Role of carotenoids and retinoids during heart development.

The nutritional requirements of the developing embryo are complex. In the case of dietary vitamin A (retinol, retinyl esters and provitamin A carotenoids), maternal derived nutrients serve as precursors to signaling molecules such as retinoic acid, which is required for embryonic patterning and organogenesis. Despite variations in the composition and levels of maternal vitamin A, embryonic tissues need to generate a precise amount of retinoic acid to avoid congenital malformations. Here, we summarize recent findings regarding the role and metabolism of vitamin A during heart development and we survey the association of genes known to affect retinoid metabolism or signaling with various inherited disorders. A better understanding of the roles of vitamin A in the heart and of the factors that affect retinoid metabolism and signaling can help design strategies to meet nutritional needs and to prevent birth defects and disorders associated with altered retinoid metabolism. This article is part of a Special Issue entitled Carotenoids recent advances in cell and molecular biology edited by Johannes von Lintig and Loredana Quadro.

Evolution of nutritional status and survival in patients with cancer on tyrosine kinase inhibitors treatment. / Evolución nutricional y de la supervivencia en un grupo de pacientes oncológicos en tratamiento con inhibidores de tirosina quinasa.

BACKGROUND AND OBJECTIVE: Treatment with oral antineoplastic agents known as tyrosine kinase inhibitors (TKIs) is new and, thus, little is known about their impact on nutritional status (NS), dietary intake, quality of life, and survival. The aim of this study was to provide information on these components in order to guide future nutritional recommendations. PATIENTS AND METHOD: A prospective, observational study in adults who start treatment with TKIs, in whom NS was assessed using the Patient-Generated Subjective Global Assessment (PG-SGA), anthropometric measures, biochemical parameters, and dietary intake (24-hour dietary recall). The EORTC QLQ-C30 was used to assess quality of life. Nonparametric tests were used in statistical analysis, and survival was analyzed using Kaplan-Meier and log-rank curves. RESULTS: Of the overall sample, 21.7% had moderate malnutrition according to PG-SGA, and 74.2% moderate weight loss at 6 months, but no patient had BMI<18.5kg/m2. Patients with moderate malnutrition had lower survival at four years of diagnosis (log-rank=0.015). Energy intake was lower than recommended by the ESPEN 2017 congress, and no patient covered the protein requirements (1.5g protein/kg weight) during follow-up. A worse score on the global health scale of the EORTC QLQ-C30 was related to worse NS. CONCLUSIONS: Treatment with TKIs does not appear to have a significant impact on NS and quality of life after 6 months of follow-up. Malnutrition should be prevented through individualized nutritional advice because it is related to shorter survival.

Effect of anti-fibroblast growth factor 23 antibody on phosphate and calcium metabolism in adenine gavaged laying hens.

Dietary factors such as adenine have been linked to phosphate-calcium metabolism disturbance and adverse productive outcomes. Anti-fibroblast growth factor 23 (FGF-23) antibody has been proposed to ameliorate adenine-induced abnormal FGF23/phosphate metabolism. This experiment was conducted to investigate the application of anti-FGF-23 antibody in adenine-gavaged laying hens. Single Comb White Leghorn laying hens with (n = 10) or without (control group, n = 10) systemic anti-FGF-23 antibody were orally gavaged with adenine (600 mg/hen/D) for 21 consecutive days. Adenine gavage increased (P ≤ 0.01) plasma phosphate and calcium levels and tended to increase (0.05 < P ≤ 0.1) plasma 1,25-dihydroxy-cholecalciferol [1,25(OH)2D3] level of hens without FGF-23 antibody. In hen with anti-FGF-23 antibody, adenine gavage increased (P ≤ 0.01) body weight and plasma calcium level and decreased (P ≤ 0.05) plasma FGF-23 level. Feed intake of hens in both treatments was suddenly decreased (control hens decreased from 111 to 55 g, P ≤ 0.01; anti-FGF-23 hens decreased from 96 to 46 g, P ≤ 0.01) 10 D after adenine gavage. Anti-FGF-23 antibody tended to increase (0.05 < P ≤ 0.1) plasma phosphorus level of hens before adenine gavage, interestingly, and decreased (P ≤ 0.01) plasma FGF-23 level and kidney index (% of body weight) of hens after adenine gavage. In conclusion, anti-FGF-23 antibody might be used (before or in the early stage) to delay the development of adenine-induced abnormal FGF23/phosphate metabolism. This is the first study to investigate the FGF-23 status in chickens suffering from dietary factors which may cause abnormal renal phosphate resorption.

Implications of phytate in plant-based foods for iron and zinc bioavailability, setting dietary requirements, and formulating programs and policies.

Plant-based diets in low-income countries (LICs) have a high content of phytic acid (myo-inositol hexaphosphate [InsP6]) and associated magnesium, potassium, and calcium salts. Together, InsP6 acid and its salts are termed "phytate" and are potent inhibitors of iron and zinc absorption. Traditional food processing can reduce the InsP6 content through loss of water-soluble phytate or through phytase hydrolysis to lower myo-inositol phosphate forms that no longer inhibit iron and zinc absorption. Hence, some processing practices can reduce the need for high-dose iron fortificants in plant-based diets and alleviate safety concerns. Dietary phytate-to-iron and phytate-to-zinc molar ratios are used to estimate iron and zinc bioavailability and to identify dietary iron and zinc requirements according to diet type. The European Food Safety Authority has set adult dietary zinc requirements for 4 levels of phytate intake, highlighting the urgent need for phytate food composition data. Such data will improve the ability to estimate the prevalence of inadequate zinc intakes in vulnerable groups in LICs, which will facilitate implementation of targeted policies to alleviate zinc deficiency.

Influence of selected dietary components on the functioning of the human nervous system

The diet is directly connected not only with the physical status but also with the functioning of the brain and the mental status. The potentially beneficial nutrients with a protective effect on the nervous system function include amino acids (tryptophan, phenylalanine, tyrosine, taurine), glucose and vitamins C, E, D and beta-carotene, B group vitamins (vitamin B12, vitamin B6, vitamin B4, vitamin B1) and minerals (selenium, zinc, magnesium, sodium, iron, copper, manganese, iodine). The presence of antioxidants in the diet protects against oxidative damage to nervous system cells. Biochemical data indicate that polyunsaturated fatty acids such as arachidonic acid (AA), docosahexaenoic acid (DHA), eicosapentaenoic acid (EPA) and gamma-linolenic acid (GLA) as structural components of the nervous system play a key role in its function. The nutrition of the entire body also influences the production of neurotransmitters in the brain. A diet without an appropriate supply of protein, mineral nutrients or vitamins may result in a failure to form appropriately balanced numbers of neurotransmitters, which, as a result, may lead to neurotransmission dysfunction. This is the reason why proper nutrition is based on vegetables, fruits, whole-grain cereal products supplemented with products providing full-value protein (dairy products, fish, lean meat) and high-quality fat products (vegetable oils, fish fats).

Hypovitaminosis C and vitamin C deficiency in critically ill patients despite recommended enteral and parenteral intakes.

BACKGROUND: Vitamin C is an essential water-soluble nutrient which cannot be synthesised or stored by humans. It is a potent antioxidant with anti-inflammatory and immune-supportive roles. Previous research has indicated that vitamin C levels are depleted in critically ill patients. In this study we have assessed plasma vitamin C concentrations in critically ill patients relative to infection status (septic shock or non-septic) and level of inflammation (C-reactive protein concentrations). Vitamin C status was also assessed relative to daily enteral and parenteral intakes to determine if standard intensive care unit (ICU) nutritional support is adequate to meet the vitamin C needs of critically ill patients. METHODS: Forty-four critically ill patients (24 with septic shock, 17 non-septic, 3 uncategorised) were recruited from the Christchurch Hospital Intensive Care Unit. We measured concentrations of plasma vitamin C and a pro-inflammatory biomarker (C-reactive protein) daily over 4 days and calculated patients' daily vitamin C intake from the enteral or total parenteral nutrition they received. We compared plasma vitamin C and C-reactive protein concentrations between septic shock and non-septic patients over 4 days using a mixed effects statistical model, and we compared the vitamin C status of the critically ill patients with known vitamin C bioavailability data using a four-parameter log-logistic response model. RESULTS: Overall, the critically ill patients exhibited hypovitaminosis C (i.e., < 23 µmol/L), with a mean plasma vitamin C concentration of 17.8 ± 8.7 µmol/L; of these, one-third had vitamin C deficiency (i.e., < 11 µmol/L). Patients with hypovitaminosis C had elevated inflammation (C-reactive protein levels; P < 0.05). The patients with septic shock had lower vitamin C concentrations and higher C-reactive protein concentrations than the non-septic patients (P < 0.05). Nearly 40% of the septic shock patients were deficient in vitamin C, compared with 25% of the non-septic patients. These low vitamin C levels were apparent despite receiving recommended intakes via enteral and/or parenteral nutritional therapy (mean 125 mg/d). CONCLUSIONS: Critically ill patients have low vitamin C concentrations despite receiving standard ICU nutrition. Septic shock patients have significantly depleted vitamin C levels compared with non-septic patients, likely resulting from increased metabolism due to the enhanced inflammatory response observed in septic shock.

Nutrition for adventure racing.

Adventure racing requires competitors to perform various disciplines ranging from, but not limited to, mountain biking, running, kayaking, climbing, mountaineering, flat- and white-water boating and orienteering over a rugged, often remote and wilderness terrain. Races can vary from 6 hours to expedition-length events that can last up to 10-consecutive days or more. The purpose of this article is to provide evidence-based nutritional recommendations for adventure racing competitors. Energy expenditures of 365-750 kcal/hour have been reported with total energy expenditures of 18 000-80 000 kcal required to complete adventure races, and large negative energy balances during competitions have been reported. Nutrition, therefore, plays a major role in the successful completion of such ultra-endurance events. Conducting research in these events is challenging and the limited studies investigating dietary surveys and nutritional status of adventure racers indicate that competitors do not meet nutrition recommendations for ultra-endurance exercise. Carbohydrate intakes of 7-12 g/kg are needed during periods of prolonged training to meet requirements and replenish glycogen stores. Protein intakes of 1.4-1.7 g/kg are recommended to build and repair tissue. Adequate replacement of fluid and electrolytes are crucial, particularly during extreme temperatures; however, sweat rates can vary greatly between competitors. There is considerable evidence to support the use of sports drinks, gels and bars, as they are a convenient and portable source of carbohydrate that can be consumed during exercise, in training and in competition. Similarly, protein and amino acid supplements can be useful to help meet periods of increased protein requirements. Caffeine can be used as an ergogenic aid to help competitors stay awake during prolonged periods, enhance glycogen resynthesis and enhance endurance performance.

[Effect of ethanol adminstration in the consumption of proteins and nitrogen balance in normal subjects with normoprotein diet]. / Efecto de la administración de etanol en la utilización protéica y balance nitrogenado en sujetos normales con dietas normoprotéicas.

The effect of excessive alcohol intake on the protein requirements and metabolism in normal subjects has not been clearly determined. In this study we measured the nitrogen balance, the hematrocrit, the hemoglobin, the serum albumin, the cholesterol, and the plasmatic amino acids in 7 non-alcoholic subjects of 25 +/- 5 years of age. A comparison was made of a diet containing 0.8 g of protein per k of weight and 40 Kcal per k of weight administered during 11 days with a period of the same length in which the 1.400 Kcal provided during the control period by carbon hydrates was provided by ethanol (200 g). During the alcoholic period no importants changes were observed in the nitrogen balance, a tendency towards greater positivity being registered. There was a decrease in the serum albumin of 4, 69 +/- 0.31 vs 3, 90 +/- 0,32 g/100 ml and an increase in globulin 1,74 +/- 0,70 vs 2,69 +/- 0,22 g/100 ml. The results showed that in a short period of time the excessive alcohol intake in normal subjects does not increase the protein requirements in spite of a decrease in the serum albumin being observed.