Hello
I kindly ask for some information from some knowledgable members before i proceed and possibly do myself harm so.........
I suffered a spinal cord injury at C3 level some years ago due to surgery to remove a tumour and radiation to stop residual tumour growth. As with any spinal injury we take a bunch of different medication to help with various issues that come with spinal injuries, muscle relaxers, anti-epileptics(for neuro pain), anticholinergic meds for bladder incontinence amongst others
Ive used lsd, 1p, al-lad and some other all with great effects, but my DMT journeys have been rather underwhelming, and recently I tried some Cubensis.
I tried 2 grams of P Cubensis, lemon tek, with very little effects, actually just a few tracers, so a couple weeks later i tried them again but this time 4 grams lemon tek, this time with exactly the same, very minimal tracers and some shaking of the eye vision, very meh. At first i thought it to be dud cubes but i doubt that to be the case.
So i tried to do some research on the effects of Psilocybin with my medication and found very little information and I'm pretty useless in understanding how things affect serotonin, dopamine etc etc. I was always under the impression that i was reasonably safe as i stopped taking any anti-depresants/ssri's, but i believe i am wrong and could very well have ended up in a bad situation.\
Please can you guys chime in here and help me understand better what is blocking my Psilocybin trips from dong anything. I understand it will take some reading but I'm here for harm reduction for myself and for any others that might be taking any of the same meds.
Current medication I take:
Oxybutynin (anticholinergic for bladder spasms) - Oxybutynin contains one stereocenter. Commercial formulations are sold as the racemate. The (R)-enantiomer is a more potent anticholinergic than either the racemate or the (S)-enantiomer, which is essentially without anticholinergic activity at doses used in clinical practice.[6][7] However, (R)-oxybutynin administered alone offers little or no clinical benefit above and beyond the racemic mixture. The other actions (calcium antagonism, local anesthesia) of oxybutynin are not stereospecific. (S)-Oxybutynin has not been clinically tested for its spasmolytic effects, but may be clinically useful for the same indications as the racemate, without the unpleasant anticholinergic side effects.
Baclofen (muscle relaxer/anti spasms) - Baclofen produces its effects by activating the GABAB receptor, similar to the drug phenibut which also activates this receptor and shares some of its effects. Baclofen is postulated to block mono-and-polysynaptic reflexes by acting as an inhibitory neurotransmitter, blocking the release of excitatory transmitters. However, baclofen does not have significant affinity for the GHB receptor, and has no known abuse potential.[18] The modulation of the GABAB receptor is what produces baclofen's range of therapeutic properties.
Similarly to phenibut (?-phenyl-GABA), as well as pregabalin (?-isobutyl-GABA), which are close analogues of baclofen, baclofen (?-(4-chlorophenyl)-GABA) has been found to block ?2? subunit-containing voltage-gated calcium channels (VGCCs).[19] However, it is weaker relative to phenibut in this action (Ki = 23 and 39 ?M for R- and S-phenibut and 156 ?M for baclofen).[19] Moreover, baclofen is in the range of 100-fold more potent by weight as an agonist of the GABAB receptor in comparison to phenibut, and in accordance, is used at far lower relative dosages. As such, the actions of baclofen on ?2? subunit-containing VDCCs are likely not clinically-relevant.[19]
Tizanidine aka Zanaflex (muscle relaxer) - Concomitant use of tizanidine and moderate or potent CYP1A2 inhibitors (such as zileuton, certain antiarrhythmics (amiodarone, mexiletine, propafenone, verapamil), cimetidine, famotidine, aciclovir, ticlopidine and oral contraceptives) is contraindicated. Concomitant use of tizanidine with fluvoxamine, a potent CYP1A2 inhibitor in humans, resulted in a 33-fold increase in the tizanidine AUC (plasma drug concentration-time curve).[1] Fluoroquinolone antibiotics such as moxifloxacin, levofloxacin, and ciprofloxacin should also be avoided due to an increased serum concentration of tizanidine when administered concomitantly.[5] Tizanidine has the potential to interact with other central nervous system depressants. Alcohol should be avoided, particularly as it can upset the stomach. The CNS-depressant effects of tizanidine and alcohol are additive.[1]
Pregabalin aka Lyrica (new age anti epileptic used for nerve pain among other uses) - Pregabalin is a GABAergic anticonvulsant and depressant of the central nervous system (CNS). It is classified as a GABA analogue and gabapentinoid.[50] It is a close analogue of the inhibitory neurotransmitter ?-aminobutyric acid (GABA).[51][52][53][19] Pregabalin binds with high affinity to the ?2? subunit-containing voltage-gated calcium channels (VDCC). It increases extracellular GABA concentrations in the brain by producing a dose-dependent increase in L-Glutamic acid decarboxylase (GAD), the enzyme responsible for making GABA.[54][54][55][56] Although pregabalin is an analogue of GABA, it does not bind directly to GABAA, GABAB, GABA?, or benzodiazepine receptors. Nor does it block sodium channels and is not active at opioid receptors. Gabapentinoids, such as pregabalin, are ?2? subunit modifiers that affect GABA. In contrast to the distribution of ?2?-1 and ?2?-2 subunits binding correlates partially with GABAergic neurons.[57] Pregabalin increases the density of GABA transporter proteins and increases the rate of functional GABA transport.[58] It also increases extracellular GABA concentrations in the brain by producing a dose-dependent increase in L-Glutamic acid decarboxylase.[54]
From limited knowledge and what information i could find i suspect the Baclofen and Oxybutynin to be the culprits in blocking the effects of the P Cubensis.
I think i really did dodge a bullet, maybe something was looking over me, or maybe I was lucky, or were the cubes just spent of any actives?
Thank you
I kindly ask for some information from some knowledgable members before i proceed and possibly do myself harm so.........
I suffered a spinal cord injury at C3 level some years ago due to surgery to remove a tumour and radiation to stop residual tumour growth. As with any spinal injury we take a bunch of different medication to help with various issues that come with spinal injuries, muscle relaxers, anti-epileptics(for neuro pain), anticholinergic meds for bladder incontinence amongst others
Ive used lsd, 1p, al-lad and some other all with great effects, but my DMT journeys have been rather underwhelming, and recently I tried some Cubensis.
I tried 2 grams of P Cubensis, lemon tek, with very little effects, actually just a few tracers, so a couple weeks later i tried them again but this time 4 grams lemon tek, this time with exactly the same, very minimal tracers and some shaking of the eye vision, very meh. At first i thought it to be dud cubes but i doubt that to be the case.
So i tried to do some research on the effects of Psilocybin with my medication and found very little information and I'm pretty useless in understanding how things affect serotonin, dopamine etc etc. I was always under the impression that i was reasonably safe as i stopped taking any anti-depresants/ssri's, but i believe i am wrong and could very well have ended up in a bad situation.\
Please can you guys chime in here and help me understand better what is blocking my Psilocybin trips from dong anything. I understand it will take some reading but I'm here for harm reduction for myself and for any others that might be taking any of the same meds.
Current medication I take:
Oxybutynin (anticholinergic for bladder spasms) - Oxybutynin contains one stereocenter. Commercial formulations are sold as the racemate. The (R)-enantiomer is a more potent anticholinergic than either the racemate or the (S)-enantiomer, which is essentially without anticholinergic activity at doses used in clinical practice.[6][7] However, (R)-oxybutynin administered alone offers little or no clinical benefit above and beyond the racemic mixture. The other actions (calcium antagonism, local anesthesia) of oxybutynin are not stereospecific. (S)-Oxybutynin has not been clinically tested for its spasmolytic effects, but may be clinically useful for the same indications as the racemate, without the unpleasant anticholinergic side effects.
Baclofen (muscle relaxer/anti spasms) - Baclofen produces its effects by activating the GABAB receptor, similar to the drug phenibut which also activates this receptor and shares some of its effects. Baclofen is postulated to block mono-and-polysynaptic reflexes by acting as an inhibitory neurotransmitter, blocking the release of excitatory transmitters. However, baclofen does not have significant affinity for the GHB receptor, and has no known abuse potential.[18] The modulation of the GABAB receptor is what produces baclofen's range of therapeutic properties.
Similarly to phenibut (?-phenyl-GABA), as well as pregabalin (?-isobutyl-GABA), which are close analogues of baclofen, baclofen (?-(4-chlorophenyl)-GABA) has been found to block ?2? subunit-containing voltage-gated calcium channels (VGCCs).[19] However, it is weaker relative to phenibut in this action (Ki = 23 and 39 ?M for R- and S-phenibut and 156 ?M for baclofen).[19] Moreover, baclofen is in the range of 100-fold more potent by weight as an agonist of the GABAB receptor in comparison to phenibut, and in accordance, is used at far lower relative dosages. As such, the actions of baclofen on ?2? subunit-containing VDCCs are likely not clinically-relevant.[19]
Tizanidine aka Zanaflex (muscle relaxer) - Concomitant use of tizanidine and moderate or potent CYP1A2 inhibitors (such as zileuton, certain antiarrhythmics (amiodarone, mexiletine, propafenone, verapamil), cimetidine, famotidine, aciclovir, ticlopidine and oral contraceptives) is contraindicated. Concomitant use of tizanidine with fluvoxamine, a potent CYP1A2 inhibitor in humans, resulted in a 33-fold increase in the tizanidine AUC (plasma drug concentration-time curve).[1] Fluoroquinolone antibiotics such as moxifloxacin, levofloxacin, and ciprofloxacin should also be avoided due to an increased serum concentration of tizanidine when administered concomitantly.[5] Tizanidine has the potential to interact with other central nervous system depressants. Alcohol should be avoided, particularly as it can upset the stomach. The CNS-depressant effects of tizanidine and alcohol are additive.[1]
Pregabalin aka Lyrica (new age anti epileptic used for nerve pain among other uses) - Pregabalin is a GABAergic anticonvulsant and depressant of the central nervous system (CNS). It is classified as a GABA analogue and gabapentinoid.[50] It is a close analogue of the inhibitory neurotransmitter ?-aminobutyric acid (GABA).[51][52][53][19] Pregabalin binds with high affinity to the ?2? subunit-containing voltage-gated calcium channels (VDCC). It increases extracellular GABA concentrations in the brain by producing a dose-dependent increase in L-Glutamic acid decarboxylase (GAD), the enzyme responsible for making GABA.[54][54][55][56] Although pregabalin is an analogue of GABA, it does not bind directly to GABAA, GABAB, GABA?, or benzodiazepine receptors. Nor does it block sodium channels and is not active at opioid receptors. Gabapentinoids, such as pregabalin, are ?2? subunit modifiers that affect GABA. In contrast to the distribution of ?2?-1 and ?2?-2 subunits binding correlates partially with GABAergic neurons.[57] Pregabalin increases the density of GABA transporter proteins and increases the rate of functional GABA transport.[58] It also increases extracellular GABA concentrations in the brain by producing a dose-dependent increase in L-Glutamic acid decarboxylase.[54]
From limited knowledge and what information i could find i suspect the Baclofen and Oxybutynin to be the culprits in blocking the effects of the P Cubensis.
I think i really did dodge a bullet, maybe something was looking over me, or maybe I was lucky, or were the cubes just spent of any actives?
Thank you
