Psychology
Research into the neuroscience of social rejection has shown that the brain regions that activate when a person is excluded, rejected, or grieving a lost relationship are the same regions that activate during physical injury, with the overlap being so substantial that a standard over-the-counter painkiller measurably reduces both kinds of pain, because the human brain has co-opted the physical pain system to register damage to social bonds
The popular framing of emotional pain treats it as something metaphorical. The broken heart of unrequited love, the sting of rejection, the ache of grief, the cutting remark, the wound that will not heal: the language…
By Space Daily Editorial Team · Editorial process, Published June 17, 2026

The popular framing of emotional pain treats it as something metaphorical. The broken heart of unrequited love, the sting of rejection, the ache of grief, the cutting remark, the wound that will not heal: the language of physical injury used to describe emotional injury is so widespread across cultures and languages that it has been treated, until quite recently, as a poetic convention rather than a scientific claim. People who use the language to describe their suffering are usually understood to be reaching for a metaphor that captures something about the intensity of what they feel.
The peer-reviewed neuroscience of the past two decades has substantially complicated this picture.
What the brain imaging evidence has shown, across multiple research teams, multiple methodologies, and multiple populations, is that emotional pain is not metaphorically similar to physical pain. The two states activate substantially overlapping neural systems, produce substantially similar behavioral and physiological responses, and respond to substantially the same pharmacological interventions. The language of broken hearts and stinging rejection is, on the strongest current reading of the evidence, more literally accurate than the popular framing has assumed.
The 2003 Cyberball study
The foundational peer-reviewed study of the neuroscience of social pain was published in October 2003 by Naomi Eisenberger, Matthew Lieberman, and Kipling Williams in the journal Science. The team designed an experiment to induce social rejection in a controlled laboratory setting while participants were inside a functional magnetic resonance imaging scanner. They used a computer game called Cyberball, in which the participant played a virtual ball-tossing game with what they believed were two other human players. After a brief inclusion phase in which all three players passed the ball to each other, the two other players began passing the ball only to each other, excluding the participant for the remainder of the game.
The two other players were not, in fact, human. They were computer-controlled. The exclusion was a designed feature of the experiment. From the participant’s subjective experience, however, they had just been deliberately excluded from a social activity by two people they had been interacting with moments earlier.
The brain activation pattern during the exclusion phase was the most significant finding of the study. The dorsal anterior cingulate cortex, a region of the brain that processes the affective component of physical pain, was significantly more active during exclusion than during inclusion. The level of activation correlated positively with the participant’s self-reported distress at being excluded. The same region of the brain that becomes active when a person is burned, cut, or struck became active when the same person was ignored in a virtual ball-tossing game.
The Eisenberger team’s interpretation, supported by the subsequent literature, was that the human brain treats social exclusion as a form of injury. The neural alarm system that evolved to alert humans to physical damage to their bodies is, on the available evidence, the same alarm system that alerts humans to damage to their social bonds.
The 2010 Tylenol study
The strongest follow-up evidence for the Eisenberger thesis came from a different direction. In 2010, a team led by Nathan DeWall at the University of Kentucky, with colleagues at Toronto, Florida, UCLA, Florida State, and Georgia College, published a study in Psychological Science that asked a simple question. If social pain and physical pain activate the same neural systems, then a pharmacological intervention that reduces physical pain should also reduce social pain. The team tested this prediction directly.
Participants in the first experiment took either 1,000 milligrams of acetaminophen, the active ingredient in Tylenol and Panadol, or a placebo, every day for three weeks. They reported their daily experience of social pain (feelings of rejection, exclusion, hurt feelings) on a standardized scale throughout the study period. The participants who took acetaminophen reported significantly lower social pain than those who took placebo, with the difference emerging gradually over the three weeks and becoming statistically significant by the end of the study.
The second experiment, also with three weeks of acetaminophen or placebo, used functional magnetic resonance imaging at the conclusion of the dosing period. Participants played the same Cyberball exclusion game while being scanned. The acetaminophen group showed significantly reduced neural activation in the dorsal anterior cingulate cortex and the anterior insula during the exclusion condition, compared with the placebo group. The pharmacological intervention designed to reduce physical pain had reduced both the felt experience and the brain activation associated with social pain.
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