Can Vitamin D cure Hashimoto’s Disease?

Mushrooms soup with noodles and parsley on the top in the plate on the table. Mushrooms are a great source of vitamin D from food. Mushrooms contain much more of it if they are sun-dried. Another health benefit of their consumption is that they are also a source of sulfur-containing amino acid. Thus, they might stimulate glutathione synthesis. Both compounds, which are vitamin D and glutathione are important in Hashimoto's disease treatment and prevention. Vitamin D and glutathione are often decreased in the diseases, and mushrooms might alleviate the serum concentration of both of them. Moreover, glutathione is essential for vitamin D metabolism and vice versa.

Hashimoto’s disease is one of the most often reported autoimmune diseases. However, most people don’t know what this disease is about even when they got id diagnosed. You can hear from a patient, that she has “thyroid”. Everyone got the thyroid gland. She only means that has thyroid disease.

Why is that happening? Because we are lacking health education. We know barely a thing about how to care about ourselves. If you find yourself confused about what you can do for yourself or what diet for hypothyroidism you should eat. Don’t worry, there are millions of people like you.

You may not even know what hypothyroidism is. Follow the article, slowly you’ll know what to do. One of the most important nutrients for Hashimoto’s disease treatment is vitamin D. You can take from supplements, you can take sunbath to get more of it, and you can eat better to increase its intake and to improve its metabolism.

Highlights

  • Vitamin D (VD) deficiency is often a case in Hashimoto’s Thyroiditis,
  • Vitamin D status improvement improves thyroid function, decreases antithyroid antibodies titers and TSH level,
  • You should do a blood test before initiation of VD supplementation,
  • The dose of 1.000 IU of VD daily should increase VD serum concentration by 10 ng/mL but its highly individual,
  • The normal status of VD is equal to or above 30 ng/mL.

Why hypothyroidism is dangerous?

Hashimoto’s Disease is one of the most diagnosed autoimmune diseases. Thyroid dysfunction caused by the disease affects the whole body: nervous system, gut function, decrease bone density or even causes infertility. Despite many scientific studies done on the disease the main one that patients receive is thyroid hormone replacement. If you want to treat the causes of the disease instead of symptoms, you are in a good place.

Before you start reading the whole article, you can go directly to the scientific publication I published with colleagues in the Journal of Food and Nutrition Research titled Supplementation in Autoimmune Thyroid Hashimoto’s Disease. Vitamin D and Selenium (DOI: 10.12691/jfnr-7-8-6). This article is a simplified version of the one above. If you are not familiar with nutrition or you just got here to understand what this Hashimoto’s Disease you got is – Stay here.

Warning note: As you probably heard, vitamin D (VD) has plenty of properties in the human body. Nowadays almost everyone writes about it on his blog like it intake would treat any disease. Surprise. In plenty of cases, it doesn’t. Moreover, it’s risky to do so without blood test control. It is similar to selenium (Se), though it takes a longer time to develop type 2 diabetes or increase cancer risk. However, if that VD is taken smartly and under control, you can benefit a lot from it. Please remember, that the best way to treat is not following what media claims. Always consult your thoughts with an educated medical professional.

What Hashimoto’s thyroiditis is

Hashimoto’s disease (HT) occurs when the immune system increases production on cells that disrupts the thyroid gland. Those compounds are called antithyroid antibodies titers and two main are:

  • Thyroglobulin antibodies (TG-Ab),
  • Thyroperoxidase antibodies (TPO-Ab).

Thyroglobulin is a structure on which thyroid hormones are synthesized by adding iodine. As a result of this biosynthesis triiodothyronine (T3) and tetraiodothyronine (T4) called also thyroxine are produced. T3 has 3 atoms of iodine and T4 four of them. As a result of disease, hypothyroidism can develop which means decreased free T4 level in the serum and concomitantly with that increase of thyroid function stimulating hormone called thyrotropin (TSH).

What Vitamin D has to do with HT development

The production of those antibodies and destruction of the thyroid gland is caused by the interaction of environmental factors (such as stress, toxins, infections, poor dietary habits, and others) with particular genes in susceptible patients. Among those factors are vitamin D, iodine, and selenium status.

Some nutritional compounds like iodine, VD, Se, iron, vitamin B, and others are necessary for thyroid function. As a result of poor dietary habits, you can become undernourished and deficient in them. Which is often a case. The immune system can’t perform its function properly and might lose its self-tolerance. It is a case as well when you are Se deficient and thyroid is out of destructive protection that stimulates the immune system. That is what you want to work on if you are a patient or avoid if you are at an increased risk of developing autoimmune thyroiditis.

Vitamin D is one of the most deficient nutrients even in sunny countries. Insufficiency or deficiency of this compound is correlated with many diseases like cancer, cardiovascular, and others. It is because VD regulates the production of many proteins that regulate physiological functions. Some of them relate to the immune system, thus VD yields an anti-inflammatory effect and regulates the function of immune cells.

Vitamin D is the compound that metabolism and activation depend on both glutathione and magnesium. If your diet is nutritionally poor and lacks glutathione synthesizing substrates, your glutathione level is decreased and thus vitamin D serum concentration. No doubt, magnesium is one of the most important nutritional minerals in your diet. Make sure your intake is appropriate.

Vitamin D status

As you probably know VD is synthesized in the skin when you expose yourself to sunlight. Then it is transported through the cardiovascular system to the liver where it gets to cholecalciferol which is 25(OH)D or 25-hydroxyvitamin D. That’s the one you measure concentration in the serum to know what you VD status is. Generally, it is accepted that:

Vitamin D deficiency status is concentration less than 20 ng/mL, <50 nmol/L, Insufficient: 20-29 ng/mL, 50-72.5 nmol/L,

Normal: 30-100 ng/mL, 75-200 nmol/L

Potentially toxic: above 100 ng/mL, above 200 nmol/.

Counts:

  • 1 ng/ml – 2.5 nmol/l,
  • 1 ug = 2.5 nmol,
  • 1 ug = 40 IU.

But the biologically active form of VD is produced from cholecalciferol in the kidney and it is called calcitriol which is 1,25(OH)2D.

Low VD serum concentration is not a good thing for the autoimmune patient. It increases the risk of HT development in healthy people and stimulates disease on those who are already sick.

The studies done on HT patients shows that most of them are VD deficient. Moreover, the severity of deficiency correlates with duration of the disease, thyroid gland volume and antithyroid antibodies titers.

How much Vitamin D HT patient needs?

In non-HT people, it was found that each 2 ng/mL increase of VD lvl in the serum is associated with a 62% reduction in HT risk development. Moreover, a level above 50 ng/mL (125 nmol/L) which still is in normal status was associated with a 30% reduced risk of antithyroid antibodies titers positive test results and 32% reduced risk of development of hypothyroidism.

It seems reasonable to achieve a VD serum concentration of 50 ng/mL at least to expect the highest benefits of it. It is also recommended to keep the upper limit of serum VD 60 ng/mL (125-150 nmol/L), though the (potentially) toxic concentration is 100 ng/mL and above. 50-60 ng/mL seems to be safe.

By taking 3.000-5.000 IU VD daily you should obtain such level but it’s really hard to tell how you would respond. Remember, that individual response might be wide different between two people.

Also take note, that obese people should take 2.5-3 times more VD than the recommended dose for normal-weight people. Thus if you can’t see results of VD supplementation maybe you don’t take enough of it.

VD dose should be adjusted to the person dependently, among other factors on regional and national recommendations, the weight of the person and ethnicity with the treatment duration of 1 to 3 months. It is recommended that the VD serum level concentration should be tested after 8-12 weeks.

1000 IU of daily intake of VD should increase VD serum lvl by 10 ng/mL.

So if your level is, for example, 25 ng/mL and you want to increase it to the 55 ng/mL you should take 3000 IU VD daily. But remember, that’s theoretically. The body response is highly individual and depends on genes too. Other factors, like undernourishment of essential nutrients for VD metabolism, might completely blunt the effects of VD supplementation. You’ll know about them from other articles on my blog.

READ: Vitamin D can’t work without magnesium

READ: You won’t increase Vitamin D level without glutathione

In one study, HT patients were given 50.000 IU VD weekly (what is 7.143 IU daily) for 3 months. The VD serum concentration increased from 26 mg/mL to 42 ng/mL. We could expect more, again, theoretically but you see as an example in this study that they didn’t raise their VD level in the blood as it could be expected.

In another study, patients who had VD level on average 11 ng/mL increased their concentration to 21 ng/mL on 1.000 IU VD taken daily in one month. 21 ng/mL is barely insufficient and they should be given higher doses. Although the 10 ng/mL increase of VD is equal to that VD supplementation of 1.000 IU increases 10 ng/mL in the blood.

Please note, that one person with insufficient status, let’s say again 25 ng/mL can increase its level to 120 ng/mL (toxic status) by taking “safe dose” like 2.000 IU VD daily while another person might increase it only to 30 ng/mL if at all.

Individual response to VD supplementation is highly wide and you should be aware of that.

Decrease TPO-Ab by Vitamin D status improvement

Thyroid peroxidase antibodies titers are most important in HT. Although, anti-TG also plays a role in pathogenesis and a diagnosis of the disease. However, negative antithyroid antibody titers, especially TPO-Ab, low TSH, and normal thyroid function are what you need.

There is, as usual, a lack of studies in the literature. However, on those that were done, VD supplementations show that HT patients can benefit a lot from it. For example, in one study it was found that TPO-Ab tends to get lower with the increase of VD serum concentration.

Among patients with autoimmune thyroiditis but normal thyroid hormone level, the highest level of antithyroid titers was found in those HT euthyroid patients, who were VD deficient (<20 ng/mL). When those patients were given 1.200-4.000 IU VD daily to achieve 40 ng/mL, their TPO-Ab decreased by 20% after 4 months, though still was elevated.

It’s still better being insufficient (20-30 ng/m) than deficient (>20 ng/mL). As one study found, VD deficient patients (11 ng/mL) increased their VD level to 21 ng/mL by taking 1000 IU/d for a month and decreased TPO-Ab and TG-Ab only by 4 and 17%.

It doesn’t seem to have clinical value but still shows that it has an impact, besides other health benefits. Moreover, TPO-Ab titers are the most important in the management of HT. Thyroid hormones level didn’t increase too. If you are VD deficient, you need more than 1.000 daily IU of VD, and the duration of one-month supplementation definitely might be too short.

Even one month longer can have a significant difference for you. In one study 60.000 IU VD taken weekly (less than 1.000 IU daily) with 500 mg calcium taken daily for 8 weeks (2 months) decreased TPO-AB by 47% compared to 17% in the control group (they were taking only calcium, but not VD). A significant difference. They decreased TPO antibody titers almost by half.

In another study, patients received 2.000 IU/d VD with calcium 1.000 mg/d for 12 weeks (3 months). Almost all of them were VD deficient at the beginning. The study duration was only 4 weeks longer than in the previous study but patients were taking twice more VD. As a result, their TPO-Ab level dropped by 48%. Again a significant difference.

As you see, ones can take much more VD than you and still have similar results from supplementation. The higher your antithyroid antibody levels the better results from intervention you can expect.

Also if you have subclinical Hashimoto’s thyroiditis – which means increased TSH level but with normal thyroid hormone concentration, it’s worth checking VD status. If needed, supplement VD or improve its metabolism. Subclinical form of the disease usually leads to clinical hypothyroidism when left without treatment. Once those patients, when given 50.000 VD weekly, increased VD serum concentration from 14 to 52 ng/mL. This is the level highly desirable in thyroiditis.

A meta-analysis of the studies, which is a form for collective assessment of the effectiveness of intervention concludes that VD supplementation for 6 months in patients with autoimmune thyroid diseases significantly decreases antithyroid antibody titers. If you don’t see results within 8-12 weeks it is possible that you simply need to wait longer or improve a whole intervention. Hashimoto’s treatment it’s not only in a pill but reflects the whole lifestyle and eating habits.

Usually, HT treatment is based on levothyroxine intake without any other changes in the life or diet of the patient. In fact, many patients have multiple dietary deficiencies and poor eating habits and this the area they can improve their health meaningly. However, ones who want only to take pills as a treatment core, levothyroxine works with VD too.

In a clinical study, hypothyroid patients were taking 50.000 IU VD weekly for 12 weeks. As they were on their stable levothyroxine therapy, their TSH level was normal (0.5-5 mIU/L). They increased the VD level from 17 to 43 ng/mL and calcium level by 0.4 mg/dL. TSH decreased on average by 0,4 mIU/L according to parathormone decrease by 3.8 pg/mL. Although there were no changes in thyroid hormones level – they significantly improved their VD status and decreased TSH. From other articles, you’ll find out that TSH level, even in high buy still in the normal range is not a good sign for HT patients.

As you can see if you have thyroid autoimmune disease, like HT it is worth taking a blood test for VD status. If you are deficient or insufficient of it – consider the improvement of the status under medical supervision. Moreover, the increase of VD serum concentration might bring positive results even in patients with normal VD status (above 30 ng/mL).

Vitamin D deficient and insufficient patients often decrease their serum TPO-Ab concentration in a result of improvement of VD status. But note that you may not increase VD serum level at all if you are undernourished. The nutritive diet is the core of the treatment.

Vitamin D supplementation in Hashimoto's Thyroiditis. Picture descrives steps in vitamin D supplementation in hypothyroidism. Before any supplementation you should do blood test to adjust the dose of vitamin D you need. After 8-12 weeks you should make another blood test to assess how effective supplementation is. If vidamin D serum concentration exceeds 100 ng/mL you should stop supplementation immediately and test your kidneys function.

Be careful with Vitamin D supplementation

Vitamin D participates in calcium and phosphorus metabolism in your body. They might also increase in the blood following vitamin D supplementation and that is a thing that you need to have under control. Why? Because it might increase soft tissue calcification.

That means that your blood vessels or kidneys and other tissues will deposit calcium. Thus uncontrolled VD supplementation may give you atherosclerosis or kidney stones.

Vitamin D serum concentration up to 100 ng/mL is considered safe for children and adults. Although, some people are hypersensitive to VD and those are patients with:

  • Idiopathic infantile hypercalcemia,
  • Williams-Beuren syndrome,
  • Granulomatous disorders,
  • Some lymphomas.

If you have any of this, you are at a higher risk of VD toxicity.

Generally, it is recommended that after initiation of VD supplementation its level should be measured after 8-12 weeks. Personally if with an agreement with your doctor, you might test VD status even after 4 weeks (1 month) and found it well too high even when not hypersensitive to VD.

When your VD serum concentration exceeds more than 100 ng/mL, stop VD supplementation immediately. Test calcium and phosphorus concentration and test your kidneys function.

Conclusion

Vitamin D deficiency is often a case in HT patients. If you have subclinical or clinical thyroid autoimmune disease, you should do a blood test for vitamin D status. By starting supplementation you can increase VD serum concentration easily to the normal range. Following that, thyroid function and antithyroid antibodies titers may improve as well as your disease symptoms. Remember, that uncontrolled vitamin d supplementation may increase calcium and phosphorus level in the blood and cause tissue calcification and damage. Thus, you shouldn’t do it without medical supervision.

Sources & References

All references can be found in the original article published in Journal of Food and Nutrition Research “Supplementation in Autoimmune Thyroid Hashimoto’s Disease. Vitamin D and Selenium (DOI: 10.12691/jfnr-7-8-6).