DATE: October 7, 2026 at 09:00AM
SOURCE: PSYPOST.ORG
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TITLE: Researchers probe the oxytocin system for clues to functional neurological disorder
A recent study investigated whether the body’s oxytocin system acts as a biological risk factor for Functional Neurological Disorder. The findings indicate that while genetic variations do not appear to directly cause the condition, interactions between genetics, epigenetics, and circulating hormones might explain how patients process physical sensations and childhood trauma. The research was published in Comprehensive Psychoneuroendocrinology.
Natascha Stoffel, a researcher at the University of Fribourg in Switzerland, led the investigation. She and her colleagues wanted to understand the biological mechanisms behind Functional Neurological Disorder. This condition sits at the boundary between psychiatry and neurology.
Patients with the disorder experience physical symptoms like tremors, weakness, or non-epileptic seizures. These symptoms are genuine and debilitating, but they are not caused by traditional structural brain diseases. People with the condition frequently report a history of adverse life events, such as childhood trauma or emotional neglect.
Patients also often struggle with interoception, which is the brain’s ability to sense and process internal bodily signals. Interoception allows a person to feel when they are hungry, when their heart is racing, or when their breathing changes. In many stress-related conditions, this internal sensory system becomes disrupted.
To explore potential biological mechanisms, Stoffel and her team focused on the oxytocin system. Oxytocin is a hormone and chemical messenger that regulates stress, emotional responses, and social behavior. The researchers suspected that changes in how the body processes oxytocin might alter a person’s stress response and their internal bodily awareness.
The team looked at three distinct components of the oxytocin system. First, they looked at genetics, specifically examining variations in the oxytocin receptor gene. Second, they examined epigenetics, which are chemical tags added to DNA that change how a gene functions without altering the genetic code itself. Epigenetic changes are influenced by a person’s environment and life experiences.
For the epigenetic component, the team specifically measured methylation, a type of chemical tag that typically reduces a gene’s activity. Finally, the researchers measured the actual levels of oxytocin circulating in the participants’ bodies.
To conduct the first part of their research, the scientists analyzed data from 89 adults, after three of the 92 originally enrolled participants were excluded because of missing genetic data. The group included 41 patients diagnosed with Functional Neurological Disorder and 48 healthy control participants. The research team collected blood samples to extract and analyze the participants’ DNA.
From the blood samples, the team identified each participant’s genetic variants for the oxytocin receptor gene. They also measured the degree of epigenetic methylation at two specific regions of this gene. To measure circulating hormones, the researchers collected saliva samples at four different times during the day.
The scientists compared the genetic and epigenetic data between the two groups. When looking at the genetic variants alone, the models showed no difference in how the gene variations were distributed between the patients and the healthy controls. They also found no statistically significant differences in the average epigenetic methylation rates between the two groups.
While the baseline genetic and epigenetic markers did not differ, the researchers found an interaction when they included the salivary oxytocin levels. Patients with the disorder who carried a specific variant of the oxytocin receptor gene (the GG genotype) had elevated levels of oxytocin in their saliva compared to healthy controls with the same genetic variant.
In healthy individuals, oxytocin levels typically rise in response to specific contexts, like social bonding, parenting, or physical exercise. For the patients in this study, the elevated oxytocin levels appeared independently of these specific triggers. The researchers suggest that a specific genetic variant might act as a vulnerability factor, causing an abnormal release of oxytocin in response to daily stress.
In the second part of the investigation, the researchers tested whether combining the genetic and epigenetic data could help explain the participants’ interoceptive abilities. Participants completed a breathing task that measured their physical sensitivity to respiratory resistance. They also filled out a questionnaire that assessed how accurately they felt they could detect their own bodily sensations.
The researchers used statistical models to see if combining the oxytocin receptor genetics, methylation data, and salivary oxytocin levels would predict the interoceptive test scores. The addition of these biological markers did not improve the models. The genetic and epigenetic variables did not explain the interoceptive dysfunction observed in the patient group.
The team then applied the same statistical approach to look at childhood trauma. Participants completed a standard questionnaire to self-report their history of childhood trauma and emotional neglect. The researchers built a model to see if the biological markers aligned with the variation in these trauma scores.
In this case, the addition of the biological markers improved the statistical model. Including the epigenetic methylation data and the salivary oxytocin levels helped explain the variance in the self-reported childhood trauma scores. Higher levels of methylation at a specific region of the oxytocin receptor gene were associated with lower reported trauma scores.
The researchers noted a few caveats regarding their findings. Because the investigation relied on a modest sample size of 89 adults, it lacked the statistical power needed to make definitive claims about genetic associations. A simulation conducted by the researchers indicated that a study would need about 400 participants to confidently detect the genetic effects they observed.
The study measured epigenetic markers using blood samples, which might not accurately reflect the methylation levels present in brain tissue. The levels of oxytocin measured in saliva also might not perfectly mirror the concentrations of the hormone functioning directly within the central nervous system.
The statistical models linking the oxytocin system to childhood trauma do not establish a directional mechanism. The researchers cannot say whether experiencing trauma causes changes to the oxytocin system, or if an altered oxytocin system changes how a person processes and reports traumatic memories. Future research will need to track larger groups of people over time to understand how stress, genetics, and hormones interact to trigger the condition.
The study, “The Oxytocinergic System in Functional Neurological Disorder: Preliminary Testing of Associations with Interoception and Childhood Trauma,” was authored by Natascha Stoffel, Juan Ansede-Bermejo, Cristina Concetti, Ángel Carracedo, and Selma Aybek.
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