The Role of Vitamin D Deficiency in Thyroid Disorders

This article is part of a special report on Thyroid Disorders. To see the other articles in this series, click here.

Note: This will be my last post until the end of August. My wife and I are going up to the Sierras to hike and soak in the hot springs for a few days before the big acupuncture licensing exam next Tuesday. The day after that we head to southern Mexico to surf and relax on the beach for a couple of weeks.

I won’t have time to respond to comments while I’m away, but please do leave them and I’ll answer when I come back. I’ve got a few more articles in the thyroid series, and next up after that will be type 2 diabetes & metabolic syndrome. Have a great August!

Vitamin D is all the rage. It seems like every day another article is published in medical journals or the mainstream press about the dangers of vitamin D deficiency, and the benefits of supplementation. In this article we’re going to discuss the impacts of vitamin D on thyroid physiology and wade into the increasingly murky topic of vitamin D supplementation – specifically as it relates to thyroid disorders.

Vitamin D deficiency has been associated with numerous autoimmune diseases in the scientific literature. Vitamin D plays an important role in balancing the Th1 (cell-mediated) and Th2 (humoral) arms of the immune system. It does this by influencing T-regulatory (Th3) cells, which govern the expression and differentiation of Th1 and Th2 cells.

Vitamin D deficiency is also specifically associated with autoimmune thyroid disease (AITD), and has been shown to benefit autoimmune-mediated thyroid dysfunction.

Vitamin D has another little-known role. It regulates insulin secretion and sensitivity and balances blood sugar. This recent paper showed that vitamin D deficiency is associated with insulin resistance. And as we saw in a previous article, insulin resistance and dysglyemcia adversely affect thyroid physiology in several ways.

“Okay, big deal,” you say. “I’ll just take vitamin D supplements or get more sun.”

Not so fast. Research over the past two decades has identified a variety of mechanisms that reduce the absorption, production and biologic activity of vitamin D in the body.

• Since vitamin D is absorbed in the small intestine, a leaky and inflamed GI tract – which is extremely common in people with low thyroid function – reduces the absorption of vitamin D.
• High cortisol levels (caused by stress or medications like steroids) are associated with lower vitamin D levels. They synthesis of active vitamin D from sunlight depends on cholesterol. Stress hormones are also made from cholesterol. When the body is in an active stress response, most of the cholesterol is used to make cortisol and not enough is left over for vitamin D production.
• Obesity reduces the biologic activity of vitamin D. Obese people have lower serum levels of vitamin D because it gets taken up by fat cells.
• Not eating enough fat or not digesting fat properly reduces absorption of vitamin D. Vitamin D is a fat-soluble vitamin, which means it requires fat to be absorbed. People on low-fat diets, and people with conditions that impair fat absorption (like IBS, IBD, gall bladder or liver disease) are more likely to have low levels of vitamin D.
• A variety of drugs reduce absorption or biologic activity of vitamin D. Unfortunately, these include drugs that are among the most popular and frequently prescribed – including antacids, replacement hormones, corticosteroids, anticoagulants and blood thinners.
• Aging reduces the conversion of sunlight to vitamin D becomes.
• Inflammation of any type reduces the utilization of vitamin D.

“Okay, fine,” you say. “I’ll just get my vitamin D measured, and if it’s low, I’ll take supplements.”

If only it were that simple. We now know that certain people with normal serum levels of vitamin D still suffer from deficiency symptoms. How is this possible?

In order for circulating vitamin D to perform its functions, it must first activate the vitamin D receptor (VDR). The problem is that many people with autoimmune disease have a genetic polymorphism that affects the expression and activation of the VDR and thus reduces the biologic activity of vitamin D. Studies have shown that a significant number of patients with autoimmune Hashimoto’s disease have VDR polymorphisms.

“Okay, I get it,” you say. “I may need higher vitamin D levels than the average person if I have one of those genetic defects. So tell me what my levels should be!”

Well, this is where we venture into murky territory. The question of how high vitamin D levels should be is very difficult to answer in the case of someone with autoimmune thyroid disease. Studies suggest the optimal 25(OH)D level is 35 ng/mL for the average person. Some researchers (notably Dr. John Cannell and colleagues at the Vitamin D Council) have suggested that 50 ng/mL should be the minimum level.

The bulk of the evidence, however, doesn’t support that claim. For starters, the other authors of the study Dr. Cannell used as the basis for his 50 ng/mL recommendation came to a very different conclusion from the same data. In the paper they published in the American Journal of Clinical Nutrition, they wrote that their data confirmed the previously acknowledged optimal level of 35 ng/mL – not the 50 ng/mL suggested by Dr. Cannell.

What’s more, some recent studies have shown that higher isn’t better when it comes to vitamin D. A study in the American Journal of Medicine found that, in most people, maximum bone density occurs at 25(OH)D levels between 32-40 ng/mL. When levels are pushed above 45 ng/mL, as recommended by Dr. Cannell, bone density starts to decrease. Another study published in the European Journal of Epidemiology found that South Indians 25(OH)D levels above 89 ng/mL were three times more likely to have suffered from heart disease than those with lower levels.

If you’ve been following this blog for a while, you know that we don’t put too much faith in epidemiological studies. They don’t prove causation. They only show a relationship between two variables. But the relationship of vitamin D to calcium levels also provides a plausible mechanism by which high 25(OH)D levels could increase the risk of heart disease.

Complicating the matter further, recent work by researcher Chris Masterjohn suggests that the harmful effects of vitamin D toxicity are at least in part caused by a corresponding deficiency in vitamins A & K2. The fat-soluble vitamins A, D & K2 work synergistically, as Masterjohn has described in his Cod Liver Oil Debate article and a recently published scientific paper.

Masterjohn’s hypothesis, which has been confirmed by others, raises the possibility that the higher levels of 25(OH)D that were linked with lower bone density and heart disease may be safe if vitamin A & K2 levels are sufficient. Unfortunately, there is no clinical evidence (that I’m aware of) that helps us to answer this question.

“Okay, okay,” you say. “Just tell me how much to take already!”

I wish it were easier to answer this question. Really, I do. I think about it a lot for my own patients.

They often have GI disorders, inflammation, stress, excess weight, VDR polymorphisms and other factors that impair their production, absorption and utilization of vitamin D. This suggests that the minimum 25(OH)D level for those with AITD may be significantly higher than for healthy people.

My current approach with these patients is to do a cautious trial of raising their serum levels to a range of 60-70 ng/mL. If their symptoms improve at this level, I will then switch them to a maintenance dose while watching for clinical signs of vitamin D toxicity. These include kidney stones (also a sign of vitamin K2 deficiency), low appetite, nausea, vomiting, thirst, excessive urination, weakness and nervousness. I will also monitor serum calcium levels, because elevated calcium in the blood is a sign of vitamin D toxicity and a significant risk factor for cardiovascular disease (especially in the presence of vitamin K2 deficiency). Calcium levels above 11-12 mg/dL (or 2.8-3 mmol/L) are indicative of vitamin D toxicity.

I will also make sure these patients are getting adequate amounts of vitamin K2 and vitamin A in their diets. Sources of vitamin A include organ meats, cod liver oil and full-fat milk and cream from grass-fed cows. Sources of vitamin K2 include fermented foods like natto, hard cheeses and kefir as well as egg yolks and butter from grass-fed cows. I may also use a vitamin K2 supplement (MK-4/MK-7 combo) if patients can’t tolerate fermented foods.

Finally, if you’re interested in finding out if you have a VDR polymorphism that could be affecting your metabolism of vitamin D, Genova Diagnostics has an Osteogenomics panel that tests for them. I’m not sure how much value this test has clinically, however, since it doesn’t provide any information about how the VDR polymorphism affects vitamin D metabolism in each specific case. That’s still something that would have to be figured out using the “trial and error” process I described above.

In time we can hope that the explosion of research being conducted on vitamin D will lead to more clarity on the question of appropriate serum 25(OH)D levels for people with autoimmune diseases. For now, we have to make our best guess based on clinical results and anecdotal reports.

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