Effect of vitamin D3 supplementation on iron status: a randomized, double-blind, placebo-controlled trial among ethnic minorities living in Norway

Abstract

BackgroundBoth vitamin D and iron deficiencies are widespread globally, and a relationship between these deficiencies has been suggested. However, there is a paucity of randomised controlled trials assessing the effect of vitamin D supplementation on iron status.PurposeWe aimed to investigate whether 16 weeks of daily vitamin D3 supplementation had an effect on serum ferritin, haemoglobin, serum iron and transferrin saturation.MethodsOverall, 251 participants from South Asia, Middle East and Africa aged 18–50 years who were living in Norway were randomised to receive daily oral supplementation of 10 μg vitamin D3, 25 μg vitamin D3, or placebo for 16 weeks during the late winter. Blood samples from baseline and after 16 weeks were analysed for serum 25-hydroxyvitamin D (s-25(OH) D), serum ferritin, haemoglobin and serum iron. In total, 214 eligible participants completed the intervention (86 % of those randomised). Linear regression analysis were used to test the effect of vitamin D3 supplementation combined (10 or 25 μg) and separate doses 10 or 25 μg compared to placebo on change (T2-T1) in each outcome variable adjusted for baseline s-25(OH)D values.ResultsThere was no difference in change in the levels of s-ferritin (1.9 μg/L, 95 % CI: -3.2, 7.0), haemoglobin (-0.02 g/dL, 95 % CI: -0.12, 0.09), s-iron (0.4 μg/L, 95 % CI: -0.5, 1.3) or transferrin saturation (0.7 %, 95 % CI: -0.6.1, 2.0) between those receiving vitamin D3 or those receiving placebo. Serum 25-hydroxyvitamin D increased from 29 nmol/L at baseline to 49 nmol/L after the intervention, with little change in the placebo group.ConclusionsIn this population of healthy ethnic minorities from South Asia, the Middle East and Africa who had low vitamin D status, 16 weeks of daily supplementation with 10 or 25 μg of vitamin D3 did not significantly affect the haemoglobin levels or other markers of iron status.Electronic supplementary materialThe online version of this article (doi:10.1186/s12937-016-0192-7) contains supplementary material, which is available to authorized users.

The effect of vitamin D supplementation on hemoglobin concentration: a systematic review and meta-analysis

“…Cholecalciferol was the main form of vitamin D that were supplemented in these studies. The duration of supplementation with vitamin D also varied from 3 h to 6 months [40][41][42][43][44][45][46][47][48][49][50][51][52][53].…”

“…Different types of vitamin D were used in these studies, four studies received vitamin D fortified food with cholecalciferol [40,[46][47][48], eight studies received oral vitamin D (cholecalciferol) supplements [42,44,45,[49][50][51][52][53] and in one study subjects were supplemented with ergocalciferol and another one with calcitriol [41,43]. The minimum vitamin D dosage was 20 IU and maximum was 500,000 IU according to these studies ( Table 1).…”

Vitamin D Status Is Associated with Hepcidin and Hemoglobin Concentrations in Children with Inflammatory Bowel Disease

“…This is consistent with several studies in chronic kidney disease, cardiovascular disease, and the general population, which have described a positive association between vitamin D status and hemoglobin and/or an inverse association between vitamin D status and anemia (9–13, 15, 39, 40). Data from clinical trials have been mixed (39–42), but recent studies in CKD and critically ill adult patient populations found that treatment with vitamin D or its analogues resulted in significant increases in hemoglobin concentrations (24, 43). This association has not been previously studied in IBD animal models or clinical studies.…”

Vitamen D Assessment In Iron Dificiency Anemic Pregnant Women and Their Newborn Compared to Controls

“…Therefore,vitamin D deficiency may affect the regulation ofhepcidin, which could accelerate the decrease in haemoglobinand increase the incidence of anaemia (Zughaier et al, 2014). Iron deficiency anaemia is the last end stage of progressionfrom normal iron status to frank deficiency (Madar et al, 2016).…”