An autoimmune condition that affects the thyroid gland, known as autoimmune hypothyroidism, is the most common autoimmune disease in the world.
Despite affecting millions of people, especially women, it has not been studied as deeply as many other diseases.
This condition occurs when the body’s immune system mistakenly attacks the thyroid, a small gland in the neck that produces hormones controlling metabolism, energy levels, and body temperature.
When the thyroid is damaged, hormone production drops, leading to symptoms such as fatigue, weight gain, feeling cold, and depression.
Now, a major international study led by scientists from the Broad Institute and the University of Helsinki has uncovered new details about the genetic causes of this disease.
By analyzing genetic data from more than 81,000 people with autoimmune hypothyroidism, researchers identified over 400 genetic markers linked to the condition. This is far more than previously known and provides a clearer picture of why some people develop the disease while others do not.
The scientists used large health databases from Finland and the United Kingdom, which contain genetic information and medical records from hundreds of thousands of volunteers.
These resources allowed them to compare people with thyroid disease to those without it and identify differences in their genes. Nearly 50 of the genetic markers they found directly affect proteins involved in immune responses and thyroid function, suggesting that both the immune system and the organ itself play important roles.
One of the most surprising discoveries was a connection between thyroid disease risk and cancer risk. Some of the genetic changes that increase the chance of developing autoimmune hypothyroidism appear to reduce the likelihood of developing skin cancer. This finding suggests that the immune system may act differently in people depending on their genetic makeup.
In autoimmune diseases, the immune system becomes overactive and attacks healthy tissues. In contrast, cancer often develops when the immune system fails to recognize and destroy abnormal cells.
The study suggests that certain genetic changes may push the immune system toward being more aggressive, which could increase the risk of autoimmune conditions but also help the body fight cancer more effectively.
The researchers found that some of the genes involved control proteins known as immune checkpoints. These proteins act like brakes that prevent the immune system from attacking normal cells.
When these brakes are weaker, the immune system may attack both cancer cells and healthy tissues. This could explain why some cancer treatments that remove these brakes can cause autoimmune side effects, including thyroid problems.
Doctors have observed that cancer patients treated with certain immunotherapy drugs sometimes develop thyroid disease as a side effect. Interestingly, these patients often respond well to treatment. The new study offers a possible explanation, showing that genetics may influence how strongly a person’s immune system reacts.
The research also revealed that autoimmune hypothyroidism is not caused by a single factor. About one-third of the genetic signals were linked to general immune system activity, while others were specific to the thyroid gland. This helps explain why autoimmune diseases often affect certain organs while leaving others untouched.
Scientists believe these findings could lead to better ways of predicting who is at risk and developing more targeted treatments in the future. Understanding the genetic differences behind the disease may also help explain why symptoms and severity vary from person to person.
Although much more research is needed, the study shows how large genetic databases can uncover hidden connections between diseases. By learning how the immune system is controlled, researchers hope to develop therapies that balance protection against infections and cancer while preventing the body from attacking itself.
This work marks an important step toward understanding one of the most common autoimmune conditions and its surprising links to cancer risk, offering new hope for improved diagnosis, prevention, and treatment in the future.
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