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

Pregnant Dutch Women Have Inadequate Iodine Status and Selenium Intake

Iodine and selenium are essential for thyroid hormone synthesis. Iodine and selenium interact. Pregnancy increases the maternal iodine requirement. We previously reported inadequate iodine status in pregnant Dutch women. Since little is known about their selenium intake, we investigated the iodine status and selenium intake in relation to iodine and selenium supplement use during pregnancy. Iodine status was established in 201 apparently healthy pregnant women as 24 h iodine excretion (24H-UIE; sufficient if median ≥225 µg), iodine concentration (24H-UIC; ≥150 µg/L) and iodine/creatinine ratio (24H-UICR; ≥150 µg/g). Selenium intake was calculated from 24 h selenium excretion. Iodine status in pregnancy proved insufficient (medians: 24H-UIE 185 µg; 24H-UIC 95 µg/L; 24H-UICR 141 µg/g). Only women taking 150 µg iodine/day were sufficient (median 24H-UIE 244 µg). Selenium intake was below the Estimated Average Requirement (EAR; 49 µg/day) in 53.8%, below the Recommended Dietary Allowance (RDA; 60 µg/day) in 77.4% and below the Adequate Intake (AI; 70 µg/day) in 88.7%. Combined inadequate iodine status and selenium intake <RDA was found in 61%. Women who want to become pregnant should, consistently with WHO and ETA recommendations, be advised to use a 150 µg iodine-containing supplement. Concomitant selenium supplementation should be added to this advice, at least in The Netherlands

Low circulating concentrations of very long chain saturated fatty acids are associated with high risk of mortality in kidney transplant recipients

Kidney transplant recipients (KTR) are at increased risk of mortality, particularly from infectious diseases, due to lifelong immunosuppression. Although very long chain saturated fatty acids (VLSFA) have been identified as crucial for phagocytosis and clearance of infections, their association with mortality in immunocompromised patient groups has not been studied. In this prospective cohort study we included 680 outpatient KTR with a functional graft ≥1 year and 193 healthy controls. Plasma VLSFA (arachidonic acid (C20:0), behenic acid (C22:0) and lignoceric acid (C24:0)) were measured by gas chromatography coupled with a flame ionization detector. Cox regression analyses was used to prospectively study the associations of VLSFA with all-cause and cause-specific mortality. All studied VLSFA were significantly lower in KTR compared to healthy controls (all p < 0.001). During a median (interquartile range) follow-up of 5.6 (5.2–6.3) years, 146 (21%) KTR died, of which 41 (28%) died due to infectious diseases. In KTR, C22:0 was inversely associated with risk of all-cause mortality, with a HR (95% CI) per 1-SD-increment of 0.79 (0.64–0.99), independent of adjustment for potential confounders. All studied VLSFA were particularly strongly associated with mortality from infectious causes, with respective HRs for C20:0, C22:0 and C24:0 of 0.53 (0.35–0.82), 0.48 (0.30–0.75), and 0.51 (0.33–0.80), independent of potential confounders. VLSFA are inversely associated with infectious disease mortality in KTR after adjustment, including HDL-cholesterol. Further studies are needed to assess the effect of VLSFA-containing foods on the risk of infectious diseases in immunocompromised patient groups

Hetfaillissement van de verzadigd vethypothese van cardiovasculaire ziektes

Fat and notably saturated fatty acids (SAFA) have a poor name. The Dutch Health Council recommends: SAFA intake as low as possible [<10 energy% (en%)] and 40-70 en% carbohydrates (CHO). The AHA recommends 5-10 en% polyunsaturated fatty acids (PUFA) of the omega-6 series (i.e. linoleic acid). The general public lived up to these recommendations to a large extent. The SAFA, CHO and linoleic acid recommendations contrast with the dietary composition of our ancestors in the Paleolithic era, with whom we differ little in a genetic sense. It was recently shown that replacing SAFA with CHO is associated with higher cardiovascular disease (CVD) risk, notably because of replacement with CHO with a high glycemic index (GI). Replacing SAFA with PUFA was associated with lower CVD risk. However, reanalysis of the AHA recommendation showed a borderline insignificant higher mortality risk with linoleic acid replacement. Insufficient consumption of fish, vegetables and fruits causes an estimated 10 times higher CVD risk than consumption of too much SAFA. Recent meta-analyses showed that SAFA, milk and milk products are not associated with CVD risk. The current connection between SAFA and CVD risk is based on an association with LDL- and HDL-cholesterol. Atherogenic dyslipidemia is increasingly regarded as secondary to chronic systemic low grade inflammation, reflected by CRP. SAFA cause inflammation by interaction with our immune system. This interaction is facilitated by consumption of CHO and notably its conversion to fat. Promoting factors are a high CHO intake, CHO with high GI, fructose, alcohol and impaired insulin sensitivity. Fish oil fatty acids inhibit de novo fatty acid synthesis and promote fatty acid oxidation, while linoleic acid inhibits the synthesis of these fatty acids and their incorporation. There is no valid evidence for the adverse effects of fat and SAFA per se. Accumulation of SAFA should be prevented. The recommended 40-70 en% CHO should be reconsidered and the consumption of CHO with high GI and fructose should be limited. The recommended 5-10 en% linoleic acid also needs reconsideration. The exaggerated attention for fat and SAFA distracts from more important avoidable risk factors for the many typically Western diseases that are linked with the metabolic syndrome. A lifestyle that causes chronic systemic low grade inflammation should be avoided

Corrigendum to "Influence of a 10-Day Mimic of Our Ancient Lifestyle on Anthropometrics and Parameters of Metabolism and Inflammation: The "Study of Origin""

[This corrects the article DOI: 10.1155/2016/6935123.]

Autoantibodies to selenoprotein P in chronic fatigue syndrome suggest selenium transport impairment and acquired resistance to thyroid hormone

Chronic Fatigue Syndrome (CFS) presents with symptoms of hypothyroidism, including mental and physical fatigue, poor sleep, depression, and anxiety. However, thyroid hormone (TH) profiles of elevated thyrotropin and low thyroxine (T4) are not consistently observed. Recently, autoantibodies to the Se transporter SELENOP (SELENOP-aAb) have been identified in Hashimoto's thyroiditis and shown to impair selenoprotein expression. We hypothesized that SELENOP-aAb are prevalent in CFS, and associate with reduced selenoprotein expression and impaired TH deiodination.Se status and SELENOP-aAb prevalence was compared by combining European CFS patients (n = 167) and healthy controls (n = 545) from different sources. The biomarkers total Se, glutathione peroxidase (GPx3) and SELENOP showed linear correlations across the samples without reaching saturation, indicative of Se deficiency. SELENOP-aAb prevalence was 9.6–15.6% in CFS versus 0.9–2.0% in controls, depending on cut-off for positivity. The linear correlation between Se and GPx3 activity was absent in SELENOP-aAb positive patients, suggesting impaired Se supply of kidney. A subgroup of paired control (n = 119) and CSF (n = 111) patients had been characterized for TH and biochemical parameters before. Within this subgroup, SELENOP-aAb positive patients displayed particularly low deiodinase activity (SPINA-GD index), free T3 levels, total T3 to total T4 (TT3/TT4) and free T3 to free T4 (FT3/FT4) ratios. In 24 h urine, iodine concentrations were significantly lower in SELENOP-aAb positive than in SELENOP-aAb negative patients or controls (median (IQR); 43.2 (16.0) vs. 58.9 (45.2) vs. 89.0 (54.9) μg/L). The data indicate that SELENOP-aAb associate with low deiodination rate and reduced activation of TH to active T3.We conclude that a subset of CFS patients express SELENOP-aAb that disturb Se transport and reduce selenoprotein expression in target tissues. Hereby, TH activation decreases as an acquired condition not reflected by thyrotropin and T4 in blood. This hypothesis opens new diagnostic and therapeutic options for SELENOP-aAb positive CFS, but requires clinical evidence from intervention trials

Prevalence and effects of functional vitamin K insufficiency : The PREVEND study

Matrix Gla Protein (MGP) is a strong vitamin K-dependent inhibitor of soft tissue calcification. We assessed the prevalence of functional vitamin K insufficiency, as derived from plasma desphospho-uncarboxylated MGP (dp-ucMGP), and investigated whether plasma dp-ucMGP is associated with all-cause and cardiovascular mortality in a large general population-based cohort. We included 4275 subjects (aged 53 ± 12 years, 46.0% male) participating in the prospective general population-based Prevention of Renal and Vascular End-Stage Disease (PREVEND) study. The prevalence of functional vitamin K insufficiency (i.e., dp-ucMGP > 500 pmol/L) was 31% in the total study population. This prevalence was significantly higher among elderly and subjects with comorbidities like hypertension, type 2 diabetes, chronic kidney disease, and cardiovascular disease (~50%). After 10 years of follow-up, 279 subjects had died, with 74 deaths attributable to cardiovascular causes. We found significant J-shaped associations of plasma dp-ucMGP with all-cause (linear term: hazard ratio (HR) (95% confidence interval (CI)) = 0.20 (0.12–0.33), p < 0.001; squared term: 1.14 (1.10–1.17), p < 0.001) and cardiovascular mortality (linear term: 0.12 (0.05–0.27), p < 0.001; squared term: 1.17 (1.11–1.23), p < 0.001). These associations remained significant after adjustment for potential confounders. Whether the correction of vitamin K insufficiency improves health outcomes needs to be addressed in future prospective intervention studies