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ALL YOU NEED TO KNOW ABOUT THYROID HEALTH AND DISEASE

Mya Care Blogger 14 Jun 2022
ALL YOU NEED TO KNOW ABOUT THYROID HEALTH AND DISEASE

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The thyroid gland is perhaps one of the most underestimated vital organs, responsible for regulating critical components of overall bodily metabolism.

The following article describes the importance of the thyroid gland, insights into how it functions, as well as common thyroid diseases that affect many individuals around the world. Tips for maintaining optimal thyroid health are also included.

Roles of the Thyroid Gland in the Body

The thyroid gland constitutes a major branch of the endocrine system as part of the hypothalamic-pituitary-thyroid axis. It secretes a variety of metabolic hormones that have an effect on every cell in the body, implicating it as one of the most important endocrine organs.[1]

The 3 main functions of the thyroid include:

  • Increasing and regulating energy metabolism in every cell
  • Maintaining balanced calcium levels across all tissues
  • Regulating iodine metabolism

In response to active thyroid hormone, the energy output of every cell peaks due to increasing mitochondrial uncoupling proteins, intracellular calcium, and oxygen uptake. These metabolic effects are required for optimal thermogenesis, heart rate, blood circulation, respiratory function, nervous stimulation, muscle contraction, bone turnover and many other vital bodily functions pertaining to metabolism and growth.

Oxygenation. Thyroid hormones serve to normalize oxygen utilization and tissue delivery by stimulating hemoglobin production, red blood cell turnover and uptake of folate and cobalamin from the digestive tract.

Development. From infancy right through to adulthood, thyroid hormones are necessary factors for optimal tissue development and maintenance. Aside from their role in metabolism, these hormones signal for the release of growth hormone from the pituitary gland.

Thyroid Hormones

There are two main thyroid hormones involved in metabolism:

  • T3 (Triiodothyronine) is the active form of thyroid hormone, comprising 10-20% of thyroid hormone circulating in the system. Thyroid hormone receptors are activated only by T3 and have a much higher affinity for T3 than for T4. T3 is mostly produced in peripheral tissues through conversion from T4.
  • T4 (Thyroxine) is an inactive form of thyroid hormone that is converted in peripheral tissues to the active form (T3). T4 comprises 80-90% of thyroid hormone produced by the thyroid. T4 is converted into T3 as required by peripheral tissues. The half-life of T4 is 7-10 days on average.

Other Thyroid Hormones include:

  • Reverse T3 is an inactive form of T3, produced as a by-product of T4 degradation. rT3 usually gets broken down into diiodotyrosine, which can be recycled by the thyroid gland to produce more thyroid hormone. rT3 levels usually remain constant, with the exception of nonthyroidal illness syndrome.
  • TSH (Thyroid Stimulating Hormone) is a pituitary hormone that signals for the thyroid gland to produce thyroid hormones. TSH is secreted in response to thyrotropin-releasing hormone (TRH), which originates from the hypothalamus.[2] These hormones form a feedback loop with thyroid hormones to maintain adequate levels. Problems with TSH and TRH can result in thyroid disease.
  • Calcitonin regulates the secretion of parathyroid hormone, both of which serve to maintain balanced calcium levels throughout the body. Through opposing the action of parathyroid hormone, calcitonin reduces bone resorption and promotes calcium excretion from the body. Other sources indicate that it may assist with gut and bone calcium absorption, pH regulation, vitamin D3 production and preventing excess calcium deposition in cardiovascular tissues[3].

Hormone Synthesis

Thyroid hormone is produced from iodine and thyroglobulin (rich in tyrosine), with the aid of the main bioactive thyroidal enzyme, thyroid peroxidase.

Production can be broken down into two simple steps:

  1. Iodide Conversion. Thyroid stimulating hormone signals for thyroid hormone production and increases the thyroid’s uptake of iodide. Iodide is then converted into iodine through being oxidized by activated thyroid peroxidase and hydrogen peroxide.
  2. Enzymatic Assembly. Thyroid peroxidase is then used again to link the iodine to tyrosine (from thyroglobulin). This forms monoiodotyrosine (MIT) and diiodotyrosine (DIT), which contain iodine with one and two tyrosine residues respectively. These compounds are further joined to form T3 (MIT + DIT) and T4 (2 x DIT).[4]

While capable of producing T3, the thyroid mostly produces T4. Both forms of thyroid hormone are stored bound to thyroglobulin. The thyroglobulin is removed via proteolysis before the hormones are released. Excess MIT, DIT, thyroglobulin and iodine are recycled back into the gland’s pool.

Most Common Thyroid Diseases

Thyroid conditions are amongst the most common diseases to affect all populations globally.[5] Due to the thyroid’s extensive role in metabolism, thyroid conditions affect nearly every organ in the body.[6]

The two main types of thyroid conditions are hypothyroidism (thyroid hormone deficiency) and hyperthyroidism (thyroid hormone excess). Other conditions typically refer to thyroid inflammation, abnormal growth or malignancy.

Diagnostic Caution. Testing for thyroid hormone levels is used for diagnostic purposes. However, test results that meet ranges for disease do not guarantee the presence of thyroid disease. A qualified physician is required to interpret the results and rule out other potential causes.

General Risk factors

  • Endocrine disruptors. Chemical agents, such as pesticides, plastic compounds and flame retardants, have been shown to disrupt thyroid endocrine function[7] and increase the risk for developing thyroid disease.[8]
  • Radiation. Exposure of the thyroid gland to radiation increases the risk for all forms of thyroidal disease.[9]
  • Poor Sleep Quality. Disturbed or poor-quality sleep can increase the risk of thyroid disease through promoting hypothalamic-pituitary imbalances. Likewise, thyroid diseases may induce sleep disorders through affecting the hypothalamic-pituitary-thyroid axis.[10]
  • Medications. Some medications interfere with thyroid hormone levels, which may increase the risk for thyroid disease in susceptible individuals.
  • Autoimmunity. Those with underlying autoimmune conditions are at an increased risk for the most common thyroid diseases, hypothyroidism and hyperthyroidism.
  • Anemia. Anemia is a risk factor for thyroid disease as well as a common condition that can develop through the course of any thyroid condition. Thyroid hormone production requires iron and heme, while bone marrow requires thyroid hormones for optimal red blood cell production. Iron deficiency is a shared risk factor for thyroid disease and anemia.[11]
  • Iodine Excess or Deficiency. Chronic excess or deficient iodine levels promote the incidence of all thyroid diseases. Iodine uptake is facilitated by low dietary intake that meets adequate nutritional requirements. Excessive intake is able to inhibit absorption, iodation of thyroglobulin and thyroid hormone production. Long-term excess intake of iodated salt may increase the risk of iodine deficiency, as well as autoimmune thyroiditis through promoting immune reactivity towards overly iodated thyroglobulin. [12]
  • Gender. Women are at the highest risk for acquiring any disease of the thyroid.[13] This is largely owing to a culmination of independent risks pertaining to women, such as pregnancy, lower fat-free mass and having higher genetic risk profile for autoimmunity.
  • Aging. Elderly women appear to be at an increased risk for thyroid autonomy in which the thyroid enlarges with excess follicular growth.
  • Genetics. Some individuals are predisposed genetically to contracting thyroid conditions, especially if predisposed to any associated condition. Those with inherited genetic conditions, such as Down’s Syndrome and Turner’s Syndrome, are equally at an increased risk.
  • Pregnancy. Some women are prone to contracting hypothyroidism post-partum and this is often connected to post-partum depression. The risk is associated with estrogen fluctuations and nutritional deficiencies that follow pregnancy.

Hypothyroidism

Hypothyroidism refers to a clinical condition of thyroid hormone deficiency.[14]

The vast majority of hypothyroidism cases fall into the primary category, pertaining to deficits within the thyroid gland itself. Rarer types of hypothyroidism include: secondary (pituitary TSH deficit), tertiary (hypothalamic TRH deficit) and peripheral (thyroid hormone metabolism issue).

Testing. In those with primary hypothyroidism, testing reveals highly elevated TSH with extreme deficiency in T4 (often seen with T3 excess). In subclinical hypothyroidism, T4 levels may appear normal alongside elevated TSH.

Symptoms

Common symptoms of hypothyroidism:

  • Bradycardia
  • Cold intolerance
  • Constipation
  • Shortness of breath
  • Fatigue
  • Weight gain
  • Deepening of the voice
  • Dry skin
  • Hair loss

Those with hypothyroidism often present with cardiovascular and metabolic symptoms such as hypertension and dyslipidemia. As hypothyroidism is potentially able to affect all organs, symptoms vary across individuals and become less specific in aging patients.

Rarer symptoms include decreased taste, vision or hearing, depression, anxiety, impaired memory, sleep disturbance, paresthesia, fertility problems, weakness, muscle cramps and wasting, pain in joints, increased tendency for bleeding and reduced kidney function.

If severe and left untreated, hypothyroidism can lead to myxedema coma and eventual death due to multiple organ failure.

Causes

Iodine deficiency is the most common cause of hypothyroidism, while chronic excesses are a significant risk factor for autoimmune hypothyroidism.

Hashimoto’s Autoimmune Thyroiditis is an autoimmune condition that causes hypothyroidism and is the most common cause in those with adequate iodine levels or excessive levels. The condition is characterized by autoantibodies against thyroid peroxidase and thyroglobulin, which effectively reduces thyroid hormone production. Lymphocytes typically invade the thyroid and promote the gland’s degeneration.

Risk Factors

Aside from the general risk factors mentioned above, hypothyroidism risk is elevated in those with the following:

  • Vitamin D3 Deficiency. Deficiencies in vitamin D3 are known to increase the risk for autoimmune diseases, including autoimmune thyroiditis.
  • Selenium Deficiency. Selenoproteins are crucial for the production of thyroid hormones, promoting optimal iodination of thyroglobulins. Deficiency in selenium serves as a risk factor for hypothyroidism and autoimmune thyroiditis.[15]
  • Iron Deficiency. Iron is required for the production of the heme protein, which is necessary for the activation of thyroid peroxidase and subsequently, thyroid hormone production. When iron and heme are deficient, thyroid peroxidase under-functions, promoting hypothyroidism.
  • Zinc Deficiency. Zinc is another micronutrient that regulates thyroid hormone production.[16] Deficiency of zinc may predispose individuals to hypothyroidism, while hypothyroidism may also predispose one to zinc deficiency.[17]
  • Premature birth can serve as a risk factor for hypothyroidism.[18]
  • Depression. Hypothyroidism has a long-standing association with depression, with either condition seemingly increasing the risk for contracting the other.[19]
  • Medications and Therapies associated with increasing the risk for primary hypothyroidism include: amiodarone, lithium, thalidomide, tyrosine kinase inhibitors, certain antibiotics and antiepileptics, radiotherapy, surgery, as well as a portion of immune-boosting therapies such as monoclonal antibodies and interferon administration.

The condition is more prevalent in women, those of European descent, and older people. This trend may be related to differences in vitamin D metabolism across these populations, which predispose these individuals to an increased risk for deficiency.

Treatment and Prognosis

Prognosis for hypothyroidism is excellent if treated and potentially fatal if left untreated. Symptoms usually reverse within weeks to months following treatment onset.[20] Treatment typically consists of thyroid hormone replacement and occasionally, nutritional and lifestyle interventions.

  • Levothyroxine is a synthetically-produced T4 hormone equivalent that is most commonly prescribed for thyroid conditions. Through the course of treatment, T4 levels increase which serves to regulate TSH and overall hormone production. Once normalized, treatment stops, and the patient is usually monitored for 6-12 more months. Appropriate dosages differ between patients and over-treatment can result in hyperthyroidism. Levothyroxine is contraindicated for patients with adrenal insufficiency and may be contraindicated on several classes of medication. Designing a protocol with a healthcare provider to facilitate absorption and prevent complications is essential when undergoing levothyroxine therapy.
  • Iodine supplementation could be prescribed if the underlying cause of hypothyroidism is deficiency. If this is the case, the patient is then treated for deficiency and symptoms typically normalize in tandem with iodine status.
  • Iron supplementation appears to help in two thirds of women with hypothyroidism, who did not respond to treatment with levothyroxine and who were not iodine deficient. Ferritin levels were below normal in these cases and were normalized through supplementation.
  • Selenium. While not officially recommended, many physicians prescribe organic selenium supplements to their patients with autoimmune thyroiditis. Selenoproteins have been shown to enhance production of thyroid hormones and inhibit thyroid peroxidase antibodies; thereby improving symptoms of hypothyroidism and autoimmune thyroiditis. Pregnant women with low selenium status may benefit from supplementation as it is known to protect against post-partum and congenital hypothyroidism.[21]

Hyperthyroidism

Hyperthyroidism refers to a thyroid condition in which the thyroid gland produces excess thyroid hormone. It often causes thyrotoxicosis, a condition in which peripheral tissues are exposed to excessive levels of thyroid hormone.

Testing. Blood tests for hyperthyroidism often reflect significantly elevated T4 and reduced TSH levels. T3 is also often tested for and in some conditions, the ratio of T3:T4 may be disproportionately increased. Subclinical hyperthyroidism will reflect low TSH with normal T4/T3. Other tests are required to diagnose the cause of hyperthyroidism.[22]

Symptoms

Symptoms of hyperthyroidism reflect an elevated metabolism. They include:

  • Fine tremor
  • Nervousness
  • Muscle weakness
  • Shortness of breath
  • Excessive sweating
  • Heat intolerance
  • Heart palpitations
  • Increased appetite
  • Weight loss
  • Diarrhea

A goiter may be present or an indication of thyroidal swelling. Other symptoms may manifest depending on the etiology of the condition.

Causes

Grave’s Disease is the leading cause in young individuals with hyperthyroidism. It is an autoimmune disorder characterized by autoantibodies that activate TSH receptors, mimicking the actions of TSH and subsequently create thyroid hormone excess. Patients with Grave’s Disease can go on to acquiring hypothyroidism, particularly if having undergone prolonged or excessive treatment with radioactive iodine.

Toxic Multinodular Goiter is the most common cause amongst elderly patients. This refers to a condition in which the thyroid has accumulated multiple growths or nodules which produce extra thyroid hormone. The nodules often produce thyroid hormone irrespective of inhibitory feedback mechanisms, leading to a state of endocrine excess.[23]

Iodine Excess. By contrast to hypothyroidism, excessive iodine levels can cause hyperthyroidism, while deficiency serves as a risk factor for both conditions. As excessive dietary intake often inhibits iodine’s absorption and hormone production, iodine excess is usually the result of iodine-containing medications that are known to be toxic to the thyroid.

Rarer causes of hyperthyroidism include:

  • Thyroid adenoma (a single benign growth or nodule that produces excess hormone)
  • Subacute, post-partum and/or factitious thyroiditis (types of thyroid inflammation)
  • Ectopic thyroid tissue (thyroid tissue developed at a distant body site, able to produce thyroid hormone)
  • Levothyroxine overtreatment

Pregnancy, estrogen hormone replacement therapy, infections, medications, and altitude sickness may induce a temporary state of hyperthyroidism that tends to resolve without requiring intervention.

Risk Factors

Hyperthyroidism risk factors are specific to the underlying cause. General risk factors include physiological stress, female sex, iodine excess, aging, infection, smoking[24] and ingestion of exogenous thyroid hormone. [25]

For Grave’s Disease, risk factors include estrogen excess, autoimmune diseases, as well as selenium and vitamin D3 deficiency[26].

Treatment and Prognosis

The prognosis is generally good overall for those being treated for Grave’s Disease, multinodular goiter and other types of hyperthyroidism.[27] If left untreated, hyperthyroidism may be fatal.

Treatment options for primary hyperthyroidism include:

  • Radioactive iodine therapy is the standard prescription for overt hyperthyroidism; unless contraindicated, as with pregnant and breast-feeding mothers. This is an extremely potent therapy in which administered radioactive iodine effectively destroys thyroid tissue. The patient will be monitored every 4-6 weeks after therapy takes place to ensure hormone normalization, which can take up to several months to achieve following one dose. Repeat administration is only required if T4 levels fail to normalize in the months following the first administration. Over-treatment can induce hypothyroidism.

Therapy may be contraindicated in patients with cardiovascular disease as initial administration of radioactive iodine promotes transient T4 elevations and can increase arrhythmias. These patients are often prescribed antithyroid medications before radioactive iodine therapy, in order to lower T4 and avoid cardiac complications. If on antithyroid medication, its important for the patient to stop treatment 1 week before receiving radioactive iodine therapy.

  • Antithyroid drugs, such as thionamide, are used to treat patients who are unable to receive radioactive iodine therapy, who require transient thyroid suppression, or those with amiodarone-induced thyrotoxicosis type 1. These drugs typically inhibit the production of thyroid hormone and serve to lower T4 levels. Antithyroid medications do not treat the underlying cause of hyperthyroidism, with symptoms returning in the majority of individuals who discontinue treatment. If severe side effects occur as a result of treatment, it’s important to notify your doctor immediately.
  • Steroids are specifically used to treat amiodarone-induced thyrotoxicosis type 2 and may be prescribed for autoimmune thyroid diseases.
  • Beta-Blockers may be prescribed to patients with hyperthyroidism who also have cardiovascular disease. If these are contraindicated, calcium channel blockers or ACE inhibitors may be prescribed instead.
  • Selenium. Grave’s disease patients may benefit from low dose supplementation with selenium if suffering mild to moderate eye abnormalities.[28] Despite these findings, selenium has the potential to increase thyroidal output and is more commonly prescribed for hypothyroidism. It’s advisable to get your selenium levels checked with your healthcare practitioner first before opting for selenium supplementation.
  • Thyroid surgery (subtotal thyroidectomy) is used for long-term control of hyperthyroidism, thyroid cancer or for extreme presentations of hyperthyroidism. A portion of the gland is removed, and this effectively suppresses excess T4 production. Hypothyroidism is the most common complication of thyroid surgery, followed by damage to surrounding structures including the parathyroid glands and vocal cords.

T4 monitoring throughout any of the above treatments is essential to avoid complications, such as over-treatment and hypothyroidism. TSH will remain suppressed until T4 levels normalize and is therefore unnecessary to monitor.

Treatment for thyroiditis usually revolves around managing symptoms, as the cause for hyperthyroidism often resolves by itself.

Other Thyroid Diseases

The most common thyroid diseases following hypothyroidism and hyperthyroidism are:

Thyroid Cancer comprises between 1-4% of cancers in the US. The majority of cancer develops in thyroid follicular cells which produce thyroid hormone, while the remainder develop in C-cells, which store thyroid hormone. A variety of genetic mutations are known to cause thyroid cancer and risk factors include female sex, family incidence, hyperthyroidism and extreme radiation exposure to the thyroid during childhood. Treatments include surgery, radioactive iodine therapy, chemotherapy, and thyroid hormone suppression.[29]

Euthyroid Sick Syndrome refers to unbalanced thyroidal function caused by critical illness and is often seen in up to 75% of hospitalized or intensive care patients. T3 is often low, with increased rT3 and normal levels of TSH and T4. Causes vary, and can include post-surgical recovery, trauma, sepsis, heart or kidney failure, starvation, hypothermia, and more. Prognosis is generally reliant on the success of treating the cause, as well as T4 levels. If T4 levels become critically low, risk of mortality is high. This condition is sometimes known as Nonthyroidal Illness Syndrome.  [30]

5 Tips for Maintaining Thyroid Health

The five below tips summarize ways in which one may support thyroid health and overall well-being.

1. Thyroid-Supportive Nutrients

The below list denotes nutrients that support optimal thyroid metabolism in healthy individuals. The list is not exhaustive.

Note: If you have a thyroid condition, it’s best to consult with a qualified healthcare practitioner about your specific nutritional status and requirements.

  • Iodine is a main ingredient in thyroid hormone production. The diet ought to contain small quantities that facilitate optimal uptake and utilization. Both excess and deficient consumption result in iodine deficiency in the long-term.
  • Selenium assists with thyroid function by promoting the production of selenoproteins. As with iodine, too little or too much selenium in the diet can be problematic for thyroid health. High doses of selenium are especially known to be toxic. Selenium ought to be consumed in an organic form, preferably from dietary sources such as seafood, nuts (especially brazil nuts), grains, and animal products.
  • Iron, Copper, Folate (Vit B9) and Cobalamin are required for red blood cell production and blood proteins that play a vital role in optimal thyroid hormone production and transportation. Animal products typically contain the highest sources of these nutrients, however they are found prolifically throughout plant-based wholefoods as well.
  • Zinc also helps to regulate thyroid function and hormone production. Sources include proteinaceous foods such as meat, oysters, whole grains, dairy, and legumes. Nuts are also a good source of zinc.
  • Vitamin D3 and K2. Vitamin D3 deficiency is a prominent risk factor for autoimmune thyroid diseases. It plays a vital role in regulating immune functions and musculoskeletal metabolism. Administration of vitamin D3 to animals with autoimmune thyroiditis showed an immediate improvement in thyroid inflammation and symptoms.[31]

2. Avoid Thyroid Endocrine Disruptors

Many pollutants, medications and food components serve to disrupt thyroid function and promote thyroid diseases. Where possible, it’s important to avoid these substances to ensure optimal thyroid function:

  • Anti-Nutrients are non-nutritional components of food that typically oppose the function of nutrients. Some antinutrients have been associated with disrupting thyroid function[32], while others have been shown to prevent thyroid disruption by inhibiting the absorption of toxins[33]. While not possible to avoid in many kinds of food, the consumption of antinutrients can be limited through proper food preparation and cooking. Examples of antinutrients include phytates, lectin, oxalates and saponins. They are most commonly found in whole grains, seeds, and the skins of fruits and vegetables.
  • Goitrogens refer to any nutrient that inhibits the uptake of iodine and that promotes goiter or thyroid dysfunction[34]. Many whole foods contain goitrogens in negligible quantities and are not a cause for concern. Soy and foods from the cruciferous family of vegetables tend to contain higher levels of goitrogenic compounds, which can be reduced through proper cooking. Similar foods include millet, cassava, peanut oil, bamboo shoots, water hyacinth, onion and garlic. Sulfites and E. Coli metabolites may also pose goitrogenic effects.[35]
  • Chemical Pollutants are known to disrupt thyroid function and include plastic compounds, pesticides and heavy metals. Examples of such compounds include PCB’s, PBDE’s, phthalates, BPA, perchlorate, organophosphates, DDT, pyrethroids, nitrates, cadmium, lead, arsenic and mercury.[36] [37] Exposure to these compounds can be reduced through rinsing foods prior to cooking, opting for non-refined nutritious wholefoods, supporting gut health, living in areas with little chemical pollution, and reducing plastic use.
  • Certain Medications will inhibit thyroid function. These include: tyrosine kinase inhibitors, immune checkpoint inhibitors (chemotherapy), antithyroid drugs, lithium, iodide, amiodarone, aminoglutethimide, sunitinib, interferon, steroids, dopamine agonists, metformin, rexinoids, NSAIDs, furosemide, etc[38]. In addition to thyroid suppression, other medications may also interfere with thyroid hormone replacement therapy. It’s best to consult with your doctor about any potentially contradictory medication prior to starting therapy.

3. Exercise in Moderation

Regular, moderate-intensity exercise is an important component of maintaining overall health and well-being, with thyroid health being no exception. It is well-known that exercise is required for optimal metabolism. In healthy subjects, ordinary physical activity has been linked with stable thyroid hormone levels[39] [40].

Exercise has been shown to improve the quality of life for those with hypothyroidism[41] and thyroid cancer[42]. Studies on athletes reveal that intensive exercise is able to increase thyroid hormone expression[43] [44] and suggest that exercise may be beneficial for those with hypothyroidism. In Grave’s Disease patients, regular structured exercise improved their thyroid hormone profile and reduced the need for antithyroid medication after 6 months.[45]

Nonetheless, those who already have thyroid disease are usually exercise intolerant. Therefore, patients ought to exercise with caution and avoid overexertion[46].

4. Limit Radiation Exposure

Radiation exposure serves to increase the risk for all thyroid diseases and ought to be minimized for optimal thyroidal function. Radioactive sources documented to promote disease usually emit ionizing radiation and include radiotherapy, X-rays and nuclear fallout.

A recent meta-analysis of research papers revealed that non-ionizing mobile phone radiation is capable of inducing thyroid hormone insufficiency and of disrupting the hypothalamic-pituitary-thyroid axis.[47] Electronic devices that emit similar types of radiation, such as microwave ovens, computers, televisions and laptops, may also be capable, but to a lesser degree due to being less in contact with the head and neck. Animal studies suggest that children may be particularly susceptible to the effects of non-ionizing radiation.[48]

5. Maintain a Stable Circadian Rhythm

The release of thyroid hormone is dependent on circadian signaling, which regulates and is regulated by signals from both the hypothalamus and pituitary gland. Sleep disturbances are able to disrupt circadian signaling and affect the function of these brain structures, resulting in abnormal thyroid function and hormone release. Both long and short sleep durations were associated with incidence of thyroid disease[49]. Likewise, thyroid disorders promote sleep disruptions.[50]

Getting to bed at the right time and making sure to get 7-9 hrs sleep is vital to the function of the thyroid. Exposure to natural light during the day and less exposure to artificial light at night are also able to help with regulating sleep.

When to see a doctor about your Thyroid

Thyroid problems typically affect all systems of the body and may therefore be difficult to identify alone. However, the symptoms are likely to be persistent and resistant to the implementation of healthy lifestyle measures.

If you find that you are constantly fatigued, battling to breathe or perform basic tasks, are experiencing rapid weight gain or loss, are having difficulty with regulating temperature, are predisposed to rapid mood swings, or have a swollen throat; then you ought to consult with a healthcare physician about your symptoms.

Conclusion

The thyroid gland plays an extensive role in the majority of cellular processes, as it is a regulator of energy metabolism. The most common thyroidal illnesses are hypothyroidism and hyperthyroidism, which pertain to thyroid hormone deficiency and excess respectively. Women, elderly individuals, those with autoimmune or metabolic diseases and those that lead an unbalanced lifestyle are at the highest risk for contracting thyroidal illness. Exercising, sleeping adequately, and consuming a healthy, nutritionally-balanced diet all serve to maintain optimal thyroid function. Limiting exposure to environmental pollutants and radiation also contribute towards improved thyroid health and help to lower the risk for disease.

If thyroid disease is suspected, it’s best to consult with your healthcare practitioner about a comprehensive protocol that suites your needs.

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