Hypothyroidism: An integrative approach

Hypothyroidism is a condition in which the thyroid gland is unable to produce sufficient thyroid hormone, thyroxine (T4) and triiodothyronine (T3), to fulfill the body’s metabolic demands. According to the National Health and Nutrition Examination Survey, hypothyroidism affects approximately one in every 300 individuals in the United States. Additionally, almost 13 million Americans are suspected to have undiagnosed hypothyroidism. (25)

Hypothyroidism is often described as primary or secondary. Primary hypothyroidism, the most common form, is caused by a dysfunction of the thyroid gland. Hashimoto’s thyroiditis, an autoimmune condition, is the most common cause of primary hypothyroidism. Secondary hypothyroidism is caused by pathogenic mechanisms involving the hypothalamus and/or pituitary gland. (52) Secondary hypothyroidism accounts for only about five percent of cases. (25)

Primary hypothyroidism may also be “overt” or “subclinical”. (52) The typical thyroid marker presentation for overt, subclinical, and secondary hypothyroidism are provided further in this article.

Hypothyroidism is a condition in which the thyroid gland is unable to produce sufficient thyroid hormone.

Clinical manifestations: Signs, symptoms, and complications

As thyroid hormones play a key role in regulating numerous physiological processes, clinical manifestations are often broad and non-specific. Signs and symptoms may also vary depending on the gender and age of an individual. (25)

Signs and symptoms

The most common symptoms of hypothyroidism are cold intolerance and fatigue. Other possible signs and symptoms of hypothyroidism include:

  • Alopecia (hair thinning, hair loss) and lateral eyebrow thinning 
  • Abnormal laboratory values 
  • Arthralgias (joint pain) 
  • Bradycardia (slow heart rate) 
  • Coarse facies (coarse facial features) (25)
  • Carotenodermia (45)
  • Constipation 
  • Delayed Achilles reflex 
  • Depression 
  • Diastolic hypertension 
  • Dry skin 
  • Edema, periorbital edema 
  • Elevated creatine kinase (CK) levels 
  • Elevated C-reactive protein (CRP) levels 
  • Elevated low-density lipoprotein (LDL) cholesterol 
  • Elevated triglycerides (25)
  • Follicular hyperkeratosis (35)
  • Goiter 
  • Hypothermia 
  • Hyperprolactinemia (elevated prolactin)
  • Hyponatremia (low sodium) (25)
  • Low basal body temperature (38)
  • Low-voltage electrocardiography 
  • Macroglossia (unusually large tongue) 
  • Memory impairment  
  • Menorrhagia (menstrual irregularities) 
  • Myalgias (muscle pain) 
  • Normocytic anemia 
  • Pericardial effusion (accumulation of fluid in the pericardial cavity) 
  • Pleural effusion (excess fluid between pleura around the lungs) 
  • Poor concentration 
  • Proteinuria (elevated protein in urine) 
  • Weakness 
  • Weight gain (25)


Untreated hypothyroidism can result in a number of consequences, including:

  • Cognitive impairment
  • Dyslipidemia
  • Hypertension
  • Infertility
  • Myxedema coma (rare, medical emergency)
  • Neuromuscular dysfunction (25)

Other considerations

Some patients with other conditions (outlined below) may present with symptoms of hypothyroidism but normal TSH levels.

  • Adrenal insufficiency (rare)
  • Anemia
  • Chronic kidney disease
  • Liver disease
  • Mental disorders (e.g., depression, anxiety disorder, and/or somatoform disorders)
  • Nutrient deficiencies (e.g., B12, iron, vitamin D)
  • Obstructive sleep apnea
  • Viral infection (e.g., HIV/AIDS, Lyme disease, mononucleosis) (25)
Low basal body temperature is among the possible signs of hypothyroidism.

Causes and contributing factors

Primary thyroid gland failure or dysfunction may be attributed autoimmune destruction (e.g., Hashimoto’s thyroiditis), congenital abnormalities, iodine deficiency, infiltrative cardiomyopathies, and a number of iatrogenic causes, such as thyroid surgery, radioiodine therapy, and neck irradiation. 

Hypothyroidism may also be the result of inadequate stimulation of the thyroid gland by the hypothalamus and/or pituitary gland (secondary hypothyroidism). In these cases, symptoms of hypothalamic-pituitary insufficiency would also be present. 

Transient hypothyroidism is characterized by a temporary deficiency in thyroid hormone. This form of hypothyroidism is associated with a number of disorders, including:

  • Postpartum thyroiditis
  • Subacute thyroiditis (acute inflammatory thyroid condition, likely caused by a virus)
  • Silent thyroiditis
  • Thyroiditis associated with TSH receptor-blocking antibodies (25)

Risk factors 

Risk factors for hypothyroidism include:

  • Age: higher risk with increasing age, particularly after age 60 (49)(54
  • Gender: more common in females than males (49)(54
  • Pre-existing thyroid-related condition (e.g., goiter)
  • Certain medical procedures (e.g., thyroid surgery, radioiodine therapy, and irradiation)
  • Genetic predisposition, family history
  • Pregnancy within last six months
  • Other medical conditions (e.g., Turner syndrome, Sjögren’s syndrome, pernicious anemia, rheumatoid arthritis, type 1 diabetes, lupus) (49)
  • Viral infections: may be associated with autoimmune thyroiditis (e.g., hepatitis C) (11)(31)(63)(64)

The following tables further outline environmental toxins, dietary factors, and medications that may negatively impact thyroid function. 

Environmental toxins 

The following table outlines a number of toxins, their effects on thyroid function, and environmental sources. 

A number of environmental toxins may negatively impact thyroid function.


The following table outlines a number of pharmaceutical medications and their effects on thyroid function.

Several pharmaceutical medications have been associated with thyroid dysfunction.

Dietary factors 

The following table outlines several foods and compounds that may contribute to hypothyroidism, their effects on thyroid function, and common dietary sources.

Certain dietary factors, such as gluten and iodine, may contribute to thyroid dysfunction.

Developing a diagnosis: Thyroid markers and functional tests

The standard for diagnosing hypothyroidism is a serum thyroid-stimulating hormone (TSH) test and a serum free thyroxine (T4) test if TSH is elevated. (25) Measuring thyroid markers, tracking basal body temperature, and conducting an Achilles reflex test may assist in developing a diagnosis.

Thyroid markers 

The table above outlines the typical ranges for various thyroid markers. (62)(66)

Typical marker presentation

The table above outlines the typical marker presentation for overt primary, secondary, and subclinical forms of hypothyroidism. (25)(53)

Functional tests

Basal Body Temperature (BBT) test

Thyroid hormones play an important role in the regulation of energy homeostasis, metabolism, and thermogenesis, a process by which heat is produced in the body. (33) Hypothyroidism has been associated with reductions in oxygen consumption, nutrient oxidation, metabolic rate, heart rate, and body temperature. (57)

Tracking BBT over time may provide an indication of thyroid function. Based on patient preferences, BBT may be recorded using a phone app or a printable chart. 

Download a BBT chart.

Achilles reflex test

The Achilles reflex test can assist in the diagnosis of hypothyroidism. An absent or decreased Achilles reflex provides evidence of a dysfunction of the deep tendon reflex of the S1 nerve, and may indicate the presence of certain conditions, such as hypothyroidism.  

In order to perform the test, a reflex (neurological) hammer is needed. The following steps outline the standard technique and most commonly used method to conduct a reflex test:

1. Ask the patient to lie supine on the examination table, with knee flexed, hip rotated externally, and the Achilles tendon area exposed and relaxed. 

2. With one hand, hold the hammer firmly by the handle. Typically, the dominant thumb and forefinger should be holding most of the weight. With the other hand, hold the patient’s foot, slightly dorsiflexed from the plantar aspect. 

3. Using the flat part of the top of the hammer, strike the Achilles tendon. Contraction of the calf muscle and plantarflexion of the foot indicates a positive result. (23)

The solution: Diet, lifestyle, and supplementation

Conventionally, the treatment approach to hypothyroidism aims to alleviate symptoms with lifelong administration of synthetic thyroid hormone (e.g., levothyroxine). (25) An integrative approach, however, may include evidence-based dietary and lifestyle interventions, supplementation, and detoxification support. 

General diet and lifestyle guidelines for patients

The following are general diet and lifestyle guidelines that may help your patients support thyroid function.

1. Patients should follow a diet of whole, minimally-processed foods. Consider recommending an autoimmune protocol diet, particularly in cases of autoimmune dysfunction such as Hashimoto’s thyroiditis. (2) Considering many individuals with celiac disease also present with thyroid dysfunction, a gluten-free diet may be an effective intervention in these cases. (59)

2. Patients should avoid or reduce consumption of dietary factors that negatively affect thyroid function. Refer to the Dietary factors table above for further information.

3. Patients should consume adequate amounts of thyroid-supportive nutrients from dietary sources and supplement their diets when necessary to prevent or address deficiency. The table below outlines thyroid-supportive nutrients, their functions, and examples of dietary sources. 

Intake of certain nutrients may support thyroid function and prevent the development of hypothyroidism.

*Caution: Excess iodine may also result in decreased thyroid hormones. (41)

4. Engaging in regular physical activity has been shown to improve thyroid hormone levels (e.g., decreased TSH, increased T4 and T3). (8) The physical activity guidelines developed by the U.S. Department of Health and Human Services provide general recommendations for activity type, frequency, and duration by population. It’s important to note that certain factors, such as health status and life events (e.g., pregnancy), may impact individual recommendations.

5. Increases in cortisol levels as a result of stress have been shown to affect thyroid hormone levels. More specifically, there appears to be a positive correlation between TSH and cortisol. (67)The diagram below depicts the pathways between the hypothalamus, pituitary gland, adrenal glands, and thyroid gland. 

The diagram above depicts the hypothalamus-pituitary-adrenal-thyroid axis.

Help your patients recognize signs of stress (e.g., low energy, changes in mood, difficulty sleeping) and incorporate stress-reduction techniques into their daily routines, such as:

  • Mindfulness practices (e.g., meditation, yoga, tai chi)
  • Regular moderate exercise (e.g., 30 minutes of walking)
  • Realistic goal-setting to reduce overwhelm
  • Social support from family, friends, colleagues, and community or religious associations (50)

Top ingredients for autoimmune thyroid support

Research examining the use of selenium, vitamin D, and Cordyceps sinensis have noted beneficial effects on thyroid autoimmunity and function. 


The thyroid organ contains a high concentration of selenium and selenoproteins involved in the metabolism of thyroid hormone. (55) Studies suggest that selenium supplementation may improve thyroid function, particularly in cases of autoimmune (or Hashimoto’s) thyroiditis. 

A randomized-controlled, double-blind study examined the effects of selenium supplementation on levels of serum thyroid peroxidase antibodies (TPOAb) in patients with chronic autoimmune thyroiditis. Patients received 200 μg per day of selenomethionine or a placebo. While patients in the placebo group did not demonstrate any changes in serum TPOAb levels, TPOAb decreased by 5% after three months and by 20% after six months in those receiving supplemental selenomethionine. (20) In another randomized-controlled, prospective study, 196 patients with autoimmune thyroiditis and subclinical hypothyroidism (TSH levels less than (10 mU/L) received selenomethionine supplementation or a placebo. Of the 192 patients who completed the study, thyroid function improved in only three out of 96 patients in the placebo group. Comparatively, the number of responders in the treatment group was ten times greater than those in the placebo group. Approximately one third of patients receiving selenomethionine (30/96) demonstrated restoration of normal thyroid function. (55)

Furthermore, a systematic review and meta-analysis reviewed the evidence from scientific trials comparing the administration of selenium in autoimmune thyroiditis patients with or without levothyroxine treatment. Serum TPOAb levels were reduced in both untreated and levothyroxine-treated patients. However, the authors also noted that it was not determined whether or not these results were clinically relevant. (69)

Preliminary research demonstrates that Cordyceps sinensis may provide immunomodulatory effects in patients with autoimmune thyroid conditions.

Vitamin D

Research has demonstrated an association between autoimmune thyroid disease and low levels of vitamin D, suggesting that vitamin D deficiency may be involved in the pathogenesis of this condition. (46)(68) As a result, a number of studies have examined whether vitamin D supplementation is effective in the treatment of Hashimoto’s thyroiditis. In one trial, 186 vitamin D deficient patients with Hashimoto’s thyroiditis were given 1200-4000 IU of oral vitamin D3 per day for four months. Patients experienced a significant reduction (20.3%) in serum TPOAb levels. (46) Similarly, when compared to a placebo, vitamin D supplementation decreased concentrations of thyroid antibodies in Hashimoto’s disease patients with normal vitamin D status who were being treated with levothyroxine. (39)

When used concomitantly, administration of vitamin D and statins may provide superior clinical outcomes when hypercholesterolemia coexists with Hashimoto’s thyroiditis. In one trial, the effects of vitamin D supplementation (2000 IU per day), simvastatin treatment (40 mg per day), and a combination of both were compared in women with Hashimoto’s thyroiditis and low vitamin D status. Results found that simvastatin alone had no effect on thyroid antibodies, vitamin D reduced TPOAb and thyroglobulin antibodies (TgAb), and the combination of simvastatin and vitamin D resulted in the greatest reduction of TPOAb and TgAb. (40)

Cordyceps sinensis

Preliminary research demonstrates that Cordyceps sinensis may provide immunomodulatory effects in patients with autoimmune thyroid conditions, namely Hashimoto’s disease and Grave’s disease. One study examined the effects of Corbrin Capsule, a medication derived from C. sinensis, in 56 patients with Hashimoto’s disease and 44 patients with Grave’s disease. Patients were randomly assigned to receive 2 g of Corbrin Capsule three times per day with their medication (methimazole or levothyroxine), or a placebo (medication only). Following Corbrin Capsule administration, individuals with both autoimmune thyroid disorders demonstrated a significant decrease in serum TPOAb levels. Corbrin Capsule also appeared to restore helper T and cytotoxic T cell balance, indicating an immunomodulatory effect. (28)

For more information on dosing and administration, see Fullscript’s Thyroid Health protocol. 

Key nutrients to support detoxification

Thyroid conditions are often associated with liver test abnormalities and dysfunction, and vice versa. (30) The liver is an integral component of our body’s detoxification system, and dysfunction may impair its ability to effectively remove potentially harmful toxins, including those associated with hypothyroidism. For example, environmental chemicals may affect thyroid hormone levels by decreasing the function of sulfotransferases, a family of enzymes involved in detoxification. (29)

The following graphic provides an overview of key nutrients that support liver function and the detoxification process.

The diagram above depicts the body's liver detoxification pathways and supportive nutrients.

The bottom line

Integrative modalities have been shown to be beneficial in the treatment of hypothyroidism, including cases of autoimmune or Hashimoto’s thyroiditis. An integrative approach to treatment may include certain dietary interventions, regular exercise, stress-reduction techniques, and supplementation of key nutrients or botanicals to support thyroid function and liver detoxification processes. 

  1. Abbott, R. D., Sadowski, A., & Alt, A. G. (2019). Efficacy of the autoimmune protocol diet as part of a multi-disciplinary, supported lifestyle intervention for Hashimoto’s thyroiditis. Cureus, 11(4), e4556.
  2. Agency for Toxic Substances & Disease Registry. (1999). ToxFAQsTM for Mercury. Retrieved from https://www.atsdr.cdc.gov/toxfaqs/TF.asp?id=113&tid=24#
  3. Agency for Toxic Substances & Disease Registry. (2003). Public health statement for fluorides, hydrogen fluoride, and fluorine. Retrieved from https://www.atsdr.cdc.gov/phs/phs.asp?id=210&tid=38
  4. Agency for Toxic Substances & Disease Registry. (2008). Public health statement for perchlorates. Retrieved from https://www.atsdr.cdc.gov/phs/phs.asp?id=892&tid=181
  5. Agency for Toxic Substances & Disease Registry. (2010). Public health statement for chlorine. Retrieved from https://www.atsdr.cdc.gov/phs/phs.asp?id=683&tid=36
  6. Aghini Lombardi, F., Fiore, E., Tonacchera, M., Antonangeli, L., Rago, T., Frigeri, M., … Vitti, P. (2013). The effect of voluntary iodine prophylaxis in a small rural community: The pescopagano survey 15 years later. The Journal of Clinical Endocrinology & Metabolism, 98(3), 1031–1039,
  7. Bajaj, J. K., Salwan, P., & Salwan, S. (2016). Various possible toxicants involved in thyroid dysfunction: A review. Journal of Clinical and Diagnostic Research, 10(1), FE01–FE3. 
  8. Bansal, A., Kaushik, A., Singh, C.M., Sharma, V., & Singh, H. (2015). The effect of regular physical exercise on the thyroid function of treated hypothyroid patients: An interventional study at a tertiary care center in Bastar region of India. Archives of Medicine & Health Sciences, 3(2), 244-246. 
  9. Bercz, J. P., Jones, L. L., Harrington, R. M., Bawa, R., & Condie, L. (1986). Mechanistic aspects of ingested chlorine dioxide on thyroid function: Impact of oxidants on iodide metabolism. Environmental Health Perspectives, 69, 249–254. 
  10. Betsy, A., Binitha, M., & Sarita, S. (2013). Zinc deficiency associated with hypothyroidism: An overlooked cause of severe alopecia. International Journal of Trichology, 5(1), 40–42. 
  11. Blackard, J. T., Kong, L., Huber, A. K., & Tomer, Y. (2013). Hepatitis C virus infection of a thyroid cell line: Implications for pathogenesis of hepatitis C virus and thyroiditis. Thyroid: Official Journal of the American Thyroid Association, 23(7), 863–870. 
  12. Bolarinwa, I.F., Oke, M.O., Olaniyan, S.A., & Ajala, A.S. (2016). A review of cyanogenic glycosides in edible plants. In M. Larramendy, & S. Soloneski (Eds.), Toxicology: New aspects to this scientific conundrum. IntechOpen. 
  13. Brent G. A. (2010). Environmental exposures and autoimmune thyroid disease. Thyroid: Official Journal of the American Thyroid Association, 20(7), 755–761. 
  14. Bülow Pedersen, I., Laurberg, P., Knudsen, N., Jørgensen, T., Perrild, H., Ovesen, L., & Banke Rasmussen, L. (2007). An increased incidence of overt hypothyroidism after iodine fortification of salt in Denmark: A prospective population study. The Journal of Clinical Endocrinology & Metabolism, 92(8), 3122–3127. 
  15. Centers for Disease Control and Prevention. (2015). Thimerosal in flu vaccine. Retrieved from https://www.cdc.gov/flu/prevent/thimerosal.htm
  16. Chandra, A.K. (2010). Goitrogen in food: Cyanogenic and flavonoids containing plant foods in the development of goiter. In R.R. Watson, & V.R. Preedy (Eds.), Bioactive foods in promoting health: Fruits and vegetables. Academic Press. 
  17. Ch’ng, C. L., Jones, M. K., & Kingham, J. G. (2007). Celiac disease and autoimmune thyroid disease. Clinical Medicine & Research, 5(3), 184–192.
  18. Coperchini, F., Awwad, O., Rotondi, M., Santini, F., Imbriani, M., & Chiovato, L. (2017). Thyroid disruption by perfluorooctane sulfonate (PFOS) and perfluorooctanoate (PFOA). Journal of Endocrinological Investigation, 40(2), 105-121.
  19. Curtis, S.W., Terrell, M.L., Jacobson, M.H., Cobb, D.O., Jiang, V.S., Neblett, M.F., … Marcus, M. (2019). Thyroid hormone levels associate with exposure to polychlorinated biphenyls and polybrominated biphenyls in adults exposed as children. Environmental Health, 18(75). 
  20. de Farias, C.R., Cardoso, B.R., de Oliveira, G.M., de Mello Guazzelli, I.C., Catarino, R.M., Chammas, M.C., … Knobel, M. (2015). A randomized-controlled, double-blind study of the impact of selenium supplementation on thyroid autoimmunity and inflammation with focus on the GPx1 genotypes. Journal of Endocrinological Investigation, 38(10), 1065-1074. 
  21. Divi, R. L., & Doerge, D. R. (1996). Inhibition of thyroid peroxidase by dietary flavonoids. Chemical Research in Toxicology, 9(1), 16–23.
  22. Doerge, D. R., & Sheehan, D. M. (2002). Goitrogenic and estrogenic activity of soy isoflavones. Environmental Health Perspectives, 110 Suppl 3(Suppl 3), 349–353. 
  23. Figliuzzi, A., & Al-Dhahir, M. A. (2018). Achilles reflex. StatPearls [Internet]. Treasure Island, FL: StatPearls Publishing. 
  24. Gaitan, E., Lindsay, R.H., Reichert, R.D., Ingbar, S.H., Cooksey, R.C., Legan, J., … Kubota, K. (1989). Antithyroid and goitrogenic effects of millet: Role of C-glycosylflavones. The Journal of Clinical Endocrinology and Metabolism, 68(4), 707-714.
  25. Gaitonde, D.Y., Rowley, K.D., Sweeney, L.B., & Eisenhower, D.D. (2012). Hypothyroidism: An update. American Family Physician, 86(3), 244-251. International Journal of Dermatology, 42(3), 178-181.
  26. Ghassabian, A., & Trasande, L. (2018). Disruption in thyroid signaling pathway: A mechanism for the effect of endocrine-disrupting chemicals on child neurodevelopment. Frontiers in Endocrinology. 
  27. Gonçalves, C., de Freitas, M. L., & Ferreira, A. (2017). Flavonoids, thyroid iodide uptake and thyroid cancer-A review. International Journal of Molecular Sciences, 18(6), 1247. 
  28. He, T., Zhao, R., Lu, Y., Li, W., Hou, X., Sun, Y., … Chen, L. (2016). Dual-directional immunomodulatory effects of corbrin capsule on autoimmune thyroid diseases. Evidence-Based Complementary and Alternative Medicine, 2016, 1360386. 
  29. Hodges, R. E., & Minich, D. M. (2015). Modulation of metabolic detoxification pathways using foods and food-derived components: A scientific review with clinical application. Journal of Nutrition and Metabolism, 2015, 760689. 
  30. Huang, M.J., & Liaw, Y.F. (1995). Clinical associations between thyroid and liver diseases. Canadian Journal of Gastroenterology and Hepatology, 10(3), 344-350.
  31. Indolfi, G., Stagi, S., Bartolini, E., Salti, R., De Martino, M., Azzari, C., & Resti, M. (2008). Thyroid function and anti‐thyroid autoantibodies in untreated children with vertically acquired chronic hepatitis C virus infection. Clinical Endocrinology, 68(1), 117-121.
  32. Iwen, K. A., Oelkrug, R., & Brabant, G. (2018). Effects of thyroid hormones on thermogenesis and energy partitioning. Journal of Molecular Endocrinology, 60(3).
  33. Jabbar, A., Yawar, A., Waseem, S., Islam, N., Ul Haque, N., Zuberi, L., … Akhter, J. (2008). Vitamin B12 deficiency common in primary hypothyroidism. Journal of Pakistan Medical Association, 58(5). 258-261.
  34. Jacobson, M. H., Darrow, L. A., Barr, D. B., Howards, P. P., Lyles, R. H., Terrell, M. L., … Marcus, M. (2017). Serum polybrominated biphenyls (PBBs) and polychlorinated biphenyls (PCBs) and thyroid function among Michigan adults several decades after the 1973-1974 PBB contamination of livestock feed. Environmental Health Perspectives, 125(9), 097020. 
  35. Kasumagic-Halilovic, E., & Begovic. B. (2012). Thyroid autoimmunity in patients with skin disorders. In N.K. Agrawal (Ed.), Thyroid hormone. IntechOpen. 
  36. Kheradpisheh, Z., Mirzaei, M., Mahvi, A. H., Mokhtari, M., Azizi, R., Fallahzadeh, H., & Ehrampoush, M. H. (2018). Impact of drinking water fluoride on human thyroid hormones: A case-control study. Scientific Reports, 8(1), 2674. 
  37. Kim D. (2017). The Role of Vitamin D in Thyroid Diseases. International Journal of Molecular Sciences, 18(9), 1949. 
  38. Kostoglou-Athanassiou, I., & Ntalles, K. (2010). Hypothyroidism: New aspects of an old disease. Hippokratia, 14(2), 82–87.
  39. Krysiak, R., Szkróbka, W., & Okopień, B. (2017). The effect of vitamin D on thyroid autoimmunity in levothyroxine-treated women with hashimoto’s thyroiditis and normal vitamin D status. Experimental and Clinical Endocrinology & Diabetes, 125(4), 229-233. 
  40. Krysiak, R., Szkróbka, W., & Okopień, B. (2018). Moderate-dose simvastatin therapy potentiates the effect of vitamin D on thyroid autoimmunity in levothyroxine-treated women with Hashimoto’s thyroiditis and vitamin D insufficiency. Pharmacological Reports, 70(1), 93-97. 
  41. Leung, A. M., & Braverman, L. E. (2014). Consequences of excess iodine. Nature Reviews Endocrinology, 10(3), 136–142.
  42. Li, S., Gao, X., Wei, Y., Zhu, G., & Yang, C. (2016). The relationship between iron deficiency and thyroid function in Chinese women during early pregnancy. Journal of Nutritional Science and Vitaminology, 62(6), 397–401.
  43. Liontiris, M.I., & Mazokopakis, E.E. (2017). A concise review of Hashimoto thyroiditis (HT) and the importance of iodine, selenium, vitamin D and gluten on the autoimmunity and dietary management of HT patients: Points that need more investigation. Hellenic Journal of Nuclear Medicine, 20(1), 51-56. 
  44. Mackawy, A. M., Al-Ayed, B. M., & Al-Rashidi, B. M. (2013). Vitamin D deficiency and its association with thyroid disease. International Journal of Health Sciences, 7(3), 267–275. 
  45. Maharshak, N., & Shapiro, J., & Trau, H. (2003). Carotenoderma: A review of the current literature. International Journal of Dermatology, 42(3), 178-181.
  46. Mazokopakis, E.E., Papadomanolaki, M.G., Tsekouras, K.C., Evangelopoulos, A.D., Kotsiris, D.A., & Tzortzinis, A.A. (2015). Is vitamin D related to pathogenesis and treatment of Hashimoto’s thyroiditis? Hellenic Journal of Nuclear Medicine, 18(3), 222-227.
  47. Moncayo, R., Kroiss, A., Oberwinkler, M., Karakolcu, F., Starzinger, M., Kapelari, K., … Moncayo, H. (2008). 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 Endocrine Disorders, 8, 2.
  48. Mughal, B. B., Fini, J. B., & Demeneix, B. A. (2018). Thyroid-disrupting chemicals and brain development: An update. Endocrine Connections, 7(4), R160–R186.
  49. National Institute of Diabetes and Digestive and Kidney Diseases. (2016). Hypothyroidism (underactive thyroid). Retrieved from https://www.niddk.nih.gov/health-information/endocrine-diseases/hypothyroidism#who
  50. National Institute of Mental Health. (n.d.). 5 things you should know about stress. Retrieved from https://www.nimh.nih.gov/health/publications/stress/index.shtml
  51. Nishida, M., Muraoka, K., Nishikawa, K., Takagi, T., & Kawada, J. (1989). Differential effects of methylmercuric chloride and mercuric chloride on the histochemistry of rat thyroid peroxidase and the thyroid peroxidase activity of isolated pig thyroid cells. Journal of Histochemistry and Cytochemistry, 37(5), 723-727.
  52. Nygaard, B. (2014). Hypothyroidism (primary). BMJ Clinical Evidence, 2014, 0605.
  53. Paoletti, J. (2008). Differentiation and treatment of hypothyroidism, functional hypothyroidism, and functional metabolism. International Journal of Pharmaceutical Compounding, 12(6), 488–497.
  54. Patil, N., Rehman, A., & Jialal, I. (2019). Hypothyroidism. StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing. 
  55. Pirola, I., Gandossi, E., Agosti, B., Delbarba, A., & Cappelli, C. (2016). Selenium supplementation could restore euthyroidism in subclinical hypothyroid patients with autoimmune thyroiditis. Endokrynologia Polska, 67(6), 567-571.
  56. Rothstein, A., Auran, J.D., & Flynn, J.T. (2003). Mercury in ophthalmic medications. Investigative Ophthalmology & Visual Science, 44, 4452. 
  57. Ruiz-Núñez, B., Tarasse, R., Vogelaar, E. F., Dijck-Brouwer, D. A. J., & Muskiet, F. A. J. (2018). Higher prevalence of “low T3 syndrome” in patients with chronic fatigue syndrome: A case–control study. Frontiers in Endocrinology, 9.
  58. Sarne, D. (2016). Effects of the environment, chemicals and drugs on thyroid Function. In K.R. Feingold, B. Anawalt, A. Boyce, et al. (Eds.). Endotext [Internet]. South Dartmouth (MA): MDText.com.
  59. Sategna-Guidetti, C., Volta, U., Ciacci, C., Usai, P., Carlino, A., De Franceschi, L., … Brossa, C. (2001). Prevalence of thyroid disorders in untreated adult celiac disease patients and effect of gluten withdrawal: An Italian multicenter study. American Journal of Gastroenterology, 96(3), 751-757.
  60. Søkilde Pedersen, I., Knudsen, N., Carlé, A., Vejbjerg, P., Jørgensen, T., Perrild, H., … Laurberg, P. (2011). A cautious iodization programme bringing iodine intake to a low recommended level is associated with an increase in the prevalence of thyroid autoantibodies in the population. Clinical Endocrinology.
  61. Soldin, O. P., O’Mara, D. M., & Aschner, M. (2008). Thyroid hormones and methylmercury toxicity. Biological Trace Element Research, 126(1-3), 1–12. 
  62. Spencer, C. A. (2017). Assay of thyroid hormones and related substances. In Endotext [Internet]. South Dartmouth, MA: MDText.com, Inc. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK279113/ 
  63. Tomer, Y. (2010). Interferon induced thyroiditis. Journal of Autoimmunity, 34(3), J322-J326. 
  64. Tomer, Y., & Menconi, F. (2009). Interferon induced thyroiditis. Best practice & research. Clinical Endocrinology & Metabolism, 23(6), 703–712. 
  65. Torino, F., Maria Corsello, S., Longo, R., Barnabei, A., & Gasparini, G. (2009). Hypothyroidism related to tyrosine kinase inhibitors: An emerging toxic effect of targeted therapy. Nature Reviews Clinical Oncology, 6(4), 219-228. 
  66. UpToDate. (2019). Laboratory test normal reference ranges in adults. Retrieved from https://www.uptodate.com/contents/laboratory-test-normal-reference-ranges-in-adults
  67. Walter, K. N., Corwin, E. J., Ulbrecht, J., Demers, L. M., Bennett, J. M., Whetzel, C. A., & Klein, L. C. (2012). Elevated thyroid stimulating hormone is associated with elevated cortisol in healthy young men and women. Thyroid Research, 5(1), 13. 
  68. Wang, J., Lv, S., Chen, G., Gao, C., He, J., Zhong, H., & Xu, Y. (2015). Meta-analysis of the association between vitamin D and autoimmune thyroid disease. Nutrients, 7(4), 2485–2498.
  69. Wichman, J., Winther, K.H., Bonnema, S.J., & Hegedüs, L. (2016). Selenium supplementation significantly reduces thyroid autoantibody levels in patients with chronic autoimmune thyroiditis: A systematic review and meta-analysis. Thyroid, 6(12), 1681-1692.
  70. Zimmermann, M.B., Wegmüller, R., Zeder, C., Chaouki, N., & Torresani, T. (2004). The effects of vitamin A deficiency and vitamin A supplementation on thyroid function in goitrous children. The Journal of Clinical Endocrinology and Metabolism, 89(11), 5441-5447.
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