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Thyroid disturbances: is it really lack of iodine or a “clamavi de profundis” for help?

Speaking of thyroid disease, iodine deficiency is always the factor that is put at the center of attention. Who doesn’t know some friend, relative or occasional acquaintance who has been diagnosed with a thyroid problem to be corrected with drugs? In most cases it is a question of greater or reduced function, more or less associated with the presence of nodules, but this is not in all cases. In another percentage of cases, a situation of autoimmunity is diagnosed, with the presence of auto-antibodies. The blood tests in this regard declare altered values ​​of antibodies against the three major thyroid antigens: TSH, TGL and TPO. It is also not uncommon to find auto-antibodies but with hormonal values ​​(T3 and T4) perfectly within the limits.

Finally, there are cases in which there is a declared autoimmune condition, which is also evident from the symptoms and clinical signs associated with the disorder. Autoimmune diseases of the thyroid include a group of disorders characterized by the immune system that produces antibodies that attack this gland. Graves’ disease and Hashimoto’s thyroiditis are the best known. They are much more common in women than men, in the 40-60 age range. The diagnosis of these disorders is confirmed by the presence of thyroid autoantibodies in the serum. Although thyroid autoimmunity is responsible for many cases of hypothyroidism, a proportion of patients may be hyper- or normo-thyroid.

Autoimmune thyroid disorders are generally associated with those of other organs or systems. Thyroid disease and vitamin B-12 deficiency is likely related to the presence of atrophic gastritis and / or pernicious anemia; both, in fact, compromise the absorption of this vitamin. Atrophic gastritis has been found to be prevalent in 35-40% of patients with thyroid autoimmunity in separate studies. Hypothyroidism is relatively common but is more prevalent in older women. While iodine deficiency is a major cause of hypothyroidism worldwide, the most common cause in the United States, where iodine food fortification is widespread, is AITD. Other causes include congenital thyroid disease, previous thyroid surgery, and medications (amiodarone and lithium).

Research has been published on the association between the prevalence of thyroid defect and vitamin B12 deficiency: many of these studies have reported that patients with hypothyroidism and B-12 deficiency often have common symptoms. Thus, hypothyroidism can potentially mask the deficiency of this vitamin. Symptoms, which include weakness, memory difficulties, sleepiness, and peripheral numbness / tingling, do not go away with hormone therapy. Additionally, neurological or psychiatric manifestations of deficiency, such as motor difficulties, easy irritability, and memory loss, can be mistaken for normal symptoms of aging.

Another underestimated factor, but proven to be a partial cause of thyroid defects, is vitamin D deficiency. Research results have shown that patients with Graves’ disease had lower levels of vitamin D, or a higher prevalence of vitamin D deficiency. Other studies have not found that deficiency of this vitamin increased the risk of the disease. Strange as it may sound that vitamin D has anything to do with the thyroid, there is nothing wrong with a probable connection between them. Vitamin D regulates practically every organ from the embryonic state, conditioning the nervous, immune, hematopoietic, renal, cardiac and, of course, the bone system. Wide cellular and genomic correlations between the vitamin D receptor and that of thyroid hormones derive from belonging to the vast family of steroid receptors.

Only after binding the corresponding hormones, these receptors translocate in the nucleus and trigger a specific genetic response for each of them. Furthermore, vitamin D is a powerful regulator of the immune system and that, experimentally, it has been found to be effective in correcting autoimmune disorders such as multiple sclerosis and rheumatoid arthritis. Only one study asked whether vitamin D could be a valuable aid in the treatment of Hashimoto’s thyroiditis. The authors found an inverse correlation between plasma vitamin D levels and the prevalence of anti-TPO antibodies in all 218 patients involved. In 80% of these patients, vitamin D administration for 4 months brought anti-TPO antibody levels back to near normal.

Instead of iodine deficiency (impossible in coastal regions, despite the presence of thyroid disorders in these), the possibility that a thyroid deficiency hides the deficiency of another element is often ignored: selenium. The daily requirement of selenium in humans is about 70 micrograms, but these are necessary for the functioning of some very important cellular enzymes. The human organ with the highest concentration of selenium is the liver, but with the same size immediately after there is the thyroid because selenium is the enzymatic cofactor of thyroperoxidase, the enzyme that triggers the synthesis of the hormone T3. Several studies have associated the prevalence of low selenium content in the soil and low selenium diets (especially vegetables and fruit), not counting the contribution of water.

There are, in fact, regions of Asia, Africa and the Americas whose soil is very poor in selenium. It is therefore not surprising that certain groups of populations, even large ones, can develop selenium deficiency and thyroid disorders with an often high prevalence. It should also be considered that even the aquifers of soils poor in selenium have a very low level of this mineral. Considering that selenium deficiency does not have clinical characteristics characterized by many disorders, it is easy to understand how its deficiency can manifest itself in the form of pathologies not apparently connected to it, including thyroid autoimmunity.

Finally, there is the possibility that another exogenous factor may contribute to the onset of thyroid disorders, at least in predisposed subjects: gluten. It is certainly surprising to associate gluten with thyroid disorders, considering that it is usually considered the cause of celiac disease, intolerances, allergies and herpetiform dermatitis. Very recent meta-analyses (Sun X et al., 2016; Sharma R et al., 2016), on the other hand, found an increased incidence of thyroid autoimmune diseases in celiac patients and, viceversa, the appearance of gluten intolerances in patients already suffering from thyroid autoimmunity. How gluten can interfere with thyroid function, or whether it stimulates the immune system to attack the thyroid, is still a mystery. It can only be disclosed that gluten is a highly antigenic protein complex.

According to some research groups, a permeabilization of the intestine caused by the subtle inflammation induced by gluten (leaky gut), would allow the passage into the blood of protein fragments of the gluten that is not completely digested. Depending on the genetic terrain of the host, this could direct a preferential autoimmune response towards the thyroid cells. The phenomenon would be facilitated by the concomitant intestinal dysbiosis, or an alteration of the gut bacterial community (microbiota) induced by a bad lifestyle or diet, daily stress, trauma, etc. In light of these revelations, it is advisable for patients with thyroid disorders to investigate certain diagnostic profiles in order to correctly identify what really lies beneath their problem.

  • Edited by Dr. Gianfrancesco Cormaci, PhD, specialist in Clinical Biochemistry.

Scientific references

Wang S, Wu Y et al. Endocrine 2018 Mar; 59(3):499-505.

Bakr HG, Meawed TE. Egypt J Immunol. 2017; 24(2):53-62.

Liontiris MI et al. Hellas J Nucl Med. 2017; 20(1):51-56.

Sharma BR et al. Indian J Endocr Metab. 2016; 20:97-100.

Sun X et al. PLoS One. 2016 Dec 28; 11(12):e0168708.

Winther KH et al. Eur J Endocrinol. 2015; 172(6):657-67.

Wu Q, et al. J Clin Endocrinol Metab. 2015; 100:4037-47.

Virili C, Centanni M. Endocrine. 2015 Aug; 49(3):583-87.

Muscogiuri G et al. Eur J Endocrinol 2014; 171(3):101-10.

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Dott. Gianfrancesco Cormaci

Medico Chirurgo, Specialista; PhD. a CoFood s.r.l.
- Laurea in Medicina e Chirurgia nel 1998 (MD Degree in 1998) - Specialista in Biochimica Clinica nel 2002 (Clinical Biochemistry residency in 2002) - Dottorato in Neurobiologia nel 2006 (Neurobiology PhD in 2006) - Ha soggiornato negli Stati Uniti, Baltimora (MD) come ricercatore alle dipendenze del National Institute on Drug Abuse (NIDA/NIH) e poi alla Johns Hopkins University, dal 2004 al 2008. - Dal 2009 si occupa di Medicina personalizzata. - Guardia medica presso strutture private dal 2010 - Detentore di due brevetti sulla preparazione di prodotti gluten-free a partire da regolare farina di frumento enzimaticamente neutralizzata (owner of patents concerning the production of bakery gluten-free products, starting from regular wheat flour). - Responsabile del reparto Ricerca e Sviluppo per la società CoFood s.r.l. (Leader of the R&D for the partnership CoFood s.r.l.) - Autore di articoli su informazione medica e salute sul sito www.medicomunicare.it (Medical/health information on website) - Autore di corsi ECM FAD pubblicizzati sul sito www.salutesicilia.it
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