Hyperthyroidism is defined as a disease characterized by Thyroid gland overactivity, leading to increased production and action of thyroid gland hormones. In general, this leads to increased energy levels, due to metabolism acceleration and fast burning. This hyper-metabolic condition caused by the organism, due to the increased availability and action of thyroid hormones, is defined as Thyrotoxicosis.
Diagnosis of Real Causes & Treatment of Hyperthyroidism
- Gradual restoration of cellular function
- Personalized therapeutic protocols, without chemical residues and excipients
- Treating the real causes
- Therapeutic formulas that work alone or in combination with any other medication
- Adopting a Molecular / Therapeutic Nutrition Plan
The human organism could be easily likened to a factory. It constantly works and produces energy. The function of each part of the body influences its overall performance and production of the factory as a whole.
The thyroid gland is part of this factory. It produces hormones, which then influence the proper functioning of the body as a whole.
These hormones affect all cell types. Maintaining these hormones at proper levels is important for our overall health, as they are for the proper operation of the “factory”. These hormones help our body to produce and consume energy.
When the thyroid gland is overactive (Hyperthyroidism), each function of the body is accelerated due to thyroid hormones excess.
This is why the thyroid gland is characterized as a “mime organ”. Because it mimics the signs and symptoms of other diseases, in multiple systems and organs of our body. As a result they are often attributed incorrectly to other diseases, leading to misdiagnoses.
The onset of thyroid gland disease is usually a slow and insidious process, and symptoms are not promptly recognized by the patient and the doctor.
Hyperthyroidism diagnosis is characteristically confusing for both Patients and Doctors.
Hyperthyroidism, the symptoms include:
Hot flashes, unintentional sweating and weight loss with increased appetite.
Heat intolerance, frequent bowel movements, bowel hyperactivity and watery – loose stools or diarrhea
Difficulty sleeping and insomnia, stress, irritability and nervousness
Hyperactivity and emotional instability
Muscle weakness, tremors (trembling hand) and constant tiredness – fatigue.
Visual disorders, eye twitching (due to upper eyelid spasms), or even exophthalmos (bulging or protruding eyeballs).
Increased heart rate – tachycardia and other heart rhythm disorders.
Brittle and oily hair, together with skin thinning
Difficulties in speaking
Increased bone absorption and calcium transfer from the bones to the blood, hypocalcaemia and hypercalciuria
Increased catabolism of proteins and lipids and glucose intolerance
Insulin resistance and hyperinsulinemia
Increase of free fatty acids and cholesterol reduction
Menstruation disorders (such as oligomenorrhea, infrequent menstrual cycles)
Reduced libido (sexual desire)
Subfertility, erectile dysfunction in men, or even oligospermia, infertility and gynecomastia.
The size of the thyroid gland increases gradually, its texture changes, but it develops nodules, ending up to nodular goiter.
The proper functioning of the “factory” is disrupted.
To date, thyroid gland dysfunction is treated using drugs. The patient should be receiving drugs throughout his or her life, while the problem is never restored, and at the same time there is a risk of side effects from the chemical substances.
Hyperthyroidism and Types of Thyroid Hormones
The thyroid gland produces three hormones: Τ3 (triiodothyronine), Τ4 (thyroxine or tetraiodothyronine) and calcitonin (thyrocalcitonin).
T3 hormone (triiodothyronine) is thyroid gland’s active hormone and it regulates the metabolism of all tissues of the body. It is responsible for all the above mentioned symptoms and with their corresponding functions.
Τ4 hormone (thyroxine or tetraiodothyronine) is the inactive thyroid hormone It does not function on its own, it just waits to be converted to Τ3.
Calcitonin is an entirely separate hormone from both Τ3 and Τ4, and its action focuses on blood calcium levels regulation, preventing it from reaching pathological high values.
Hormones of our body may be in two states, free or bound. A free hormone means that it is active and it can do what it is supposed to do, i.e. deliver oxygen and energy in the case of T3 or be converted to Τ3 in the case of Τ4.
Hyperthyroidism and its possible causes
Gluten is an endosperm protein of soft wheat, barley and rye. Today it is one of the major nutritional problems for people. This is because it in included in most marketed foods or are available for consumption by the general public.
Continuous and increasing gluten consumption causes intestinal permeability (Leaky gut syndrome). The intestine is lined with a monocellular layer, which functions as a barrier, preventing the outflow of microbes to the blood. A permeable intestine is a gate for infections, while toxins and food substances, such as gluten, may cause systematic inflammation, leading to autoimmunity.
Given that the structural elements of gluten have similar molecular structure with structural elements of the thyroid gland, the immune system gets confused and often attacks the thyroid gland (Autoimmune thyroiditis). This process is called molecular mimicry. Apart from gluten, infections, drugs and stress may also cause intestinal damage, allowing the inflow of toxins, microbes and undigested food particles directly in the blood.
Other causes of Hyperthyroidism:
Mercury, which is a heavy metal, can alter or destroy cellular structure in tissues and organs. Destroyed cells are identified by the immune system as foreign elements, i.e. like intruders, and starts attacking them. According to many statistical studies, people that are more exposed to mercury have a greater risk of developing autoimmune thyroid disease. A drug that is often used but acts in a toxic way and causes immunological reaction against thyroid cells is the antiarrhythmic amiodarone.
Infections from Herpes Simplex Virus (HSV) family and the Epstein-Barr Virus (EBV) have been implicated as a possible cause of autoimmune thyroid disease, through inflammation and molecular mimicry.
The case of iodine is slightly controversial. It seems that if very little iodine is present (iodopenia), goiter and Hypothyroidism may be caused, while greater doses of Iodine cause Hyperthyroidism. When the body detects increased iodine availability, the thyroid gland may be stimulated to produce more thyroid hormone. If someone with usual low iodine intake suddenly consumes a very rich in iodine diet, then too much thyroid hormone is produced, resulting in an overactive thyroid.
All the above causes lead to hormonal aberration and overactivity of the thyroid gland, resulting in dysfunction of the whole body. Hyperthyroidism is now here.
Types of Thyrotoxicosis:
Diffuse Toxic Goiter (Graves Disease), a clearly autoimmune disorder, which is present in the 70% of patients with hyperthyroidism, Multinodular Toxic Goiter, in which one or more nodules (lumps) grow on the thyroid gland and overproduce hormones, Toxic Adenoma, Hyperthyroid phase of the autoimmune Hashimoto’s thyroiditis, Subacute thyroiditis in the acute phase (De Quervain’s thyroiditis), exogenous overdose of thyroid hormones and Thyroid Cancer
Hyperthyroidism – Treatment
Up until now, hyperthyroidism is managed with various treatments that include antithyroid drugs, such as methimazole, carbimazole, or propylthiouracil, which inhibit thyroid functioning. They cause side effects, including rash, hair loss, vertigo, aplastic anemia, lupus-like syndrome and hepatitis. Furthermore, treatments that involve taking radioactive iodine isotopes (131I) affect the patient due to the radiation, while the patient should then receive for life replacement therapy. Finally, total or partial surgical excision of the thyroid gland is also suggested in many cases.
These therapeutic methods that are being used for many decades against Hyperthyroidism, are mainly used in order to eliminate the symptoms, but not the causes that led to thyroid gland deregulation.
Patients remain patients and they are in constant suffering, due to their health’s imbalance. The result of the non-causal and non-permanent treatment of their problem is the psychological and financial burden for life. Everyday life changes significantly. Symptoms usually reappear. Their focus is constantly on their diet and on ways to maintain their fragile health in good status.
Hyperthyroidism can be treated
Thyroid gland’s biochemical and functional restoration, so that hormonal production returns to normal levels, is a permanent treatment. Its duration is from six to eighteen months.
Mean duration changes according to the causes that led to biochemical aberration (the disease), as well as patient’s overall status and habits.
The combination of Micro-Μacro Nutrients therapeutic protocols with Molecular nutrition and a heavy metals removal program is often required.
Treatments aim at cellular restoration, and biochemical balance of cells, through the gradual correction of chronic deficiencies with micronutrients.
Furthermore, neurotransmitters are fixed and hormonal balance is restored using Biomimetic hormones only. Additional guidance is provided for exercise and nutrition during this period.
Molecular nutrition includes anti-inflammatory foods, rich in nutrients, with low contents in carbohydrates and gluten.
At the same time, treatment of the Permeable Bowel Syndrome is achieved, all infections are managed, and the immune system is strengthened.
Finally, the treatment applied to remove heavy metals or other chemical compounds, which have been identified through the exams as the causes of Hyperthyroidism, lasts three weeks and its results are amazing.
- Nobuyuki Amino 4 Autoimmunity and hypothyroidism Bailiére’s Clinical Endocrinology and Metabolism Volume 2, Issue 3 August 1988. doi:10.1016/S0950-351X(88)
- van Rijn LE, Pop VJ, Williams GR. Low bone mineral density is related to high physiological levels of free thyroxine in peri-menopausal women. Eur J Endocrinol. 2014;170(3):461‐468. Published 2014 Feb 7. doi:10.1530/EJE-13-0769
- Yaylali O, Kirac S, Yilmaz M, et al. Does hypothyroidism affect gastrointestinal motility?. Gastroenterol Res Pract. 2009;2009:529802. doi:10.1155/2009/529802
- NHS “Erectile dysfunction (impotence)” 16 August 2017 https://www.nhs.uk/conditions/
- Kalra S, Unnikrishnan AG, Sahay R. The hypoglycemic side of hypothyroidism. Indian J Endocrinol Metab. 2014;18(1):1‐3. doi:10.4103/2230-8210.126517
- Abrams JJ, Grundy SM. Cholesterol metabolism in hypothyroidism and hyperthyroidism in man. J Lipid Res. 1981;22(2):323‐338.
- CJ Gardner, P Richardson, et al. Hypothyroidism in a patient with non-alcoholic fatty liver disease BMJ 2011; 342 doi: https://doi.org/10.1136/bmj.
- Sintzel F, Mallaret M, Bougerol T. Potentialisation par les hormones thyroïdiennes des traitements tricycliques et sérotoninergiques dans les dépressions résistantes [Potentializing of tricyclics and serotoninergics by thyroid hormones in resistant depressive disorders]. Encephale. 2004;30(3):267‐275. doi:10.1016/s0013-7006(04)
- Berent D, Zboralski K, Orzechowska A, Gałecki P. Thyroid hormones associated with depression severity and clinical outcome in patients with major depressive disorder. Mol Biol Rep. 2014;41(4):2419‐2425. doi:10.1007/s11033-014-3097-6
- Brănişteanu DE, Dimitriu A, Vieriu M, et al. Cutaneous manifestations associated with thyroid disease. Rev Med Chir Soc Med Nat Iasi. 2014;118(4):953‐958.
- B. Winsa, MD, A. Karlsson, MD et al. Stressful life events and Graves’ disease The Lancet VOLUME 338, ISSUE 8781, P1475-1479, DECEMBER 14, 1991 doi: https://doi.org/10.1016/0140-
- Matos‐Santos, A., Nobre, E.L., Costa, J.G.E., Nogueira, P.J., Macedo, A., Galvão‐Teles, A. and De Castro, J.J. (2001), Relationship between the number and impact of stressful life events and the onset of Graves’ disease and toxic nodular goitre★. Clinical Endocrinology, 55: 15-19. doi:10.1046/j.1365-2265.2001.
- Sategna-Guidetti C, Bruno M, Mazza E, et al. Autoimmune thyroid diseases and coeliac disease. Eur J Gastroenterol Hepatol. 1998;10(11):927‐931. doi:10.1097/00042737-
- Mainardi E, Montanelli A, Dotti M, Nano R, Moscato G. Thyroid-related autoantibodies and celiac disease: a role for a gluten-free diet?. J Clin Gastroenterol. 2002;35(3):245‐248. doi:10.1097/00004836-
- Roland Gärtner, Barbara C. H. Gasnier, Johannes W. Dietrich, Bjarne Krebs, Matthias W. A. Angstwurm, Selenium Supplementation in Patients with Autoimmune Thyroiditis Decreases Thyroid Peroxidase Antibodies Concentrations, The Journal of Clinical Endocrinology & Metabolism, Volume 87, Issue 4, 1 April 2002, Pages 1687–1691, https://doi.org/10.1210/jcem.
- Baeke F, Takiishi T, Korf H, Gysemans C, Mathieu C. Vitamin D: modulator of the immune system. Curr Opin Pharmacol. 2010;10(4):482‐496. doi:10.1016/j.coph.2010.04.001
- Arrieta MC, Bistritz L, Meddings JB. Alterations in intestinal permeability. Gut. 2006;55(10):1512‐1520. doi:10.1136/gut.2005.085373
- Langer P, Kocan A, Tajtaková M, et al. Fish from industrially polluted freshwater as the main source of organochlorinated pollutants and increased frequency of thyroid disorders and dysglycemia. Chemosphere. 2007;67(9):S379‐S385. doi:10.1016/j.chemosphere.
- Martin I. Surks, M.D., and Rubens Sievert, M.D. Drugs and Thyroid Function N Engl J Med 1995; 333:1688-1694 DOI: 10.1056/NEJM199512213332507
- Boukis MA, Koutras DA, Souvatzoglou A, Evangelopoulou A, Vrontakis M, Moulopoulos SD. Thyroid hormone and immunological studies in endemic goiter. J Clin Endocrinol Metab. 1983;57(4):859‐862. doi:10.1210/jcem-57-4-859
- Tomer Y, Huber A. The etiology of autoimmune thyroid disease: a story of genes and environment. J Autoimmun. 2009;32(3-4):231‐239. doi:10.1016/j.jaut.2009.02.007
- Vestergaard P, Rejnmark L, Weeke J, et al. Smoking as a risk factor for Graves’ disease, toxic nodular goiter, and autoimmune hypothyroidism. Thyroid. 2002;12(1):69‐75. doi:10.1089/105072502753451995
- Wajner SM, Goemann IM, Bueno AL, Larsen PR, Maia AL. IL-6 promotes nonthyroidal illness syndrome by blocking thyroxine activation while promoting thyroid hormone inactivation in human cells. J Clin Invest. 2011;121(5):1834‐1845. doi:10.1172/JCI44678
- Farhangi MA, Keshavarz SA, Eshraghian M, Ostadrahimi A, Saboor-Yaraghi AA. The effect of vitamin A supplementation on thyroid function in premenopausal women. J Am Coll Nutr. 2012;31(4):268‐274. doi:10.1080/07315724.2012.
- Hedrén E, Diaz V, Svanberg U. Estimation of carotenoid accessibility from carrots determined by an in vitro digestion method. Eur J Clin Nutr. 2002;56(5):425‐430. doi:10.1038/sj.ejcn.1601329
- Olivieri O, Girelli D, Stanzial AM, Rossi L, Bassi A, Corrocher R. Selenium, zinc, and thyroid hormones in healthy subjects: low T3/T4 ratio in the elderly is related to impaired selenium status. Biol Trace Elem Res. 1996;51(1):31‐41. doi:10.1007/BF02790145
- Drutel A, Archambeaud F, Caron P. Selenium and the thyroid gland: more good news for clinicians. Clin Endocrinol (Oxf). 2013;78(2):155‐164. doi:10.1111/cen.12066
- Zimmermann MB, Köhrle J. The impact of iron and selenium deficiencies on iodine and thyroid metabolism: biochemistry and relevance to public health. Thyroid. 2002;12(10):867‐878. doi:10.1089/105072502761016494
- Jain RB. Thyroid function and serum copper, selenium, and zinc in general U.S. population. Biol Trace Elem Res. 2014;159(1-3):87‐98. doi:10.1007/s12011-014-9992-9
- Abdel-Dayem, M.M., Elgendy, M.S. Effects of chronic estradiol treatment on the thyroid gland structure and function of ovariectomized rats. BMC Res Notes 2, 173 (2009). https://doi.org/10.1186/1756-
- Understanding Local Control of Thyroid Hormones: (Deiodinases Function and Activity) NAHIS https://www.nahypothyroidism.
- Nobuyuki Amino 4 Autoimmunity and hypothyroidism Baillière’s Clinical Endocrinology and Metabolism Volume 2, Issue 3, August 1988, Pages 591-617 doi: https://doi.org/10.1016/S0950-
- Yang, J., Yang, X. & Li, M. Baicalin, a natural compound, promotes regulatory T cell differentiation. BMC Complement Altern Med 12, 64 (2012). https://doi.org/10.1186/1472-
- Asvold BO, Bjøro T, Nilsen TI, Gunnell D, Vatten LJ. Thyrotropin levels and risk of fatal coronary heart disease: the HUNT study. Arch Intern Med. 2008;168(8):855‐860. doi:10.1001/archinte.168.8.855
- Anthony Martin Gerdes and Giorgio Iervasi Thyroid Replacement Therapy and Heart Failure Circulation 2010;122:385–393 https://doi.org/10.1161/
- Hiroaki Kimura and Patrizio Caturegli Chemokine Orchestration of Autoimmune Thyroiditis Thyroid 2007 17:10, 1005-1011 https://doi.org/10.1089/thy.
- Molnár I, Balázs C, Szegedi G, Sipka S. Inhibition of type 2,5′-deiodinase by tumor necrosis factor alpha, interleukin-6 and interferon gamma in human thyroid tissue. Immunol Lett. 2002;80(1):3‐7. doi:10.1016/s0165-2478(01)
- Kjellman BF, Ljunggren JG, Beck-Friis J, Wetterberg L. Reverse T3 levels in affective disorders. Psychiatry Res. 1983;10(1):1‐9. doi:10.1016/0165-1781(83)
- Mebis L, van den Berghe G. The hypothalamus-pituitary-thyroid axis in critical illness. Neth J Med. 2009;67(10):332‐340.
- Rannem T, Ladefoged K, Hylander E, Hegnhøj J, Staun M. Selenium depletion in patients with gastrointestinal diseases: are there any predictive factors?. Scand J Gastroenterol. 1998;33(10):1057‐1061. doi:10.1080/003655298750026750
- Vitamin B12 Health Sheet NIH March 30, 2020 https://ods.od.nih.gov/
- Schroeder AC, Privalsky ML. Thyroid hormones, t3 and t4, in the brain. Front Endocrinol (Lausanne). 2014;5:40. Published 2014 Mar 31. doi:10.3389/fendo.2014.00040
- Moncayo R, Kroiss A, Oberwinkler M, et al. The role of selenium, vitamin C, and zinc in benign thyroid diseases and of selenium in malignant thyroid diseases: Low selenium levels are found in subacute and silent thyroiditis and in papillary and follicular carcinoma. BMC Endocr Disord. 2008;8:2. Published 2008 Jan 25. doi:10.1186/1472-6823-8-2
- Guy E. Abraham, M.D. (1)and David Brownstein, M.D. Evidence that the administration of Vitamin C improves a defective cellular transport mechanism for iodine: A Case Report Optimox https://www.optimox.com/
- Anna J Duffield, Christine D Thomson, Kristina E Hill, Sheila Williams, An estimation of selenium requirements for New Zealanders, The American Journal of Clinical Nutrition, Volume 70, Issue 5, November 1999, Pages 896–903, https://doi.org/10.1093/ajcn/
- Hossein-nezhad A, Spira A, Holick MF. Influence of vitamin D status and vitamin D3 supplementation on genome wide expression of white blood cells: a randomized double-blind clinical trial. PLoS One. 2013;8(3):e58725. doi:10.1371/journal.pone.