Calcitonin is a hormone that lowers calcium levels in your blood by slowing the breakdown of bone and helping your kidneys flush out excess calcium. Your body produces it naturally, and a synthetic version is used as a medication for bone disorders. Here’s how it works at each level.
Where Calcitonin Comes From
Calcitonin is made by specialized cells in your thyroid gland called C-cells (or parafollicular cells). These sit alongside the follicular cells that produce the better-known thyroid hormones T3 and T4, but they have a completely different job. C-cells act as calcium sensors. When calcium in your blood rises above normal, C-cells release calcitonin into the bloodstream to bring it back down.
The primary trigger is elevated blood calcium, though other signals like the gut hormone gastrin can also stimulate release. Normal baseline calcitonin levels are quite low: 8.4 pg/mL or less in men and 5.0 pg/mL or less in women.
How It Slows Bone Breakdown
Your bones are constantly being remodeled. Cells called osteoclasts break down old bone tissue, releasing calcium and other minerals into the bloodstream. Calcitonin’s main job is to put the brakes on this process.
Osteoclasts have calcitonin receptors on their surface. These belong to a family of receptors that work through a signaling molecule called a G protein. When calcitonin binds to these receptors, it sets off a chain of internal signals. The cell produces a messenger molecule (cyclic AMP) that activates enzymes inside the osteoclast, ultimately telling the cell to stop dissolving bone. The osteoclast essentially pauses its resorption activity. Less bone breakdown means less calcium flooding into your blood, which is how calcitonin brings elevated calcium levels down.
What It Does in the Kidneys
Calcitonin also acts on your kidneys, though its effects there are more nuanced than you might expect. Rather than simply dumping calcium into urine, calcitonin actually increases the reabsorption of calcium and magnesium in the kidney tubules, conserving these minerals. At the same time, it promotes a small but measurable increase in phosphate excretion. The net result is that calcitonin helps redistribute calcium rather than waste it, pulling it out of the blood while preserving some through kidney conservation. This makes calcitonin, like parathyroid hormone, a calcium-conserving hormone in the kidneys.
The Balance With Parathyroid Hormone
Calcitonin doesn’t work alone. It operates as part of a feedback system with parathyroid hormone (PTH), and the two hormones act as physiological antagonists. When blood calcium drops too low, your parathyroid glands release PTH, which increases bone breakdown, boosts calcium reabsorption in the kidneys, and indirectly increases calcium absorption from food through vitamin D activation. When blood calcium rises too high, your thyroid C-cells release calcitonin, which does roughly the opposite: it suppresses bone breakdown and adjusts kidney handling of calcium.
Think of it like a thermostat with two settings. PTH turns the heat up (raises calcium), calcitonin turns it down (lowers calcium). Together, they keep blood calcium within a tight range that your muscles, nerves, and heart need to function properly. PTH is considered the more dominant regulator in everyday calcium balance, while calcitonin plays a stronger role when calcium spikes acutely.
How Synthetic Calcitonin Works as a Medication
The calcitonin used in medications is a synthetic version modeled after salmon calcitonin, not the human form. This matters because salmon calcitonin is about 50 times more potent than human calcitonin. Researchers believe this is because the salmon version folds into its active shape more readily, allowing it to bind receptors more effectively.
Synthetic calcitonin is available as a nasal spray or injection and is used in two main situations: treating high blood calcium (hypercalcemia) and managing postmenopausal osteoporosis. For hypercalcemia, calcitonin works faster than most other options, lowering calcium within about 2 hours of the first dose. Its peak effect occurs at 24 to 48 hours, with the blood-calcium-lowering action lasting 4 to 7 days in most cases.
For osteoporosis, calcitonin nasal spray is reserved for women who are more than 5 years past menopause and cannot use or tolerate other treatments. It’s considered a second-line option because it has not been shown to reduce fracture risk, and it doesn’t increase bone mineral density in women who are in early menopause.
Side Effects of Calcitonin Therapy
The nasal spray and injectable forms have different side effect profiles. The nasal spray most commonly causes nasal symptoms: runny nose, crusting, dryness, irritation, and occasionally nosebleeds. About 12% of patients in clinical studies experienced nasal inflammation, and roughly 11% reported other nasal symptoms. Back pain, joint pain, and headache each occurred in 3% to 5% of patients. Rare cases of nasal ulceration have been reported, sometimes requiring a temporary break from treatment.
The injectable form causes more systemic side effects. Nausea occurs in about 10% of patients receiving injections, compared to less than 2% with the nasal spray. Flushing affects 2% to 5% of injection users but under 1% of nasal spray users. Because calcitonin is a protein, allergic reactions are possible with either form, though they are uncommon.