buildingpaul
New member
Thought that this maybe of interest to some of the members......
Benzodiazepines (Diazepam, Clonazepam, Oxazepam, Nitrazepam, Temazepam, etc.): No direct negative interactions with anabolicsteroids. However, some clinical evidence suggests that some anabolic steroids seem to interact with the peripheral benzodiazepine receptors (PBRs), inhibiting them. One particular study on rats demonstrated that Stanozolol (Winstrol) inhibited the PBR up to 75% and 17beta-Testosterone Cypionate inhibited the PBR up to 40%, while the administration of 17alpha-methyltestosterone and Nortestosterone Decanoate did not demonstrate any significant inhibition of the PBR-specific ligand(4). Although the study does not make any conclusions about what result this might have on the effect of benzodiazepines in the body, it suggests that the use of certain anabolic steroids might reduce the effectiveness of different benzodiazepines due to the inhibition of the benzodiazepine receptors. However, anecdotal evidence would suggest that people who are prescribed benzodiazepines while on a cycle of anabolic steroids do not report any significant reduction in effectiveness. Even if some anabolic steroids do seem to inhibit the PBR, the fact that different benzodiazepine drugs exist with different strengths of activity would mean that various benzodiazepines might not be affected by this effect, and still bind quite strongly to the PBR despite any inhibition caused by AAS. For example, the PBR is actually Diazepam's secondary binding site, not its primary one(5). Furthermore (and this is going slightly off-topic here), the PBR controls many different functions in the human body and is not yet completely understood, but because benzodiazepines bind to the PBR and cause CNS depression (thus enabling the user to sleep), it might very well be possible that the 'Trensomnia' that is caused by Trenbolone might actually be due to Trenbolone possibly expressing strong inhibition of the PBR. The result would then of course be an inhibition of depressive effects on the CNS, thus disrupting sleep patterns.
Benzodiazepines (Diazepam, Clonazepam, Oxazepam, Nitrazepam, Temazepam, etc.): No direct negative interactions with anabolicsteroids. However, some clinical evidence suggests that some anabolic steroids seem to interact with the peripheral benzodiazepine receptors (PBRs), inhibiting them. One particular study on rats demonstrated that Stanozolol (Winstrol) inhibited the PBR up to 75% and 17beta-Testosterone Cypionate inhibited the PBR up to 40%, while the administration of 17alpha-methyltestosterone and Nortestosterone Decanoate did not demonstrate any significant inhibition of the PBR-specific ligand(4). Although the study does not make any conclusions about what result this might have on the effect of benzodiazepines in the body, it suggests that the use of certain anabolic steroids might reduce the effectiveness of different benzodiazepines due to the inhibition of the benzodiazepine receptors. However, anecdotal evidence would suggest that people who are prescribed benzodiazepines while on a cycle of anabolic steroids do not report any significant reduction in effectiveness. Even if some anabolic steroids do seem to inhibit the PBR, the fact that different benzodiazepine drugs exist with different strengths of activity would mean that various benzodiazepines might not be affected by this effect, and still bind quite strongly to the PBR despite any inhibition caused by AAS. For example, the PBR is actually Diazepam's secondary binding site, not its primary one(5). Furthermore (and this is going slightly off-topic here), the PBR controls many different functions in the human body and is not yet completely understood, but because benzodiazepines bind to the PBR and cause CNS depression (thus enabling the user to sleep), it might very well be possible that the 'Trensomnia' that is caused by Trenbolone might actually be due to Trenbolone possibly expressing strong inhibition of the PBR. The result would then of course be an inhibition of depressive effects on the CNS, thus disrupting sleep patterns.
