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Hallucinogen Persisting Perception Disorder (HPPD) Support Forum

dasitmane

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Everything posted by dasitmane

  1. DMT is why I am here. I had an amazing life with so much potential. It turned it all to complete hell, a flame of torment in my brains senses daily, sleeping was the only time I had peace for months, and waking was my nightmare. Based on that I think you can reason for yourself if it’s a good idea.
  2. Everything in our universe is quite simple, Push/pull concept, up down black white red blue north pole south pole day night sun black hole etc etc etc... well with our receptors its the same concept, agonist inverse agonist, I was thinking that maybe these very potent agonist of the 5ht2a receptors cause such an extreme push that things become out of balance, just like if you decreased suns gravity the earth would fall away, maybe we can utilize inverse 5ht2a agonists to accomplish the rebalancing of our receptors. unfortunately these dont exist that are on the market today, only in clinical trials, for the treatment of insomnia. Anyone have any ideas? Update: Full documentation of this disease can be found on page 24 post #478
  3. "In a survey of sixty five users of LSD, Holsten found fifty users who described post LSD disturbances eighteen months to four years later3." HPPD is wayyy more prevalent than people are estimating among LSD users. http://www.bjmp.org/content/25-years-hallucinogen-persisting-perception-disorder-diagnostic-challenge Its incredible to me that these findings arent more widely published. Hallucinogens are clearly neurotoxic. Holsten, F. (1976) Flashbacks: Clinical and social significance 1 ½-4 years after the first admission , Journal of Norwegian Medical Association; 96: 875-878
  4. dasitmane

    need help and hope..

    It could be possibly theorized, but its not a possibility to be honest because the symptoms would go away int he case of sensitivity. like I already said, receptors in the brain can be modified, by the brain. So your receptors have gone back to normal, you're brain however, clearly is not. This shows that its not caused by sensitivity. So Dr. Nichols is unfortunately inaccurate in his thoughts on what might be the cause of HPPD. No one knows whats causing the visuals right now. There is very little research on it and its unlikely that there will be much primarily because you're dealing with illegal substances. The hard answer of whats most probable is 5HT2A neurotoxicity(through glutamate modifications), so neuronal loss.
  5. dasitmane

    HPPD Case Studies

    Just google it and you will find a couple. Most of them are from single users that report their disturbances to physicians and the physicians document the information/findings. Tbh I dont think there are going to be many due to governmental regulations on the scheduled substances known to lead to HPPD.
  6. For now sedatives work just fine. Anything thats relaxing to the nervous system. GABA agonists of course, like benzos, or natural ones if you can find any. Lemon balm always helped my anxiety and I pretty much carry it with me everywhere I go. I've noticed that cowslip, which is good for sleeping, if I drink it at night the next day my anxiety is not so bad, but cowslip is hard to find so its not the best choice really. As for visuals I cant really comment because mine eventually went away and so did the DR/DP. Unless I drink A LOT of coffee then the DR/DP comes back slightly. I'm working on some other things but nothing that I will post on here as of yet. If I think of anything else I'll let you know.
  7. “Danjoking, you're right. I apologize for my behavior” - TheMythos Yah post it if you want, it’s beneficial to compile all information we can. To be honest though I think everything is pretty much summed up and come to an end as far as the cause of HPPD. If you haven’t read the last couple pages, it’s gone over pretty thoroughly. Not that you’ll agree. Also please do not be rude to productive members like dayum_son.
  8. dasitmane

    HPPD question for who had been recovered

    No not really. For me personally though I don’t think the visual sector of my brain was affected as much as others. My anxiety was the worst by far and still is. I never got halos or drifters. Tbh I would trade you any day for the visual snow vs my anxiety, so be grateful lol. The visual snow also didn’t even set in for a couple weeks so idk, it could have even just been a symptom of rewiring. It also could have been from the scar formation process or the phagocytes cleaning up etc. who knows, but I haven t had any visual snow for years.
  9. dasitmane

    need help and hope..

    I'm just now seeing that. The 5ht2a receptor excitotoxicity is the most probable reason for this. Still its a guess. Its what I outline as the most probable case in my large thread if you haven't read it. The glutamate "acceleration" theory is definitely improbable if you mean it in terms of post drug use. If you mean during drug use you are basically rehashing exactly what I've said in my thread, so its already been covered. Glutamate levels after drugs use will stabilize, so its not a degenerative disease. Also glutamate "acceleration" and receptor sensitivity are not exactly comparable terms. If you mean specifically receptor sensitivity, its hardly likely that its caused by receptor sensitivity, as receptors will increase or decrease in time, or adjust. Its been four years so your glutamate receptors also have returned to normal. The only other alternative that they mention is GABA transmission disruption. Which I suppose could be a case but i dont exactly understand how it could be permanent. Unless like Dr. Abraham stated with GABA interneurons. Also, I think what you may not understand is that the excitotoxicity mentioned is cause for permanent neuronal loss, and it only occurs during the time of drug use.
  10. If I understand this article right, it shows that hallucinogenic effects, are infact, just like I said directly linked to glutamate. Its super hard to understand though. 5-HT2A–mGluR2 Heteroreceptor Complexes Heteroreceptor complexes between 5-HT2A and mGlu2 receptors were demonstrated in cellular models and implicated in psychosis (Gonzalez-Maeso et al., 2008). mGlu2 receptors were also shown to form heterocomplexes with 5-HT2B but not with 5-HT2C receptors (Delille et al., 2012). Three residues at the intracellular end of transmembrane four (Ala-677(4.40), Ala-681(4.44), and Ala-685(4.48)) were essential for the 5-hydroxytryptamine 2A–metabotropic glutamate 2 (5-HT2A–mGlu2) receptor heteromerization and its psychoactive behavioral function (Moreno et al., 2012). Viral-mediated overexpression in the frontal cortex of wild-type mGlu2 receptor but not of a mutant mGlu2 receptor, which cannot heteromerize with 5-HT2A, rescued the behavioral actions of LSD and other related hallucinogenic drugs in mGlu2 knockout rodents (Moreno et al., 2011, 2012). An allosteric receptor–receptor interaction exists in this complex since mGlu2 receptor activation produces an increase in the affinity of hallucinogenic 5-HT2A agonists for the 5-HT2A protomer binding site (Gonzalez-Maeso et al., 2008). A bidirectional receptor–receptor interaction is present since 5-HT2A agonistsreduce the affinity of mGlu2 agonists for the mGlu2 protomer binding site. It is of substantial interest that the allosteric receptor–receptor interactions in these heteroreceptor complexes are dysregulated in postmortem brains from schizophrenia subjects (Moreno et al., 2012; Muguruza et al., 2013). Subsequent work from this group suggests that the 5-HT2A–mGluR2 heteroreceptor complexes make possible a Gq–Gi balance through signaling cross talk, which could be determined by using ion channels in oocytes from Xenopusas markers for Gi/o- and Gq/11-dependent signaling (Fribourg et al., 2011). A drug-induced pattern dominated by high Gi/o signaling predicts antipsychotic potential, while a pattern dominated by high Gq signaling predicts propsychotic potential. In a recent randomized phase II clinical trial (Patil et al., 2007), it was found that an mGlu2/3 agonist prodrug improved negative and positive symptoms of schizophrenia. However, this trial has so far not been confirmed. Selective 5-HT receptor antagonists also produce therapeutic effects, but they are rather weak in contrast to the therapeutic effects of atypical antipsychotic drugs that block 5-HT2A receptors with high potency (Meltzer, 2012, 2013; Meltzer et al., 1989, 2004). However, the biological relevance of the 5-HT2A–mGluR2 heteroreceptor complexes has been challenged since their formation inter alia does not always lead to effects on second messengers (Delille et al., 2012). Also in view of a limited colocation of 5-HT2A and mGlu2 receptors in the brain, interactions of the two signaling receptor systems through functional brain pathways independent of heteromerization probably play a significant role (Delille et al., 2013). Nevertheless, the molecular integration of the signaling in the 5-HT2A–mGluR2 heteroreceptor complexes via receptor–receptor interactions (Gonzalez-Maeso et al., 2008) remains one relevant mechanism for functional interactions according to the available evidence summarized earlier in the text. Future work will determine which of the two mechanisms operating at the molecular and network level, respectively, plays the leading role in mediating the integration of 5-HT2A and mGlu2 signaling of relevance for psychosis and its treatment.
  11. My initial thought, is thats just some guys blog. I'm not saying that we should increase sensitivity, honestly I dont think 5ht2a receptors should be messed with at all. But if you wanted to counter balance serotonin neuronal loss specifically linked to 5ht2a receptors you would want to mildly increase sensitivity to attempt to make up for it, theoretically. I do not however think this would accomplish much. Although.... Ashwaganda might actually be a good choice for anti anxiety. I have no idea if it would work though. Also I believe that antipsychotic drugs tend towards antagonist of 5ht2a. But this is different than increasing or decreasing receptors. Also I think that Dr. Abraham's thoughts on interneuronal loss(I think he just states they're modified or something though) associated with GABA production is accurate as well. So increasing GABA mildly would be a good idea as well.
  12. I could be wrong but I think you would want increased sensitivity. In the case that I make, which could eventually turn out to be wrong but I’m sticking with it from here on out, the Axons simply are just gone, so I honestly don’t see modulating 5ht2a receptors helping very much either way. You could try it but if the axons aren’t there it will do nothing lol. Basically you’ll need neurogenesis, and even that may have limitations.
  13. 5-HT2A receptors are found postsynaptically to serotonergic neurons, and are particularly concentrated in the frontal cortex. 5-HT2Areceptors are also found in high density in the claustrum, a region that is connected to the visual cortex, in parts of the limbic system (i.e., amygdala and hippocampus), and in the basal ganglia (Table 15-2). In the cortex, the 5-HT2Areceptor is located on local GABAergic interneurons, as well as on pyramidal projection neurons, which are known to be glutamatergic. The amygdala is probably the area effected causing severe anxiety. The claustrum maybe is the area effected causing visual symptoms?
  14. I can add too that in the case of Risperodone, a 5ht2a inverse agonist, and other anti convulsion medications which are 5ht2a antagonists there is a correlation with palinopsia. Palinopsia being obviously common with HPPD, the most probable reason being, that the 5ht2a specific neurons that underwent glutamate excitotoxic apoptosis, are now gone, and therein laying a lack of 5ht2a input, which would be similar to that of these drugs, being inverse agonists and antagonists. So this gives even more credence that HPPD is caused by 5ht2a induced glutamate excitotoxic apoptosis.
  15. dasitmane

    need help and hope..

    HPPD is definitely not a degenerative disease. Unless you continue drug use. As long as you aren't doing drugs still your glutamate levels have normalized. Also Im not seeing anything on the wiki about palinopsia being directly related to 5ht2a receptors.
  16. dasitmane

    my success story

    You've been posting this for weeks now. Why not just post it when you post it.....
  17. Sounds like pretty much the best information he could have gave you for this condition. Theres really not anything else they have to offer. I dont completely agree with his stance on benzos if people feel their anxiety is bad enough that they need them. But there are alternatives in herbal medicine that would work as well. Hes right about alcohol too, but if you dont want to consume it thats not bad either. If you are trying to limit even minute amounts though that are in other foods its a bit unnecessary, as you should know, your body produces some ethyl alcohol in its own metabolism.
  18. They could be considered for possibility, however ion channel damage directly from hallucinogen use would be repairable by the brain. Indirect ion mutation through dna changes from hallucinogens would easily ruled out as well due to the fact that it would then be a progressive onset, not overnight like HPPD.
  19. Well guys, I've pretty much figured it all out. This condition is actually quite simple as to the cause. I sometimes pray for an answer as to the cause, so that we can better understand the condition. Yesterday during my usual walk, I did the same. Last night I decided to do some quick reading and found 1 thing after another within a short amount of time and everything adds up. Researchers dont have any information on what hallucinogens do to the brain seemingly, but this isn't quite the case. We know for certain that take for example LSD, acts on 5ht2a receptors, we know this for sure because 5ht2a antagonists taken before LSD ingestion, will prevent hallucinations. As to the reason for the hallucinations they aren't quite sure, but they do know that 5ht2a activation exhibits increases in glutamate. Glutamate is the most available receptor in the brain, it also is notorious for excitotoxic apoptosis. The clear answer is that LSD and other hallucinogens increase neuronal output of glutamate, the hallucinations are probably from the overly excessive production of glutamate, and its stimulant effects. This is the cascade effect leading to overexcitation of neurons, and their eventual course to apoptosis, leading to the condition of HPPD. Now, some may argue that there are some who don't get HPPD, and that HPPD is rare. This is true, and creates a bit of elusiveness. The most possible reasons for this is that for one, many people are pretty complacent as to their actual cognitive function, and deficits created therein, this is one possible reason for less reports of HPPD. Granted however, I dont think this is the primary case for the rarity of HPPD, but rather, that glutamate requires breakdown, and utilizes P5P, or vitamin B6, for its breakdown with glutamate decarboxylase. Thus, the most probable explanation for HPPD is that the sufferers most likely have a variable amount of metabolic deficiency for the production of P5P or glutamate decarboxylase. This would explain why the condition is rare, and why some people come out seemingly unscathed by hallucinogens. I hardly doubt that they come out completely unscathed, but I am sure that their neuronal loss is most likely quite limited. The most likely explanation for MRIs having little to no findings is most probably due to the fact that the neuronal loss is scattered. Thus it will hardly show on MRIs, if at all, and this is why a small percentage actually do seem to have some minor findings of scattered white matter micro lesions, commonly associated with migraines. I'd like to comment too, that in my own personal case, the most likely cause for my HPPD was that I consistently, for years, would always take folinic acid, which I always noticed had a strong stimulant effect, not really knowing the reason for it however. Now I have found that folinic acid and other folate compounds are directly linked to the availability of free glutamate, hence during the use of hallucinogen use incombinate with high glutamate availability, you're going to be more prone to excitotoxicity leading to apoptosis and HPPD. Folate supplementation is also readily found in breads, and multivitamins. The cause for some people developing HPPD simply could be eating high amounts of folate in breads and grains unknowingly, and then taking hallucinogens, buffering glutamate production and excitotoxicity. Like I said, super simple, and easily explained. I should add too that people who experience recovery is due to neuronal plasticity. I'm not going to explain what that is here but its pretty simple to google and is pretty limited to the amount of recovery. From here I will try to find out if long distance axonal tracts can be repaired, if not even with neurogenesis and even stem cell research we will be limited to recovery based on that alone. Long distance axonal tracts are very important. As I've stated before, the Axolotl Salamander, who can regenerate large chunks of his brain, is incapable of repairing long distance axonal tracts after blunt trauma. This most certainly will inhibit functional regrowth of the brain. Also I'd like to add that the areas of the brain effected, are the cortico limbic systems. So frontal cortex, hipp, thalamus, etc. Heres a good read for understanding the limbic system https://www.interaction-design.org/literature/article/our-three-brains-the-emotional-brain. It all pretty much makes perfect sense. Heres for frontal lobe, https://en.wikipedia.org/wiki/Frontal_lobe#Function. Just skip to function and damage. I think we all will see a lot of our symptoms correlate or fall in to place in these areas of the brain.
  20. Shit bros the more I read and learn the more confused I am. It could be so many things that cause HPPD. Some people do so much LSD and have zero symptoms after. I think that we must have some susceptibility, it may not even be brain damage. I was thinking that other possibilities could be allergic reaction related swelling causing microvascular ischemia in the brain, starving scattered neurons(neuronal loss). Another possibility really could be possible gene/DNA changes that create ion channel mutations, I dont know how it coiuld be that since it seems to come on over nice, but I did notice a progression in my symptoms from day one, so I dont know. But ion channel mutations could cause this. This is an impossible disease. Heres some stuff that ive found to be pretty interesting lately Posterior visual pathway cortical lesions (tumor,[1] abscess,[3] hemorrhage,[4] infarction,[1] arteriovenous malformation,[5]cortical dysplasia,[6] aneurysm[1]) and various seizure causes (hyperglycemia,[7] ion channel mutations,[8] Creutzfeldt–Jakob disease,[9] idiopathic seizures,[10] etc.) cause focal cortical hyperactivity or hyperexcitability, resulting in inappropriate, persistent activation of a visual memory circuit. Illusory palinopsia is a dysfunction of visual perception, resulting from diffuse, persistent alterations in neuronal excitability that affect physiological mechanisms of light or motion perception. Illusory palinopsia is caused by migraines, HPPD, prescription drugs, head trauma, or may be idiopathic. Trazodone,[11] nefazodone,[12] mirtazepine,[13] topiramate,[14]clomiphene,[15] oral contraceptives, and risperidone[16] have been reported to cause illusory palinopsia. A patient frequently has multiple types of illusory palinopsia, which represent dysfunctions in both light and motion perception. Light and motion are processed via different pathways, suggesting diffuse or global excitability alterations. https://en.wikipedia.org/wiki/Palinopsia This information could send us in an accurate general direction of whats going on here.
  21. dasitmane

    The Long and Winding Road

    Id say were definitely masters of suffering. Bro can you please respond? Can you please post the video of the shaman or try to find it or give more details?
  22. dasitmane

    The Long and Winding Road

    Go on........ Can you find the show again??
  23. Heres a Danish study that did tests on 400 different people, 154 complained about long term problems years later. AKA HPPD sufferers. Some even committed suicide. And they lean toward potential neurotoxicity. "two-thirds of the patients had flashbacks." http://journals.sagepub.com/doi/10.1177/0957154X16629902
  24. Haha, no not that long. Some may be pertaining to medicine. Ill see what I have when I have time.
  25. Interesting. I may have some old German manuscripts that maybe you could help me understand? Might, its been a long time since I've looked at my non english stuff.
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