Your brain’s internal thermostat, located in a region called the hypothalamus, gets deliberately reset to a higher temperature when you’re fighting an infection. That mismatch between where your body temperature actually is and where the brain now wants it to be is what produces the alternating waves of chills and heat. You feel freezing cold while your temperature climbs toward the new, higher target, then uncomfortably hot once you overshoot it or your brain resets the target back down. The whole cycle is orchestrated by your immune system, and it serves a purpose that goes well beyond making you miserable.
How Your Brain’s Thermostat Gets Reset
When a virus or bacterium invades your body, immune cells detect the threat and release signaling molecules called cytokines. Three of the most important fever-inducing cytokines are interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha). These molecules act on the brain both directly and indirectly, ultimately reaching the hypothalamus and triggering it to raise the body’s temperature set point.1PubMed. Cytokines and fever. Mechanisms and sites of action Research using antibodies that block IL-1 and IL-6 has shown that when you neutralize these signals, fevers are consistently reduced, confirming their role as the body’s internal fever-starters.2PubMed. Invited review: cytokine regulation of fever: studies using gene knockout mice
The cytokines don’t simply flip a switch. They trigger the production of prostaglandin E2 (PGE2) in the preoptic area of the hypothalamus, which is the specific zone responsible for monitoring and regulating core temperature. PGE2 suppresses the neurons that normally keep your temperature stable, effectively telling the brain: “The current temperature is too low. Heat up.”3PubMed. Physiology, Fever This is also why drugs like aspirin and ibuprofen can bring a fever down. They block prostaglandin production, which lowers the thermostat back toward normal without addressing the underlying infection.
Why You Feel Cold First
The chills that come at the start of a fever are counterintuitive. You’re about to get hot, so why do you feel like you’ve been dropped into an ice bath? The answer is that your brain has just raised the target temperature, but your body hasn’t caught up yet. From the hypothalamus’s perspective, your normal 37°C is now below the new set point. Your brain interprets that gap the same way it would interpret actually being cold: it activates every warming mechanism it has.
The first response is cutaneous vasoconstriction, a narrowing of the blood vessels near your skin’s surface. This traps warm blood deeper in your body to prevent heat loss through the skin.4Handbook of Clinical Neurology. Efferent thermoregulatory pathways regulating cutaneous blood flow and sweating – Section: Efferent neural pathways for fever Your skin turns pale and feels cold to the touch, which reinforces the subjective sensation of freezing. Then comes shivering, your muscles contracting rapidly and involuntarily to generate heat. Research has traced both the shivering and the vasoconstriction during fever to the same brain circuits that drive ordinary cold-defense responses. Neurons in the dorsomedial hypothalamus and a brainstem region called the rostral raphe pallidus fire up to produce thermogenesis, increased heart rate, and constricted skin blood vessels, all driven by excitatory signals that are normally held in check but get released when PGE2 enters the picture.5PubMed Central. Central efferent pathways for cold-defensive and febrile shivering
This is also why you instinctively pile on blankets and curl up when a fever is rising. Your brain is receiving a genuine “you’re too cold” signal, even though your actual temperature is normal or already elevated. Behaviorally and physiologically, the chill phase of a fever is nearly identical to what happens when you step outside on a freezing day without a coat.
Why the Heat Comes Next
Once your body temperature reaches the new set point, the chills stop and you enter a plateau phase. You feel warm, your skin flushes, and you may start to sweat. The hypothalamus is now satisfied that your temperature matches its target, so it stops driving heat-generating mechanisms. When the set point eventually starts dropping, either because the immune system is gaining the upper hand or because you’ve taken a fever-reducing medication, the process reverses. Your body now has more heat than the thermostat calls for, so the brain triggers heat-loss responses: blood vessels in the skin dilate, sending warm blood toward the surface, and your sweat glands kick in.6PubMed. Central circuitries for body temperature regulation and fever
This is the “hot flash” phase of being sick, and it can be just as uncomfortable as the chills. You might soak through your sheets overnight as your body dumps the excess heat. A qualitative study of fever experiences found that about three-quarters of patients reported feeling warm during fevers, while nearly two-thirds described clamminess and perspiration. Roughly four out of five people reported feeling cold, having chills, or shivering at some point during their febrile episodes.7PubMed Central. Beyond Intuition: Patient Fever Symptom Experience Most people cycle through both sensations, sometimes multiple times in a day, because fever set points often fluctuate as immune signaling ebbs and flows.
Why Your Body Bothers With All This
Fever is not a malfunction. It’s a defense strategy that has been conserved in warm-blooded and cold-blooded vertebrates for over 600 million years of evolution, which is a strong hint that it provides a real survival advantage.8PubMed Central. Fever and the thermal regulation of immunity: the immune system feels the heat The elevated temperature does several useful things simultaneously. It boosts the mobility and killing power of immune cells like neutrophils and natural killer cells. It increases the production of interferons, which have direct antiviral activity. It stresses pathogens and infected cells by inducing heat shock proteins, which then help flag those cells for destruction. And it makes rapidly dividing microbes more vulnerable to other immune attacks, creating a kind of combined assault that is greater than the sum of its parts.9PubMed Central. Let fever do its job: The meaning of fever in the pandemic era
That said, this defense comes with a real cost.
The Energy Price of Running a Fever
Heating your body above its normal temperature takes fuel. Calorimetry studies have shown that fever and infection together lead to measurably higher metabolic heat production, which, combined with the reduced appetite that typically accompanies illness, creates a significant energy deficit.10PubMed. The metabolic cost of fever One study of children on intravenous nutrition found that energy expenditure increased by about 11% for every degree Celsius of fever, and protein breakdown rose as well, reflecting the body’s need to fuel the immune response even at the expense of its own tissues.11Clinical Nutrition. Energy cost of fever in children on total parenteral nutrition
The metabolic burden can be even more dramatic in malnourished individuals. Research on children with acute malaria found that resting energy expenditure rose by an average of 30% during febrile episodes, with the magnitude of the increase influenced by the child’s nutritional status. Kids who were more underweight showed a different metabolic response, underscoring how illness and malnutrition compound each other.12Pediatric Research. Effect of Malaria and Fever on Energy Metabolism in Gambian Children This metabolic cost helps explain why you feel so wiped out after even a moderate fever. Your body has been burning through calories at an accelerated rate while simultaneously diverting resources to immune function.
How Fever Changes With Age
The hot-and-cold cycle described above is a robust response in young, healthy adults, but it shifts considerably in older people. Research consistently shows that older adults are less able to mount an effective fever.13PubMed Central. Altered Febrile Responses in Older Adults: A Systematic Review Where a younger person with a serious infection might spike a temperature of 39°C or higher along with vigorous chills, an older adult with the same infection might run only a low-grade fever or none at all. The classic chills-and-sweats pattern may be replaced by subtler symptoms like confusion, weakness, or a general decline in function.14Journal of the Indian Academy of Geriatrics. Fever in Older Persons – Section: DIFFERENCE BETWEEN THE YOUNG AND THE OLDER INDIVIDUALS
This blunted response is partly due to age-related changes in the immune system, which produces fewer and less potent cytokine signals. It’s a double-edged problem: the very mechanism that makes young people uncomfortable during a fever, that aggressive thermostat reset, is also what mobilizes a strong immune defense. When the signal weakens, both the discomfort and the protective benefit diminish. For caregivers, the practical takeaway is that the absence of a high fever in an older person does not mean the absence of a serious infection. In that age group, even a small rise in temperature can be clinically meaningful.
Fever Is Not the Same as Overheating
There’s a meaningful distinction between fever and other forms of elevated body temperature, and it matters for understanding the hot-and-cold experience. Fever involves a regulated increase, meaning the hypothalamic set point moves upward and the body uses normal thermoregulatory mechanisms to reach the new target. The cold sensations, shivering, and vasoconstriction are all part of that regulated process. Aspirin-type drugs can bring the temperature back down precisely because the thermostat is still functional, just set higher.15PubMed. Fever versus hyperthermia
Hyperthermia, by contrast, is what happens when the body gains heat faster than it can shed it, but the set point hasn’t changed. Heatstroke, for example, overwhelms the cooling system without any thermostat reset. You don’t get chills with heatstroke because the brain isn’t sending a “you’re too cold” signal. The body is just failing to keep up with the heat load. This matters practically: fever-reducing medications won’t help with hyperthermia because there’s no elevated set point to lower. And the progression to dangerous temperatures is different. In fever, the body rarely lets core temperature exceed about 41°C because the thermostat, though set high, is still regulating. In hyperthermia, there’s no ceiling, and temperatures can climb to life-threatening levels more quickly.
Where heat generation does exceed the hypothalamic set point, or when fever reaches extreme levels, the consequences can be serious: cellular damage, organ dysfunction, and, if severe or sustained, death.16PubMed Central. The pathophysiological basis and consequences of fever This is part of why the body normally keeps fever within a controlled range and why extremely high fevers always warrant medical attention.
When Stress Raises Your Temperature Without an Infection
Not all temperature spikes come from fighting germs. Acute psychological stress can produce a genuine rise in core body temperature, a phenomenon seen across mammals including humans.17PubMed. Stress-induced hyperthermia and anxiety: pharmacological validation These psychogenic fevers work through a different pathway than infectious fever. Instead of cytokines and prostaglandins, the sympathetic nervous system drives the temperature increase, largely by activating heat production in brown fat tissue via specific adrenergic receptors.18PubMed Central. Psychogenic fever: how psychological stress affects body temperature in the clinical population
Because the mechanism is different, the experience can differ too. Classic antipyretics like ibuprofen, which target the prostaglandin pathway, tend to be less effective against stress-related temperature rises. People with chronic stress or anxiety disorders sometimes present with persistent low-grade elevations in body temperature that resist standard fever treatments, which can lead to frustrating diagnostic odysseys before the psychological component is recognized. The subjective sensation may include feeling flushed and warm, though the characteristic chills-then-heat cycling of an infectious fever is often less pronounced or absent, since there isn’t the same dramatic thermostat reset happening in the hypothalamus.
The Gut Connection to Fever’s Defenses
One of the more surprising recent findings in fever research involves the gut microbiome. A 2023 study explored why higher body temperatures help mice and hamsters survive influenza and SARS-CoV-2 infections. The researchers found that the protective effect of elevated temperature wasn’t simply the heat itself. Mice that were kept at high ambient temperatures but had depleted gut bacteria or were fed a low-fiber diet lost the survival advantage, even though their body temperatures were just as elevated as those of control animals.19Nature Communications. High body temperature increases gut microbiota-dependent host resistance to influenza A virus and SARS-CoV-2 infection
The key turned out to be what the gut bacteria were producing. Higher body temperatures boosted gut microbial metabolism, increasing levels of bile acids and other metabolites that appear to support the immune response. In other words, the fever created conditions for the gut microbiome to generate protective compounds, and without the microbiome doing its part, the fever alone wasn’t enough. This finding is still being explored and has mostly been demonstrated in animal models, but it adds a layer to our understanding of why fever matters. The hot-and-cold misery you feel during an illness isn’t just about heating up your tissues. It may also be reshaping the chemical environment inside your gut in ways that help you fight the infection.
How Fever and Menopausal Hot Flashes Overlap
If the hot flashes during illness remind you of menopausal hot flashes, you’re picking up on a real physiological similarity. Both involve sudden vasodilation and sweating driven by the thermoregulatory centers in the brain. But the triggers are different, and the two phenomena actually interact in an interesting way. A study tracking menopausal women during febrile illness found that hot flashes decreased during the fever itself. There were fewer of them, and those that did occur tended to be less intense. Once the fever broke, hot flashes returned to their usual pattern.20PubMed. Effect of fever on menopausal hot flashes
The researchers proposed several explanations. The elevated core temperature during fever might suppress whatever mechanism normally triggers a menopausal hot flash. Alternatively, the competing thermoregulatory drive of fever, which is pushing the body to retain heat, might override the vasodilation signal of a hot flash. Or some byproduct of the fever process itself might mask the hot flash response. Whatever the cause, the observation highlights that the brain’s temperature-control system can only juggle so many competing demands at once. When infectious fever commandeers the thermostat, the hormonal fluctuations that normally cause hot flashes seem to get pushed to the background, a small silver lining during an otherwise uncomfortable experience.
How Different Pathogens Shape the Fever Pattern
Not every infection produces the same fever profile. Clinicians have long noticed that certain infections generate characteristic temperature patterns: some cause steadily sustained fevers, others produce dramatic spikes and crashes, and still others create a slow undulating wave. Part of this variation comes from the fact that viruses and bacteria activate different branches of the immune system. Research comparing gene activity in the white blood cells of febrile children found that viral infections uniquely activated interferon signaling pathways, while bacterial infections uniquely activated integrin signaling pathways.21PubMed Central. Gene expression profiles in febrile children with defined viral and bacterial infection These different immune programs produce different cytokine mixes, different prostaglandin dynamics, and therefore different patterns of thermostat adjustment.
For you as the person sweating through a fever, this means the rhythm of your hot-and-cold flashes partly reflects what you’re infected with. A fast-cycling pattern of chills and sweats every few hours suggests a different immune conversation than a steady, sustained warmth with a single dramatic sweat at the end. Malaria is the extreme example: the parasite’s replication cycle times the release of immune-activating debris to produce fevers that spike at predictable intervals. Most common infections aren’t that rhythmic, but the general principle holds. Your body isn’t just “hot” or “cold” when sick. It’s running a dynamic, fluctuating thermoregulatory program that shifts as the immune response evolves over hours and days, producing the waves of discomfort that make illness feel like such an unpredictable ordeal.