Natural Management of Graves' Disease

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Natural Management of Graves’ Disease

All too often Graves’ disease patients are rushed into a life-altering procedure as this issue is surrounded with fear and pressure.

Often time’s patients are scared and make quick decisions under the pressure of their doctor. Unfortunately, these decisions are often not well informed leaving the patient regretting the radioactive or surgical procedure months later, after they have had time to think and get another opinion.


Even more unfortunate is once these procedures are done, there is no going back. If you have Graves’ and are reading this, take a deep breath. Allow yourself the time to read this article and obtain a second opinion. In this article I will discuss what Graves’ disease is, what causes it, the risks associated with Graves’ and both conventional and alternative treatment options. It does not matter if you were just diagnosed or if you have had this condition for 10 years and have already had your thyroid removed; you should still read this article for important information on this disease.

What is Graves’ Disease?

Graves’ disease is a form of thyroid autoimmunity that causes hyperthyroidism. More specifically, it is a process in which your body makes immune cells that attack your thyroid gland and this attack causes your thyroid to produce excessive amounts of thyroid hormone, causing hyperthyroidism. Hyperthyroid means too much thyroid hormone.

What are the signs and symptoms of hyperthyroidism or Graves’?

The Mayo clinic provides a concise list [1]:
• Anxiety
• Irritability
• Difficulty sleeping
• Fatigue
• A rapid or irregular heartbeat
• A fine tremor of your hands or fingers
• An increase in perspiration or warm, moist skin
• Sensitivity to heat
• Weight loss, despite normal eating habits
• Enlargement of your thyroid gland (goiter)
• Change in menstrual cycles
• Erectile dysfunction or reduced libido
• Frequent bowel movements or diarrhea
• Graves’ ophthalmopathy (eye complications -Eye bulging, tearing, dryness, irritation, puffy eyelids, inflammation, light sensitivity, blurred vision, pain)
• Thick, red skin usually on the shins or tops of the feet (Graves’ dermopathy)

What are the risks?

If the hyperthyroidism caused by Graves’ disease is not managed it can cause significant damage. Because one of the symptoms of Grave’s is increased heart rate it can cause problems with your heart including changes in heart rhythm, changes in the structure and function of the heart and even congestive heart failure. If a woman is pregnant with Graves’ it can cause complications such as preterm birth, problems with the child’s thyroid, poor growth or preeclampsia.

Thyroid storm is a rare-but life threatening complication of Graves’ in which one becomes severely hyperthyroid. It can cause sudden fever, profuse sweating, delirium, confusion, weakness, tremors, highly irregular heartbeat, low blood pressure and even coma. This is considered a medical emergency and one should seek immediate care. Brittle bones are also associated with untreated Grave’s disease.

Those who have one autoimmune disease are at heightened risk to develop another autoimmune disease [1a, 1b, 1c, 1d, 1e, 1f1g]. Some common autoimmune diseases are; multiple sclerosis, rheumatoid arthritis, type I diabetes, celiac disease, Crohn’s disease and eczema/psoriasis. In fact, autoimmune disease are now more common than cancer [1h].

Conventional Treatment

Initial Conventional Treatment; Managing Hyperthyroidism with Pharmaceuticals

In conventional medicine, thyroid suppressing drugs and beta blockers are usually the initial treatment. Anti-thyroid medications interfere with your thyroids ability to use iodine; iodine is needed to make thyroid hormone so blocking iodine will lower thyroid hormone levels. An example is Tapazone (Methimazole). Conversely, beta blockers do not affect thyroid hormone levels rather they temporarily block the effects of excessive thyroid hormone on the heart. Examples include Propranolol (Inderal), Atenolol (Tenormin), Metoprolol, Nadolol (Corgard).

What are the side effects of anti-thyroid drugs?

The Mayo clinic list the “more common” side effects of Methimazole as [2]:
• Black, tarry stools
• Chest pain
• Chills
• Cough
• Fever
• Painful or difficult urination
• Shortness of breath
• Sore throat
• Sores, ulcers, or white spots on the lips or in the mouth
• Swollen glands
• Unusual bleeding or bruising
• Unusual tiredness or weakness

What are the side effects of Beta Blockers?

The Mayo clinic list the “more common” side effects of Beta Blockers as [3]:
• Fatigue
• Cold hands
• Headache
• Upset stomach
• Constipation
• Diarrhea
• Dizziness

Secondary Conventional Treatment; Targeting Your Thyroid Gland

For over 50% of patients these therapies will not work [4] prompting either surgical removal of the thyroid gland or destruction of the gland using radioactive iodine. Radioactive iodine gets absorbed by the thyroid gland and thus causes damage and destruction of the gland. Unfortunately, because the thyroid gland is either removed or destroyed patients usually become hypothyroid, this is actually the goal of either surgery or radioactive iodine. These patients will then require thyroid replacement hormone for the rest of their lives [4].

What are the risks of radioactive iodine or surgery?

One of the drawbacks to radioactive iodine therapy is the fact that it can worsen eye complications associated with Grave’s disease. There are also risks associated with the surgery including damage to your vocal cords and your parathyroid glands. Unfortunately, most who undergo radioactive iodine or surgery will need thyroid hormone replacement medication for the rest of their lives. For many, these options are far from ideal. Fortunately there are some alternatives to these conventional options.

Functional Medicine Treatment

There are two main goals of functional medicine management of Graves’. Firstly, we have to suppress the hyperthyroidism. The goal here is to provide immediate relief so that:

  1. no damage occurs, and
  2. you as a patient can relax, think clearly and not feel like you have to make a treatment decision today

Secondly, we need to investigate the cause of the Graves’ disease. Once we determine and treat the cause your thyroid may return to normal and you will not require any ongoing treatment. To recap, first we buy some time by naturally treating the symptoms and then we fix the problem by treating the cause.

What if I have already had my thyroid gland removed or irradiated?
It is still a very good idea to read this article and pursue what caused the Graves’ to begin with. Removing or irradiating the thyroid gland does not treat any of the underlying problems that cause this disease. Investigating and treating the cause will help prevent any other forms of autoimmune disease from developing in the future and can significantly increase your overall health and well being.

Let’s first discuss how to suppress the hyperthyroidism (treating the symptoms). This would be the natural equivalent of using thyroid suppressing drugs Tapazone, (methimazole) and/or beta blockers [Propranolol (Inderal), Atenolol (Tenormin), Metoprolol, Nadolol (Corgard)].

Initial Functional Medicine Treatment; Managing Hyperthyroidism Naturally

The most effective and well studied compounds shown to suppress hyperthyroidism are:

• L-carnitine
Selenium
• Bugleweed and Lemon Balm
• Iodine

L-carnitine

A randomized, double-blind, placebo-controlled clinical trial (with a crossover arm) was performed in a group of 50 women [5]. In this study researchers induced hyperthyroidism in the study participants. This study used different doses of L-carnitine, for different lengths of time making it excellent in evaluating the effects of L-carnitine on hyperthyroidism. This study showed:

L-carnitine had significant positive effects on
• weakness and fatigue
• shortness of breath
• palpitations
• nervousness
• insomnia
• tremors
• heart rate
• bone mineral density
L-carnitine did not affect thyroid hormone levels (TSH, fT4, fT3)

The authors of this study concluded, “L-carnitine is effective in both reversing and preventing symptoms of hyperthyroidism.” The authors also comment that carnitine can be safely used in pregnant women with Graves’. Additionally they comment that carnitine can be used to prevent and treat even the most severe form of hyperthyroidism known as thyroid storm [5, 6]. Carnitine has no known toxicity, contraindications or interactions with other drugs or significant side effect [5].

How long until L-carnitine will start working?
I have observed patients feeling a difference within days of starting L-carnitine, although the maximum benefit may take weeks to months to realize according to some studies [5].

Selenium

The most research regarding selenium and thyroid has examined selenium’s effect on Hashimoto’s [7]. That being said there have also been some promising findings regarding selenium’s effect on Graves’ disease [8, 9, 1011, 12, 13]. While the data do not appear to be 100% conclusive, evidence is suggesting the following:

  • Selenium has the ability to lower the antibodies associated with Hashimoto’s [8]
  • Selenium has the ability to lower the antibodies associated with Grave’s [9]
  • Selenium can be used by pregnant women with thyroid disease to help prevent regression of thyroid health postpartum, and has no effect on the fetus and maybe a slight benefit [8]
  • Selenium can lower the eye complications associated with Grave’s [8, 9, 10]
  • Selenium can lower the eye complications associated with Grave’s radioactive iodine treatment [911]
  • Higher blood selenium levels correlate with a lower relapse rate of Grave’s [12]
  • Patients with Grave’s tend to have lower selenium levels [13]
  • Selenium appears to lower the symptoms associated with Graves’ [9]
  • Patients given selenium along with radioactive iodine or anti-thyroid drugs (Methimizole) achieve normal thyroid status faster than those not receiving selenium. [911)

Update April 2019:

  • A landmark study was published in April 2019.  It found selenium + methimazole lead to greater improvements that methimazole alone.  The improvements were in: free T3, free T4, TPO antibodies, thyroglobulin antibodies (TG) and thyroid receptor antibodies.

Bugleweed & Lemon Balm

Bugleweed and Lemon Balm, also known as Lycopus europaeus and Melissa officinalis respectively, have been used for a long time in the management of mild hyperthyroidism. Despite their positive history there are not many modern studies examining these compounds.

This being said Bugleweed and Lemon Balm appear to be safe and have a positive impact in managing hyperthyroidism. Here are some highlights from what we know about these herbs:

  • Bugleweed and Lemon Balm may actually work to block TSH and cause a lowering of T4 and T3 [14]
  • Short term animal studies have shown an ability to decrease TSH, T4 and T3 [14]
  • Decreased heart rate with no side effects in prospective human studies [15]
  • Bugleweed was shown to reduce the increased heart rate and blood pressure associated with Grave’s. It was found to be as effective as the prescription beta block, Atenolol, in an animal study [16]

Iodine

Natural Management of Graves’ Disease - AdobeStock 180191805 Iodine L

Iodine should not be used as a primary therapy, although it does seem to have utility as a short term addition to help manage hyperthyroidism. One study showed that 150mg per day of potassium iodide led to reversal of hyperthyroidism. The effects, however, were short lived; only lasting for 21 days in some but up to 6 weeks in others. Because of this it appears Iodide is best used as a temporary add on to existing therapies to help dampen a flare up of hyperthyroidism [17].

In summary we see four natural medicines as treatment options for managing the hyperthyroidism associated with Graves’ disease. I have found these compounds to be effective for many patients and also to be well tolerated meaning they cause no side effects with the exception to L-carnitine which can cause loose stools in high doses. Fortunately this resolves immediately when decreasing the dose.

We have established there are two options (natural and pharmaceutical) for managing the hyperthyroidism aspect of Graves’ in the short term. Why not just try to cover up the symptoms and hope it goes away? The relapse rate for patients who are treated with thyroid suppressing drugs can approach 68%. This means there may be roughly a 70% chance you need to have your thyroid removed or destroyed. This gives weight to how important it is to do everything possible to treat this at the cause [18].

Secondary Functional Medicine Treatment; Treating the Underlying Cause

Why do I have Grave’s disease? This is the most important question to ask and answer. This van diagram illustrates the factors associated with thyroid autoimmunity, remember Graves’ disease is a form of thyroid autoimmunity. Please note not all of these factors are ones that can be treated. From this list the most important and treatable factors are:

• Selenium deficiencies
• Infections
• Stress
• Gluten
• Vitamin Deficiencies (Vitamin D, omega 3, folate)
• Gut Microflora
• Leaky gut

Infections

Several different bacteria and viruses have been associated with autoimmunity. Some of the most well studied are:

BacteriaViruses
• Yersinia enterocolitis
• Helicobacter pylori
• Epstein Barr
• Cytomegalovirus
• Herpes Simplex Virus

This has caused researchers to identify these infections as one of the contributors to developing autoimmunity [19, 20, 21, 22, 23, 24, 25]. Some studies have even shown as infection activity increases, so does the severity of the autoimmune process [25].

A meta analysis examining the association of H. Pylori infections and thyroid autoimmunity concluded, “Overall, H. pylori infection was associated with autoimmune thyroid disease; the association was significant for Graves’ disease… These findings suggest that H. pylori infection potentially plays a part in the development of ATDs.” [19ATD means autoimmune thyroid disease (Hashimoto’s and Graves’ being the most common forms).

Three case studies were published showing that all three women with Graves’ had concurrent Epstein Barr virus reactivation. Note severe Epstein Barr is also known as mononucleosis.

“Although the etiology of Graves’ disease is still not clear, it is generally suggested that environmental factors such as infections contribute to the development of Graves’ disease. We report here three cases of Graves’ disease which presented simultaneously with infectious mononucleosis due to primary EBV infection [26].” 

Some researchers are theorizing the reason why Epstein Barr virus might cause autoimmunity is essentially because the virus actually gets inside the thyroid gland thus stimulating your immune cells to attack the gland and cause autoimmunity [27].

While we have great studies showing the correlation between infections and autoimmunity; and there is a suggested causal relationship, we are still lacking some data. Published studies showing a decrease of autoimmune activity after treating infections are sparse but impressive.

A study was conducted in Italy that illustrated how powerful treatment of infections can be in halting the autoimmune process. Ten patients who had Hashimoto’s autoimmune thyroid disease and also had an H. Pylori infection were selected. Five underwent treatment and five did not. Here is a breakdown of the findings (please note adequate data was only available for three patients from each group) [28].

Again the patients all had thyroid disease and a H. Pylori bacterial infection. The three in green (on top) were treated for the infection. The three in red (on bottom) were not treated. The numbers you see are the patients’ levels of TPO antibodies. TPO antibodies tell us how severe the autoimmune process is; the higher the number the higher the damage, under about 35 is ideal. As you see here ALL of the patients’ levels were elevated to start. But, those who underwent treatment for bacteria had a significant drop in their antibody levels while the patients who were not treated did not. So treating an infection helped to dampen or stop the autoimmune process that damages the thyroid.

How important are the antibody levels?

A large study, known as meta-analyses, showed that high antibodies levels are predictive of Graves’ relapse; so whatever we can do to lower these antibodies will be a good idea [29].

While there may not yet be any large scale randomized control trials looking at this, there are many clinicians in the field, myself included, who report that screening for and treating these infections seems to contribute greatly to halting the autoimmune process. It’s a simple inference to draw that removing a pathogenic bacteria overgrowth like Helicobacter Pylori, could be beneficial. Remember Hashimoto’s and Graves’ are immune disorders, infections cause activation of the immune system, clearance of an infection allows the immune system to calm down.

The H. Pylori bacterium has been shown to cause stomach burning, ulcers and inflammation. Fortunately, H. Pylori and many of these other infections can be safely eradicated with a course of antibiotic herbs. So there is good reason to screen for and treat these infections especially when we know for certain they have a strong relationship to autoimmunity. Additionally, most every infection will cause fatigue and treating an infection will almost always help with patients energy levels.

Leaky Gut

The subject of infections ties in with that of gut health. Why is this? Well, many of these infections can live in your gut, so this means they act not only as an infection which stimulated the already over stimulated immune systems but also damages your gut. H. Pylori and Yersinia are two examples of this.

Why is gut health linked to my thyroid? Well again the connection is via the immune system. Some researchers have said that it is not even possible to develop autoimmunity unless the gut is first damaged [30].

But why exactly is this? While we don’t know for sure just yet, there are some highly plausible hypotheses. In this picture you see a sample of intestinal tissue. The blue and green cells are immune cells. As you can see there is a tremendous concentration of immune cells in the gut, about 70% of our immune system is contained in gut [31].

(Click slide to enlarge)

This is because the gut is the barrier between you and the outside world. Remember ‘stuff’ from the outside world gains entry to your blood stream via the gut so we need to have plenty of border patrol aka immune cells. When you have ‘leaky gut’ the boarder or gut barrier is compromised and too much ‘stuff’ is allowed in. This stuff may be bacteria, viruses, fungus, food particles, chemicals, etc… Well who then comes to the rescue once too much ‘stuff’ gets into your blood? You guessed it, your immune cells. So if you have an underlying predisposition to autoimmunity (see “Gene Factors” in van diagram above) and then you develop leaky gut, the stage may be set for you to develop autoimmunity, or specifically Graves’. I will go into much more detail about this in the book.

Gut Microflora

Here is a very simplified overview of a very exciting and complex topic. Good bacteria and fungus live in your intestines, more so in your colon. They are needed to help crowd out the bad bacteria, fungus and other infections. They are also needed to prevent leaky gut. Additionally they help breakdown nutrients and increase nutrient absorption. As if this isn’t enough, the good microflora has also been shown to have a direct impact on certain types of autoimmunity.

In a 2012 review published in the International Journal of Immunopathology and Pharmacology the authors commented, “Alterations in both the structure and function of intestinal microbiota could be one of the common causative triggers of autoimmune and/or autoinflammatory disorders [32].”

Dr. David Brady, ND, DC recorded a very well referenced lecture going into great detail on the gut microflora-autoimmune connection. Brady does a great job covering how the medical literature shows a strong association between gut flora and autoimmunity. Unfortunately, this is seldom mentioned in medical practice.

Stress

Stress in known to provocate almost any health condition. The effects of stress are far reaching, but specifically stress can effect Graves’ via two main mechanisms. Firstly, stress can weaken your immune system, which can make you more susceptible to acquiring an infection or can cause an infection you already have to become even more problematic. Secondly, we also know that stress modulates what is known as the Th1/Th2 balance in the immune system. One of the predominant theories of autoimmunity suggests that a shift in this balance is a predisposing factor to developing autoimmunity.

Gluten

Gluten intolerance may be connected to autoimmune thyroid, and specifically Graves’ disease by way of a gene or genes. A gene known as the CLTA-4 gene is known to be associated with Graves’.

A study published in 2012 showed that 60% of those with AIT (autoimmune thyroid) disease had this gene, while only 25% of healthy controls had this gene [34].

How does this link to gluten intolerance? In 2013 a meta-analysis was published showing a link between the CTLA-4 gene and celiac disease, celiac disease being the highest level of gluten intolerance one can have [35]. These finding have been confirmed in other reviews as well [36].

Other studies, in Hashimoto’s patients, have shown that a gluten free diet can decrease one’s need for medication and dampen the autoimmune attack [37].

Irrespective of the exact gene or genes involvement, observational data is fairly clear that those with celiac disease have a high incidence of autoimmune thyroid disease (Graves’ and Hashimoto’s).

Now it’s important to mention that there is a growing subset of our population that does not have full blown celiac disease but does have what’s known as ‘gluten intolerance’ [38].

Recent medical studies support the idea that those with ‘gluten intolerance’ may also derive health benefit from a gluten free diet [39].

Vitamin Deficiencies

Vitamin D is becoming progressively more agreed upon that vitamin D helps fight autoimmunity to a greater or lesser extent. Lets look at a few details.

A 2012 study published in the journal Endocrine showed that patients who relapse after Graves’ treatment have lower vitamin D levels, while those who do not relapse have higher levels of vitamin D [40].

Interestingly other studies are suggesting that autoimmunity may be due to defects in the vitamin D receptor thus making the vitamin D in your body less effective. A 2013 study performed in Turkey showed that a certain defect in the vitamin D receptor left patients at higher risk for Hashimoto’s thyroid autoimmunity [41]. Along these same lines, certain viral infections may actually block the vitamin D receptor and this may be another mechanism through which chronic infections lead to autoimmunity [42].

Omega 3s

Omega 3 fatty acids have become an important dietary and supplemental considerations because they have become deficient in the diet in industrialized nations. Omega 3s serve numerous functions, regarding autoimmunity the most important function they confer is likely their effect on inflammation.

omega 3s Animal and vegetable sources of omega-3 acids as salmon, avocado, linseed, eggs, butter, walnuts, almonds, pumpkin seeds, parsley leaves and rapeseed oil

Every cell of your body has a coating around it know as a cell membrane. The cell membrane is comprised of fatty acids. If the cell membrane is composed of too much omega 6 and not enough omega 3 fats, then the cell is more prone in inflammation. Increasing consumption of omega 3s will help restore balance to your cell membranes and make you less prone to inflammation and autoimmunity. But how does inflammation tie in with autoimmunity? Remember one of the hallmarks of autoimmunity is on overzealous immune response. Your body mounts an immune response by sending out white blood cells that essentially shoot inflammation at ‘bad guys’ to destroy them. This is good when it is controlled, but in those with autoimmunity the process rages out of control. Restoring proper levels of omega 3s is like taking bullets out of your immune systems guns thus preventing your immune system from getting out of control. Please remember its all about balance and over consumption of omega 3s may cause problems just like a deficient intake.

There is a wealth of data available on the health benefits of omega 3s. Just to quote one study regarding omega 3s effect on autoimmunity, the available evidence show that increased daily intake of dietary n-3 FA decreases the severity of autoimmune disorders…[43]”

Folate/MTHFR

Some patients have a gene mutation known as the MTHFR mutation. Essentially this mutation decreases one’s ability to break down folic acid. Folic acid is a synthetic form of the naturally occurring vitamin called folate. Because food processing damages folate, the synthetic form (folic acid), is added back to our food. Patients with this gene mutation cannot absorb folic acid and they become deficient in this vitamin.

Data on this topic is sparse and I question if treating this gene mutation will have any significant impact on thyroid autoimmunity. Some studies show an association with this mutation and autoimmune thyroid; one study showed that 30% of autoimmune thyroid patients had the MTHFR gene mutation [44].

However other studies show no correlation with this specific gene mutation and thyroid autoimmunity [45]. Fortunately treating this gene polymorphism is inexpensive and safe as the preferred treatment is via diet and vitamin therapy. While this may not be the first item to address, it may be worthwhile to discuss this with your doctor if your doctor is up to date on this topic.

In Summary

We have reviewed information discussing conventional and natural treatment options. The first and most important action you can take is to undergo “Initial Treatment” for the symptoms of Graves’, the hyperthyroidism. This can be done with natural or pharmaceutical treatments. Once this is achieved you have bought yourself some time to decide on your next step of treatment.

Click on the supplement names for more information.

NameDoseTimes Per DayWith FoodNotes
Selenium11Yes 
L-Carnitine11YesCan cause loose stools. If it does reduce your dose until this subsides

*Disclaimer: This content is for informational purposes only. You should consult with your doctor before using any of these products.

The next step is to decide on “Secondary Treatment”; whether conventional or natural treatment will be your choice for addressing the thyroid itself. Likely the most important decision in this whole scenario regards the secondary treatment. Because conventional secondary treatment means permanent loss of your thyroid gland and subsequent need for thyroid medication for the rest of your life (in most cases) many would prefer this as a last resort.

Undergoing the functional medicine secondary treatment has the potential to save ones thyroid gland. The main criticism of this approach will be it is less well studied then the conventional approach. This is true, however it has more to do with funding. Natural treatments do not have the large research funding that drug and surgical procedures do. That being said we have covered a fair amount of research supporting the functional medicine approach. The functional medicine approach is natural and has the potential to allow one to avoid permanent loss of their thyroid, so it appears this is a highly logical first choice. You can always have the surgery/radiation later, but once it’s done there is no going back. Hopefully this review of Graves’ disease will enable you to make an informed decision that you feel comfortable with. Feel free to contact my office should you have any questions.

➕ Links & References

RISKS

1. Mayo Clinic: Graves’ disease

2. Mayo Clinic: Methimazole (Oral Route)

3. Mayo Clinic: Beta-blockers

Conventional TREATMENTS

4. Graves Disease Treatment & Management

Functional Medicine TREATMENTS: Initial

5. Usefulness of L-carnitine, a naturally occurring peripheral antagonist of thyroid hormone action, in iatrogenic hyperthyroidism: a randomized, double-blind, placebo-controlled clinical trial

6. Effects of carnitine on thyroid hormone action

7. Selenium supplementation for Hashimoto’s thyroiditis

8. Selenium and the thyroid gland: more good news for clinicians

9. The evolving role of selenium in the treatment of graves’ disease and ophthalmopathy

10. Selenium and the course of mild Graves’ orbitopathy

11. The effect of antioxidant supplementation on superoxide dismutase activity, Cu and Zn levels, and total antioxidant status in erythrocytes of patients with Graves’ disease

12. Serum selenium levels in patients with remission and relapse of graves’ disease

13. Serum selenium is low in newly diagnosed Graves’ disease: a population-based study.

14. Extracts and auto-oxidized constituents of certain plants inhibit the receptor-binding and the biological activity of Graves’ immunoglobulins

15. Lycopus europaeus (Gypsywort): effects on the thyroidal parameters and symptoms associated with thyroid function

16. Extract of Lycopus europaeus L. reduces cardiac signs of hyperthyroidism in rats

17. The effect of iodide on serum thyroid hormone levels in normal persons, in hyperthyroid patients, and in hypothyroid patients on thyroxine replacement

18. Is there a methimazole dose effect on remission rate in Graves’ disease? Results from a long-term prospective study. The European Multicentre Trial Group of the Treatment of Hyperthyroidism with Antithyroid Drugs.

Functional Medicine TREATMENTS: 2nd

INFECTIONS

19. Associations of Helicobacter pylori infection and cytotoxin-associated gene A status with autoimmune thyroid diseases: a meta-analysis

20. Helicobacter pylori infection is markedly increased in patients with autoimmune atrophic thyroiditis

21. Helicobacter pylori infection and autoimmune thyroid disease in young patients: the disadvantage of carrying the human leukocyte antigen-DRB1*0301 allele

22. The influence of selenium supplementation on postpartum thyroid status in pregnant women with thyroid peroxidase autoantibodies

23. Why is the thyroid so prone to autoimmune disease?

24. Epstein-Barr virus in systemic lupus erythematosus, rheumatoid arthritis and multiple sclerosis—association and causation

25. Homologies between proteins of Borrelia burgdorferi and thyroid autoantigens.

26. Graves’ disease associated with infectious mononucleosis due to primary Epstein-Barr virus infection: report of 3 cases

27. CD8+ T-Cell Deficiency, Epstein-Barr Virus Infection, Vitamin D Deficiency, and Steps to Autoimmunity: A Unifying Hypothesis

28. Decrease in thyroid autoantibodies after eradication of Helicobacter pylori infection.

29. Meta-analysis evaluation of the impact of thyrotropin receptor antibodies on long term remission after medical therapy of Graves’ disease.

Leaky Gut & Microflora

30. Mechanisms of disease: the role of intestinal barrier function in the pathogenesis of gastrointestinal autoimmune diseases

31. Allergy and the gastrointestinal system

32. Gut microbiota and the immune system: an intimate partnership in health and disease

Gluten

34. CTLA-4 gene polymorphisms and their influence on predisposition to autoimmune thyroid diseases (Graves’ disease and Hashimoto’s thyroiditis).

35. Association between CTLA-4 polymorphisms and susceptibility to Celiac disease: a meta-analysis.

36. Celiac disease and autoimmune thyroid disease

37. Prevalence of coeliac disease in patients with thyroid autoimmunity

38. Small-intestinal histopathology and mortality risk in celiac disease

39. Non-celiac wheat sensitivity: separating the wheat from the chat!

Vitamin Deficiencies

Vitamin D

40. Serum vitamin D levels are decreased in patients without remission of Graves’ disease

41. Vitamin D receptor gene ApaI, TaqI, FokI and BsmI polymorphisms in a group of Turkish patients with Hashimoto’s thyroiditis.

42. Epstein-Barr virus encoded EBNA-3 binds to vitamin D receptor and blocks activation of its target genes.

43. Effects of n-3 fatty acids on autoimmunity and osteoporosis.

44. MTHFR mutations in female patients with autoimmune thyroiditis

45. Association of polymorphisms in DNMT1, DNMT3A, DNMT3B, MTHFR and MTRR genes with global DNA methylation levels and prognosis of autoimmune thyroid disease.

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