Stop Taking Vitamin D Until You Learn This! The Risks and Deficiencies You Need To Know

At this point, I assume most people have heard about the importance of vitamin D and its correlation to increased health risks and diseases. And especially after the covid pandemic, there has been more attention put on the link between vitamin D deficiency and Covid-19 comorbidities. When assessing for deficiency, most physicians check 25 (OH) vitamin D. If vitamin D is found to be low (and according to some studies, around 41% of Americans are vitamin D deficient (1), doctors will either prescribe vitamin D or recommend that you supplement. This recommendation typically comes from one lab marker: a serum 25 (OH)D. However, I will explain why we may need to rethink this approach and how this philosophy could potentially do more harm in the long run than good.

When I worked in the hospital as a dietitian over ten years ago, vitamin D recommendations were very common for me to write in my patients’ charts for the doctors. As the years went by, even more research started coming out on the importance of Vitamin D in our health, and more people began supplementing with it based on this single marker. However, I learned a lot about vitamin D over the years that has now changed the way I recommend this supplement so freely. It stems beyond just ensuring to take the proper form of vitamin D, which is D3 for enhanced absorption, and alongside vitamin K2 for transport to bones and teeth. Maybe this awakening came as a huge wake-up call with my own health, which pushed me down a path of extensive vitamin D research that led me to be cautious when recommending this vitamin. 

Why Checking 25 (OH) Vitamin D Levels Alone to Determine Deficiency May Not Be a Good Model of Care
25 (OH)D is considered the best measure of vitamin D status in the blood, this is why it’s the most commonly ordered form of vitamin D by physicians to see if you’re getting enough vitamin D from food, sunshine, or supplements. However, this is in the storage form that is stored in the liver. 25 (OH)D is preferred because it has a longer half-life (~2-3 weeks) compared to 1,25-dihydroxyvitamin D (1,25 (OH)2 D) (~4 hours), providing a more stable indicator of overall vitamin D status. However, critics argue that relying solely on 25 (OH)D may overlook issues in vitamin D metabolism, such as impaired conversion to its active form or increased degradation, which can mask underlying health issues.

Your body makes vitamin D in the skin from a molecule when UVB sunlight hits your skin. You can also get vitamin D from foods or supplements. UVB light from the sun triggers the conversion of this molecule, 7-DHC, into vitamin D—it’s not driven by an enzyme. Once vitamin D enters your bloodstream (from the skin or diet), it gets converted to 25-hydroxyvitamin D (25 (OH)D), which is the storage form of vitamin D. A few different enzymes can do this, but the main one appears to be CYP2R1 (2).

How Vitamin D Becomes the Active Hormone
After vitamin D is converted to 25 (OH)D, it undergoes another step to become 1,25-dihydroxyvitamin D (1,25(OH)₂D)—the active form of vitamin D. 1,25 (OH)2D is primarily produced in the kidneys and is responsible for most of the 1,25 (OH)2D circulating in the blood. However, 1,25 (OH)2D can also be produced outside the kidneys by certain immune cells in inflammatory states or infections (3). In those who have chronic kidney disease, this is the marker that is checked to assess vitamin D levels because they have difficulty producing enough active vitamin D. Other conditions where 1,25 (OH)2D levels are commonly checked include hyperparathyroidism, sarcoidosis, certain malignancies, vitamin D-dependent rickets, or if there is a suspicion of vitamin D toxicity. Other than those conditions, 25 (OH)D is the main form of vitamin D that is checked, and 1,25 (OH)2D rarely gets ordered.

Why the Topic of Vitamin D Is Not Black and White
For 25 (OH)D to be effective, it must be converted to 1,25 (OH)2D. Measuring only 25 (OH)D does not give you the complete picture, and here’s why:

• If 25 (OH)D is low, we are unable to determine if it’s low because of insufficient vitamin D production in the skin, or if you are not taking in enough through your diet.
  
• It does not tell us if we’re magnesium deficient, which is important because magnesium is needed to convert 25 (OH)D into 1,25 (OH)2D.
  
• It does not indicate whether 25 (OH)D is being actively deactivated and converted to 1,25 (OH)₂D by immune cells during inflammatory responses (also known as the cell danger response) or being metabolized through other pathways. 
  

I can guarantee you that your physician is not paying this much attention to your vitamin D or assessing it at this level! But why is this important? Because most people who get their vitamin D level checked are being prescribed mega doses of vitamin D or told to supplement. I have seen mega doses prescribed as high as 50,000 IU once a week for up to 12 weeks. However, even much smaller doses of vitamin D (5,000-10,000 IU) when you really don’t need additional vitamin D, could increase intestinal calcium absorption and bone resorption, leading to hypercalcemia and tissue damage (4, 5). In the long run, this could increase the risk of osteoporosis and osteopenia, worsen mineral imbalances (like magnesium and potassium deficiencies), and overall worsen dysregulation, leading to more inflammatory cascades in the body (6,7,8). So, is more vitamin D always better or the answer? I would say no. This is where we need to stop and challenge the current model of healthcare, because vitamin D supplementation alone does not solve all vitamin D deficiency problems.

Under normal conditions, or homeostasis, 25 (OH)D levels are higher, often significantly so, than 1,25 (OH)2D. Dr. Eric Balcavage, who wrote the book The Thyroid Debacle, says 25 OHD should be 1.3 times higher than 1,25 (OH)2D. Further, if 1,25 (OH)2D is elevated and 25 (OH)D is low or within range but lower than 1,25 OHD, this can be a sign of dysregulated vitamin D metabolism, often influenced by inflammation, autoimmunity, or granulomatous conditions (such as sarcoidosis). (9)

Other Markers Need to Be Checked Besides Just 25 (OH)D
Magnesium is needed to convert 25 (OH)D to 1,25 (OH)2D, (10) so it would make sense to check this mineral along with vitamin D, wouldn’t it? However, the only way to measure magnesium accurately is to look at the intracellular stores of magnesium, known as red blood cell (RBC) magnesium (11). This is also a marker I rarely see ordered in conventional medicine. This test gives you a more accurate picture of your blood magnesium levels. You also don’t want RBC magnesium just within normal range; you want to aim for the optimal range, which is the upper portion of the range, 6.0 mg/dL or higher (12). If RBC magnesium is lower than this, and both 25 (OH)D and 1,25 (OH)2D are low, then it would be wise to supplement with magnesium first since it’s needed for vitamin D conversion. Continue to hold off on the vitamin D supplementation until after rechecking all levels again in 30 days. At this point, you can see if magnesium is optimized and then add additional vitamin D if still necessary or if no improvements in 25 (OH)D. 

1,25 OHD can give us critically important information regarding our vitamin D status, so this marker is recommended for testing as well. If 1,25 (OH)2D is greater than 25 (OH)D, then it’s not recommended to supplement with vitamin D (13). As mentioned, inflammation is most often behind this cause if not due to other medical conditions. Checking other markers of inflammation such as CRP HS, homocysteine, fibrinogen, etc. can be helpful in this case and addressing the sources of inflammation is how you correct this. Unfortunately, this is where conventional medicine falls short and often leaves you with no answers. In functional medicine, we recognize that many factors—such as toxins, pathogens, and other physiological stressors—can cause inflammation in the body. Conventional medicine does not generally investigate these factors. They wait to diagnose so that a drug or surgery can be recommended. If you want to look for the cause behind the inflammation, the diagnosis, or the symptoms, you will need to pursue alternative paths to health.

Conclusion
In recent years, a vast amount of information has emerged in the field of health and disease, much of which challenges our traditional way of thinking. Despite advancements in technology and science, it can take decades for these findings to be fully integrated into medical textbooks and curricula. Consequently, many physicians remain unaware of this newer research, so if you discuss these insights about Vitamin D with a conventional doctor, you may receive a skeptical response. Functional medicine practitioners, on the other hand, are generally more open to this information and may already be familiar with it. Ultimately, it’s crucial to be your own health advocate—continue asking questions and seeking knowledge to ensure the best possible outcomes for your well-being.

If you want to screen for vitamin D deficiency, it’s recommended to look beyond 25 (OH)D alone. Consider asking for:

• 1,25 (OH)2D: The active form of vitamin D that can offer a clearer picture of your overall vitamin D metabolism.
  
• RBC Magnesium: A more accurate measure of magnesium status, which is necessary to convert 25 (OH)D into 1,25 (OH)2D.
  

By checking these three markers (25 (OH)D, 1,25 (OH)2D, RBC Magnesium), you can gain deeper insight into how your body is handling vitamin D, helping you make more informed decisions about supplementation and other interventions.


References:
Vitamin D metabolism, mechanism of action, and clinical applications
Vitamin D metabolites as clinical markers in autoimmune and chronic disease
(13) Balcavage, Halderman, The Thyroid Debacle, 2022, Balboa Press, pg 263