For years, when a woman said she felt pain for longer after surgery, an accident or physical trauma, the explanation remained suspended between cultural stereotypes and psychological interpretations. Too much sensitivity, they said. Greater emotionality. A different pain threshold.
Today science definitively shifts the center of gravity of the discussion and does so with a clear fact: the difference in the duration of pain between men and women has a precise biological basis, rooted in the functioning of the immune system.
A new study published in Science Immunology suggests that the male body has a faster mechanism to “turn off” pain after an injury, thanks to specific immune cells regulated by testosterone. It is not a question of perception, nor of suggestion. It’s physiology. And this discovery, in addition to having important clinical implications, touches a cultural nerve that affects millions of women.
The biological switch that turns off pain
When we hurt ourselves, pain is not just a nervous signal that starts from the injured area and reaches the brain. It is the result of a continuous dialogue between the nervous system and the immune system.
After trauma, immune cells migrate into the damaged tissue and release molecules that can amplify inflammation or reduce it, thus modulating the intensity and duration of suffering. It is in this subtle balance that the difference between men and women is played out.
The researchers focused on a molecule called interleukin-10 (IL-10), known for its powerful anti-inflammatory action. In experimental mouse models with induced skin inflammation, males began to recover more rapidly than females approximately one week after the onset of injury.
The amount of inflammation was similar in both groups. The real difference lay elsewhere: more immune cells capable of producing IL-10 were present in the males’ tissues.
This molecule, released in particular by monocytes – a type of white blood cell – binds to receptors present on sensory neurons, attenuating the transmission of the painful signal. When the researchers blocked IL-10 or prevented the nerves from “receiving” it, the pain was prolonged in both sexes, demonstrating that this mechanism works as a real biological brake.
Testosterone influences the immune system
At this point the question was inevitable: why are these monocytes more active in males? The answer appears to involve testosterone, which not only affects muscle development or secondary sexual characteristics but also influences the behavior of the immune system.
When female mice were given a synthetic androgen similar to testosterone, they produced more IL-10-positive monocytes and their recovery from pain was faster. On the contrary, by eliminating or blocking the testosterone signal in males, the advantage was eliminated.
To test whether the same pattern was also observable in humans, the researchers analyzed data from the AURORA study, which follows US patients after major traumas such as car accidents. Men and women reported similar levels of pain immediately after the traumatic event. In the following months, however, the pain decreased more rapidly in the men.
Higher levels of IL-10 were also present in male blood samples, and this higher concentration was associated with a more significant reduction in pain over time.
The research does not claim to explain every form of chronic pain, because physiology is always a complex mix of genetic, hormonal and environmental factors. However, it adds an important piece in an area where gender differences have often been trivialized.
A medical question, but also a cultural one
Chronic pain affects millions of people and many painful conditions affect women to a greater extent. Yet, those who work in healthcare know how often their reports are minimized or interpreted as excessive.
Knowing that there is an immune mechanism that can slow down the turning off of pain in women changes the perspective, because it restores scientific dignity to an experience that is too often belittled.
This awareness also opens up interesting therapeutic scenarios. In animal models, a molecule called resolvin D1, involved in resolving inflammation, increased the production of IL-10-positive monocytes, speeding recovery in both sexes and narrowing the observed gap.
According to the authors, topical treatments – such as testosterone patches – could in the future offer localized benefits, limiting the systemic effects of the hormones. The road is still long, but one thing appears clear: the female and male bodies respond to pain through partly different immune pathways, and ignoring this evidence means giving up truly personalized medicine.
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