top of page

A Primer on Thyroid Dysfunction

This blog post accompanies the 6th episode of my BioBros Podcast, featuring Derek of More Plates More Dates and Vigorous Steve. During the episode, I discuss thyroid function because (1) both Dallas the alleged growth hormone abusers Dallas McCarver and Dave Palumbo developed it, and (2) GH use lowers TSH levels in most people. Until now, it is my impression that no one in the PED or biohacking community has ever explained how growth hormone lowers TSH, and whether it is dangerous for the thyroid.

Without knowing anything about thyroid function, I assumed that pro-growth forces could accelerate cancer development, leading me to conclude upregulating TSH chronically could produce hyperplasia. It turns out that I was right, but the situation is much worse than that. And who knew that cabergoline/pramipexole are potent growth hormone inhibitors?


1. Hypothalamus releases thyrotropin-releasing hormone (TRH).

a. Binds to the thyrotropin-releasing hormone receptor (TRHR) in the anterior pituitary.

2. Pituitary releases thyroid-stimulating hormone (TSH) into the bloodstream.

3. TSH stimulates the thyroid to produce thyroxine (T4) and triiodothyronine (T3), which stimulates the metabolism.

4. T3 and T4 act via somatostatin to inhibit hypothalamic TRH in a negative feedback loop.


1. Chronic TSH stimulation can produce hyperplasia of the thyroid gland[1][2].

2. Catecholamines: not fully understood, except at the dopamine receptor.

a. Norepinephrine[3] stimulates the release of TRH from the hypothalamus, which is likely how the cold speeds up our metabolism faster.

b. Dopamine regulates TSH[4].

i. Dopamine[5] and dopamine receptor agonists[6] suppress TSH synthesis while dopamine antagonists[7] minorly enhance TSH synthesis.

1. Schizophrenics have higher T3[8] and T4[9] levels.

ii. Note that dopamine may lower GH[10] pulses.

1. Dopamine agonists are used to treat gigantism, inhibiting GH more effectively than IGF-1[11] - think of using nandrolone sans GH now!

2. Acutely, they cause growth hormone release in healthy people[12].

3. IGF-1:

a. Type 1 IGF-1 receptor is mostly expressed in the thyroid gland[13].

b. IGF-1R overexpression in the thyroid increases gland weight, decreases TSH, increases serum T4, suggesting that IGF-1 and the IGF-1R stimulate thyroid function[14].

c. Epidemiologic studies reveal IGF-1 levels are associated with goiter[15].

d. In acromegaly:

i. Acromegalic people have increased thyroid vascularity[16].

ii. In a study of 62 Italian acromegalics: thyroid volume is associated with the duration of acromegaly, 78% of patients had thyroid disorders (particularly non-toxic nodular disorder), and thyroid carcinoma was more common[17].

iii. A study of 37 acromegalics found goiters to be common.

1. Early in the course of the disease, a diffuse goiter develops.

2. Thyroid autonomy and nodule formation begin – growth can continue without TSH.

3. Attenuating GH secretion can reduce thyroid size, but this is limited by the extent of nodularity[18].

e. In hypopituitary patients given GH, IGF-1 does not independently stimulate thyroid growth but enhanced proliferation of thyroid cells by potentiation the mitogenic effects of TSH.

f. In women[19] but not obese[20] people, GH administration suppresses TSH.

g. IGF-1 levels are dose-dependently associated with the risk of thyroid enlargement and nodule formation in non-acromegalic people[21].


1. When iodine sufficient, about 5% of people have thyroid nodules, though 68% harbor occult nodules.

2. 65% with ultrasound, 15% with CT or fMRI, and 1-2% with positron emission tomography (PET).

3. Solitary in 50% of cases.

4. More nodules in older people, females, and larger people.

5. 16 million Americans have a palpable nodule: about 10% have cancer, 5% cause compressive problems, and 5% cause thyroid dysfunction.


1. 211% increase from 1975-2013, 3% annually.

2. Most new diagnoses are of papillary thyroid cancer (PTC), the least aggressive and most common type.

3. Doctors hypothesized that over-surveillance of small tumors that would not cause pathologies may be responsible.

4. This meta-analysis finds a true increase in both the thyroid cancer rate and mortality from advanced-stage papillary thyroid cancers.


1. Nitrate exposure[25]:

a. Nitrates compete with iodide for the sodium-iodide symporter on thyroid follicles, reducing T3 and T4 and increasing TSH[26][27].

b. Due to TSH elevation, thyroid hypertrophies[28] (even from nitrate in drinking water[29]).

c. This is aside from the N-nitroso carcinogens[30].

2. Polychlorinated biphenyls (PCBs): synthetic, lipophilic compounds mainly found in large fish and they disrupt the thyroid function[31].

3. Plastics:

a. Phthalates in cosmetics, food packaging, cleaning agents, medical equipment[32].

i. They don’t accumulate but are excreted through urine.

ii. They can activate the estrogen receptor and upregulate VEGF.

b. Bisphenol A (BPA):

i. Structurally similar to 17-B-estradiol, competes with endogenous estrogens at the ER[33].

ii. Inhibits thrombopoietin (TPO) activity.

iii. Binds to the thyroid hormone receptor (TR) weakly, antagonizing the activity of T3.

4. Radiation[34], particularly for papillary thyroid cancers.

5. Perfluorinated compounds (PFCs): Stain repellent products (usually used to resist stains or oils) associated with thyroid disease[35].

6. Metals:

a. Cadmium most strongly (chocolate)[36]; lead[37].

7. Pesticides[38].


1. Excess iodine intake increases AITD prevalence[39].

2. Autoimmune disease sufferers are 85+% female; only early childhood incidence of T1D is nearly equalin both sexes.

a. Males have greater immune suppression than females in most species[40].

b. Females have more immunoreactivity to insult (antigens).

i. Over half of the immune genes that are overexpressed in them have estrogen response elements, compared to less than 10% of the men’s immune genes that are overexpressed following a challenge[41].

3. Grave’s disease (GD) and Hashimoto’s thyroiditis (HT) are the most common[42].

a. Grave’s has a sudden onset and is usually controlled within 2 years.

b. Hashimoto’s has a slower onset and titers of antibodies can be very high.

i. Even with levothyroxine treatment, titers of anti-TSPO antibodies decrease slowly (i.e. over 5 years) and remain within the pathological range[43].

4. Primary antibodies:

a. Ranges[44]:

i. Anti-TSHR > 1.75 U/mL

ii. Anti-TPO > 35 U/l

iii. Anti-Tg > 20 U/l

b. Anti-thyroid-stimulating hormone receptor (TSHR):

i. The first anti-TSHR antibody to be identified was later called immunoglobulin G (IgG)[45].

ii. Anti-TSHR antibodies found in 90% of GD, 0-20% of HT, and 10-75% of atrophic thyroiditis patients[46].

iii. GD:

1. Autoantigen initiation in GD to the TSHR seems to occur when A-subunits are shed during the normal function of the receptor on the thyrocyte[47].

2. Stimulating antibodies are found in 73-100% of GD patients, while blocking antibodies are found in 25-75%[48][49][50] - always more stimulatory antibodies[51].

3. High anti-TSHR antibodies at diagnoses or cessation of therapy is an indication for recurrence of GD and more severe therapy (i.e. surgery/radioiodine)[52].

c. Anti-thyroid peroxidase (TPO):

i. More common and critical than Anti-Tg antibodies[53].

ii. Detected in 90-95% of AITD, 80% of GD, and only 10-15% of healthy people[54].

iii. They can be of any class of immunoglobulin G (IgG), though IgG1 and IgG4 are more common[55], and low levels of IgAs have also been reported[56].

iv. Anti-TPO antibodies increase oxidative stress[57], but cause less damage to the thyroid than T-cell of cytokine-mediated apoptosis[58].

1. While cytotoxic to thyrocytes in GD, that has not been shown in HT[59].

d. Anti-thyroglobulin (Tg):

i. Tg is a heterogenous glycoprotein made of dimers (two attached molecules), usually with 2-4 T4 and 0.3 T3 molecules.

ii. Anti-Tg antibodies in GD are mostly IgG4[60], with low levels of IgA[61].

iii. In HT, the IgG2 class may be dominant[62].

iv. Anti-Tg antibodies are found in 10% of healthy people, 15% of people over 60, 50-60% in GD, and 60-80% in HT (CITATION)

v. They do not cause thyrocyte destruction.

5. Antibodies against thyroid antigens (rarely detected)[63]:

a. Anhydrase 2, megalin, T3 and T4, sodium iodide symporter (NIS), and pendrin.

6. Environment:

a. Differences:

i. Smoking is protective for HT but increases likelihood of GD by 3.3x.

1. Lowers anti-Tg and anti-TPO antibody levels.

2. (Similar to how it helps colitis but worsens Crohn’s[64]).

ii. Stress increases the prevalence of GD but not HT[65].

b. Protective:

i. Teetotalers are 2.17x more likely to develop AITD[66][67].

1. High alcohol consumption suppresses the immune system[68].

c. Harmful:

i. Infection with viruses[69] and bacteria (e.g. H. Pylori[70]) increases AITD prevalence.

ii. Interferon gamma (IFN-y), IL-2, and granulocyte-macrophage colony-stimulating factor (GM-CSF) levels[71].

iii. Polyaromatic hydrocarbon exposure elevates circulating antibodies against TPO and Tg[72].

iv. The use of lithium[73]:

1. It becomes concentrated in thyrocytes and either reduces or increases iodine uptake to the thyroid.

a. Reduction: Lithium causes more iodide retention and competes for the iodide transport in the thyroid.

b. Increase: Due to decreased thyroid function and consequent increased TSH secretion[74].

2. Reduces thyroid hormone synthesis via inhibiting the action of TSH on cyclic adenosine monophosphate (cAMP) and via other mechanisms.

v. Therapeutic or environmental radiation[75].

d. Iodine supplementation:

i. Humans contain 25-50 mg of iodine, 50-70% stored outside the thyroid, mostly in the gastrosalivary pool.

ii. Iodine can be attached to sodium, potassium, lipids, or proteins (i.e. iodotyrosin, idiolactone).

iii. Iodine intake of 400-600 mcg/day or more can induce or worsen autoantibody formation, increasing the immunogenicity of Tg[76].

iv. Higher iodine concentrations can induce oxidative stress via TPO activation[77].

v. Iodinization increases anti-TPO antibodies from 14-24% and anti-Tg antibodies from 14-20% in epidemiological studies[78].

vi. Increased iodine supplementation also increases cytokine secretion, T cells, and antibody production by B cells[79].

vii. Iodine has 10x the antioxidant potential of vitamin C and 50x that of iodide[80].

1. Most supplements either contain iodide alone or a combination of the two.

2. Breast cancer cells can take up iodine by facilitated diffusion, and Lugol’s solution (5% iodine, 10% kalium iodide) has a net anti-estrogenic effect.

7. Genetics:

a. 79% of GD manifestation can be explained by genetics; antibody formation among twins is 73% positively correlated[81].

b. It around 55% for HT and AT[82], with antibody formation among monozygotic twins at 80% and among dizygotic twins at 40%.

[1] Capen, C. C. (1992). Pathophysiology of chemical injury of the thyroid gland. Toxicology letters, 64, 381-388. [2] Capen, C. C. (1997). Mechanistic data and risk assessment of selected toxic end points of the thyroid gland. Toxicologic Pathology, 25(1), 39-48. [3] DIEGUEZ, C., FOORD, S. M., PETERS, J. R., HALL, R., & SCANLON, M. F. (1984). Interactions among epinephrine, thyrotropin (TSH)-releasing hormone, dopamine, and somatostatin in the control of TSH secretion in vitro. Endocrinology, 114(3), 957-961. [4] Scanlon, M. F., Weightman, D. R., Shale, D. J., Mora, B., Heath, M., Snow, M. H., ... & Hall, R. (1979). Dopamine is a physiological regulator of thyrotrophin (TSH) secretion in normal man. Clinical endocrinology, 10(1), 7-15. [5] Cooper, D. S., KLIBANSKI, A., & Ridgway, E. C. (1983). Dopaminergic modulation of TSH and its subunits: in vivo and in vitro studies. Clinical Endocrinology, 18(3), 265-275. [6] Haugen, B. R. (2009). Drugs that suppress TSH or cause central hypothyroidism. Best practice & research Clinical endocrinology & metabolism, 23(6), 793-800. [7] Delitala, G., Devilla, L., Canessa, A., & D'asta, F. (1981). On the role of dopamine receptors in the central regulation of human TSH. European Journal of Endocrinology, 98(4), 521-527. [8] Sim, K., Chong, S. A., Chan, Y. H., & Lum, W. M. (2002). Thyroid dysfunction in chronic schizophrenia within a state psychiatric hospital. Annals of the Academy of Medicine, Singapore, 31(5), 641-644. [9] Baumgartner, A., Pietzcker, A., & Gaebel, W. (2000). The hypothalamic–pituitary–thyroid axis in patients with schizophrenia. Schizophrenia research, 44(3), 233-243. [10] Van den Berghe, G., De Zegher, F., Lauwers, P., & Veldhuis, J. D. (1994). Growth hormone secretion in critical illness: effect of dopamine. The Journal of Clinical Endocrinology & Metabolism, 79(4), 1141-1146. [11] Howlett, T. A., Willis, D., Walker, G., Wass, J. A., Trainer, P. J., & UK Acromegaly Register Study Group (UKAR‐3). (2013). Control of growth hormone and IGF 1 in patients with acromegaly in the UK: responses to medical treatment with somatostatin analogues and dopamine agonists. Clinical endocrinology, 79(5), 689-699. [12] Jaffe, C. A., & Barkan, A. L. (1992). Treatment of acromegaly with dopamine agonists. Endocrinology and metabolism clinics of North America, 21(3), 713-735. [13] Cissewski, K., Wolf, M., & Moses, A. C. (1992). Characterization of insulin-like growth factor receptors in human thyroid tissue. Receptor, 2(3), 145-153. [14] Clément, S., Refetoff, S., Robaye, B., Dumont, J. E., & Schurmans, S. (2001). Low TSH requirement and goiter in transgenic mice overexpressing IGF-I and IGF-I receptor in the thyroid gland. Endocrinology, 142(12), 5131-5139. [15] Völzke, H., Friedrich, N., Schipf, S., Haring, R., Lüdemann, J., Nauck, M., ... & Wallaschofski, H. (2007). Association between serum insulin-like growth factor-I levels and thyroid disorders in a population-based study. The Journal of Clinical Endocrinology & Metabolism, 92(10), 4039-4045. [16] Bogazzi, F., Manetti, L., Bartalena, L., Gasperi, M., Grasso, L., Cecconi, E., ... & Martino, E. (2002). Thyroid vascularity is increased in patients with active acromegaly. Clinical endocrinology, 57(1), 65-70. [17] Gasperi, M., Martino, E., Manetti, L., Arosio, M., Porretti, S., Faglia, G., ... & Liuzzi, A. (2002). Prevalence of thyroid diseases in patients with acromegaly: results of an Italian multi-center study. Journal of endocrinological investigation, 25(3), 240-245. [18] Cheung, N. W., & Boyages, S. C. (1997). The thyroid gland in acromegaly: an ultrasonographic study. Clinical endocrinology, 46(5), 545-549. [19] Giannoulis, M. G., Boroujerdi, M. A., Powrie, J., Dall, R., Napoli, R., Ehrnborg, C., ... & Sonksen, P. H. (2005). Gender differences in growth hormone response to exercise before and after rhGH administration and the effect of rhGH on the hormone profile of fit normal adults. Clinical endocrinology, 62(3), 315-322. [20] Maccario, M., Ramunni, J., Oleandri, S. E., Procopio, M., Grottoli, S., Rossetto, R., ... & Ghigo, E. (1999). Relationships between IGF-I and age, gender, body mass, fat distribution, metabolic and hormonal variables in obese patients. International journal of obesity, 23(6), 612-618. [21] Völzke, H., Friedrich, N., Schipf, S., Haring, R., Lüdemann, J., Nauck, M., ... & Wallaschofski, H. (2007). Association between serum insulin-like growth factor-I levels and thyroid disorders in a population-based study. The Journal of Clinical Endocrinology & Metabolism, 92(10), 4039-4045. [22] Durante, C., Grani, G., Lamartina, L., Filetti, S., Mandel, S. J., & Cooper, D. S. (2018). The diagnosis and management of thyroid nodules: a review. Jama, 319(9), 914-924. [23] Lim, H., Devesa, S. S., Sosa, J. A., Check, D., & Kitahara, C. M. (2017). Trends in thyroid cancer incidence and mortality in the United States, 1974-2013. Jama, 317(13), 1338-1348. [24] Fiore, M., Oliveri Conti, G., Caltabiano, R., Buffone, A., Zuccarello, P., Cormaci, L., ... & Ferrante, M. (2019). Role of emerging environmental risk factors in thyroid cancer: a brief review. International journal of environmental research and public health, 16(7), 1185. [25] Ward, M. H., Kilfoy, B. A., Weyer, P. J., Anderson, K. E., Folsom, A. R., & Cerhan, J. R. (2010). Nitrate intake and the risk of thyroid cancer and thyroid disease. Epidemiology (Cambridge, Mass.), 21(3), 389. [26] Bloomfield, R. A., Welsch, C. W., Garner, G. B., & Muhrer, M. E. (1961). Effect of dietary nitrate on thyroid function. Science, 134(3491), 1690-1690. [27] Bloomfield, R. A., Welsch, C. W., Garner, G. B., & Muhrer, M. E. (1962). Thyroid compensation under the influence of dietary nitrate. Proceedings of the Society for Experimental Biology and Medicine, 111(2), 288-290. [28] Tajtáková, M., Semanová, Z., Tomková, Z., Szökeová, E., Majoroš, J., Rádiková, Ž., ... & Langer, P. (2006). Increased thyroid volume and frequency of thyroid disorders signs in schoolchildren from nitrate polluted area. Chemosphere, 62(4), 559-564. [29] van Maanen, J. M., van Dijk, A., Mulder, K., de Baets, M. H., Menheere, P. C., van der Heide, D., ... & Kleinjans, J. C. (1994). Consumption of drinking water with high nitrate levels causes hypertrophy of the thyroid. Toxicology letters, 72(1-3), 365-374. [30] Bogovski, P., & Bogovski, S. (1981). Special report animal species in which n‐nitroso compounds induce cancer. International journal of cancer, 27(4), 471-474. [31] Meeker, J. D. (2010). Exposure to environmental endocrine disrupting compounds and men's health. Maturitas, 66(3), 236-241. [32] Zuccarello, P., Conti, G. O., Cavallaro, F., Copat, C., Cristaldi, A., Fiore, M., & Ferrante, M. (2018). Implication of dietary phthalates in breast cancer. A systematic review. Food and Chemical Toxicology, 118, 667-674. [33] Zhang, Y., Wei, F., Zhang, J., Hao, L., Jiang, J., Dang, L., ... & Jiang, L. (2017). Bisphenol A and estrogen induce proliferation of human thyroid tumor cells via an estrogen-receptor-dependent pathway. Archives of biochemistry and biophysics, 633, 29-39. [34] Ron, E. (1996). II Cancer Epidemiology and Prevention/Eds D. Schottenfeld, JF Fraiimeni. New York, 1000-1018. [35] Melzer, D., Rice, N., Depledge, M. H., Henley, W. E., & Galloway, T. S. (2010). Association between serum perfluorooctanoic acid (PFOA) and thyroid disease in the US National Health and Nutrition Examination Survey. Environmental health perspectives, 118(5), 686-692. [36] Buha, A., Matovic, V., Antonijevic, B., Bulat, Z., Curcic, M., Renieri, E. A., ... & Wallace, D. (2018). Overview of cadmium thyroid disrupting effects and mechanisms. International journal of molecular sciences, 19(5), 1501. [37] Li, H., Li, X., Liu, J., Jin, L., Yang, F., Wang, J., ... & Gao, Y. (2017). Correlation between serum lead and thyroid diseases: papillary thyroid carcinoma, nodular goiter, and thyroid adenoma. International journal of environmental health research, 27(5), 409-419. [38] Han, M. A., Kim, J. H., & Song, H. S. (2019). Persistent organic pollutants, pesticides, and the risk of thyroid cancer: systematic review and meta-analysis. European Journal of Cancer Prevention, 28(4), 344-349. [39] Camargo, R. Y., Tomimori, E. K., Neves, S. C., Rubio, I. G., Galrao, A. L., Knobel, M., & Medeiros-Neto, G. (2008). Thyroid and the environment: exposure to excessive nutritional iodine increases the prevalence of thyroid disorders in Sao Paulo, Brazil. European journal of endocrinology, 159(3), 293. [40] McKean, K. A., & Nunney, L. (2005). Bateman's principle and immunity: phenotypically plastic reproductive strategies predict changes in immunological sex differences. Evolution, 59(7), 1510-1517. [41] Hewagama, A., Patel, D., Yarlagadda, S., Strickland, F. M., & Richardson, B. C. (2009). Stronger inflammatory/cytotoxic T-cell response in women identified by microarray analysis. Genes & Immunity, 10(5), 509-516. [42] McLeod, D. S., & Cooper, D. S. (2012). The incidence and prevalence of thyroid autoimmunity. Endocrine, 42(2), 252-265. [43] Schmidt, M., Voell, M., Rahlff, I., Dietlein, M., Kobe, C., Faust, M., & Schicha, H. (2008). Long-term follow-up of antithyroid peroxidase antibodies in patients with chronic autoimmune thyroiditis (Hashimoto's thyroiditis) treated with levothyroxine. Thyroid, 18(7), 755-760. [44] Elhomsy, G., & Staros, E. (2014). Antithyroid Antibody. Laboratory Medicine. [45] Adams, D. D. (1956). Abnormal responses in the assay of thyrotropin. In Proc Univ Otago Med School (Vol. 34, pp. 11-12). [46] De Carvalho, G., Perez, C., & Ward, L. S. (2013). The clinical use of thyroid function tests. Arq Bras Endocrinol Metabol, 57, 193-204. [47] Rapoport, B., & McLachlan, S. M. (2016). TSH receptor cleavage into subunits and shedding of the A-subunit; a molecular and clinical perspective. Endocrine reviews, 37(2), 114-134. [48] TADA, H., IZUMI, Y., WATANABE, Y., TAKANO, T., FUKATA, S., KUMA, K., ... & AMINO, N. (2001). Blocking type anti-TSH receptor antibodies detected by radioreceptor assay in Graves' disease. Endocrine journal, 48(6), 703-710. [49] Kim, W. B., Chung, H. K., Park, Y. J., Park, D. J., Tahara, K., Kohn, L. D., & Cho, B. Y. (2000). The prevalence and clinical significance of blocking thyrotropin receptor antibodies in untreated hyperthyroid Graves' disease. Thyroid, 10(7), 579-586. [50] Roti, E., Braverman, L. E., & DeGroot, L. J. (1998). TSH Receptor Antibody Measurement in the Diagnosis and Management of Graves’ Disease Is Rarely Necessary b. The Journal of Clinical Endocrinology & Metabolism, 83(11), 3781-3784. [51] Laurberg, P., Nygaard, B., Andersen, S., Carlé, A., Karmisholt, J., Krejbjerg, A., ... & Andersen, S. L. (2014). Association between TSH-receptor autoimmunity, hyperthyroidism, goitre, and orbitopathy in 208 patients included in the remission induction and sustenance in Graves’ disease study. Journal of Thyroid Research, 2014. [52] Tun, N. N. Z., Beckett, G., Zammitt, N. N., Strachan, M. W., Seckl, J. R., & Gibb, F. W. (2016). Thyrotropin receptor antibody levels at diagnosis and after thionamide course predict Graves' disease relapse. Thyroid, 26(8), 1004-1009. [53] Balucan, F. S., Morshed, S. A., & Davies, T. F. (2013). Thyroid autoantibodies in pregnancy: their role, regulation and clinical relevance. Journal of thyroid research, 2013. [54] De Carvalho, G., Perez, C., & Ward, L. S. (2013). The clinical use of thyroid function tests. Arq Bras Endocrinol Metabol, 57, 193-204. [55] Xie, L. D., Gao, Y., Li, M. R., Lu, G. Z., & Guo, X. H. (2008). Distribution of immunoglobulin G subclasses of anti‐thyroid peroxidase antibody in sera from patients with Hashimoto's thyroiditis with different thyroid functional status. Clinical & Experimental Immunology, 154(2), 172-176. [56] Balucan, F. S., Morshed, S. A., & Davies, T. F. (2013). Thyroid autoantibodies in pregnancy: their role, regulation and clinical relevance. Journal of thyroid research, 2013. [57] Ruggeri, R. M., Vicchio, T. M., Cristani, M., Certo, R., Caccamo, D., Alibrandi, A., ... & Gangemi, S. (2016). Oxidative stress and advanced glycation end products in Hashimoto's thyroiditis. Thyroid, 26(4), 504-511. [58] Zaletel, K., & Gaberscek, S. (2011). Hashimoto's thyroiditis: from genes to the disease. Current genomics, 12(8), 576-588. [59] DeGroot, L. J. (2015). Graves’ disease and the manifestations of thyrotoxicosis. [60] Caturegli, P., Kuppers, R. C., Mariotti, S., BUREK, C. L., Pinchera, A., Ladenson, P. W., & Rose, N. R. (1994). IgG subclass distribution of thyroglobulin antibodies in patients with thyroid disease. Clinical & Experimental Immunology, 98(3), 464-469. [61] Balucan, F. S., Morshed, S. A., & Davies, T. F. (2013). Thyroid autoantibodies in pregnancy: their role, regulation and clinical relevance. Journal of thyroid research, 2013. [62] Caturegli, P., Kuppers, R. C., Mariotti, S., BUREK, C. L., Pinchera, A., Ladenson, P. W., & Rose, N. R. (1994). IgG subclass distribution of thyroglobulin antibodies in patients with thyroid disease. Clinical & Experimental Immunology, 98(3), 464-469. [63] Marcocci, C., & Marino, M. (2005). Thyroid directed antibodies. [64] Ueno, A., Jijon, H., Traves, S., Chan, R., Ford, K., Beck, P. L., ... & Ghosh, S. (2014). Opposing effects of smoking in ulcerative colitis and Crohn's disease may be explained by differential effects on dendritic cells. Inflammatory bowel diseases, 20(5), 800-810. [65] Swain, M., Swain, T., & Mohanty, B. K. (2005). Autoimmune thyroid disorders—an update. Indian Journal of Clinical Biochemistry, 20(1), 9. [66] Carlé, A., Bülow Pedersen, I., Knudsen, N., Perrild, H., Ovesen, L., Rasmussen, L. B., ... & Laurberg, P. (2013). Graves′ hyperthyroidism and moderate alcohol consumption: evidence for disease prevention. Clinical Endocrinology, 79(1), 111-119. [67] Carlé, A., Pedersen, I. B., Knudsen, N., Perrild, H., Ovesen, L., Rasmussen, L. B., ... & Laurberg, P. (2012). Moderate alcohol consumption may protect against overt autoimmune hypothyroidism: a population-based case–control study. European journal of endocrinology, 167(4), 483-490. [68] Romeo, J., Wärnberg, J., Nova, E., Díaz, L. E., Gómez-Martinez, S., & Marcos, A. (2007). Moderate alcohol consumption and the immune system: a review. British Journal of Nutrition, 98(S1), S111-S115. [69] Desailloud, R., & Hober, D. (2009). Viruses and thyroiditis: an update. Virology journal, 6(1), 1-14. [70] de Luis, D. A., Varela, C., de La Calle, H., Cantón, R., de Argila, C. M., San Roman, A. L., & Boixeda, D. (1998). Helicobacter pylori infection is markedly increased in patients with autoimmune atrophic thyroiditis. Journal of clinical gastroenterology, 26(4), 259-263. [71] Hoekman, K., Wagstaff, J., Pinedo, H. M., von Blomberg-van der Flier, B. M. E., & Drexhage, H. A. (1991). Reversible thyroid dysfunction during treatment with GM-CSF. The Lancet, 338(8766), 541-542. [72] Bahn, A. K., Mills, J. L., Snyder, P. J., Gann, P. H., Houten, L., Bialik, O., ... & Utiger, R. D. (1980). Hypothyroidism in workers exposed to polybrominated biphenyls. New England Journal of Medicine, 302(1), 31-33. [73] Kibirige, D., Luzinda, K., & Ssekitoleko, R. (2013). Spectrum of lithium induced thyroid abnormalities: a current perspective. Thyroid research, 6(1), 1-5. [74] Lazarus, J. H. (1998). The effects of lithium therapy on thyroid and thyrotropin-releasing hormone. Thyroid, 8(10), 909-913. [75] Hancock, S. L., Cox, R. S., & McDougall, I. R. (1991). Thyroid diseases after treatment of Hodgkin's disease. New England Journal of Medicine, 325(9), 599-605. [76] Carroll, R., & Matfin, G. (2010). Endocrine and metabolic emergencies: thyroid storm. Therapeutic advances in endocrinology and metabolism, 1(3), 139-145. [77] Žarković, M. (2012). The role of oxidative stress on the pathogenesis of Graves' disease. Journal of thyroid research, 2012. [78] Effraimidis, G., & Wiersinga, W. M. (2014). Autoimmune thyroid disease: old and new players. Eur J Endocrinol, 170(6), R241-R252. [79] Zaletel, K., & Gaberscek, S. (2011). Hashimoto's thyroiditis: from genes to the disease. Current genomics, 12(8), 576-588. [80] Winkler, R. (2015). Iodine—a potential antioxidant and the role of Iodine/Iodide in health and disease. Natural Science, 7(12), 548. [81] Hansen, P. S., Brix, T. H., Iachine, I., Kyvik, K. O., & Hegedüs, L. (2006). The relative importance of genetic and environmental effects for the early stages of thyroid autoimmunity: a study of healthy Danish twins. European journal of endocrinology, 154(1), 29-38. [82] Brix, T. H., Kyvik, K. O., & Hegedüs, L. (2000). A population-based study of chronic autoimmune hypothyroidism in Danish twins. The Journal of Clinical Endocrinology & Metabolism, 85(2), 536-539.


bottom of page