Thyroid Health

Thyroid Health: A Nutritional and Natural-Health Reference

1. Definition and Overview

The thyroid gland is a vital endocrine (hormone-producing) gland that plays a major role in the metabolism, growth, and development of the human body. It is a small, butterfly-shaped gland located at the front of the neck under the skin, and is a part of the endocrine system that controls many of the body's important functions by producing and releasing certain hormones. The thyroid gland is found at the front of the neck, under the voice box; it is butterfly-shaped, with the two lobes on either side lying against and around the windpipe (trachea), and connected at the front by a narrow strip of tissue known as the isthmus.

The gland functions as an endocrine organ, producing thyroid hormone and calcitonin, thereby regulating metabolism, growth, and serum calcium concentrations. It plays an essential role in regulating the basal metabolic rate (BMR) and stimulating somatic and psychic growth, besides having a vital role in calcium metabolism.

The thyroid gland secretes three hormones: the two thyroid hormones — triiodothyronine (T3) and thyroxine (T4) — and a peptide hormone, calcitonin. The thyroid hormones influence the metabolic rate and protein synthesis and growth and development in children. Calcitonin plays a role in calcium homeostasis.

2. Hormone Synthesis and the HPT Axis

The thyroid produces approximately 90% inactive thyroid hormone, or thyroxine (T4), and 10% active thyroid hormone, or triiodothyronine (T3). T4 is converted to T3 peripherally by type 1 deiodinase in tissues with high blood flow, such as the liver and kidneys. In the brain, T4 is converted to active T3 by type 2 deiodinase produced by glial cells. The third iodothyronine is called reverse T3, or rT3; rT3 is inactive and forms by type 3 deiodinase activity on T4.

These iodothyronines are composed of thyroglobulin and iodine. Thyroglobulin is formed from amino acids in a basal to apical fashion within the thyroid cells. Like the catecholamines epinephrine and norepinephrine, thyroid hormones are synthesized from the amino acid tyrosine. The synthesis of thyroid hormones requires the iodination of tyrosine molecules and the combination of two iodinated tyrosine residues.

Regulation of thyroid hormone starts at the hypothalamus. The hypothalamus releases thyrotropin-releasing hormone (TRH) into the hypothalamic-hypophyseal portal system to the anterior pituitary gland. TRH stimulates thyrotropin cells in the anterior pituitary to release thyroid-stimulating hormone (TSH). The pituitary gland uses the hormone TSH to control the amount of hormones the thyroid gland releases into the bloodstream. This represents the hypothalamic-pituitary-thyroid (HPT) axis, a classic endocrine feedback loop.

Thyroid hormones affect the following bodily functions: how the body uses energy (metabolism), heart rate, body temperature, brain development, mental activity, and skin and bone maintenance.

3. Principal Thyroid Conditions

3.1 Hypothyroidism

Hypothyroidism is a very common endocrine disorder that causes under-secretion of thyroid hormones, mainly thyroxine (T4) and triiodothyronine (T3). It affects people of every age group but is more commonly found in women and older people. The National Health and Nutrition Examination Survey (NHANES III) study found the prevalence of overt hypothyroidism among individuals aged 12 years and older in the US to be 0.3%, and subclinical hypothyroidism 4.3%.

The symptoms of hypothyroidism can go unnoticed, may not be specific, and may overlap with other conditions. Common symptoms include fatigue, weight gain, increased sensitivity to cold (cold intolerance), irregular bowel movements (constipation), and dry skin. A thorough inquiry into a patient's symptoms should be performed, including dry skin, voice changes, hair loss, constipation, fatigue, muscle cramps, cold intolerance, sleep disturbances, menstrual cycle abnormalities, weight gain, and galactorrhea.

Nearly all the major organs are affected by hypothyroidism, but the cardiovascular system has been most extensively researched. Patients present with an increase in vascular resistance, a diminishing of left ventricular function, and lower cardiac output. Patients with hypothyroidism frequently have symptoms of metabolic syndrome, such as increased blood pressure, waist circumference expansion, and elevated cholesterol levels (dyslipidemia), as well as a greater incidence of cardiovascular risk factors.

The most common cause of hypothyroidism in the developed world is Hashimoto's thyroiditis. In addition to cell-mediated destruction, anti-thyroid autoantibodies (anti-thyroglobulin and anti-TPO) are produced, leading to antibody-dependent cell-mediated cytotoxicity. During the early stage of the disease, the patient may develop a non-tender, symmetrical, and painless goiter. As inflammation continues, thyroid follicles are damaged and can rupture. When thyroid follicles rupture, the patient may be asymptomatic or can experience hashitoxicosis. As the disease progresses, the thyroid gland may become normal-size or small, depending on the extent of fibrosis, and the patient can develop the symptoms of hypothyroidism.

Autoimmune thyroiditis (Hashimoto's) is associated with other immune-mediated diseases such as diabetes mellitus type 1, pernicious anemia, myasthenia gravis, celiac disease, rheumatoid arthritis, and systemic lupus erythematosus. In the developing world, the most common cause of hypothyroidism is iodine deficiency.

3.2 Hyperthyroidism

Common symptoms of hyperthyroidism include heat intolerance, excessive sweating, tachycardia, palpitations, anxiety, unintentional weight loss, tremor, menstrual irregularities, and ocular findings such as exophthalmos and diplopia. In excess, thyroid hormones both overstimulate metabolism and disrupt the normal functioning of the sympathetic nervous system, causing speeding up of various body systems and symptoms resembling an overdose of epinephrine (adrenaline).

Hyperthyroidism is characterized by excessive secretion of thyroid hormones; the most common cause is the autoimmune disorder Graves' disease. Graves' disease is an autoimmune disease caused by the production of TSH receptor antibodies that stimulate thyroid gland growth and thyroid hormone release.

3.3 Goiter and Thyroid Nodules

Sometimes the whole thyroid gland becomes enlarged (diffuse goiter), and sometimes individual lumps called nodules grow in the gland (nodular goiter). Common etiologies for goiter include iodine deficiency, hyperthyroidism, and hypothyroidism.

4. Contributing and Associated Factors

4.1 Autoimmune Factors and Genetic Susceptibility

Autoimmune thyroid diseases are polygenic diseases resulting from a combination of genetic predisposition (thyroid-specific genes and immune-modulating genes) and environmental triggers (iodine, selenium, drugs, irradiation, smoking, infections, stress, etc.), characterized by lymphocytic infiltration into the thyroid gland and production of thyroid-specific autoantibodies. Although the etiology of Hashimoto's thyroiditis is not known exactly, it is thought to be related to the interaction between genetic factors, environmental factors, and epigenetic effects, and is 7–10 times more common in women than in men.

4.2 Iodine Status (Deficiency and Excess)

Iodine is an important substance that is needed to make the thyroid hormones T3 and T4. The body cannot produce this trace element, so adequate amounts must be obtained through the diet. Iodine is absorbed into the bloodstream from food in the bowel and then carried to the thyroid gland, where it is used to make thyroid hormones. Lack of iodine in the diet leads to hypothyroidism.

Iodine exhibits a classic dual role in autoimmune thyroid disease, characterized by a U-shaped dose-response curve. Chronic exposure to excess iodine intake induces autoimmune thyroiditis, partly because highly iodinated thyroglobulin (Tg) is more immunogenic. For this reason, the American Thyroid Association recommends avoiding supplements containing more than 500 μg/day of iodine.

4.3 Sex and Age

The NHANES III study found the prevalence of overt hypothyroidism in the US to be 0.3% and subclinical hypothyroidism 4.3%. Female gender and increasing age are associated with a higher risk for abnormal TSH and an increased prevalence of antithyroid antibodies. Autoimmune destruction of follicular cells often affects women at rates up to 7 times higher than men.

4.4 Gut Microbiota and the Diet–Gut–Thyroid Axis

Thyroid function is closely linked to nutrition through the diet–gut–thyroid axis. This narrative review highlights the influence of nutritional components and micronutrients on thyroid development and function, as well as on the gut microbiota. Dietary changes can alter the gut microbiota, leading not just to dysbiosis and micronutrient deficiency but also to changes in thyroid function through immunological regulation, nutrient absorption, and epigenetic changes. Nutritional imbalance can lead to thyroid dysfunction and/or disorders, such as hypothyroidism and hyperthyroidism, and possibly contribute to autoimmune thyroid diseases.

4.5 Pregnancy

If the body needs more energy in certain situations — for instance, if it is growing or cold, or during pregnancy — the thyroid gland produces more hormones. After women give birth, about 5% develop postpartum thyroiditis, which can occur up to nine months afterwards. This is characterized by a short period of hyperthyroidism followed by a period of hypothyroidism; 20–40% remain permanently hypothyroid.

5. Key Nutrients in Relation to Thyroid Health

Micronutrients such as iodine, selenium, iron, zinc, copper, magnesium, vitamin A, and vitamin B12 influence thyroid hormone synthesis and regulation throughout life.

5.1 Iodine

Role and evidence: In order to make thyroid hormones, the thyroid gland needs iodine, an element found in food (most commonly iodized table salt) and water. The thyroid gland traps iodine and transforms it into thyroid hormones. If there is too little or too much iodine in the body, it can affect the level of hormones the thyroid makes and releases. The normal European daily dietary intake of iodine is about 150 μg, of which approximately 125 μg is taken up by the thyroid gland and used for hormone synthesis.

The role of iodine deficiency as a global cause of goiter and hypothyroidism is among the most firmly established relationships in nutritional endocrinology. Significant success was observed in the management of thyroid disorders with the worldwide iodization of salt in the late 20th century. Research has found that many supplements are mislabeled and do not contain the iodine content stated on the label.

5.2 Selenium

Role: Selenium is an essential trace element required for thyroid hormone synthesis and exerts antioxidant effects. Selenium and iodine have a synergistic relationship that is especially important for a healthy thyroid. Iodine is a component of thyroid hormone, and selenium as a selenoprotein helps to convert the thyroid hormone into its active form. Both minerals are needed by the thyroid in adequate amounts; too much of one can contribute to a deficiency of the other.

Scientific evidence — Hashimoto's thyroiditis: A 2024 systematic review and meta-analysis (Huwiler et al., published in Thyroid) examined 35 randomized controlled trials. The meta-analysis showed a significant decrease in TPOAb (SMD −0.96 [CI −1.36 to −0.56]; 29 cohorts; 2,358 participants; I² = 90%) after selenium supplementation. However, of the 31 cohorts that reported on TPOAb, 10 (32%) observed a significant decrease in TPOAb titers, while 21 (68%) found no significant effect after selenium supplementation compared with the control group. No significant changes were observed in fT4, T4, fT3, T3, TGAb, thyroid volume, interleukin-2, and IL-10. Overall, certainty of evidence was moderate.

A second 2025 meta-analysis across 21 RCTs with 1,610 participants reported: serum TPOAb was significantly reduced after selenium supplementation after 3 months (SMD = −0.46, 95% CI: −0.74 to −0.18, P = .001) and 6 months (SMD = −0.80, 95% CI: −1.38 to −0.21, P = .008). Serum TgAb levels decreased at 3 months but not at 6 months. The etiology of HT is multifactorial, with selenium deficiency being a potential contributing factor. However, the exact role of selenium in HT pathogenesis remains unclear, and further research is needed.

Limitations: High heterogeneity between studies (I² = 90%) is a consistent finding. Of the studies that checked blood selenium levels at baseline, participants were severely selenium-deficient in 50%, mildly deficient in 39%, and only selenium-sufficient in 11%. This suggests the benefit may be conditional on prior deficiency status. Adequate selenium intake is considered vital in areas of iodine deficiency or excess, and in regions of low selenium intake a supplement of 50–100 μg/day of selenium may be appropriate.

5.3 Iron

Inadequate intake of iodine impairs thyroid function and results in a spectrum of disorders. Other common deficiencies of micronutrients such as iron, selenium, vitamin A, and possibly zinc may interact with iodine nutrition and thyroid function. Randomized controlled intervention trials in iodine- and iron-deficient populations have shown that providing iron along with iodine results in greater improvements in thyroid function and volume than providing iodine alone. Treatment of anemic women with impaired thyroid function with iron improves thyroid-hormone concentrations, while thyroxine and iron together are more effective in improving iron status.

With regard to nutritional factors, evidence implicates high iodine intake and deficiencies of selenium and iron, with a potential relevance of vitamin D status, in Hashimoto's thyroiditis.

5.4 Zinc

Regarding zinc, there is limited evidence of its relationship with iodine status, although zinc is essential for proper thyroid function. Animal research has shown combined deficiencies of selenium, zinc, and iodine have compounding effects: serum T3 was significantly lower than in controls in zinc-deficient, selenium-zinc-deficient, and selenium-iodine-deficient groups. Single and multiple deficiencies of selenium, zinc, and iodine have distinct effects on thyroid metabolism and structure; however, these findings are largely from animal models, and human evidence is limited.

5.5 Vitamin D

Recent evidence suggests that vitamin D deficiency, which is common worldwide, could have non-skeletal actions including an important role in autoimmune diseases, cancers, metabolic syndromes, and cardiovascular disease. Low levels of vitamin D have also been associated with autoimmune thyroid diseases (AITD) such as Hashimoto's thyroiditis (HT) and Graves' disease (GD).

A meta-analysis including 25 studies comprising 2,695 cases and 2,263 controls showed that Hashimoto's thyroiditis patients had lower vitamin D serum levels compared to control groups; however, there was significant heterogeneity between the studies. Lower vitamin D status has been found in HT patients than in controls, and inverse relationships of serum vitamin D with TPO/Tg antibodies have been reported. However, other data and the lack of trial evidence suggest that low vitamin D status is more likely the result of autoimmune disease processes that include vitamin D receptor dysfunction.

Supplementation evidence: A study reported that supplementation with cholecalciferol (vitamin D3) significantly reduced TPO antibody levels in vitamin D-deficient patients with Hashimoto's thyroiditis, indicating an improvement in autoimmune activity. However, the effect of vitamin D on thyroid function appears to vary significantly across different studies. Only three of the included studies in one systematic review demonstrated significant changes in TSH levels, indicating the need for further research to establish a definitive conclusion.

5.6 Vitamin A

Vitamin A supplementation given alone or in combination with iodized salt can have a beneficial impact on thyroid function and thyroid size. This evidence comes primarily from studies in iodine-deficient populations and is considered preliminary.

6. Herbs and Botanical Ingredients

6.1 Ashwagandha (Withania somnifera)

Traditional use: Ashwagandha (Withania somnifera), a traditional medicine in Ayurveda, is often prescribed for thyroid dysfunctions. Withania somnifera has been used in traditional medicine for thousands of years. Due to the wide range of its activities, there has been interest in its possible beneficial effects on the human body.

Scientific evidence: A prospective, randomized, double-blind, placebo-controlled study was performed in India. Fifty subjects with elevated serum TSH levels (4.5–10 μIU/L) aged between 18 and 50 were randomized in either a treatment (n = 25) or placebo (n = 25) group for an 8-week treatment period. The intervention was ashwagandha root extract (600 mg daily) or starch as placebo. Eight weeks of treatment with ashwagandha improved serum TSH (p < 0.001), T3 (p = 0.0031), and T4 (p = 0.0096) levels significantly compared to placebo.

Ashwagandha appears to elevate thyroid hormones in hypothyroid contexts. However, there is a case report of ashwagandha treatment associated with thyrotoxicosis, a hypermetabolic syndrome where excess thyroid hormones are produced and released into the blood. Evidence is limited to small single-center trials and requires replication in larger, more diverse populations.

6.2 Bugleweed (Lycopus europaeus / Lycopus virginicus)

Traditional use: Bugleweed is a traditional herbal medicine that has been used to treat the tremors and rapid heartbeat associated with hyperthyroidism. Bugleweed can be taken as tea or tincture and is used to relieve some of the symptoms associated with an overactive thyroid gland, such as a rapid pulse, palpitations, nervousness, anxiety, and insomnia.

Scientific evidence: A 2019 review concluded that bugleweed exhibited actions correlating with its use in both traditional and modern herbal practices, including endocrine modulation; particularly with regard to the thyroid. The study suggests that rosmarinic acid, a predominant constituent found in bugleweed, has significant actions on thyroid function. Lemon balm has been shown in vitro to interact with and prevent the binding of autoantibodies to the TSH receptor. Freeze-dried and aqueous extracts of related herbs have demonstrated TSH-binding and hormone conversion-preventing effects in vitro. Studies dating back to the 1950s support the current clinical usage of this herb, having evidenced its efficacy for reducing the symptoms of hyperthyroidism including cardiac-related symptoms. Overall, human clinical trial data remain sparse, and existing evidence is primarily preclinical or observational.

6.3 Lemon Balm (Melissa officinalis)

Traditional use: Lemon balm is a perennial herb belonging to the mint family, celebrated for its gentle lemon scent and long history of use in herbal medicine. The lemon balm plant has been traditionally valued as a calming herb.

Scientific evidence: Lemon balm has been shown in vitro to interact with and prevent the binding of autoantibodies to the TSH receptor, suggesting the plant may have some use in Graves' disease. The mechanism of action may be inhibition of TSH-stimulated cyclic adenosine monophosphate (cAMP) production. Another in vitro study revealed that aqueous extract of lemon balm inhibited the peripheral conversion of T4 to T3. No human trials have yet evaluated the efficacy of lemon balm for hyperthyroidism.

A case report described two women with overactive thyroid who were treated with herbal remedies including lemon balm and bugleweed: in the first case, a 64-year-old woman with Graves' disease took an herbal combination of lemon balm and bugleweed for nine months, and her thyroid tests both improved and then remained normal, without the need for any other thyroid medication. These are case reports only and do not constitute controlled evidence.

6.4 Bladderwrack (Fucus vesiculosus)

Traditional use: Bladderwrack is a seaweed or kelp rich in organically bound iodine, which is considerably more potent at stimulating the thyroid gland than mineral iodine. It has been traditionally used for the treatment of low thyroid function and to aid in weight loss when associated with hypothyroidism, as iodine can stimulate the production of thyroxine and increase the body's basal metabolic rate.

Scientific evidence: Bladderwrack occupies a unique place in therapy in that the herb is used for treating both hyperthyroidism and hypothyroidism, although the seaweed's effects are poorly understood. Its primary mechanism of action is iodine provision. Bladderwrack should only be used sparingly and under medical supervision, as excessive iodine consumption can be hazardous and exacerbate some thyroid problems. Formal clinical trials in human populations are lacking.

6.5 Motherwort (Leonurus cardiaca)

Traditional use and regulatory status: Motherwort is traditionally known as a heart tonic and uterine stimulant. It is approved by the German Commission E for nervous cardiac disorders and as an adjuvant for thyroid hyperfunction. In vitro the plant has demonstrated negative chronotropic effects. There are no complete studies in humans for motherwort.

6.6 Myo-Inositol

Myo-inositol (myo-Ins) has gained much attention in recent years due to its endocrinological function in modulating insulin, FSH, and importantly TSH activity. Research discusses the use of myo-Ins in autoimmune thyroiditis, reporting that myo-Ins administration combined with selenium induces immunomodulatory effects by reducing levels of thyroid antibodies, pro-inflammatory chemokines, and oxidative stress. A deficiency in myo-Ins was associated with increased cancer risk, while myo-Ins and selenium supplementation reduced thyroid nodule size, number, and elasticity. Evidence to date is preliminary and largely from small trials.

7. Dietary Factors

7.1 Goitrogenic Foods: Cruciferous Vegetables

The term "goitrogen" refers to any substance that can produce goiter, the enlargement of the thyroid gland. Glucosinolates, found in cruciferous vegetables like broccoli, cabbage, kale, and Brussels sprouts, can break down into isothiocyanates, which inhibit iodine uptake by the thyroid. These compounds can inhibit the uptake of iodine, which is essential for thyroid hormone production.

The enzyme that creates these iodine-blocking compounds when vegetables are chopped is rapidly deactivated by cooking, so there is less concern about eating too many cooked crucifers. In individuals with sufficient iodine intake, moderate consumption of goitrogenic foods is unlikely to cause significant thyroid dysfunction. However, in people with an iodine deficiency or those who already have an underactive thyroid, excessive consumption of goitrogens could exacerbate thyroid problems. There is currently very little evidence about what is "reasonable" regarding cruciferous vegetable consumption and thyroid health.

7.2 Goitrogenic Foods: Soy

Dietary soy products — including soy milk, tofu, soy sauce, tempeh, and miso — contain isoflavones. Because isoflavones can inhibit the action of thyroid peroxidase, which is required for thyroid hormone synthesis, it has been proposed that dietary soy intake may increase the risk for hypothyroidism in euthyroid individuals, or that a higher dose of thyroid hormone replacement may be required in patients being treated for hypothyroidism. There is little evidence that soy isoflavones present a problem for people with normal thyroid function who are getting enough iodine.

7.3 Gluten and Autoimmune Thyroiditis

Hashimoto's thyroiditis is the most common autoimmune disease. It may be associated with non-thyroidal autoimmune diseases, including celiac disease or other gluten-related conditions. In recent years, interest in the gluten-free diet has increased for its supposed extra-intestinal anti-inflammatory effect; thus, many patients with HT initiate a gluten-free diet on their own.

A pilot study found that the gluten-free diet reduced thyroid antibody titers, as well as slightly increased 25-hydroxyvitamin D levels. The results suggest that the gluten-free diet may bring clinical benefits to women with autoimmune thyroid disease. However, when analyzing the available literature, researchers found no basis for introducing a gluten-free diet for the standard management of all Hashimoto's patients. There is insufficient evidence to support a gluten-free diet for all HT patients.

7.4 Mediterranean and Anti-Inflammatory Dietary Patterns

The recommended dietary approach for Hashimoto's is an anti-inflammatory diet that levels the supply (to compensate for deficiencies) of vitamin D, iodine, and selenium, which are found in plant products rich in polyphenols, antioxidants, and omega-3 fatty acids. Literature analysis has concluded that the Mediterranean diet has a potentially protective effect against thyroid autoimmunity and that low consumption of animal foods has a protective effect on thyroid autoimmunity.

8. Lifestyle Factors

8.1 Stress

Environmental triggers for autoimmune thyroid disease include stress, in addition to iodine, selenium, drugs, irradiation, smoking, and infections. The HPT axis is sensitive to stress-related hormonal changes, and stress-response pathways (e.g., cortisol elevation) can interact with thyroid regulation, though clinical evidence specifically quantifying this in humans remains limited.

8.2 Smoking

Smoking is recognized among the environmental triggers for autoimmune thyroid diseases. Epidemiological associations between smoking and both Graves' disease and Hashimoto's thyroiditis have been described in the literature, though causality is difficult to isolate from confounders.

8.3 Iodine Supplementation Caution

Iodine-induced thyroid dysfunction is found to be common in those who have a history of endemic iodine deficiency or pre-existing thyroid disease. Accumulating evidence indicates that early assessment and correction of trace element imbalances — particularly involving iodine, selenium, and vitamin D — may provide a cost-effective adjunct strategy to slow disease progression and improve patient outcomes.

8.4 Overall Dietary Quality

Apart from the definitive role of iodine and selenium deficiency in the causation of hypothyroidism, the role of other dietary factors in affecting thyroid health remains inconclusive based on available scientific evidence. There is still no specific diet recommended for patients with Hashimoto's thyroiditis, but a protective effect of an anti-inflammatory diet rich in vitamins and minerals and low in animal foods has been suggested. Pharmacotherapy, along with appropriate nutrition and supplementation, are important elements of medical care for patients with HT. These factors may decrease autoantibody levels, improve thyroid function, slow down the inflammatory process, maintain proper body weight, relieve symptoms, and prevent nutritional deficiencies.

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