The Important Role of Vitamin D in Graves’ Disease

Graves’ disease is an autoimmune disease of the thyroid gland, which was described by the Irish physician Robert James Graves in 1835. It was first recognized in the 19th century as a syndrome involving an overactive thyroid gland, manifested by goiter, palpitations and various types of eye pathological conditions. Many characteristic signs and symptoms of Graves’ disease result from high levels of thyroid hormones. It is diagnosed by low levels of thyroid stimulating hormone (TSH) and high levels of free thyroxine (FT4).

Graves’ disease occurs as a result of complex interactions between genetic and environmental factors and it is a more severe form of autoimmune thyroid disease than Hashimoto’s autoimmune thyroiditis,  mainly due to the adverse effects of high thyroid hormones on vital functions, which may endanger the patient’s life.

Vitamin D and Graves’ Disease

It is widely known that the most important role of Vitamin D is to maintain the homeostasis of calcium and phosphorus to enhance bone health. However, its beneficial effect is not limited to this. Adequate reserves of Vitamin D in the body strengthen its defenses and consequently prevent or limit the development of autoimmune diseases, which are associated with thyroid dysfunction.

Recent evidence suggests that Vitamin D may play a vital role in endocrine disorders, particularly type 1 and 2 diabetes and polycystic ovary syndrome. This is because Vitamin D greatly contributes to the body’s immunity. In recent years, it has been claimed that it strengthens the cells of the immune system and consequently has anti-inflammatory function.

In particular, Vitamin D has been shown to inhibit the stimulation of T and B lymphocytes. In particular, it reduces the production of cytokines, such as interleukin IL -12 and IL-23.

Therefore, when Vitamin D is within normal levels, the risk of developing autoimmune thyroid diseases, such as Graves’ disease, can be prevented or reduced. So, according to recent scientific data, it seems that Vitamin D deficiency, especially when levels are less than 12.5ng / ml, should be considered a very important risk factor for the development of autoimmune thyroid disease.

How important is Vitamin D after all?

Very recent scientific findings show today that Western Europe, and of course Greece, is facing a “pandemic” of Vitamin D deficiency. Although Vitamin D is synthesized through the effects of sunlight on the skin, some genetic factors interfere with its proper synthesis. An inhibitory factor, for example, is the widespread use of sunscreen, as it blocks the action of sunlight on our skin. Thus, the human body is deficient in Vitamin D.

Given that 80% of Vitamin D is synthesized by the sun, while only 20% is absorbed through the diet, eating foods rich in Vitamin D is not the only way to boost its levels in the human body. However, we need to know that foods rich in omega fatty acids have high Vitamin D stores. So, it is contained in large quantities in fatty fish, but also in some fruit.

It is recommended to measure the levels of Vitamin D in almost every age group and the timely intervention with its supplementary administration, where there is necessity, because its adequate values ​​in the human body help prevent the development of autoimmune diseases. It is also of the outmost importance to focus the attention of physicians on understanding the pathophysiology of Graves’ disease, on its early diagnosis, on treatment strategies and on the prevention of recurrence of the disease, in order to achieve optimal and integrated management of patients with Graves’ disease.

Dr. Nikoleta Koini, M.D.

Doctor of Functional, Preventive, Anti-ageing and Restorative Medicine.
Diplomate and Board Certified in Anti-aging, Preventive, Functional and Regenerative Medicine from A4M (American Academy in Antiaging Medicine).

References:

1. Weetman AP. Graves’ disease. N Eng J Med. 2000;343(17):1236-48.
2. Barnett PS, McGregor AM. Immunological factors. Disease of the thyroid: pathophysiology and management. In: Wheeler MH, Lazarus JH, eds. Cambridge UK: Chapman & Hall Medical; 1994. p. 85-103.
3. Plum, L.A.; DeLuca, H.F. Vitamin D, disease and therapeutic opportunities. Nat. Rev. Drug Discov. 2010, 9, 941–955.
4. Muscogiuri, G.; Tirabassi, G.; Bizzaro, G.; Orio, F.; Paschou, S.A.; Vryonidou, A.; Balercia, G.; Shoenfeld, Y.; Colao, A. Vitamin D and thyroid disease: To D or not to D? Eur. J. Clin. Nutr. 2015, 69, 291–296.
5. Li, Y.-B.; Xue, X.-H.; Liu, S.-W.; Xi, G.-X.; Zhao, L.-X.; Zhang, X.-L. Clinical research of serum vitamin D in early Graves’ disease. Chin. Rem. Clin. 2014, 14, 242–243.
6. Liu, X.-H. Correlation between Serum Level of 25-(OH)D3 and Humoral Immunity in Patients with Autoimmune Thyroid Diseases. Master’s Thesis, Zhengzhou University, Zhengzhou, China, 2012.
7. Brandt F, Almind D, Christensen K, Green A, Brix TH, Hegedüs L. Excess mortality in hyperthyroidism: the influence of preexisting comorbidity and genetic confounding: a Danish nationwide register-based cohort study of twins and singletons. J ClinEndocrinolMetab 2012; 97:4123-9.
8. Bahn RS, Burch HB, Cooper DS, et al. Hyperthyroidism and other causes of thyrotoxicosis: management guidelines of the American Thyroid Association and American Association of Clinical Endocrinologists. EndocrPract 2011;17:456-520.
9. Hewison M. An update on vitamin D and autoimmunity.ClinEndocrinol 2012;76: 424 315–25. 425
10. Carlberg C, Campbell MJ. Vitamin D receptor signaling mechanisms: integrated ac- 426 tions of a well-defined transcription factor. Steroids 2013;78:127–36.