Hearing that your immune system is attacking your thyroid can sound alarming. And if you search online for information about Hashimoto’s thyroiditis, you are very likely to come across long lists of symptoms, strict diets, supplements, and claims about “healing” or curing the thyroid.
The reality is both simpler and more complex.
Hashimoto’s thyroiditis is an autoimmune disease of the thyroid gland. Over time, the immune response can damage thyroid tissue and reduce the gland’s ability to produce thyroid hormones. However, this process is usually gradual, and some people may have Hashimoto’s for years while their thyroid hormone levels remain completely normal.1, 2, 3
Understanding this distinction is important because having Hashimoto’s does not automatically mean that a person already has hypothyroidism.
What Is Hashimoto’s Thyroiditis?
Hashimoto’s thyroiditis, also known as chronic autoimmune thyroiditis or chronic lymphocytic thyroiditis, develops when the immune system loses tolerance to components of the thyroid and mounts an autoimmune response against thyroid tissue.1, 2, 3
It is one of the most common autoimmune disorders of the thyroid gland and an important cause of primary hypothyroidism in areas where iodine intake is adequate.1, 2, 5
Hashimoto’s can affect anyone, but it is significantly more common in women. A large systematic review and meta-analysis estimated the overall prevalence in adults at around 7.5%, although estimates varied considerably depending on geographic region, population, and diagnostic criteria. Women were affected nearly four times more often than men.4
What Happens to the Thyroid?
The immune process involved in Hashimoto’s is much more complex than simply the presence of thyroid antibodies.
Immune cells infiltrate the thyroid gland and recognize thyroid antigens as targets. T lymphocytes, B lymphocytes, inflammatory signaling pathways, and autoantibodies all form part of a complex immune response that can gradually damage thyroid follicular cells.1, 2, 3
The two antibodies most commonly associated with Hashimoto’s are:
Anti-TPO antibodies are the most characteristic and are detected in the majority of people with Hashimoto’s.1
However, antibodies should not be viewed as the entire disease. They are important markers of thyroid autoimmunity, while immune cell-mediated mechanisms also play a major role in damage to thyroid tissue.2, 3
As the damage progresses, the thyroid may eventually become unable to produce adequate amounts of thyroid hormones.
This is when hypothyroidism develops.
Hashimoto’s and Hypothyroidism Are Not the Same Thing
This is one of the most important distinctions for patients to understand.
Hashimoto’s is the autoimmune disease.
Hypothyroidism describes the functional state that develops when the thyroid can no longer produce enough thyroid hormone.
A person can therefore have positive thyroid antibodies and evidence of Hashimoto’s while still having normal TSH and free T4 levels. This state is called euthyroidism.1
In some people, thyroid function remains normal for a long time. In others, progressive thyroid damage eventually leads to subclinical or overt hypothyroidism.1, 5, 9
What Symptoms Can Hashimoto’s Cause?
Hashimoto’s itself may cause no symptoms at all in its early stages.
Most of the well-known symptoms associated with the condition become more noticeable when thyroid hormone production falls and hypothyroidism develops.1, 5
Possible symptoms include:
- fatigue and reduced energy
- increased sensitivity to cold
- constipation
- dry skin
- thinning hair or hair loss
- muscle weakness or muscle aches
- weight gain
- changes in the menstrual cycle
- mood changes
- difficulty concentrating or a feeling of mental slowing.1, 5
Some people may also develop enlargement of the thyroid gland, known as a goiter, which can cause a feeling of pressure or fullness in the neck.1
These symptoms are not specific to Hashimoto’s. Fatigue, weight changes, hair loss, and mood changes can occur for many different reasons.
That is why symptoms alone cannot diagnose thyroid disease.
How Is Hashimoto’s Diagnosed?
Diagnosis is usually based on a combination of several pieces of information rather than a single test.
TSH
Thyroid-stimulating hormone (TSH) is usually the most important initial laboratory test for assessing thyroid function.
When the thyroid begins to produce insufficient amounts of hormone, the pituitary gland typically responds by increasing TSH production in an effort to stimulate the thyroid.5, 9
Free T4
Free thyroxine (FT4) helps determine whether thyroid hormone production has actually declined.
A high TSH combined with a low FT4 is consistent with overt primary hypothyroidism.5
If TSH is elevated but FT4 remains within the reference range, the condition is called subclinical hypothyroidism.9
Thyroid Antibodies
Testing for anti-TPO antibodies can help establish that thyroid autoimmunity is the underlying cause.
Thyroglobulin antibodies may provide additional information in some cases, but anti-TPO antibodies are generally more useful for identifying autoimmune thyroiditis.1, 2
An important point is that antibody levels do not need to be measured repeatedly simply to monitor whether Hashimoto’s is getting “better” or “worse.” Thyroid function is generally monitored with TSH, with additional tests when clinically necessary.1
What About Thyroid Ultrasound?
A thyroid ultrasound is not automatically necessary for every person with Hashimoto’s.
It can reveal characteristic changes in thyroid tissue and may be useful when the diagnosis is unclear, when the thyroid is enlarged, when a nodule is suspected, or when there is another clinical reason to image the gland.1
However, if the biochemical findings and antibody tests are clear and there is no concern about a structural abnormality, ultrasound may not provide useful additional information.
How Is Hashimoto’s Treated?
There is currently no established treatment that selectively switches off the autoimmune process and permanently restores damaged thyroid tissue.
Instead, treatment focuses primarily on thyroid function.1, 5, 10
If Thyroid Function Is Normal
If a person has elevated thyroid antibodies but normal TSH and FT4 levels, thyroid hormone treatment is usually not required.
Thyroid function is monitored over time because hypothyroidism may develop later.1
If Hypothyroidism Develops
When Hashimoto’s causes overt hypothyroidism, the standard treatment is levothyroxine, a synthetic form of the T4 hormone normally produced by the thyroid.1, 5, 10
The aim is to replace the hormone that the thyroid can no longer produce in sufficient amounts and bring TSH back into an appropriate range.
The dose is individualized and adjusted according to repeat blood tests.10
For many people whose hypothyroidism is caused by Hashimoto’s, treatment is long term.
What About Subclinical Hypothyroidism?
This situation is less straightforward.
When TSH is mildly elevated but FT4 remains normal, the decision to start levothyroxine depends on factors such as the degree of TSH elevation, symptoms, age, cardiovascular risk, pregnancy or plans for pregnancy, and other clinical considerations.9
In other words, a mildly elevated TSH does not automatically mean that medication is required.
Can Hashimoto’s Occur Alongside Other Autoimmune Diseases?
Yes.
Autoimmune diseases have a tendency to cluster, partly because several of them share common genetic and immunological susceptibility factors.3, 7
People with autoimmune thyroid disease are more likely than the general population to have another autoimmune condition.7
Associations have been reported with conditions including:
- type 1 diabetes
- celiac disease
- Addison’s disease
- pernicious anemia / autoimmune gastritis
- vitiligo
- rheumatoid arthritis
- systemic lupus erythematosus.7, 8
This does not mean that every person with Hashimoto’s should assume they have or will develop another autoimmune disease.
Screening for additional conditions is usually guided by symptoms, medical history, family history, and individual risk.
Celiac disease deserves particular attention because its association with autoimmune thyroid disease has been extensively studied. A meta-analysis of 6,024 people with autoimmune thyroid disease found biopsy-confirmed celiac disease in approximately 1.6% overall, although prevalence varied considerably across populations and was higher in children.8
What About Gluten?
This is probably one of the most common questions surrounding Hashimoto’s.
You may have heard that everyone with Hashimoto’s should stop eating gluten.
The available scientific evidence does not support this recommendation.
A gluten-free diet is medically necessary for people who also have celiac disease.
For people with Hashimoto’s who do not have celiac disease, the evidence remains limited.
A 2025 systematic review and meta-analysis specifically examined randomized studies of gluten-free diets in people with Hashimoto’s without celiac disease. Only three studies, involving a total of 110 participants, were available for meta-analysis, and the certainty of the evidence was rated as very low because of methodological limitations and imprecision.6
The analysis found no significant improvement in TSH, free T3, or free T4.6
At present, therefore, there is not enough high-quality scientific evidence to routinely recommend a gluten-free diet as a treatment for Hashimoto’s in people without celiac disease.
And there is no proven “Hashimoto’s diet” that can cure the autoimmune condition.
What matters is adequate overall nutrition and a dietary pattern that supports general health.
Highly restrictive diets should not be adopted simply because they are promoted online as a way to “heal” the thyroid.
Conclusion
Hashimoto’s thyroiditis is an autoimmune disease in which the immune system targets the thyroid gland.
But having Hashimoto’s does not automatically mean having hypothyroidism.
Some people maintain normal thyroid function for years, while others gradually develop thyroid hormone deficiency and require levothyroxine treatment.
Diagnosis is based mainly on thyroid function tests and evidence of thyroid autoimmunity. Ultrasound can be useful in selected cases, but it is not mandatory for everyone.
Hashimoto’s can occur alongside other autoimmune diseases, particularly conditions such as type 1 diabetes and celiac disease, but having one autoimmune disease does not mean that developing another is inevitable.
And despite claims commonly made online, there is currently no convincing evidence that removing gluten treats Hashimoto’s in people who do not have celiac disease.
The goal of care is not to chase antibody levels or follow increasingly restrictive diets.
It is to monitor thyroid function, identify hypothyroidism when it develops, and treat it appropriately.
References
1. Klubo-Gwiezdzinska J, Wartofsky L. Hashimoto thyroiditis: an evidence-based guide to etiology, diagnosis and treatment. Pol Arch Intern Med. 2022;132(3):16222.
2. Ragusa F, Fallahi P, Elia G, et al. Hashimoto’s thyroiditis: epidemiology, pathogenesis, clinic and therapy. Best Pract Res Clin Endocrinol Metab. 2019;33(6):101367.
3. Weetman AP. An update on the pathogenesis of Hashimoto’s thyroiditis. J Endocrinol Invest. 2021;44(5):883–890.
4. Hu X, Chen Y, Shen Y, Tian R, Sheng Y, Que H. Global prevalence and epidemiological trends of Hashimoto’s thyroiditis in adults: a systematic review and meta-analysis. Front Public Health. 2022;10:1020709.
5. Chaker L, Papaleontiou M. Hypothyroidism: a review. JAMA. 2025;334(19):1750–1760.
6. Araújo EMQ, Coutinho-Lima CRO, de Sousa AS, et al. Effects of gluten-free diet in non-celiac Hashimoto’s thyroiditis: a systematic review and meta-analysis. Nutrients. 2025;17(21):3437.
7. Boelaert K, Newby PR, Simmonds MJ, et al. Prevalence and relative risk of other autoimmune diseases in subjects with autoimmune thyroid disease. Am J Med. 2010;123(2):183.e1–183.e9.
8. Roy A, Laszkowska M, Sundström J, et al. Prevalence of celiac disease in patients with autoimmune thyroid disease: a meta-analysis. Thyroid. 2016;26(7):880–890.
9. Biondi B, Cappola AR, Cooper DS. Subclinical hypothyroidism: a review. JAMA. 2019;322(2):153–160.
10. Jonklaas J, Bianco AC, Bauer AJ, et al. Guidelines for the treatment of hypothyroidism: prepared by the American Thyroid Association Task Force on Thyroid Hormone Replacement. Thyroid. 2014;24(12):1670–1751.
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