Hashimoto’s disease develops when your immune system mistakenly attacks your thyroid gland, but no single cause explains why this happens. It results from a combination of genetic predisposition, hormonal factors, and environmental triggers that together push the immune system to turn against healthy thyroid tissue. The disease affects 1 to 2 percent of people in the United States, with most cases diagnosed between ages 30 and 60.
What Happens Inside the Thyroid
In Hashimoto’s, certain immune cells (B cells and T cells) infiltrate the thyroid gland and begin destroying the cells that produce thyroid hormones. This destruction is gradual. Over months or years, the thyroid loses its ability to keep up with your body’s hormone needs, eventually leading to hypothyroidism, where hormone levels drop too low.
The hallmark of the disease is follicular destruction. The tiny sacs inside your thyroid that store and release hormones are progressively broken down. Nearly all patients with Hashimoto’s show a dense, widespread immune cell infiltration throughout the gland. Your body essentially treats the thyroid like a foreign invader and slowly dismantles it.
Genetics Set the Stage
Hashimoto’s runs in families. If a close relative has the disease or another autoimmune condition, your own risk is significantly higher. Several gene variants related to immune system regulation have been linked to increased susceptibility. These genes influence how your immune system distinguishes your own tissues from genuine threats, and certain inherited versions make that distinction less reliable.
Having the genetic predisposition alone isn’t enough to cause the disease. Most researchers describe Hashimoto’s as requiring a “second hit,” some environmental or hormonal trigger that activates the autoimmune process in someone already genetically vulnerable.
Why Women Are Affected Far More Often
Hashimoto’s is significantly more common in women than in men. Estrogen plays a direct role in this imbalance. It influences both the number and behavior of immune cells and can stimulate the production of thyroid antibodies, the very molecules that drive the autoimmune attack. Estrogen also affects the signaling pathway between the brain and the thyroid gland, which helps explain why the disease often emerges or worsens during periods of hormonal change like pregnancy, postpartum, and perimenopause.
Viral Infections as a Trigger
Certain viral infections appear to set off Hashimoto’s in genetically susceptible people. The Epstein-Barr virus (EBV), best known for causing mono, is the most studied example. Parts of the virus share a structural resemblance to proteins found in the thyroid, specifically thyroid peroxidase and thyroglobulin. When the immune system mounts a response against EBV, it can accidentally “learn” to attack those similar-looking thyroid proteins. This case of mistaken identity, called molecular mimicry, leads to the production of anti-thyroid antibodies.
Studies have found elevated levels of EBV-related antibodies in Hashimoto’s patients. EBV also appears to weaken the specific immune cells responsible for clearing infected cells, allowing the virus to linger and continuously provoke the immune system. This persistent stimulation can sustain and worsen the autoimmune response over time.
Iodine and Other Dietary Factors
Iodine has a complex relationship with Hashimoto’s. Your thyroid needs iodine to make hormones, but too much can actually trigger or worsen autoimmune thyroiditis. This has been observed in populations that consume large amounts of seafood, sea vegetables, or iodine supplements. Excess iodine can cause a form of hypothyroidism that resolves once intake drops back to normal, but in someone with genetic susceptibility, it may also kickstart a lasting autoimmune process.
Selenium, a trace mineral, plays a protective role in thyroid function. There is evidence that selenium supplementation can reduce levels of TPO antibodies (the main marker of Hashimoto’s) and improve mood and overall well-being in people with the disease. However, taking selenium when you’re also iodine-deficient can backfire and worsen thyroid function, so the two nutrients need to be considered together.
Stress and the Thyroid Connection
Chronic stress affects the thyroid indirectly through the adrenal glands. When you’re under sustained stress, your adrenal glands release cortisol. Elevated cortisol suppresses the production of thyroid-stimulating hormone (TSH), which disrupts the balance of thyroid hormones throughout your body. While stress alone probably doesn’t cause Hashimoto’s, it can worsen thyroid dysfunction and may act as one of several triggers in someone who is already predisposed.
Other Autoimmune Conditions Raise Your Risk
Hashimoto’s rarely exists in isolation. If you already have one autoimmune condition, your chances of developing another are higher. Celiac disease is one of the most common companions. The prevalence of celiac disease in people with autoimmune thyroid disorders is about four times greater than in the general population. Type 1 diabetes, rheumatoid arthritis, and lupus are also associated with increased Hashimoto’s risk. This clustering suggests shared underlying immune system dysfunction rather than completely separate disease processes.
How Hashimoto’s Is Confirmed
The diagnosis relies on blood tests that measure two things: thyroid hormone levels and specific antibodies. The most important antibody is thyroid peroxidase antibody (TPOAb). Normal levels fall below 5.6 IU/ml. If your TPOAb is elevated and your TSH is high (meaning your thyroid is underperforming), that combination points strongly to Hashimoto’s. Thyroglobulin antibodies (TgAb), normally below 4 IU/ml, can also signal the disease.
An interesting nuance: you can test positive for TPO antibodies while your thyroid hormone levels are still normal. This means the autoimmune process has started, but your thyroid hasn’t been damaged enough yet to affect hormone output. People in this situation have a higher likelihood of developing full hypothyroidism later in life, which is why doctors sometimes monitor antibody-positive patients over time even before symptoms appear.
Putting It All Together
There’s no single way you “get” Hashimoto’s. The disease emerges from a layered combination of inherited genetic risk, hormonal environment (particularly estrogen), and one or more external triggers like viral infections, excess iodine, or prolonged stress. Some of these factors you can’t control, like your genes or a past EBV infection. Others, like iodine intake and stress management, offer at least some room for influence. Most people diagnosed with Hashimoto’s will never pinpoint exactly which trigger tipped the balance, because it’s typically several factors converging over years.