5ht2Antogonist
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Is "SS" abbreviated to "Social Suicide" or am I wrong?
Leukoencephalopathy caused by NBOMe?
- Thread starter 5ht2Antogonist
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Is "SS" abbreviated to "Social Suicide" or am I wrong?
Angstknauel
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Could you please say, why do you think that you could have this rare disease?
Have you been to a doctor yet?
How much did you use?
Have you been to a doctor yet?
How much did you use?
PriestTheyCalledHim
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Please see a doctor and tell him/her how you took NBOMe, and about any other drugs you currently take, have taken in the past, or are prescribed and take, symptoms you are having, concerns, etc.
Good luck.
Good luck.
5ht2Antogonist
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Because, ever since I had that NBOMe experience, I kinda feel outta space. Like, living in another dimension or something. My eye sight got worse. Working memory used to be a lot worse too, but it's been 4 and half months now and can say it's slightly better. I can understand this as it WAS caused by possibly a neurotoxic chemical and I quote:
The symptoms of acute and chronic toxic encephalopathy do not resolve with cessation of exposure and can include memory loss, small personality changes/increased irritability, insidious onset of concentration difficulties, involuntary movements (parkinsonism), fatigue, seizures, arm strength problems, and depression.
Increased exposure time and increased concentration of the chemicals will worsen the effects of toxic encephalopathy, due to the associated structural CNS damage and direct functional impairment consequences.
Long term studies have demonstrated residual cognitive impairment (primarily attention and information-processing impairment resulting in dysfunction in working memory) up to 10 years following cessation of exposure.[5]
Sorry for the font change.Anyway Well yes, I know that I need a diagnosis so that's why I have an appointment from the Neurologist for the upcoming week.
Also,
"Toxic encephalopathy is just the medical word for the under recognized, under-diagnosed brain fog. This classic symptom is often erroneously chalked up to normal aging, stress, poor memory, or a bad personality. Many people do not know that there is a cause and a cure for brain fog or toxic encephalopathy. But unfortunately, many do not know that they even have it, for there is a silent epidemic of toxic encephalopathy.
What are the symptoms of brain fog? Dopey, dizzy, spacy, can't think clearly, "feel like there's a bag over my head," can't concentrate, poor memory, depressed for no reason, fatigue for no reason, or unexplained mood swings out of proportion to the trigger."
http://www.burningissues.org/car-www/medical_effects/toxic-brain.htm
As to your question about the dosage, It was probably below 500 ug. It didn't make me hallucinate, maybe it acted as antagonist? IDK.
In addition to these, I had to see ED that night when it happened. Rising temperature was just unbearable.
Lastly, I might be OCD ing right now.
5ht2Antogonist
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So.. the considerations for treatment of Leukoencephalopathy is
"The only known way to prevent drug-related encephalopathy is strict adherence to prescription guidelines for legal drugs and strict avoidance of illegal drugs of abuse."
^^That's hell of a designer drug disease here with no known ways to treat :D
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Serotonin syndrome I would imagine.
LucidSDreamr
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you say it was a single dose, how high was the dosage? How long has it been since you dosed
PriestTheyCalledHim
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Well, as someone else wrote earlier in this thread we're not medical professionals here. Google is not good at diagnosing Leukoencephalopathy, encephalopathy, or other medical issues like that, and you're not a medical professional either.
What you're describing with your memory issues, etc. can be caused by a number of things that are not related to you taking NBOME or any other drugs you use. It could be from anxiety and stress due to obsession/OCD that you posted about having.
It would not be a bad idea to avoid using all drugs until you see a doctor and figure out what's happening. Good luck.
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5ht2Antogonist
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Uhmm.. probably below 500 micrograms. The guy had said that he was giving me the half of the amount. I believe the dosage was around 250 ug -ish though, as it didn't make me trip at all (no OEV's CEV'S) I mean, hue effect on my vision and increased euphoria was present at the time. Then it all turned to a bad trip, felt like I wouldn't get out of it. And I remember I was so scared of "dying" , the idea of which, normally didn't scare me so much before.
So.. what could be the other substances that re sold on blotter papers? Like, maybe it wasn't an NBOMe at all.
Are there any other chemicals that make your tongue go numb?
Bromo DragonFly anyone?
Bigazznugz
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Lots of chems taste bitter and make you trip. I seriously doubt you had bromodragonfly, it's too rare and nbomes are more popular, but that's besides the point.
What do you want? Do you want medical help cuz if so you're in the wrong spot, seriously there is nothing we can do here, if you think something is wrong go to a doctor....
What do you want? Do you want medical help cuz if so you're in the wrong spot, seriously there is nothing we can do here, if you think something is wrong go to a doctor....
5ht2Antogonist
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A possible therapy method here maybe?
**Autophagy is the natural, regulated, destructive mechanism of the cell that disassembles unnecessary or dysfunctional components.
STUDY
Sporadic short-term fasting, driven by religious and spiritual beliefs, is common to many cultures and has been practiced for millennia, but scientific analyses of the consequences of caloric restriction are more recent. Published studies indicate that the brain is spared many of the effects of short-term food restriction, perhaps because it is a metabolically privileged site that, relative to other organs, is protected from the acute effects of nutrient deprivation, including autophagy.17 We show here that this is not the case: short-term food restriction induces a dramatic upregulation of autophagy in cortical and Purkinje neurons. To our knowledge, this is the first demonstration that food restriction leads to in vivo neuronal autophagy. Our data extend recent reports in tissue culture systems,18,20 and have implications for individuals who, by choice or necessity, have limited food intake. Our findings also may have therapeutic implications, as outlined below. Autophagy is sometimes referred to as cellular “cleansing”, and our observations provide an attractive neuronal parallel to the organismal benefits that, historically, are perceived to derive from fasting.
In this study we describe a novel technique to identify and characterize autophagosomes in the tissues of GFP-LC3 mice, using vibratome sections and confocal microscopy. The changes that we report using this method are confirmed using the standard technique of TEM; this both validates the new approach, and confirms the conclusions that we have drawn therefrom. Herein, we make at least three novel observations.
First, we identify and localize autophagosomes in cortical and Purkinje neurons of normal-fed mammals.
Second, we show that, in these CNS neurons, short-term food restriction leads to a marked increase in the number of autophagosomes, together with changes in their physical characteristics. In principle, the observed changes could result either from increased production of autophagosomes, or from reduced fusion of autophagosomes with lysosomes. We believe that the former explanation is the more likely, because the activity of mTOR, a key protein that restrains autophagy, is reduced in the Purkinje cells of food-restricted mice (Fig. 3B). Thus, our data favor the interpretation that the increased abundance of autophagosomes results from upregulation of the autophagy pathway in neurons, rather than from the blockade of autophagosome maturation, although some contribution from the latter cannot be excluded.
Third, we demonstrate that the changes that are induced by food restriction differ somewhat depending on the neuronal cell type. This is consistent with the recent proposal that autophagy pathways may differ among cell types, as a result of evolutionary adaptation to the specific physiological needs of the cell.14 Published studies in which autophagy was inhibited have shown that the outcome varies with cell or tissue type. For example, interruption of neuronal autophagy can lead to degenerative disease,1,2 but an equivalent block in pancreatic acinar cells causes no overt dysfunction.21 However, until now it has been thought that increased autophagy would result in phenotypically-similar changes in closely-related cell types. Here we show that this appears not to be the case in vivo. Following food restriction, we observed both similarities and differences in the size and distribution of autophagosomes in cortical neurons and Purkinje cells. The fact that the observed changes in autophagy differed between these two neuronal cell types suggests that a more extensive analysis is warranted, to determine the extent to which short-term food restriction induces autophagy—and, possibly, other changes—in the mammalian CNS.
Our observation that a brief period of food restriction can induce widespread upregulation of autophagy in CNS neurons may have clinical relevance. As noted above, disruption of autophagy can cause neurodegenerative disease, and the converse also may hold true: upregulation of autophagy may have a neuroprotective effect. For example, in vitro models have shown that starvation in neuronal cell lines can remove toxic molecules and damaged mitochondria from neurons.22–24 Other tissue culture studies, of mutant huntingtin and α-synuclein proteins (which are associated with Huntington disease and familial Parkinson disease respectively), have identified autophagy substrates that can be removed by drug-induced enhancement of autophagy. Most importantly, some neuroprotective effects of drug-enhanced autophagy also have been observed in vivo, in a D. melanogaster model of Huntington disease.25 Finally, it has been suggested that intermittent fasting might improve neuronal function by means that are entirely independent of caloric intake, and may instead reflect an intrinsic neuronal response that is triggered by fasting;26,27 we speculate that the reported improvement of neuronal function may be related to the upregulation of autophagy that we show here. The above findings have encouraged the development of drugs that might enhance neuronal autophagy, thereby protecting against disease. Such drugs must: (i) be able to cross the intact blood-brain barrier; (ii) upregulate neuronal autophagy; and (iii) be harmless to the recipient. Food restriction is a simple, reliable, inexpensive and harmless alternative to drug ingestion and, therefore, we propose that short-term food restriction may represent an attractive alternative to the prophylaxis and treatment of diseases in which candidate drugs are currently being sought. However, caution is counseled, because studies in rat brain have suggested that chronic starvation might inhibit autophagy,28 an outcome that could damage, rather than protect, neurons.28,29
**Autophagy is the natural, regulated, destructive mechanism of the cell that disassembles unnecessary or dysfunctional components.
STUDY
Sporadic short-term fasting, driven by religious and spiritual beliefs, is common to many cultures and has been practiced for millennia, but scientific analyses of the consequences of caloric restriction are more recent. Published studies indicate that the brain is spared many of the effects of short-term food restriction, perhaps because it is a metabolically privileged site that, relative to other organs, is protected from the acute effects of nutrient deprivation, including autophagy.17 We show here that this is not the case: short-term food restriction induces a dramatic upregulation of autophagy in cortical and Purkinje neurons. To our knowledge, this is the first demonstration that food restriction leads to in vivo neuronal autophagy. Our data extend recent reports in tissue culture systems,18,20 and have implications for individuals who, by choice or necessity, have limited food intake. Our findings also may have therapeutic implications, as outlined below. Autophagy is sometimes referred to as cellular “cleansing”, and our observations provide an attractive neuronal parallel to the organismal benefits that, historically, are perceived to derive from fasting.
In this study we describe a novel technique to identify and characterize autophagosomes in the tissues of GFP-LC3 mice, using vibratome sections and confocal microscopy. The changes that we report using this method are confirmed using the standard technique of TEM; this both validates the new approach, and confirms the conclusions that we have drawn therefrom. Herein, we make at least three novel observations.
First, we identify and localize autophagosomes in cortical and Purkinje neurons of normal-fed mammals.
Second, we show that, in these CNS neurons, short-term food restriction leads to a marked increase in the number of autophagosomes, together with changes in their physical characteristics. In principle, the observed changes could result either from increased production of autophagosomes, or from reduced fusion of autophagosomes with lysosomes. We believe that the former explanation is the more likely, because the activity of mTOR, a key protein that restrains autophagy, is reduced in the Purkinje cells of food-restricted mice (Fig. 3B). Thus, our data favor the interpretation that the increased abundance of autophagosomes results from upregulation of the autophagy pathway in neurons, rather than from the blockade of autophagosome maturation, although some contribution from the latter cannot be excluded.
Third, we demonstrate that the changes that are induced by food restriction differ somewhat depending on the neuronal cell type. This is consistent with the recent proposal that autophagy pathways may differ among cell types, as a result of evolutionary adaptation to the specific physiological needs of the cell.14 Published studies in which autophagy was inhibited have shown that the outcome varies with cell or tissue type. For example, interruption of neuronal autophagy can lead to degenerative disease,1,2 but an equivalent block in pancreatic acinar cells causes no overt dysfunction.21 However, until now it has been thought that increased autophagy would result in phenotypically-similar changes in closely-related cell types. Here we show that this appears not to be the case in vivo. Following food restriction, we observed both similarities and differences in the size and distribution of autophagosomes in cortical neurons and Purkinje cells. The fact that the observed changes in autophagy differed between these two neuronal cell types suggests that a more extensive analysis is warranted, to determine the extent to which short-term food restriction induces autophagy—and, possibly, other changes—in the mammalian CNS.
Our observation that a brief period of food restriction can induce widespread upregulation of autophagy in CNS neurons may have clinical relevance. As noted above, disruption of autophagy can cause neurodegenerative disease, and the converse also may hold true: upregulation of autophagy may have a neuroprotective effect. For example, in vitro models have shown that starvation in neuronal cell lines can remove toxic molecules and damaged mitochondria from neurons.22–24 Other tissue culture studies, of mutant huntingtin and α-synuclein proteins (which are associated with Huntington disease and familial Parkinson disease respectively), have identified autophagy substrates that can be removed by drug-induced enhancement of autophagy. Most importantly, some neuroprotective effects of drug-enhanced autophagy also have been observed in vivo, in a D. melanogaster model of Huntington disease.25 Finally, it has been suggested that intermittent fasting might improve neuronal function by means that are entirely independent of caloric intake, and may instead reflect an intrinsic neuronal response that is triggered by fasting;26,27 we speculate that the reported improvement of neuronal function may be related to the upregulation of autophagy that we show here. The above findings have encouraged the development of drugs that might enhance neuronal autophagy, thereby protecting against disease. Such drugs must: (i) be able to cross the intact blood-brain barrier; (ii) upregulate neuronal autophagy; and (iii) be harmless to the recipient. Food restriction is a simple, reliable, inexpensive and harmless alternative to drug ingestion and, therefore, we propose that short-term food restriction may represent an attractive alternative to the prophylaxis and treatment of diseases in which candidate drugs are currently being sought. However, caution is counseled, because studies in rat brain have suggested that chronic starvation might inhibit autophagy,28 an outcome that could damage, rather than protect, neurons.28,29
Incunabula
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Yes, at one point it was very fashionable with angsty teenagers, to come on here and claim they'd had SS from a handfull of mushrooms or what not. I guess leukoencephalopathy is going to be the new black.
5ht2Antogonist
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That's true. I was just trying to sort out what my best move could be here , in case.. (you know
)
5ht2Antogonist
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It's really amazing how scientists recently found that Psilocybin had effect on Hippocampal Neurogenesis.
https://www.youtube.com/watch?v=iC-tFPMeVHk
So.. Psilocybin also might cause -basically- demyelination on the white-matter? A double edge sword maybe.
Moreover.. it's interesting that, on that study, they also had 25I-NBOMe.
I'm just really curious how this'll turn up.
( I think severity of the toxicity might have to do with genetic predisposition and, overall, duration that one exposes himself/herself AND overexcitement on their Seratonergic neurons might have to do with this too. )
Chronic users of Seratonergic drugs are probably on higher risk.
There's just .. lots of research that needs to be done IMO
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Go to a doctor, reading stuff online is only feeding into your obsessive worrying. There is nothing we can do except try to tell you that in all likelihood, the only thing wrong with you is that you're experiencing obsessive thoughts. The mind is a powerful thing, and if you convince yourself that you're damaged, you're going to feel like you're damaged. Long-term anxiety has profoundly negative effects on mental and physical health. If you don't escape this loop you've fallen into, it will be bad for you. You're creating a prison for yourself here. Go to a doctor already and discover the truth, all this speculation and Internet searching is exacerbating what's going on here. I'm telling you, this happens with regularity in this forum, the signs to me are clear that what you've got going on is a disordered obsessive thought process, and you need to sort that out.
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^ Best advice on this thread from Xorkoth. Pupnik and a few others too. Hypochondria is real. The problem with that is if you stay a hypochondriac you may make peace with this issue but the mind will find something else to worry about. I was a nuerotic when I was younger and found reasons to worry about my heart, stomach, mind. I remember feeling my hearbeat when I was tripping and because it was not a perfect rhythm like a song I had a problem. Unbelievable thinking. The heart speeds up and slows down all the time. But I remember really worrying about that. I thought I had an ulcer once too and read all up on it. I was not even close. I am talking 35-40 years ago. You do outgrow this type of worry and then it changes to financial worries. And financial worries I need to make peace with too. If you think about it all life is is making peace with things. (ex- a parent finds out their son or daughter is homosexual and in order to live a peaceful life the parent will have to make peace with that. I just saw that with a family member and it was beautiful how the old homophobic uncle accepted his son after a period of time and opened up his love again) ((sorry about the parenthesis, I code all day in SQL so it is a habit. ))
I guess as I got older I found what to make peace with. If I were the OP I would have a little faith my your body and how it is always healing in a basically healthy state. Some diseases that is not true I know , but unless you really have a disease I would get comfortable with the notion of Not worrying. That probably means you need a doctor to tell you that instead of us, who have been through it. It is a process. Good luck, stay well.
))I guess as I got older I found what to make peace with. If I were the OP I would have a little faith my your body and how it is always healing in a basically healthy state. Some diseases that is not true I know , but unless you really have a disease I would get comfortable with the notion of Not worrying. That probably means you need a doctor to tell you that instead of us, who have been through it. It is a process. Good luck, stay well.
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That happened exactly in my family. It really was very beautiful to see. My uncle had been homophobic and racist his whole life, was just sort of raised that way in the culture he grew up in. His son came out and it was terrible to see, he treated his son badly and his son hated him for it. But after a couple of years, he realized that this was HIS SON, and now they are close again and my uncle has opened up his mind so much, he's no longer a bigot in any way and he thinks so much more deeply about things.
Yeah totally off-topic... but this made me smile.
Solipsis
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It's true: there have been threads also about concerns and obsessive thought after NBOMe use that went on for many pages about what this bluelighter feared had happened. It's not to pile you guys together or anything! The lesson to learn from that though is that just like in that thread the answer has already been given:
DO: Go to a doctor and check if your symptoms are any indication for what you are worried about, or something else.
DON'T: You must not keep assuming, guessing or proceeding to considerations of treatments when you haven't even properly checked if you have something physically wrong with you.
For what it's worth, feeling spaced out is way way too little indication for leukoencephalopathy. Elevated body temperature is a sign of serotonergic instability (from inability to properly maintain body temperature), but this is normally temporary and does not automatically mean that you have serotonin syndrome. Let alone leukoencephalopathy type stuff. I am not hearing anything to suggest neurological disease but rather psychological problems in the range of OCD / derealization and depersonalization / depression, things that we see all too frequently after use of psychedelics but for some reason more with NBOMe's.
There is neurological involvement of that probably yes, but a syndrome like of leukoencephalopathy is truly next level and can include more severe problems with movement and cognition.
Anyway, the point was to not obsess over this so I'll stop enabling that now. If you keep having problems sticking to that DO / DON'T, hypochondria is indeed the likely culprit.
This is not about it 'all being in your head', the problems you seem to have are real even if they are different. But you must face the reality of the situation and that involves seeking help rather than trying to self-diagnose etc.
DO: Go to a doctor and check if your symptoms are any indication for what you are worried about, or something else.
DON'T: You must not keep assuming, guessing or proceeding to considerations of treatments when you haven't even properly checked if you have something physically wrong with you.
For what it's worth, feeling spaced out is way way too little indication for leukoencephalopathy. Elevated body temperature is a sign of serotonergic instability (from inability to properly maintain body temperature), but this is normally temporary and does not automatically mean that you have serotonin syndrome. Let alone leukoencephalopathy type stuff. I am not hearing anything to suggest neurological disease but rather psychological problems in the range of OCD / derealization and depersonalization / depression, things that we see all too frequently after use of psychedelics but for some reason more with NBOMe's.
There is neurological involvement of that probably yes, but a syndrome like of leukoencephalopathy is truly next level and can include more severe problems with movement and cognition.
Anyway, the point was to not obsess over this so I'll stop enabling that now. If you keep having problems sticking to that DO / DON'T, hypochondria is indeed the likely culprit.
This is not about it 'all being in your head', the problems you seem to have are real even if they are different. But you must face the reality of the situation and that involves seeking help rather than trying to self-diagnose etc.