. For some food categories, the Reference Amounts Customarily Consumed (RACCs) will increase to reflect portions commonly consumed on a single occasion. These regulatory changes are now effective, and product label changes will be mandatory beginning 26 July 2018. This commentary considers the potential impact of these regulatory changes on the vitamin and mineral contents of foods and dietary supplements. Case studies examined potential effects on food fortification and nutrient density. The updated DVs may lead to a reduction in the nutrient density of foods and dietary supplements with respect to 8 vitamins (vitamin A, thiamin, riboflavin, niacin, vitamin B-6, vitamin B-12, biotin, and pantothenic acid) and 6 minerals (zinc, selenium, copper, chromium, molybdenum, and chloride), and have mixed effects on 2 vitamins where the amount required per serving is affected by chemical structure (i.e., form) (natural vitamin E compared with synthetic vitamin E and folic acid compared with folate). Despite an increased DV for vitamin D, regulations limit food fortification. The adoption of Dietary Folate Equivalents for folate labeling may lead to reductions in the quantity of folic acid voluntarily added per RACC. Finally, because of increased RACCs in some food categories to reflect portions that people typically eat at one time, the vitamin and mineral density of these foods may be affected adversely. In totality, the United States is entering an era in which the need to monitor dietary intake patterns and nutritional status is unprecedented., Competing Interests: 2: Author disclosures: MI McBurney, S Hartunian-Sowa, and NV Matusheski are employed by DSM Nutritional Products, a manufacturer of vitamins and supplier to the food, dietary supplement, and pharmaceutical industries. There were no other conflicts of interest., (© 2017 American Society for Nutrition.)

Population data on long-chain omega-3 polyunsaturated fatty acid (LCn-3 PUFA) status from biomarkers of dietary intake is lacking. The objectives were to describe plasma LCn-3 PUFA concentrations and compare them to concentrations associated with cardiovascular health and dietary recommendations for two servings of seafood/week. Fasting plasma fatty acids were measured among 1386 subjects ≥20 years from the National Health and Nutrition Examination Survey, 2003-2004. LCn-3 concentrations represent the sum of eicosapentaenoic acid, docosapentaenoic acid and docosahexaenoic acid relative to total fatty acids (expressed as a percentage). Mean LCn-3 PUFA concentration was 2.07% (95% CI 1.95-2.19). Overall, 80.6% of participants had LCn-3 below concentrations recommended for cardiovascular health. Hispanic participants were the most likely to have LCn-3 PUFA below recommended levels. Nearly all participants (95.7%) had LCn-3 below concentrations associated with cardiovascular protection. Older participants (≥60 years) had higher LCn-3 PUFA concentrations than those aged 20-39 years but not aged 40-59 years. LCn-3 PUFA concentrations were lower for Hispanic participants relative to non-Hispanic black participants. Suboptimal LCn-3 concentrations are common among U.S. adults. These findings highlight the need to increase LCn-3 intake among Americans.

Vitamins play a crucial role in health, but modern lifestyles may lead to suboptimal intakes even in affluent countries. The aim of the present study is to review vitamin intakes in Germany, the UK, The Netherlands and the USA and to compare them with respective national recommendations. Data on adults from the most recently published national dietary intake surveys for the first three countries and data for adults from the US National Health and Nutrition Examination Survey from 2003 to 2008 for the USA were used as a basis for the analysis. The proportions of the populations with intakes below recommendations were categorised as < 5, 5-25, >25-50, >50-75 and >75 % for each vitamin. The data generated are presented in a 'traffic light display', using colours from green to red to indicate degrees of sufficiency. The trends found were compared with the results from the European Nutrition and Health Report 2009, even though in that report, only information on mean intakes in the different countries was available. We showed that, although inter-country differences exist, intakes of several vitamins are below recommendations in a significant part of the population in all these countries. The most critical vitamin appears to be vitamin D and the least critical niacin. The variation between the countries is most probably due to differences in recommendations, levels of fortification and local dietary habits. We show that a gap exists between vitamin intakes and requirements for a significant proportion of the population, even though diverse foods are available. Ways to correct this gap need to be investigated.

On December 17, 2018, the North American branch of the International Life Sciences Institute (ILSI North America) convened a workshop "Can We Begin to Define a Healthy Gut Microbiome Through Quantifiable Characteristics?" with >40 invited academic, government, and industry experts in Washington, DC. The workshop objectives were to 1) develop a collective expert assessment of the state of the evidence on the human gut microbiome and associated human health benefits, 2) see if there was sufficient evidence to establish measurable gut microbiome characteristics that could serve as indicators of "health," 3) identify short- and long-term research needs to fully characterize healthy gut microbiome-host relationships, and 4) publish the findings. Conclusions were as follows: 1) mechanistic links of specific changes in gut microbiome structure with function or markers of human health are not yet established; 2) it is not established if dysbiosis is a cause, consequence, or both of changes in human gut epithelial function and disease; 3) microbiome communities are highly individualized, show a high degree of interindividual variation to perturbation, and tend to be stable over years; 4) the complexity of microbiome-host interactions requires a comprehensive, multidisciplinary research agenda to elucidate relationships between gut microbiome and host health; 5) biomarkers and/or surrogate indicators of host function and pathogenic processes based on the microbiome need to be determined and validated, along with normal ranges, using approaches similar to those used to establish biomarkers and/or surrogate indicators based on host metabolic phenotypes; 6) future studies measuring responses to an exposure or intervention need to combine validated microbiome-related biomarkers and/or surrogate indicators with multiomics characterization of the microbiome; and 7) because static genetic sampling misses important short- and long-term microbiome-related dynamic changes to host health, future studies must be powered to account for inter- and intraindividual variation and should use repeated measures within individuals.

A number of studies have demonstrated that the Sirtuin family member, Sirt1, is a key integrator of growth, metabolism, and lifespan. Sirt1 directly interacts with and deacetylates key regulators of the circadian clock, positioning it to be an important link between feeding and circadian rhythms. In fact, one study suggests that Sirt1 is necessary for behavioral anticipation of limited daily food availability, a circadian process termed food anticipatory activity (FAA). In their study, mice overexpressing Sirt1 had enhanced FAA, while mice lacking Sirt1 had little to no FAA. Based on the supposition that Sirt1 was indeed required for FAA, we sought to use Sirt1 deletion to map the neural circuitry responsible for FAA. We began by inactivating Sirt1 using the cell-type specific Cre-driver lines proopiomelanocortin, but after observing no effect on body weight loss or FAA we then moved on to more broadly neuronal Cre drivers Ca2+/calmodulin-dependent protein kinase II and nestin. As neither of these neuronal deletions of Sirt1 had impaired FAA, we then tested 1) a broad postnatal tamoxifen-inducible deletion, 2) a complete, developmental knockout of Sirt1, and 3) a gene replacement, catalytically inactive, form of Sirt1; but all of these mice had FAA similar to controls. Therefore, our findings suggest that FAA is completely independent of Sirt1. [ABSTRACT FROM AUTHOR]

The SIRT1 protein deacetylase is reported to have a remarkably wide spectrum of biological functions affecting such varied processes as aging, cancer, metabolism, neurodegeneration and immunity. However, the SIRT1 literature is also full of contradictions. To help establish the role(s) of SIRT1 in these and other biological processes, we set out to create a mouse in which the SIRT1 activity could be toggled between on and off states by fusing the estrogen receptor ligand-binding domain (ER) to the C terminus of the SIRT1 protein. We found that the catalytic activity of the SIRT1-ER fusion protein increased 4–5 fold in cells treated with its ligand, 4-hydroxy-tamoxifen (4OHT). The 4OHT-induced activation of SIRT1-ER was due in large part to a 2 to 4-fold increase in abundance of the SIRT1-ER protein in cells in culture and in tissues in vivo. This increase is reversible and is a consequence of 4OHT-induced stabilization of the SIRT1-ER protein. Since changes in SIRT1 level or activity of 2–4 fold are frequently reported to be sufficient to affect its biological functions, this mouse should be helpful in establishing the causal relationships between SIRT1 and the diseases and processes it affects. [ABSTRACT FROM AUTHOR]

The protein deacetylase SIRT1 is involved in the regulation of a large number of cellular processes that are thought to be required for cancer initiation and progression. Both SIRT1 activity and tumorigenesis can be influenced by dietary fat and polyphenolics. We set out to determine whether dietary modulations of tumorigenesis are mediated by SIRT1 catalytic functions. We introduced a mammary gland tumor-inducing transgene, MMTV-PyMT, into stocks of mice bearing a H355Y point mutation in the Sirt1 gene that abolishes SIRT1 catalytic activity. Tumor latency was reduced in animals fed a high fat diet but this effect was not dependent on SIRT1 activity. Resveratrol had little effect on tumor formation except in animals heterozygous for the mutant Sirt1 gene. We conclude that the effects of these dietary interventions on tumorigenesis are not mediated by modulation of SIRT1 catalytic activity. [ABSTRACT FROM AUTHOR]

This review elucidates the importance of healthy dietary and lifestyle habits to reduce morbidity and mortality associated with coronary heart disease (CHD), stroke and cardiovascular diseases. Given published evidence of the poor compliance, increased cost, and decreased benefit/risk ratios of medical therapies, individuals (and populations) are encouraged to adopt healthy life habits. The three most atherogenic dietary risk factors are saturated fat, cholesterol and obesity. Dietary patterns associated with the consumption of grains and grain-based foods predict risk of CHD independently of other life habits. Epidemiological and intervention studies elucidating the strong protective associations of grains, cereal fibers and anti-oxidant vitamins on CHD are reviewed. In summary, the consumption of grains and grain-based cereals is repeatedly associated with the ingestion of many nutrients, e.g., dietary fiber and anti-oxidants, that alter energy balance and nutrient intakes to positively affect cardiovascular health, especially when combined with healthy life habits, [ABSTRACT FROM AUTHOR]

A letter to the editor is presented in response to the article "Increasing starch intake in the human diet increases fecal bulking" by P.S. Shetty.

To determine the long-term effect of reducing carbohydrate or increasing fiber intakes on LDL particle size and HDL composition, 69 subjects with type 2 diabetes randomly received ∼10% energy from low-fiber breakfast cereal (LF), high-fiber cereal (HF), or monounsaturated fatty acid-rich oil/margarine (MUFA) for 6mo. Compared to LF, serum-triglyceride fell by ∼12% on MUFA and increased by ∼13% on HF (p<0.05). LDL-size fell significantly on both MUFA and HF. HDL-triglyceride did not change significantly on MUFA, but increased by ∼20% on HF (p<0.05). Changes in HDL-triglyceride, but not changes in LDL-size, were significantly related to changes in serum triglyceride. Thus, modest long-term changes in carbohydrate and fiber intakes affected LDL particle size and HDL-triglyceride in type 2 diabetic subjects. The changes in HDL composition may have been driven by changes in serum triglyceride, but the changes in LDL particle size appear to have been caused by other factors. [Copyright &y& Elsevier]