Hypothyroidism

HYPOTHYROIDISM

Hypothyroidism may be either subclinical or overt (symptomatic). Subclinical hypothyroidism is characterized by a serum TSH above the upper reference limit in combination with a normal free thyroxine (T4). An elevated TSH, usually above 10 mIU/L, in combination with a subnormal free T4 characterizes overt hypothyroidism. The prevalence of subclinical disease was 4.3% and of overt disease was 0.3%. Studies have shown that 5.9% of women and 2.3% of men over the age of 60 years have TSH values over 10 mIU/L, 39% of whom had subnormal T4 levels. The incidence of hypothyroidism in women was 3.5 per 1000 per year and in men it was 0.6 per 1000 per year.

CAUSES OF HYPOTHYROIDISM:

Chronic autoimmune thyroiditis, also known as chronic lymphocytic thyroiditis or Hashimoto’s thyroiditis, is a common autoimmune disease, which most often leads to impaired function of the thyroid gland

Environmental iodine deficiency is the most common cause of hypothyroidism on a worldwide basis. In areas of iodine sufficiency, such as the United States, the most common cause of hypothyroidism is chronic autoimmune thyroiditis (Hashimoto’s thyroiditis). Hashimoto’s thyroiditis is 5–10 times more common in women than in men. Besides Hashimoto’s thyroiditis, autoimmune thyroid diseases (AITDs), include chronic autoimmune thyroiditis. Hypothyroidism may occur as a result of radioiodine or surgical treatment for hyperthyroidism, thyroid cancer, or benign nodular thyroid disease and after external beam radiation for non–thyroid-related head and neck malignancies, including lymphoma.

Central hypothyroidism occurs when there is insufficient production of bioactive TSH due to pituitary or hypothalamic tumors (including craniopharyngiomas), inflammatory (lymphocytic or granulomatous hypophysitis) or infiltrative diseases, hemorrhagic necrosis (Sheehan’s syndrome), or surgical and radiation treatment for pituitary or hypothalamic disease. In central hypothyroidism, serum TSH may be mildly elevated, but assessment of serum free T4 is usually low, differentiating it from subclinical primary hypothyroidism.

It was shown that hypothyroidism, even when adequately treated, is associated with increased morbidity and mortality (8-11). Results suggested that thyroid peroxidase antibody (TPO-Ab) positivity per se might be associated with symptomatic distress in patients with Hashimoto’s thyroiditis.

DIAGNOSIS:

Besides clinical symptoms and blood tests for thyroid function (TSH, T3, T4 levels), determining the presence of elevated anti-thyroid antibody titers which include anti-thyroglobulin antibodies (TgAb), anti–microsomal/thyroid peroxidase antibodies (TPOAb), and TSH receptor antibodies (TSHRAb) is performed.

It is important to notice that many patients with chronic autoimmune thyroiditis are biochemically euthyroid. However, approximately 75% have elevated anti-thyroid antibody titers.

SIGNS AND SYMPTOMS OF HYPOTHYROIDISM:

Dry skin, cold sensitivity, fatigue, muscle cramps, voice changes, and constipation are among the most common. Less commonly appreciated and typically associated with severe hypothyroidism are carpal tunnel syndrome, sleep apnea, pituitary hyperplasia that can occur with or without hyperprolactinemia and galactorrhea, and hyponatremia that can occur within several weeks of the onset of profound hypothyroidism.

WHEN TO TREAT HYPOTHYROIDISM:

There is general agreement that patients with primary hypothyroidism with TSH levels above 10 mIU/L should be treated. Treratment of patients with TSH levels of 4.5–10 mIU/L may benefit depending on specific patient symptoms and comorbidities and can be determine by thier physician

HOW TO TREAT HYPOTHYROIDISM:

Treatment of hypothyroidism is best accomplished using synthetic L-thyroxine sodium (Synthroid, Thyroxine). Absorbtion of levothyroixine could depend on gastric acid secretion. The liquicap preparation (Tirosint) is the least affected by changes in pH. medication should be taken in the morning and on empty stomach - 60 minutes before breakfast on an empty stomach. It should not be taken with substances or other medications because that will interfere with its absorption and metabolism.

Dose adjustments are guided by serum TSH determinations in 4–8 weeks following initiation of therapy.

Once an adequate replacement dosage has been determined, a periodic follow-up evaluations with repeat TSH testing at 6-month and then 12-month intervals are appropriate.

SELENIUM:

In a recent Danish study, serum selenium concentration was inversely associated with thyroid volume, supporting a role for selenium in the thyroid gland, which indeed has the highest selenium concentration of all tissues (13, 14)

Selenium naturally appears in water and some foods. While people only need a very small amount, selenium plays a key role in the metabolism and its antioxidant properties. Antioxidants protect cells from damage.

Studies showed that levothyroxine is only corrects low thyroid function, but it does not treat the disease! The combination of Levothyroxine and Selenium combination results in improved therapeutic effects than the levothyroxine monotherapy in preventing hashimotos thyroiditis progression (7). Selenium is a nonmetal mineral, a trace element and an essential micronutrient. Study showed that the recommended daily Selenium intake is 50 μg and 40 μg for men and women, respectively, and it is believed that 10% of adults would benefit from increasing their intake (12 -14). The majority of randomized clinical trials, selenium, in various formulations,effectively decreased serum TPO-Ab concentrations in Hashimoto’s thyroiditis patients (15-26)

WHEN TO CONSULT AN ENDOCRINOLOGIST

Although most physicians can diagnose and treat hypothyroidism, consultation with an endocrinologist is recommended
in the following situations: children and infants, patients in whom it is difficult to render and maintain a euthyroid state, pregnancy, women planning conception, cardiac disease, presence of goiter, nodule, or other structural changes in the thyroid gland, presence of other endocrine disease such as adrenal and pituitary disorders, unusual constellation of thyroid function test results, unusual causes of hypothyroidism as those induced by agents

HYPOTHYROIDISM DURING PREGNANCY:

Overt untreated hypothyroidism during pregnancy may adversely affect maternal and fetal outcomes. These adverse outcomes include increased incidences of spontaneous miscarriage, preterm delivery, preeclampsia, maternal hypertension, postpartum hemorrhage, low
birth weight and stillbirth, and impaired intellectual and psychomotor development of the fetus.

Women with positive TPO Antibodies may have an increased riskfor first trimester miscarriage, preterm delivery, and for offspring with impaired cognitive development.

Treatment with L-thyroxine before conception has been shown to reduce the miscarriage rate and to increase live birth rate in women with subclinical hypothyroidism undergoing assisted reproduction.

When a woman with hypothyroidism becomes pregnant, the dosage of L-thyroxine should be increased as soon as possible to ensure that serum TSH is 2.5 mIU/L, L-thyroxine treatment should be initiated. Serum TSH and total T4 measurements should be monitored every 4 weeks during the first half of pregnancy and at least once between 26 and 32 weeks gestation to ensure that the requirement for L-thyroxine has not changed. Some of us would continue to monitor thyroid indices after 32 weeks in order to confirm that thyroid indices are in the normal range. L-thyroxine dosages should be adjusted as indicated, aiming for TSH levels that are within the normal range for that phase of pregnancy.

HYPOTHYROIDISM AND INFERTILITY

Some patients with infertility and menstrual irregularities have underlying chronic thyroiditis in conjunction with subclinical or overt hypothyroidism. Expert endocrinologist can determine which patient will benefit from thyroid hormone replacement therapy. Thyroid hormone replacement therapy may normalize the menstrual cycle and restore normal fertility may normalize the menstrual cycle and restore normal fertility.

References:

1) Jeffrey R. Garber,Rhoda H. Cobin, Hossein Gharib, James V. Hennessey, Irwin Klein,Jeffrey I. Mechanick, Rachel Pessah-Pollack, Peter A. Singer, and Kenneth A. Woeber. Clinical Practice Guidelines for Hypothyroidism in Adults: Cosponsored by the American Association of Clinical Endocrinologists and the American Thyroid Association. THYROID Volume 22, Number 12, 2012.

2) Sawin CT, Castelli WP, Hershman JM, McNamara P, Bacharach P 1985 The aging thyroid. Thyroid deficiency in the Framingham Study. Arch Intern Med 145:1386–1388.

3) Surks MI, Ortiz E, Daniels GH, Sawin CT, Col NF, Cobin RH, Franklyn JA, Hershman JM, Burman KD, Denke MA, Gorman C, Cooper RS, Weissman NJ 2004 Subclinical thyroid disease: scientific review and guidelines for diagnosis and management. JAMA 291:228–238.

4) Rodondi N, den Elzen WP, Bauer DC, Cappola AR, Razvi S, Walsh JP, Asvold BO, Iervasi G, Imaizumi M, Collet TH, Bremner A, Maisonneuve P, Sgarbi JA, Khaw KT, Vanderpump MP, Newman AB, Cornuz J, Franklyn JA, Westendorp RG, Vittinghoff E, Gussekloo J 2010 Subclinical hypothyroidism and the risk of coronary heart disease and mortality. JAMA 304:1365–1374.

5) Razvi S, Weaver JU, Vanderpump MP, Pearce SH 2010 The incidence of ischemic heart disease and mortality in people with subclinical hypothyroidism: reanalysis of the Whickham Survey cohort. J Clin Endocrinol Metab 95:1734–1740.

6) Goldsmith RE, Sturgis SH, Lerman J, Stanbury JB 1952 The menstrual pattern in thyroid disease. J Clin Endocrinol Metab 12:846–855.

7) Yu L. Levothyroxine monotherapy versus levothyroxine and selenium combination therapy in chronic lymphocytic thyroiditis. J Endocrinol Invest. 2017 Nov;40(11):1243-1250.

8) Thvilum M, Brandt F, Brix TH, Hegedus L. A review of the evidence for and against increased mortality in hypothyroidism. Nat Rev Endocrinol. 2012;8(7):417–424.

9) Thvilum M, Brandt F, Almind D, Christensen K, Hegedus L, Brix TH. Excess mortality in patients diagnosed with hypothyroidism: a nationwide cohort study of singletons and twins. J Clin Endocrinol Metab. 2013;98(3):1069–1075.

10) Thvilum M, Brandt F, Almind D, Christensen K, Brix TH, Hegedus L. Type and extent of somatic morbidity before and after the diagnosis of hypothyroidism. A nationwide register study. PloS One. 2013;8(9):e75789.

11) Thvilum M, Brandt F, Almind D, Christensen K, Brix TH, Hegedüs L. Increased psychiatric morbidity before and after the diagnosis of hypothyroidism: a nationwide register study. Thyroid. 2014. doi:10.1089/thy.2013.0555.

12) Rasmussen LB, Mejborn H, Andersen NL, Dragsted LO, Krogholm KS, Larsen EH. Selen og Sundhed. Danmarks Fødevareforskning: Copenhagen; 2006.

13) Rayman MP. Selenium and human health. Lancet. 2012;379:1256–1268.

14) Rasmussen LB, Schomburg L, Kohrle J, Pedersen IB, Hollenbach B, Hog A, Ovesen L, Perrild H, Laurberg P. Selenium status, thyroid volume, and multiple nodule formation in an area with mild iodine deficiency. Eur J Endocrinol. 2011;164:585–590.

15) Gartner R, Gasnier BC, Dietrich JW, Krebs B, Angstwurm MW. Selenium supplementation in patients with autoimmune thyroiditis decreases thyroid peroxidase antibodies concentrations. J Clin Endocrinol Metab. 2002;87:1687–1691.

16) Duntas LH, Mantzou E, Koutras DA. Effects of a six month treatment with selenomethionine in patients with autoimmune thyroiditis. Eur J Endocrinol. 2003;148:389–393.

17) Gartner R, Gasnier BC. Selenium in the treatment of autoimmune thyroiditis. Biofactors. 2003;19:165–170.

18) Turker O, Kumanlioglu K, Karapolat I, Dogan I. Selenium treatment in autoimmune thyroiditis: 9-month follow-up with variable doses. J Endocrinol. 2006;190:151–156.

19) Mazokopakis EE, Papadakis JA, Papadomanolaki MG, Batistakis AG, Giannakopoulos TG, Protopapadakis EE, Ganotakis ES. Effects of 12 months treatment with L-selenomethionine on serum anti-TPO levels in patients with Hashimoto’s thyroiditis. Thyroid. 2007;17:609–612.

20) Karanikas G, Schuetz M, Kontur S, Duan H, Kommata S, Schoen R, Antoni A, Kletter K, Dudczak R, Willheim M. No immunological benefit of selenium in consecutive patients with autoimmune thyroiditis. Thyroid. 2008;18:7–12. doi: 10.1089/thy.2007.0127. [PubMed] [Cross Ref]
Balazs C. The effect of selenium therapy on autoimmune thyroiditis. Orv Hetil. 2008;149:1227–1232.

21) Kvicala J, Hrda P, Zamrazil V, Nemecek J, Hill M, Jiranek V. Effect of selenium supplementation on thyroid antibodies. J Radioanal Nucl Chem. 2009;280(2):275–279.

22) Nacamulli D, Mian C, Petricca D, Lazzarotto F, Barollo S, Pozza D, Masiero S, Faggian D, Plebani M, Girelli ME, Mantero F, Betterle C. Influence of physiological dietary selenium supplementation on the natural course of autoimmune thyroiditis. Clin Endocrinol (Oxf) 2010;73:535–539.

23) Krysiak R, Okopien B. The effect of levothyroxine and selenomethionine on lymphocyte and monocyte cytokine release in women with Hashimoto’s thyroiditis. J Clin Endocrinol Metab. 2011;96(7):2206–2215. doi: 10.1210/jc.2010-2986.

24) Anastasilakis AD, Toulis KA, Nisianakis P, Goulis DG, Kampas L, Valeri RM, Oikonomou D, Tzellos TG, Delaroudis S. Selenomethionine treatment in patients with autoimmune thyroiditis: a prospective, quasi-randomised trial. Int J Clin Pract. 2012;66:378–383.

25) Zhu L, Bai X, Teng WP, Shan ZY, Wang WW, Fan CL, Wang H, Zhang HM. Effects of selenium supplementation on antibodies of autoimmune thyroiditis. Zhonghua Yi Xue Za Zhi. 2012;92:2256–2260.

26) Eskes SA, Endert E, Fliers E, Birnie E, Hollenbach B, Schomburg L, Kohrle J, Wiersinga WM. Selenite supplementation in euthyroid subjects with thyroid peroxidase antibodies. Clin Endocrinol (Oxf) 2014;80:444–451.


Global Healing Center's Selenium supplement is plant-derived, highly bioavailable, and made from 100% organic materials to support your body naturally.

Our Thyroid Health Kit™ provides the essential nutrients you need to support normal, healthy thyroid levels including iodine, selenium, and more.