Thyroid problems are most often caused by the immune system attacking the thyroid gland, but nutritional imbalances, genetics, medications, pregnancy, and environmental chemicals can all play a role. The two most common thyroid conditions, Hashimoto’s thyroiditis and Graves’ disease, are both autoimmune in origin. Understanding what drives thyroid dysfunction helps you recognize risk factors and make sense of a diagnosis.
Autoimmune Disease: The Most Common Cause
The immune system is behind the majority of thyroid problems. In Hashimoto’s thyroiditis, the leading cause of an underactive thyroid (hypothyroidism), a specific type of white blood cell infiltrates the thyroid and destroys the cells that produce hormones. The immune system also produces antibodies against an enzyme called thyroid peroxidase, which the gland needs to make its hormones. These antibodies are found in over 90% of people with Hashimoto’s. Over time, this ongoing destruction leaves the thyroid unable to keep up with the body’s demand for hormones, and levels gradually drop.
Graves’ disease works in the opposite direction. The immune system produces antibodies that mimic the signal your pituitary gland normally sends to the thyroid. These rogue antibodies latch onto receptors on thyroid cells, activating the same growth and hormone-production pathways that the natural signal would. The result is an overactive thyroid (hyperthyroidism) that churns out far more hormone than the body needs. Unlike Hashimoto’s, where the gland is slowly destroyed, Graves’ disease effectively jams the thyroid’s accelerator pedal down.
Genetics and Family History
If a close relative has a thyroid condition, your own risk goes up considerably. Twin studies estimate that about 79% of the susceptibility to Graves’ disease comes from genetic factors. Researchers have identified several genes that increase risk for both Graves’ disease and Hashimoto’s, each contributing a modest bump in susceptibility. Certain immune-related gene variants roughly double the odds of developing either condition. No single gene causes thyroid disease on its own, but carrying several of these variants together, combined with environmental triggers, can tip the balance.
This is why thyroid problems tend to cluster in families. If your mother or sister has Hashimoto’s, you’re not guaranteed to develop it, but your baseline risk is meaningfully higher than someone without that family history.
Iodine: Too Little or Too Much
Your thyroid needs iodine to manufacture hormones. Adults require about 150 micrograms per day (more during pregnancy and breastfeeding). When iodine is scarce, the thyroid can’t produce enough hormone, and the pituitary gland responds by pumping out more of its signaling hormone, TSH. Persistently elevated TSH can cause the thyroid to enlarge into a visible swelling called a goiter.
But excess iodine causes problems too. In people who already get enough iodine, a sudden surplus can paradoxically suppress hormone production and lead to hypothyroidism. In people who have been iodine-deficient for a long time, the opposite can happen: the thyroid may have developed independent nodules that no longer respond to normal regulatory signals. When iodine suddenly becomes available, these nodules can overproduce hormones, triggering hyperthyroidism. This is especially common in older adults with long-standing goiters. The takeaway is that iodine balance matters in both directions.
Medications That Affect the Thyroid
Several widely prescribed drugs can disrupt thyroid function as a side effect. Amiodarone, a heart rhythm medication, causes thyroid dysfunction in roughly 2% to 24% of patients depending on the dose. It contains a large amount of iodine and can push the thyroid toward either overproduction or underproduction. At lower doses, the rate of thyroid problems drops to around 4%, but the risk never disappears entirely.
Lithium, commonly used for bipolar disorder, is another well-known culprit. Hypothyroidism occurs in anywhere from 6% to 52% of people taking lithium, a wide range that reflects differences in dosing, duration, and individual susceptibility. If you take either of these medications, your doctor will typically monitor your thyroid function with regular blood tests. Other medications, including certain cancer immunotherapies, can also trigger thyroid inflammation.
Pregnancy and Postpartum Changes
About 1 in 20 women (5% to 10%) develop postpartum thyroiditis within the first year after giving birth. It follows a distinctive two-phase pattern. The first phase, usually between one and four months postpartum, involves a temporary surge of thyroid hormone as the inflamed gland leaks stored hormone into the bloodstream. This can cause anxiety, irritability, rapid heart rate, and difficulty sleeping.
The second phase, typically between four and eight months postpartum, swings in the other direction. The gland, now depleted and damaged, underproduces hormones, leading to fatigue, weight gain, brain fog, and depressed mood. These symptoms are easily mistaken for normal postpartum exhaustion or postpartum depression. Most women eventually recover full thyroid function, but a significant percentage go on to develop permanent hypothyroidism. Women who test positive for thyroid antibodies before or during pregnancy are at the highest risk.
Thyroid Nodules
Thyroid nodules are remarkably common. Up to 60% of adults have at least one, though most are too small to feel and are discovered incidentally during imaging for something else. On physical exam alone, doctors detect nodules in about 5% to 7% of adults, but ultrasound picks them up in 20% to 76% of the population.
The vast majority of nodules are benign. Only about 5% turn out to be cancerous (roughly 4% to 6.5% in clinical series). Most nodules don’t affect thyroid function at all. However, some nodules become “autonomous,” meaning they produce thyroid hormone independently of the body’s normal feedback system. These can cause hyperthyroidism, particularly if they grow large or if iodine intake increases suddenly. When a nodule is discovered, your doctor will evaluate its size, appearance on ultrasound, and sometimes perform a fine-needle biopsy to rule out cancer.
Environmental Chemicals
Certain industrial and environmental contaminants interfere directly with thyroid function. Perchlorate, found in some drinking water supplies (particularly in dry regions of the southwestern United States), blocks the thyroid’s ability to absorb iodine. This reduces hormone production in the person exposed and, during pregnancy, limits the amount of thyroid hormone available to the developing fetus. Perchlorate also crosses the placenta and suppresses hormone production in the fetal thyroid gland directly. The effects are worse when perchlorate exposure is combined with low iodine intake, which compounds the deficiency.
Other chemicals classified as endocrine disruptors, including certain industrial compounds found in nonstick coatings, flame retardants, and plastics, can interfere with how thyroid hormones are transported and used in the body. The effects of low-level chronic exposure are still being studied, but people with borderline iodine intake or existing thyroid vulnerability may be more susceptible.
Other Contributing Factors
Radiation exposure to the head or neck, whether from medical treatment or environmental sources, damages thyroid tissue and increases the risk of both hypothyroidism and thyroid cancer. This includes radiation therapy for childhood cancers, lymphoma, or head and neck tumors. The thyroid is one of the most radiation-sensitive organs in the body, and problems may not appear until years or decades after exposure.
Sex plays a major role in thyroid disease risk. Women are five to eight times more likely than men to develop thyroid conditions, a disparity that is partly explained by hormonal influences on the immune system and partly by the X chromosome carrying immune-related genes. Age also matters: the risk of hypothyroidism rises steadily after age 60, and thyroid nodules become more common with each decade of life. Smoking has been linked to an increased risk of Graves’ disease specifically, while stress and infections may act as triggers in people who are already genetically predisposed.