Chills when you’re sick are your body’s way of generating heat to reach a higher internal temperature. When your immune system detects an infection, it essentially tricks your brain into thinking your normal body temperature is too low, triggering the same warming responses you’d experience standing outside in freezing weather. The result is shivering, goosebumps, and that deep feeling of cold, even though your actual temperature is rising.
How Your Brain Resets the Thermostat
Your brain has a built-in thermostat located in a region called the hypothalamus. Normally it keeps your body hovering around 98.6°F (37°C). When you catch an infection, your immune cells release signaling molecules called pyrogens that travel to the hypothalamus and raise that set point, sometimes to 100.4°F (38°C) or higher. At that moment, your brain perceives a gap: your actual body temperature is now “too cold” compared to the new target. So it launches the same heat-conserving strategies it would use if you were genuinely freezing.
Two things happen almost immediately. First, blood vessels near your skin’s surface narrow, pulling warm blood away from the surface and toward your core. That’s why your hands, feet, and skin feel cold and pale during a chill. Second, your brain sends signals through the spinal cord to your skeletal muscles, commanding them to contract rapidly and involuntarily. That rapid contraction is shivering, and it produces a significant burst of heat. These processes continue until the temperature of the blood flowing through the hypothalamus catches up to the new, higher set point. Once it does, the chills stop, even though you now have a fever.
The Chain Reaction Inside Your Immune System
The process starts when your immune system spots something foreign, whether it’s a virus, bacterium, or toxin. These invaders act as “exogenous pyrogens,” meaning they’re fever-triggering substances that come from outside the body. In response, your white blood cells produce their own signaling chemicals, the “endogenous pyrogens,” which are the real drivers of fever.
The key players are a handful of immune signaling molecules. One of the first to appear in the bloodstream after an infection triggers the immune response is TNF-alpha, which is considered a major regulator of fever. Shortly after, traces of IL-1 appear, followed by large amounts of IL-6, which tracks most closely with actual changes in body temperature during a fever. Each of these molecules contributes to the fever response, and blocking any one of them reduces but doesn’t completely eliminate it. They work as a team.
These signaling molecules ultimately stimulate the production of a compound called prostaglandin E2 in the hypothalamus. Prostaglandin E2 is the final messenger that actually alters the firing rate of temperature-sensitive brain cells, pushing the set point upward. This is also why common fever reducers like acetaminophen and ibuprofen work: they block the enzyme that produces prostaglandin E2 in the brain, which lowers the set point back toward normal and stops the chill cycle.
Chills vs. Rigors
Not all chills are created equal. The mild shivering and cold feeling you get with a typical cold or stomach bug is your garden-variety chill. But some infections produce something far more intense called a rigor. A rigor is a sudden, violent episode of shaking that you can’t control, often accompanied by a rapid spike in temperature. Your teeth may chatter, your whole body may tremble, and it can feel genuinely alarming.
Rigors are more commonly associated with serious bacterial infections like pneumonia, kidney infections, and bloodstream infections. They also occur with malaria and some viral infections including influenza. A true rigor almost always accompanies a fever. If you experience uncontrollable, intense shaking along with a high temperature, it typically signals that your body is mounting a strong immune response to something significant.
Why Fever (and Chills) Exist
It might seem counterproductive for your body to make you miserable when you’re already fighting an infection, but fever is actually a deliberate defense strategy. Many bacteria and viruses replicate more slowly at higher temperatures. A raised body temperature also speeds up certain immune functions, helping white blood cells move faster and work more efficiently. The chills are simply the cost of getting there: the shivering and vasoconstriction are the engines your body uses to push its temperature up to a level that’s hostile to whatever is making you sick.
Once your body temperature matches the new set point, you stop shivering and typically feel hot instead of cold. When the infection starts to resolve and your immune system dials back its signaling molecules, the set point drops back to normal. At that point, your body is now “too warm” relative to the thermostat, so you start sweating and flushing to cool down. That’s why the classic fever cycle goes: chills, then heat, then sweating.
Chills Without Fever
Sometimes you feel chills but don’t actually have a fever, which can be confusing. Several conditions unrelated to infection can trigger this. Hypothyroidism, where the thyroid gland doesn’t produce enough metabolism-regulating hormone, can make you more sensitive to cold and cause frequent chills. Iron-deficiency anemia reduces your blood’s ability to carry oxygen efficiently, and common symptoms include feeling cold, looking pale, and persistent fatigue. Low blood sugar can also trigger shivering and a cold sensation as your body responds to the energy drop.
If you’re experiencing recurring chills without any other signs of infection, like sore throat, cough, body aches, or congestion, it may point to one of these underlying issues rather than a passing illness.
When Chills Signal Something Serious
In most cases, chills accompany routine infections and resolve on their own. But chills combined with certain other symptoms can indicate sepsis, a life-threatening condition where the body’s response to infection starts damaging its own tissues. Warning signs include confusion or a sudden change in mental clarity, fast and shallow breathing, feeling lightheaded, extreme sleepiness or difficulty staying awake, and sweating without clear cause. If chills come with any of these symptoms, particularly confusion or rapid breathing, that combination requires emergency care. Sepsis progresses quickly, and early treatment dramatically improves outcomes.
How Fever Reducers Stop the Cycle
When you take acetaminophen or ibuprofen for a fever, you’re not just masking the symptom. These medications interrupt the process at its source by blocking the production of prostaglandin E2 in the brain. With less prostaglandin E2 acting on the hypothalamus, the temperature set point drops back toward normal. Once that happens, your body no longer perceives a gap between its current temperature and the target, so the shivering stops, blood flow to the skin returns, and the chills fade. The two medications work slightly differently at the molecular level (ibuprofen competes directly with the raw materials the enzyme needs, while acetaminophen deactivates the enzyme itself), but the end result is the same: the thermostat resets, and your body stops trying to warm up.