I can obtain 100 10 mg oxycodone hydrochloride and I have 30 mg of Ativan. How much of this do I take to successfully ctb.
RoseGirl
Student
- May 8, 2025
- 155
tapetum_lucidum
Member
- Mar 12, 2023
- 44
RoseGirl
Student
- May 8, 2025
- 155
R. A.
If I must die, do not let them say I did not live.
- Aug 8, 2022
- 1,449
Here's data safety sheet about oxycodone:
Lethal dose 50% (LD50) for oxycodone in mouse with oral intake is 482 mg/kg. Now if we use transferring method (mentioned here https://pmc.ncbi.nlm.nih.gov/articles/PMC4804402/), we can found that human equivalent dose (HED) for that is:
HED (mg / kg = 482 × 0.081 (mouse to human transition dose) = 39.042 mg / kg.
Same as ativan (lorazepam), here's the data safety sheet:
Lethal dose 50% (LD50) for lorazepam in mouse with oral intake is 1850 mg/kg. Now if we use the same transferring method, we can found that human equivalent dose (HED) for that is:
HED (mg / kg = 1850 × 0.081 = 149.85 mg / kg.
Now you can multiply that with your bodyweight and that's how much you should take. For instance, if you have 75 kg bodyweight you should take oxycodone around 2928,15 mg of oxycodone and/or 11238,75 mg of lorazepam. Since your stock of Ativan isn't near enough as needed, I'd suggest focus on oxycodone by stocking them up first. Now do note:
1. These are only calculation. In my opinion, the dose needed to ctb would be way lower than the predicted dose by animals. Even in the calculation paper they included notes that larger animals need far lower dose to achieve the same effect due to larger differences in the physiological process.
2. These are lethal dose 50%, meaning at that dose only 50% of the population of the samples died after ingesting the substance. Same as the transitioned dose. You could be in the upper half or lower half of the 50%. Same as many others, you should try your tolerance with the drug before you truly want to ctb
3. I think your ativan might be useful for you to turn off your SI and not as ctb method. Focus your method on oxycodone since you have bigger stocks of it.
Tldr: Use ativan, wait for it to slowly take effect, then ctb using all of your oxycodone stocks (if you can). Remember to prepare it thoroughly.
Here's the estrogen data safety sheet:
LD50 for mouse in intravenous injection is 1740 mg/kg. With the same calculation as above, we can extrapolate them by this:
HED (mg / kg = 1740 × 0.081 = 140.94 mg / kg.
Same notes as above, but do note ctb by estrogen is pretty rare and unheard of. Here's a case report of similar style if you're interested:
Pulmonary embolism due to exogenous estrogen intoxication - PubMed
We know that exogenous estrogen increase the risk of venous thromboembolism in therapeutic use. It should be kept in mind that even single ingestion of a single high-dose exogenous estrogen intake may induce pulmonary thromboembolism.
pubmed.ncbi.nlm.nih.gov
Sorry for not searching enough on testosterone. Data regarding testosterone toxicity is actually far harder to search than estrogen (don't ask me why lmao idk either). Here's one:we
In there they found LD50 for mouse with dermal injection is around 2000 mg/kg. With the same calculation we can make it's HED by:
HED (mg / kg = 2000 × 0.081 = 162 mg / kg.
Now do note that this calculation is extremely flimsy due to:
1. Its only made by using analogies related to the similar compound 4-Androstene-3,17-dione.
2. Still no case report of testosterone being used in ctb
3. The route is dermal injection, not straight up intravenous injection like in estrogen
4. All the points above about LD50 and precaution that this is only a calculation/speculation
Sorry for not searching enough on testosterone. Data regarding testosterone toxicity is actually far harder to search than estrogen (don't ask me why lmao idk either). Here's one:
In there they found LD50 for mouse with dermal injection is around 2000 mg/kg. With the same calculation we can make it's HED by:
HED (mg / kg = 2000 × 0.081 = 162 mg / kg.
Now do note that this calculation is extremely flimsy due to:
1. Its only made by using analogies related to the similar compound 4-Androstene-3,17-dione.
2. Still no case report of testosterone being used in ctb
3. The route is dermal injection, not straight up intravenous injection like in estrogen
4. All the points above about LD50 and precaution that this is only a calculation/speculation
Last edited:
RoseGirl
Student
- May 8, 2025
- 155
Freedombus'25
Hating every minute of being alive.
- Dec 8, 2019
- 1,703
Can I PM you some questions regarding meds and such. I don't really feel comfy asking in public thread. No pressure or anything....
Human equivalent dose. Since studies on toxicology can't be done on humans (obviously), the dose acquired from test animals need to be adjusted to the human level.
Sure, why not? My DM are open.
What is your knowledge on a baclofen overdose? What is does, what it's like, and if it can actually work? I plan on consuming guanfacine as well.
First of all, I want to said I'm really sorry for the long wait. College stuff and irl conditions make me busy rn.
Converting table from this publication I mentioned: https://pmc.ncbi.nlm.nih.gov/articles/PMC4804402/. I think I'll needing this more later on so I'll just post it here lol.
Your question has 3 topics, here's how it goes:
1. Baclofen overdose
Here's a data sheet about baclofen:
LD50 for oral route in rat is 50 – 300 mg/kg. From the publication above we can make its HED into this:
HED = 50 x 0.162 = 8.1 mg/kg
HED = 300 x 0.162 = 48.6 mg/kg
So we can deduct that LD50 for oral route for human is around 8,1-48,6 mg/kg.
There is actually a lot of good publications about baclofen overdose. I pick one that's a really good publication about baclofen overdose, here goes:
Baclofen therapeutics, toxicity, and withdrawal: A narrative review - PMC
Baclofen is an effective therapeutic for the treatment of spasticity related to multiple sclerosis, spinal cord injuries, and other spinal cord pathologies. It has been increasingly used off-label for the management of several disorders, including ...
pmc.ncbi.nlm.nih.gov
This study explains the symptoms, effect, and treatment of baclofen overdose. In general, ingestion as little as 200 mg a day could cause toxicity with the symptoms of degradation of consciousness (hallucinations, confusion, tremor, catatonia) that could lead up to death. Here's a case report of alleged ingestion of 15 tablet of 20 mg baclofen that ended on his death:
2. Guanfacine overdose
Different from baclofen, there's not a lot of data regarding guanfacine. I couldn't even find guanfacine LD50 on any data safety sheet.
From what I found, not a lot of guanfacine overdose can make them fatal. Here's a pretty good publication reviewing cases of guanfacine overdose:
Delayed Signs and Symptoms of Extended Release Guanfacine Overdose in Two Adolescent Patients: Implications of Monitoring on the Psychiatry Unit - PMC
Guanfacine is a selective alpha-2a adrenoreceptor agonist that with overdose can cause symptoms ranging from mild sedation to coma, respiratory depression, hyporeflexia, hypotonia, bradycardia, and hypotension. Despite a well-defined and predictable ...
pmc.ncbi.nlm.nih.gov
Guanfacine poisoning resulting in transient ST-segment elevation: a case report - International Journal of Emergency Medicine
Background Guanfacine is an alpha-2 adrenergic agonist that decreases norepinephrine release and sympathetic outflow. With the increased use of guanfacine for attention-deficit hyperactivity disorder (ADHD), reports of guanfacine poisoning have also risen. Case presentation A 15-year-old male...
intjem.biomedcentral.com
In general, I can't really make a judgement of this one. I don't think this is a good method with such no cases of dying of this so far as I can search of.
3. Baclofen and Guanfacine
There's a potential interaction on this one, usually because guanfacine can make hypotension that also can be lowered by baclofen:
Baclofen and guanfacine Interactions - Drugs.com
A Moderate Drug Interaction exists between baclofen and guanfacine. View detailed information regarding this drug interaction.
www.drugs.com
Can they work together in case of ctb? I say maybe. I can't really have a firm answer since studies on that is so low.
Thank you so much for your response! I wanted to combine the two because I knew that they both could lower blood pressure but I was scared I didn't have enough baclofen (because it's not my prescription), but I actually have more than I thought, 980 mg. I'm not sure if I should just do the baclofen or not, because the guanfacine is all wonky with it being extended release.First of all, I want to said I'm really sorry for the long wait. College stuff and irl conditions make me busy rn.
View attachment 177789
Converting table from this publication I mentioned: https://pmc.ncbi.nlm.nih.gov/articles/PMC4804402/. I think I'll needing this more later on so I'll just post it here lol.
Your question has 3 topics, here's how it goes:
1. Baclofen overdose
Here's a data sheet about baclofen:
LD50 for oral route in rat is 50 – 300 mg/kg. From the publication above we can make its HED into this:
HED = 50 x 0.162 = 8.1 mg/kg
HED = 300 x 0.162 = 48.6 mg/kg
So we can deduct that LD50 for oral route for human is around 8,1-48,6 mg/kg.
There is actually a lot of good publications about baclofen overdose. I pick one that's a really good publication about baclofen overdose, here goes:
Baclofen therapeutics, toxicity, and withdrawal: A narrative review - PMC
Baclofen is an effective therapeutic for the treatment of spasticity related to multiple sclerosis, spinal cord injuries, and other spinal cord pathologies. It has been increasingly used off-label for the management of several disorders, including ...
This study explains the symptoms, effect, and treatment of baclofen overdose. In general, ingestion as little as 200 mg a day could cause toxicity with the symptoms of degradation of consciousness (hallucinations, confusion, tremor, catatonia) that could lead up to death. Here's a case report of alleged ingestion of 15 tablet of 20 mg baclofen that ended on his death:
2. Guanfacine overdose
Different from baclofen, there's not a lot of data regarding guanfacine. I couldn't even find guanfacine LD50 on any data safety sheet.
From what I found, not a lot of guanfacine overdose can make them fatal. Here's a pretty good publication reviewing cases of guanfacine overdose:
Here's also a case report of guanfacine overdose case report that maybe interesting to you:Delayed Signs and Symptoms of Extended Release Guanfacine Overdose in Two Adolescent Patients: Implications of Monitoring on the Psychiatry Unit - PMC
Guanfacine is a selective alpha-2a adrenoreceptor agonist that with overdose can cause symptoms ranging from mild sedation to coma, respiratory depression, hyporeflexia, hypotonia, bradycardia, and hypotension. Despite a well-defined and predictable ...
In general, the symptoms of guanfacine overdose is hypotension, impaired consciousness, and bradycardia. Some can be delayed if they are using extended release version of guanfacine (as upper publication makes it)Guanfacine poisoning resulting in transient ST-segment elevation: a case report - International Journal of Emergency Medicine
Background Guanfacine is an alpha-2 adrenergic agonist that decreases norepinephrine release and sympathetic outflow. With the increased use of guanfacine for attention-deficit hyperactivity disorder (ADHD), reports of guanfacine poisoning have also risen. Case presentation A 15-year-old male...
In general, I can't really make a judgement of this one. I don't think this is a good method with such no cases of dying of this so far as I can search of.
3. Baclofen and Guanfacine
There's a potential interaction on this one, usually because guanfacine can make hypotension that also can be lowered by baclofen:
Baclofen and guanfacine Interactions - Drugs.com
A Moderate Drug Interaction exists between baclofen and guanfacine. View detailed information regarding this drug interaction.
Can they work together in case of ctb? I say maybe. I can't really have a firm answer since studies on that is so low.
mob
Student
- Jul 19, 2023
- 149
I recently overdosed on 7.2g of bupropion (extended release, if it matters), was taken to the hospital, recovered within 3 days. Had no seizures.
My question is, since the lethal range goes from 6g (at least that's where it starts getting toxic) upwards, how much does a person have to take to certainly die from it?
I don't plan on OD'ing on bupropion again, I'm just curious.
My question is, since the lethal range goes from 6g (at least that's where it starts getting toxic) upwards, how much does a person have to take to certainly die from it?
I don't plan on OD'ing on bupropion again, I'm just curious.
This is very hard question because certain death after bupropion use is absolutely hard on. The numbers are really large on its range, because its definitely depends on what patient are we're talking about:
A 19-year-old woman died with an estimated bupropion overdose of 28.2 g and possible oxcarbazepine co-ingestion.:
A 19-Year-Old Woman with a History of Depression and Fatal Cardiorespiratory Failure Following an Overdose of Prescribed Bupropion - PMC
Patient: Female, 19-year-old Final Diagnosis: Poisoning by bupropion Symptoms: Altered mental status • cardiogenic shock • seizure Medication: — Clinical Procedure: — Specialty: Toxicology Management of emergency care Bupropion is a ...
pmc.ncbi.nlm.nih.gov
A 28 year old male with history of severe depression died after consumption of 30 300mg bupropion (9 g) extended release pills as a part of a suicidal attempt:
A 26-year-old man who ingested 23 g bupropion, developed seizures and hypoxia, and died 4 d after supportive intensive care:
This range is really large, even as small as 9 g and up to >20g of buproprion (and one with possible ingestion of other substance). I'd say your attempt of 7,2g can kill someone with different subject as you (age, height, gene, sex, or dietary usage). And extended release certainly matter in terms of denying the immidiate release of bupropion of toxic concentration into the body. I'd say you're lucky surviving that attempt.
Lyn
Momentary
- Mar 1, 2025
- 293
I don't know if my question is relevant. But still...
Why are SSRIs, with all their side effects, considered first-line treatment for social anxiety, when there are alternatives that have way less side effects and can be used occasionally, instead of daily use?
Like propranolol+GABA meds for example.
What is the point of SSRI when you are dealing with anxiety, not some kind of depression or something?
In general, mechanism between anxiety and depression is closely linked, due to the root of it is the same. Both the depression and anxiety is theorized to be caused by the disruption of chemical in the brain. The monoamine hypothesis that depression is caused by decreased brain levels of serotonin (5-HT), dopamine (DA), and norepinephrine (NE). Meanwhile, the modulation of normal and pathologic anxiety states is associated with multiple regions of the brain and abnormal function in several neurotransmitter systems, including norepinephrine (NE), γ-aminobutyric acid (GABA), serotonin (5-HT), dopamine (DA), corticotropin-releasing factor (CRF), and cholecystokinin. Now why I said this is a theory? Because brain chemical is so complex that there's no complete answer on why these neurochemical mentioned causes depression and/or anxiety. One of the most debated (and rightfully so) neurotransmitter that is hotly debated in here is serotonin.
Although there are data suggesting that the 5-HT system is dysregulated in patients with anxiety disorders, definitive evidence that shows a clear abnormality in 5-HT function is lacking. In general, 5-HT is primarily an inhibitory neurotransmitter that is used by neurons originating in the raphe nuclei of the brain stem and projecting diffusely throughout the brain (eg, cortex, amygdala, hippocampus, and limbic system). Abnormalities in serotonergic functioning through release and uptake at the presynaptic autoreceptors (5-HT1A/1D), the serotonin-reuptake transporter (SERT), or effect of 5-HT at the postsynaptic receptors (eg, 5-HT1A, 5-HT2A
, and 5-HT2C) may play a role in anxiety disorders.
This is where SSRI goes into play. The mechanism of action for antidepressants in anxiety disorders is not fully understood. Antidepressants may modulate receptor activation of neuronal signal transduction pathways connected to the neurotransmitters 5-HT, DA, and NE. By activating stress-adapting pathways, SSRIs and SNRIs reduce the somatic anxiety symptoms and the general distress experienced by patients. Of course there's treatment for rapid/acute anxiety treatment, usually benzodiazepines. But antidepressants are effective in the acute and long-term management of anxiety. Data support the use of the SSRIs and SNRIs for acute therapy (8- to 12-week trials) with response rates between 60% and 68%, and remission rates of approximately 30%. This is why SSRI is the first line treatment for anxiety.
I pull most of this from DiPiro's Pharmacology book, but here's a research that shows the latest updates of serotonin in anxiety and depression:
Latest updates on the serotonergic system in depression and anxiety - PMC
Psychiatric disorders are among the leading causes of global health burden, with depression and anxiety being the most disabling subtypes. The two common disorders, depression and anxiety, usually coexist and are pathologically polygenic with ...
pmc.ncbi.nlm.nih.gov
TLDR: Anxiety is theorized because of dysfunction in neurotransmitter in the brain, one of the biggest contributor in it is serotonin. This is why SSRI is used in anxiety as to normalize the serotonin amount in the brain so that the patients experience fewer episodes due to modulated neurotransmitter.
There's an interesting thread regarding OD as a method of ctb, check this out:
sanctioned-suicide.net
I'm still conflicted because LD50 isn't a really good measure of lethality imo (due to how wild the approximation of predicted LD50 in humans and cases regarding actual death by OD), but I think its definitely a good read to add measurement in your plan.
Why ODs Fail Miserably (A Guide)
There's still a lot of questions and inquiries about ODs, and people asking about what things may facilitate a successful attempt. Let's be clear, ODs are rarely fatal. Why? For a couple of reasons: (1) modern medications are designed to be very safe, as manufacturers aim to avoid deaths that...
sanctioned-suicide.net
I'm still conflicted because LD50 isn't a really good measure of lethality imo (due to how wild the approximation of predicted LD50 in humans and cases regarding actual death by OD), but I think its definitely a good read to add measurement in your plan.
MissAbyss
"I gazed for too long.."
- Jul 20, 2025
- 26
Hello Mati,
First of all, I would like to thank you for sharing your knowledge, it is very valuable.
Before I start asking questions, may I ask if you have any knowledge regarding Post-Acute Withdrawal Syndrome caused by long-term use and abrupt discontinuation of antidepressants (SSRIs)?
First of all, I would like to thank you for sharing your knowledge, it is very valuable.
Before I start asking questions, may I ask if you have any knowledge regarding Post-Acute Withdrawal Syndrome caused by long-term use and abrupt discontinuation of antidepressants (SSRIs)?
Hi, thanks for asking here.Hello Mati,
First of all, I would like to thank you for sharing your knowledge, it is very valuable.
Before I start asking questions, may I ask if you have any knowledge regarding Post-Acute Withdrawal Syndrome caused by long-term use and abrupt discontinuation of antidepressants (SSRIs)?
First of all, I truly don't know about Post-Acute Withdrawal Syndrome (therefore will be shortened as PAWS) up until you asked. After some bit of research, I find this phenomenon is interesting. Not only due to lack of studies in PAWS, but the effects are so long passed after the treatment that it's really hard to be detected in the first place. So far I only found three relevant papers on PAWS on antidepressants, all of them have its own quirks.
This is a review on PAWS on the scale of systematic review. It use 7 studies which is detailed in Table 1. This is the most updated resource on PAWS on antidepressants. It includes the severity of the symptoms up to strategic treatments of PAWS itself. Generally, the treatment of PAWS is the reinstatement of antidepressants involved before, or switching to a low-dose benzodiazepine until the symptom slowly gone and the discontinuation can slowly begun.
Maintenance or Discontinuation of Antidepressants in Primary Care | NEJM
Patients with depression who are treated in primary care practices may receive antidepressants for prolonged periods. Data are limited on the effects of maintaining or discontinuing antidepressant ...
Protracted withdrawal syndrome after stopping antidepressants: a descriptive quantitative analysis of consumer narratives from a large internet forum - PMC
Protracted withdrawal syndrome (PWS) after stopping antidepressants (frequently also referred to as post-acute withdrawal syndrome or PAWS) has been described in a few case reports. However, a detailed quantitative analysis of specific symptom ...
pmc.ncbi.nlm.nih.gov
"The two suicides reported among our subjects were verified by public records. Both were women who had been active on several Internet sites dealing with psychiatric drug withdrawal and were explicit about their extreme distress. Both had medical treatment subsequent to developing PWS from antidepressants. One initiated sertraline at age 16; after 16 months on the drug, her 1-month medically supervised taper was uneventful, except for post-SSRI sexual dysfunction (PSSD), which persisted, despite treatment with mianserin, for 38 months, until her suicide. In multiple Internet support groups, she had expressed distress about her ongoing sexual dysfunction. Her last post on SurvivingAntidepressants.org was in October 2019: "To be honest, now I'm in absolute hell. I don't see much hope in this situation anymore. It's been 3+ years and I'm still in pretty much the same situation. I don't know how much longer I'll be here honestly". The next day, she killed herself. She had recently turned 21 years old. The second woman took 15 mg mirtazapine for 69 months despite initial and ongoing adverse effects from the drug. Her lengthy and difficult taper brought no relief of symptoms. In her sixth year of PWS, she saw some improvement, but in May 2020 had an adverse reaction to an antibiotic-steroid ear drop that revived her most severe withdrawal symptoms, one of them akathisia. In Internet forums, she clearly expressed anguish over her iatrogenic condition. After 69 months of PWS, in August 2020, she killed herself."
To me, this is so sad because its not only because this study is the only one having suicides (or at least I'm not searching further), but its also so relatable to me. I'm also on my SSRI rn, and I too experience some of the symptom mentioned here when I'm abruptly discontinuing my meds a month ago (I'm more experiencing mood changes and brain fog). Right now I'm back on my meds, but the fact that this can turn into as far as a suicide is... so saddening to me. I hope two of the people died mentioned in the studies rests in peace right now.
If you're experiencing PAWS right now. I'm so sorry for your condition. I can help to make a strategy to at least try to combat them, but please keep in touch with a professional regarding this. I learned that PAWS can be a serious threat for everyone post-recovery, and the treatment must be personalized to make sure they worked. Thank you for introducing me to this topic. If you have any question more about this, feel free to ask here.
How would you rate the following concoction as a method of ctb in terms of reliability, speed, & peacefulness?
300 mg Oxycodone
18 g Tapentadol
14.5 g Carisoprodol
29 mg Alprazolam
9 g Amitriptyline
1 cup grapefruit juice (potentiator)
45-60 mins prior:
Metoclopramide 30 mg - 3 pills
Ondansetron 8 mg - 2 pills
300 mg Oxycodone
18 g Tapentadol
14.5 g Carisoprodol
29 mg Alprazolam
9 g Amitriptyline
1 cup grapefruit juice (potentiator)
45-60 mins prior:
Metoclopramide 30 mg - 3 pills
Ondansetron 8 mg - 2 pills
Similar threads
- MatiSendiri
- Suicide Discussion
Suicide Discussion
Praestat_Mori
Discussion
if you can choose your next life ...
- secretghost
- Suicide Discussion 2
Suicide Discussion
Spite
