The most common cause of low thyroid levels in developed countries is Hashimoto’s thyroiditis, an autoimmune condition where the immune system gradually destroys the thyroid gland. It affects up to 10% of the population. But autoimmune disease is far from the only cause. Surgery, medications, iodine problems, pregnancy, infections, and pituitary disorders can all drive thyroid hormone levels down.
Hashimoto’s Thyroiditis
In Hashimoto’s thyroiditis, immune cells infiltrate the thyroid and destroy the follicles that produce hormones. This isn’t a sudden event. It happens over months or years, which is why many people don’t notice symptoms until a significant amount of thyroid tissue is already damaged. The hallmark of the disease is the presence of antibodies against thyroid proteins circulating in the blood, and nearly all patients with high levels of these antibodies show intense immune cell activity in the gland itself.
The condition is far more common in women and becomes more likely with age. Its cause appears to be a combination of genetic susceptibility and environmental triggers, though the specific triggers vary from person to person. Because the destruction is gradual, some people spend years in a “subclinical” phase where their thyroid-stimulating hormone (TSH) is creeping up but their actual hormone levels haven’t dropped enough to cause obvious symptoms.
Thyroid Surgery
Removing all or part of the thyroid gland is one of the most straightforward paths to low thyroid levels. Total thyroidectomy causes permanent hypothyroidism in essentially 100% of patients, since there’s simply no tissue left to make hormones. Near-total and subtotal procedures produce similar rates, around 87% to 100%. Even a hemithyroidectomy, where only one lobe is removed, leads to permanent hypothyroidism in about 28% of patients. The remaining lobe can often compensate, but not always. Nearly half of hemithyroidectomy patients experience at least a temporary dip in thyroid function before their remaining tissue picks up the slack.
Radioactive Iodine Treatment
Radioactive iodine therapy is commonly used to treat an overactive thyroid, particularly Graves’ disease. It works by destroying thyroid cells, but the trade-off is that it frequently destroys enough tissue to cause the opposite problem. In one large study, the overall rate of permanent hypothyroidism after repeated treatments was about 51%. Most of these cases, roughly three-quarters, developed after the first dose. Higher doses were more effective at controlling the overactive thyroid but also more likely to tip patients into hypothyroidism, with rates approaching 48% after a single high-dose treatment. For most people, this outcome is expected and managed with daily thyroid hormone replacement.
Medications That Affect the Thyroid
Several widely prescribed drugs can interfere with thyroid function. Two of the best-known culprits are lithium (used for bipolar disorder) and amiodarone (used for irregular heart rhythms).
Lithium increases iodine buildup inside the thyroid while simultaneously blocking the steps needed to assemble and release thyroid hormones. The result is a gland full of raw materials but unable to produce a finished product.
Amiodarone is unusually rich in iodine. Each dose releases large amounts of iodide as it’s broken down, and that flood of iodine overwhelms the thyroid’s normal regulatory mechanisms. In a healthy thyroid, a sudden spike in iodine temporarily slows hormone production, then the gland adapts and resumes normal output. In susceptible people, that adaptation never happens, and hormone production stays suppressed. Amiodarone also interferes with enzymes that convert thyroid hormones into their active forms in tissues throughout the body.
Iodine Deficiency and Excess
Your thyroid needs iodine to build its hormones. Adults require about 150 micrograms per day, with higher needs during pregnancy (220 to 250 mcg) and breastfeeding (290 mcg). When intake drops below about 100 mcg per day, the pituitary gland ramps up TSH to push the thyroid harder. If intake falls below 10 to 20 mcg per day, even that compensatory effort fails and hypothyroidism sets in, often accompanied by a visible enlargement of the thyroid called a goiter.
Iodine deficiency remains a leading cause of hypothyroidism worldwide, though it’s uncommon in countries with iodized salt. Paradoxically, too much iodine can also suppress thyroid function in people whose glands are already vulnerable. High iodine intake inhibits hormone production and can trigger the same symptoms as deficiency, including goiter and elevated TSH.
Pituitary and Brain-Related Causes
Sometimes the thyroid gland itself is perfectly healthy, but it never receives the signal to produce hormones. That signal comes from TSH, which is made by the pituitary gland at the base of the brain. Pituitary tumors, surgery, radiation therapy, traumatic brain injuries, and inflammatory conditions can all damage the pituitary enough to reduce or eliminate TSH production. This is called secondary or central hypothyroidism.
When a pituitary tumor grows, it tends to knock out hormone production in a predictable sequence: growth hormone goes first, then the hormones controlling reproduction, and then TSH. This means that by the time someone develops low thyroid levels from a pituitary problem, they often have other hormonal deficiencies as well. Central hypothyroidism can be tricky to diagnose because TSH levels may appear normal or only mildly abnormal, even though the thyroid is genuinely underperforming.
Thyroid Inflammation
Viral infections can trigger a painful inflammation of the thyroid called subacute thyroiditis. The illness typically unfolds in phases. In the first weeks, the inflamed gland leaks stored hormone into the bloodstream, which can actually cause temporary symptoms of an overactive thyroid. As the stored hormone is depleted and the damaged gland struggles to produce more, a hypothyroid phase follows. This painful process lasts anywhere from a week to a few months.
The good news is that over 90% of people with classic subacute thyroiditis recover completely and return to normal thyroid function. Up to 10%, however, sustain enough scarring that they need permanent hormone replacement.
Postpartum Thyroiditis
About 5% to 10% of people develop thyroid inflammation in the months after giving birth. Postpartum thyroiditis follows a similar pattern to subacute thyroiditis: an initial phase of excess hormone release, followed by a hypothyroid dip, and then a gradual return to normal within 3 to 6 months. Most people recover fully, but 20% to 50% remain hypothyroid a year after delivery. The risk of permanent hypothyroidism is highest in those who already carry thyroid antibodies or have a history of autoimmune thyroid disease, with about 20% of affected individuals ultimately needing lifelong treatment.
Congenital Hypothyroidism
Some babies are born with low thyroid levels. In 80% to 85% of cases, this happens because the thyroid gland didn’t develop properly during pregnancy, and the reason is often unknown. The remaining 15% to 20% of cases are caused by genetic changes that prevent the thyroid from manufacturing hormones correctly, even when the gland itself is present. Congenital hypothyroidism can also appear as part of a broader genetic condition; babies with Down syndrome, for example, have higher rates.
Newborn screening programs catch most cases within the first few days of life, which is critical because untreated congenital hypothyroidism can impair brain development. Early treatment with thyroid hormone replacement allows normal growth and development in the vast majority of affected children.