So I failed a xanax overdose (50mg) plus generous quantities of alcohol on top of having pneumonia. While i was in the psych ward my boyfriend ghosted me, and blocked me on all forms of social media, and my kids got removed from my custody. So i came home to that. I dont feel driven and determined to keep going, if anything... coming home to nothing just made me want to redouble my efforts next time. I signed off for the hospital to send all my paperwork to my psychiatrist and i got a next day appointment and he didnt bother to read any of the paperwork and sent through a xanax refill. The only reason i survived the first attempt is because i told my (then) boyfriend immediately and he called 911. This time i'm gonna have a 45mg xanax refill but do i need to supplement with anything other than alcohol? It was pretty damn close but the pneumonia helped. Suggestions?
I learned in pharmacology classes, that one of the most dangerous and contraindicated mixtures of medication types is prescribing both benzodiazepines and barbiturates at the same time.
These two medications acting together can very quickly to shut off the respiratory drive and result in fatal overdose.
They have what is described as synergistic effect on each other.
Common benzodiazapenes are Xanax (alprazolam) prescribed for acute panic disorder and panic attacks (because it has on of the shortest half lives of benzodiazepines on the market, Valium (diazepam) prescribed for generalized anxiety, fear of public speaking, or sometimes as a sedative - mildly potent with a rather long half life (52 hrs), Lorazepam as an alternative to diazepam, Ativan (intramuscular or intravenous in emergency departments for seizures, combative patients, extreme anxiety or panic, etc...
This class of medication (benzodiazapines) works on the inhibitory neurotransmitter system GABA (gamma aminobutyric acid) receptors within the brain (also the same neurotransmitter system agonized by ethanol (drinking alcohol), facilitating inebriation and depressant effects seen caused by drinking, alongside neuronal long term depression of networks. Benzodiazapines bind to GABA receptors by class and INCREASE the FREQUENCY of CHLORIDE (anion) channel openings along the neuronal membrane. Increasing the migration of negatively charged chloride ions into the neuron facilitates REpolarization of the cellular membrane potential.
Barbiturates are a class of drug applied as a memory wiping anesthetic for procedures and small operations in which the patient must be awake responsive and mildly cooperative. I have also seen them prescribed as an assistive medication for acute opioid withdrawal/detox, or alcohol detox treatment. In the latter case phenobarbital was the barbiturate used. I have seen mild barbiturates like N-butyl barbiturate prescribed with tylenol in small doses for menstrual cramps. Other examples of barbiturate application has been in outdated interrogation by military or intelligence groups administering sodium thiopental as a hopeful "truth serum." They are also used as an anesthetic adjunct for rapid sequence intubation, or sometimes prescribed as anticonvulsants for seizure disorders.
Barbiturate class medication acts on GABA(a) receptor sites distinct from the benzodiazepine binding site, and barbiturates cause an INCREASE in the DURATION of CHLORIDE channel openings on the neuronal membrane from GABA receptors
These two effects when combined (increase in FREQUENCY of chloride channel openings from GABA receptors -from benzodiazepines- alongside increase in DURATION of chloride channel openings from GABA receptors - caused by barbiturates) is devastatingly synergistic, and causes effected neurons to repolarize MUCH more quickly than under the condition of just one drug or the other, ultimately leading to severe respiratory depression in the brainstem, and easily respiratory arrest. This dangerous contraindication could cause mortality in a similar manner as opioid overdose (which causes respiratory depression and arrest in the brainstem, leading to eventual hypoxia and cardiac arrest, followed by hypoxic brain death within 6 to 10 minutes)
These GABAergic drugs taken in conjunction with different GABAergic drugs, perhaps a simple GABA agonist (ethanol), or other CNS depressants with indirect effects on GABA systems (such as opiates and opioids) would also have a synergistic effect on one another, and compound the danger of CNS depression leading to mortality through respiratory arrest originating from the brain stem.
This is why mixtures or combinations in high doses of say, Xanax and heroine (a commonly abused combination among severe street addicts), or Alcohol and Xanax, can have alarmingly high mortality. A factor in unintentional overdose with these combinations is the GABAergic effect on memory or elimination of new short term memory formation from the hippocampus... this would cause the user to be unable to remember their last dose or figure out a safe dose, eventually leading to overdose.
Now, in my life, I was addicted to IV H. And the withdrawals would get really bad. I always had some xanax around in my detox kit, for anxiety, to help with sleep during detox etc... I found a bottle of my gfs n-butyl barbiturate prescribed for her menstrual cramps, and being in opiate withdrawal I impulsively wanted to CTB. So I took the bottle of n-butyl barbiturate with 9 xanax bars and washed it all down with a glass of wine for good measure. I have no memory after that, but I was definitely breathing, not only breathing I was up and about, I came to my wits sitting on a random park bench with no idea where I was or how I had gotten there, and walking off from there I unwittingly stumbled across my jeep which was idling in neutral keys still in ignition, abandoned with the doors open, one wheel popped up the sidewalk curb, another front wheel in the grass of a park, the back wheels and rear end still butting into the roadway.
Now there are a number of reasons this attempt to ctb was so unsuccessful. One could be that opiate withdrawal and tolerance had caused me to build up an extremely resilient respiratory drive over time. This in combination with the fact that the dosage of n-butyl barbiturate with tylenol was very low, like it was probably basically a baby dose of barbiturate, nothing serious... although I took a moderately serious amount of xanax - dosage wise- and a half hearted attempt at adding alcohol, this impulsive ctb attempt was extremely dangerous to others (I drove around apparently, still have no memory), caused negative unintended consequences for myself (I ended up explaining this in the psych ward a week later), only offered me mild temporary relief from the opioid withdrawal by erasing my memory for a short period of time, but overall really messed me up more. I'm also lucky I didn't hit and hurt or kill someone in my jeep all Xannied out of mind.
These two medications acting together can very quickly to shut off the respiratory drive and result in fatal overdose.
They have what is described as synergistic effect on each other.
Common benzodiazapenes are Xanax (alprazolam) prescribed for acute panic disorder and panic attacks (because it has on of the shortest half lives of benzodiazepines on the market, Valium (diazepam) prescribed for generalized anxiety, fear of public speaking, or sometimes as a sedative - mildly potent with a rather long half life (52 hrs), Lorazepam as an alternative to diazepam, Ativan (intramuscular or intravenous in emergency departments for seizures, combative patients, extreme anxiety or panic, etc...
This class of medication (benzodiazapines) works on the inhibitory neurotransmitter system GABA (gamma aminobutyric acid) receptors within the brain (also the same neurotransmitter system agonized by ethanol (drinking alcohol), facilitating inebriation and depressant effects seen caused by drinking, alongside neuronal long term depression of networks. Benzodiazapines bind to GABA receptors by class and INCREASE the FREQUENCY of CHLORIDE (anion) channel openings along the neuronal membrane. Increasing the migration of negatively charged chloride ions into the neuron facilitates REpolarization of the cellular membrane potential.
Barbiturates are a class of drug applied as a memory wiping anesthetic for procedures and small operations in which the patient must be awake responsive and mildly cooperative. I have also seen them prescribed as an assistive medication for acute opioid withdrawal/detox, or alcohol detox treatment. In the latter case phenobarbital was the barbiturate used. I have seen mild barbiturates like N-butyl barbiturate prescribed with tylenol in small doses for menstrual cramps. Other examples of barbiturate application has been in outdated interrogation by military or intelligence groups administering sodium thiopental as a hopeful "truth serum." They are also used as an anesthetic adjunct for rapid sequence intubation, or sometimes prescribed as anticonvulsants for seizure disorders.
Barbiturate class medication acts on GABA(a) receptor sites distinct from the benzodiazepine binding site, and barbiturates cause an INCREASE in the DURATION of CHLORIDE channel openings on the neuronal membrane from GABA receptors
These two effects when combined (increase in FREQUENCY of chloride channel openings from GABA receptors -from benzodiazepines- alongside increase in DURATION of chloride channel openings from GABA receptors - caused by barbiturates) is devastatingly synergistic, and causes effected neurons to repolarize MUCH more quickly than under the condition of just one drug or the other, ultimately leading to severe respiratory depression in the brainstem, and easily respiratory arrest. This dangerous contraindication could cause mortality in a similar manner as opioid overdose (which causes respiratory depression and arrest in the brainstem, leading to eventual hypoxia and cardiac arrest, followed by hypoxic brain death within 6 to 10 minutes)
These GABAergic drugs taken in conjunction with different GABAergic drugs, perhaps a simple GABA agonist (ethanol), or other CNS depressants with indirect effects on GABA systems (such as opiates and opioids) would also have a synergistic effect on one another, and compound the danger of CNS depression leading to mortality through respiratory arrest originating from the brain stem.
This is why mixtures or combinations in high doses of say, Xanax and heroine (a commonly abused combination among severe street addicts), or Alcohol and Xanax, can have alarmingly high mortality. A factor in unintentional overdose with these combinations is the GABAergic effect on memory or elimination of new short term memory formation from the hippocampus... this would cause the user to be unable to remember their last dose or figure out a safe dose, eventually leading to overdose.
Now, in my life, I was addicted to IV H. And the withdrawals would get really bad. I always had some xanax around in my detox kit, for anxiety, to help with sleep during detox etc... I found a bottle of my gfs n-butyl barbiturate prescribed for her menstrual cramps, and being in opiate withdrawal I impulsively wanted to CTB. So I took the bottle of n-butyl barbiturate with 9 xanax bars and washed it all down with a glass of wine for good measure. I have no memory after that, but I was definitely breathing, not only breathing I was up and about, I came to my wits sitting on a random park bench with no idea where I was or how I had gotten there, and walking off from there I unwittingly stumbled across my jeep which was idling in neutral keys still in ignition, abandoned with the doors open, one wheel popped up the sidewalk curb, another front wheel in the grass of a park, the back wheels and rear end still butting into the roadway.
Now there are a number of reasons this attempt to ctb was so unsuccessful. One could be that opiate withdrawal and tolerance had caused me to build up an extremely resilient respiratory drive over time. This in combination with the fact that the dosage of n-butyl barbiturate with tylenol was very low, like it was probably basically a baby dose of barbiturate, nothing serious... although I took a moderately serious amount of xanax - dosage wise- and a half hearted attempt at adding alcohol, this impulsive ctb attempt was extremely dangerous to others (I drove around apparently, still have no memory), caused negative unintended consequences for myself (I ended up explaining this in the psych ward a week later), only offered me mild temporary relief from the opioid withdrawal by erasing my memory for a short period of time, but overall really messed me up more. I'm also lucky I didn't hit and hurt or kill someone in my jeep all Xannied out of mind.
Last edited:
Zozo
Member
- May 4, 2020
- 45
Ghostmedic, with your knowledge of pharmacology maybe you can answer a question.
I take benzos usually once a month on a 3 day "binge." I noticed I have a pouch of powdered GABA in my cabinet (don't know where it came from). I always wondered what would happen if I were to take the GABA with the benzos. Would they potentiate each other? Would this be dangerous?
I take benzos usually once a month on a 3 day "binge." I noticed I have a pouch of powdered GABA in my cabinet (don't know where it came from). I always wondered what would happen if I were to take the GABA with the benzos. Would they potentiate each other? Would this be dangerous?
I'm so sorry you've experienced this. You were clearly over the edge as it was, to then have all that happen to you. I'm so sorry you've had basically no compassion or actual help for your life circumstances. I've been to a psych ward before because I was depressed about external circumstances. They just gave me drugs and didn't help me with any of my practical issues.
I'm glad you're able to vent here.
