Thyroidal and Extrathyroidal Requirements for Iodine and Selenium: A Combined Evolutionary and (Patho)Physiological Approach.

Iodide is an antioxidant, oxidant and thyroid hormone constituent. Selenoproteins are needed for triiodothyronine synthesis, its deactivation and iodine release. They also protect thyroidal and extrathyroidal tissues from hydrogen peroxide used in the 'peroxidase partner system'. This system produces thyroid hormone and reactive iodine in exocrine glands to kill microbes. Exocrine glands recycle iodine and with high urinary clearance require constant dietary supply, unlike the thyroid. Disbalanced iodine-selenium explains relations between thyroid autoimmune disease (TAD) and cancer of thyroid and exocrine organs, notably stomach, breast, and prostate. Seafood is iodine unconstrained, but selenium constrained. Terrestrial food contains little iodine while selenium ranges from highly deficient to highly toxic. Iodine vs. TAD is U-shaped, but only low selenium relates to TAD. Oxidative stress from low selenium, and infection from disbalanced iodine-selenium, may generate cancer of thyroid and exocrine glands. Traditional Japanese diet resembles our ancient seashore-based diet and relates to aforementioned diseases. Adequate iodine might be in the milligram range but is toxic at low selenium. Optimal selenoprotein-P at 105 µg selenium/day agrees with Japanese intakes. Selenium upper limit may remain at 300-400 µg/day. Seafood combines iodine, selenium and other critical nutrients. It brings us back to the seashore diet that made us what we currently still are.

A review of vitamin A equivalency of ß-carotene in various food matrices for human consumption.

Vitamin A equivalency of ß-carotene (VEB) is defined as the amount of ingested ß-carotene in µg that is absorbed and converted into 1 µg retinol (vitamin A) in the human body. The objective of the present review was to discuss the different estimates for VEB in various types of dietary food matrices. Different methods are discussed such as mass balance, dose-response and isotopic labelling. The VEB is currently estimated by the US Institute of Medicine (IOM) as 12:1 in a mixed diet and 2:1 in oil. For humans consuming ß-carotene dissolved in oil, a VEB between 2:1 and 4:1 is feasible. A VEB of approximately 4:1 is applicable for biofortified cassava, yellow maize and Golden Rice, which are specially bred for human consumption in developing countries. We propose a range of 9:1-16:1 for VEB in a mixed diet that encompasses the IOM VEB of 12:1 and is realistic for a Western diet under Western conditions. For a 'prudent' (i.e. non-Western) diet including a variety of commonly consumed vegetables, a VEB could range from 9:1 to 28:1 in a mixed diet.

Food matrix effects on bioaccessibility of ß-carotene can be measured in an in vitro gastrointestinal model.

Since the food matrix determines ß-carotene availability for intestinal absorption, food matrix effects on the bioaccessibility of ß-carotene from two diets were investigated in vitro and compared with in vivo data. The "mixed diet" consisted of ß-carotene-rich vegetables, and the "oil diet" contained ß-carotene-low vegetables with supplemental ß-carotene. The application of extrinsically labeled ß-carotene was also investigated. The bioaccessibility of ß-carotene was 28 µg/100 µg ß-carotene from the mixed diet and 53 µg/100 µg ß-carotene from the oil diet. This ratio of 1.9:1 was consistent with in vivo data, where the apparent absorption was 1.9-fold higher in the oil diet than in the mixed diet. The labeled ß-carotene was not equally distributed over time. In conclusion, the food matrix effects on bioaccessibility of ß-carotene could be measured using an in vitro model and were consistent with in vivo data. The application of extrinsically labeled ß-carotene was not confirmed.

Advantages and limitations of the protein digestibility-corrected amino acid score (PDCAAS) as a method for evaluating protein quality in human diets.

PDCAAS is a widely used assay for evaluating protein quality. It is a chemical score, which is derived from the ratio between the first limiting amino acid in a test protein and the corresponding amino acid in a reference amino acid pattern and corrected for true faecal N digestibility. Chemical scores exceeding 100 % are truncated to 100 %. The advantages of the PDCAAS are its simplicity and direct relationship to human protein requirements. The limitations are as follows: the reference pattern is based on the minimum amino acid requirements for tissue growth and maintenance and does not necessarily reflect the optimum intake. Truncated PDCAAS of high-quality proteins do not give any information about the power of these proteins to compensate, as a supplement, for low levels of dietary essential amino acids in low-quality proteins. It is likely that faecal N digestibility does not take into account the loss from the colon of indispensable amino acids that were not absorbed in the ileum. Anti-nutritional factors, such as lectins and trypsin inhibitors, in several plant protein sources can cause heightened endogenous losses of amino acids, an issue which is particularly relevant in animal feedstuffs. The assumption that amino acid supplementation can completely restore biological efficiency of the protein source is incorrect since the kinetics of digestion and absorption between supplemented free amino acids and amino acids present in dietary proteins, are different.

Vitamin A equivalency and apparent absorption of beta-carotene in ileostomy subjects using a dual-isotope dilution technique.

The objective was to quantify the vitamin A equivalency of beta-carotene in two diets using a dual-isotope dilution technique and the apparent beta-carotene absorption as measured by the oral-faecal balance technique. Seventeen healthy adults with an ileostomy completed the 4-week diet-controlled, cross-over intervention study. Each subject followed both diets for 2 weeks: a diet containing vegetables low in beta-carotene content with supplemental beta-carotene in salad dressing oil ('oil diet'; mean beta-carotene intake 3.1 mg/d) and a diet containing vegetables and fruits high in beta-carotene content ('mixed diet'; mean beta-carotene intake 7.6 mg/d). Daily each subject consumed a mean of 190 microg [13C10]beta-carotene and 195 microg [13C10]retinyl palmitate in oil capsules. The vitamin A equivalency of beta-carotene was calculated as the dose-corrected ratio of [13C5]retinol to [13C10]retinol in serum. Apparent absorption of beta-carotene was determined with oral-faecal balance. Isotopic data quantified a vitamin A equivalency of [13C10]beta-carotene in oil of 3.6:1 (95 % CI 2.8, 4.6) regardless of dietary matrices differences. The apparent absorption of (labelled and dietary) beta-carotene from the 'oil diet' (30 %) was 1.9-fold higher than from the 'mixed diet' (16 %). This extrinsic labelling technique can measure precisely the vitamin A equivalency of beta-carotene in oil capsules, but it does not represent the effect of different dietary matrices.

Increased consumption of fatty and lean fish reduces serum C-reactive protein concentrations but not inflammation markers in feces and in colonic biopsies.

Fish consumption is associated with a reduced colorectal cancer risk. A possible mechanism by which fish consumption could decrease colorectal cancer risk is by reducing inflammation. However, thus far, intervention studies investigating both systemic and local gut inflammation markers are lacking. Our objective in this study was to investigate the effects of fatty and lean fish consumption on inflammation markers in serum, feces, and gut. In an intervention study, participants were randomly allocated to receive dietary advice (DA) plus either 300 g of fatty fish (salmon) or 300 g of lean fish (cod) per week for 6 mo, or only DA. Serum C-reactive protein (CRP) concentrations were measured pre- and postintervention (n = 161). In a subgroup (n = 52), we explored the effects of the fish intervention on fecal calprotectin and a wide range of cytokines and chemokines in fecal water and in colonic biopsies. Serum CRP concentrations were lower in the salmon (-0.5 mg/L; 95% CI -0.9, -0.2) and cod (-0.4 mg/L; 95% CI -0.7, 0.0) groups compared with the DA group. None of the inflammation markers in fecal water and colonic biopsies differed between the DA group and the groups that consumed extra fish. In conclusion, increasing salmon or cod consumption for 6 mo resulted in lower concentrations of the systemic inflammation marker CRP. However, exploratory analysis of local markers of inflammation in the colon or feces did not reveal an effect of fish consumption.

Vitamin A equivalency of beta-carotene in healthy adults: limitation of the extrinsic dual-isotope dilution technique to measure matrix effect.

Data on the vitamin A equivalency of beta-carotene in food are inconsistent. We quantified the vitamin A equivalency (microg) of beta-carotene in two diets using the dual-isotope dilution technique and the oral-faecal balance technique. A diet-controlled, cross-over intervention study was conducted in twenty-four healthy adults. Each subject followed two diets for 3 weeks each: a diet containing vegetables low in beta-carotene with supplemental beta-carotene in salad dressing oil ('oil diet') and a diet containing vegetables and fruits high in beta-carotene ('mixed diet'). During all 6 weeks, each subject daily consumed a mean of 55 (sd 0.5) microg [13C10]beta-carotene and 55 (sd 0.5) microg [13C10]retinyl palmitate in oil capsules. The vitamin A equivalency of beta-carotene was calculated as the dose-corrected ratio of [13C5]retinol to [13C10]retinol in serum and from apparent absorption by oral-faecal balance. Isotopic data quantified a vitamin A equivalency of [13C10]beta-carotene in oil of 3.4 microg (95 % CI 2.8, 3.9), thus the bio-efficacy of the beta-carotene in oil was 28 % in the presence of both diets. However, data from oral-faecal balance estimated vitamin A equivalency as 6:1 microg (95 % CI 4, 7) for beta-carotene in the 'oil diet'. beta-Carotene in the 'oil diet' had 2.9-fold higher vitamin A equivalency than beta-carotene in the 'mixed diet'. In conclusion, this extrinsic labelling technique cannot measure effects of mixed vegetables and fruits matrices, but can measure precisely the vitamin A equivalency of the beta-carotene in oil capsules.

The Protein Digestibility-Corrected Amino Acid Score (PDCAAS)--a concept for describing protein quality in foods and food ingredients: a critical review.

Protein Digestibility-Corrected Amino Score (PDCAAS) is discussed. PDCAAS is now widely used as a routine assay for protein quality evaluation, replacing the more traditional biological methods [e.g., measurement of the Protein Efficiency Ratio (PER) in rats]. PDCAAS is based on comparison of the essential amino acid content of a test protein with that of a reference essential amino acid pattern and a correction for differences in protein digestibility as determined using a rat assay. Although PDCAAS is a rapid and useful method, it often shows discrepancies when compared to PER values. These discrepancies relate to the following issues: uncertainty about the validity of reference patterns, invalidity of correction for fecal (versus ileal) digestibility, truncation of PDCAAS values to 100%, failure to obtain full biological response after supplementation of the limiting essential amino acid, discrepancies between protein and amino acid digestibility, effects of processing on protein quality, and effects of the presence of antinutritional factors in the matrix containing the protein. Part of the discrepancy between PDCAAS and PER can be overcome by modifications of PDCAAS. This article describes some proposed modifications and puts forward the suggestion that the rat protein fecal digestibility assay be replaced by an in vitro ileal amino acid digestibility assay based on a computer-controlled gastrointestinal model.

Folic acid and 5-methyltetrahydrofolate in fortified milk are bioaccessible as determined in a dynamic in vitro gastrointestinal model.

Dairy products are a potential matrix for folate fortification to enhance folate consumption in the Western world. Milk folate-binding proteins (FBP) are especially interesting because they seem to be involved in folate bioavailability. In this study, folate bioaccessibility was investigated using a dynamic computer-controlled gastrointestinal model [TNO gastrointestinal model (TIM)]. We used both ultrahigh temperature (UHT)-processed milk and pasteurized milk, differing in endogenous FBP concentrations and fortified with folic acid or 5-methyltetrahydrofolate (5-CH(3)-H(4)folate). To study FBP stability during gastrointestinal passage and the effect of additional FBP on folate bioaccessibility, FBP-fortified UHT and pasteurized milk products were also tested. Folate bioaccessibility and FBP stability were measured by taking samples along the compartments of the gastrointestinal model and measuring their folate and FBP concentrations. Folate bioaccessibility from folic acid-fortified milk products without additional FBP was 58-61%. This was lower (P < 0.05) than that of the 5-CH(3)-H(4)folate-fortified milk products (71%). Addition of FBP reduced (P < 0.05) folate bioaccessibility from folic acid-fortified milk (44-51%) but not from 5-CH(3)-H(4)folate-fortified milk products (72%). The residual FBP levels in the folic acid- and 5-CH(3)-H(4)folate-fortified milk products after gastrointestinal passage were 13-16% and 0-1%, respectively, of the starting amounts subjected to TIM. In conclusion, milk seems to be a suitable carrier for folate, because both folic acid and 5-CH(3)-H(4)folate are easily released from the matrix and available for absorption. However, our results suggest that folic acid remains partly bound to FBP during passage through the small intestine, which reduces the bioaccessibility of folic acid from milk in this model.