26.2 an RCT and a Follow-up RCT: Epigenetic Effects of PTSD Remediation Using Clinical Emotional Freedom Therapy (EFT), and an RCT on the Effect of EFT on Stress Biochemistry

ObjectivesThis presentation will discuss 3 randomized controlled trials (RCTs) that studied the effects of emotional freedom techniques (EFTs), an evidence-based method validated in over 100 clinical trials. One RCT examined cortisol, one studied gene expression, and the third analyzed microRNAs that silence DNA base pairs.MethodsThe cortisol RCT was performed in a triple-blind fashion. Participants were randomized to a single session of either EFT, talk therapy, or rest. The other 2 RCTs used 10 sessions in a population with clinical levels of PTSD and compared EFT to treatment as usual (TAU). Blood draws for messenger RNA levels for 93 genes related to PTSD were performed before and after treatment.ResultsIn the cortisol RCT, the EFT group showed statistically significant improvements in anxiety (-58.34%; p < .05), depression (-49.33%; p < .002), the overall severity of symptoms (-50.5%; p < .001), and symptom breadth (-41.93%; p < .001). The EFT group experienced a significant decrease in cortisol level (-24.39%; standard error [SE], 2.62) compared with the decrease observed in the talk therapy (-14.25%; SE, 2.61) and rest (-14.44%; SE, 2.67) groups (p < .03). In the PTSD trials, symptom scores decreased by 25.63 points to below the clinical cutoff (p < .00001). Insomnia declined from the moderate clinical range to the mild clinical range. Treatment was associated with statistically significant differences in anxiety, depression, paranoia, hostility, and all other parameters except concussion, somatization, and physical functioning. Participants maintained their gains at the 3- and 6-month follow-up visits. Significant differences (p < .05) were found for 6 genes: chemokine receptor 3 (CXCR3); interleukin (IL)-18; IL-10 receptor beta; tumor necrosis factor (TNF)-α–induced protein 6; leukocyte-endothelial cell adhesion molecule 1 (selectin L); and interferon-induced transmembrane protein 1. A cluster of microRNAs associated with depression were inhibited after treatment.ConclusionsMonitoring gene expression, cortisol levels, and other inflammatory processes can provide objective biomarkers of the success of treatment in patients with a history of ACEs. EFT may be used as a brief nondrug epigenetic intervention in populations with PTSD.NI, PTSD, GS ObjectivesThis presentation will discuss 3 randomized controlled trials (RCTs) that studied the effects of emotional freedom techniques (EFTs), an evidence-based method validated in over 100 clinical trials. One RCT examined cortisol, one studied gene expression, and the third analyzed microRNAs that silence DNA base pairs. This presentation will discuss 3 randomized controlled trials (RCTs) that studied the effects of emotional freedom techniques (EFTs), an evidence-based method validated in over 100 clinical trials. One RCT examined cortisol, one studied gene expression, and the third analyzed microRNAs that silence DNA base pairs. MethodsThe cortisol RCT was performed in a triple-blind fashion. Participants were randomized to a single session of either EFT, talk therapy, or rest. The other 2 RCTs used 10 sessions in a population with clinical levels of PTSD and compared EFT to treatment as usual (TAU). Blood draws for messenger RNA levels for 93 genes related to PTSD were performed before and after treatment. The cortisol RCT was performed in a triple-blind fashion. Participants were randomized to a single session of either EFT, talk therapy, or rest. The other 2 RCTs used 10 sessions in a population with clinical levels of PTSD and compared EFT to treatment as usual (TAU). Blood draws for messenger RNA levels for 93 genes related to PTSD were performed before and after treatment. ResultsIn the cortisol RCT, the EFT group showed statistically significant improvements in anxiety (-58.34%; p < .05), depression (-49.33%; p < .002), the overall severity of symptoms (-50.5%; p < .001), and symptom breadth (-41.93%; p < .001). The EFT group experienced a significant decrease in cortisol level (-24.39%; standard error [SE], 2.62) compared with the decrease observed in the talk therapy (-14.25%; SE, 2.61) and rest (-14.44%; SE, 2.67) groups (p < .03). In the PTSD trials, symptom scores decreased by 25.63 points to below the clinical cutoff (p < .00001). Insomnia declined from the moderate clinical range to the mild clinical range. Treatment was associated with statistically significant differences in anxiety, depression, paranoia, hostility, and all other parameters except concussion, somatization, and physical functioning. Participants maintained their gains at the 3- and 6-month follow-up visits. Significant differences (p < .05) were found for 6 genes: chemokine receptor 3 (CXCR3); interleukin (IL)-18; IL-10 receptor beta; tumor necrosis factor (TNF)-α–induced protein 6; leukocyte-endothelial cell adhesion molecule 1 (selectin L); and interferon-induced transmembrane protein 1. A cluster of microRNAs associated with depression were inhibited after treatment. In the cortisol RCT, the EFT group showed statistically significant improvements in anxiety (-58.34%; p < .05), depression (-49.33%; p < .002), the overall severity of symptoms (-50.5%; p < .001), and symptom breadth (-41.93%; p < .001). The EFT group experienced a significant decrease in cortisol level (-24.39%; standard error [SE], 2.62) compared with the decrease observed in the talk therapy (-14.25%; SE, 2.61) and rest (-14.44%; SE, 2.67) groups (p < .03). In the PTSD trials, symptom scores decreased by 25.63 points to below the clinical cutoff (p < .00001). Insomnia declined from the moderate clinical range to the mild clinical range. Treatment was associated with statistically significant differences in anxiety, depression, paranoia, hostility, and all other parameters except concussion, somatization, and physical functioning. Participants maintained their gains at the 3- and 6-month follow-up visits. Significant differences (p < .05) were found for 6 genes: chemokine receptor 3 (CXCR3); interleukin (IL)-18; IL-10 receptor beta; tumor necrosis factor (TNF)-α–induced protein 6; leukocyte-endothelial cell adhesion molecule 1 (selectin L); and interferon-induced transmembrane protein 1. A cluster of microRNAs associated with depression were inhibited after treatment. ConclusionsMonitoring gene expression, cortisol levels, and other inflammatory processes can provide objective biomarkers of the success of treatment in patients with a history of ACEs. EFT may be used as a brief nondrug epigenetic intervention in populations with PTSD.NI, PTSD, GS Monitoring gene expression, cortisol levels, and other inflammatory processes can provide objective biomarkers of the success of treatment in patients with a history of ACEs. EFT may be used as a brief nondrug epigenetic intervention in populations with PTSD.