Help SN and Olanzapine Protocol

[ghoulcat]

Hey all.

This is my first post here, possibly my last, as I'm determined to CTB. I'm 30, paranoid, dumb as a doorknob, have nervous breakdowns on the regular, terrible social skills, feel inadequate wherever I am, have no reputation to protect, no love life, no money, no willingness to work... but I digress. I've purchased SN and have also acquired a prescription for Olanzapine. I plan to use these drugs as a poison and as an antiemetic respectively. I have also read that BZDs help a great deal with anxiety and make it so you pass out faster. I've read the PPH, so I know how much SN to take, but I'm wondering:

• How much Olanzapine would I need to take to make sure that I wouldn't throw the SN solution up?
• How long after taking Olanzapine should I take SN?
• Having access to Olanzapine, are anxiolytics even needed? Could I pass out from an Olanzapine overdose?
• Are there any OTC anxiolytics that could work as a substitute for BZDs?

Hopefully I'm not breaking any rules here, but if you know how to get BZDs on the Clear Web in Europe, please give me a hint on how I could get them. I'll try to get an anxiolytic prescription tomorrow, but I'm afraid the doctor might refuse to give me one knowing that I'm suicidal: I've recently went to the hospital, opened up about my suicidal thoughts and they had a psychiatrist see me, that's where the Olanzapine prescription comes from. I imagine that's something the doctor might have a record of, so I'm not positive I can get an anxiolytic prescription.

Any help is greatly appreciated.

 

[penguinl0v3s]

Hey there,

How much Olanzapine would I need to take to make sure that I wouldn't throw the SN solution up?

The important receptors to inhibit are 5-HT3, D2, H1 and H2 receptors. Especially D2, which is why metoclopramide is so effective. If you look at the receptor profile of metoclopramide, it is so effective because it is a strong D2 antagonist, as well as a 5HT3 antagonist. What is important for measuring its efficacy is the inhibition constant (Ki) and the smaller the Ki, the more effective it is at binding to the intended site.

Metoclopramide's Ki is 28.8 nM, which is a high affinity. Its affinity for 5HT3 is low in comparison, and antiemetic effects of serotonin only exist on higher doses--but serotonin antagonism isn't as important here, though it is good to have because serotonin antagonism does affect the vomiting centre, which can get triggered by the chemoreceptor trigger zone (CRTZ) that SN in blood will active.

Compare that to Olanzapine, which primarily blocks 5HT2A, D1, and then D2 as a secondary. It has a 5HT2A Ki of 1.32–24.2 and D2 Ki of 3.00–106 nM. I have no idea why the range is this big? It was sourced from Wikipedia, so my guess is just that studies varied in results. Given how big this range is, you would probably have to take a 1:1 ratio or 3.6x as much as the meto dosage, at worst. On the bright side, olanzapine is known to have far fewer side effects than metoclopramide, so it's probably safe.

How long after taking Olanzapine should I take SN?

6 hours. Peak olanzapine concentration is 6 hours after dosing. Source here.

Having access to Olanzapine, are anxiolytics even needed? Could I pass out from an Olanzapine overdose?

I'm not sure what your question is. Anti-anxiety meds were never necessary for the SN method. They are optional. There is no point in trying to overdose on psychiatric medications, as (almost-- see bupropion) all of them have low toxicity. Given that the people who take them are prone to being suicidal.

Are there any OTC anxiolytics that could work as a substitute for BZDs?

They are better than nothing, but benzodiazepines are the strongest by far.

I'll try to get an anxiolytic prescription tomorrow, but I'm afraid the doctor might refuse to give me one knowing that I'm suicidal: I've recently went to the hospital, opened up about my suicidal thoughts and they had a psychiatrist see me, that's where the Olanzapine prescription comes from. I imagine that's something the doctor might have a record of, so I'm not positive I can get an anxiolytic prescription.

Your doctor is going to be willing to prescribe you an anxiolytic 99%. Depressed people often have comorbidity anxiety, so it's not weird. Benzos also have 0 overdose potential by the way. But they're only good for short term anxiety, so if you have a short term problem like anxiety from adjusting to olanzapine, that's what doc would be more open to giving you benzos for.

 

[h.s.p.]

The important receptors to inhibit are 5-HT3, D2, H1 and H2 receptors. Especially D2, which is why metoclopramide is so effective. If you look at the receptor profile of metoclopramide, it is so effective because it is a strong D2 antagonist, as well as a 5HT3 antagonist. What is important for measuring its efficacy is the inhibition constant (Ki) and the smaller the Ki, the more effective it is at binding to the intended site.

Metoclopramide's Ki is 28.8 nM, which is a high affinity. Its affinity for 5HT3 is low in comparison, and antiemetic effects of serotonin only exist on higher doses--but serotonin antagonism isn't as important here, though it is good to have because serotonin antagonism does affect the vomiting centre, which can get triggered by the chemoreceptor trigger zone (CRTZ) that SN in blood will active.

Compare that to Olanzapine, which primarily blocks 5HT2A, D1, and then D2 as a secondary. It has a 5HT2A Ki of 1.32–24.2 and D2 Ki of 3.00–106 nM. I have no idea why the range is this big? It was sourced from Wikipedia, so my guess is just that studies varied in results. Given how big this range is, you would probably have to take a 1:1 ratio or 3.6x as much as the meto dosage, at worst. On the bright side, olanzapine is known to have far fewer side effects than metoclopramide, so it's probably safe.

Thank you for this information, this is very detailed. Where did you get all of this from? Seems far too detailed to belong to Wikipedia only

 

[penguinl0v3s]

Thank you for this information, this is very detailed. Where did you get all of this from? Seems far too detailed to belong to Wikipedia only

I'm a pharmacokinetics & toxicology enthusiast! Going to study medicine. I picked up a lot of random knowledge with hobbyist reading, so I used that to data gather the necessary info from the NIH library and Wikipedia.

 

[Endisclose]

6 hours. Peak olanzapine concentration is 6 hours after dosing. Source here.

I've heard Olanzapine can have a pretty strong sedatory effect. Wouldn't staying up that long cause a substantial amount of drowsiness by the time one takes SN? I'd be surprised if one is still awake .

I came across this video on youtube when I was researching about negative effects of meto.. Turns out olanzapine can have pretty much the same risks as meto as it belongs to the same class of drugs i. e., antipsychotics.

 

[h.s.p.]

I'm a pharmacokinetics & toxicology enthusiast! Going to study medicine. I picked up a lot of random knowledge with hobbyist reading, so I used that to data gather the necessary info from the NIH library and Wikipedia.

Thanks for the explanation. Would you have the time and will to answer a few questions in private, please?

 

[penguinl0v3s]

I came across this video on youtube when I was researching about negative effects of meto.. Turns out olanzapine can have pretty much the same risks as meto as it belongs to the same class of drugs i. e., antipsychotics.

All dopamine antagonists, specially D2 antagonists increase the risk of movement disorders. The D2 receptor is the antiemetic one. You can't decrease your risk much without decreasing antiemetic efficacy. Meto is the best one because it targets D2 very specifically without messing up your other dopamine receptors.

 

[Endisclose]

All dopamine antagonists, specially D2 antagonists increase the risk of movement disorders. The D2 receptor is the antiemetic one. You can't decrease your risk much without decreasing antiemetic efficacy. Meto is the best one because it targets D2 very specifically without messing up your other dopamine receptors.

I was thinking about olanzapine and domperidone combined together being a possibly effective and less riskier alternative to meto. I wonder if you think this would be viable. The prescribed dose for olanzapine for mania in bipolar disorder is 15 mg, while 20 mg is considered a high dose. As an antiemetic, the prescribed dose is from 5mg to 10 mg. 10mg may be more effective but may cause more drowsiness.

I wonder if the 36 or 48 hour regime of domperidone combined with 5mg or 10mg olanzapine taken 45 mins before SN might offer same efficacy and less risk than meto with olanzapine being a second generation Antipsychotic. Testing the Olanzapine out whichever dose one goes for would be a good idea to check for level of drowsiness anyway.

 

[penguinl0v3s]

I was thinking about olanzapine and domperidone combined together being a possibly effective and less riskier alternative to meto. I wonder if you think this would be viable. The prescribed dose for olanzapine for mania in bipolar disorder is 15 mg, while 20 mg is considered a high dose. As an antiemetic, the prescribed dose is from 5mg to 10 mg. 10mg may be more effective but may cause more drowsiness.

I wonder if the 36 or 48 hour regime of domperidone combined with 5mg or 10mg olanzapine taken 45 mins before SN might offer same efficacy and less risk than meto with olanzapine being a second generation Antipsychotic. Testing the Olanzapine out whichever dose one goes for would be a good idea to check for level of drowsiness anyway.

I do think it's viable, but why do you think it's less risky than meto? What does it being a second gen antipsychotic mean to you?

 

[Endisclose]

I do think it's viable, but why do you think it's less risky than meto? What does it being a second gen antipsychotic mean to you?

I read somewhere that second generation antipsychotics are less prone to cause EPS than first gen ones.. So I thought "less prone" meant less risky. I also saw in a video that EPS can occur with the first few doses of olanzapine with benadryl being mentioned as the antidote.. So much for being "less prone" I guess..

 

[penguinl0v3s]

I read somewhere that second generation antipsychotics are less prone to cause EPS than first gen ones.. So I thought "less prone" meant less risky. I also saw in a video that EPS can occur with the first few doses of olanzapine with benadryl being mentioned as the antidote.. So much for being "less prone" I guess..

That's because 1st gen targets D2 and 2nd gen targets both D2 and 5HT2. They are less prone to causing movement disorders when used for treatment of psychiatric disorders, because mood is affected by D2 and 5HT2. But antiemetic properties are solely reliant on the D2 receptor, so 2nd gen antipsychs aren't better for antiemetic effects. Just go with meto if possible, since it has the highest affinity to D2. Dosing your other receptors is making yourself more prone to side effects.

Yeah, you can develop TD acutely, no helping that. The tl;dr is that messing with your D2 receptors can cause movement disorders, but to get antivomitting effects you have to target D2 receptors… so it's an unavoidable risk. If you want an enhancement though, I'd get some prescription ondansetron, because it targets 5HT3 (not to be confused with 5HT2) and that can enhance D2's antiemetic effects.

I'll try to summarize the different receptors and what they do for clarity:

• D2 (Dopamine 2): dopamine receptor, is an antiemetic that targets the CRTZ, the part of the vomiting response that triggers from poisons. Also affects movement, so can cause TD acutely if affected
• Other dopamine receptors: don't seem to be very responsible for causing TD, if at all, but from what I can see the research says to try not to mess up your other dopamine receptors too much either
• 5HT1 or 5HT2 (serotonin 1 and 2): serotonin receptors that affect mood
• 5HT3 (serotonin 3): serotonin receptor that is part of the vomiting centre, it is connected to the CRTZ so it can enhance antiemetic effects of meto but can't directly prevent poison-induced vomiting

 

[Endisclose]

That's because 1st gen targets D2 and 2nd gen targets both D2 and 5HT2. They are less prone to causing movement disorders when used for treatment of psychiatric disorders, because mood is affected by D2 and 5HT2. But antiemetic properties are solely reliant on the D2 receptor, so 2nd gen antipsychs aren't better for antiemetic effects. Just go with meto if possible, since it has the highest affinity to D2. Dosing your other receptors is making yourself more prone to side effects.

Yeah, you can develop TD acutely, no helping that. The tl;dr is that messing with your D2 receptors can cause movement disorders, but to get antivomitting effects you have to target D2 receptors… so it's an unavoidable risk. If you want an enhancement though, I'd get some prescription ondansetron, because it targets 5HT3 (not to be confused with 5HT2) and that can enhance D2's antiemetic effects.

I'll try to summarize the different receptors and what they do for clarity:

• D2 (Dopamine 2): dopamine receptor, is an antiemetic that targets the CRTZ, the part of the vomiting response that triggers from poisons. Also affects movement, so can cause TD acutely if affected
• Other dopamine receptors: don't seem to be very responsible for causing TD, if at all, but from what I can see the research says to try not to mess up your other dopamine receptors too much either
• 5HT1 or 5HT2 (serotonin 1 and 2): serotonin receptors that affect mood
• 5HT3 (serotonin 3): serotonin receptor that is part of the vomiting centre, it is connected to the CRTZ so it can enhance antiemetic effects of meto but can't directly prevent poison-induced vomiting

Yeah my first choice is still meto. And guess I'd use 2nd gen antipsychotics only if I go for domperidone. Do you think there is a possibility of getting TD on a stat dose of meto? I thought it was only a long term risk more like if it's used over 12 weeks or 6 months.

I've been doing quite a bit of research on meto and I found that the TD, parkinsonism and depression were associated with chronic use. From the documented cases, I noticed that EPS like akathisia and dystonia usually happened from within a few hours of taking the first dose to within a 24 to 48 hour period. Usually they've been seen to occur after taking the second or third dose when taken orally.

First dose EPS reactions I've seen from meto were always through the IV or IM route and one case involved a child (children being a high risk group for meto).

I am also undecided on the question of testing the meto. As of the moment I am planning to just take a 10 mg dose to eliminate the risk of anaphylaxis which although rare is a risk nevertheless. If 10 mg test dose of meto causes any symptoms, imo it's better avoided. It may be a sign of high sensitivity which may cause bigger problems with a higher dose. Also if one has an allergy issue with meto taking a stat dose would be highly risky and there's no saying what reaction it might produce. I think that sort of nasty surprise is better avoided.

Also I asked chatgpt and it said that if there is no EPS upon taking a 30 mg dose of meto, there is no guarantee that one won't get EPS if one takes another 30 mg dose even if its a month later. I am therefore not sure if there is any value to testing the Stat dose beforehand and think it might be better to take it directly before ctb after testing just the 10 mg dose, provided there are no symptoms. Hopefully one is long gone by the time any EPS are supposed to manifest given they tend to occur only a few hours after taking it.

I've done some research on the meto question and would be grateful if you could go through the following thread and provide any inputs/corrections/opinions.

What are the negative effects from taking Meto before SN?

To follow up on this: Is it okay to take Adderall XR at the same time as the triple dose of 10 mg of Meto before SN 45minutes later?

sanctioned-suicide.net

Think your inputs would be more valuable to the community as you are qualified in this field compared to it coming from someone like me who is just a layman operating with logic. I hope I haven't got anything wrong that might mislead people.