Written by: Jonine Moller, M.Sc. in Sports Science
Vitamin D is subclassified into two main forms – vitamin D2 (ergocalciferol) and vitamin D3 (cholecalciferol) . Ultimately, both forms of the vitamin are converted into 25(OH)D, or calcidiol, by the liver . Therefore, Calcidiol reflects your vitamin D status.
There are more than one source of this vitamin. 80% or more of the vitamin D3 in your body is formed in the skin when exposed to UVB sunlight [2; 3]. The remaining vitamin D3 can be consumed through oily fish, egg yolk and fortified foods [2; 4].
Vitamin D2 is mostly found in fortified foods and supplements. It is, however, probably better to supplement with vitamin D3 rather than D2. Vitamin D2 has less of an impact on your blood levels of calcidiol than vitamin D3. Calcidiol is the form in which vitamin D is present in the blood . Calcidiol is also the precursor which is converted into its hormone form by the kidneys .
Vitamin D is best known for its role in the absorption and control of calcium and phosphorus levels. In addition, it is essential for proper bone growth and remodelling [1; 3]. This vitamin, however, has many more functions. For example, it plays a vital role in increasing and producing cells and modulation of the immune system . These functions are dependent on the activation of the vitamin D receptors in the respective tissues.
Vitamin D deficiency is becoming quite common worldwide, leading to a wide array of health problems .
A blood test is used to measure the levels of calcidiol [3; 5; 6]. You are considered to be deficient if your blood levels of 25(OH)D are below 50 – 75 nmol/L. Severe deficiency (below 25 – 30 nmol/L) greatly increases your risk for osteomalacia and nutritional rickets [3; 6]. Both of these conditions are related to bone health. Without sufficient vitamin D, your body's absorption of calcium and phosphorus absorption is very low .
Several other diseases and conditions are, however, also associated with vitamin D . For example, adequate levels of vitamin D are necessary to aid in fighting multitudes of infections. Vitamin D deficiency has even been found to play a role in the progression of autoimmune diseases [1; 3]. In addition, and importantly, vitamin D deficiency is an important cardiovascular risk factor .
The most typical and severe symptoms of a vitamin D deficiency are:
Muscle and bone aches and pains
Severe muscle weakness
Unfortunately, before osteomalacia develops, which involves the symptoms mentioned above, there aren't obvious symptoms that serve as a warning for deficiency. The following may all be linked to a vitamin D deficiency: getting sick often, constantly being tired, struggling with depression, obesity and type 2 diabetes, or lung disease .
Several medical conditions and medications increase your risk of being vitamin D deficient. Your greatest risk for being deficient is if:
You are critically ill,
You have chronic renal (kidney) failure,
You have liver disease or,
You have gotten a kidney or liver transplant .
Pregnant women are at risk to be vitamin D deficient since their need for it is higher. This is due to its need by the fetus for good health and development . In addition, celiac disease (gluten intolerance) increases your risk for vitamin D deficiency as it could involve malabsorption.
For the sake of vitamin D3 production, adequate sun exposure is extremely important to prevent developing a deficiency. Your skin colour's darkness greatly determines how much sun exposure you need for enough vitamin D synthesis . Someone with darker skin needs more time in the sun compared to someone with fair skin. Likewise, completely covering your skin with sunblock can block vitamin D production .
Other than the risk factors already mentioned, genes have also been found to play a large role in increasing your risk of having a deficiency of this vitamin. For example, having the applicable gene variants could increase your risk for deficiency up to four-fold .
Certain gene variations have been found to increase your likelihood of a vitamin D deficiency. The CYP2R1 and GC genes are among these . CYP2R1 codes for the enzyme responsible for converting vitamin D3 into calcidiol . The GC gene needed to make transportation of vitamin D to its target tissues possible .
Using supplements is an effective strategy to prevent becoming deficient [2; 7]. Importantly, though, vitamin D is a fat-soluble vitamin. Consequently, unlike the case with water-soluble vitamins such as vitamin C, you can take in too much of it. It is accepted that blood levels of 25(OH)D should not exceed 125 - 150 nmol/L .
Too high vitamin D levels could increase your risk of falls, fractures and mortality . Therefore, it is not recommended to take large quantities of vitamin D supplements as a blind precaution against deficiency. In addition, excessive calcium in the urine can result from taking too many supplements .
Knowing your genetic predisposition to be vitamin D deficient is essential. Knowing whether you are predisposed or not will help you ensure proper nutrition to optimise your health.
 Umar, M., Sastry, K. S., & Chouchane, A. I. (2018). Role of vitamin D beyond the skeletal function: A review of the molecular and clinical studies. International Journal of Molecular Sciences, 19(6), 1–28. https://doi.org/10.3390/ijms19051618
 Lee, J. H., O'Keefe, J. H., Bell, D., Hensrud, D. D., & Holick, M. F. (2008). Vitamin D Deficiency. An Important, Common, and Easily Treatable Cardiovascular Risk Factor? Journal of the American College of Cardiology, 52(24), 1949–1956. https://doi.org/10.1016/j.jacc.2008.08.050
 Sassi, F., Tamone, C., & D’amelio, P. (2018). Vitamin D: Nutrient, hormone, and immunomodulator. Nutrients, 10(11), 1–14. https://doi.org/10.3390/nu10111656
 Pearce, S. H. S., & Cheetham, T. D. (2010). Diagnosis and management of vitamin D deficiency. BMJ (Online), 340(7738), 142–147. https://doi.org/10.1136/bmj.b5664
 Vieth, R. (2020). Vitamin D supplementation: cholecalciferol, calcifediol, and calcitriol. European Journal of Clinical Nutrition, 74(11), 1493–1497. https://doi.org/10.1038/s41430-020-0697-1
 Amrein, K., Scherkl, M., Hoffmann, M., Neuwersch-Sommeregger, S., Köstenberger, M., Tmava Berisha, A., Martucci, G., Pilz, S., & Malle, O. (2020). Vitamin D deficiency 2.0: an update on the current status worldwide. European Journal of Clinical Nutrition, 74(11), 1498–1513. https://doi.org/10.1038/s41430-020-0558-y
 Holick, M. F., Binkley, N. C., Bischoff-Ferrari, H. A., Gordon, C. M., Hanley, D. A., Heaney, R. P., Murad, M. H., & Weaver, C. M. (2011). Evaluation, Treatment, and Prevention of Vitamin D Deficiency: an Endocrine Society Clinical Practice Guideline. The Journal of Clinical Endocrinology & Metabolism, 96(7), 1911–1930. https://doi.org/10.1210/jc.2011-0385
 Holick, M. F. (2008). Deficiency of sunlight and vitamin D. BMJ, 336(7657), 1318–1319. https://doi.org/10.1136/bmj.39581.411424.80
 Traglia, M., Windham, G. C., Pearl, M., Poon, V., Eyles, D., Jones, K. L., Lyall, K., Kharrazi, M., Croen, L. A., & Weiss, L. A. (2020). Genetic contributions to maternal and neonatal Vitamin D levels. Genetics, 214(4), 1091–1102. https://doi.org/10.1534/GENETICS.119.302792
 Slater, N. A., Rager, M. L., Havrda, D. E., & Harralson, A. F. (2017). Genetic Variation in CYP2R1 and GC Genes Associated with Vitamin D Deficiency Status. Journal of Pharmacy Practice, 30(1), 31–36. https://doi.org/10.1177/0897190015585876
 Cheng, J. B., Levine, M. A., Bell, N. H., Mangelsdorf, D. J., & Russell, D. W. (2004). Genetic evidence that the human CYP2R1 enzyme is a key vitamin D 25-hydroxylase. Proceedings of the National Academy of Sciences, 101(20), 7711–7715. https://doi.org/10.1073/pnas.0402490101