Sometimes a fever doesn’t just make you hot — it makes everything else feel cold. A room that felt comfortable an hour ago now seems drafty, pushing you to bundle up or scoot closer to the heater. That wave of chills has long been treated as a side effect of illness. But new research suggests it’s something more deliberate.
Published in The Journal of Physiology, the study links chills to the amygdala, a hub in the brain’s emotional circuitry. Researchers found that a molecule released during infection activates a pathway to this region, amplifying the sensation of cold and driving warmth-seeking behavior. The results show that chills are not merely a byproduct of rising temperature, but part of a response that blends physiology with emotion.
How Fever Triggers Chills in the Brain
When the body detects an infection, it produces a molecule called prostaglandin E₂, which helps raise body temperature. This increase is one reason fevers can slow pathogen growth and support immune defenses.
Researchers have known that this molecule acts on the brain’s temperature-control center, triggering responses such as shivering and conserving heat. But fever does not rely on internal heat alone. It also changes behavior.
To test that idea, the team gave rats a choice between two plates, one neutral and one warmer. Under normal conditions, the animals preferred the neutral surface. But when the fever-related molecule was delivered to a temperature-sensitive brain region called the lateral parabrachial nucleus, the rats began choosing the warmer plate instead.
Notably, they did this without increasing shivering or other automatic heat production. In other words, the molecule changed the animals’ behavior, not just their internal temperature.
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Where Emotion Enters the Circuit
The researchers next followed how information from this temperature-sensitive region travels through the brain. They identified a receptor called EP3 as key to the warmth-seeking response.
Nerve cells carrying EP3 may connect to the amygdala and, far less, to the brain’s temperature-control center. The same circuit is active in cold conditions, suggesting it normally helps signal when the body feels cold. During infection, that signal appears to be turned up.
When this circuit was activated, the sensation of cold intensified. That finding suggests chills are not simply about detecting lower temperatures at the skin. Instead, the brain seems to heighten how cold feels, making it uncomfortable enough to prompt action.
Rather than acting only as a thermostat, the brain draws on emotional systems to push the body toward warmth at a moment when higher internal temperature can help fight infection.
More Than a Symptom
The results point to two coordinated responses during fever. One increases heat production inside the body. The other shapes behavior, influencing how cold it feels and encouraging animals to seek warmer surroundings.
If similar pathways operate in humans, the work could reshape how scientists think about the sensory and emotional dimensions of illness. It may also offer insight into conditions involving chronic inflammation or disruptions in temperature regulation.
Chills, then, may not be an accidental byproduct of fever. They may be part of a built-in survival response, one that uses emotion to guide the body toward warmth when it matters most.
This article is not offering medical advice and should be used for informational purposes only.
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Article Sources
Our writers at Discovermagazine.com use peer-reviewed studies and high-quality sources for our articles, and our editors review for scientific accuracy and editorial standards. Review the sources used below for this article:
- This article references information from a recent study published in The Journal of Physiology: The pyrogenic mediator prostaglandin E2 elicits warmth seeking via EP3 receptor-expressing parabrachial neurons: a potential mechanism of chills
