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This post reflects my perspective as a functional medicine certified health coach with many years of experience in autoimmune conditions, immune dysregulation, and hormone health. It’s not medical advice and isn’t intended to replace the guidance of your licensed healthcare provider.

For years, Vitamin D was a near-automatic recommendation in my health coaching practice. Low D on labs? Supplement. Autoimmune condition? Definitely supplement.

It was reflexive and I certainly wasn’t alone. The functional medicine and nutrition communities have treated Vitamin D like a no-brainer and universal insurance policy for well over two decades and many have published a chart outlining…if your level is in this range, supplement with this amount, or in this range, supplement with this amount. Aka “D stacking.”

I’m sure many of you have seen these guidelines, maybe even on this blog. I’ve removed them. And yes, I understand that this post may make some heads roll.

Where things get interesting and why we need to pause

Vitamin D isn’t a vitamin, nor is it a nutrient. It’s a hormone produced from photolytic reaction with ultraviolet light, which I starting writing about in 2011.

To take things further, Vitamin D is a secosteroid hormone, structurally derived from cholesterol. It’s part of the steroid hormone axis alongside cortisol, estrogen, testosterone, and DHEA.

In other words, the “vitamin” designation is a historical artifact.

This distinction is important because when you supplement with a steroid hormone, you don’t simply raise a level, you introduce a signal into a tightly controlled feedback system that’s designed to regulate itself. We all know that when you push one hormone, you push the others. Given that D is a hormone, it can have downstream effects on the broader steroid hormone axis.

Think about how we talk about other hormones. If someone’s cortisol is low, we don’t just hand them a cortisol pill and call it a day. If estrogen is low, there should be an entire informed consent conversation about risks, dosing, delivery, and monitoring. But Vitamin D gets handed out in 5000 IU doses as a default wellness recommendation, often without a second thought.

By the way, I’ve never heard anyone refer to D as HRT (hormone replacement therapy), but maybe they should? You can read more about HRT and that tightly regulated feedback system in my recent blog post.

Low D in autoimmunity

The “if you only take one thing” crowd, of which I used to be a part of, is largely working from correlation: people with low D have worse health outcomes. Yes, that’s real. But correlation doesn’t tell us whether low Vitamin D status is driving the dysfunction or reflecting a situation where health status is already suboptimal.

Exogenous (outside) D3 suppresses endogenous (inside) synthesis and can affect VDR (Vitamin D receptor) expression in ways that are difficult to predict, particularly in someone whose immune system is already dysregulated. I wrote about VDR polymorphism (genetic variation) in my 2019 article, 3 Reasons for Vitamin D Malabsorption.

And when it comes to autoimmune conditions, research supports that low Vitamin D is often a consequence of the disease, not the cause.

Several mechanisms can be at play:

• Again, VDR polymorphisms: impair the body’s ability to utilize D, regardless of serum level, and are common in the autoimmunity community
• Chronic inflammation: drives D into tissue, pulling it out of circulation
• Dysregulated conversion: doesn’t tell you what’s actually happening at the receptor level

I now understand that chasing a lab value with supplementation doesn’t resolve any of these. In other words, it addresses a number, but not someone’s biology.

So before we start taking a secosteroid hormone to help with immune dysregulation, we want to know why D is low.

If supplemental D is acting as an unmonitored intervention, particularly in autoimmune populations with VDR dysfunction, the potential ramifications are further immune dysregulation, suppression of your own Vitamin D synthesis, and disrupted calcium handling.

In no way the same: sun exposure vs. supplementation

This is where the conversation usually goes something like, “But I never go in the sun. I wear SPF 50 every day. What am I supposed to do?”

Firstly, did you know that most sunscreen on the market is highly toxic and the companies making this toxic sludge have never been required to prove it’s safe? Several ingredients are endocrine disruptors, exceed FDA safety thresholds for systemic absorption, and in some cases are known carcinogens. Carcinogens. You know, cancer-causing agents. #facepalm

Please, get educated on this. I wrote this article, A Chemical Coat of Armor, in 2012 and I’m sure it can use some updates in terms of the list of toxic ingredients, but it’s a start.

Back to the glorious sun…

Sun exposure and D supplementation aren’t equivalent interventions—not even close.

Cutaneous Vitamin D synthesis from UVB exposure is certainly one benefit of getting out in the sun, but it’s not the only one. Sun exposure also drives nitric oxide release, supports melatonin synthesis, and regulates circadian rhythm.

Low D has also been associated with depression and cognitive decline, including dementia, Alzheimer’s, and psychosis, which you can read more about here. So those avoiding the sun are missing an entire cascade of benefits, not just a single “nutrient.”

Additionally, SPF 8 (which most sunscreen companies don’t even make anymore) and above blocks the majority of UVB needed for D synthesis.

My non-medical recommendation is to forget the capsule. Stop “D stacking.” Fifteen to 20 minutes of unprotected midday sun on significant skin surface area (arms, legs, back) is mechanistically different than pumping IUs of D3.

According to Dr. Greg Plotnikoff, “We know that Vitamin D is free from the sun. A general guide is that you can make Vitamin D from sun exposure if your shadow is shorter than you are tall.” 

I’ve been baking in the sun for over 40 years. I’m 56 and thankfully, many people think I’m about a decade younger than I am. (I don’t know how much longer this will last.) I get out there every chance I get and I never, ever wear makeup with sunscreen. Ever.

And oh yeah, you can’t overdose on sun-derived Vitamin D. When your skin has synthesized enough, the body breaks down the excess—there’s a built-in shutoff valve. We don’t have this protection when we’re swallowing it.

What about Minnesota in January?

I live in Minnesota. Geography and season are real variables for a lot of people and I’m not going to pretend meaningful UVB exposure is available here from October through April.

That said, Vitamin D is fat-soluble, meaning it’s stored in adipose tissue and released gradually over time. If you’re getting adequate sun exposure from spring through fall, without sunscreen blocking synthesis, those stores can carry you through the winter months.

If sun exposure is difficult and you just can’t get out there as much as you’d like to, I’m not going to say that supplementation is never appropriate. It’s that it shouldn’t be automatic. Again, if adequate exposure is genuinely impossible and we’re looking at someone with documented deficiency and no significant VDR dysfunction, the conversation can look different.

But even then, we want the full hormonal picture because D doesn’t exist in isolation. It cross-talks with magnesium (required for D conversion), Vitamin K2 (essential for proper routing), and with the broader steroid hormone axis.

So I liken recommending D without this context to adjusting one instrument in the orchestra and calling it good.

What if it’s already in a blend?

This is a fair question because many aren’t taking isolated D3, they’re taking an immune support formula, a multi, or a targeted blend where D is one ingredient among a few.

Context matters and I don’t want to absolutist about this.

When Vitamin D appears alongside thoughtful cofactors, it can be a different conversation than reflexive, isolated high dose (or even moderate dose) D3 supplementation. Again, “D stacking.”

The presence of K2 for proper routing, magnesium for conversion support, and other synergistic compounds can change the risk profile.

What I’ve completely moved away from is D as the lead recommendation. The “just take D” reflex, the routine 5000–10,000 IUs without context, the assumption that a low number on a lab always means more D is the answer. I now know that this thinking is sloppy.

But again, if you’re using a well-formulated blend and it’s working for you, that’s not what I’m pushing back on. I’m pushing back on D in isolation, dosed aggressively, without asking why it’s low in the first place.

Finally, food sources?

It’s simply not worth trying to get sufficient D levels with food. That said, cod liver oil wins with 1360 IUs per tablespoon. And in a distant second, at 566 IUs, is 3 oz. of swordfish. From there, the numbers decrease significantly—forget egg yolks and shiitakes as a source of D. None of these foods will ever replace the benefits of safe sun exposure. 

Low D is a signal and the goal is to consider it correctly. It requires looking at VDR genetics, inflammatory markers, sun exposure history, and the broader hormonal environment. Because these questions lead somewhere real.