Fawkinchit

I remember when I was reading studies done about hallucinogens changing the way we learn etc..... Anyone involved in those studies I would remove from practicing medicine or doing research if I could. Personally I'd say this sounds pretty dumb.

If you're referring to Hope's thread he doesn't specifically say they did, he says what if, and only eludes to the possibility of the sort. Also classifications of whats actually meant by "reversing" are very broad. "reversing" could simply just mean taking a specific antipsychotic, treating the symptoms etc. Maybe they did though! That would be great. Also for all we know it could just be hypothesis from the doctors. But, ya, I agree, I dont like how this world works either. Also, I dont think the hypothesis here are very crazy, they have a lot of potential!

This is a good question, but I just wanted to add that not all infections are transmitted.

Because I posted it? lol

Anyone else listen to this stuff?

You dont....

This too is amazing, I never considered a breach in the blood brain barrier. Mainly just the epithelial. And yah, exactly Alzheimer's, and Parkinson's too. There was a study that showed they all had one strain of bacteria in common in their gut. Its extremely interesting. You're completely understanding why I'm talking about this lol, its great. Theres definitely potential here. That guy brought up a really interesting note as well, as to how drugs effect the microbiome. We should try to find more studies as well on how drugs effect bacteria, in and or outside of the body. We should try too, to find information or studies done that show effects of drugs on the blood brain barrier as well. I wasn't really even aware that there could be any disruption of it. Good job! Btw... if you dont have HPPD, what made you decide to come here and study this?

This is good! I actually for a while there was using probiotic kefir. Its not bad. I dont know if it improved my symptoms at all but the health benefits all around are enormous. Certain strains to also help weed out invasive bacteria such as S. Aureus etc. I tried making my own as well, but it made me feel kind of sick when I made my own, but I also let it ferment longer than usual, but it was too much for me so I stuck with the kind they sell at walmart, plus it tastes better. Regardless, gut dysbiosis and epithelial barrier inconsistencies can definitely lead to a lot of health issues. I think that kefir is good and could possibly be beneficial for sure. From all the reading I did on it, I would say health wise it should be a staple in every family household, no joke.

Imagine for a moment, a bacterial infection of the gut, or the central nervous system, that produces indolethylamine N-methyltransferase, breaking down serotonin and tryptamine in to Bufotenine and DMT. It would be a constant feed of these compounds, a constant high, HPPD. The more I read the more potential I'm believing this may have... https://www.ncbi.nlm.nih.gov/pubmed/16095048 Potentially hallucinogenic 5-hydroxytryptamine receptor ligands bufotenine and dimethyltryptamine in blood and tissues. Kärkkäinen J1, Forsström T, Tornaeus J, Wähälä K, Kiuru P, Honkanen A, Stenman UH, Turpeinen U, Hesso A. Author information 1 Peijas Hospital, Helsinki University Central Hospital, Vantaa, Finland. jorma.karkkainen@helsinki.fi Abstract Bufotenine and N,N-dimethyltryptamine (DMT) are hallucinogenic dimethylated indolethylamines (DMIAs) formed from serotonin and tryptamine by the enzyme indolethylamine N-methyltransferase (INMT) ubiquitously present in non-neural tissues. In mammals, endogenous bufotenine and DMT have been identified only in human urine. The DMIAs bind effectively to 5HT receptors and their administration causes a variety of autonomic effects, which may reflect their actual physiological function. Endogenous levels of bufotenine and DMT in blood and a number of animal and human tissues were determined using highly sensitive and specific quantitative mass spectrometric techniques. A new finding was the detection of large amounts of bufotenine in stools, which may be an indication of its role in intestinal function. It is suggested that fecal and urinary bufotenine originate from epithelial cells of the intestine and the kidney, respectively, although the possibility of their synthesis by intestinal bacteria cannot be excluded. Only small amounts of the DMIAs were found in somatic or neural tissues and none in blood. This can be explained by rapid catabolism of the DMIAs by mitochondrial monoamino-oxidase or by the fact that the dimethylated products of serotonin and tryptamine are not formed in significant amounts in most mammalian tissues despite the widespread presence of INMT in tissues.

Here is another very extremely interesting article about a fungal infection of Cicadas, that produces cathinone, an amphetamine like compound, and also psylosybin. This is interesting because it shows a possibility of maybe an infection of the gut, or other areas of the body, by fungi, bacteria, or parasites that produce stimulant like compounds, and could very well be the cause of HPPD. It really makes a lot of sense if there were some type of bacteria that grows on hallucinogenic compounds, and or feeds off of them, and then are ingested, causing bad trips, and then infecting the host, aka perpetual trip. The article is also hilarious. Maybe if we could get Hope's research team on this. https://www.theatlantic.com/science/archive/2018/07/massospora-parasite-drugs-its-hosts/566324/ This Parasite Drugs Its Hosts With the Psychedelic Chemical in Shrooms It also makes their butts fall off. A cicada infected by MassosporaMATT KASSON Imagine emerging into the sun after 17 long years spent lying underground, only for your butt to fall off. That ignominious fate regularly befalls America’s cicadas. These bugs spend their youth underground, feeding on roots. After 13 or 17 years of this, they synchronously erupt from the soil in plagues of biblical proportions for a few weeks of song and sex. But on their way out, some of them encounter the spores of a fungus called Massospora. A week after these encounters, the hard panels of the cicadas’ abdomens slough off, revealing a strange white “plug.” That’s the fungus, which has grown throughout the insect, consumed its organs, and converted the rear third of its body into a mass of spores. The de-derriered insects go about their business as if nothing unusual has happened. And as they fly around, the spores rain down from their exposed backsides, landing on other cicadas and saturating the soil. “We call them flying saltshakers of death,” says Matt Kasson, who studies fungi at West Virginia University. Massospora and its butt-eating powers were first discovered in the 19th century, but Kasson and his colleagues have only just shown that it has another secret: It doses its victims with mind-altering drugs. Perhaps that’s why “the cicadas walk around as if nothing’s wrong even though a third of their body has fallen off,” Kasson says. To study these fungi, “you really have to be in the right place at the right time,” Kasson says. For him, the time was May 2016, when billions of periodical cicadas emerged throughout the northeastern United States. He and his colleagues collected around 150 of the unfortunate saltshakers. And a year later, a colleague supplemented this collection with infected banger-wing cicadas—a different species that emerges annually. Greg Boyce, a member of Kasson’s team, looked at all the chemicals found in the white fungal plugs of the various cicadas. And to his shock, he found that the banger-wings were loaded with psilocybin—the potent hallucinogen found in magic mushrooms. “At first, I thought: There’s absolutely no way,” he says. “It seemed impossible.” After all, no one has ever detected psilocybin in anything other than mushrooms, and those fungi have been evolving separately from Massospora for around 900 million years. The surprises didn’t stop there. “I remember looking over at Greg one night and he had a strange look on his face,” Kasson recalls. “He said, ‘Have you ever heard of cathinone?’” Kasson hadn’t, but a quick search revealed that it’s an amphetamine. It had never been found in a fungus before. Indeed, it was known only from the khat plant that has long been chewed by people from the Middle East and the Horn of Africa. But apparently, cathinone is also produced by Massaspora as it infects periodical cicadas. The team took great pains to check that Massospora really does contain these unexpected drugs. They showed that the substances are found only in the infected cicadas and not in the uninfected ones. They found that the fungus has the right genes for making these chemicals, and contains the precursor substances that you’d expect. And at some point during this work, it dawned on Kasson that he was working with illicit substances. Psilocybin, in particular, is a Schedule I drug, and researchers who study it need a permit from the Drug Enforcement Administration. “I thought: Oh, crap,” he says. “Then I thought: OH CRAP. The DEA is going to come in here, tase me, and confiscate my flying saltshakers.” He sent them an email. “This is … interesting,” read the initial response. “You have to understand that this is not something we normally get emails about.” After some discussion, the agency decided that no permit was required, since the drug is found in such small quantities within the cicadas, and since Kasson had no plans for concentrating it. I asked Kasson if it’s possible to get high by eating Massospora-infected cicadas. Surprisingly, he didn’t say no. “Based on the ones we looked at, it would probably take a dozen or more,” he said. But it’s possible that earlier in the infections, before the conspicuous saltshaker stage, the fungus might pump out higher concentrations of these chemicals. Why? Kasson suspects that the drugs help the fungus control its hosts. Infected cicadas behave strangely. Despite their horrific injuries, males become hyperactive and hypersexual. They frenetically try to mate with anything they can find, including with other males. They’ll even mimic the wing-flicking signals of females to lure males toward them. None of this does them any good—their genitals have either been devoured by the fungus or have fallen off with the rest of their butts. Instead, this behavior only benefits the fungus, allowing its spores to find new hosts. Kasson suspects that cathinone and psilocybin are responsible for at least some of these behaviors. “If I had a limb amputated, I probably wouldn’t have a lot of pep in my step,” he said. “But these cicadas do. Something is giving them a bit more energy. The amphetamine could explain that.” Psilocybin’s role is harder to explain. The drug might make humans hallucinate, but no one knows if cicadas would similarly trip. There is, however, a theory that magic mushrooms evolved psilocybin to reduce the appetites of insects that might compete with them for decaying wood. Perhaps by suppressing the appetites of cicadas, Massospora nudges them away from foraging and toward incessant mating. There are many parasitic fungi that manipulate the behavior of insect hosts, including the famous Ophiocordyceps fungi, which can turn ants into zombies. “There’s a lot of curiosity about how these fungi might actually manipulate behavior, and this is the first time that anyone has identified chemical compounds that could play that role,” says Kathryn Bushley from the University of Minnesota. “That’s really significant.” The discovery opens up a lot of questions, says Corrie Moreau from the Field Museum of Natural History. What exactly do these drugs do to the cicadas? And, she wonders, “do other cicada-infecting fungi share these same molecules, or has each manipulating fungus evolved a unique compound to induce the desired behavior?” “And maybe there are other players involved,” Kasson added. He pointed to another study, which I wrote about last week, in which a different fungus seems to use a virus to control the minds of flies. “We might think that it’s just a host and a fungus, but maybe it’s more complicated than that.”

Whoa... What... let me get this straight. You did cocaine after getting HPPD? Lmao wtf. So this is really intriguing though... it didn't make it worse??? And other people have mentioned this??

This exactly, holy fuck.

Thanks! Glad to be back, I hope the same. just wanted to add to this thread the infection idea may not be as far fetched as I believed This is an excerpt about the parasite T. Gondii. IL-12 is produced during T. gondii infection to activate natural killer (NK) cells.[36] Tryptophan is an essential amino acid for T. gondii, which it scavenges from host cells. IFN-γ induces the activation of indole-amine-2,3-dioxygenase (IDO) and tryptophan-2,3-dioxygenase (TDO), two enzymes that are responsible for the degradation of tryptophan.[45] Immune pressure eventually leads the parasite to form cysts that normally are deposited in the muscles and in the brain of the hosts.[36] Immune response and behaviour alterationsEdit The IFN-γ-mediated activation of IDO and TDO is an evolutionary mechanism that serves to starve the parasite, but it can result in depletion of tryptophan in the brain of the host. IDO and TDO degrade tryptophan to N-formylkynurenine and administration of L-kynurenine is capable of inducing depressive-like behaviour in mice.[45] T. gondii infection has been demonstrated to increase the levels of kynurenic acid (KYNA) in the brains of infected mice and KYNA has also been demonstrated to be increased in the brain of schizophrenic persons.[45] Low levels of tryptophan and serotonin in the brain were already associated to depression.[46] really interesting what they say with schizophrenia. i also hardly doubt chlorine dioxide has much potential, as i believe there is always small amounts in the drinking water.

See and thats really interesting because when I take opiod related pain killers it doesn't bother me in the slightest lol. Coffee however I think we can all agree lmao.

I once found a study they did on hallucinogens where a large percentage, like way more than you would expect out of about 400 people got HPPD, they pretty much ignored the negative results if I remember, I think 2 even had it so bad they committed suicide. None of it appeared to be mentioned for the most part.

Yah, definitely, you have a far greater chance of recovery, nothing is guaranteed here however, as rarely anything is in medicine. You'll really just have to wait it out and see. By the way, don't be a dope and try hallucinogens again if the symptoms recede, you're clearly vulnerable to HPPD, doing more drugs could put you here indefinitely, and the symptoms can be far worse than you describe, take some time to find new hobbies and other things you enjoy in life, and live life happily. FYI my visual snow eventually went away and has never come back, though I do get very slight reminiscences of it if I drink a lot of caffeine etc. My HPPD clearly was worse than yours though.

It doesn't appear to be a progressive disorder, there however, things that can make it worse, or trigger it.

The Lewy Body Dementia is really unique. Maybe thats a potential for the cause of this condition as well, some deposits of a chemical or protein of some sort that has difficulty being broken down once deposited, and disrupting brain function. Again, I doubt it, but maybe. The first hypothesis sounds a lot like what I have been saying, but I attribute it to a loss of white matter which is the communication circuits between gray matter, causing deficiencies in the sensory cycle that they explain. Also if I remember correctly, Acetylcholine typically has a lot to do with motor function and bodily control. Its clearly noticed that people with Lewy Body Dementia begin having motor control issues, incontinence, and extreme muscle rigidity. Sufferers of HPPD typically have no motor or body movement/function issues, so I would believe this rules out any regulation disorders specifically with Acetylcholine.

Wait I'm confused.... so they have reversed it? Or no? Also congrats on the success! I remember talking to you about all this a couple years ago.

All good candidates, gingko actually used to be one of my favorites when I was young, great for memory and adding mental clarity. The two herbs that I'm posting though are different from those, one more common, the other less common. The first one is common sage, the second is cowslip. Sage is clearly far easier to get and you can just make a tea out of it every day, its shown a lot of evidence for the brain and treatment for dementia as well. Theres a lot more that I know about these herbs but i dont care to get very far in depth on them, anyone who wants to try them can try them. The cowslip is really rare and hard to get, I think I had to have some shipped from eastern europe or something, but it has a better sedative effect, so its helps promptly. Don't anyone think that this is for immediate treatment for the symptoms though, this is a long term treatment, I would say minimum one year if you want to do it. Whether it will work for others I dont know, but I have had improvement that I wasn't really expecting after so long and do attribute to the various treatments I was trying. Sage will improve your memory as well, which its well known to do, I can tell too that my mental cognition is far improved from what it was as well too. One symptom that I noticed after improvement which is prevalent and often missed is the cognitive and mental blunting of this condition so to speak, there are emotional disturbances as well, an incapacity to properly conceive of the evident reality facing the person whatever it may be, as if there were some sort of block in the frontal processing and reception of the brain, which is very interesting and typically unnoticed by your average patient with HPPD. What is most interesting about sage as well, is that it has a very strong antimicrobial activity, better than that of Ampicillin against MDRS Staphylococcus Aureus. After doing a lot of research on microbiology I started to realize that there are a LOT of conditions that we consider "immune" or "genetic" which are clearly just caused by bacterial imbalances and infections. As a matter of fact we constantly have roughly 2 pounds of bacteria living in our intestines our whole lives! They all have very unique functions and metabolisms, many symbiotic, others, infectious. Eczema is a bacterial infection by MRSA or MDRS Staphylococcus Aureus, the immune system is just there in response to the bacteria. 90%+ of eczematic lesions have this bacteria. I began to postulate the possibility of HPPD being caused by a bacterial infection, by possibly a bacteria that feeds and metabolizes catecholamines, its a really far fetched idea and highly unlikely, but, regardless, still possible and would explain why so few get HPPD from usage, maybe being more susceptible to the bacteria, such as that as eczema patients. Think too, 2 pounds of bacteria, and where does 90% of serotonin come from in the body? The gut! All fairly interesting stuff. I could elaborate on this a lot more but for the sake of time I'm going to refrain. For anyone that wants to try this just buy sage, you can get a pound for less than 20$ online, take it in a tea daily, and report your findings, I don't guarantee anyone success by this, but its something that everyone can try. If you do try it, and care to share results, please give it time to work, give atleast 3 months to report anything. Good luck!

Hello everyone! Hope everyone is doing well. Been wanting to make a post for months now but just haven't been able to find time. The main reasons for my post is to share my progress and share what my methods were for the progress in hopes that others can possibly benefit from the same treatments. With very little notoriety and/or profit for medical science HPPD gets very little to no coverage at all, so I hope this is something to help those who are destitute in this insufferable and most terrible disorder and condition which could be described by none other than the manifestation of hell itself. To start I just want to explain that at the beginning of my condition I could scarcely drink 1/4 - 1/2 a cup of 12 oz coffee, I would often just discard the rest, anything more would initiate massive anxiety and increases in other symptoms involved with HPPD. Now, however, things have changed! I didn't really have much progress after about a year, things stayed relatively the same. I would, however, like to share a photo of how much caffeine I can consume, and explain how much I do consume daily, as a proof of improvement, that I do attribute to a various degree of long term treatment that is available to everyone. [ Here you can see the maximum amount of caffeine that I can now consume daily if I choose, it will give me minor amounts of anxiety, but its not beyond what I can handle, where before I could come nothing close to this. Don't be confused either, the coke I can drink whole as well, and the coffee thermos is 24 oz.. This is no where near what I was capable of consuming before, and took about 2-3 years to accomplish. On average daily since this is a bit much for me, I only drink the 24oz coffee, which I make every morning, coupled with a few supplements that have a mild stimulant effect. I've even been able to take minor amounts of stimulants that I always enjoyed before my condition(all legal of course). Its been a long road. So, here I will share two herbs that may potentially help you, I don't claim that it will resolve all your symptoms all together, I do still have issues, but they are significantly decreased from what they were. I do believe that this is a neurological disorder, but I atop the two herbs to share in potentially assisting the progression of the suffering from this disease, I do also have a possible alternative to the diagnosis to this disorder after researching very significantly microbiology for other reasons not involved with HPPD. Tomorrow in my next post I will explain the two herbs, I want to elaborate more so on the other possible diagnosis involving microbiology which is a possibility and will tie in to the treatment for both possibilities involved which I think everyone will be somewhat intrigued about. I hope everyone the best and hope you're all hanging in there and doing your research trying to improve this condition. Tomorrow I will post more and for sure elaborate on this condition and the possible treatments. I would like to shout out to Jay, Hope, Kozin, dayum_son, and a few others too but its been a while and I'll have to look up the screen names. Sorry for anyone that has PM'd me and I haven't responded I haven't been on for a while but I will try to be on more. I also wanted to post old information which is basically a sum up of my old post that I typed up for someone in an email which will save me a lot of time than typing it again. In my next post I will make an alternative possible diagnosis that is far different from the foregoing. I want everyone to know too that you're the greatest even if everyone abandons and leaves you in your suffering. Keep fighting to save yourself and bare your infirmities with this terrible disease and I hope anyone that leaves or abandons you adjourns their due justice in the universal law of karma to the fullest extent and then some if God so feels it. I hope too that you're all relieved of this curse that destroys lives and that people will supplicate to the suffering of the nightmare that we live waking. I hope to help you all in the next post. My heart goes out to everyone with this condition. Stay strong. The actual etiology, though often argued, is most likely to be a form of excitotoxic apoptosis following glutamate receptor overstimulation. It could also include variable causes including neuronal hyperthermia due to the overstimulation. This is commonly neglected as a possibility in health, research, and media, due to the fact that in MRI studies of HPPD sufferers and hallucinogenic users there is no "notable" damage that can be perceived. However I was able to accumulate quite a lot of MRIs from actual HPPD sufferers and there is a decent yield for white matter hyperintensities, enough to be suspect for possible neuronal degeneration. The white matter lesions also appear to be long standing ruling out temporary axonal demyelination. Another point to be shown that it neuronal loss should not be ruled out is the obvious fact that MRIs are only subject to detecting larger unscattered masses of neuronal lost such as that found in blunt trauma victims and stroke victims etc, but unbeknownst to your average physician its incapable of showing minute scattered neuronal loss which can be seen in the link of this lithium overdose patent. Case Report A 45-year-old Mr. S presented with a history of altered sensorium for the past 2 days. The patient had a history of five episodes of mania and two episodes of depression in the last 15 years. Six weeks ago he had an episode of mania, for which he was treated at a tertiary care center as inpatient and given a tablet each of olanzapine 20 mg, lithium 900 mg, and chlorpromazine 300 mg daily. A week after he was discharged from the center, while still on regular medication, he developed coarse tremors affecting the whole body and was unable to walk. When he was brought to the Accident and Emergency Department of our hospital, he was afebrile and was not responding to painful commands. His pulse rate was 105/min with exaggerated deep tendon reflexes. His investigations showed a raised serum lithium level of 3.9 mEq/L, creatinine of 1.8 mg/dl, and raised white blood cells of 24,800/μl. His liver function tests and sugar level were within the normal range. All his previous medications, including lithium were stopped, and he was treated with intravenous (IV) normal saline, IV ceftriaxone 2 g, and vancomycin 500 mg twice a day for 2 weeks. In order to rule out any infection, his blood was sent for culture, and a cerebrospinal fluid (CSF) analysis was done to rule out any neuro-infection. However, both blood culture and CSF results were found to be normal. A magnetic resonance imaging (MRI) of the brain showed T2 and flair hyperintensities in the bilateral parietal lobe and periventricular white matter changes, both suggestive of lithium toxicity [Figure 1]a. In view of his low Glasgow coma scale (8/15), the patient was intubated. Also, because of the severe lithium toxicity, hemodialysis was started. After two cycles of hemodialysis, the patient started responding to painful commands. His serum lithium level fell to 1.8 mEq/L. He was extubated on day 5 of admission. From day 6 onward, he started responding to oral commands, even though his speech was slurred. However, he had coarse tremors, truncal ataxia, and difficulty in deglutition. Subsequently, the patient was shifted to the psychiatry ward of our hospital for further management and for observation of manic symptoms. Physiotherapy was started, and within 2 weeks of intensive physiotherapy the patient started walking with support. His speech too improved. After 3 weeks, when his blood serum lithium level fell to 0.2 mEq/L, he started showing symptoms of mania. He was then treated with oral quetiapine, which was gradually increased to 300 mg/day. Thirty-six days after the first MRI, a second MRI was done. The second MRI showed up to 40% reduction in periventricular white matter hyperintensities in the bilateral parietal lobes [Figure 1]b. Even after about 6 months of follow-up the patient continues to have coarse tremors, dysarthria, and significant limb ataxia. Brain MRI showing hyperintensities.  So even after 6 months he was showing symptoms, which clearly demonstrates damage to the neural tissue. A clear example that MRIs are not completely effective and accurate in diagnosing neuronal loss. There are countless examples that be given to prove this, another is even in epileptic patients who are taking anticonvulsant medications as treatment, proven neurotoxic compounds, MRIs will only show neuronal loss after 10-20 years and will only show it as encephalopathy. So media and medicine claiming that this hallucinogenic compound are "safe" are ignoring a LOT of information. Heres just one of many abstracts that show through the study of MDMA that activation of 5ht2a receptions(those activated in hallucinogens) are neurotoxic Abstract 3,4-Methylenedioxymethamphetamine (MDMA or "Ecstasy") and 2,5-dimethoxy-4-iodoamphetamine hydrochloride (DOI) are hallucinogenic amphetamines with addictive properties. The hippocampus is involved in learning and memory and seems particularly vulnerable to amphetamine's neurotoxicity. We evaluated the neurotoxicity of DOI and MDMA in primary neuronal cultures of hippocampus obtained from Wistar rat embryos (E-17 to E-19). Mature neurons after 10 days in culture were exposed for 24 or 48 h either to MDMA (100-800 μM) or DOI (10-100 μM). Both the lactate dehydrogenase (LDH) release and the tetrazolium-based (MTT) assays revealed a concentration- and time-dependent neuronal death and mitochondrial dysfunction after exposure to both drugs. Both drugs promoted a significant increase in caspase-8 and caspase-3 activities. At concentrations that produced similar levels of neuronal death, DOI promoted a higher increase in the activity of both caspases than MDMA. In the mitochondrial fraction of neurons exposed 24h to DOI or MDMA, we found a significant increase in the 67 kDa band of apoptosis inducing factor (AIF) by Western blot. Moreover, 24h exposure to DOI promoted an increase in cytochrome c in the cytoplasmatic fraction of neurons. Pre-treatment with an antibody raised against the 5-HT(2A)-receptor (an irreversible antagonist) greatly attenuated neuronal death promoted by 48 h exposure to DOI or MDMA. In conclusion, hallucinogenic amphetamines promoted programmed neuronal death involving both the mitochondria machinery and the extrinsic cell death key regulators. Death was dependent, at least in part, on the stimulation of the 5-HT(2A)-receptors. https://www.ncbi.nlm.nih.gov/pubmed/22983118 Risperodone is a good case too for showing excitotoxic damage, 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. So unfortunately for these sufferers is most likely that their diagnosis is neuronal loss. A sad day for anyone regardless if they are a drug addict or a one times user. Heres a study that shows the areas likely to be affected Brain imaging studies Until recently, many neural circuit models were based on animal studies, and implications for the effects of hallucinogenic drugs or disease models in humans were based on inferences from these studies. However, functional neuroimaging studies enable one to examine these neural circuit models directly and test specific hypotheses about the role of specific neural systems in the expression of ASC. PET with the radiotracer 18F-fluorodcoxyglucose (18FDG) was used to assess drug-induced changes in the regional cerebral metabolic rate of glucose (CMRglu), as an index of cerebral activity. We found that a hallucinogenic dose of racemic ketamine increased neuronal activity in the prefrontal cortex (hyperfrontality) and associated limbic regions, as well as in striatal and thalamic structures in healthy volunteers, giving the first evidence that functional alterations in CSTC loops may underlie the symptomatology of drug-induced ASC.50 This hyperfrontality finding was corroborated and extended in subsequent studies in healthy volunteers in which the effects of hallucinogens and NMDA antagonists including psilocybin, racemic ketamine, and S-ketamine were compared. In particular, we found that, despite different primary mechanisms of action, the two classes of drugs produced strikingly similar brain activation patterns as indexed by normalized CMRglu. Both psilocybin and ketamine markedly increased brain activity bilaterally in the frontomedial and frontolateral cortex, including the anterior cingulate. Lesser increases were found in the temporomedial, superior, and inferior parietal cortices, striatum, and thalamus. Decreases were found in the left caudate nucleus, bilaterally in the ventral striatum, occipital lobe, and visual pathway.9-11 A correlational analysis revealed that the metabolic hyperfrontality in ketamine and psilocybin subjects was associated with a depersonalization/derealization syndrome, thought disturbances, and mania-like symptoms.9-11 The hyperfrontality finding in ASC was further supported by evidence from brain imaging studies with ketamine and psilocybin in healthy volunteers27,51 and was also found in subjects treated with the classic pheny le thyl amine hallucinogen mescaline.52 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3181663/ Prognosis is typically really bad with little recovery in patients that have extensive damage. Mainly the only saving grace is synaptic hyper plasticity. If you then take in to account the possibility for future advancements in neurogenesis and stem cell research there is some hope but there is the unfortunate case that regeneration of damage to the white matter shown in Axolotl Salamanders is structural deficient when taken in to account long distance axonal tracts. The Axolotl being capable to regenerating neurons sadly only can fill the area of these damaged long tracts with short neurons typically found in gray matter, making structural integrity likely deficient in functional regrowth. So even with neurogenesis prognosis is likely grim for these patients. There is a certain drug that I found that ends the cascade event of hallucinations right at the core of the matter and would in the event of a "bad trip" save these patients a great deal of permanent neuronal loss if they made it to the ER in time. I cant find the drug at the moment and I don't have time to find it but I believe it was simply an reverse 5htp2a receptor agonist. I was actually able to find some treatments in extremely old medical books too, which lead me to believe that the physicians were actually stimulating neurogenesis in their patients, but still even with that recovery is limited due to axonal tracts being lost in white matter, but it would certainly improve their lives. Instead of educating people of these dangers they promote hallucinogens as potential for all kinds of treatments and ignore negative effects. One study showed in 400 people who were given hallucinogens 157 report long term effects that did not resolve, some committed suicide. Heres the axolotl research The axolotl can regenerate multiple organs, including the brain. It remains, however, unclear whether neuronal diversity, intricate tissue architecture, and axonal connectivity can be regenerated; yet, this is critical for recovery of function and a central aim of cell replacement strategies in the mammalian central nervous system. Here, we demonstrate that, upon mechanical injury to the adult pallium, axolotls can regenerate several of the populations of neurons present before injury. Notably, regenerated neurons acquire functional electrophysiological traits and respond appropriately to afferent inputs. Despite the ability to regenerate specific, molecularly-defined neuronal subtypes, we also uncovered previously unappreciated limitations by showing that newborn neurons organize within altered tissue architecture and fail to re-establish the long-distance axonal tracts and circuit physiology present before injury. The data provide a direct demonstration that diverse, electrophysiologically functional neurons can be regenerated in axolotls, but challenge prior assumptions of functional brain repair in regenerative species. https://doi.org/10.7554/eLife.13998.001 This how complex the tracts are Interneurons a possibility, Dr. Abraham comments on this LSD and the phenethylamine hallucinogen DOI are potent partial agonists at 5-HT2A receptors on interneurons in rat piriform cortex. Marek GJ1, Aghajanian GK. Author information Abstract Correlations between 5-hydroxytryptamine (5-HT) receptor binding affinities and human hallucinogenic potency have suggested that 5-HT2 receptors mediate the hallucinogenic effects of lysergic acid diethylamide (LSD) and phenethylamine hallucinogens. Electrophysiological studies have suggested that a subpopulation of gamma-aminobutyric acid (GABA)ergic interneurons in layer III of the rat piriform cortex are excited by serotonin (5-HT) via 5-HT2A receptors. These interneurons have inhibitory inputs on pyramidal cells in layer II. In the present study, we tested low concentrations of both LSD (3-100 nM) and the phenethylamine hallucinogen 1-(2,5-dimethoxy-4-iodophenyl-2-aminopropane (DOI; 0.3-10 microM) on rat piriform cortical interneurons that were excited by 5-HT. Both LSD (3-100 nM) and DOI (0.3-10 microM) excited almost every cell excited by 5-HT. The maximal excitation achieved with LSD and DOI was 39% and 55% of the effect of a near-maximal 5-HT concentration (100 microM). Consistent with a partial agonist action, LSD and DOI blocked the 5-HT excitation of piriform cortical interneurons only at the higher hallucinogen concentrations tested. A specific 5-HT2A receptor antagonist, MDL 100,907, blocked excitation of these interneurons by 5-HT, LSD and DOI, but not by norepinephrine or alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionate. Again, consistent with a partial agonist action of the hallucinogens, intracellular experiments showed that a maximal concentration of DOI (10 microM) induced fewer postsynaptic inhibitory currents than did 5-HT (100 microM) in pyramidal neurons in layer II of the piriform cortex. Based on the present electrophysiological studies, we conclude that LSD and DOI, a phenethylamine hallucinogen, act as highly potent partial agonists at cortical 5-HT2A receptors.

I had dizziness in the beginning as well. I had to lean on things if I wasn’t moving, or at least that made it better. It went away though eventually so yours could too. Give it some time and stay very clear of drugs. You seem to be susceptible to HPPD. Good luck

Delucid is a complete moron. I wouldn’t listen to him and it seems like he is trolling. Thanks for opening up. I thin you should let your family know if they will be understanding, that way you will have help if you need someone there for you. The only reason really to see a doctor is if you feel like you need benzos which is typical if you experience terrible anxiety as a symptom. Other than that there is nothing they can do for you. Lemon balm in my experience was a decent supplement to help with the anxiety.

It’s sounds like yes you do. I do not believe that delucid knows what he is talking about. You’re visual snow is a classic symptom. In rare cases people do get HPPD from smoking weed. Incombanant with Prozac it could have amplified effects etc. I would say yes you do to some degree have HPPD.

Whoa, thanks.