Deep Dive Into the Complex Disease Process of Hashimoto’s Thyroiditis

Deep Dive Into the Complex Disease Process of Hashimoto’s Thyroiditis

By Maranda Gadbois, written in June 2023

Thyroid disorders have become more widely recognized over the past several years. Whether it is Grave’s disease, hypothyroidism, hyperthyroidism, autoimmune thyroiditis (Hashimoto’s thyroiditis), or thyroid cancer, it has become easier to identify these disorders due to our understanding of the thyroid gland and the hormones that it produces. These conditions can be easily identified using a simple lab test. Physicians are ordering these labs to help diagnose these conditions more regularly.

Autoimmune thyroiditis was discovered by Hakaru Hashimoto in 1912 after he discovered lymphocytes infiltrating the thyroid gland.1 Autoimmune thyroiditis, also known as chronic lymphocytic thyroiditis, will be referred to as Hashimoto’s thyroiditis throughout this article. Hashimoto’s thyroiditis is particularly interesting because there is an autoimmune component to this condition. The immune system begins to attack this vital gland and wreaks havoc on the body if left undiagnosed. This article will explain Hashimoto’s thyroiditis in detail and how it impacts the body, creates vitamin and mineral deficiencies, and the best way to manage this disease.

Primary Condition

Autoimmune thyroiditis, Hashimoto’s thyroiditis, or chronic lymphocytic thyroiditis is a complex condition. The thyroid gland is the most common gland within the body that is impacted by an autoimmune disease.2 When Hakaru Hashimoto first recognized this condition, he found that the thyroid gland was infiltrated by lymphocytes which resulted in the production of anti-thyroid antibodies.2 The thyroid gland relies on the enzymatic reaction of thyroid peroxidase to oxidize iodide to iodine in order to make thyroid hormones.2 The anti-thyroid antibodies, thyroid peroxidase antibodies (TPO Ab) are found in individuals with Hashimoto’s thyroiditis.2 These antibodies basically target the enzyme that creates thyroid hormones in the thyroid. Another form of antibodies often found in individuals with Hashimoto’s thyroiditis are called thyroglobulin antibodies (TG Ab), due to the relationship between thyroid hormones and iodination of tyrosine molecules.2

Signs and Symptoms of Hashimoto’s

Many people associate thyroid diseases with goiters, however, individuals with Hashimoto’s thyroiditis will likely not present with a goiter; although there is always exceptions and in some cases small goiters have been found3,4 The thyroid gland can present as asymmetrical and appear enlarged and firm at first glance prior to diagnosis.3 It is important to note that Hashimoto’s thyroiditis causes hyperthyroidism initially, then the thyroid is unable to produce the thyroid hormone causing hypothyroidism.3,4 The signs and symptoms of Hashimoto’s thyroiditis will present differently due to the different levels of thyroid hormone found within the individual, however, there are several common symptoms.3

Individuals commonly present with unexplained weight gain even with diminished appetite, fatigue, lethargy, depression, weakness, breathing difficulty (dyspnea) during anything that causes exertion, muscle or joint pain (arthralgias / myalgias), muscle cramps, heavy menstrual bleeding (menorrhagia), constipation, dry skin, headache, cold intolerance, carpal tunnel syndrome and Raynaud’s syndrome.3,4 There are some physical signs as well that will be seen in these patients with undiagnosed Hashimoto’s. These physical signs are low heart rate (bradycardia); diastolic hypertension; thin, brittle nails; thinning hair that is also dry; peripheral edema (also called myxedema) which causes nonpitting edema and a puffy face and eyelids; skin pallor or yellowing of the skin (carotenemia).3,4

There are some less common symptoms that present but also need to be discussed. Some individuals have a diminished appetite with weight loss, hoarseness of the voice, decreased sense of taste and smell, diminished auditory acuity, loss of eyelashes or eyebrows, thickening of the tongue, hard pitting edema, cardiac enlargement (also referred as “myxedema heart”), and even psychosis (also referred as “myxedema madness”).3 Obviously many of these symptoms are extreme and will not occur in most cases, however, there will always be exceptions. The “myxedema madness” or psychosis is usually caused when there is severe hypothyroidism and the thyroid essentially just stops working.3,4

Diagnosis of Hashimoto’s

Autoimmune thyroiditis or Hashimoto’s thyroiditis is diagnosed using lab values. Subclinical hypothyroidism is diagnosed as having an elevated TSH (thyroid-stimulating hormone) that is elevated outside of the normal range value of 0.4-4.0 mIU/L.3,4 Clinical hypothyroidism is diagnosed when TSH is >10 mIU/L and is considered more severe.3,4 The main difference between clinical hypothyroidism and Hashimoto’s thyroiditis is that there are no anti-thyroid antibodies (TPO Ab) found in someone with hypothyroidism, therefore, these anti-thyroid antibodies need to be present in an individual with an elevated TSH for a diagnosis of HT.3,4 Again, there are always exceptions to the rule and 5% of individuals with Hashimoto’s thyroiditis will have no detectable levels of TPO Ab.3 Generally, an individual will present with elevated serum TSH with either normal TPO or decreased TPO, indicating Hashimoto’s thyroiditis.3,4

Hashimoto’s thyroiditis typically has an excellent prognosis as over time as it usually progresses to hypothyroidism, which is easily manageable.3 When autoimmune thyroiditis is first detected within the body, there tends to be a passive release of stored thyroid hormones which causes hyperthyroidism.3,4 This elevates serum free T4 levels with higher than normal free T3 levels with suppressed TSH levels.3,4 Basically the thyroid gland is burned out due to hyperactivity that will switch over to underactivity leaving the individual with lasting hypothyroidism. The main difference is the autoimmune component that impacts the body as well and this should be explored further.

Hashimoto’s thyroiditis is an autoimmune disorder, therefore, an individual with Hashimoto’s thyroiditis is at a higher risk of developing or already having another autoimmune disorder. Therefore, these individuals should be screened for other autoimmune disorders, especially if they are displaying other symptoms of different autoimmune disorders. Additionally, 15% of individuals diagnosed with Hashimoto’s thyroiditis have elevated serum IgA transglutaminase (tTG) antibody and ~5% have significant celiac disease.3 Although it may be less common, some other diseases to consider are dermatitis herpaformitis, chronic active hepatitis, rheumatoid arthritis, SLE (lupus), myasthenia gravis, Addison’s disease, type I diabetes, pernicious anemia and Sjorgen’s syndrome.3,4 More research continues to be done on the relationship between celiac disease and Hashimoto’s thyroiditis. It should certainly be explored as a potential cause of the condition, considering the etiology of Hashimoto’s thyroiditis continues to remain a mystery.

Physiological and Metabolic Causes

Hashimoto’s thyroiditis is the most common cause of hypothyroidism, therefore, individuals diagnosed with hypothyroidism should also be tested for Hashimoto’s thyroiditis to rule out an autoimmune cause of this condition.3 Currently, 1% of the general population and ~5% of individuals over the age of 60 have hypothyroidism; 85% of this statistic are women.3,4 For every 4 per 1000 women and every 1 per 1000 men have hypothyroidism, whereas individuals from Asian descent, specifically from Japan, have a higher incidence due to their diet being high in iodine and low in selenium as children.4

There are several factors that can influence the development of Hashimoto’s thyroiditis. Several genetic, environmental, and lifestyle factors have been found as a potential contribution to development of this disease. Hashimoto’s thyroiditis appears to be involved in major histocompatibility genes (HLA class I and II), immunoregulatory genes (TLA4, PD1, CD40) and genes associated with thyroid specific genes and TPO Ab synthesis.5 Several HLD-DR polymorphisms are found within those diagnosed with Hashimoto’s disease, specifically HLD-DR3, DR4, and DR5.4Hashimoto’s thyroiditis causes lymphocytic infiltration which means that the immune system begins to active the T cells and the B cells to attack the thyroid gland.4,6 Cell destruction is caused from CD8+ cytoxic T cells and the cytokines tumor necrosis factor (TNF), interleukin-1 (IL-1), and interferon.4,6 Some environmental factors include smoking status, excessive iodine intake, alcohol use, selenium intake, vitamin D deficiency.5

The thyroid gland has two primary functions; to produce and release thyroid hormones that balance of metabolism and secreting calcitonin, which is a hormone that regulates calcium.7 The primary hormones secreted from the thyroid gland are thyroxine (T4) and triiodothyronine (T3)7 These hormones do require iodine-containing amino acids, therefore, adequate iodine intake is necessary for these hormones to be produced.7 Thyroid-stimulating hormone (TSH) is the primary hormone that regulates how well or poorly the thyroid gland will function.7 This hormone is produced by the pituitary gland in the brain. When the thyroid gland is functioning poorly, circulating TSH levels will begin to rise and this indicates low thyroid function (hypothyroidism), conversely if the TSH levels begin to lower this indicates hyper function of the thyroid gland (hyperthyroidism).7 TSH is the driver of how well thyroid gland functions, however it impacts all of the other thyroid hormones and how they function throughout the whole body. If it is not functioning properly it will begin to effect metabolism, the cardiovascular system, nervous system, adrenal system, skeletal muscles, carbohydrate and cholesterol metabolism, and growth.6 There are significant consequences when the thyroid gland is not balanced and it will affect the whole body, therefore, it is crucial to monitor the thyroid function to maintain health.

Nutrition and Lifestyle

            When any autoimmune disorder is diagnosed, there is usually some sort of nutritional protocol that is recommended for that condition. Several studies have been conducted for diets associated with Hashimoto’s thyroiditis, however, there is a lack of research in the area of Hashimoto’s thyroiditis and no protocol is recommended at this time.8However, if 15% of individuals diagnosed with Hashimoto’s thyroiditis test positive for serum IgA transglutaminase (tTG) antibody, following a gluten-free diet may be beneficial.3

Although there is no specific nutritional protocol recommended for Hashimoto’s thyroiditis, there have been some studies that have been conducted on several ones. A lactose-restricted regimen has been studied and found that TSH levels were decreased in individuals with hypothyroidism, however there was no significant change in PTH (parathyroid hormone), free T4, and calcium.8 Therefore, there isn’t significant evidence to recommend  lactose restriction diet for those with hypothyroidism or Hashimoto’s thyroiditis.8 Gluten avoidance has been found to be beneficial for those with Hashimoto’s thyroiditis. Studies have found that serum titers of TPO Ab and Tg Ab antibodies were reduced and vitamin D levels increased with no differences in TSH, free T3 and T4 when individuals did not consume gluten.8 This seems like a promising protocol as the antibodies were decreased, which can indicate that the inflammation has decreased and the thyroid isn’t under as much attack. A Paleo-style diet, that did not allow grains or dairy products with micronutrient supplementation, showed a significant reduction in TPO Ab and Tg Ab and participants reported alleviation of symptoms.8 The Paleo diet basically is a gluten-free diet that also does not allow for dairy products to be consumed, therefore, this could be a diet for HT. It is important to note that the participants were supplemented with micronutrients which may contribute to adequate nutritional intake, but the Paleo diet seems like it may be the best option as a diet for those with Hashimoto’s thyroiditis; more research should be done on this.

It appears promising that a gluten-free diet may be beneficial for individuals diagnosed with Hashimoto’s thyroiditis. There is some conflicting data within the research as it does not appear to be as beneficial to those who are not diagnosed with celiac disease or wheat/gluten hypersensitivity.9 Following a long-term gluten-free diet can lead to dietary and nutritional deficiencies, whereas supplementation of vitamins and minerals that have been found in an individual with HT would be more beneficial than following a restrictive diet.9

Another component to consider in overall health of those with Hashimoto’s thyroiditis is the health of the gut microbiota and how this may impact the disease process of HT. Some research suggests that intestinal dysbiosis, bacterial overgrowth, and increased intestinal permeability can promote inflammation and increase risk for developing autoimmune disorders, such as Hashimoto’s thyroiditis.8,10 Several studies found that patients with Hashimoto’s thyroiditis have increased zonulin levels, which indicates “leaky gut”, and had increased Bacteroides species and less Bifidobacterium within their guts, suggesting intestinal dysbiosis.8,10 As a society that does not consume adequate amounts of fiber daily, intestinal dysbiosis has become increasingly more common. Because of this, increased rates of autoimmune disorders continue to rise, including Hashimoto’s thyroiditis. It is important for anyone who does have a diagnosis of Hashimoto’s thyroiditis that they at least consume enough fiber every day to fuel their gut microbiome. More and more research continues to be conducted on the role of the gut microbiota for overall health.

Treatment Plan

Treatment for Hashimoto’s thyroiditis appears to be rather simple from a medical standpoint. However, this condition is complex and there are other factors that need to be considered, such as diet and lifestyle. Current medical management for Hashimoto’s thyroiditis is a prescription of Levothyroxine, which  is prescribed for both hypothyroidism and Hashimoto’s thyroiditis.3,4

Levothyroxine is dosed at 0.05-2.0 mg and is to be taken orally daily, preferably 30 minutes to 1 hour prior to eating breakfast.3,4 If there happens to be a goiter present, a suppressive dose of T4 may be prescribed with levothyroxine to shrink the goiter.3,4 There is another medication found on the market that continues to be used as treatment for hypothyroidism, but it hasn’t been approved by the FDA for treatment. This medication is called Armour Thyroid and it is made up of desiccated animal thyroid preparations (or thyroid extract) and is not recommended for treatment because of the ratio of T3 and T4 is not balanced for our human bodies.4 However, this medication continues to be prescribed by some physicians.

Another important factor for treatment plan would be testing for and identifying any vitamin or mineral deficiencies. There are some deficiencies that are common with Hashimoto’s thyroiditis and these deficiencies can exacerbate symptoms. It may not be conventional at this time to test for micronutrient deficiencies; however it would be beneficial to have this be a standard practice. Individuals sometimes have to be their own advocate to request this kind of testing, but diagnosing and treating micronutrient deficiencies is essential for treatment of Hashimoto’s thyroiditis.

Vitamin and Minerals of Concern

As mentioned above, there are several micronutrient concerns that are associated with Hashimoto’s thyroiditis. Some of these deficiencies may be recognized on a nutrition focused physical exam, while others may be symptomatic and diagnosed via lab work. Although there is no known cause of Hashimoto’s thyroiditis, there has been some speculation and theories revolved around whether or not vitamin D or selenium deficiency may be the cause of Hashimoto’s thyroiditis.11 Therefore, monitoring for vitamin and mineral deficiencies is critical for individuals with Hashimoto’s thyroiditis.


Iodine is an important mineral to mention in regard to the thyroid gland, however, it is not really associated with Hashimoto’s thyroiditis, as deficiency generally does not cause Hashimoto’s thyroiditis. Furthermore, it is important to mention this vital mineral because of its involvement with the thyroid gland, and without it, the thyroid would not be able to produce important hormones needed throughout the body. Often times iodine and iodide are used interchangeably because iodide is the ionic form of iodine.12 Iodine is needed especially for T4, which is a pro-hormone, and T3, which is a hormone.2 Iodine deficiency isn’t always associated with Hashimoto’s thyroiditis, however, a high iodine diet may cause damage to the thyroid gland.2 Although individuals with Hashimoto’s thyroiditis do not commonly present with having a goiter, iodine deficiency is associated with development of goiters.2 Following a diet that is balanced with iodine is the most beneficial because deficiency can cause goiters and toxicity can increase the risk of developing thyroid disease.2 Often times there is an association with iodine and selenium. A diet high in iodine and low in selenium further increases the risk of developing Hashimoto’s thyroiditis, as selenium is involved in dozens of metabolic processes that are involved within our immune system.11

Sources of iodine can vary due to the mineral content of where the soil is that the food has been grown in.12Drinking water is also a source of iodine and this also varies greatly worldwide.12 Some foods high in iodine are seafood, meat, eggs, dairy products, grains and legumes.12 Worldwide there was a problem with individuals being chronically low in iodine, causing goiters, therefore, table salt was fortified with iodine in order to provide adequate amounts of iodine to everyone.12 There are foods known as goitrogens because they interfere with iodide metabolism and it will cause the thyroid gland to become enlarged.12 These foods are cruciferous vegetables, such as cabbage, kale, cauliflower, broccoli, rutabaga, turnips, Brussels sprouts and mustard greens.12 If an individual is having an issue with thyroid production it may be a good idea to avoid these foods in their raw form until the thyroid is balanced out again.

The amount of iodide needed to prevent a goiter from developing is ~50-75 mcg/day; however, the RDA for adults is 150 mcg/day.12 Pregnant women do need a higher amount of iodide while pregnant and lactating; 220-290 mcg/day.12Now that iodine is added to table salt, there has been less issues with iodine deficiency, however, iodine deficiency continues to be problematic throughout the world and affects 200-300 million individuals worldwide.12 Without iodine, our bodies would not be able to produce thyroid hormones, therefore, iodine is the most crucial mineral needed for good thyroid health.

Iodine supplementation is not recommended to prevent autoimmune thyroiditis because excessive iodine intake has been associated as a potential cause for the disease when coupled with a selenium deficiency.2 Signs of an iodine toxicity include burning of the mouth, throat and stomach; nausea, vomiting, diarrhea, and fever.12 These symptoms may not be easily identified as an iodine toxicity, as they are fairly common symptoms of many other illnesses. High iodine intake may impact how well the thyroid can function; thus toxicity should be avoided.12 Individuals with Hashimoto’s thyroiditis might consider using unrefined sea salt as opposed to iodized refined salt, while still consuming natural foods that contain iodine..

Vitamin D

            Vitamin D appears to be the next very important vitamin in regard to thyroid health and the development of Hashimoto’s thyroiditis. Vitamin D, which is a fat-soluble vitamin but acts like a steroid hormone, is involved within many processes in the body. Vitamin D regulates gene expression, bone metabolism, and calcium/phosphorus homeostasis.13 Vitamin D receptors (VDR) are found is most tissues within our bodies, meaning basically all tissues need vitamin D in order to function.12,13 There is a correlation between vitamin D intake and of Hashimoto’s thyroiditis, because vitamin D supplementation can reduce TPO Ab levels in individuals that are already deficient in vitamin D and have Hashimoto’s thyroiditis.11Vitamin D is one the natural immunomodulators that the body has and it regulates many immune-mediated processes. Because of this, it has been theorized that vitamin D deficiency could be a cause of of Hashimoto’s thyroiditis.11 Vitamin D is responsible for the proper circadian rhythm involving the immune and endocrine axes, therefore, insufficiency of vitamin D may increase the production of cytokines and chemokines found within the body.14

The main source of vitamin D is through our skin when it is exposed to sunlight.12 There are several parts of the world that go long periods of time with little sunlight and cold weather, therefore, vitamin D deficiency can be common in those areas. Many foods are fortified with vitamin D because deficiency of vitamin D causes rickets in children and osteomalacia in adults.12 Food sources of vitamin D include fatty fish, such as swordfish, salmon, tuna and sardines, shitake mushrooms, and dairy products, cereals, and breads because they can be fortified.12 Cutaneous production of vitamin D is by far the most efficient way of obtaining vitamin D as only 15-30 minutes of sun exposure can provide 10,000-20,000 IU of vitamin D, which is about 100 times more than what is found in milk.12

Deficiency of vitamin D is diagnosed via a lab test of serum 25-OH D concentration <10 ng/mL.12 Treatment of vitamin D deficiency is usually treated with high doses of vitamin D given over 8-12 weeks at 50,000 IU weekly.12Research suggest that supplementing with 2000 IU daily, even while getting sunlight exposure, is not harmful to individuals to take year round and should prevent vitamin D deficiency.11,12


            Selenium is another key component of thyroid and immune function, therefore, there is a huge correlation between selenium intake and development of Hashimoto’s thyroiditis. Selenium is a major antioxidant for the body and is needed for over 30 enzymatic reaction, hence the term selenoproteins was created and now known for the processes within the body.11,12 The highest concentration of selenium within the body is found in the thyroid gland and the thyroid gland can retain this weight even when there is a deficiency.10,11 Several studies have shown that supplementation with selenium has improved inflammatory and immune responses in the body, as well as reduce TPO Ab in those with Hashimoto’s thyroiditis.2,11 Glutathione peroxidase is expressed in the thyroid gland and it is one of the antioxidants that requires selenium to function.2,12 In regards to the thyroid gland, selenium is required for iodine metabolism, including creation of thyroid hormones, through various iodothyronine 5’-Deiodinases (IDI or ID).12 These deiodinases remove iodine from T4to create T3, which is the primary regulator of metabolism and normal growth.12 A selenium deficiency decreases T3concentrations while inadvertently increasing T4 concentrations which will begin to disrupt metabolism and normal growth parameters.12

Adequate selenium intake is vital for the health of not only the thyroid gland but for the whole body system. Without selenium, several enzymatic reactions would not be able to occur in the body and this can lead to activation of the immune system, that will be difficult to turn off if deficiencies continue. Similar to iodine, selenium is sourced in our soil which varies greatly across the world.12 Foods containing selenium include meat, seafood, nuts and seeds, dairy products, grains, and eggs.12 Brazil nuts and yellowfin tuna are the best sources of selenium.2,11,12

Selenium deficiency continues to be prevalent worldwide. In China, central Asia, and parts of Europe, selenium deficiency leads to Keshan disease and Kashin-Beck disease which leads to cardiomyopathy and unfortunately, death.12In the United States, most selenium deficiency is within the population of individuals receiving total parenteral nutrition; those whom are receiving calories, protein, fat, and micronutrient via a port or central line.12 Selenium deficiency can cause poor growth, muscle pain and weakness, loss of pigmentation of hair and skin, and whitening of the nail bed.12 It is thought that poor growth related to thyroid disease is likely due to lack of selenium.12 Selenium can be supplemented 100-200 mcg/day; preferably selenomethionine versus selenite as selenomethionine is better absorbed.12 Some providers suggest 200 mcg/day selenium to those with Hashimoto’s thyroiditis because it has been shown to reduce serum TPO Ab levels.3,11 However, selenium toxicity would want to be avoid as it causes several negative side effects that will be discussed later.


            Iron is a mineral that is found within our bodies and used for several processes within. Our bodies contain a substantial amount of iron; 2-4 grams of iron or ~38 mg iron/kg body weight for women and ~50 mg iron/kg body weight for men.12 Most of our iron is found in hemoglobin, myoglobin, as parts of enzymes, within our blood, and the rest is stored.12 Iron and thyroid hormones work closely together, therefore iron deficiency impacts the thyroids ability to produce hormones. Thyroid peroxidase (TPO) is an enzyme that catalyzes thyroid hormone production and is essential for creation of all the thyroid hormones.2,12 Iron plays an important role in thyroid health because TPO is heme-dependent, and iron is required for thyroid hormone synthesis.2,10,12 Iron deficiency impacts the storage of the hormones and the secretion due to low oxygen transport.2,10,12 Not only does TPO need iron, but T3 is needed for the creation of erythrocyte precursors as it promotes production of erythropoietin.2  Lack of iron will decrease TPO activity which inherently impacts the production of T3 and T4.12 Iron deficiency is common in those with Hashimoto’s thyroiditis, especially when there is a secondary underlying autoimmune condition, such as celiac disease or autoimmune gastritis.2

There are two different forms of iron that we receive from food sources: heme and nonheme.12 Animal products, such as meat, poultry, and fish are the best sources of heme iron, whereas nonheme food sources are found from plants; such as whole grains, nuts, legumes, peas, some fruits and vegetables, and tofu.2,12 Many foods, such as cereals and grain products, are fortified with iron in order to promote adequate intake of iron and decrease incidence of iron deficiency.12

Iron status is typically monitored via serum hemoglobin levels, but ferritin can also be monitored for deficiency too.12 Symptoms of iron deficiency primarily found in children include pallor, listlessness, behavioral disturbances, impaired cognition, impaired learning, and short attention span.12 In adults, often times it is difficult to complete work tasks, stay focused and be productive, and complain of fatigue.12 Iron can be given orally to correct deficiency. Iron supplementation of 30-65 mg daily appears to be sufficient, however some may require up to 120 mg daily.12

The Tolerable Upper Intake Level set for iron in the adult population is 45 mg.12 Iron toxicity can be deathly because iron begins to become free radical causing damage to the gastrointestinal tract and other soft tissues.12 Symptoms of acute toxicity are abdominal pain, vomiting, diarrhea, and blood in stool.12

Vitamin B12

            Vitamin B12, also known as cobalamin, is a vitamin of concern for individuals diagnosed with Hashimoto’s thyroiditis. Vitamin B12 is synthesized within our intestines via anaerobic microorganisms, however, dietary intake of vitamin B12 is also important to maintain adequate levels within our body.10,12 It has been theorized that the gut microbiota of those with Hashimoto’s thyroiditis may be compromised; leading to gut dybiosis and bacterial overgrowth.10 If the gut microbiota is compromised, not only will the immune system become triggered, but synthesis of vitamins, such as vitamin B12, vitamin K, folic acid, and other B vitamins, may be compromised, leading to deficiencies. Vitamin B12 deficiency is often times found within individuals with Hashimoto’s thyroiditis because of the correlation between other autoimmune disorders that may not be diagnosed in that individual, such as celiac disease.15,16Approximately 18% of individuals diagnosed with Hashimoto’s thyroiditis have a vitamin B12 deficiency, therefore it is important to monitor and check vitamin B12 levels when first diagnosed.15 Vitamin B12 deficiency causes an increased amount of homocysteine which is harmful because it can lead to atherosclerosis; this is often overlooked when first diagnosed with Hashimoto’s thyroiditis.16

Adequate gut health is essential for the synthesis of several vitamins within our body, including vitamin B12. Focusing on gut health is the best way to ensure our immune system is functioning properly and vitamins are able to be synthesized.10 Vitamin B12 is able to be absorbed when consumed and 50% of our vitamin B12 requirements are obtained orally.15 Food sources of vitamin B12 come primarily from meat and meat products, with very little absorbed from plant foods.12 Vitamin B12 is needed for nutrient metabolism and energy production; purines and pyrimidines required for synthesis of nucleic acid require vitamin B12.12 Although this is an indirect relationship due to vitamin B12’s relationship with folate.12

As mentioned above, vitamin B12 deficiency may be overlooked in individuals with Hashimoto’s thyroiditis because it is not known to cause Hashimoto’s thyroiditis, but rather caused secondary to another autoimmune disorder that could be present.16 Again, ruling out a secondary autoimmune disorder during diagnosis of Hashimoto’s thyroiditis is crucial to avoid vitamin and mineral deficiencies. Vitamin B12 deficiency is serious. It impacts both hematologic and neurological system; which can have permanent and irreversible damage to the nervous system.12 Pernicious anemia can be identified via blood work because this results in megaloblastic macrocytic anemia.12 Other symptoms of vitamin B12deficiency related to pernicious anemia include fatigue, skin pallor, and some cardiorespiratory effects, such as shortness of breath.12 More serious symptoms impact the neurological system and can be irreversible. These symptoms include clumsiness, poor coordination, numbness and/or pain in the extremities, irritability, memory loss, disorientation, hallucinations, and even dementia.12

Treatment of vitamin B12 deficiency will be dependent on whether or not the deficiency is caused from malabsorptive issue from another autoimmune disorder, such a celiac disease.12,15 Treatment for vitamin B12 is 1 mg vitamin B12 for approximately one week with the dose decreased slightly for about 1-2 months.12 If there is a malabsorptive component causing the deficiency then monthly intramuscular injections will be administered at 500-1,000 mcg or an increased dose of 1,000-2,000 mcg orally.12

Prescription of Vitamin and Mineral Supplementation


            Iodine supplementation is not recommended for individuals with Hashimoto’s Thyroiditis. However, adequate intake is also necessary for proper function of the thyroid gland. Now that iodine has been added to table salt, there has been a lower incidence of iodine deficiency, although it does continue to exist. The amount of iodide needed to prevent a goiter from developing is ~50-75 mcg/day; however, the RDA for adults is 150 mcg/day.12 Pregnant women do need a higher amount of iodide while pregnant and lactating; 220-290 mcg/day.12 Good food sources containing iodine are seafood, meat, eggs and dairy products, grains, and legumes.12 The benefit of maintaining adequate amounts of iodine is the normal production of thyroid hormones that are necessary for several parts of the body. The thyroid gland can continue functioning normally and can reduce symptoms associated with hypothyroidism.

Vitamin D

            Vitamin D supplementation is recommended for those with Hashimoto’s Thyroiditis that present with a deficiency. If an individual is deficient, 50,000 IU vitamin D is recommended to take weekly for 8-12 weeks.12 A maintenance dose of 2,000 to upwards of 4,000 IU daily is recommended, even if the individual has exposure to sunlight, as this will likely not lead to a vitamin D toxicity.12 Food sources of vitamin D are fatty fish (swordfish, salmon, mackerel, tuna, and sardines), liver, fortified dairy products (milk and yogurt), eggs, and cheese.12 Vitamin D is essential for the function of the immune system. Adequate amount of vitamin D will allow the immune system to function properly and has been shown to decrease serum TPO Ab levels in those diagnosed with Hashimoto’s Thyroiditis.9,14


            Selenium supplementation has been studied extensively due to its involvement with production of thyroid hormones. 100-200 mcg/day of selenium is recommended for supplementation for a deficiency; preferably in the form selenomethionine because it is best absorbed.12 It is safe to take 200 mcg/day of selenium in order to lower TPO Ab levels and improve thyroid gland function.3,11 Foods containing selenium are meat, seafood, dairy products, grains, eggs, nuts and seeds; with Brazil nuts being one of the best sources of selenium.2,11,12 Adequate selenium intake not only helps the thyroid gland produce vital thyroid hormones, but is needed for over 30 different enzymatic reactions, therefore, contributing to overall function of the human body. Selenium intake should be monitored to avoid toxicity, however, this is one of the most important minerals in regards to thyroid function.


            Iron supplementation is recommended for individuals with Hashimoto’s Thyroiditis that are deficient. Supplementation of 30-65 mg/day of iron appears to be sufficient, however, up to 120 mg/day may be necessary for some people.12 There are two types of food sources for iron: heme and non-heme. Food sources that provide heme are animal products, mainly meat, poultry and fish, whereas non-heme food sources are derived from plants such as whole grains, nuts, legumes, peas and tofu.12 Adequate iron levels will prevent anemia and allow the production of red blood cells. If someone has an iron deficiency, they may feel fatigued, thus correction of this deficiency may provide some much needed energy.

Vitamin B12

            Vitamin B12 supplementation is required once a deficiency has been detected. Often times this deficiency can be overlooked in individuals with Hashimoto’s Thyroiditis, therefore it is even more important to check these levels regularly. Vitamin B12 is mainly sourced from meat and meat products as very little is absorbed from plant sources.12 The gut can synthesize vitamin B12, however, if the gut is compromised in any way, then it would not be able to produce this vitamin. Treatment of vitamin B12 is 1 mg vitamin B12 orally daily and to continue for approximately 1-2 months (dosage may be decreased slightly during this time frame).12 If malabsorptive issues occur, intramuscular injections are recommended at 500-1,000 mcg per month for better absorption and can continue until deficiency is resolved. As there is no Tolerable Upper Intake Level set at this time for vitamin B12, the risk of toxicity is low. Vitamin B12 deficiency can have irreparable and lasting neurological deficits, therefore, adequate intake of this vitamin is critical.

Recommendations for Follow-Up Care

            Follow-up care for individuals diagnosed with Hashimoto’s Thyroiditis should be dependent on the person and the symptoms they are showing. Treating based off symptoms appears to be the best way to manage this disease, as everyone presents differently. Follow-up with primary care physician should occur approximately every 3 months in order to have full thyroid panel, including TSH, free T4 and free T3, and TPO Ab be drawn.3,4 Monitoring of vitamin D, selenium, iron, and vitamin B12 is recommended to ensure no deficiencies are present.

Although some would argue that serum TPO Ab levels don’t need to be monitored, decreasing TPO Ab levels indicate less inflammation occurring, thus, less damage being caused to the thyroid gland.3,4 Some individuals may want to try a specific diet, such as anti-inflammatory diet, Paleo diet, or gluten-free diet; therefore, referral to a dietitian or nutrition professional may be beneficial to this population. Depression is prevalent in the Hashimoto’s Thyroiditis population; therefore, it is recommended to treat this in order to preserve good mental health.3,4

Additional Testing

            Due to the nature of Hashimoto’s thyroiditis being an autoimmune disorder, it would be important to rule out any additional autoimmune disorders present. It appears that the development of HT is secondary to another autoimmune disorder, such as celiac disease. As HT is often times diagnosed as a secondary autoimmune disease, individuals who have already been diagnosed with an autoimmune disorder should be tested for HT, especially if those individuals present with hypothyroidism.

There is a correlation between abnormal lipid metabolism and Hashimoto’s thyroiditis. Monitoring of these lab values may be of benefit to see how well the treatment for this condition is working because cholesterol metabolism is impacted when serum T3is low.17 Individuals who are treated with levothyroxine and have normal levels of TSH and other thyroid hormones can continue to show signs and symptoms of hypothyroidism.17 One of the chief complaints is weight gain and continued slow metabolism with basal metabolic rate (BMR) ~10% slower than that of individuals that do not have hypothyroidism.17 Free T3 levels appear to have a correlation between both abnormal lipid metabolism and slower BMR, therefore, frequent monitoring of free T3 is recommended.17 Additionally, there may even be more value in following up with a registered dietitian or nutritional professional in order to educate on a proper nutrition and exercise regimen to improve overall health.

Adequate gut health appears to be a common theme within the treatment for Hashimoto’s thyroiditis, therefore, it may be beneficial to follow-up with a gastrointestinal specialist that could test for intestinal dysbiosis or bacterial overgrowth. They may be able to recommend specific probiotics that would be beneficial to that specific individual if they do happen to have either one of those conditions.

Outcome Measures

            Obvious outcome measures are lab values that are within normal limits (WNL). Tolerance to treatment, i.e. levothyroxine treatment and potential supplementation of vitamin and minerals to combat deficiencies, should be monitored. If possible, vitamin and mineral panels should be drawn by primary care physician to monitor for any and all deficiencies. If there are deficiencies present, proper repletion of those vitamins and minerals is necessary. These measures are able to be assessed objectively, as labs can be drawn and tested against normal range values. Some subjective measures would be the individual’s symptoms and whether or not they persist.

I hope you enjoyed this thorough review of this disease process as I enjoyed putting it together myself and learning about Hashimoto’s thyroiditis.


  1. Hiromatsu Y, Satoh H, Amino N. Hashimoto’s thyroiditis: history and future outlook. Hormones (Athens). 2013;12(1):12-18. doi:10.1007/BF03401282
  2. Rayman MP. Multiple nutritional factors and thyroid disease, with particular reference to autoimmune thyroid disease. Proc Nutr Soc. 2019;78(1):34-44. doi:10.1017/S0029665118001192
  3. Papadakis, MA., McPhee, ST., Rabow, MW. Current medical diagnosis and treatment. McGraw Hill, 62nd edition; 2023.
  4. Jameson, L., Kasper, DL., Longo, DL., Fauci, As., Hauser, SL., Loscalzo, J. Harrison’s principles of internal medicine, volume 2. McGraw Hill, 12th ed; 2018.
  5. Weetman AP. An update on the pathogenesis of Hashimoto’s thyroiditis. J Endocrinol Invest. 2021;44(5):883-890. Doi:10.1007/s40618-020-01477-1
  6. Ralli M, Angeletti D, Fiore M, et al. Hashimoto’s thyroiditis: An update on pathogenic mechanisms, diagnostic protocols, therapeutic strategies, and potential malignant transformation. Autoimmun Rev. 2020;19(10):102649. Doi:10.1016/j.autrev.2020.102649
  7. Barrett, KE., Barman, SM., Brooks, HL., Yuan, JXJ. Ganong’s review of medical physiology. McGraw Hill, 26thed; 2019.
  8. Mikulska, AA, Karazniewicz-Lada M, Filipowicz D, Ruchala M, Glowka FK. Metabolic characteristics of Hashimoto’s thyroiditis patients and the role of microelements and diet in the disease management-An overview. Int J Mol Sci. 2022;23(12):6580. Published 2022 Jun 13. doi: 10.3390/ijms23126580
  9. Szczuko M, Syrenicz A, Szymkowiak K, et al. Doubtful Justification of the Gluten-Free Diet in the Course of Hashimoto’s Disease. Nutrients. 2022;14(9):1727. Published 2022 Apr 21. doi:10.3390/nu14091727
  10. Knezevic J, Starchl C, Tmava Berisha A, Amrein K. Thyroid-Gut-Axis: How Does the Microbiota Influence Thyroid Function?. Nutrients. 2020;12(6):1769. Published 2020 Jun 12. doi:10.3390/nu12061769
  11. Liontiris MI, Mazokopakis EE. A concise review of Hashimoto thyroiditis (HT) and the importance of iodine, selenium, vitamin D and gluten on the autoimmunity and dietary management of HT patients. Points that need more investigation. Hell J Nucl Med. 2017;20(1):51-56. doi:10.1967/s002449910507
  12. Gropper, S., Smith, J., Carr, T. Advanced Nutrition and Human Metabolism. 7thCengage; 2018.
  13. Kim D. The Role of Vitamin D in Thyroid Diseases. Int J Mol Sci. 2017;18(9):1949. Published 2017 Sep 12. doi:10.3390/ijms18091949
  14. Danailova Y, Velikova T, Nikolaev G, et al. Nutritional management of thyroiditis of Hashimoto. Int J Mol Sci.2022;23(9):5144. Published 2022 May 5. doi: 10.3390/ijms23095144
  15. Benites-Zapata VA, Ignacio-Cconchoy FL, Ulloque-Badaracco JR, et al. Vitamin 12 levels in thyroid disorders: A systemic review and meta-analysis. Front Endrocrinol (Lausanne). 2023;14:1070592. Published 2023 Feb 22. doi: 10.3389/fendo.2023.1070592
  16. Aktas HS. Vitamin B12 and vitamin D levels in patients with autoimmune hypothyroidism and their correlations with anti-thyroid peroxides antibodies. Med Princ Pract. 202;29(4):364-370. doi: 10.1159/000505094
  17. Ettleson MD, Bianco AC. Individualized therapy for hypothyroidism: Is T4 enough for everyone?. J Clin Endocrinol Metab. 2020;105(9):e3090-e3104. doi: 10.1210/clinem/dgaa430