Research ArticleClinical Studies
Open Access

Effects of Short-term High-dose Vitamin D Supplementation on Mineral Homeostasis in Healthy Young Adults

MARKÉTA KRÁLOVÁ, PAVLÍNA ČERNÁ, HEDVIKA MIKOLÁŠOVÁ, MICHAL JIRÁSKO, EVA DĚDEČKOVÁ, RADEK KUČERA and LADISLAV PECEN
In Vivo May 2026, 40 (3) 1645-1653; DOI: https://doi.org/10.21873/invivo.14315

Abstract

Background/Aim: High-dose vitamin D supplementation is increasingly used to achieve extraskeletal effects, but its safety regarding mineral metabolism remains under discussion. This study assessed the effects of vitamin D on serum calcium, magnesium, and parathyroid hormone (PTH) concentrations in young healthy individuals.

Materials and Methods: Sixty-five healthy volunteers received cholecalciferol drops in doses ranging from 1,000 to 8,000 IU/day across two winter seasons. Serum concentrations of 25-hydroxyvitamin D [25(OH)D], calcium, magnesium, and PTH were measured at defined intervals.

Results: Supplementation resulted in a dose-dependent increase in serum 25(OH)D, reaching a maximum of 208.5 nmol/l. Despite the high intake, all measured parameters remained within physiological ranges. A significant inverse association between 25(OH)D and PTH levels confirmed physiological suppression of PTH at higher vitamin D concentrations, though all values stayed within reference limits.

Conclusion: The absence of clinically relevant disturbances in calcium, magnesium, or PTH levels supports the safety of high-dose vitamin D supplementation when appropriately monitored in young healthy adults, even at the upper limits of therapeutic dosing. These findings highlight the need for further research to delineate the long-term effects of high-dose vitamin D supplementation on mineral metabolism across diverse patient populations.

Keywords:

Introduction

Vitamin D is a fat-soluble vitamin obtained from diet and synthesized in the skin via UVB radiation. It exists mainly as ergocalciferol (D2) and cholecalciferol (D3), the latter being predominant in humans. Both forms are biologically inactive and require hydroxylation in the liver to 25(OH)D (calcidiol) and then in the kidney to 1,25(OH)2D (calcitriol), the active form (1). Vitamin D regulates calcium-phosphate metabolism and exerts extraskeletal effects, including immune modulation, metabolic processes, cell proliferation, differentiation, and apoptosis (2, 3).

Limited sun exposure, particularly in regions at latitudes above 33°, which includes European populations, and reduced dietary intake may contribute to hypovitaminosis D (4). This has become a global health concern and may lead to various health issues, including hypocalcemia and impaired bone mineralization. Recently, increasing attention has been directed toward vitamin D deficiency due to its association with a higher risk of developing autoimmune, malignant, metabolic, cardiovascular, and infectious diseases (5-7).

A general consensus on the optimal dosage of vitamin D for supplementation has not been established (6). Serum 25(OH)D levels are widely recognized as the standard measure of vitamin D status, though definitions of sufficiency vary across clinical guidelines. Deficiency is typically defined as concentrations below 50 nmol/l, with severe deficiency classified as levels under 30 nmol/l – thresholds linked to a markedly increased risk of rickets and osteomalacia. For the general population under the age of 65, levels between 50 and 150 nmol/l are considered sufficient, while individuals with increased vulnerability are advised to maintain concentrations within the 75-150 nmol/l range (8). To achieve the extraskeletal effects attributed to vitamin D, serum 25(OH)D concentrations generally need to be sustained within the range of 75-125 up to 150 nmol/l, which typically requires regular supplementation with vitamin D doses of 3,000-5,000 IU/day (9).

Elevated vitamin D intake, particularly daily doses ≥4,000 IU, poses potential health risks (10). A primary concern associated with vitamin D toxicity is hypercalcemia resulting from enhanced intestinal calcium absorption, which can lead to severe gastrointestinal disturbances and multisystem complications with potentially life-threatening consequences (11, 12). In addition to increasing serum calcium levels, high doses of vitamin D may also suppress parathyroid hormone (PTH) activity and potentially affect magnesium levels (13-15). However, multiple studies indicate that high-dose vitamin D supplementation (up to 10,000 IU/day) can be considered safe and rarely leads to hypercalcemia in healthy individuals; when it occurs, symptoms are typically mild and transient (10). The likelihood of hypercalcemic intoxication and associated complications rises significantly when serum 25(OH)D levels exceed 250 nmol/l (8).

The aim of this study was to assess the impact of vitamin D supplementation, administered at doses targeting extraskeletal effects, on serum concentrations of calcium, magnesium, and PTH in young healthy individuals.

Materials and Methods

Study population. Sixty-five healthy volunteers of Caucasian ethnicity, without chronic diseases, metabolic disorders, or cancer, participated in this study. Pregnant women were not included. The initial screening involved the assessment of body mass index (BMI). A detailed overview of patient characteristics is provided in Table I. The study was conducted between October 2021 and April 2023, with data collected exclusively during October-April periods each year to minimize the confounding effect of solar UVB radiation on endogenous cutaneous synthesis of vitamin D3 in study participants. An over-the-counter form of cholecalciferol drops in an oil-based solution was used for supplementation. The dosing schedule is presented in Table II. Only participants who completed all scheduled blood draws were included in the study. The participants were not allowed to take any additional vitamin D, calcium, or magnesium supplements. The study was approved by the Ethics Committee of University Hospital Pilsen and the Faculty of Medicine in Pilsen, Charles University, under the number 374/2020, August 6, 2020.

View this table:
Table I.

Patient characteristics.

View this table:
Table II.

Dosing schedule and blood draw description.

Sample collection. Blood sampling was conducted according to the dosing regimen. Blood samples were collected in the morning hours at approximately the same time for each participant, with fasting recommended prior to sampling. A total of ten blood samples were collected during the two supplementation periods (see Table II). Peripheral blood samples were drawn into VACUETTE® CAT Serum Separator Clot Activator tubes (Greiner Bio-One, Kremsmünster, Austria). Within two hours of collection, the tubes were centrifuged at 1,700 rpm for 10 min to separate the serum. Each serum sample was then divided into three aliquots of equal volume (500 μl each): two reserved for analysis and one archived. Samples were either processed on the same day for ion analysis or stored at −80 °C for further analysis.

Vitamin D, Ca, Mg, and PTH measurement. Total 25(OH)D levels were assessed using the chemiluminescent ACCESS 25(OH) Vitamin D Total kit (Beckman Coulter, Brea, CA, USA), and PTH levels were measured with the ACCESS Intact PTH kit on the Unicel® DxI 800 Analyzer (Beckman Coulter). All samples were thawed simultaneously and analyzed in a single batch. Calcium and magnesium concentrations were quantified using the Cobas system (Cobas 8000, Cobas c702, Roche Diagnostics, Basel, Switzerland). The intra- and inter-assay coefficients of variation were <10.0% for 25(OH)D, <2.0% for calcium, <2.0% for magnesium, and <8.0% for PTH, according to manufacturer specifications. Samples designated for ion measurement were processed immediately on the day of collection. Unlike the other serum parameters, serum levels of PTH were measured only during the second part of the study period, from October 2022 to March 2023. Physiological reference ranges for comparison were derived from the official documentation provided by the manufacturers of the instruments employed in data analysis.

Statistical analysis. Statistical analysis was conducted using SAS software (version 9.4, SAS Institute Inc., Cary, NC, USA). Normality of data distribution was assessed using the Shapiro-Wilk test. For relationships between serum 25(OH)D and calcium, magnesium, PTH, and BMI, simple linear regression analysis was conducted. Each bivariate relationship was visualized using scatterplots with superimposed linear regression lines, 95% confidence intervals, and 95% prediction bands. p-Values <0.05 were considered statistically significant. Because multiple samples were obtained per participant, observations are not statistically independent. Simple linear regression was used for exploratory visualization, while recognizing that a mixed-effects model would better account for within-subject correlation.

Results

Vitamin D and calcium. Statistical analysis revealed a highly significant positive correlation between serum vitamin D and calcium levels (p<0.0001) (Figure 1). The effect was however modest, and even at the highest vitamin D concentration observed in this study (208.5 nmol/l), serum calcium levels remained within the physiological range of 2.20-2.60 mmol/l. A hypothetical extrapolation beyond the observed range suggested that hypercalcemia would occur only at 25(OH)D concentrations above ~545 nmol/l.

Figure 1.
Figure 1.

Vitamin D and calcium levels. Positive correlation between serum 25(OH)D (nmol/l) and serum calcium (mmol/l) in healthy young adults. A scatterplot with a linear regression line, 95% confidence interval (blue) and 95% prediction bands (p<0.0001; r2=0.0451).

Vitamin D and magnesium. Statistical assessment identified a slight but significant inverse relationship between serum vitamin D and magnesium levels (p=0.0141) (Figure 2). Normal physiological levels of serum magnesium range between 0.76 and 1.15 mmol/l. A hypothetical extrapolation beyond measured values suggested that achieving critically low serum magnesium concentrations (<0.66 mmol/l) would require extremely high vitamin D levels (~989.6 nmol/l).

Figure 2.
Figure 2.

Vitamin D and magnesium levels. Negative correlation between serum 25(OH)D (nmol/l) and serum magnesium (mmol/l) in young healthy adults. A scatterplot with a linear regression line, 95% confidence interval (blue) and 95% prediction bands (p<0.0141; r2=0.0097).

Vitamin D and PTH. A statistically significant negative correlation (p<0.0001) was observed between vitamin D and PTH levels in the studied cohort, indicating that PTH concentrations declined with increasing vitamin D levels (Figure 3). The physiological reference range for PTH is defined as 1.3-9.3 pmol/l. Model extrapolation suggests that serum PTH value of ≤1.6 pmol/l would only be reached at a vitamin D concentration of 285.6 nmol/l, whereas the highest vitamin D level recorded in this study was 208.5 nmol/l.

Figure 3.
Figure 3.

Vitamin D and PTH levels. Negative correlation between serum 25(OH)D (nmol/l) and serum PTH (pmol/l) in young healthy adults. A scatterplot with a linear regression line, 95% confidence interval (blue) and 95% prediction bands (p<0.0001; r2=0.0592).

Serum calcium and BMI. As part of a secondary, exploratory analysis, statistical evaluation indicated a significant negative correlation between BMI and serum calcium levels (p=0.0008). This finding suggests that higher BMI levels are associated with lower serum calcium concentrations.

Discussion

Vitamin D plays a central role in human physiology, traditionally recognized for its critical involvement in calcium homeostasis and bone health. Beyond its well-established skeletal effects, an increasing number of studies have highlighted the hormone-like actions of vitamin D in various extraskeletal tissues, including the immune, cardiovascular, and endocrine systems (16). However, many of these extraskeletal benefits appear to require serum levels of 25(OH)D that exceed those necessary for bone maintenance, often necessitating higher supplemental doses. This brings forth concerns regarding the safety of such regimens, especially in light of their capacity to disturb mineral metabolism.

Excessive vitamin D supplementation results in elevated serum levels of 25(OH)D and its active metabolite 1,25(OH)2D, both of which synergistically enhance intestinal calcium absorption and may contribute to the development of hypercalcemia, a potentially life-threatening condition that can manifest with a wide range of symptoms (17). In our study, despite a statistically significant correlation between serum vitamin D and calcium concentrations, serum total calcium levels remained within the physiological range even following relatively high vitamin D supplementation (8,000 IU/day for two months). Model extrapolation indicated that a serum calcium level of 2.75 mmol/l, regarded as abnormally elevated, would only be reached at a vitamin D concentration of approximately 545.5 nmol/l. This projection should be interpreted cautiously, as such values were not observed.

Dudenkov et al. reported no significant association between serum 25(OH)D and calcium concentrations (p=0.20), nor with the risk of hypercalcemia (p=0.24), based on an analysis of over 20,000 vitamin D measurements (18). In contrast, our study focused on a relatively homogeneous group of 65 young, healthy individuals, which may have minimized interindividual variability and allowed the detection of a weak but statistically significant dose-dependent relationship between serum 25(OH)D and calcium. While this homogeneity reduced biological variability, it also limits external validity. The findings should not be generalized to older adults, individuals with renal impairment, or those on medications affecting calcium metabolism.

Shirvani et al. conducted a randomized, double-blind, controlled clinical trial involving 30 healthy adults receiving daily supplementation of 600, 4,000, or 10,000 IU of vitamin D3 over a 24-week period. Despite achieving substantially elevated serum 25(OH)D concentrations – up to 196.5 ± 33.8 nmol/l in the highest-dose group – the study reported no statistically significant changes in serum calcium levels across any of the intervention arms (p>0.05), which differs from our findings (19). This discrepancy may be attributable to distinctions in study design, population characteristics, and statistical methodology, which may have influenced the ability to detect subtle physiological associations.

There is growing evidence supporting the safety of high-dose vitamin D supplementation. In a randomized open-label study, Fassio et al. investigated high-dose vitamin D supplementation in otherwise healthy individuals with vitamin D deficiency, using the highest approved regimens in Italy (up to 10,000 IU/day for 8 weeks or 100,000 IU every other week for 12 weeks), and observed no serious adverse events or cases of hypercalcemia (referring to total serum calcium >2.63 mmol/l) (20).

Calcium levels were assessed as serum total calcium in our study. Although ionized calcium is the physiologically most relevant marker, its limited availability and higher cost restrict its routine use in clinical practice. Because ionized calcium and urinary calcium excretion were not evaluated, subclinical hypercalciuria or altered renal calcium handling cannot be excluded. Future studies should incorporate ionized calcium and urinary calcium/creatinine ratios to better assess renal safety.

Magnesium is essential for the enzymatic conversion of vitamin D into its active and inactive forms (21). Reddy et al. suggest that high doses of vitamin D may substantially reduce magnesium levels (14). These findings align with our study, which found that higher vitamin D levels may be associated with a modest decrease in serum magnesium, yet the clinical relevance is likely negligible. In contrast, Al-Daghri et al. found that six months of daily vitamin D supplementation (2,000 IU) in patients with type 2 diabetes mellitus led to a significant increase in serum magnesium levels, particularly among women (22). Farhangi et al. administered a single high-dose vitamin D injection (600,000 IU) and found that serum magnesium levels significantly increased in obese but not in non-obese women, while vitamin D levels rose in both groups (23). Changes in serum magnesium in our study were small and may fall within analytical variability, as serum magnesium is an insensitive biomarker of total body magnesium status. Further research is needed to clarify the impact of vitamin D supplementation on magnesium levels, as it remains unclear whether vitamin D directly increases or decreases magnesium or whether the effects result from combined changes in calcium, PTH, or other factors.

PTH helps control calcium and phosphate levels partly by promoting the formation of active vitamin D in the kidneys, and its secretion responds to changes in calcium, phosphate, and vitamin D status (24). Supplementation with 25(OH)D has been shown to reduce PTH concentrations (19, 22). Our findings confirmed the inverse association between serum 25(OH)D and PTH, in line with previous reports (25), underscoring the inhibitory effect of increasing vitamin D levels on PTH secretion. However, the clinical impact appeared minimal in our study, as PTH concentrations remained within the physiological range even at higher vitamin D doses (8,000 IU/day). Even in the absence of hypercalcemia, vitamin D-induced suppression of PTH could influence neuromuscular function, especially in older adults. Therefore, our results support safety only within the specific context of young, healthy individuals under short-term monitoring.

The mathematical extrapolations predicting serum levels of calcium, magnesium and PTH at supraphysiological 25(OH)D levels are intended as sensitivity analyses rather than predictive evidence. Several methodological considerations should be noted. Because repeated measurements were obtained from the same individuals, the p-values derived from simple linear regression models should be interpreted as exploratory. No formal adjustment for multiple testing was applied. Furthermore, although some associations reached statistical significance, the explained variance was low (r2=0.0097-0.0592), indicating modest effect sizes. Fasting prior to sample collection was recommended according to the study protocol; however, adherence to fasting was self-reported and not objectively confirmed. This represents a potential limitation of the study.

The results of our study revealed a statistically significant inverse relationship between BMI and serum calcium levels, suggesting a potential influence of increased body mass on calcium metabolism. Similar findings were reported by Jafari-Giv et al., who identified a negative association between these variables (26). However, it should be emphasized that this analysis was exploratory and not a predefined primary objective of the study. Therefore, these findings should be interpreted with caution. Further research specifically designed to investigate this relationship is warranted to clarify its magnitude, clinical relevance, and underlying mechanisms.

Conclusion

Our study identified significant associations among serum vitamin D, calcium, magnesium, and PTH levels in a homogeneous cohort of young, healthy adults. Serum total calcium showed a modest positive relationship with 25(OH)D, while magnesium and PTH exhibited inverse trends consistent with established physiological mechanisms. Importantly, all parameters remained within their respective reference ranges throughout the supplementation period, even at doses up to 8,000 IU/day. These results indicate that short-term, high-dose vitamin D supplementation can be biochemically safe in healthy adults when administered under proper monitoring. The findings contribute to the growing evidence that higher therapeutic vitamin D intakes, within monitored frameworks, do not necessarily disrupt calcium–magnesium–PTH homeostasis. Additionally, an inverse relationship between BMI and serum calcium levels was demonstrated, indicating a potential modulatory effect of adiposity on calcium metabolism. The results highlight the need for further research to delineate the long-term effects of high-dose vitamin D supplementation on mineral metabolism across diverse patient populations.

Footnotes

  • Authors’ Contributions

    Conceptualization: M.K., R.K., P.Č. Data curation: L.P., M.J. Formal analysis: M.K. H.M. Funding Acquisition: R.K. Investigation: P.Č., E.D., M.J. Methodology: H.M., E.D. Project administration: R.K. Resources: R.K. Software: L.P. Supervision: R.K., M.J. Validation: L.P. Visualization: M.J. Writing - original draft: P.Č., M.K., H.M. Writing - review and editing: M.J., L.P.

  • Conflicts of Interest

    The Authors declare no conflicts of interest in relation to this study.

  • Funding

    This study was supported by the Ministry of Health, Czech Republic-conceptual development of research organization (Faculty Hospital in Pilsen-FNPl, 00669806), BBMRI-CZ: Biobank net-work – a versatile platform for the research of the etiopathogenesis of diseases CZ.02.1.01/0.0/0.0/16_0 13/000167 and LM2015089, and by the “Cooperatio” Program, research area Pharmaceutical Sciences.

  • Artificial Intelligence (AI) Disclosure

    During the preparation of this manuscript, a large language model ChatGPT (OpenAI, version GPT-5) was used solely for language editing and stylistic improvements in select paragraphs. No sections involving the generation, analysis, or interpretation of research data were produced by generative AI. All scientific content was created and verified by the authors. Furthermore, no figures or visual data were generated or modified using generative AI or machine learning–based image enhancement tools.

  • Received November 5, 2025.
  • Revision received February 19, 2026.
  • Accepted March 2, 2026.

This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

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Effects of Short-term High-dose Vitamin D Supplementation on Mineral Homeostasis in Healthy Young Adults
MARKÉTA KRÁLOVÁ, PAVLÍNA ČERNÁ, HEDVIKA MIKOLÁŠOVÁ, MICHAL JIRÁSKO, EVA DĚDEČKOVÁ, RADEK KUČERA, LADISLAV PECEN
In Vivo May 2026, 40 (3) 1645-1653; DOI: 10.21873/invivo.14315
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