Progesterone was very successful in treating traumatic brain injury in animal models and human clinical trials stages I & II but showed no effect at all in 2 large stage III trials. Stage I & II trials used, respectively, 1 and 2 mg/kg/day intravenously. The stage III trials both increased the intravenous dosage to 12mg/kg/day. It has been proposed that this 6x dose increase is responsible for eliminating the neuroprotective effect because progesterone may have a U-shaped dose response curve.
Ray Peat however seems to suggest that more progesterone is always more protective. Perhaps brain glycogen was depleted by the high dose but I have trouble believing that this alone would eliminate ALL protective effect.
Does anybody have any thoughts on why this would occur? This failure in clinical trials seems like a huge blow to the possible acceptance of a major use of progesterone by the mainstream medical system since there may not be any more attempted. I would really like to ask Ray what he thinks but I can't find his contact information.
Randy B. Howard, Iqbal Sayeed, Donald G. Stein. Suboptimal dosing parameters as possible factors in the negative Phase III clinical trials of progesterone for TBI. J Neurotrauma 2016. doi: 10.1089/neu.2015.4179
Ray Peat however seems to suggest that more progesterone is always more protective. Perhaps brain glycogen was depleted by the high dose but I have trouble believing that this alone would eliminate ALL protective effect.
Does anybody have any thoughts on why this would occur? This failure in clinical trials seems like a huge blow to the possible acceptance of a major use of progesterone by the mainstream medical system since there may not be any more attempted. I would really like to ask Ray what he thinks but I can't find his contact information.
Randy B. Howard, Iqbal Sayeed, Donald G. Stein. Suboptimal dosing parameters as possible factors in the negative Phase III clinical trials of progesterone for TBI. J Neurotrauma 2016. doi: 10.1089/neu.2015.4179