Totally New Protocols For SN From Nitschke in Sept update

[TydalWave]

Regarding the removal of propanolol, Dr Nitschke may have been influenced by the replacement of propanolol by amitriptyline in the American Clinicians' Academy on Medical Aid in Dying's (ACAMAID) 4-drug lethal mixture.

The data compiled by the ACAMAID in December 2019 suggest that amitriptyline leads to a quicker death: 90% of patients died under 4 hours (average 1.1 h, max 4.4 h) as opposed to 81% with propanolol (average 1.3 h, max 5.1 h).

Consistent with this, Dr Nitschke explains that tachycardia may lead to a faster death "presumably because of cardiac arrest", similarly to the ACAMAID ("Propanolol from D-DMP2 was switched to amitriptyline from D-DMA because: In aid in dying, tachyarrhythmias are more quickly lethal than bradyarrhythmias").

In August 2020, Dr Lonny Shavelson of the ACAMAID recommended retiring DDMP2 altogether in favor of DDMA.

I have seen this article cited on a few posts now, and I don't understand how these conclusions from this case study are being directly applied to SN. This involves a completely different lethal agent (digoxin) which has a different effect on the body from what I understand.

When ingested at high doses digoxin toxicity causes irregularly heart beat with the most common cause of death being by cardiac arrythmia (National Library of Medicine). By definition, this is when the heart beats too fast (tachyardia) or too slow (bradychardia). So the use of propranolol will clearly have a direct impact on the speed of this process.

I just don't see how the same conclusion can be directly applied to sodium nitrite poisoning. Sodium nitrite reacts with blood to create methemoglobin, which deprives your body of oxygen as concentrations increase in your bloodstream. The hearts job is to pump blood and oxygen, so tachyardia is a natural reaction to a lack of oxygen. High doses of propranolol would then combat your bodies natural defense mechanism to this and potentially accelerate the deprivation of oxygen.

I am not advising anyone either way. I just think if you are going to cite conclusions from a case study for a completely different drug, you should atleast prefice it as your opinion and explain why it is relevant to SN. Personally, I am still planning on using propranolol in my exit plan. I'm happy to share more of my reasoning over PM if anyone out there is stuck in the same boat as me.

Digitalis Toxicity - StatPearls - NCBI Bookshelf

www.ncbi.nlm.nih.gov

https://www.health.state.mn.us/communities/environment/water/docs/contaminants/nitratmethemog.pdf

 

[well2hell]

I have seen this article cited on a few posts now, and I don't understand how these conclusions from this case study are being directly applied to SN. This involves a completely different lethal agent (digoxin) which has a different effect on the body from what I understand.

When ingested at high doses digoxin toxicity causes irregularly heart beat with the most common cause of death being by cardiac arrythmia (National Library of Medicine). By definition, this is when the heart beats too fast (tachyardia) or too slow (bradychardia). So the use of propranolol will clearly have a direct impact on the speed of this process.

I just don't see how the same conclusion can be directly applied to sodium nitrite poisoning. Sodium nitrite reacts with blood to create methemoglobin, which deprives your body of oxygen as concentrations increase in your bloodstream. The hearts job is to pump blood and oxygen, so tachyardia is a natural reaction to a lack of oxygen. High doses of propranolol would then combat your bodies natural defense mechanism to this and potentially accelerate the deprivation of oxygen.

I am not advising anyone either way. I just think if you are going to cite conclusions from a case study for a completely different drug, you should atleast prefice it as your opinion and explain why it is relevant to SN. Personally, I am still planning on using propranolol in my exit plan. I'm happy to share more of my reasoning over PM if anyone out there is stuck in the same boat as me.

Digitalis Toxicity - StatPearls - NCBI Bookshelf

www.ncbi.nlm.nih.gov

https://www.health.state.mn.us/communities/environment/water/docs/contaminants/nitratmethemog.pdf

The ACAMAID's reasoning is detailed in their paper (bolding mine):

The reason for most of the longer deaths with D-DMP2 is that the myocardium tolerates bradycardias caused by the dig[oxin]/propranolol (we use small EKG rhythm monitors with our patients, so we see the pharmacologic effects on the myocardium). We then took out propranolol and added amitriptyline, to formulate D-DMA (amitriptyline induces tachyarrhythmias and impairs cardiac contractility, as well as causing profound hypotension). And the results are again impressive: See D-DMP2 vs. D-DMA on the graph.Our times to death again dropped significantly by using D-DMA, now with 90% of deaths occurring in <2 hours. D- DMA is both faster and more reliable than D-DMP2, and markedly better than DDMP2.
In summary: D-DMP2 improves DDMP2 by 33%. D-DMA improves D-DMP2 by another 33%. Compare D-DMA with DDMP2: It's 69% better—a very significant difference.

Their study was controlled, in the sense that the fourth drug of the lethal mixture was the only variable (i.e. amitriptyline vs propanolol; the rest of the regimen did not change, and in particular both groups received digoxin). As in this study, taking a large dose of propanolol with SN leads to bradycardia. Then, the effects of amitriptyline are in part similar to SN: both lead to profound hypotension and consequently tachycardia, since SN causes the mass formation of nitric oxide, a potent vasodilator. These three reasons are why extrapolating from this paper to SN is viable.

Edit: also note that both the lethal drug mixture and SN work by causing hypoxia, albeit by different mechanisms (ischemic vs hypemic hypoxia, respectively). It makes sense that tachycardia accelerates death — not only does it lead to cardiac arrest, but it also helps sodium nitrite be absorbed from the gut faster and this speeds up methemoglobinemia (i.e. depriving the blood from oxygen) in turn.

 

[TydalWave]

The ACAMAID's reasoning is detailed in their paper (bolding mine):


Their study was controlled, in the sense that the fourth drug of the lethal mixture was the only variable (i.e. amitriptyline vs propanolol; the rest of the regimen did not change, and in particular both groups received digoxin). As in this study, taking a large dose of propanolol with SN can lead to bradycardia. Then, the effects of amitriptyline are in part similar to SN: both lead to profound hypotension and consequently tachycardia, since SN causes the mass formation of nitric oxide, a potent vasodilator. These three reasons are why extrapolating from this paper to SN is viable.

The role of amitriptyline in this case study is entirely different than SN so I don't see how their similarity is relevant. The lethal agent in this study is the digoxin and digoxin toxicity is no the same as sodium nitrite poisoning. They react entirely differently.

Tachyardia is not the driving force in death from SN; atleast not for those who have been following the PPH through the April 2022 release. We know this because of the vast number of people who have followed these guidelines and included propranolol in their exit plan. The latest update to the PPeH essentials does opt for a high dose of benzos in lieue of propranolol. But the purpose of these are to "shorten the time to conciousness loss". Assuming one will be unconscious by the time tachyardia spikes, reducing this side effect is not necessary.

 

[well2hell]

The role of amitriptyline in this case study is entirely different than SN so I don't see how their similarity is relevant. The lethal agent in this study is the digoxin and digoxin toxicity is no the same as sodium nitrite poisoning. They react entirely differently.

Tachyardia is not the driving force in death from SN; atleast not for those who have been following the PPH through the April 2022 release. We know this because of the vast number of people who have followed these guidelines and included propranolol in their exit plan. The latest update to the PPeH essentials does opt for a high dose of benzos in lieue of propranolol. But the purpose of these are to "shorten the time to conciousness loss". Assuming one will be unconscious by the time tachyardia spikes, reducing this side effect is not necessary.

The point of the study is that tachycardia is preferable to bradycardia caused by propanolol because it leads to a quicker death. Tachycardia is not the driving force of SN poisoning, indeed, but this shows that it is helpful and so it shouldn't be suppressed.

As for benzodiazepines, tachycardia should kick in before unconsciousness because the latter only happens when the methemoglobomin blood level is above 50% (compared to <1% in normal circumstances):

Symptoms and signs of slightly elevated methemoglobinemia are non-specific. Patients are usually asymptomatic when MetHb is less than 20%, in the absence of co-existing cardiovascular or pulmonary conditions. Cyanosis can be detected when the MetHb is between 10% and 20%. Blood becomes chocolate brown at about 15–20% [11]. This feature can be detected in the clinical setting before the skin and nails change color. Symptoms of hypoxia begin at levels of about 35%. Patients experience fatigue and muscle weakness. Myoglobin is a muscle protein that contains one heme subunit. This single subunit is able to bind one oxygen molecule. The myoglobin contained in muscle can be oxidized like Hb in the presence of nitrites, leaving the molecule less able to bind oxygen. Consequentially, muscle hypoxia ensues and patients may feel weak, lethargic, and crampy.

At increasing metHgb levels, patients experience the effects of low oxygen tension: fatigue, tachypnea, dyspnea, tachycardia, altered mental status, nausea, and vomiting. For case #1, the presence of heartburn medications the home and in close proximity to her body may indicate that she was experiencing some of the gastrointestinal symptoms for a period of time before dying or took some before she took the sodium nitrite to avoid vomiting. Above 50%, patients develop severe symptoms of tissue hypoxia including cardiac arrhythmia, seizures and coma (a). Literature reports suggest that levels above about 50% can be fatal and levels over 70% are generally expected to be so, [1] with some potential variability [5]. Some patients with levels of greater than 94% have survived [1].

https://onlinelibrary.wiley.com/doi/10.1111/1556-4029.14689

They could be helpful to fall asleep and avoid tachycardia, but I am also concerned that taking one might slow down the absorption of SN because of the extra water. The ACAMAID showed that when drunk with 60mL water as opposed to 120mL, the average time to death with their lethal drug mixture is cut by half — that may apply to SN too. https://www.acamaid.org/wp-content/uploads/2022/10/DDMAPh-Update-10-11-22.pdf

One could mix the SN and the benzodiazepine in the same glass of water but that could reduce the solubility, and thus absorption, of SN. In my view, the most sensible approach may be that which Stan recommended — taking a normal dose of benzodiazepine ahead of time, so that 1) it has kicked in by the time SN is ingested, 2) it prevents anxiety and SI from tachycardia and 3) it doesn't interfere with the absorption of SN.

EDIT: benzodiazepines can also prevent seizures from methemoglobinemia, so that may be an argument in favor of taking a large dose along with SN.

 

[TydalWave]

They could be helpful to fall asleep and avoid tachycardia, but I am also concerned that taking one might slow down the absorption of SN because of the extra water. The ACAMAID showed that when drunk with 60mL water as opposed to 120mL, the average time to death with their lethal drug mixture is cut by half — that may apply to SN too. https://www.acamaid.org/wp-content/uploads/2022/10/DDMAPh-Update-10-11-22.pdf

One could mix the SN and the benzodiazepine in the same glass of water but that could reduce the solubility, and thus absorption, of SN. In my view, the most sensible approach may be that which Stan recommended — taking a normal dose of benzodiazepine ahead of time, so that 1) it has kicked in by the time SN is ingested, 2) it prevents anxiety and SI from tachycardia and 3) it doesn't interfere with the absorption of SN.

I was looking into that too since a key takeaway from the study was taking the digoxin 30 minutes earlier to increase absorption. I was curious if the order of operations so to speak with sodium nitrite, benzos, betas could play a similar role...

One key difference though I think is that SN is absorbed at a much higher rate than the lethal drug mixture they used. The oral bioavailability of digoxin is 70-80% whereas sodium nitrite is 98%. I am not sure if there is a direct correlation between absorption rate and how likely a drugs absorption can be interfered by the absorption of other substances, but I would lean to think that SN would be less likely to be stunted in the same way digoxin was.

 

[well2hell]

I was looking into that too since a key takeaway from the study was taking the digoxin 30 minutes earlier to increase absorption. I was curious if the order of operations so to speak with sodium nitrite, benzos, betas could play a similar role...

One key difference though I think is that SN is absorbed at a much higher rate than the lethal drug mixture they used. The oral bioavailability of digoxin is 70-80% whereas sodium nitrite is 98%. I am not sure if there is a direct correlation between absorption rate and how likely a drugs absorption can be interfered by the absorption of other substances, but I would lean to think that SN would be less likely to be stunted in the same way digoxin was.

It is an interesting question that merits further investigation but unfortunately we have no way of collecting data on CTB by SN (though in the PPeH, Exit International invite people to have their CTB recorded and sent to them).

A word of caution, though; the oral bioavailability of a drug is the amount that ends up in the blood after first and second-pass metabolism, not how much is absorbed from the small intestine.

Looking at the ACAMAID's paper, they say the small quantity of digoxin (100mg) was getting "lost" among the rest of the lethal mixture (24g for DMA) and as such it wasn't being well absorbed. That may also be the case for any drug taken along SN since it will be in small quantity compared to the dose of SN (25-35g). For example, it could be that 400mg propanolol or 1g diazepam with SN is absorbed as absorbed as digoxin with the other drugs in the lethal mixture. Who knows.

Though a noteworthy point is that 5g phenobarbital accelerates the time to death per the ACAMAID's data, but they propose that is because 1) it can be absorbed directly from the stomach rather than the small intestine (at least in part), 2) it strongly potentiates respiratory depression:

Phenobarbital is a barbiturate that can be transported across the gastric mucosa13 14 15, making it the only drug in the current aid-in-dying regimens that can be partially absorbed before reaching the small intestine. 16 17 18 19 20 This might be helpful in patients with delayed gastric emptying (gastroparesis), which is present in many of our dying patients.
Upon reaching the brain, phenobarbital binds with the GABA receptors and affects them differently than benzodiazepines or opiates, 21 Thus, the addition of phenobarbital to the morphine and diazepam of D-DMA/DDMA can augment the sedative and respiratory suppression effects of those protocols.

https://www.acamaid.org/wp-content/uploads/2021/12/1-12-21-Adding-phenobarbital-to-DDMA-protocols.pdf

So perhaps the solution to avoiding any unpleasant effect from SN is phenobarbital (since it will put one to sleep quickly) +/- a benzodiazepine. Plus it prevents seizures from SN. It is more difficult to acquire, though.

 

[TydalWave]

It is an interesting question that merits further investigation but unfortunately we have no way of collecting data on CTB by SN (though in the PPeH, Exit International invite people to have their CTB recorded and sent to them).

A word of caution, though; the oral bioavailability of a drug is the amount that ends up in the blood after first and second-pass metabolism, not how much is absorbed from the small intestine.

Looking at the ACAMAID's paper, they say the small quantity of digoxin (100mg) was getting "lost" among the rest of the lethal mixture (24g for DMA) and as such it wasn't being well absorbed. That may also be the case for any drug taken along SN since it will be in small quantity compared to the dose of SN (25-35g). For example, it could be that 400mg propanolol or 1g diazepam with SN is absorbed as absorbed as digoxin with the other drugs in the lethal mixture. Who knows.

Though a noteworthy point is that 5g phenobarbital accelerates the time to death per the ACAMAID's data, but they propose that is because 1) it can be absorbed directly from the stomach rather than the small intestine (at least in part), 2) it strongly potentiates respiratory depression:

https://www.acamaid.org/wp-content/uploads/2021/12/1-12-21-Adding-phenobarbital-to-DDMA-protocols.pdf

So perhaps the solution to avoiding any unpleasant effect from SN is phenobarbital (since it will put one to sleep quickly) +/- a benzodiazepine. Plus it prevents seizures from SN. It is more difficult to acquire, though.

That is interesting.... The PPH originally advised propranolol to be taken at the same time as SN too which I always found odd... I know a number of users have opted to take it earlier in an effort to have the effects kick in by the time SN is absorbed; however, it sounds taking this before would also greatly increase the rate of absorption for the propranolol--so I would assume less would need to be taken to get the same effects.

Wish we had more hard data on this. It is a damn shame that society makes us do this in hiding--because with how many people have followed these methods with their own twists on the ratio's and timing, we could have the largest case study on this and understand it so much better.

 

[silentdude122]

Are you supposed to take 20 tablets of 30 mg Oxazepam?? Did I read that correctly

 

[Himalayan]

This guy don't even research his shit. Why do we trust him

 

[Himalayan]

Desperation. There are little ZERO doctors or medical professionals on this site but all the blind leading the blind randomly answering people's questions with such certainty.

Doctors aren't too sure either. There's no suicidology.
Also, what kill one. Doesnt kill the other, bro. I will have to start facing the slave wage reality, because it doesn't seem like suicide is coming at all

 

[BipolarExpress]

Doctors aren't too sure either. There's no suicidology.
Also, what kill one. Doesnt kill the other, bro. I will have to start facing the slave wage reality, because it doesn't seem like suicide is coming at all

There is a field called suicidology, but it's research on causes and prevention, rather than suicide methods.

 

[littlelady774]

PN is getting pretty old.. maybe he's going senile

 

[Obliviate]

From these pics it looks like the new ppeh may be from September

 

[NotADrill]

God I wish these methods would stop changing every 15mins. Ultimately, I guess large amounts of SN would kill you regardless but the conflicting reports on how to make it less traumatic are so confusing.
If Oxazepam or Diazepam are the new orders of the day in that quantity; Does anyone know of a good source to get them in the UK? I got Diazepam delivered yesterday but after taking one 5mg tab last night, I'm doubting their validity. I'm going to try and get my GP to prescribe me Diazepam next week but they're quite conservative about that sort of thing.

 

[cherry7]

I'm sticking with Stan. I'm done listening to nitz.

Why's that?

 

[cherry7]

I know the PPH is considered pretty definitive, but does it bother anyone else the frequency and severity of typos in there? Maybe it's my professional background but it's hard to take something so important seriously when there are glaring errors like "during the weight time"...

I noticed that too

 

[diyCTB]

Hold on...

"Drugs such as oxazepam (20x30mg tablets), Valium (Diazepam, 50x10mg)
and the off-licence, bromazolam (10mg), can lessen anxiety and signifcantly
shorten the time to consciousness loss."

I heard if someone did not take Xanax/Alprazolam can pass out from 4mg (4000 micrograms) soon. 250 (0.25) micrograms of Alprazolam is approximately equivalent to Diazepam 5mg. And Oxazepam 10mg is approximately equivalent to Diazepam 5mg. Source: https://www.sps.nhs.uk/articles/choosing-an-equivalent-dose-of-oral-benzodiazepine/

Here they are talking about taking 100x10mg tablets of Oxazepam that would equate 50x10mg Diazepam. That would also be 250 (0.25) micrograms of Alprazolam 100 tablets. I am not in a normal cognitive state of mind to do the math properly but don't you think such benzo dose would be an overkill and it will be moments before you pass out and vomit? Blacking out first before experiencing the discomfort that comes with SN sounds like a more peaceful way to exit but if you vomit (which is likely to happen even with antiemetic) you won't be able to take another SN drink. I think the purpose of benzos is not to fall asleep quickly but to be calm enough to not panic.

 

[Tsunami]

It's crazy how much information and counter-information there is about SN. After 1 month of intensive and daily reading (PPH, all threads with the keyword SN and all "guides" proposed) I am just completely lost.