Thyroid cancer starts when cells in the thyroid gland develop DNA mutations that cause them to grow out of control. In most cases, there’s no single clear cause. Instead, a combination of genetic predisposition, environmental exposures, and sometimes just bad luck drives the process. Women are nearly three times more likely to develop thyroid cancer than men, with about 20 new cases per 100,000 women annually compared to 7.4 per 100,000 men. The median age at diagnosis is 51.
What Happens Inside the Thyroid
Your thyroid is a butterfly-shaped gland at the base of your neck that produces hormones regulating metabolism. Thyroid cancer develops through a multistep process where normal thyroid cells accumulate genetic changes over time. Early mutations may produce a slow-growing, well-behaved tumor. Additional mutations can push those cells toward more aggressive behavior.
One of the most common genetic changes is a mutation called BRAF, which flips on a growth-signaling pathway and keeps it permanently active. This mutation is especially common in papillary thyroid cancer, the most frequent type. Other mutations in growth-regulating genes (like RAS) play a role in different subtypes. When cells pile up enough of these genetic errors, they lose the ability to stop dividing, forming a tumor that can eventually spread to lymph nodes or other organs.
Radiation Exposure, Especially in Childhood
The strongest known environmental risk factor for thyroid cancer is exposure to ionizing radiation during childhood. Children’s thyroid glands are still developing, which makes the cells more vulnerable to radiation-induced DNA damage. Studies of atomic bomb survivors in Hiroshima and Nagasaki, children who received radiation treatments for head and neck conditions, and populations exposed to nuclear fallout all show elevated thyroid cancer rates decades later.
Radioactive iodine (I-131) from nuclear fallout is particularly relevant because the thyroid absorbs iodine to make hormones. Children in the Mountain West, Midwest, and Eastern United States who drank milk during the era of aboveground nuclear testing (1945 to 1963) likely received higher thyroid doses from contaminated pastures. The risk increases with younger age at exposure and with repeated exposures. Adult thyroid tissue, by contrast, appears much more resistant to radiation-induced cancer.
Inherited Genetic Risk
Most thyroid cancers are not inherited, but genetics can load the dice. Having a first-degree relative with thyroid cancer raises your own risk. The clearest hereditary link involves medullary thyroid cancer, a less common type that originates from different cells than the other subtypes. About 25% of medullary thyroid cancers are inherited through mutations in the RET gene, which is passed down in families as part of a condition called multiple endocrine neoplasia type 2 (MEN2). People with known RET mutations are often offered genetic counseling and preventive monitoring or surgery.
For the more common papillary and follicular types, the genetic picture is murkier. No single gene drives most cases, but a family history of thyroid disease in general, including noncancerous conditions, is considered a risk factor.
Iodine Intake and Thyroid Function
Iodine, the mineral your thyroid needs to produce hormones, plays a complex role. Both too little and too much may influence risk. In a case-control study, excessive iodine intake was associated with an 18-fold higher odds of papillary thyroid cancer compared to adequate intake. When excessive iodine combined with high levels of circulating thyroid hormone, the odds climbed even higher. Iodine deficiency, meanwhile, has been linked to follicular thyroid cancer in regions where it’s common, though it was rare in the study populations examined.
This doesn’t mean iodine-rich foods are dangerous. The relationship likely matters most at extremes and may interact with other thyroid conditions. For most people eating a varied diet, iodine intake falls within normal range.
Existing Thyroid Conditions
Several benign thyroid problems are associated with a higher chance of eventually developing thyroid cancer. These include an enlarged thyroid (goiter), Hashimoto’s disease (an autoimmune condition that attacks the thyroid), and thyroid nodules. That said, thyroid lumps are extremely common, and only about 5 out of 100 turn out to be cancerous. Most people with these conditions will never develop cancer, but having them does warrant closer monitoring.
Environmental Chemicals
A growing body of research points to certain environmental pollutants that disrupt hormone signaling and may contribute to thyroid cancer risk. A large meta-analysis found positive associations between thyroid cancer and exposure to flame retardants (polybrominated diphenyl ethers), phthalates (found in plastics and personal care products), and several heavy metals including cadmium, lead, mercury, and arsenic. Bisphenol A (BPA), despite being a known endocrine disruptor, did not show a statistically significant link to thyroid cancer in the same analysis.
These chemicals are widespread in household products, industrial settings, and contaminated water. The strength of these associations varies, and exposure levels matter. But for people with occupational exposure to heavy metals or flame retardants, the connection is worth being aware of.
The Four Main Types
Not all thyroid cancers behave the same way, and the type you develop partly depends on which cells mutate and which genetic changes accumulate.
- Papillary thyroid cancer accounts for the majority of cases. It grows slowly and has an excellent prognosis, even when it has spread to nearby lymph nodes.
- Follicular thyroid cancer is the second most common type. It’s more likely than papillary cancer to spread to distant sites like the lungs and bones, though outcomes are still generally favorable.
- Medullary thyroid cancer arises from a different cell type (C cells that produce a hormone called calcitonin rather than thyroid hormone). About 75% of cases are sporadic, with the remaining 25% linked to inherited RET gene mutations.
- Anaplastic thyroid cancer is rare and aggressive. It sometimes develops from a pre-existing papillary or follicular cancer that accumulates additional mutations driving it toward rapid, undifferentiated growth. Average survival is about six months, though some patients do survive longer.
How Thyroid Cancer Gets Detected
Thyroid cancer often produces no symptoms in its early stages. Many cases are found incidentally during imaging for something else entirely, or when a lump is noticed in the neck during a routine physical exam. When a nodule is found, the standard evaluation involves a blood test measuring thyroid-stimulating hormone (TSH) and an ultrasound of the thyroid and surrounding lymph nodes.
On ultrasound, features that raise suspicion for cancer include a solid nodule that appears darker than surrounding tissue, irregular margins, tiny calcium deposits (microcalcifications), and a shape that’s taller than it is wide. Purely cystic (fluid-filled) nodules are rarely cancerous and typically don’t need a biopsy. For suspicious nodules 1 cm or larger, a fine-needle aspiration biopsy is used to collect cells for examination under a microscope. Spongy or mostly cystic nodules generally aren’t biopsied unless they reach 2 cm or more.
Because thyroid nodules are so common and the vast majority are benign, finding a lump doesn’t mean you have cancer. But nodules that meet the size and appearance criteria above do warrant further evaluation to rule it out.