Introduction

Hashimoto's thyroiditis is an autoimmune condition in which the cells of the thyroid are destroyed. Initially the destruction of the thyroid cells causes a release of larger than normal amounts of thyroid hormone, resulting in transient acute hyperthyroidism. As destruction of the thyroid cells continues, eventually too few cells will remain to produce normal amounts of thyroid hormone and the patient will develop a hypothyroid state.

Hashimoto's thyroiditis is associated with other autoimmune conditions, such as:

  • Adrenal insufficiency (Schmidt's syndrome)
  • Inflammatory bowel disease
  • Celiac disease
  • Pernicious anemia
  • Diabetes Mellitus type I
  • Graves disease

Please see conventional, complementary, and alternative medical treatments for important background information regarding the different types of medical treatments discussed on this page. Naturopathic, Complementary, and Alternative treatments that may be considered include:

Epidemiology

[Taylor2024] states that Hashimoto's thyroiditis is now the most common cause of hypothyroidism, although historically the most common cause was iodine deficiency.

According to [Wyne2022  🕮 ], the prevalence of [diagnosed] cases of Hashimoto's thyroiditis in the United States has "significantly increased over the past two decades." Medical claims data as of 2019, suggests that 11.7% of the US population is affected by Hashimoto's thyroiditis, which increases with age, as shown below:

Prevalence
18-29 1.7%
30-39 4.2%
40-49 7.2%
50-59 11.2%
60+ 17.8%
The data also shows that 76.1% of the patients [treated] for Hashimoto's thyroiditis were female, and that 14.4% of persons diagnosed with Hashimoto's thyroditis were untreated.

See also [Vanderpump2011] [Ragusa2019  🕮 ] and [Taylor2018  🕮 ].

Pathophysiology

The exact cause of the autoimmune condition is unknown, but naturopaths and functional medicine practioners think that leaky gut syndrome, dysbiosis, and food allergies may play an important role both in initiating and maintaining the autoimmune process.

Hashimoto's thyroiditis is due to an autoimmune process that results in inflammatory damage to the thyroid follicles that store thyroid hormones (T4 and T3). This damage causes excess amounts of T4 and T3 to be released into the bloodstream, causing hyperthyroid symptoms. The elevated T4 and T3 levels exert a negative feedback effect on the pituitary, causing a suppression of TSH. This phase may last several weeks.

As the inflammation continues to destroy more thyroid follicles, the thyroid gland's ability to make and store T4 and T3 declines until the thyroid gland is incapable of maintaining an euthyroid state, and the temporary (acute) hyperthyroid state transitions through a subacute phase in which TSH may be elevated, while T4 and T3 remain within the reference range. This state may resolve within a year, or may progress to a chronic hypothyroid state that is characterized by depressed T4 and T3 levels accompanied by elevated TSH and symptoms of a hypothyroid state which may be permanent.

If left untreated, the chronic elevation in TSH may stimulate hypertrophy of the thyroid gland, resulting in goiter. Treatment with appropriatly titrated amount of thyroid hormone replacement therapy will lower TSH and prevent formation of the goiter.

Susceptibility to subclinical thyroiditis has been associated with the Human Leukocyte Antigen genes HLA-B*35, HLA-B*18:01, HLA-DRB1*01 and HLA-C*04:01 [Stasiak2021  🕮 ].

New onset of subclinical thyroiditis has been associated with viral infection 2–6 weeks prior in genetically predisposed individuals. A number of viruses have been implicated, including Coxsackie, Echo, adenoviruses, influenza, measles, mumps, rubella, parvovirus B19, orthomyxovirus, HIV, Epstein-Barr, hepatitis E, Dengue, and SARS. In particular, SARS-CoV-2 exhibits high affinity to thyroid tissue [Stasiak2021  🕮 ].

Clinical Presentation

  • Chronic hypothyroid signs/symptoms: fatigue, weakness, cold intolerance, decreased memory, constipation, muscle and joint pain, hoarseness, weight gain, dry skin and sparse hair, depression, carpal tunnel syndrome, decreased sweating, swollen tongue, eyes, hands and feet, burning, prickling, itching, or tingling sensations, and hearing impairment. Slow heart rate, decreased pulse pressure, low body temperature, delayed relaxation of deep tendon reflexes.
  • Acute hyperthyroid signs/symptoms: Nervousness and emotional distress, shortness of breath, increased sweating and heat intolerance, night sweats, rapid heart rate, heart palpitations, fatigue, weakness, weight loss despite increased appetite, tremors or inward trembling [Kharrazian2010], atrial fibrillation, loss of bone density, bulging eyes (exophthalmos).
  • Physical Exam: Thyroid gland is usually non-tender, diffusely enlarged with fine nodularity, possibly asymmetrically.

Diagnosis

  • Hashimoto's thyroiditis may present as:
    • an acute hyperthyroid condition (low TSH, high free T4),
    • a chronic hypothyroid condition in the standard thyroid screening panel (TSH, low free T4),
    • as a subclinical hypothroid condition (high TSH while T4 and T3 remain within their reference ranges). [Stasiak2021  🕮 ] has noted a correlation between subclinical Hashimoto's thyroiditis and COVID19.
  • Elevated anti-thyroperoxidase (TPO) levels (95%).
  • Elevated antithyroglobulin antibodies (60-80%).
  • Hashmoto's thyroiditis has characteristic features under ultrasound that can aid in excluding other forms of thyroiditis [Wang2023].
  • Thyroid gland nodularities upon palpation merit further evaluation (to rule out concomitant cancer) with ultrasound or fine needle biopsy, especially if isolated or unilateral, or patient has a history of head/neck radiation exposure.
  • Follow-up labs for associated conditions:
    • CBC (anemia).
    • Lipid panel (elevated cholesterol).
    • Metabolic Chemistry Panel (elevated CPK [creatine phosphokinase], LDH, AST, Hyponatremia).
    • IgA anti-endomysial antibodies and IgA tissue transglutaminase (Celiac).
    • Adrenal Stress Index (adrenal insufficiency).
    • Intestinal Permeability Test (leaky gut) [Naturopathic/Functional medicine only].
    • Food Allergy Test (autoimmune triggers) [Naturopathic/Functional medicine only].
    •  >   
      Organic Acid Test (gut dysbiosis)[Naturopathic/Functional medicine only].

Differential Diagnosis

  • With hyperthyroid symptoms:
    • Acute phase Hashimoto's thyroiditis: Depressed TSH and elevated T4, elevated TPOAb or TgAb, but not TSI.
    • Grave's disease: Depressed TSH and elevated T4 and TSI but not elevated TPOAb or TgAb.
    • Pituitary tumor: Elevated TSH and elevated T4.
    • Pheochromocytoma: Elevated 24-hour urine VMA, catecholamines, and metanephrine.
    • Toxic multi-nodular goiter: (Iodine deprivation followed by repletion).
  • With hypothyroid symptoms:
    • Iodine-deficient goiter.
    • Drug-induced: Lithium, amiodarone, propylthiouracil, methimazole, phenylbutazone, sulfonamides, interferon-alpha, iodine, aminosalicylic acid, aminoglutethimide.
    • Genetic.
    • Ablation of thyroid gland.
    • Subacute thyroiditis: Elevated Erythrocyte Sedimentation Rate (ESR) and low antithyroid antibody titer.
    • Pregnancy or post-partum.

Differential Diagnosis

  • With hyperthyroid symptoms:
    • Acute phase Hashimoto's thyroiditis: Depressed TSH and elevated T4, elevated TPOAb or TgAb, but not TSI.
    • Grave's disease: Depressed TSH and elevated T4 and TSI but not elevated TPOAb or TgAb.
    • Pituitary tumor: Elevated TSH and elevated T4.
    • Pheochromocytoma: Elevated 24-hour urine VMA, catecholamines, and metanephrine.
    • Toxic multi-nodular goiter: (Iodine deprivation followed by repletion).
  • With hypothyroid symptoms:
    • Iodine-deficient goiter.
    • Drug-induced: Lithium, amiodarone, propylthiouracil, methimazole, phenylbutazone, sulfonamides, interferon-alpha, iodine, aminosalicylic acid, aminoglutethimide.
    • Genetic.
    • Ablation of thyroid gland.
    • Subacute thyroiditis: Elevated Erythrocyte Sedimentation Rate (ESR) and low antithyroid antibody titer.
    • Pregnancy or post-partum.

Management

Conventional Treatments

Acute hyperthyroid condition

When anti-TPO or anti-Tg antibodies are present, treatment is different from that of Graves' disease. Since elevated T4 is due to destruction of thyroid tissue, rather than the action of TSI, treatment with antithyroid drugs methimazolem propylthiomethimazole, radioactive iodine, etc are not indicated. Instead, beta-blockers such as propranolol or atenolol can provide symptomatic relief. Continue monitoring TSH, T4, and symptoms every 4-6 weeks, because at some point the acute hyperthyroid phase will transition to the chronic hypothyroid phase, requiring different treatment [? cite].

Chronic hypothyroid condition

If the patient is symptomatic or TSH > 10 mIU/L, the standard of care recommended by the Go to external Internet siteAmerican Thyroid Association is hormone replacement therapy with approximately 1.6mcg/Kg/day of levothyroxine. Dosing should start low and slowly increase to the a target of TSH within the reference range and (free) T4 and T3 in the upper half of the reference rangen [? cite]. Continued monitoring of antibody levels is unnecessary; but TSH levels should be checked every 6–12 months. Special considerations for infants, children, elderly, and pregnant patients are discussed in [Kaur2025], [Quintero2021  🕮 ], [Ross2016  🕮 ], [Sweeney2014  🕮 ], [Pearce2003  🕮 ], Go to external Internet siteATA.

Subclinical hypothroid condition

Subclinical hypothroid is also called granulomatous thyroiditis or de Quervain`s thyroiditis [Stasiak2021  🕮 ].

The ATA does not recommend active treatment of subclinical hypothyroid conditions, but instead watchful waiting while monitoring TSH [and free T4] every 6 to 12 months [Sweeney2014  🕮 ], Go to external Internet siteMedscape, [Stasiak2021  🕮 ], [Fatourechi2003  🕮 ].

Secondary hypothroid condition

In cases of pituitary failure, TSH is an unreliable guide, so the ATA recommends that treatment should aim to maintain free-thyroid hormones in the upper half of the reference range.

Naturopathic, Complementary, and Alternative Treatments

    Nutritional Medicine

    Naturopathic philosophy prioritizes removing obstacles to cure. While individual needs and case management strategies may vary, it is a good idea to address nutritional deficiencies early in the treatment plan. In particular, when treating Hashimoto's thyroditis, the following nutrients should be optimized:

  • Treat adrenal insufficiency first, if present (supplementing T4 or T3 in the presence of adrenal insufficiency is contraindicated).
  • Hormone replacement therapy: Start with 1.6mcg/Kg/day levothyroxine (T4, Synthroid, Levothroid) and titrate up 25mcg/day every 4-6 weeks until TSH is normalized. Some patients get better results with a T4/T3 blend from a compounding pharmacy). Drug interactions with thyroid HRT requiring dosage adjustments: oral anticoagulants, insulin, oral hypoglycemics, estrogens and oral contraceptives, cholestyramine, iron and calcium supplements. Start with 33% lower doses in the elderly.
  • Gluten-free diet if Celiac is a comorbidity [Kharrazian2010].
  • Treat dyslipidemia (cholesterol imbalance) if present; however Dr. Weyrich notes that correcting T4 levels will often correct dyslipidemia without further intervention.
  • Treat dysbiosis if present.
  • Heal the leaky gut if present.
  • Identify and avoid problem foods.

Low Dose Naltrexone (LDN)

According to the Low Dose Naltrexone home page [LDN], LDN has been seen to benefit Hashimoto's thyroiditis, which is considered to be an autoimmune disease.

Dr. Weyrich has been trained to use Low Dose Naltrexone (LDN) and offers these protocols as a complement to other therapies; however, at this time Dr. Weyrich has only treated one confirmed case of Hashimoto's thyroiditis using LDN (in addition to thyroid hormone replacement therapy). The patient reported significant improvement in symptoms, and auto-antibody markers were seen to be substantially reduced.

Please see What is Low Dose Naltrexone? for more information.

Immune System Balancing

[McCulley2018, pp 28, 35, 61, 89] reports that Hashimoto's thyroiditis is a TH1-dominant, localized, autoimmune disorder, and proposes an approach to treating this disease, which should be supervised by a properly trained medical professional. Dr. Weyrich has considerable interest in this topic, and has treated several cases of Hashimoto's thyroiditis with Immune System Balancing.

Please see What is Immune System Balancing? for more information.

ICD-10

References