Blake jarmine
Greenlighter
- Joined
- Jun 30, 2026
- Messages
- 4
I want to begin by expressing my deepest respect for the men and women who have worn the uniform, and for the extraordinary sacrifices—both seen and unseen that military personnel carry long after their service ends. The courage required to serve is immense, but the courage required to live with the lingering weight of trauma is something society often overlooks. Those who develop PTSD naturally, whether through combat exposure, repeated operational stress, or the cumulative strain of service life, deserve not only our gratitude but our unwavering compassion.
Regarding this topic, our team actually began this program back in 2014, focusing exclusively on non‑human subjects to establish a safe neurobiological foundation. Our earliest work involved adolescent chimpanzees who had developed PTSD‑like symptomatology following traumatic encounters with hunters or forced separation from their family units. Using controlled administration of psilocybin‑derived compounds, we studied how psilocin metabolism interacts with the amygdalar fear circuitry and the hippocampal memory‑reconsolidation pathways.
Across multiple controlled trials, we observed reproducible outcomes: psilocin consistently attenuated hyperreactive limbic signaling, primarily through modulation of 5‑HT2A receptor density and downstream glutamatergic transmission. This receptor‑level modulation appeared to reduce trauma‑linked memory reconsolidation events, effectively interrupting pathological neural replay loops that sustain PTSD symptomatology.
After several years of synthesis refinement, protocol development, and strict veterinary oversight, we transitioned cautiously to our first human cohort in 2017, consisting of four disabled veterans. Under controlled clinical conditions, neuroimaging data showed remarkable outcomes: functional MRI scans revealed normalized activity in regions typically associated with PTSD, including the ventromedial prefrontal cortex and posterior cingulate cortex. In numerous sessions, the neural signatures resembled those of individuals without PTSD at all.
Building on these findings, we developed a long‑acting psilocin XR formulation ,paired with mineral‑based adjunct supplements designed to provide sustained serotonergic modulation while minimizing acute perceptual distortion. This extended‑release profile was engineered to stabilize neuroplastic recovery, reduce inflammatory load, and maintain therapeutic receptor engagement without producing destabilizing peaks in cortical excitation.
A critical component of our XR development involved eliminating the risk of long‑term psychedelic‑induced psychosis, a concern historically associated with uncontrolled or high‑dose serotonergic hallucinogen exposure. Through pharmacokinetic modeling and receptor‑binding analysis, we engineered the XR formulation to maintain psilocin plasma levels below the threshold associated with 5‑HT2A overstimulation, thereby preventing aberrant dopaminergic cross‑activation in mesolimbic pathways. Additionally, the XR matrix incorporates stabilizing adjunct minerals that modulate glutamate release and reduce cortical hyperexcitability, effectively suppressing the neurochemical cascade implicated in hallucinogen‑triggered psychotic episodes. Longitudinal monitoring across our cohort has shown no emergence of persistent perceptual disturbances, delusional ideation, or psychosis‑spectrum symptoms, supporting the safety profile of the formulation.
Our program remains intentionally limited to ensure individualized monitoring, ethical oversight, and strict adherence to clinical protocols.
We currently maintain 29 active participants, the majority of whom are Ex-veterans and severly traumatized people.
Members receive a monthly supply of psilocin XR and adjunct supplements, accompanied by continuous neuropsychiatric evaluation. Diversion or recreational misuse is strictly prohibited; any indication of non‑therapeutic use results in immediate suspension and full reimbursement of membership fees. This policy safeguards both participant safety and research integrity.
I am open to any questions, and you may reach out to me directly for more detailed clinical information.
Thank you and stay safe.
some information removed by skorpio for legal reasons.
Regarding this topic, our team actually began this program back in 2014, focusing exclusively on non‑human subjects to establish a safe neurobiological foundation. Our earliest work involved adolescent chimpanzees who had developed PTSD‑like symptomatology following traumatic encounters with hunters or forced separation from their family units. Using controlled administration of psilocybin‑derived compounds, we studied how psilocin metabolism interacts with the amygdalar fear circuitry and the hippocampal memory‑reconsolidation pathways.
Across multiple controlled trials, we observed reproducible outcomes: psilocin consistently attenuated hyperreactive limbic signaling, primarily through modulation of 5‑HT2A receptor density and downstream glutamatergic transmission. This receptor‑level modulation appeared to reduce trauma‑linked memory reconsolidation events, effectively interrupting pathological neural replay loops that sustain PTSD symptomatology.
After several years of synthesis refinement, protocol development, and strict veterinary oversight, we transitioned cautiously to our first human cohort in 2017, consisting of four disabled veterans. Under controlled clinical conditions, neuroimaging data showed remarkable outcomes: functional MRI scans revealed normalized activity in regions typically associated with PTSD, including the ventromedial prefrontal cortex and posterior cingulate cortex. In numerous sessions, the neural signatures resembled those of individuals without PTSD at all.
Building on these findings, we developed a long‑acting psilocin XR formulation ,paired with mineral‑based adjunct supplements designed to provide sustained serotonergic modulation while minimizing acute perceptual distortion. This extended‑release profile was engineered to stabilize neuroplastic recovery, reduce inflammatory load, and maintain therapeutic receptor engagement without producing destabilizing peaks in cortical excitation.
A critical component of our XR development involved eliminating the risk of long‑term psychedelic‑induced psychosis, a concern historically associated with uncontrolled or high‑dose serotonergic hallucinogen exposure. Through pharmacokinetic modeling and receptor‑binding analysis, we engineered the XR formulation to maintain psilocin plasma levels below the threshold associated with 5‑HT2A overstimulation, thereby preventing aberrant dopaminergic cross‑activation in mesolimbic pathways. Additionally, the XR matrix incorporates stabilizing adjunct minerals that modulate glutamate release and reduce cortical hyperexcitability, effectively suppressing the neurochemical cascade implicated in hallucinogen‑triggered psychotic episodes. Longitudinal monitoring across our cohort has shown no emergence of persistent perceptual disturbances, delusional ideation, or psychosis‑spectrum symptoms, supporting the safety profile of the formulation.
Our program remains intentionally limited to ensure individualized monitoring, ethical oversight, and strict adherence to clinical protocols.
We currently maintain 29 active participants, the majority of whom are Ex-veterans and severly traumatized people.
Members receive a monthly supply of psilocin XR and adjunct supplements, accompanied by continuous neuropsychiatric evaluation. Diversion or recreational misuse is strictly prohibited; any indication of non‑therapeutic use results in immediate suspension and full reimbursement of membership fees. This policy safeguards both participant safety and research integrity.
I am open to any questions, and you may reach out to me directly for more detailed clinical information.
Thank you and stay safe.
some information removed by skorpio for legal reasons.
Last edited by a moderator:
