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Studies Provide Insights

This Is the Biological Reason Why Women and Men Perceive Pain Differently

Pain often lasts longer in women than in men. In this context, research may have uncovered some intriguing findings.
Pain often lasts longer in women than in men. In this context, research may have gained intriguing insights. Photo: Getty Images
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July 15, 2026, 8:02 am | Read time: 6 minutes

When it comes to pain, there seem to be gender-specific differences. Women suffer more often from chronic pain, while men are often considered less sensitive to pain—whether due to social conditioning or biological reasons. Recent research shows that certain immune cells in men actually reduce pain faster than in women. FITBOOK delves into the study and has also asked an independent pain expert for her assessment.

When the Pain Subsides, the Body Keeps Working

Pain doesn’t just subside because everything in the body returns to how it was before. A recent study on rats from Würzburg shows: After a nerve injury, immune cells, support cells, and gene activities in the nervous system reorganize—and apparently in different ways in male and female animals.1 Study author Robert Blum emphasizes: “I didn’t expect individual genes to go through the roof. Thus, pain regression is not a reversal of the injury, not a return to the original state, but a completely new genetic and gender-specific program.”2

In female rats, immune cells remained active directly on the nerve cells for longer. In male animals, however, so-called glial cells showed longer changes. These are support cells that surround nerve cells and can influence their activity.

Since the results come from an animal model, they cannot be directly transferred to humans. However, they align with another recent study suggesting that certain immune cells in men may reduce pain faster than in women.

Not Just a Matter of Perception in Men and Women

Women report persistent pain more often than men after injuries and inflammations. One assumption is that women and men express pain differently, which likely also has sociocultural reasons.3 After all, in many cultures, expressions of pain are considered a sign of weakness.

However, newer findings focus more on biological processes: Apparently, not only the perception of pain differs, but also its processing and regression in the body. Earlier studies showed that immune cells and their messengers—called cytokines—play an important role in pain processing.4 Particularly, the cytokine interleukin-10 (IL-10) acts like a “pain inhibitor.” It can dampen inflammation and simultaneously influence the activity of pain receptors. Building on these insights, a recent study by Michigan State University examined whether IL-10–producing monocytes contribute differently to pain resolution in men and women.5

Details of the Study

The aim of the study was to identify the cellular and molecular mechanisms behind the potentially faster pain resolution in men. To do this, the researchers combined preclinical models of inflammation and traumatic injury in mice with clinical data from humans after accidents.

Part 1: Experiments on Mice

In the animal models, the researchers induced pain in mice, on one hand through inflammatory stimuli and on the other through a traumatic model under stress. They recorded the pain reactions using standardized mechanical tests. Additionally, they used genetically modified mice to visualize IL-10–producing monocytes and specifically investigate their activity. They also tested the influence of male sex hormones—called androgens—and their receptors on these cells.

It was found that male mice reduced pain from inflammatory or traumatic stimuli significantly faster than females. The researchers were able to demonstrate that IL-10–producing monocytes play a key role: The more of these cells were present, the faster the pain subsided. The IL-10 signals released by the monocytes act directly on receptors of sensory nerve cells, thus contributing to the dampening of pain signals.

Androgens Promote Pain-Relieving Immune Cells

Male sex hormones increased both the number and activity of these monocytes. Conversely, blocking androgen receptors or removing IL-10 significantly delayed pain resolution. Furthermore, it was shown that the messenger Resolvin D1 stimulates the IL-10 production of monocytes and thereby accelerates pain resolution. This effect occurred in mice of both sexes.

Part 2: Human Study

Additionally, the researchers evaluated data from the AURORA study, in which 245 people were examined after traumatic accidents–mostly traffic accidents.6 Participants reported their pain intensity immediately after the accident and in the following weeks on a scale from zero to ten. In addition, the researchers analyzed blood samples and determined both the IL-10 levels and the estimated proportions of various immune cells, including monocytes. The results mirrored the findings from the animal models. Men reported a faster decrease in their pain over the course of the study than women. At the same time, they showed higher IL-10 levels and larger proportions of monocytes in the blood.

IL-10 and Monocytes Also Linked to Pain Resolution in Humans

Further analyses showed that higher IL-10 values were associated with a stronger decrease in pain. Statistical models also suggested that IL-10 mediates the relationship between monocytes and pain resolution. This indicates that immune cells also play an important role in the regulation of pain in humans.

More on the topic

Possible Significance of the Results

The study shows for the first time that IL-10–producing monocytes play an important role in the resolution of pain. This could at least partially explain why pain subsides faster on average in men than in women. One possible explanation is that male sex hormones promote the formation and activity of these monocytes and thus also increase the production of the anti-inflammatory messenger IL-10. Women could therefore—at least under certain conditions—be more susceptible to longer-lasting pain.

Additionally, the results provide new insights into how the immune system directly interacts with the nervous system. The communication between immune cells and nerve cells via the IL-10 signal could therefore be a potential target for future pain therapies. It might be conceivable to specifically promote the activity of IL-10–producing monocytes—for example, through agents like Resolvin D1.

Limitations

The study also has some limitations. Results from mouse models can only be transferred to humans to a limited extent. While local inflammatory reactions in the skin were examined in mice, the human data is based on self-reported pain and blood analyses.

Additionally, in the human study, only correlations between IL-10 levels, monocyte proportions, and pain progression could be observed. A direct proof that monocytes are indeed the main source of IL-10 in humans was not possible in this analysis. The type and location of injuries also varied among participants, making it difficult to compare pain progressions.

This article is a machine translation of the original German version of FITBOOK and has been reviewed for accuracy and quality by a native speaker. For feedback, please contact us at info@fitbook.de.

Sources

  1. Schlott, F., Hartmannsberger, B., Bischler, T. et al. (2026). Sex-specific molecular and cellular phenotypes during resolution of neuropathic pain in dorsal root ganglia. Cell Reports. ↩︎
  2. Uniklinikum Würzburg. Männer und Frauen lösen Schmerzen unterschiedlich auf. (accessed on July 10, 2026) ↩︎
  3. Deutsche Schmerzgesellschaft: Schmerz bei Frauen und Männer (aufgerufen am 10.9.2026) ↩︎
  4. Laumet, G., Bavencoffe, A., Edralin, J. et al. (2020). Interleukin-10 resolves pain hypersensitivity induced by cisplatin by reversing sensory neuron hyperexcitability. Pain ↩︎
  5. Sim, J., O’Guin, E., Sugimoto, C. et al. (2026). Monocyte-derived IL-10 drives sex differences in pain duration. Science Immunology ↩︎
  6. McLean, S., Ressler, K., Koenen, K. et al. (2021). Correction: The AURORA Study: a longitudinal, multimodal library of brain biology and function after traumatic stress exposure. Molecular Psychiatry ↩︎
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