Background: This study is based on the hypothesis, that the toxic or physiological effects of an optical isomer may be counteracted or reversed by the administration of a potentized preparation of one of its stereoisomers. In the present study the enantiomer was used. Methods: 154 ICR conventional mice were used. 77 mice were administered (R)-(+)-propranolol HCl homeopathic potency prior to and during the experiment, and the other 77 were administered indistinguishable placebo. On the day of the experiment the mice were sedated with intraperitoneal Rometar. Once sedated they were injected intraperitoneally with the LD50 dose of (S)-(–)-propranolol HCl. Results: The end point for statistical analysis was the difference in survival between the placebo and treatment mice. The odds ratio for survival of treatment mice relative to placebo mice was 1.64. The hypothesis of equal survival proportions gave a chi-square of 2.0916 (1 degree of freedom), which has a p-value of 0.1481. The analysis was then adjusted for mouse weight and intraperitoneal (–)-propranolol dosage using a logistic regression (LR) model. The LR treatment odds ratio was 2.017 and the LR treatment chi-square was 2.8864 (1 degree of freedom), which has a p-value of 0.0893. Consequently we accept the null hypothesis of no treatment effect on survival. The odds ratio estimates show that the treatment mice are 2.02 times more likely to survive than placebo mice, but this was not statistically significant with p = 0.089. Nine percent more treatment mice survived than placebo mice. The investigators accustomed to handling rodents noted that mouse recovery seemed substantially faster in the treatment mice than in the placebo mice.

Background: A previous pilot study was performed to see if toxicity of (S)-(–)-propranolol hydrochloride may be inhibited by a potentized preparation of its enantiomer. The present study is based on the hypothesis that the toxic effects of an optical isomer, may be counteracted or reversed by the administration of a potentized preparation of one of its stereoisomers, and in particular the enantiomer. Methods: 508 ICR conventional mice were used. 254 mice were administered (R)-(+)-propranolol HCl homeopathic potency prior to and during the experiment, and the other 254 were administered indistinguishable placebo. On the day of the experiment mice were anesthetized with intraperitoneal Rometar. Once sedated the mice were administered the LD50 dose of (–)-propranolol HCl intraperitoneally. Results: The end point for statistical analysis was the difference in survival between the placebo and treatment mice. The odds ratio for survival of treatment mice relative to placebo mice was 1.52. The hypothesis of equal survival proportions gave a chi-square of 5.0429 (1 degree of freedom), which has a p-value of 0.0247. The analysis was then adjusted for mouse weight and intraperitoneal (–)-propranolol dosage using a logistic regression (LR) model. The LR treatment odds ratio was 1.51 and the LR treatment chisquare was 4.8112 (1 degree of freedom), which has a p-value of 0.0283. Consequently, we reject the null hypothesis of no treatment effect on survival. Eleven percent more treatment mice survived than placebo mice. Conclusion: We conclude that the toxicity of intraperitoneal (–)-propranolol HCl, may be counteracted by administration of a potency of its enantiomer, in ICR conventional mice which have survived preceding intraperitoneal Rometar injection, and pre-dosing with (+)-propranolol HCl homeopathic potency.

Background: Previous studies have been performed to see if toxicity of optically active compounds may be inhibited by potentized preparations of their enantiomers. The present study is based on the hypothesis that the toxic effects of an optical isomer may be counteracted or reversed by the administration of a potentized preparation of one of its stereoisomers and in particular the enantiomer (patent applied for). Methods: The design was prospective, blind, randomized, and placebo-controlled. 210 ICR conventional mice were used. 105 mice were administered a mixture of (+)-U50488 hydrochloride homeopathic potencies prior to and during the experiment, and the other 105 were administered indistinguishable placebo. The first 52 mice were used to establish an LD₅₀ of intraperitoneally administered (–)-U50488 hydrochloride under the conditions of this experiment. The estimated LD₅₀ was 25 mg/kg. The remaining 158 mice were then administered this LD₅₀ of (–)-U50488 HCl intraperitoneally. One mouse from the placebo group was excluded from the analysis because it died immediately after the possibly intravenous injection of (–)-U50488 HCl. Results: 67% of homeopathy mice survived compared with 47% of placebo mice. The end point for statistical analysis was the difference in survival between the placebo and homeopathy mice. The analysis was adjusted for mouse weight using a logistic regression (LR) model. The LR treatment odds ratio for survival of treatment mice relative to placebo mice was 2.301 and the LR treatment chi-square was 6.2030 (1 degree of freedom), which has a p-value of 0.0128. Consequently, we reject the null hypothesis of no treatment effect on survival. Conclusion: We conclude that toxicity of intraperitoneal injection of (–)-U50488 hydrochloride may be inhibited by administration of a mixture of potencies of its enantiomer.

We conclude that enantiomeric potencies are superior to identically produced isopathic potencies, in inhibiting toxicity of (-)-U-50488 HCl. Homeopathic inhibition of toxicity may be stereospecific.

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