fbpx
 

Hashimoto’s Thyroiditis

 

Hashimoto’s Thyroiditis or Hashimoto’s Disease

Hashimoto’s disease is an autoimmune pathological condition that affects the thyroid gland. During this condition the human body produces antibodies (auto-antibodies) that act against the thyroid gland.

 

Inflammation caused by this phenomenon is also known as chronic lymphocytic thyroiditis and can often result in an underactive thyroid gland (hypothyroidism).

 

Diagnosis of Real Causes & Treatment of Hashimoto’s Thyroiditis

  • 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

 

Symptoms

Symptoms of Hashimoto’s disease may not be evident in the beginning as the disease can progress slowly over a course of many years.

 

The symptoms that usually lead a physician to test for Hashimoto’s disease are similar to those of Hypothyroidism and include dizziness, skin dryness, constipation, fatigue, cold intolerance, fluid retention, decreased libido, fragile hair, irregular period, weight gain/ difficulty losing weight, palpitations or hoarse voice.

 

Previous thyroid gland problems or a goiter can also indicate the existence of Hashimoto’s disease.

 

hashimoto's thryroiditis treatment

 

Pathophysiology of Hashimoto’s Disease

The thyroid is a butterfly-shaped gland located at the base of the larynx. This gland can be parallelized as the power house of the metabolism. The thyroid uses iodine and tyrosine in order to produce two basic hormones, thyroxine (T4) and triiodothyronine (T3).

 

During Hashimoto’s disease, the levels of T3 and T4 are very low and subsequently the levels of TSH (thyroid stimulating hormone) are too high. Being classified as an autoimmune disease, means that the immune system mistakenly attacks the thyroid gland. More specifically, the influx of CD4 and T helper cells along with the action of auto-antibodies produced by B cells against thyroglobulin (TG) and thyroid peroxidase (TPO), cause the gradual destruction of the thyroid gland.

 

Epidemiology and risk factors

Hashimoto’s disease is one of the most common endocrine disorders. It is estimated that in the USA, approximately 4.78% of the population have an undiagnosed thyroid dysfunction. In Europe an estimated 1-2% of the population suffers from this disease.

 

Hashimoto’s is more common among women aged 30 to 50 years old and can coexist along with other autoimmune diseases such as Rheumatoid arthritis, lupus and type 1 Diabetes. Other risk factors include a positive family history for Hashimoto’s and exposure to irradiation.

Hashimoto – Treatment

 

Classical therapeutic approach

The usual treatment of Hypothyroidism includes medicines, typically substitutions of T4 hormone that regulate the levels of TSH. Dosage is usually regulated according to the levels of TSH and only. It is extremely usual in Hashimoto disease that the thyroid function is far from restored based on regulation of TSH values alone.

In most cases, patients need to take medicines throughout their lifetime and be monitored extremely closely for thyroid hormones’ fluctuations that are attributed to the disease itself.

This can impact the patients’ psychology as they feel that the disease can never be treated effectively. Many patients express concerns about the effects medicines may have on their health in the long run.

 

Hashimoto’s Disease – Treatment

The general view concerning Hashimoto disease – as well as all thyroid disorders-  is that there is no effective treatment available just effective management. That is not true.

The usual administration of medications aims to provide the body with the missing hormones that can be no longer produced by the thyroid gland. That’s achieved through prescription of synthetic thyroid hormones and it’s the only treatment available the last decades. In day to day clinical practice it is evident that the patient is often de-regulated every now and then. A constant change in drug dosages is required in order to manage the symptoms.

 

The key to a successful therapeutic approach is to light on the underlying causes.

The patients make no radical adaptations to their daily life. Instead it’s progressively improved along with their health status.

  • Personalized therapeutic protocols, without chemical residues and excipients
  • Treatments that can be combined with other approaches, without side-effects

 

Hashimoto’s Disease – Examination

Your personalized treatment plan will be based upon the symptoms described, your medical history overall and most importantly through specialized diagnostic testing. This way it’s possible to uncover the molecular causes and factors that led to the manifestation of Hashimoto disease.

After filling in a detailed Medical Questionnaire, your Health Specialist will address a series of targeted questions to you, to assess your symptoms and the general health status. Through biochemical, hormonal and specialized molecular examination, all malfunctions are detected.

The combination of therapeutic schemes can include:

  • Macro-micronutrients medications
  • Molecular Nutrition strategies
  • Hormone Restoration through Bioidentical hormones
  • Regulation of the gastro-intestinal system

The proposed therapeutic protocols are based on specific medical algorithms that utilize the diagnostic tests’ results. Depending on the laboratory tests findings, the type of treatment, its duration and any other possible combination or regimen are individually defined.

The therapeutic protocols are successfully established in clinical use since 1997, first used in US. Treatment protocols can be applied solely or combined with any other medication the patient is currently undergoing.

The suitable treatment and nutrition plan will aim towards achieving even higher levels of health and well-being along with alleviating not only the symptoms but the true causes of Hashimoto’s disease.

Functional Corporation
Partners

Read more:


The Impact of Nutrition on Hashimoto Disease

 

References


  • Cooper DS. Subclinical Hypothyroidism. NEJM. 2001 Jul 26;345: 260– 265.
  • Persky VW, Turyk ME, Wang L, Freels S, Chatterton R Jr, Barnes S, Erdman J Jr, Sepkovic DW, Bradlow HL, Potter S. Effect of soy protein on endogenous hormones in postmenopausal women. Am J Clin Nutr. 2002 Jan; 75( 1): 145– 153. Erratum in: Am J Clin Nutr. 2002 Sep; 76( 3): 695
  • Toscano V, Conti FG, Anastasi E, Mariani P, Tiberti C, Poggi M, Montuori M, Monti S, Laureti S, Cipolletta E, Gemme G, Caiola S, Di Mario U, Bonamico M. Importance of gluten in the induction of endocrine autoantibodies and organ dysfunction in adolescent celiac patients. Am J Gastroenterol. 2000 Jul; 95( 7): 1742–1748.
  • 4Ellingsen DG, Efskind J. Effects of low mercury vapour exposure on the thyroid function in chloralkali workers. J Appl Toxicol. 2000 Nov– Dec; 20( 6): 483– 489.
  • WJ, Pan Y; Johnson AR, et al. Reduction of chemical sensitivity by means of heat depuration, physical therapy and nutritional supplementation in a controlled environment. J Nutr Env Med. 1996;6:141– 148.
  • Pelletier C, Imbeault P, Tremblay A. Energy balance and pollution by organochlorines and polychlorinated biphenyls. Obes Rev. 2003 Feb; 4( 1): 17– 24. Review.
  • Bland J. Nutritional Endocrinology, Normalizing Hypothalamus-Pituitary-Thyroid Axis Function, 2002 Seminar Series Syllabus.
  • Gaby AR. Sub-laboratory hypothyroidism and the empirical use of Armour thyroid. Altern Med Rev. 2004 Jun; 9( 2): 157– 179.
  • Goglia F. Biological effects of 3,5-diiodothyronine (T( 2)). Biochemistry (Moscow). 2005 Feb; 70( 2): 164– 172.
  • Trbojević B, Djurica S. Diagnosis of autoimmune thyroid disease. Srp Arh Celok Lek 2005;133 Suppl 1:25-33.
  • Duntas LH. Environmental factors and autoimmune thyroiditis. Nat Clin Pract Endocrinol Metab 2008;4(8):454-460.
  • Wiersinga WM. Clinical relevance of environmental factors in the pathogenesis of autoimmune thyroid disease. Endocrinol Metab (Seoul) 2016;31(2):213-222.
  • Kawicka A, Regulska-Ilow B. Metabolic disorders and nutritional status in autoimmune thyroid diseases. Postepy Hig Med Dosw (Online) 2015;69:80-90.
  • Wang L, Wang B, Chen SR, et al. Effect of selenium supplementation on recurrent hyperthyroidism caused by Graves’ disease: a prospective pilot study. Horm Metab Res 2016;[Epub ahead of print].
  • Dharmasena A. Selenium supplementation in thyroid associated ophthalmopathy: an update. Int J Ophthalmol 2014;7(2):365-375.
  • Marcocci C, Kahaly GJ, Krassas GE, et al. Selenium and the course of mild Graves’ orbitopathy. N Engl J Med 2011;364(20):1920-1931.
  • Hwang S, Byun JW, Yoon JS, et al. Inhibitory effects of α-lipoic acid on oxidative stress-induced adipogenesis in orbital fibroblasts from patients with Graves ophthalmopathy. Medicine (Baltimore) 2016;95(2):e2497.
  • Chen K, Yan B, Wang F, et al. Type 1 5′-deiodinase activity is inhibited by oxidative stress and restored by alpha-lipoic acid in HepG2 cells. Biochem Biophys Res Commun 2016;472(3):496-501.
  • Sharma BR, Joshi AS, Varthakavi PK, et al. Celiac autoimmunity in autoimmune thyroid disease is highly prevalent with a questionable impact. Indian J Endocrinol Metab 2016;20(1):97-100.
  • Roy A, Laszkowska M, Sundström J, et al. Prevalence of celiac disease in patients with autoimmune thyroid disease: a meta-analysis. Thyroid 2016;26(7):880-890.