Vitamin D is not technically a true vitamin. By definition, a vitamin is something you can’t make yourself and so has to be acquired from food or supplements. It got lumped in with vitamins early on before it wasn’t well understood.

There are five forms of Vitamin D. The one we’re concerned with, the one important to health, is cholecalciferol. Cholecalciferol is a secosteroid, a steroid molecule with one ring open. (I’m sure you remembered this from biochem.)

Synthesis 

Cholecalciferol is synthesized in the skin from 7-dehydrocholesterol when the skin is subject to ultraviolet B (UVB) light. How much cholecalciferol is made depends on several things: the intensity of the UVB as determined by the latitude, season, cloud cover, and altitude, and the age and amount of pigmentation of the skin. Equilibrium can be reached in the skin within a few minutes of exposure. After that, cholecalciferol degrades as fast as it’s made, making it impossible to get vitamin D overdose from UV exposure.

It’s generally accepted that 5–30 minutes of exposure of the face, arms, and legs twice a week provides enough vitamin D for most people. I’m at 4,700 feet elevation. I can burn in the spring at 15-20 minutes if I’m not careful as we regularly have a UV index of 10. The higher the altitude, the less atmosphere to filter out UVB rays. Cholecalciferol can also be produced from UV lamps in tanning beds, though at much lower levels as most tanning beds produce only 4–10% UVB. Blood levels have been found higher in people who tan frequently.

Cholecalciferol is inactive. It travels from the skin to the liver, where it’s converted to calcifediol, also known as 25-(OH)D, by the enzyme 25-hydroxylase. Conversion to 25-(OH)D is loosely regulated, if at all. Calcifediol is what’s measured in the blood to determine a patient’s vitamin D status and is the sum of what was produced in the skin as well as any ingested D2 or D3. After a typical daily intake of vitamin D3, it takes about seven days to convert it to calcifediol.

Although we measure 25-(OH)D in the blood, it’s not the active form of the vitamin. It travels to the kidney where it’s converted into calcitriol (1,25-(OH)2 vitamin D3), the bioactive form, by an enzyme called 1-alpha-hydroxylase and under the influence of parathyroid hormone. Unlike calcifediol, this conversion is tightly regulated. When these metabolites travel through the blood they’re bound to vitamin D-binding protein.

Functions

Calcitriol is very important for maintaining calcium levels and promotes bone health and development. It increases the absorption of calcium from the intestines, promotes reabsorption of lost calcium back into bones, and increases the production of brain-derived neurotrophic factor (influences the brain and peripheral nervous system), nitric oxide (an important vasodilator), and glutathione (the body’s main antioxidant). Lastly, calcitriol promotes the formation and differentiation of new cells. Pretty important substance, wouldn’t you say?

Low levels of vitamin D have been associated with multiple sclerosis, asthma, flu, tuberculosis, and certain cancers. And, as we’ll discuss, certain autoimmune conditions.
For vitamin D to act, it needs to bind to a set of receptors called, not surprisingly, vitamin D receptors (VDRs), principally located in the nuclei. VDRs can be found in most organs, including the brain, heart, skin, gonads, prostate, and breast. And, here’s one tie-in to the thyroid: VDRs are a subset of thyroid hormone receptors.

Deficiency

In general, vitamin D deficiencies are caused by decreased exposure of the skin to sunlight. Far fewer people work outdoors now than before and the use of a sunscreen with an SPF of only 8 can block 95% of vitamin D production. The following conditions are considered risk factors for vitamin D deficiency:

1. Age: The elderly have a higher risk due to decreased sunlight exposure, decreased intake of vitamin D in the diet, and thinner skin, which leads to decreased manufacturing of vitamin D. The elderly are generally exposed to less sunlight due to hospitalization and institutionalization, immobility, and being housebound.
2. Malnutrition: Increased rickets shows up in populations that leave the traditional omnivore diet with high intakes of meat, fish, and eggs, and low intakes of refined cereals, to diets high in cereals and limited access to dairy products.
3. Obesity: For reasons not well understood but likely due to available vitamin D being taken up by fat cells.
4. Decreased sun exposure: We have been scared out of the sun and told to apply sunscreen when we do get sun exposure. People living in regions farther from the equator can experience seasonal variations in vitamin D status. 
5. Darker skin color: Darker skin has more melanin, which acts like sunblock.
6. Malabsorption: Untreated celiac disease, inflammatory bowel disease, pancreatic insufficiency, and surgical procedures that reduce absorption from the intestines can lead to low vitamin D levels. Lastly, keep in mind that hypothyroidism can cause issues with proper absorption from the gut, including vitamin D.
7. Critical illness: People who take vitamin D supplements before being admitted for intensive care are less likely to die than those who don’t. Also, vitamin D levels decline during stays in intensive care. (Keep this in mind when you or a loved one is looking at a hospital stay.)

Vitamin D and Autoimmune Thyroid Disease

I found several studies that establish a relationship between low vitamin D levels and autoimmune disease (both Hashimoto’s thyroiditis and Graves’ disease). Vitamin D deficiency was 3–5 times as common in patients with an autoimmune thyroid disease than in controls.
The results of the studies indicate:

• Low levels of vitamin D can cause thyroid disorders, especially autoimmune disorders.
• Low levels of vitamin D increase the amount of antithyroid antibodies found in the bloodstream. 

VDRs are found on activated T and B cells and monocytes, which get activated when the immune system goes after something it doesn’t think belongs in the body. In this manner, vitamin D reduces chronic inflammation, the cause of most disease, by suppressing T and B cell and monocyte activity.

Vitamin D needs to be present in adequate amounts for T3, the active thyroid hormone, to get into and energize the cell. They both work in the cell nucleus. Put another way, thyroid hormones won’t work well when vitamin D levels aren’t optimal.

However, vitamin D’s involvement in autoimmune thyroid disorders goes deeper still.
Autoimmune diseases are thought to be caused by genetic polymorphism: small changes at the genetic level that affect the structure and function of important cells and proteins, including VDRs.
In fact, several studies have shown that VDR polymorphism is common in those with autoimmune thyroid disease. This means the biological activity of vitamin D is reduced, even when it properly binds to receptors. If VDRs in the thyroid gland are polymorphic, even normal levels of vitamin D can’t produce the same effects as it can on normal VDRs.

Therefore, people with polymorphic VDRs need higher than normal serum levels of vitamin D to avoid deficiency. We’ll visit this topic again when discussing vitamin D therapy.

Assessment of and Ideal Vitamin D Levels

The test to order is the 25-hydroxy vitamin D test. Most labs will have a normal range of 30–100. Many, if not most, MDs won’t consider vitamin D therapy if levels are with the normal range, even just inside the normal range. 1,25()H)D is not tested because it’s regulated by other hormones, such as parathyroid hormone. 1,25(OH)D levels can be normal in a vitamin D-deficient individual.

Research is clear that 35 ng/ml is the minimum level for optimum function, for healthy people. But people with an autoimmune thyroid condition aren’t healthy.

They often have stress, excess weight, GI problems, high inflammation, VDR polymorphisms, and other factors that inhibit production, absorption, and utilization of vitamin D. So, the minimal 25-hydroxy vitamin D level for those with Hashimoto’s thyroiditis may be significantly higher. But how high?

Too much vitamin D is toxic. Get too much of it and it can increase odds of heart disease and, oddly, lower bone density. 

What gives?

There appears to be a close relationship of vitamin D to vitamins A and K2. Higher D levels increase the demand for demand for K2 and A so increasing D intake, especially the higher amount commonly recommended, in the presence of inadequate A and K2 intake is probably unwise.
 
Vitamin D Therapy

How much and what kind of vitamins D, A, and K2 turned out to be a more complicated topic than expected, so I’ll cover this in a future post. We'll also discuss the SET-DB™ approach to improving vitamin D (and A and K2) levels.

Hypothyroidism and iron deficiency have more in common than you might know or think. This brief post will examine their relationship and how SET-DB™ can help.

Hypothyroidism is a condition where:

1. You don’t make enough thyroid hormone to be healthy, or 
2. You make enough but don’t covert it into its active form, T3, or
3. You aren’t able to use it on a cellular level (for any number of reasons).

Some of the symptoms of hypothyroidism—fatigue, cold intolerance, hair loss—are also possible symptoms of iron deficiency. Iron-deficient individuals may also experience irregular heart beat, anxiety, and restless leg syndrome.

Did you know the thyroid is closely connected to the gut? When there is adequate T3 supply to stomach cells they produce hydrochloric acid, which, among other things, helps break down protein. Most of the iron we eat (at least the most bioavailable iron) is found in animal protein. If we don’t digest the protein, we can’t get at the iron in it.

So, low T3 is tied to low stomach acid and low iron.

And, iron is an an important mineral to test for sensitivity, and treat if necessary with SET-DB™. It’s a must-do treatment in the SET-DB™ Thyroid Protocol and is found in the Minerals Category/BioSurvey.

How is low thyroid hormone availability connected to hair loss?

The answer may be ferritin. From Wikipedia:

“Ferritin is a universal intracellular protein that stores iron and releases it in a controlled fashion. The protein is produced by almost all living organisms, including algae, bacteria, higher plants, and animals. In humans, it acts as a buffer against iron deficiency and iron overload. Ferritin is found in most tissues as a cytosolic (dissolved in the cell’s cytoplasm) protein, but small amounts are secreted into the serum where it functions as an iron carrier. Plasma ferritin is also an indirect marker of the total amount of iron stored in the body, hence serum ferritin is used as a diagnostic test for iron-deficiency anemia.”

Emphasis is mine.

Here is a direct connection between ferritin and hair loss, as found on Dr. Philip Kingsley’s site:

“Correct ferritin levels maximize your hair’s ‘anagen’ or ‘growing’ phase and encourage your hairs to grow to their full length. When you aren’t getting enough iron through your diet, your body takes ferritin stored in non-essential tissue, like your hair bulb, and gives it to essential tissue, such as your heart. Because your hair bulb is where all your hair cells are produced, this leeching of ferritin can cause your hair to shed before it reaches its maximum length.

The average reference ranges for ferritin are 14-170 micrograms per litre, but our research shows that ferritin should be at least 80 ug/L (micrograms per litre) in women for hair follicles to function at their best.”

After some research on the subject, like most lab values, optimal ferritin levels for individuals can vary. One thing I did learn is ferritin can be high for reasons other than excess iron. Systemic inflammation can raise ferritin levels due to its role as an acute phase reactant that up-regulates in response to inflammation or oxidative stress.

So, if one wants to be really careful, they wouldn’t have their ferritin checked when they’re sick, or get a hs-CRP test that measures overall inflammatory status. If hs-CRP is elevated, the ferritin level may say nothing about iron status.

Furthermore, on this subject, Mark Sisson writes:

“Come to think of it, if elevated ferritin can be a marker of inflammation and oxidative stress, the inflammation could be responsible for some of the negative health effects linked to high ferritin. Or, if having too much iron in the body can increase oxidative damage, it may be that high iron levels are increasing inflammation which in turn increases ferritin even further. Biology gets messy. Lots of feedback loops.”

Biology can indeed get messy and science is still learning much about the role iron plays in the human body.

Here is Sisson's follow-up post on Iron.

As for SET-DB™ and ferritin, I couldn’t find ferritin in ZYTO’s library so I added it to the Thyroid Protocol library. It’s not yet in a BioSurvey so you’ll have to test it separately. Sorry Select owners. Eventually I’ll have it in a BioSurvey, when I figure out what else to put it with.

Supplementation

I wouldn’t recommend anyone start on an iron supplement or purposely increase their consumption of iron-containing foods until they’ve had their iron and ferritin tested. A complete anemia panel should include serum iron, transferrin, TIBC, and the saturation percentage. 

Diet

As a side note, part of the ongoing attack on meat eating is the claim that the iron in meat promotes colon cancer. Sisson unpacks that in the post I referenced earlier, but here’s the gist of it: 

The relationship between heme iron (the kind found in meat) and colon cancer is conditional on iron oxidating fatty acids in the colon. Not just any fatty acids, though. The kind found in seed oils, polyunsaturated fatty acids. In fact, studies seeking to prove that heme iron promotes colon cancer can’t get the cancer to “take” unless the lab animals are fed high-PUFA oils, like safflower oil. Feed them olive or coconut oil with the heme iron and the study can’t proceed because no cancer occurs.

Another good reason not to eat industrial seed oils, aside from their effect on the thyroid.

Final comments

While researching this topic, and the thyroid in general, I took the time to read through the comments section of the posts. You should, too. It’s a real eye-opener. Skip the snark and pay attention to the ones from people who have been suffering with health problems despite improving their diet, seeing their MD (in most cases), and taking the supplements and/or medications they were told to take. Many have negative reactions to the pills and many just don’t get better.

Based on my experience, this is likely due to sensitivities to the nutrients they need to enjoy improved health, but also to all the nutrient groups as well as foods. This is where SET-DB™ can help. Clearing a sensitivity to iron or ferritin could well allow someone to better handle those substances, which could be a big part in them enjoying better thyroid health, and better health in general.

My wife and I have been on a ketogenic diet for about eight weeks, for weight loss and to help us gain control over our diet again (perhaps I should just speak for myself on that last one). In the past we always did the homeopathic version of the hCG diet, the one from DesBio we put patients on while in practice. It always worked well for us and we knew it inside and out, but we decided to try something different.

It was a little tough for a couple of weeks, mainly because we didn’t supplement with enough electrolyte replacements, but we’re humming along now. We’re at the point where we’re starting to add more carbs from starchier but healthy sources, like sweet potatoes. (We’ve been eating plenty of vegetables but no fruit). I’m down 17 pounds, my wife about 10 (but she looks like she’s lost more).

Anyway, this isn’t a keto diet post, it’s a thyroid post. While researching for my upcoming SET-DB™ Thyroid Protocol, I ran across some interesting information regarding dietary fat and the thyroid gland.

“It turns out the linoleic acid suppresses thyroid signaling.”

Here are some highlights of the post I linked above (Mark’s Daily Apple—great site):

1. Rats on a corn oil diet convert less T4 to active T3 than rats on a lard diet.
   - You’ll recall that about 90% of the hormone made and released by the thyroid gland is T4. The body has to convert T4 into the active T3. Corn oil inhibits this conversion.
2. Rats on a safflower oil diet have a more greatly reduced metabolic response to T3 than rats on a beef fat diet.
   - Beef fat also reduced the metabolic response, just not as much as safflower oil.
   - The rats were fed a high-glucose and otherwise fat-free diet. Nasty, even for rats.
   - Last sentence in the abstract: “These data support the hypothesis that polyunsaturated fats uniquely suppress the gene expression of lipogenic enzymes by functioning as competitive inhibitors of T3 action, possibly at the nuclear receptor level.”
3. Rats on a high-PUFA (polyunsaturated fatty acids) diet have brown fat that’s less responsive to thyroid hormone. Remember, brown fat is the type that generates heat to keep us warm.
   - Click this link if you need a primer in what brown fat is (I had to).
4. Rats on a long-term diet high in soybean oil have terrible body temperature regulation, which thyroid function in large part controls.
5. The more rapeseed meal (from which PUFA-rich canola oil is derived) you feed turkeys, the worse their thyroid signaling gets and the less meat/eggs they produce.
   - The researchers didn’t state whether this negative effect would apply to humans.
6. Back in the 70s, researchers proposed using vegetable oil as a treatment for hyperthyroidism.
7. This reduced thyroid signaling isn’t a function of all polyunsaturated fats, however. Omega-3 PUFAs, found in seafood, increase thyroid signaling in the liver. Keep eating fish, folks.

What’s all this mean? For one, people concerned about their thyroid health should eat as little PUFAs as possible (except Omega-3). In fact, since PUFAs are easily oxidized, and rancid fat is bad for you, PUFAs should also be avoided by anyone concerned with their health in general.

When I developed my highly effective fibromyalgia treatment program, I didn’t feel the need to include dietary recommendations, for a number of reasons.

One, getting people to change their diet is difficult. Most have to be backed into a corner, facing serious health problems, before they’ll give up their favorite fast food meals and daily quarts of sugary soft drinks.

Two, the program is very effective without a change of diet. This suggests that diet doesn’t cause or greatly contribute to fibromyalgia, but I realize that may not be completely true. While the average patient sees a 67% decrease in their overall symptom profile, the fact is most had some symptom(s) at the end of the program, albeit far less than they had when they began. Diet modification could well have resolved some of those residual symptoms.

Three, sometimes you have to pick your battles. Those who raised or are raising children understand this. Do you want to spend your energy getting patients to come in for their treatments (which actually isn’t difficult at all because we got the money issue out of the way at the start) and take the few supplements you give them, which proved to be effective, or spend your time begging and pleading with them to stop eating at Burger King every day?

This won’t be the case with my upcoming thyroid protocol. As you just read (and there’s more to come, diet-wise), there’s enough evidence that diet does affect thyroid and thyroid hormone function.

The most important part of the program will, of course, be eliminating a person’s sensitivities to things like iodine, thyroid tissue (80–90% of hypothyroid sufferers have Hashimoto’s thyroiditis), T3, T4, TSH, adrenal hormones, certain amino acids, etc. If this isn’t done, it’s likely supplementation with hormones or nutritionals will not work as well as they could, or at all.