The most common cause of low thyroid (hypothyroidism) is an autoimmune condition called Hashimoto’s thyroiditis, where the immune system attacks and gradually destroys the thyroid gland. But autoimmunity is far from the only cause. Surgical removal of the thyroid, radiation treatment, certain medications, iodine imbalances, pregnancy, and even problems with the pituitary gland can all lead to an underactive thyroid.
Hashimoto’s Thyroiditis
In Hashimoto’s, the immune system mistakes thyroid tissue for a threat. A specific type of immune cell infiltrates the thyroid, causing inflammation and steadily killing the hormone-producing cells. At the same time, the body creates antibodies that target the gland. The most common of these, thyroid peroxidase antibodies, show up in over 90% of people with Hashimoto’s. Another type, thyroglobulin antibodies, appears in 50% to 80% of cases.
The destruction doesn’t happen overnight. Most people lose thyroid function gradually over months or years, sometimes passing through a stage called subclinical hypothyroidism where blood levels of thyroid hormone are still normal but the pituitary gland is already working harder to compensate. A key part of what goes wrong is that the immune cells responsible for keeping the system in check are suppressed, while the cells that drive inflammation are ramped up. This imbalance lets the attack continue unchecked.
Iodine: Too Little or Too Much
Your thyroid needs iodine to build its hormones, and the recommended daily intake for adults is 150 micrograms. In many parts of the world, iodine deficiency remains a leading cause of hypothyroidism and goiter. In countries where salt is iodized, outright deficiency is uncommon, but it still affects people with restricted diets or those who avoid iodized salt entirely.
Interestingly, too much iodine can also shut down thyroid hormone production. When the gland is flooded with iodine, it temporarily blocks the process of incorporating iodine into hormones as a protective mechanism. For most people this effect is temporary, but in those with underlying thyroid vulnerability, excess iodine can trigger lasting hypothyroidism.
Surgery and Radiation Treatment
Removing part or all of the thyroid through surgery (thyroidectomy) is one of the most straightforward causes of hypothyroidism. If the entire gland is removed, hypothyroidism is guaranteed and lifelong hormone replacement becomes necessary. Partial removal may or may not leave enough tissue to maintain normal hormone levels.
Radioactive iodine therapy, commonly used to treat an overactive thyroid, destroys thyroid tissue from the inside. The resulting hypothyroidism depends on the condition being treated. For Graves’ disease, 5% to 50% of patients develop hypothyroidism within the first year, with an additional 3% to 5% becoming hypothyroid each year after that. For a single overactive thyroid nodule, fewer than 10% develop permanent hypothyroidism. For a toxic multinodular goiter, the risk is higher, ranging from roughly 20% to 75% over eight years depending on the radiation dose used.
Medications That Affect the Thyroid
Several commonly prescribed drugs can interfere with thyroid function. Amiodarone, a heart rhythm medication, is one of the most significant. It contains a large amount of iodine and directly affects how the body processes thyroid hormones. It blocks the conversion of the less active form of thyroid hormone into its more potent form, and it can cause direct toxicity to thyroid cells. Roughly 15% to 20% of patients on amiodarone develop some form of thyroid dysfunction. Hypothyroidism specifically occurs in 10% to 20% of patients on short-term therapy and 5% to 10% of those taking it for more than a year.
Lithium, used to treat bipolar disorder, is another well-known culprit. It concentrates in thyroid tissue and inhibits hormone release. Other medications that can contribute include certain cancer immunotherapy drugs, tyrosine kinase inhibitors, and interferon-based treatments.
Postpartum Thyroiditis
Some women develop thyroid problems in the months after giving birth. Postpartum thyroiditis is an autoimmune inflammatory condition where antibodies and immune cells attack the thyroid, causing stored hormones to leak out of damaged cells. This creates a characteristic two-phase pattern.
The first phase, occurring one to four months after delivery, involves a temporary surge of thyroid hormone that can cause symptoms like anxiety, rapid heartbeat, and weight loss. This is followed by a hypothyroid phase, typically between four and eight months postpartum, as the damaged gland struggles to produce enough hormone. Many women recover full thyroid function within a year, but a significant percentage develop permanent hypothyroidism.
Pituitary and Brain-Related Causes
The thyroid doesn’t operate independently. It takes orders from the pituitary gland, a pea-sized structure at the base of the brain that releases thyroid-stimulating hormone (TSH). The pituitary itself takes direction from the hypothalamus, a region higher up in the brain. If either of these structures is damaged, the thyroid never gets the signal to produce hormones, even though the gland itself is perfectly healthy.
Pituitary tumors are the most common cause. They can compress the hormone-producing cells, block the blood supply that carries signals from the hypothalamus, or, rarely, bleed internally in a sudden event called pituitary apoplexy. Brain surgery, radiation to the head, traumatic brain injury, and certain infiltrative diseases can also damage these structures. This type of hypothyroidism, called central hypothyroidism, is trickier to diagnose because TSH levels may appear normal or even low rather than elevated.
Environmental Chemicals
Certain environmental contaminants interfere with the thyroid’s ability to absorb iodine, which is the essential first step in making thyroid hormones. Perchlorate, found in rocket fuel residue, fireworks, and some fertilizers, is among the most potent. It blocks the channel that transports iodine into thyroid cells and also suppresses the genes involved in hormone production.
Nitrate, widespread in drinking water and processed foods, inhibits the same iodine transport channel, though less powerfully than perchlorate. Thiocyanate, a compound found in cigarette smoke and certain foods like cassava, has a similar blocking effect and also interferes with how iodine is incorporated into thyroid hormones once inside the cell. For most people with adequate iodine intake, these exposures pose minimal risk. But in people who are already borderline iodine-deficient, the combined effect of these chemicals can tip the balance toward hypothyroidism.
Congenital Hypothyroidism
About 1 in 4,000 babies is born with a thyroid that didn’t form properly, a condition called thyroid dysgenesis. The gland may be missing entirely, underdeveloped, or located in the wrong place in the neck. Only 2% to 5% of these cases have an identifiable genetic cause, meaning most occur spontaneously during fetal development for reasons that aren’t fully understood.
Another 30% to 40% of babies identified through newborn screening have a thyroid gland in the right location but with a defect in the hormone-making machinery, known as dyshormonogenesis. These cases are more likely to have a clear genetic basis, involving mutations in genes responsible for various steps of hormone production. Newborn screening programs catch most cases within the first few days of life, allowing treatment to begin before any developmental harm occurs.
How Hypothyroidism Is Identified
Diagnosis centers on a blood test measuring TSH and free thyroxine (T4). When the thyroid is underperforming, the pituitary pumps out more TSH to try to compensate. Elevated TSH with low T4 confirms overt hypothyroidism. In subclinical hypothyroidism, TSH is elevated but T4 remains in the normal range.
Treatment guidelines from the American Thyroid Association and the American Association of Clinical Endocrinology recommend starting hormone replacement when TSH rises above 10 mIU/L, when symptoms of hypothyroidism are present, when thyroid antibodies test positive, or in women of reproductive age. The decision to treat milder elevations depends on the individual situation and whether symptoms are affecting quality of life.