Vitamin D: Global Deficiency, Immunity and Muscle Function

Vitamin D occupies a special place among nutrients: technically it is a steroid hormone whose receptors are found in almost every cell of the body — from immune cells to muscle cells. At the same time, its primary source of synthesis is not food, but skin exposed to ultraviolet B radiation. This is precisely what makes its deficiency a structural problem for a significant portion of humanity.

How widespread is vitamin D deficiency worldwide?

A large-scale pooled analysis by Cui A. and co-authors, published in Frontiers in Nutrition in 2023, combined data from 308 population-based studies across 81 countries for the years 2000–2022 — a total of 7.9 million participants. The authors used three threshold values for blood 25-hydroxyvitamin D concentration:

• Below 30 nmol/L (severe deficiency): 15.7% of the world's population (95% CrI: 13.7–17.8%).
• Below 50 nmol/L (clinical insufficiency): 47.9% of the world's population (95% CrI: 44.9–50.9%).
• Below 75 nmol/L (suboptimal level): 76.6% of the world's population.

The most vulnerable groups are residents of the Eastern Mediterranean (35.2% with levels below 30 nmol/L), low- and middle-income countries, and women: their risk of deficiency is 1.3 times higher than in men. In winter and spring, deficiency prevalence is 1.7 times higher than in summer and autumn. This explains why the problem is relevant not only in the tropics — residents of temperate and high latitudes are virtually deprived of the main source of vitamin D during the dark season.

How does vitamin D affect muscle strength in athletes?

The meta-analysis by Han Q. and co-authors (Frontiers in Nutrition, 2024) synthesized data from 10 randomized controlled trials involving 318 athletes — 166 in the vitamin D3 group and 152 in the placebo group. The central question: does supplementation improve measurable strength outcomes?

The results were heterogeneous. The combined analysis across four categories of strength tests did not reach significance: SMD 0.18 (95% CI: −0.02 to 0.37; p=0.08). However, when broken down by individual measurements the picture changes:

• Isometric quadriceps contraction: significant improvement — SMD 0.57 (95% CI: 0.04–1.11; p=0.04).
• Maximum bench press strength (1RM): no significant change — SMD −0.15 (95% CI: −0.57–0.26; p=0.47).
• Vertical jump: no significant change — SMD 0.21 (95% CI: −0.09–0.50; p=0.17).
• Handgrip strength: no significant change — SMD 0.21 (95% CI: −0.23–0.64; p=0.35).

Important context: blood 25(OH)D levels in participants did rise significantly after the intervention — by an average of 14.76 nmol/L (95% CI: 8.74–20.77; p<0.0001). This means the supplement works biochemically — the question is whether this is sufficient for a strength effect in mixed athlete populations.

A parallel question — the association between baseline 25(OH)D and muscle strength in observational data — was investigated by Ong MTY and co-authors (BMC Sports Science, Medicine and Rehabilitation, 2024). Their meta-analysis covered 28 studies with 5,752 participants and found a robust positive correlation between serum 25(OH)D and isokinetic quadriceps strength at 180°/s: r=0.245 (95% CI: 0.078–0.398; p=0.004). Combined isokinetic correlation across five studies (n=401): r=0.261 (p<0.001). The data are observational — reverse causality and confounders cannot be excluded.

What does the science say about immune function?

Vitamin D receptors (VDR) are expressed on T cells, B cells, macrophages, and dendritic cells — making it biologically relevant to the immune response. The most systematic data available as of 2025 concern the prevention of acute respiratory infections.

The systematic review and meta-analysis by Jolliffe DA and co-authors (Lancet Diabetes & Endocrinology, February 2025, volume 13, issue 4, pp. 307–320) synthesized the accumulated evidence base from several dozen RCTs involving hundreds of thousands of patients. The authors documented a moderate protective effect of daily vitamin D supplementation, most pronounced in individuals with baseline deficiency. Bolus administration (infrequent large doses) produced less consistent results. An important caveat: the effect is heterogeneous across studies — the quality of evidence is limited by heterogeneity of designs and populations.

Why supplements don't always work and what this means for practice

The key argument that recurs in most meta-analyses: the effect of supplementation depends on the baseline level of deficiency. In people with normal or high 25(OH)D levels, additional supplementation produces virtually no measurable benefit — neither on muscle parameters nor on immune markers. The situation is entirely different for those who start with severe deficiency.

The second factor is dose and form. Vitamin D3 (cholecalciferol) is more bioavailable than D2 (ergocalciferol) and more effectively raises serum 25(OH)D. Daily intake of moderate doses maintains levels more consistently than periodic boluses.

The third factor is co-nutrients. Vitamin D works in tandem with vitamin K2 (menaquinone) and magnesium: without sufficient magnesium, the enzyme that converts vitamin D to its active form functions inefficiently. Isolated vitamin D supplementation in the presence of magnesium deficiency predictably yields a smaller result.