Unraveling the effect of recreational fear on inflammation: A prospective cohort field study.

A fear reaction is fundamental for survival and naturally activates the adrenergic system, prompting an acute and vital flight-or-fight response. While sustained stress is associated with unhealthy low-grade inflammation, more acute and transient activation of the adrenergic system has been suggested to impact the immune system and subsequently attenuate low-grade inflammation, e.g. through cold exposure or hyperventilation. Voluntary exposure to frightening stimuli, such as scary entertainment, is another reliable activator of the adrenergic system, yet its impact on the immune system and low-grade inflammation is unknown. The objectives of this study are to i. assess proportional changes of participants with low-grade inflammation at and three days after a voluntary frightening event, and ii. explore mean value alterations in inflammatory markers and immune cells over time. We recruited adult participants among visitors to a real-life intense frightening haunted house attraction, located in Vejle, Denmark. The overall fright potential of the exposure was estimated through heart rate (HR) monitoring and self-reported levels of fear. Low-grade inflammation (defined as high sensitive C-reactive protein (hs-CRP) > 3 mg/L)) and immune cells (subtypes of leukocytes) were measured from blood samples immediately before, immediately after, and three days after the haunted house event. A total of 113 participants, 69 females (61.1 %), and 44 males (38.9 %), with a mean age of 29.7 (SD 10.1) were included in the analyses. The average duration of exposure was 50 min and 51 s, while the mean HR throughout the event was 111.1 BPM (mean SD 10.1), and the mean subjective reported scare level was 5.4 (SD 1.9) on a Likert scale ranging from 1 to 9. Twenty-two participants exhibited low-grade inflammation (hs-CRP > 3 mg/L) at the event, with 10 participants normalizing their hs-CRP levels three days post-event. Seven participants had normal hs-CRP levels at the event, but low-grade inflammation three days post-event. Thus, we found no proportional difference between participants with low-grade inflammation at the event (19.5 %) and three days after the event (16.8 %) (diff. -2.7 %; 95 % CI: -10.7 to 5.4, p = 0.47). For the 22 participants exhibiting low-grade inflammation at the event, 18 participants (82 %) decreased their hs-CRP levels, with a mean decrease in hs-CRP from 5.7 mg/L pre-event to 3.7 mg/L three days post-event (diff. -2.0, 95 % CI: -3.2 to -0.7, p = 0.003). Supporting an overall attenuation of inflammation, total leukocytes and lymphocytes decreased for both participants with low-grade inflammation and with normal inflammatory levels, when comparing levels pre- and three days post-event, although all mean levels remained within the normal range. Conclusively, we find no proportional differences in participants exhibiting low-grade inflammation (hs-CRP > 3) when comparing levels at and three days after exposure to a voluntary frightening event. However, explorative analyses suggest that recreational fear exposure may attenuate immune cells across the entire cohort (N = 113) and decrease hs-CRP levels for participants who exhibit low-grade inflammation at the event (N = 22).