***UPDATE: Cornell looked at 1.4 million COVID cases and found no link between vitamin D levels and risk of COVID infection or severity of infection
Full disclosure, my family and I all had COVID-19 back in March of 2020 before there was testing available. Rachel lost her sense of taste, and Milo and I had mild upper respiratory symptoms. Mine came on with a blinding headache for an afternoon and about 3 days of symptoms.
Several years ago, we stopped supplementing with vitamin D. But not before Rachel got pregnant with our first child, and we took D and a multivitamin throughout the pregnancy. The combination of all the vitamin A, beta carotene, zinc, and vitamin D calcitriol may very well have contributed to her fibroid growing from 5cm to 12cm in just a few short weeks after she got pregnant. These all combined to create the perfect environment for the fibroid, as well as the type of conditions that could make someone far more vulnerable to worse outcomes from viral infections.
First thing to understand is that when someone says “vitamin D,” they are referring to a group of steroid hormones that contains at least 24 different forms. However, only one form is ever actually tested for in the blood or administered as a supplement or hormone therapy drug. That is 1,25(OH)D3, or D3 for short. Most people have rejected the idea that D2 is a suitable supplement for this purpose, and the emphasis is only on D3. But this form is an “active” form that means it is capable of binding with receptor sites on cells to cause an effect. The precursor to this form is 25(OH)D which is a stored form that remains in tissues until it is converted to the active form to circulate in the blood. They’re hormones, just like all our others, that the body carefully regulates to keep the body in proper functioning balance.
Also recall that until 2011, the “normal range” for D3 was 20-30 and only people with severe illness ever fell below this range. Then, after being turned down elsewhere, Dr. Michael Holick convinced the Endocrine Society to accept a range of 30-100 as “normal.” This made almost everyone deficient overnight, and launched a multi-billion dollar industry of testing and supplements. Point is, if you’re otherwise healthy, it’s extremely unlikely you’re deficient. In fact, if you’ve been supplementing or eating fortified foods, it’s far more likely you’re well over the range for normal, healthy people.
As a hormone, the primary function of D3 is to increase the level of calcium in the blood by increasing absorption from the intestines. Do our bodies necessarily want more calcium? The condition known as hypercalcemia can cause a lot of acute symptoms, which are similar to that of thyroid disorders, kidney failure, or tuberculosis. According to the Mayo Clinic:
What are the symptoms of hypercalcemia?
“Although having symptoms of hypercalcemia is uncommon, symptoms can include:
- More frequent urination and thirst
- Fatigue, bone pain, headaches
- Nausea, vomiting, constipation, decrease in appetite
- Lethargy, depression, memory loss or irritability
- Muscle aches, weakness, cramping and/or twitches”
When I was taking D3 on a regular basis, I had all of these symptoms. Long term, calcification continues in the soft tissues, joints, nervous system, and arteries.
The primary function of D3 is to increase blood calcium, but what if there’s not enough calcium in the intestines to match the level indicated by the dose or natural levels? This triggers the parathyroid to release calcium from the bones to achieve the “desired” calcium level. But now, this calcium has nowhere to go, leaving it to deposit in tissues where it’s not needed. That’s because building bone is a regulated process that requires other cofactors, and doesn’t just happen because there’s more calcium available.
Let’s jump into how this affects our health when it comes to potential upper respiratory infections. First of all, “[r]esearchers have now discovered that calcium induces the switch from acute to chronic infection.” I have personally spoken or worked with several people who experienced chronic symptoms following COVID-19 who had been taking a D3 supplement.
“Elevated coronary artery calcium (CAC) is a marker for worse prognosis among patients hospitalized for COVID-19, according to a French analysis.” If these patients already had calcification from excess calcium in their blood, the natural response of the body would be to reduce it’s active “vitamin” D3 levels. That’s how the body protects itself from dangerous conditions, by creating the appropriate response to attempt to mitigate harm. So it should be no surprise that other researchers found that “[p]atients with lower serum calcium levels (especially ≤2.0 mmol/L) had worse clinical parameters, higher incidences of organ injury and septic shock, and higher 28-day mortality.” In fact, these patients had an average D3 of 10.20. Unfortunately for these folks, both low D and calcium levels are indicative of underlying “pre-existing conditions,” including endocrine disorders, diabetes, and kidney disease. Certainly, we could increase their D3 and calcium levels with supplementation, but would that be counter to the body’s innate wisdom and cause more harm than good?
Since active D3 calcitriol opens calcium channels, we can look at what relationship that has with viruses. Turns out, that most viruses manipulate the calcium channels to improve their reproduction and survivability. Dysregulated calcium is a consistent feature of comorbidities like obesity, diabetes, and cardiovascular disease (including the microvascular complications like bruising, ruptured capillaries and blood vessels, and blood clots). Researchers now assert that calcium channel blocking (CCB) drugs may be extremely beneficial in treating COVID. One researcher asserts that CCB “have been reported to inhibit viral entry as well as its replication. More interestingly, the recent clinical investigation of COVID-19 patients revealed that the CCB amlodipine besylate administration was associated with reduced fatality rate of patients with hypertension.”
Unfortunately, “[u]tility [of “vitamin D”] as a therapeutic agent is limited by hypercalcemic effects and attempts to circumvent this problem have used vitamin D superagonists, with increased efficacy and reduced calcemic effect.” Meaning, if you’re going to use D3 as a COVID-19 prophylactic, you’d better be taking something to block it’s effect on calcium levels, too, which as far as I can tell are not readily available for consumer use. Otherwise, the hypercalcemia is inevitable.
Are we shooting ourselves in the foot with D3 supplementation? Some may assert the benefits outweigh the risks, and that taking vitamin K2 with the D3 mitigates any harm. I agree that K2 is critical to overall health, and resistance to infection by helping keep calcium at appropriate levels and getting it to where it’s truly needed. However, K2 is an antidote to both hypervitaminosis A and hypercalcemia (also a symptom of hypervitaminosis A). So, if we are supplementing both D3 and K2, it is cancelling the benefits of the K2.
Now you may be wondering why all these studies show the benefits of D3 supplementation for reducing morbidity and mortality from COVID. Researchers at Weill Cornell Medical College asked the same thing, and their conclusion was that administering vitamin D reduces inflammation caused by pathogenic infections, the same way other secosteroids suppress inflammation. “While this results in short-term palliation, persistent pathogens that may influence disease progression, proliferate over the long-term.”
We do know quite a lot about what’s happening here. Calcitriol D3 directly affects the balance between Th1 and Th2 immune responses by suppressing Th1 and increasing Th2. This is important, because Th1 is our initial defense against infections and is an inflammatory response. Th2 is the “allergy” or anti-inflammatory cytokine response. Th1 is also associated with autoimmune conditions. Excess Th2 response will in fact suppress Th1 response, which could suppress autoimmune symptoms. But if this is being manipulated through steroids like D3, the immune response is no longer free to self-regulate and choose the appropriate response to various conditions. This may be desirable short-term, but what is going to be the result of suppressing these responses without changing the underlying conditions in the long run? Increased vulnerability to pathogenic infection and chronic infection are most likely.
If I was suddenly stricken with terminal COVID, I may want to be treated with D3 in combination with other therapies, as it does suppress inflammation and the cytokine response that would actually be killing me. But the best strategy is to minimize my risk of being in that situation in the first place. It’s clear to me that prophylactic supplementation of secosteroid hormone D3 is not in interest of minimizing my risk, and would in fact be increasing it.