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Kaniksha Desai, MD, FACE
Stanford University
Palo Alto, CA

August 24, 2021

Thyroid hormone replacement is a critical element in the overall management of patients with thyroid cancer. For a long period of time, aggressive TSH suppression with long-term high doses of thyroid hormone was advocated for all thyroid cancer patients to prevent cancer recurrence by reducing the stimulation of cancer cells. Recently, a growing body of evidence has suggested a limited benefit to aggressive TSH suppression in many patients. In addition, there appears to be significant risks of long-term TSH suppression to cardiovascular health, bone health, and mental health including the development of osteoporosis, atrial fibrillation, and mood disorders, which can significantly impact Quality of Life in thyroid cancer patients. Benefits of preventing cancer recurrence should be balanced with risks of excessive thyroid hormone replacement. Therefore, thyroid hormone replacement should be tailored to provide appropriate levels of TSH suppression based on a dynamic risk stratification in thyroid cancer patients.

Currently best practice for the management of thyroid cancer patients determines individualized thyroid hormone replacement therapy based on risk stratification of cancer recurrence following initial surgery and the patient’s response to subsequent treatment.

After initial surgery, patients are risk-stratified based upon their surgical pathology and extent of tumor metastasis. They are categorized into three groups for their risk of recurrence: low (<5%), intermediate (5-30%) and high (30-50+%). Thyroid hormone replacement is initiated with TSH goals based upon this risk stratification. Low risk patients that have had their cancer completely resected, including lobectomy patients, are given replacement doses to make them euthyroid with a TSH goal of 0.5 to 2.0 mu/L. Intermediate risk patients, often with lymph node involvement, have mild suppression of their TSH with thyroid hormone replacement dosed to a TSH goal of 0.1 to 0.5 mu/L. High risk patients including those who have extensive metastatic disease or incomplete resection are given higher doses of thyroid hormone with a TSH goal of <0.1 mu/L to prevent cancer recurrence.

At subsequent follow up visits, patients are evaluated for their response to overall cancer treatment and are categorized into four groups: 1) excellent response to treatment (no evidence of cancer recurrence), 2) biochemical incomplete response (elevations in thyroglobulin tumor marker levels), 3) structural incomplete response (local or metastatic disease present) or 4) indeterminate response (nonspecific imaging findings or slight elevations in tumor marker levels). Patients with high risk of recurrence, as well as those with structural incomplete response benefit the most from aggressive TSH suppression and are treated accordingly. In patients with excellent response to treatment with no evidence of disease, thyroid hormone treatment can be decreased, even in initially high-risk patients after 5 years. If a patient has a recurrence, then a higher dose of thyroid hormone treatment may be recommended in the future.

In summary, thyroid hormone replacement should be tailored to patients individually based on their initial risk for thyroid cancer recurrence as well as their response to treatment over time to avoid under treatment of high-risk patients and overtreatment of low risk patients. Risk of thyroid cancer growth and recurrence should be balanced with risk of long-term side effects of over-suppression.

References:
1. Haugen BR, Alexander EK, Bible KC, Doherty GM, Mandel SJ, Nikiforov YE, Pacini F, Randolph GW, Sawka AM, Schlumberger M, Schuff KG, Sherman SI, Sosa JA, Steward DL, Tuttle RM, Wartofsky L. 2015 American Thyroid Association Management Guidelines for Adult Patients with Thyroid Nodules and Differentiated Thyroid Cancer: The American Thyroid Association Guidelines Task Force on Thyroid Nodules and Differentiated Thyroid Cancer. Thyroid. 2016 Jan;26(1):1-133.
2. Tarasova VD, Tuttle RM. A Risk-adapted Approach to Follow-up in Differentiated Thyroid Cancer. Rambam Maimonides Med J. 2016 Jan 28;7(1):e0004. doi: 10.5041/RMMJ.10231. PMID: 26886955; PMCID: PMC4737510.
3. Tuttle RM, Alzahrani AS. Risk Stratification in Differentiated Thyroid Cancer: From Detection to Final Follow-up. J Clin Endocrinol Metab. 2019 Mar 15;104(9):4087–100.
4. Grani G, Ramundo V, Verrienti A, Sponziello M, Durante C. Thyroid hormone therapy in differentiated thyroid cancer. Endocrine. 2019 Oct;66(1):43-50.
5. Biondi B, Cooper DS. Thyroid Hormone Suppression Therapy. Endocrinol Metab Clin North Am. 2019 Mar;48(1):227-237.
6. Grani G, Zatelli MC, Alfò M, Montesano T, Torlontano M, Morelli S, Deandrea M, Antonelli A, Francese C, Ceresini G, Orlandi F, Maniglia CA, Bruno R, Monti S, Santaguida MG, Repaci A, Tallini G, Fugazzola L, Monzani F, Giubbini R, Rossetto R, Mian C, Crescenzi A, Tumino D, Pagano L, Pezzullo L, Lombardi CP, Arvat E, Petrone L, Castagna MG, Spiazzi G, Salvatore D, Meringolo D, Solaroli E, Monari F, Magri F, Triggiani V, Castello R, Piazza C, Rossi R, Ferraro Petrillo U, Filetti S, Durante C. Real-World Performance of the American Thyroid Association Risk Estimates in Predicting 1-Year Differentiated Thyroid Cancer Outcomes: A Prospective Multicenter Study of 2000 Patients. Thyroid. 2021 Feb;31(2):264-271.

Disclaimer:
The ideas and opinions expressed on the ATA Blogs do not necessarily reflect those of the ATA. None of the information posted is intended as medical, legal, or business advice, or advice about reimbursement for health care services. The mention of any product, service, company, therapy or physician practice does not constitute an endorsement of any kind by ATA. ATA assumes no responsibility for any injury or damage to persons or property arising out of or related to any use of the material contained in, posted on, or linked to this site, or any errors or omissions.

For more information on Thyroid Topics please visit: https://www.thyroid.org/thyroid-information/

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Benjamin Gigliotti, MD
University of Rochester Medical Center, NY
January 15, 2021

A common clinical dilemma is the management of patients with treated hypothyroidism and/or Hashimoto’s thyroiditis who feel unwell despite normal thyroid function tests. Weight gain, fatigue, brain fog, depressed mood, cold intolerance, constipation, dry skin, joint/muscle aches, hair loss, and brittle nails may be reported. These symptoms are commonly referred to as “thyroid symptoms,” and an internet search will reveal innumerable sources that reinforce a link between these and inadequate treatment or thyroid autoimmunity itself. However, clinicians must be cautious not to reflexively infer causation from correlation since:

– Even the most classic symptoms of hypothyroidism are non-specific and are commonly found in other diseases and in the general population.
– Anti-thyroid antibodies are often ordered in patients with unexplained symptoms, so autoimmune thyroid disease is disproportionately diagnosed in this setting; it remains unclear if this causes symptoms in and of itself.
– Most online resources emphasize the voices of people with thyroid disease who feel unwell since those who feel well do not tend to seek out or contribute to these resources.

In my experience, vague symptoms in this setting often have a multifactorial explanation, and thyroid disorders are rarely the dominant or only cause. Although the severity or number of symptoms can be daunting to evaluate, it is critical to meet the patient’s frustration with compassion, longitudinal relationship-building and thoughtful inquiry. Asking the following questions may prove helpful in determining the source(s) of symptoms:

-Is the normal TSH truly reflective of the patient’s thyroid axis?

• Repeating the TSH over time can exclude spuriously or transiently normal results.
• The upper limit of the TSH reference range (4-5mIU/L for most assays) is debated and may be lower in young patients or higher in older or obese patients. Regardless, I have never seen resolution of severe symptoms from treatment of a TSH that is within (or even slightly above or below) the reference range; several studies support this observation.(1)
• Checking a free T4 level at least once can ensure concordance with the TSH and exclude assay interference (e.g. biotin or heterophile antibodies) or rare cases of central hypothyroidism).(2)
• Total T3, free T3, and reverse T3 assays perform poorly in hypothyroidism and are rarely helpful, especially if the TSH and free T4 are normal

-Could there be an alternative explanation for each symptom that warrants workup, treatment, or counseling?

• Weight gain and/or fatigue are particularly common, occurring in up to half of all adults. Inadequate or poor-quality sleep, excessive work, suboptimal diet, and inadequate exercise are common causes. Menopause can also contribute, especially if vasomotor symptoms disrupt sleep.
• Hashimoto’s is associated with a higher rate of other clinically significant autoimmune diseases (e.g. lupus, rheumatoid arthritis, celiac disease) and numerous functional disorders (e.g. depression, migraines, irritable bowel syndrome, fibromyalgia).
• Iron deficiency is common in menstruating women, a population enriched in autoimmune thyroid disease, and can cause a similar spectrum of symptoms, even without anemia or frankly low ferritin levels.

– Can thyroid hormone therapy be optimized?

• Some patients on levothyroxine report improved symptoms after targeting a “low normal” TSH, although it is increasingly unclear if this approach is effective, and caution should be used in patients at risk for harm from iatrogenic hyperthyroidism.(3)
• Many patients express interest in therapies other than standard-of-care levothyroxine (4); Dr. Shrestha recently wrote a thoughtful blog post on thyroid hormone formulations (https://www.thyroid.org/thyroid-prescription-levothyroxine/). It is prudent to consult with an experienced endocrinologist familiar with the literature and pros/cons of using T3 and T4+T3 combination therapy to determine their appropriateness on a case-by-case basis.

While there is rarely a panacea, engaging in supportive listening, initiating an appropriately comprehensive evaluation, setting realistic expectations, and seeking consultation with endocrinology (especially when questions about assay reliability or optimal thyroid hormone replacement arise) can prove beneficial.

References:
1. Biondi B 2013 The normal TSH reference range: what has changed in the last decade? J Clin Endocrinol Metab 98:3584-3587.
2. Burch HB 2019 Drug Effects on the Thyroid. N Engl J Med 381:749-761.
3. Samuels MH, Kolobova I, Niederhausen M, Janowsky JS, Schuff KG 2018 Effects of altering levothyroxine (L-T4) doses on quality of life, mood and cognition in L-T4 treated subjects. J Clin Endocrinol Metab. ePub 2018 Mar 2.
4. Jonklaas J, Bianco AC, Bauer AJ, Burman KD, Cappola AR, Celi FS, Cooper DS, Kim BW, Peeters RP, Rosenthal MS, et al. 2014 Guidelines for the treatment of hypothyroidism: prepared by the american thyroid association task force on thyroid hormone replacement. Thyroid 24:1670-1751.

Disclaimer:
The ideas and opinions expressed on the ATA Blogs do not necessarily reflect those of the ATA. None of the information posted is intended as medical, legal, or business advice, or advice about reimbursement for health care services. The mention of any product, service, company, therapy or physician practice does not constitute an endorsement of any kind by ATA. ATA assumes no responsibility for any injury or damage to persons or property arising out of or related to any use of the material contained in, posted on, or linked to this site, or any errors or omissions.

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Rupendra T. Shrestha, MD
University of Minnesota, Minneapolis, MN
December 20, 2020

Many patients try to avoid synthetic products and processed food as much as possible. This might imply that a hormone replacement considered natural is better. How do “natural” animal-derived thyroid hormone products differ from “synthetic” levothyroxine?

To understand this, we must understand some of the basics. The main hormone a thyroid gland produces is thyroxine – a molecule of tyrosine with four iodine bound to it. Thyroxine has left and right enantiomers – the same exact molecule rotated either to the left or to the right – levo- and dextro, respectively. Our bodies make thyroxine that is left rotated (or levothyroxine). The right rotated dextrothyroxine does not have any thyroid hormone action.

Levothyroxine brands and generics are all molecularly identical to levothyroxine — exactly the same molecule that the thyroid would be producing if it was to function normally! Therefore, if the manufactured compound is the exact compound that which we make naturally, is it synthetic or natural?

“Natural thyroid hormones” (such as Armour®, Nature-Throid®, or others) contain both levothyroxine and liothyronine. In these products, the levothyroxine is exactly the same as the synthetic versions, but the product is derived from a sheep or pig rather than from a machine. The liothyronine, or T3, is the more active form of thyroid hormone. Naturally, the thyroid produces a very small amount of T3. Most T3 is converted from T4 on an as-needed basis by various organs. Different organs require different amounts of T3 based on their metabolic state.

There are many people who do not get adequate symptom relief with levothyroxine and try animal thyroid extracts. These drugs are not approved by the FDA, and people who take them can end up overdosing thyroid hormone. This excess thyroid hormone is not without risks. Symptoms can include feeling warm, obtaining less sleep, and restlessness (which many perceive as increased energy). It also increases the risk of heart problems such as atrial fibrillation and can increase the risk of osteoporosis. Despite this, there may be some individuals who actually do benefit from T3. However, research has shown these patients are in the minority. Therefore, if taking animal thyroid extracts seem to give symptomatic improvement by giving higher dose of thyroid, it may come at a price.

If thyroid labs are normal on levothyroxine but a patient has persistent symptoms, one important step is to assess for other confounding problems such as sleep issues, lack of exercise and other chronic medical problems prior to considering a change in thyroid hormone.

In summary, while levothyroxine is made artificially, it is the exact molecule that our natural thyroid gland would have produced. On the other hand, the thyroid hormone extracts that are advertised as “natural products” are produced from the glands of animals, and the dosing is difficult to match to human requirements. Some patients may end up getting more hormone than is required and that can give a false sense of “improvement.” There may be some individuals who might benefit from additional T3, and more research is needed in this area.

For Further Reference:
American Thyroid Association Thyroid Hormone Treatment Brochure

Disclaimer:
The ideas and opinions expressed on the ATA Blogs do not necessarily reflect those of the ATA. None of the information posted is intended as medical, legal, or business advice, or advice about reimbursement for health care services. The mention of any product, service, company, therapy or physician practice does not constitute an endorsement of any kind by ATA. ATA assumes no responsibility for any injury or damage to persons or property arising out of or related to any use of the material contained in, posted on, or linked to this site, or any errors or omissions.

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Monday, October 19, 2015 – 1:15 pm ET (embargoed) –

The American Thyroid Association (ATA) will present Takashi Yoshimura, Ph.D. with the 2015 Van Meter Award at the 85th Annual Meeting of the ATA, held in conjunction with the International Thyroid Congress, October 18-23, 2015, in Lake Buena Vista (Orlando), FL. Established in 1930, The Van Meter Award recognizes outstanding contributions by a young clinical scientist to research on the thyroid gland and hormones. The award recipient delivers the only ATA prize lecture this year, the Van Meter Award Lectureship, at the 15th International Thyroid Congress on Monday, October 19. Dr. Yoshimura’s talk is entitled “Novel roles for TSH and TH identified by discovery-driven approach”.

The Van Meter Award receives support from Mary Ann Liebert, Inc., publishers of the journal Thyroid.
Dr. Yoshimura’s remarkable contributions to thyroid research relate to a series of fascinating discoveries made in birds, mammals, and fish that link photoreceptors in the brain to thyroid hormone-based regulation of seasonal reproduction. He holds a Ph.D. in Agricultural Sciences and is a Professor in the Graduate School of Bioagricultural Sciences and Director of the Avian Bioscience Research Center at University of Nagoya, Japan. Sparking Dr. Yoshimura’s interest in the thyroid and thyroid hormones was his seminal discovery in birds–published in Nature in 2003–that the light-induced conversion of thyroxine (T4) to triiodothyronine (T3) in the brain regulates gonadal activity as the days get longer and shorter. He then identified the molecular mechanism associated with this phenomenon, which involves the enzyme deiodinase 2, and went on to show that extended daylight induced the synthesis of the same enzyme in mammals, suggesting that the mechanism regulating seasonal reproduction had been conserved throughout evolution.

Systems biology analytical methods led to the unexpected finding in birds that thyroid stimulating hormone (TSH) secreted from the pituitary gland is the “springtime hormone” that triggers expression of DIO2 ,the gene that controls deiodinase 2 production in the hypothalamus. Dr. Yoshimura then demonstrated that in mammals, TSH produced by the pituitary gland mediates the action of the pineal hormone melatonin, which had previously been shown to play a crucial role in regulating seasonal reproduction. More recently, Dr. Yoshimura’s group has uncovered the regulatory mechanism by which TSH secreted by two different compartments of the pituitary gland can carry out different regulatory activities without functional crosstalk.

Further pursuing this line of investigation, Dr. Yoshimura subsequently described the mechanism for seasonal regulation of TSH and DIO2 in fish, describing the physiological role of the saccus vasculosus as a seasonal sensor in fish.

This comprehensive body of work is likely to have a great impact on future research related to human reproductive health and mood disorders, such as seasonal affective disorder (also known as SAD or winter depression).

###

The American Thyroid Association (ATA) is the leading worldwide organization dedicated to the advancement, understanding, prevention, diagnosis, and treatment of thyroid disorders and thyroid cancer. ATA is an international membership medical society with over 1,700 members from 43 countries around the world. Celebrating its 92^nd anniversary, the ATA delivers its mission — of being devoted to thyroid biology and to the prevention and treatment of thyroid disease through excellence in research, clinical care, education, and public health — through several key endeavors: the publication of highly regarded professional journals, Thyroid, Clinical Thyroidology, and VideoEndocrinology; annual scientific meetings; biennial clinical and research symposia; research grant programs for young investigators, support of online professional, public and patient educational programs; and the development of guidelines for clinical management of thyroid disease and thyroid cancer. The ATA promotes thyroid awareness and information through its online Clinical Thyroidology for the Public (distributed free of charge to over 11,000 patients and public subscribers) and extensive, authoritative explanations of thyroid disease and thyroid cancer in both English and Spanish. The ATA website serves as the clinical resource for patients and the public who look for reliable information on the Internet.  Every fifth year, the American Thyroid Association joins with the Latin American Thyroid Society, the European Thyroid Association, and the Asia and Oceania Thyroid Association to co-sponsor the International Thyroid Congress (ITC).  This year the ITC is hosted by the American Thyroid Association at the Walt Disney World Swan and Dolphin Resort.  More information about the 15^th ITC can be found at http://www.thyroid.org/itc2015/.

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The American Thyroid Association (ATA), in its support of young scientists working in the field of thyroidology, awarded grants in 2013 to researchers studying a range of topics related to thyroid disease, thyroid cancer, and thyroid biology, including two young researchers whose studies will contribute to our understanding of the role thyroid hormones play in regulating cholesterol levels in the blood and the physiology of skeletal muscle. The ATA Research committee has recently reviewed their progress and approved funding for the second year grant.

Binding of thyroid hormones to the thyroid gland can cause a lowering of blood levels of total cholesterol and low density lipoprotein (LDL or “bad”) cholesterol. This has implications for the development of novel cholesterol-lowering therapies, particularly for individuals in whom statins are not safe or effective. Kevin Phillips, PhD and colleagues at Methodist Hospital, Houston, TX, have proposed a new mechanism to explain this cholesterol lowering effect of thyroid h ormones. The grant award to support Dr. Phillips’ research proposal entitled “The Contribution of Cyp7a1 to the Cholesterol Lowering Actions of TR Agonists” will fund studies to test the hypothesis that this mechanism is independent of functional LDL receptors and involves induction of the enzyme cholesterol 7a-hydroxylase (CYP7a). Bio

Joao Pedro Saar Werneck-de-Castro, PhD, University of Miami, Florida, received an ATA grant award for his research proposal entitled “What Is the Role of Type II Deiodinase (D2)-Mediated T3 Production in Skeletal Muscle.” His group has created a strain of mouse that is deficient in type II deiodinase (D2), an enzyme that converts the prohormone thyroxine (T4) to the bioactive thyroid hormone T3. They have proposed a dual source of D2 in skeletal muscle: muscle cells (myocytes), and fat cells (brown adipocytes) and aim to show that mouse skeletal muscle contains intermingled brown adipocytes that express high levels of D2. Bio

“These studies are very interesting because they expand our knowledge into the role of thyroid hormone in particular tissues and may lead to new and exciting treatment strategies based on thyroid hormone or related analogs,” says Ronald Cohen, MD, Associate Professor, Section of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Chicago, Illinois.

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What is the thyroid gland?

The thyroid gland located in the neck produces thyroid hormones which help the body use energy, stay warm and keep the brain, heart, muscles, and other organs working normally.

Thyroid hormone is used:

1. to replace the function of a failing, or failed, thyroid gland (replacement therapy), and
2. to prevent further growth of thyroid tissue (suppression therapy), particularly in patients with a history of thyroid cancer

Why do I need thyroid hormone pills?

Hypothyroidism is the most common reason for needing thyroid hormone replacement (see Hypothyroidism brochure). Pure synthetic thyroxine (T4), taken once daily by mouth, successfully treats the symptoms of hypothyroidism in most patients.

How is the dose of thyroxine chosen?

The initial T4 dose is carefully selected based on your weight, age, and other medical conditions. The dose is then adjusted based on your thyroid hormone levels and your symptoms. The current branded forms of T4 are Synthroid® Levoxyl® Levothyroid®, Tirosint® and Unithroid®. Although these all contain the same synthetic T4, there are different inert ingredients in each of brand names. In general, it is best for you to stay on the same brand name.

How do I take thyroxine?

T4 is taken just once a day and results in very stable levels of thyroid hormone in the blood stream. The best time to take T4 is probably first thing in the morning on an empty stomach. However, the most important thing is to be consistent when you take it. If you miss a dose of T4, it is usually best to take the missed dose as soon as you remember.

Does thyroxine interact with any other medications?

Medications that may cause a change in your T4 dose include birth control pills, estrogen, testosterone, some anti-seizure medications, and some medications for depression. Iron, calcium, soy, and some cholesterol-lowering medications can decrease the absorption of thyroid hormone.

Should I take thyroxine while I am pregnant?

Since T4 is a hormone normally present in the body, it is absolutely safe to take it while pregnant. You often need an increased dose of T4 during pregnancy, so it is important to have thyroid hormone and TSH levels measured once you know that you are pregnant.

What about “natural” thyroid hormones?

Desiccated (dried and powdered) animal thyroid (Armour®), now mainly obtained from pigs, was the most common form of thyroid therapy before the individual active thyroid hormones were discovered. While desiccated thyroid contains both T4 and T3, the balance of T4 and T3 in animals is not the same as in humans, so the hormones in animal thyroid pills aren’t necessarily “natural” for the human body. Further, the amounts of both T4 and T3 can vary in every batch of desiccated thyroid, making it harder to keep blood levels right. Finally, even dessicated thyroid pills have chemicals (binders) in them to hold the pill together, so they are not completely “natural”. Desiccated animal thyroid is rarely prescribed today, and there is no evidence that desiccated thyroid has any advantage over synthetic T4.

What about T3?

While most actions of thyroid hormone are most likely due to T3, most T3 in the body comes from the conversion of T4. The conversion of T4 to T3 is normal in hypothyroid patients, so the body can regulate to levels of T4 just as if the T4 was being produced from the thyroid gland. T3 has a very short life span in the body, while the life span of T4 is much longer, ensuring a steady supply of T3. There is no indication for the use of T3 alone for the treatment of hypothyroidism.

What about combined T4 and T3 treatment?

There has been interest in whether addition of a low amount of T3 given twice or three times a day in combination with T4 may benefit those patients that do not feel completely normal on T4 alone. A trial period of 3 – 6 months is reasonable to determine if combination T4 and T3 therapy will help.

Will thyroid hormone help me if I have hypothyroid symptoms but normal thyroid hormone levels?

In several scientific studies, there was no difference between T4 and a placebo (sugar pill) in improving symptoms, depression or well-being in patients with “hypothyroid” symptoms and normal thyroid hormone levels.

Why would I need to go on thyroid hormone suppression therapy?

Thyroxine can also be used to keep the TSH level in the low, or low normal, range. In the past, such thyroid hormone suppression therapy was used to prevent benign thyroid nodules and enlarged thyroid glands from growing. More recent evidence has shown that this practice is not effective in regions of the world that have adequate iodine intake (such as the USA). Moreover, excess thyroid hormone can increase the risk or heart rhythm problems and bone loss making the use of thyroxine for suppressing benign thyroid tissue more risky than beneficial in iodine sufficient populations.

Thyroid hormone suppression therapy is also an important part of the treatment of thyroid cancer and is effective in stopping the growth of microscopic thyroid cancer cells or residual thyroid cancer. In this case, the benefit of suppression therapy outweighs the risks.

Thyroid Hormone Treatment FAQ for Saving and Printing (PDF File, 130 KB)

Thyroid Hormone Treatment FAQ for Saving and Printing (PDF File, 75 KB)

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What is the thyroid gland?

The thyroid gland is a butterfly-shaped endocrine gland that is normally located in the lower front of the neck. The thyroid’s job is to make thyroid hormones, which are secreted into the blood and then carried to every tissue in the body. Thyroid hormone helps the body use energy, stay warm and keep the brain, heart, muscles, and other organs working as they should.

Thyroid hormone Treatment

Thyroid hormone is used in two situations:

1. to replace the function of the thyroid gland, which is no longer functioning normally (“replacement therapy”) and
2. to prevent further growth of thyroid tissue (“suppression therapy”). Suppression therapy is used primarily in patients with thyroid cancer to prevent recurrence or progression of their cancer.

Definition, Therapy & Treatment

Thyroid hormone replacement therapy

Many people have a thyroid gland that cannot make enough thyroid hormone for the body’s needs. This is called Hypothyroidism and may be caused by a non-functioning thyroid gland (for example Hashimoto’s disease), by destruction of thyroid gland by surgery or radiation treatment or by a non-functioning pituitary gland (see Hypothyroidism Brochure). Hypothyroidism, is the most common reason for needing thyroid hormone replacement.

The goal of thyroid hormone treatment is to closely replicate normal thyroid functioning. Pure, synthetic thyroxine (T4) works in the same way as a patient’s own thyroid hormone would. Thyroid hormone is necessary for the health of all the cells in the body. Therefore, taking thyroid hormone is different from taking other medications, because its job is to replace a hormone that is missing. The only safety concerns about taking thyroid hormone are taking too much or too little. Your thyroid function will be monitored by your physician to make sure this does not happen.

How is the dose of thyroid hormone chosen?

When someone is first started on thyroid hormone the initial dose is carefully selected based on information such as a person’s weight, age, and other medical conditions. The dose will then need to be adjusted by a physician to keep the thyroid function normal. The physician will make sure the thyroid hormone dose is correct by performing a physical examination and checking TSH levels.

There are several brand names of thyroid hormone available. Although these all contain the same synthetic T4, there are different inactive ingredients in each of the brand names. In general, it is best for you to stay on the same brand name. If a change in brand name is unavoidable, you should be sure your physician is aware of the change, so that your thyroid function can be re-checked. If your pharmacy plan changes your thyroid hormone to a generic preparation, it is important for you to inform your physician.

How do I take thyroid hormone?

Thyroid hormone is easy to take. Because it stays in your system for a long time, it can be taken just once a day, and this results in very stable levels of thyroid hormone in the blood stream. When thyroid hormone is used to treat hypothyroidism, the goal of treatment is to keep thyroid function within the same range as people without thyroid problems. Keeping the TSH level in the normal range does this. The best time to take thyroid hormone is probably first thing in the morning on an empty stomach. This is because food in the stomach can affect the absorption of thyroid hormone. However, the most important thing is to be consistent, and take your thyroid hormone at the same time, and in the same way, every day. If you are taking several other medications, you should discuss the timing of your thyroid hormone dose with your physician. Sometimes taking your thyroid hormone at night can make it simpler to prevent your thyroid hormone from interacting with food or other medications.

Do not stop your thyroid hormone without discussing this with your physician. Most thyroid problems are permanent, and therefore most patients require thyroid hormone for life. If you miss a dose of thyroid hormone, it is usually best to take the missed dose as soon as you remember. It is also safe to take two pills the next day; one in the morning and one in the evening. It is very important that your thyroid hormone and TSH levels are checked periodically, even if you are feeling fine, so that your dose of thyroid hormone can be adjusted if needed.

Does thyroid hormone interact with any other medications?

Taking other medications can sometimes cause people to need a higher or lower dose of thyroid hormone. Medications that can potentially cause people to need a different dose of thyroid hormone include birth control pills, estrogen, testosterone, some anti-seizure medications (for example Dilantin and Tegretol), and some medications for depression. Yet other products can prevent the absorption of the full dose of thyroid hormone. These include iron, calcium, soy, certain antacids and some cholesterol-lowering medications. For all these reasons, it is important for people taking thyroid hormone to keep their physician up to date with any changes in the medications or supplements they are taking.

Should I take thyroid hormone while I am pregnant?

Since thyroid hormone is a hormone normally present in the body, it is absolutely safe to take while pregnant. Indeed, it is very important for pregnant women, or women who are planning to become pregnant, to have normal thyroid function to provide the optimum environment for her baby. Women who are taking thyroid hormone often need an increased dose of thyroid hormone during their pregnancy, so it is important to have thyroid hormone and TSH levels measured once you know that you are pregnant. You should discuss the timing of thyroid blood tests with your physician, but often thyroid function is checked at least every trimester.

What about “natural” thyroid hormones?

Desiccated (dried and powdered) animal thyroid (Armour®), now mainly obtained from pigs, was the most common form of thyroid therapy before the individual active thyroid hormones were discovered. People can still buy it over the Internet—legally if it’s sold as a food supplement, but illegally if it’s sold as a medicine. It is also available still as a prescription. Since pills made from animal thyroid are not purified, they contain hormones and proteins that never exist in the body outside of the thyroid gland. While desiccated thyroid contains both T4 and T3, the balance of T4 and T3 in animals is not the same as in humans, so the hormones in animal thyroid pills aren’t necessarily “natural” for the human body. Further, the amounts of both T4 and T3 can vary in every batch of desiccated thyroid, making it harder to keep blood levels right. Finally, even desiccated thyroid pills have chemicals (binders) in them to hold the pill together, so they are not completely “natural”. Desiccated animal thyroid is rarely prescribed today, and there is no evidence that desiccated thyroid has any advantage over synthetic T4.

What about T3?

While most actions of thyroid hormone are most likely due to T3, most T3 in the body comes from the conversion of T4. The conversion of T4 to T3 is normal in hypothyroid patients. T3 has a very short life span in the body, while the life span of T4 is much longer, ensuring a steady supply of T3. A preparation of synthetic T3 (Cytomel®) is available. After taking a tablet of Cytomel® there are very high levels of T3 for a short time, and then the levels fall off very rapidly. This means that T3 has to be taken several times each day, and even doing this does not smooth out the T3 levels properly. In addition, it is impossible to avoid having too much thyroid hormone in the system soon after each dose of T3 is taken. High T3 levels can lead to unpleasant symptoms such as rapid heart beat, insomnia and anxiety. High T3 levels also can harm the heart and the bones. Another concern with using T3 treatment is that the body is deprived of the ability to adjust the conversion of T4 to T3 to regulate the supply of T3 according to the body’s own needs. Thus, there is no indication for the use of T3 alone for the treatment of hypothyroidism.

What about combined T4 and T3 treatment?

Some hormone preparations containing both T4 and T3 are available in the United States (Thyrolar®). Combination T4/T3 preparations contain much more T3 than is usually produced naturally within the body. Because of this, they can have the same side effects as T3 given by itself. It is also given once a day, ignoring the short life span of T3 in the body. There has been interest in whether a combination of T4 and T3, with a lower amount of T3 given more than once a day, might result in better treatment of hypothyroidism, especially in those patients that do not feel completely normal on T4 alone. In these cases, Cytomel® (T3) is taken in addition to T4. A trial period of 3 – 6 months is reasonable to determine if combination T4 and T3 therapy will help.

Will thyroid hormone help me if I have hypothyroid symptoms but normal thyroid hormone levels?

Some people with normal thyroid blood tests have symptoms that are similar to symptoms of hypothyroidism. Several scientific studies have looked at whether T4 therapy would be of benefit to patients with symptoms that overlap with hypothyroid symptoms and normal thyroid function. In all cases, there was no difference between T4 and a placebo (sugar pill) in improving symptoms or well-being.

Thyroid hormone suppression therapy for benign nodules and goiter

In the past, thyroid hormone suppression therapy was used to prevent benign thyroid nodules and enlarged thyroid glands from growing. More recent evidence has shown that this practice is not effective in regions of the world that have adequate iodine intake (such as the USA). Moreover, excess thyroid hormone can increase the risk or heart rhythm problems and bone loss making the use of thyroxine for suppressing benign thyroid tissue more risky than beneficial in iodine sufficient populations.

Treatment of thyroid cancer

After surgery for thyroid cancer, thyroid hormone is needed both to replace the function of the removed thyroid gland and to keep any small or residual amounts of thyroid cancer cells from growing (see Thyroid Cancer brochure). Thyroid hormone suppression therapy is also an important part of the treatment of thyroid cancer and is effective in stopping the growth of microscopic thyroid cancer cells or residual thyroid cancer. In this case, the benefit of preventing the growth of residual thyroid cancer cells outweighs the risks of a mild increase in the risk of fast, irregular heart rhythms, exacerbation of chest pain and decreased bone density. A physician should closely monitor this kind of treatment. The duration of suppression therapy in cancer patients currently being debated.

Further Information

Further details on this and other thyroid-related topics are available in the patient information section on the American Thyroid Association website at www.thyroid.org.

Thyroid Hormone Treatment Brochure for Saving and Printing (PDF File, 453 KB)

Thyroid Hormone Treatment Brochure for Saving and Printing (PDF File, 182 KB)

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