What Causes Hashimoto's?

A Hashimoto’s diagnosis often comes with a question: why did this happen? You may look back at a pregnancy, infection, stressful period, or new supplement and wonder whether it played a role. The timing can be worth exploring, but it rarely tells the whole story.

What’s the short answer on the cause of Hashimoto’s?

Hashimoto’s develops when the immune system attacks the thyroid. Genes influence susceptibility, while factors such as iodine intake, immune changes after pregnancy, and certain medicines may contribute to thyroid autoimmunity or dysfunction. For most people, no single cause can be identified. The useful question is which factors are supported by evidence and whether reviewing them could change your care. [2–4]

Understanding the evidence can help you decide which parts of your history deserve attention, what to ask your clinician, and how to fact-check medical information or claims you might see online.

What is Hashimoto’s?

Hashimoto’s thyroiditis is an autoimmune disease in which immune cells damage the thyroid gland. Blood tests for thyroid peroxidase (TPO) antibodies, and sometimes thyroglobulin antibodies, help identify this immune response. Damage from this autoimmunity can eventually reduce thyroid hormone production, causing hypothyroidism. However, thyroid autoimmunity can be present even while hormone production is still normal. [3]

Hashimoto’s is a leading cause of hypothyroidism in countries with sufficient iodine intake. A 2022 meta-analysis estimated adult prevalence at about 7.5%, but results varied substantially by population and diagnostic method. The 7.5% figure is a pooled research estimate, not a precise worldwide count. [3,5]

How much of Hashimoto’s is genetic?

Genes explain an important part of susceptibility, but they do not determine who will eventually develop Hashimoto’s. A study of 110,814 Swedish twins estimated the heritability of overt Hashimoto’s at 65%. Heritability describes how much variation in susceptibility across a population is attributable to genetic differences. It does not mean that 65% of your disease came from genes or that the remaining 35% came from identifiable exposures. [2]

Identical twins help illustrate this distinction. A small Danish study reported about 55% concordance for chronic autoimmune hypothyroidism, while the larger Swedish study reported 29% for overt Hashimoto’s. Concordance describes how often both twins were affected. Although the estimates differ, neither shows that identical genes guarantee the same outcome. [1,2]

Other heritability estimates for autoimmune thyroid disease have been around 70–80%, depending on the population, disease definition, and methods. Several genes involved in immune regulation, including HLA, CTLA-4, and PTPN22, have been implicated. There is no single universal “Hashimoto’s gene.” [4]

The takeaway? Tell your clinician if thyroid disease runs in your family. That history can help guide evaluation, but it cannot establish a diagnosis. Some people develop Hashimoto’s without known family cases, while others with affected relatives never develop it.

What are the main risk factors and triggers for Hashimoto's?

A “trigger” can mean different things in thyroid research. A study might measure diagnosed Hashimoto’s, new thyroid antibodies, low hormone production, or small hormone changes within the normal range. Before interpreting a finding, check what the researchers actually measured. Evidence that something affects thyroid hormones is not automatically evidence that it causes Hashimoto’s.

The table summarizes the evidence for each stated outcome. “Strong” means the relationship is well established; “moderate” means human studies support an association but important uncertainties remain; “emerging” means findings are preliminary or inconsistent; and “weak” means support for the specific claim is limited. These are editorial assessments from our scientific perspective, not formal clinical grades or estimates of your personal risk.

As you read, note factors that apply to your history, along with dates, doses, and any thyroid results from that time. The checklist later in this article can help you turn those details into focused questions.

Iodine excess

Iodine is essential for making thyroid hormones, but more is not always better. In a five-year Chinese study, autoimmune thyroiditis developed in 0.2% of participants in a mildly iodine-deficient region, compared with 1.0% in a region with more-than-adequate intake and 1.3% in an excessive-intake region. These were regional comparisons, not a randomized controlled trial where iodine supplementation was assigned. . [6]

The relationship is not simply “less iodine is better.” A later survey of more than 78,000 Chinese adults found higher thyroid-antibody positivity in iodine-deficient groups. The studies measured different outcomes over different periods, but together they show why both excess and inadequate intake deserve attention. [7]

Action item: Start your review with concentrated sources: kelp capsules, iodine drops, and “thyroid support” supplements. You can use EXPIN's Cabinets feature to track your supplement intake - labels, daily doses, and dates of use - for your next doctor's appointment. Ask whether your total intake needs adjusting; do not try to remove all iodine from your diet, especially during pregnancy. [3]

Pregnancy and the postpartum period

Pregnancy and the months after delivery involve major immune changes. Postpartum thyroiditis can develop within the first year after birth, with an overactive thyroid phase, an underactive phase, or both. It is closely related to autoimmune thyroid disease, although its course can differ from chronic Hashimoto’s. [8]

A clinical review estimated that postpartum thyroiditis affects approximately 5% of women, with some later developing permanent hypothyroidism. The proportion varies across populations and follow-up periods. Persistent symptoms after childbirth deserve assessment; for example, fatigue could be a symptom and should not automatically be attributed to interrupted sleep. [8]

Action item: Record when symptoms began relative to delivery and bring any thyroid results from before or during pregnancy. Earlier results may help your clinician assess whether thyroid changes were already present.

Medications that affect the thyroid

Some medicines have well-established thyroid effects, but they act through different mechanisms. Immune checkpoint inhibitors, used in cancer treatment, can provoke immune-related thyroid dysfunction. A 2023 meta-analysis of newer checkpoint inhibitors reported hypothyroidism in approximately 10% of treated patients. Because several widely used agents were excluded, that number does not describe the risk for every regimen. [9]

Lithium can impair thyroid hormone release. Amiodarone can cause underactive or overactive thyroid disorders, with underlying thyroid disease affecting risk. Interferon-alpha can cause autoimmune and nonautoimmune thyroiditis. So as you can see, a medication-related thyroid problem needs to be identified more precisely before calling it Hashimoto’s. [10–12]

Action item: Bring the medicine name, start date, and dose changes to your prescribing clinician. You can use EXPIN Cabinets to track these medications just as you do your supplements Ask what thyroid monitoring is appropriate and whether earlier results help explain the timing. Do not stop treatment on your own; a thyroid problem can often be managed while the necessary medicine continues.

Low selenium

Selenium helps proteins involved in thyroid hormone metabolism and protection against oxidative damage function properly. In a Chinese study comparing two counties, a group of thyroid disorders affected 30.5% of people in the low-selenium county and 18.0% in the county with adequate selenium. Those percentages covered several conditions, not Hashimoto’s alone; higher selenium status was also associated with lower odds of autoimmune thyroiditis. [13]

Supplement trials answer a different question. A 2024 meta-analysis found that selenium reduced TPO antibodies and, in participants not taking thyroid hormone replacement, thyroid-stimulating hormone (TSH). Improving a blood marker does not by itself show that patients feel better, avoid thyroid damage, or can stop treatment. The findings do not establish that selenium prevents or cures Hashimoto’s. [14]

Action item: Before adding selenium, review what you already get from food and supplements. Ask whether there is a reason to suspect inadequate intake and what benefit supplementation is expected to provide. More is not necessarily better: excessive selenium can be harmful. [29]

Quitting smoking

Some studies have found a temporary increase in autoimmune hypothyroidism after people stop smoking. In a Danish case-control study, the odds were higher during the first two years after quitting; the increase was not observed in the three-to-ten-year category. The estimates were imprecise, so the size of the association should be interpreted cautiously. [15]

A separate prospective study linked smoking cessation with the development of thyroid antibodies. Neither finding means that most people who quit will develop thyroid disease, or that resuming smoking would be an appropriate response. [16]

Action item: Continue with smoking cessation. If persistent symptoms develop after quitting, include your quit date when discussing them with your clinician so thyroid function can be considered alongside other explanations.

Infections

Infections can activate the immune system, but the evidence differs by organism. Hepatitis C has a recognized association with thyroid autoimmunity; historical studies also need to separate the infection’s effects from those of interferon treatment. [12]

Findings for H. pylori are inconsistent: one meta-analysis found no statistically significant association with Hashimoto’s, while another did. Differences in the populations and methods make the disagreement difficult to resolve. Evidence that Epstein–Barr virus specifically causes Hashimoto’s is also uncertain. [4,17,18]

A large matched cohort found more newly diagnosed Hashimoto’s after COVID-19 infection. That observation raises a research question, but it cannot fully separate a biological effect from increased testing, more healthcare visits, or disease that was already present but undetected. Thyroid inflammation after infection is also not always Hashimoto’s. [19]

Action item: Add significant infections and their dates to your timeline, then compare them with your earliest thyroid results. Be sure to tell us about any infections during your EXPIN interviews. An infection before diagnosis is useful context; by itself, it does not establish a need for broad infection testing or treatment.

Vitamin D

Many studies find low vitamin D more often in people with Hashimoto’s. One meta-analysis reported approximately threefold higher odds of vitamin D deficiency than in healthy controls. That statistic describes how often deficiency was found; it does not mean low vitamin D triples the risk of developing Hashimoto’s. [20]

Researchers still need to establish which way the relationship runs. Low vitamin D might precede disease, follow changes in health or activity, or share another underlying factor. If you have a documented deficiency, ask how to correct it and assess the response. Treating deficiency is a separate goal from preventing Hashimoto’s or reversing thyroid damage.

Everyday chemicals

Research on thyroid health includes PFAS, phthalates, BPA, PCBs, perchlorate, and mercury. These substances differ in how people encounter them and how they may affect the body. They should not be grouped into a single “toxin” explanation. Interference with thyroid hormone signaling is also a different outcome from an autoimmune attack on the gland. [4,21,22]

For example, a US study found an association between PFAS levels and thyroid hormone changes in a subgroup with elevated TPO antibodies and low iodine status. It raised the possibility that existing thyroid autoimmunity or iodine status could influence susceptibility to hormone effects; it did not show that PFAS caused the antibodies. [21]

A Korean population study found associations between phthalates or phenolic compounds and thyroid-related measures, but no association with TPO or thyroglobulin antibodies. A later US analysis likewise found no antibody association for the pollutants it examined. This is why a headline about “thyroid disruption” needs closer reading before it is applied to Hashimoto’s. [23,24]

Action item: For a specific concern, record the substance or product, how you encountered it, how often, and for how long. Tell us this information during your EXPIN interview. A named workplace chemical is more useful information than “high toxin exposure.” The evidence does not justify concluding that cosmetics or food packaging caused your Hashimoto’s, or promising that replacing household products will reverse it.

Radiation

Radiation effects depend on the type, dose, and context of exposure. In a study of children and adolescents after Chernobyl, thyroid antibodies were more common in the more heavily exposed area: 19.5% versus 3.8%. The investigators did not find corresponding thyroid dysfunction in those groups. [25]

Action item: These findings concern antibodies after fallout exposure, not the risk from routine diagnostic imaging. If you have received radiation treatment or had another substantial documented exposure, record the type, body area, and approximate date for your clinician. Those details matter more than the broad label “radiation.”

Stress

Stress is often described online as a root cause of Hashimoto’s, but direct evidence is limited. A prospective study followed women with a family history of autoimmune thyroid disease and found no association between measured stress and new thyroid antibodies or overt thyroid dysfunction. This weakens a simple causal claim without ruling out every possible role for stress. [26]

Stress still deserves attention when it affects sleep, coping, or daily functioning. Feeling worse during a stressful period does not establish when thyroid autoimmunity began. You can seek help for stress as a way to alleviate autoimmunity symptoms without treating it as proof that you caused, or could have prevented, the disease.

Alcohol

A Danish observational study linked moderate alcohol consumption with lower odds of overt autoimmune hypothyroidism. Inherent differences between drinkers and nondrinkers could help explain the association, and the study does not establish that alcohol prevents disease. It provides no basis for starting to drink or increasing consumption for thyroid health. [27]

Why it is rarely one cause

The search for a single root cause can miss how Hashimoto’s develops over time. Inherited susceptibility likely interacts with several influences, and the disease may go unnoticed until symptoms or a blood test bring it to attention. Your diagnosis date is not necessarily the date autoimmunity began. [3,4]

Imagine someone diagnosed a few months after childbirth and shortly after an infection. Both events belong on the timeline. But an older abnormal thyroid test might show that changes began before either event. That earlier result can be more informative than whichever event happened closest to diagnosis.

Dose matters too. Ordinary dietary iodine and concentrated iodine drops are different exposures. Record amounts where possible, and distinguish a brief exposure from repeated use. Life stages such as puberty or perimenopause may be relevant context, but timing alone cannot identify a cause.

Population trends need the same care. A 2026 Tehran Thyroid Study report found that TPO-antibody positivity rose from 11.7% to 16.3% over approximately 18 years. That is a trend in one cohort’s antibodies, not proof of an equivalent worldwide rise in Hashimoto’s. Aging and study methods matter, and the finding alone cannot identify testing practices or chemical exposure as the explanation. [28]

How to review your own history

Start with what you can document: your earliest abnormal thyroid tests, antibody results, and diagnosis date. Then add when you first noticed symptoms and any relevant events or exposures, including those well before diagnosis. Approximate dates are useful; mark them as estimates so they remain distinct from recorded results.

For supplements, record the product name, daily dose, and dates of use. For a workplace concern, name the substance and task if you can. “Started iodine drops in March” or “used a named solvent weekly for six months” gives your clinician something specific to assess.

Use these ten questions to organize the review. Answer yes, no, or unsure, then add dates and details where relevant.

1. Does a close relative have Hashimoto’s or another autoimmune thyroid condition?

2. Did symptoms or abnormal results appear during pregnancy or within a year after childbirth?

3. Did you use kelp, iodine drops, or a supplement marketed for thyroid support?

4. Did you start or change lithium, amiodarone, interferon, or cancer immunotherapy?

5. Did you stop smoking in the two years before symptoms or diagnosis?

6. Was there a significant infection before the first thyroid changes?

7. Have you had a documented nutrient deficiency or a diet that substantially limits nutrient sources?

8. Have you received radiation treatment involving the neck or had another substantial documented radiation exposure?

9. Did work, hobbies, or a move introduce a specific, identifiable chemical exposure?

10. Do you have earlier thyroid results showing that changes preceded the event you currently suspect?

Use this checklist to organize a conversation, not to calculate a risk score. It is not a validated assessment, and the number of “yes” answers cannot identify the cause of your disease. Focus on details that could change a decision about testing, monitoring, or treatment.

What to bring to your doctor

Bring your timeline, laboratory reports, medication list, supplement labels, relevant family history, and EXPIN expotype report. Start the appointment with your main concern: confirming the diagnosis, reviewing a particular exposure, or understanding persistent symptoms. That helps keep the discussion focused on what you need now.

Useful questions include:

• What do my TSH and free T4 results show about current thyroid function?
• Do my antibody results and clinical history support Hashimoto’s, or another thyroid condition?
• Could any medication or supplement affect my thyroid or the interpretation of my tests?
• Does my history suggest a reason to assess iodine intake, selenium status, or another nutritional concern?
• Would investigating a suspected exposure change my treatment or monitoring?

Ask what would change if a suspected contributor were confirmed. The answer can help you and your clinician decide whether further testing is worthwhile. Investigating the past should not delay treatment for current hypothyroidism. [30]

Frequently asked questions

Is Hashimoto’s genetic or environmental?

Both can contribute. Twin studies show a substantial genetic influence, but identical twins do not always both develop the disease. The often-quoted 65% heritability estimate describes variation in susceptibility across a population, not a percentage breakdown of one person’s illness. [1,2]

Can stress cause Hashimoto’s?

Stress has not been established as a direct cause. One prospective study found no association between measured stress and new thyroid autoimmunity or overt dysfunction. That does not exclude every possible role of stress in autoimmunity, but it does not support blaming stress for an individual case. [26]

Can quitting smoking trigger Hashimoto’s?

Studies have observed a temporary increase in diagnosed autoimmune hypothyroidism or thyroid antibodies after quitting. They cannot determine what caused an individual case. Continue with smoking cessation and discuss persistent symptoms with your clinician. Restarting smoking is not a thyroid treatment. [15,16]

Does too much iodine cause Hashimoto’s?

Excess iodine can contribute to thyroid problems, including autoimmune thyroiditis in susceptible people. However, iodine is essential, and deficiency is also harmful. Review high-dose iodine and kelp supplements with your clinician rather than trying to eliminate all dietary iodine. [3,6,7]

Why do more women get Hashimoto’s?

Sex-related differences in immune regulation, genetic susceptibility, and reproductive biology likely contribute. There is no single established explanation for the difference. Female predominance is well documented, but it does not mean all women face the same risk or that men are protected. [2,4,5]

Can Hashimoto’s be prevented?

There is no proven strategy that reliably prevents Hashimoto’s. Avoiding unnecessary excess iodine and reviewing relevant medicines or nutritional concerns are reasonable clinical discussions, but they cannot guarantee prevention. Developing the disease does not mean you failed to manage your lifestyle or exposures correctly. [3,4]

Put your history in context

Understanding risk factors can help you recognize a supplement worth reviewing, identify a reason for thyroid monitoring, or bring better records to an appointment. Those are useful outcomes even when no single cause can be found.

Explore your exposure history with EXPIN - our interviews use all of the questions above to guide your review in an easy conversational format. Bring relevant details to your clinician and ask which, if any, could change your care. The goal is a clearer health history and more focused decisions, rather than certainty about why Hashimoto’s developed.

References

Numbered citations correspond to the article and evidence table. Links lead to journal records or authoritative clinical resources.

[1] Brix TH et al. A population-based study of chronic autoimmune hypothyroidism in Danish twins. JCEM. 2000. DOI: 10.1210/jcem.85.2.6385

[2] Skov J et al. Limited genetic overlap between overt Hashimoto’s thyroiditis and Graves’ disease in twins. JCEM. 2021; published online December 2020. DOI: 10.1210/clinem/dgaa956

[3] NIDDK. Hashimoto’s disease. Patient information.

[4] Wiersinga WM. Clinical relevance of environmental factors in the pathogenesis of autoimmune thyroid disease. Endocrinol Metab. 2016. DOI: 10.3803/enm.2016.31.2.213

[5] Hu X et al. Global prevalence and epidemiological trends of Hashimoto’s thyroiditis in adults. Front Public Health. 2022. DOI: 10.3389/fpubh.2022.1020709

[6] Teng W et al. Effect of iodine intake on thyroid diseases in China. NEJM. 2006. DOI: 10.1056/NEJMoa054022

[7] Teng D et al. An inverse relationship between iodine intake and thyroid antibodies. Thyroid. 2020. DOI: 10.1089/thy.2020.0037

[8] Stagnaro-Green A. Approach to the patient with postpartum thyroiditis. JCEM. 2012. DOI: 10.1210/jc.2011-2576

[9] Yoo WS et al. Incidence of endocrine-related dysfunction in patients treated with new immune checkpoint inhibitors. Endocrinol Metab. 2023. DOI: 10.3803/enm.2023.1785

[10] Lazarus JH. Lithium and thyroid. Best Pract Res Clin Endocrinol Metab. 2009. DOI: 10.1016/j.beem.2009.06.002

[11] Trip MD et al. Incidence, predictability, and pathogenesis of amiodarone-induced thyrotoxicosis and hypothyroidism. Am J Med. 1991. DOI: 10.1016/0002-9343(91)90187-3

[12] Tomer Y. Hepatitis C and interferon induced thyroiditis. J Autoimmun. 2010. DOI: 10.1016/j.jaut.2009.11.008

[13] Wu Q et al. Low population selenium status is associated with increased prevalence of thyroid disease. JCEM. 2015. DOI: 10.1210/jc.2015-2222

[14] Huwiler VV et al. Selenium supplementation in patients with Hashimoto thyroiditis: systematic review and meta-analysis of randomized trials. Thyroid. 2024. DOI: 10.1089/thy.2023.0556

[15] Carlé A et al. Smoking cessation is followed by a sharp but transient rise in the incidence of overt autoimmune hypothyroidism. Clin Endocrinol. 2012. DOI: 10.1111/j.1365-2265.2012.04455.x

[16] Effraimidis G et al. Discontinuation of smoking increases the risk for developing thyroid peroxidase antibodies and/or thyroglobulin antibodies: a prospective study. 2009. PMID: 19141579

[17] Associations of Helicobacter pylori infection and cytotoxin-associated gene A status with autoimmune thyroid diseases: a meta-analysis. 2013. PMID: 23544831

[18] Meta-analysis of the correlation between Helicobacter pylori infection and autoimmune thyroid diseases. 2017. PMID: 29383192

[19] Incident autoimmune diseases in association with SARS-CoV-2 infection: a matched cohort study. 2023. PMID: 37335408

[20] Štefanić M, Tokić S. Serum 25-hydroxyvitamin D concentrations in relation to Hashimoto’s thyroiditis: systematic review, meta-analysis and meta-regression. Eur J Nutr. 2020. DOI: 10.1007/s00394-019-01991-w

[21] Cross-sectional associations of serum perfluoroalkyl acids and thyroid hormones in US adults: variation according to TPOAb and iodine status. 2016. PMID: 26517287

[22] Relationship between urinary phthalate and bisphenol A concentrations and serum thyroid measures in US adults and adolescents. 2011. PMID: 21749963

[23] Thyroxine-binding globulin, peripheral deiodinase activity, and thyroid autoantibody status in association of phthalates and phenolic compounds with thyroid hormones. 2020. PMID: 32464474

[24] Association of exposure to a mixture of phenols, parabens, and phthalates with altered serum thyroid hormone levels. 2024. PMID: 39047362

[25] Pacini F et al. Prevalence of thyroid autoantibodies in children and adolescents from Belarus exposed to Chernobyl fallout. Lancet. 1998. DOI: 10.1016/S0140-6736(97)11397-6

[26] Effraimidis G et al. Involvement of stress in the pathogenesis of autoimmune thyroid disease: a prospective study. 2012. PMID: 22226433

[27] Carlé A et al. Moderate alcohol consumption may protect against overt autoimmune hypothyroidism: a population-based case-control study. Eur J Endocrinol. 2012. DOI: 10.1530/eje-12-0356

[28] Tarighat-Payma M et al. Long-term natural history of thyroid peroxidase antibodies: 18 years of follow-up in the Tehran Thyroid Study. J Transl Autoimmun. 2026. DOI: 10.1016/j.jtauto.2026.100358

[29] NIH Office of Dietary Supplements. Selenium fact sheet for health professionals.

[30] American Thyroid Association. Hashimoto’s thyroiditis.