Ketamine Cures Depression By Reducing Serotonin, Increasing Dopamine

haidut

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As many of my readers know, FDA recently approved the party drug ketamine (known as Special-K on the street) as a rapidly-acting antidepressant. The rapid antidepressant effects of ketamine have been known since the 1960s but FDA denied that those effects are relevant in humans and refused to consider "scheduled" illicit drugs for therapeutic uses. Ketamine, together with ecstasy (MDMA), LSD, GHB, etc is a highly illegal drug and FDA/DEA ruthlessly enforce laws against the possession, distribution and sale of such drugs by the general public. However, the pharmaceutical industry has been growing increasingly desperate over the last two decades since many new studies came out demonstrating its blockbuster antidepressant drugs (most notably the SSRI class) are no better than placebo while at the same time turning patients into violent criminals. As a result of this desperation, pharma companies began lobbying FDA/DEA to ease restrictions on performing studies with those "evil" illicit drugs young people "ruin" their lives with and the results have been just spectacular. Ketamine was shown to rapidly cure depression in humans, LSD was shown to eliminate violent behavior and recidivism in felons, MDMA was shown to cure post-traumatic stress disorder (PTSD), GHB was shown to cure alcoholism, etc. So, Big Pharma managed to get the best of both worlds - on one hand it got all of these highly effective and relatively safe drugs banned for the general public, while on the other it is allowed to re-introduce these drugs in proprietary formulations for use in the general population at costs thousands of times higher than what they cost on the street. However, this is not the whole story. As it turns out, there may be another reason for the banning of these drugs that is now coming out. That reason is related to the proposed mechanism of antidepressant action for ketamine. Big Pharma and its regulatory accomplices have been trumpeting for decades that ketamine's antidepressant effects are manifested through antagonism of the NMDA receptor - i.e. that ketamine acts as glutamate antagonist. This mechanism is plausible since other NMDA antagonists, such as magnesium, are also rapidly acting antidepressants. However, the benefits of those NMDA antagonists still take at least 2-3 days to start manifesting, while ketamine works in hours and sometimes even in mere minutes after admnistration. That extremely rapid onset of action suggests that some other mechanism may be the primary route through which ketamine works. And now, the new study below materializes the worst nightmares of Big Pharma and its regulatory ilk. Namely, the study below demonstrates that ketamine produces its rapid and potent antidepressant effects by lowering serotonin and increasing dopamine. No wonder FDA/DEA want to ban all access to the drug - the inconvenient truth about serotonin is too profitable to allow to perish! As such, we now have at least one officially approved drug that unequivocally demonstrates what medicine and medical authorities have been concealing for decades - that serotonin is a CAUSE of depression and lowering its levels and/or raising the levels of its "antagonist" dopamine cures depression. I would not be surprised if that study below ends up being the straw that breaks the SSRI camel's back and unleashes a flurry of class-action lawsuits against the fraudulent serotonin industry and all people/companies/agencies that support and profit from it.

A randomized placebo-controlled PET study of ketamine´s effect on serotonin 1B receptor binding in patients with SSRI-resistant depression | Translational Psychiatry
New study shows how ketamine combats depression

"...The anaesthetic drug ketamine has been shown, in low doses, to have a rapid effect on difficult-to-treat depression. Researchers at Karolinska Institutet now report that they have identified a key target for the drug: specific serotonin receptors in the brain. Their findings, which are published in Translational Psychiatry, give hope of new, effective antidepressants. Depression is the most common psychiatric diagnosis in Sweden, affecting one in ten men and one in five women at some point during their lives. Between 15 and 30 per cent of patients are not helped by the first two attempts at therapy, in which case the depression is designated difficult to treat. Studies have shown that low doses of the anaesthetic drug ketamine are rapid acting on certain sufferers, but exactly how it works is unknown. A nasal spray containing ketamine has recently been approved in the USA and EU for patients with treatment-resistant depression."

"...Serotonin plays a key role in depression and low levels are thought to be linked to more serious disease. There are 14 different kinds of receptor for this neurotransmitter on the surface of neurons. For their PET imaging, the researchers used a radioactive marker that binds specifically to serotonin 1B receptors. They found that the ketamine operated via these receptors in a formerly unknown mechanism of action. Binding to this receptor reduces the release of serotonin but increases that of another neurotransmitter called dopamine. Dopamine is part of the brain's reward system and helps people to experience positive feelings about life, something that is often lacking in depression. "We show for the first time that ketamine treatment increases the number of serotonin 1B receptors," says the study's last author Johan Lundberg, research group leader at the Department of Clinical Neuroscience, Karolinska Institutet."
 

Mauritio

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Agmatine should be able to do the same, since it it targets the same suggested receptor. And to my knowledge it has fewer side effects.
 
Joined
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8,510
Agmatine should be able to do the same, since it it targets the same suggested receptor. And to my knowledge it has fewer side effects.

yes that is interesting.

The Clinical Antidepressant Effect of Exogenous Agmatine Is Not Reversed by Parachlorophenylalanine: A Pilot Study - PubMed

Objectives
To examine and record the clinical antidepressant effect of exogenous agmatine, an amino acid derived central glutamaergic modulator in endogenously depressed subjects. It was also the author's intention to examine the effects of parachlorophenylalanine (PCPA) in therapeutic responders to determine if serotonergic mechanisms mediate agmatine's antidepressant effect.

Methodology
Exogenous agmatine was ingested in doses of 2‐3mg/day by depressed subjects with Major Depresssive Disorder (MDD), clinically assessed using the 21 item Hamilton Rating Scale for Depression (HAM‐D), the Clinical Global Impression (CGI) and the Brief Psychiatric Rating Scale (BPRS). Antidepressant responders volunteered to concommittantly ingest parachlorophenylalanine (PCPA) at starting doses of 250mg/day, and increased until depressive relapse, mitigating side effects, or a maximum dosage of 1250mg/day.

Results
Three depressed subjects showing total illness remission with exogenous agmatine did not relapse after concomitantly adding PCPA. Effective in relieving both psychomotor agitation and retardation, the antidepressant effect was free of physical or behavioural side effects: gastrointestinal discomfort and loose stools in one subject resolved spontaneously within days. All three subjects refused to risk depressive relapse by temporarily stopping agmatine after PCPA was stopped.

Conclusion
The antidepressant effect of exogenous agmatine was documented in a small number of MDD subjects, and was not reversed/modified by PCPA confirming findings in animals that therapeutic response is not mediated by serotonergic mechanisms. A NAMDA (N‐methyl‐D‐aspartate) receptor antagonist, agmatine's recognized function in brain as inhibitory modulator of excitatory glutamatergic transmission suggests a pivotal role for brain glutamate, contributing to the ripening glutamatergic basis of depression, and a rational basis for future antidepressant pharmacotherapy.
 

orewashin

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Jun 16, 2020
Messages
327
Is Ketamine now covered by insurance companies, or do you have to pay out-of-pocket? If it's the latter, I'm guessing it's very expensive.
 

Atman

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Dec 10, 2016
Messages
294
So, Big Pharma managed to get the best of both worlds - on one hand it got all of these highly effective and relatively safe drugs banned for the general public, while on the other it is allowed to re-introduce these drugs in proprietary formulations for use in the general population at costs thousands of times higher than what they cost on the street.
How does that work? They can't patent it right? So generics from different companies should pop up eventually, pushing down the prices to production cost plus a small premium.
 

Frankdee20

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Ketamine is basically a cousin of PCP and eventually replaced PCP as a clinically used anesthetic in the 50’s.... Its basically a strong NMDA blocker... I’ve snorted it during my drug days, but it was meh...
 

orewashin

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Jun 16, 2020
Messages
327
Ketamine is basically a cousin of PCP and eventually replaced PCP as a clinically used anesthetic in the 50’s.... Its basically a strong NMDA blocker... I’ve snorted it during my drug days, but it was meh...
DXM in cough syrup is the weakest NMDA blocker, followed by Ketamine in the middle, and PCP being the strongest. I've never heard of anyone committing wild criminal acts on Ketamine before, unlike PCP.
 

Andman

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Aug 1, 2017
Messages
570
DXM in cough syrup is the weakest NMDA blocker, followed by Ketamine in the middle, and PCP being the strongest. I've never heard of anyone committing wild criminal acts on Ketamine before, unlike PCP.

yeah kinda hard to do nasty stuff when youre in the hole haha
 

Frankdee20

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Sun Coast, USA
DXM in cough syrup is the weakest NMDA blocker, followed by Ketamine in the middle, and PCP being the strongest. I've never heard of anyone committing wild criminal acts on Ketamine before, unlike PCP.

Yes, ketamine is milder, and not as notorious.... but those PCP stories could also be due to the fact that PCP is commonly smoked, not snorted, which makes it more intense, but also could’ve been smoked with crack cocaine .... who knows
 

Frankdee20

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I was looking at binding sites and affinities for PCP, in addition to NMDA, it appears to be a D2 agonist, also a DRI, but perhaps most significantly is the alpha 2 adrenal agonist quality... making users aggressive and violent.... Ketamine seems to block all muscarinic acetylcholine receptors, which could contribute to inability to move
 

Rick K

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Feb 18, 2019
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As many of my readers know, FDA recently approved the party drug ketamine (known as Special-K on the street) as a rapidly-acting antidepressant. The rapid antidepressant effects of ketamine have been known since the 1960s but FDA denied that those effects are relevant in humans and refused to consider "scheduled" illicit drugs for therapeutic uses. Ketamine, together with ecstasy (MDMA), LSD, GHB, etc is a highly illegal drug and FDA/DEA ruthlessly enforce laws against the possession, distribution and sale of such drugs by the general public. However, the pharmaceutical industry has been growing increasingly desperate over the last two decades since many new studies came out demonstrating its blockbuster antidepressant drugs (most notably the SSRI class) are no better than placebo while at the same time turning patients into violent criminals. As a result of this desperation, pharma companies began lobbying FDA/DEA to ease restrictions on performing studies with those "evil" illicit drugs young people "ruin" their lives with and the results have been just spectacular. Ketamine was shown to rapidly cure depression in humans, LSD was shown to eliminate violent behavior and recidivism in felons, MDMA was shown to cure post-traumatic stress disorder (PTSD), GHB was shown to cure alcoholism, etc. So, Big Pharma managed to get the best of both worlds - on one hand it got all of these highly effective and relatively safe drugs banned for the general public, while on the other it is allowed to re-introduce these drugs in proprietary formulations for use in the general population at costs thousands of times higher than what they cost on the street. However, this is not the whole story. As it turns out, there may be another reason for the banning of these drugs that is now coming out. That reason is related to the proposed mechanism of antidepressant action for ketamine. Big Pharma and its regulatory accomplices have been trumpeting for decades that ketamine's antidepressant effects are manifested through antagonism of the NMDA receptor - i.e. that ketamine acts as glutamate antagonist. This mechanism is plausible since other NMDA antagonists, such as magnesium, are also rapidly acting antidepressants. However, the benefits of those NMDA antagonists still take at least 2-3 days to start manifesting, while ketamine works in hours and sometimes even in mere minutes after admnistration. That extremely rapid onset of action suggests that some other mechanism may be the primary route through which ketamine works. And now, the new study below materializes the worst nightmares of Big Pharma and its regulatory ilk. Namely, the study below demonstrates that ketamine produces its rapid and potent antidepressant effects by lowering serotonin and increasing dopamine. No wonder FDA/DEA want to ban all access to the drug - the inconvenient truth about serotonin is too profitable to allow to perish! As such, we now have at least one officially approved drug that unequivocally demonstrates what medicine and medical authorities have been concealing for decades - that serotonin is a CAUSE of depression and lowering its levels and/or raising the levels of its "antagonist" dopamine cures depression. I would not be surprised if that study below ends up being the straw that breaks the SSRI camel's back and unleashes a flurry of class-action lawsuits against the fraudulent serotonin industry and all people/companies/agencies that support and profit from it.

A randomized placebo-controlled PET study of ketamine´s effect on serotonin 1B receptor binding in patients with SSRI-resistant depression | Translational Psychiatry
New study shows how ketamine combats depression

"...The anaesthetic drug ketamine has been shown, in low doses, to have a rapid effect on difficult-to-treat depression. Researchers at Karolinska Institutet now report that they have identified a key target for the drug: specific serotonin receptors in the brain. Their findings, which are published in Translational Psychiatry, give hope of new, effective antidepressants. Depression is the most common psychiatric diagnosis in Sweden, affecting one in ten men and one in five women at some point during their lives. Between 15 and 30 per cent of patients are not helped by the first two attempts at therapy, in which case the depression is designated difficult to treat. Studies have shown that low doses of the anaesthetic drug ketamine are rapid acting on certain sufferers, but exactly how it works is unknown. A nasal spray containing ketamine has recently been approved in the USA and EU for patients with treatment-resistant depression."

"...Serotonin plays a key role in depression and low levels are thought to be linked to more serious disease. There are 14 different kinds of receptor for this neurotransmitter on the surface of neurons. For their PET imaging, the researchers used a radioactive marker that binds specifically to serotonin 1B receptors. They found that the ketamine operated via these receptors in a formerly unknown mechanism of action. Binding to this receptor reduces the release of serotonin but increases that of another neurotransmitter called dopamine. Dopamine is part of the brain's reward system and helps people to experience positive feelings about life, something that is often lacking in depression. "We show for the first time that ketamine treatment increases the number of serotonin 1B receptors," says the study's last author Johan Lundberg, research group leader at the Department of Clinical Neuroscience, Karolinska Institutet."

Hello George. In the land of igloos and all things holy that are hockey, ketamine can be prescribed by doctors treating depression. If you pm me I will give you more relevant info on this as I am very familiar with someone who will switch from ssri's this week to ketamine and is suffering from severe depression among other things.
 

Shontelle

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Joined
Feb 10, 2016
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Hi
As many of my readers know, FDA recently approved the party drug ketamine (known as Special-K on the street) as a rapidly-acting antidepressant. The rapid antidepressant effects of ketamine have been known since the 1960s but FDA denied that those effects are relevant in humans and refused to consider "scheduled" illicit drugs for therapeutic uses. Ketamine, together with ecstasy (MDMA), LSD, GHB, etc is a highly illegal drug and FDA/DEA ruthlessly enforce laws against the possession, distribution and sale of such drugs by the general public. However, the pharmaceutical industry has been growing increasingly desperate over the last two decades since many new studies came out demonstrating its blockbuster antidepressant drugs (most notably the SSRI class) are no better than placebo while at the same time turning patients into violent criminals. As a result of this desperation, pharma companies began lobbying FDA/DEA to ease restrictions on performing studies with those "evil" illicit drugs young people "ruin" their lives with and the results have been just spectacular. Ketamine was shown to rapidly cure depression in humans, LSD was shown to eliminate violent behavior and recidivism in felons, MDMA was shown to cure post-traumatic stress disorder (PTSD), GHB was shown to cure alcoholism, etc. So, Big Pharma managed to get the best of both worlds - on one hand it got all of these highly effective and relatively safe drugs banned for the general public, while on the other it is allowed to re-introduce these drugs in proprietary formulations for use in the general population at costs thousands of times higher than what they cost on the street. However, this is not the whole story. As it turns out, there may be another reason for the banning of these drugs that is now coming out. That reason is related to the proposed mechanism of antidepressant action for ketamine. Big Pharma and its regulatory accomplices have been trumpeting for decades that ketamine's antidepressant effects are manifested through antagonism of the NMDA receptor - i.e. that ketamine acts as glutamate antagonist. This mechanism is plausible since other NMDA antagonists, such as magnesium, are also rapidly acting antidepressants. However, the benefits of those NMDA antagonists still take at least 2-3 days to start manifesting, while ketamine works in hours and sometimes even in mere minutes after admnistration. That extremely rapid onset of action suggests that some other mechanism may be the primary route through which ketamine works. And now, the new study below materializes the worst nightmares of Big Pharma and its regulatory ilk. Namely, the study below demonstrates that ketamine produces its rapid and potent antidepressant effects by lowering serotonin and increasing dopamine. No wonder FDA/DEA want to ban all access to the drug - the inconvenient truth about serotonin is too profitable to allow to perish! As such, we now have at least one officially approved drug that unequivocally demonstrates what medicine and medical authorities have been concealing for decades - that serotonin is a CAUSE of depression and lowering its levels and/or raising the levels of its "antagonist" dopamine cures depression. I would not be surprised if that study below ends up being the straw that breaks the SSRI camel's back and unleashes a flurry of class-action lawsuits against the fraudulent serotonin industry and all people/companies/agencies that support and profit from it.

A randomized placebo-controlled PET study of ketamine´s effect on serotonin 1B receptor binding in patients with SSRI-resistant depression | Translational Psychiatry
New study shows how ketamine combats depression

"...The anaesthetic drug ketamine has been shown, in low doses, to have a rapid effect on difficult-to-treat depression. Researchers at Karolinska Institutet now report that they have identified a key target for the drug: specific serotonin receptors in the brain. Their findings, which are published in Translational Psychiatry, give hope of new, effective antidepressants. Depression is the most common psychiatric diagnosis in Sweden, affecting one in ten men and one in five women at some point during their lives. Between 15 and 30 per cent of patients are not helped by the first two attempts at therapy, in which case the depression is designated difficult to treat. Studies have shown that low doses of the anaesthetic drug ketamine are rapid acting on certain sufferers, but exactly how it works is unknown. A nasal spray containing ketamine has recently been approved in the USA and EU for patients with treatment-resistant depression."

"...Serotonin plays a key role in depression and low levels are thought to be linked to more serious disease. There are 14 different kinds of receptor for this neurotransmitter on the surface of neurons. For their PET imaging, the researchers used a radioactive marker that binds specifically to serotonin 1B receptors. They found that the ketamine operated via these receptors in a formerly unknown mechanism of action. Binding to this receptor reduces the release of serotonin but increases that of another neurotransmitter called dopamine. Dopamine is part of the brain's reward system and helps people to experience positive feelings about life, something that is often lacking in depression. "We show for the first time that ketamine treatment increases the number of serotonin 1B receptors," says the study's last author Johan Lundberg, research group leader at the Department of Clinical Neuroscience, Karolinska Institutet."
Hi!
It’s shontelle (Ornella’s daughter) my gf is a doctor and she admitted that ketamine is now being microdosed with her peers :)
What do you think of GHB ?
 

sladerunner69

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May 24, 2013
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28
Location
Los Angeles
As many of my readers know, FDA recently approved the party drug ketamine (known as Special-K on the street) as a rapidly-acting antidepressant. The rapid antidepressant effects of ketamine have been known since the 1960s but FDA denied that those effects are relevant in humans and refused to consider "scheduled" illicit drugs for therapeutic uses. Ketamine, together with ecstasy (MDMA), LSD, GHB, etc is a highly illegal drug and FDA/DEA ruthlessly enforce laws against the possession, distribution and sale of such drugs by the general public. However, the pharmaceutical industry has been growing increasingly desperate over the last two decades since many new studies came out demonstrating its blockbuster antidepressant drugs (most notably the SSRI class) are no better than placebo while at the same time turning patients into violent criminals. As a result of this desperation, pharma companies began lobbying FDA/DEA to ease restrictions on performing studies with those "evil" illicit drugs young people "ruin" their lives with and the results have been just spectacular. Ketamine was shown to rapidly cure depression in humans, LSD was shown to eliminate violent behavior and recidivism in felons, MDMA was shown to cure post-traumatic stress disorder (PTSD), GHB was shown to cure alcoholism, etc. So, Big Pharma managed to get the best of both worlds - on one hand it got all of these highly effective and relatively safe drugs banned for the general public, while on the other it is allowed to re-introduce these drugs in proprietary formulations for use in the general population at costs thousands of times higher than what they cost on the street. However, this is not the whole story. As it turns out, there may be another reason for the banning of these drugs that is now coming out. That reason is related to the proposed mechanism of antidepressant action for ketamine. Big Pharma and its regulatory accomplices have been trumpeting for decades that ketamine's antidepressant effects are manifested through antagonism of the NMDA receptor - i.e. that ketamine acts as glutamate antagonist. This mechanism is plausible since other NMDA antagonists, such as magnesium, are also rapidly acting antidepressants. However, the benefits of those NMDA antagonists still take at least 2-3 days to start manifesting, while ketamine works in hours and sometimes even in mere minutes after admnistration. That extremely rapid onset of action suggests that some other mechanism may be the primary route through which ketamine works. And now, the new study below materializes the worst nightmares of Big Pharma and its regulatory ilk. Namely, the study below demonstrates that ketamine produces its rapid and potent antidepressant effects by lowering serotonin and increasing dopamine. No wonder FDA/DEA want to ban all access to the drug - the inconvenient truth about serotonin is too profitable to allow to perish! As such, we now have at least one officially approved drug that unequivocally demonstrates what medicine and medical authorities have been concealing for decades - that serotonin is a CAUSE of depression and lowering its levels and/or raising the levels of its "antagonist" dopamine cures depression. I would not be surprised if that study below ends up being the straw that breaks the SSRI camel's back and unleashes a flurry of class-action lawsuits against the fraudulent serotonin industry and all people/companies/agencies that support and profit from it.

A randomized placebo-controlled PET study of ketamine´s effect on serotonin 1B receptor binding in patients with SSRI-resistant depression | Translational Psychiatry
New study shows how ketamine combats depression

"...The anaesthetic drug ketamine has been shown, in low doses, to have a rapid effect on difficult-to-treat depression. Researchers at Karolinska Institutet now report that they have identified a key target for the drug: specific serotonin receptors in the brain. Their findings, which are published in Translational Psychiatry, give hope of new, effective antidepressants. Depression is the most common psychiatric diagnosis in Sweden, affecting one in ten men and one in five women at some point during their lives. Between 15 and 30 per cent of patients are not helped by the first two attempts at therapy, in which case the depression is designated difficult to treat. Studies have shown that low doses of the anaesthetic drug ketamine are rapid acting on certain sufferers, but exactly how it works is unknown. A nasal spray containing ketamine has recently been approved in the USA and EU for patients with treatment-resistant depression."

"...Serotonin plays a key role in depression and low levels are thought to be linked to more serious disease. There are 14 different kinds of receptor for this neurotransmitter on the surface of neurons. For their PET imaging, the researchers used a radioactive marker that binds specifically to serotonin 1B receptors. They found that the ketamine operated via these receptors in a formerly unknown mechanism of action. Binding to this receptor reduces the release of serotonin but increases that of another neurotransmitter called dopamine. Dopamine is part of the brain's reward system and helps people to experience positive feelings about life, something that is often lacking in depression. "We show for the first time that ketamine treatment increases the number of serotonin 1B receptors," says the study's last author Johan Lundberg, research group leader at the Department of Clinical Neuroscience, Karolinska Institutet."

I am wondering if ketamine would be worth a try for us PFS sufferers. GHB has seemed to help a lot of us through re-activating the GABA system. It is difficult to obtain though, and not legal. Would you think ketamine could have some potential in this regard?
 

James b

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Joined
May 10, 2018
Messages
1,141
I am wondering if ketamine would be worth a try for us PFS sufferers. GHB has seemed to help a lot of us through re-activating the GABA system. It is difficult to obtain though, and not legal. Would you think ketamine could have some potential in this regard?

I know it’s probably not an exact science, but could you help share some info on suggested dosage and duration for reactivating the GABA system with GHB?
 
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