Onemorestep

I’m sorry to hear you are suffering. It is a very tough road we are on. I promise you, however, there is absolutely hope. I experience a lot of good days and feelings today that I never dreamed possible. And I have taken more hallucinogens and drugs than I think most people would dream. Really pushed the envelope. I even huffed a bunch of air duster as a kid lol. it sounds like someone you rely on abandoned you? If so I’m sending you love. I know that sometimes doesn’t mean much when you are where you are. I have had similar experiences with people too. Those who took on my pain and suffering and it was too much for them. That doesn’t mean there isn’t love out there for you. When you are ready for it, and you put yourself out there, it will come.

Unfortunately, alcohol is also just really really bad for the brain... if you must use it then take DHM to help with the toxic aldehydes. That is at least one way to practice harm reduction. I can attest as well that alcohol really retarding my recovery at certain points. I had my first brush with HPPD from triple c’s. I’m sorry to hear you are experiencing HPPD. Fortunately, I was young at the time and recovered eventually. Stay sober. Exercise. Practice as good sleep hygiene as humanly possible (says he at 4:30 am lol). antipsychotics have been known to worsen peoples symptoms. But have also helped some. It might depend on your personal hppd and intensity etc. if you have a little cash you can spare, I highly recommend you get your genes tested. They can tell you, at least pre hppd, if you would respond favorably to antipsychotic medications. It’s not an absolute guide, but it can help. Especially teaching you how to take care of yourself to promote healing. They will send you personalized guides on how to live a healthy lifestyle according to your genetics. https://selfdecode.com

Indeed I often found conflicting information, especially when dealing with anecdotal reports. I always just erred on the side of caution when my hppd was in its acute phase. even in scientific research, there is a lot of bias. Wish it were otherwise. Best of luck in your research

Ah, Im sorry to hear that If its any consolidation it is a very mild hallucinogen through Gaba B receptors I think and not 5ht2a but i really have no idea. Amanita mushroom's psychedelic effects are purportedly through gaba. Z drugs such as ambien also can cause hallucinations and hppd and they work through gaba as well. It is possible these drugs/supplements also have currently unexplored MOA's. Often drug companies only account for the MOA they are trying to push and those they learn about through side effects.. or computer programs designed to imitate binding on receptors. I recommend that before you take a supplement or drug, do very thorough research on google and google scholar and reddit. I use search terms such as the following combined with the supplement or drug name. As you learn more about what you respond negatively to, and their MOA's, you can also search for those terms too. I reacted very poorly to anything that increased acetylcholine for a while, so I always searched " ________________ acetylcholine" to make sure it wouldnt raise those levels. Important to check all three of those places! "bad reaction" "negative reaction" "permanent" "hallucinogenic" "hallucinogen" "gaba antagonist" "excitotoxic" "excitotoxicity" If you search Lemon balm hallucinogenic you'll find some interesting stuff.

Wish I had seen this in june-- Yes i had the hair loss. It really helped my mind. I felt cured. Ruined my body though I do not think i was healthy enough physically at the time to handle keppra. I recommend you get on rogaine asap. Idk why it screws with hair so much but it took me quite a while to return and didn't fully. Rogaine has brought a lot back though. I don't even use it on my head-- Im just trying to grow a beard! seems to help with the head even if applied to the face though hehe. Some people also report lessening of hair loss with b vitamin supplementation. Remember to watch your b6 as keppra is known to effect that

Indeed, luckily I can handle the trace (and not so trace) amounts after 7 years of healing. Additionally, there are a multitude of trace cannabinoids besides cbd in Hemp flower that can make you feel all sorts of stuff if youre sensitive. Fascinating I was not aware of the pooping out component. We know so little about how the endocannabinoid system works. I havent had that experience with cbd, although it does have a tolerance for me certainly. It doesn't do much of jack shit for my physical problems by itself though anyway ahha. Thank you for the info something interesting to note--- I have a friend with mdma induced hppd and he suffered from panic attacks for quite some time afterwards until he took cbd and they just stopped. Recently, they have returned though and are not responsive to the cbd. This could be indicative of what you are describing, but he has also been social distancing for a year and his mother fell ill with cancer so its not exactly a fair case study...

Be careful with high doses of Lemon Balm as it can be hallucinogenic (I dont remember how much is a high dose tbh) Bacopa should be sourced well to avoid toxic metal exposure. As a plant, it pulls these out of the soil, so if your bacopa is being sourced from less agricultural responsible third world countries, this can be a problem. There is almost no oversight or testing in the supplement business that is enforced.

I wrote elsewhere about a negative reaction to Delta-8-thc through overuse. I have taken the steps to recover from it successfully afaik. There are some important things I need to note about my experience with it, both over time and the negative reaction. The negative reaction brought on a host of hppd symptoms. Some were exacerbation of current ones, new symptoms (faded luckily), and resurgence of old symptoms (also gone). Now that things have calmed down, I want to say that delta 8 still continues to effect my life in profoundly positive ways even after complete cessation of drug for 10 days. Some of the worst and older permanent symptoms of hppd have been significantly reduced or faded completely. Most notable being anxiety and disassociation and difficulty empathizing. This is fascinating to me as it’s almost identical to in structure to thc... but I realize in the world of the brain and body that means little. My relief is palpable. Now onto more things of note during my experience. 1) I take a drug called pregabalin for muscle issues but it tends to leave me in a state of kindling for a period afterwords. This is noticeable for a few days, then regresses to the point I don’t notice it for a few more days. However, in that noticeable and unnoticeable state, if I intake cannabinoids such as delta8 or delta9, cbd, or even large doses of cbd I enter a panicked state that lasts until the cannabinoids have left my system or decreased enough for my brain to achieve homeostasis again. 2) I take a drug called selegiline that acts as an mao-b inhibitor in doses under 10mg in the brain (includes accumulated doses in the brain I would expect) and an dual mao-a and b inhibitor above that. I generally take 1-2 mg every few days. Sublingual is much much stronger so I generally just do one mg if that is the route. Sometimes I have been known to take 5mg sublingual, however, when the depression is bad and I haven’t taken it in more than a few days. My experience with taking too much selegiline results in a, I’m assuming dopamine induced, panic attack that will not cease for hours after ingestion. Once my brain readjusts, the panic fades quickly. This has happed only handful of times over the years, mostly during my early days with it. while not comfortable when I screw up the dosing, I am accustomed to the feeling and can tolerate it pretty easily. This generally only occurs when I take 5mg two days in a row. While I cannot prove that this panic is dopamine induced, I have felt almost every type of anxiety that can be caused by the major neurotransmitters due to my prior experience with highly targeted drug withdrawals and overdoses, and that experience is they are quite different in their subjective feelings. (Low serotonin (ssri withdrawal), low or high dopamine (excess amphetamine dose and withdrawal, but more so excess live selegiline dose and withdrawal (more targeted moa), low gaba (benzodiazepine and to a lesser extent glutamate decarboxylase deficient states from gabapentin withdrawal (dirtier MOA)), high glutamate (genetics, ampakines, nmda agonists), high norepinephrine (excess Norepinephrine Reuptake Inhibitor dose). (Important to note that none of this past experience was within the last three years if not seven years or longer). Normally if I’m in the state of kindling, I avoided cannabinoids. However, one day I misjudged how deep in kindling I was. Upon my intake of cannabinoids I experienced the usual high anxiety I was used to in that brain state. In my anxiety fog, I accidentally put a full 5 mg pill in my mouth along with my routine b12 sublinguals. I take a lot bad tasting drugs, so I didn’t really notice the selegiline until I had been sublingually absorbing for 20 min. I figured I might be fine, as I have taken 5mg before. what occurred next was something I had not experienced since my days of using hallucinogens. Very suddenly I entered a state that was identical to a bad mushroom trip. I felt myself losing control of my grip on reality. It felt exactly the same as when I took 6.5 grams of shrooms (I know, I belong on this site clearly) during my foolish youthful experimentation 7 years ago. Had I not been accustomed to years and years of disassociative anxiety, I believe I would have lost it. Through breathing techniques, a lot of calming music, and a call to a loved one I trust, I was able to keep myself from falling over that mental fence, thank god. This state only lasted for about 30 min, before it faded to reasonable levels where I could be alone without spiraling. So what. The hell. Happened. I’ve taken d8 by itself. I’ve taken d8 in kindling. I’ve had selegiline induced panic before.... ...but all combined, it was too identical to hallucinogenic freak out to not mention it here. My hope is, that through this experience, we can identify a key factor in what can cause a hallucinogenic freak out—extremely high levels of dopamine activity coupled with low gabergic activity (and subsequent high glutamate) in the presence of a hallucinogenic drug. Granted, while there are some unknowns here, with the information I have at my disposal I think it assumptive to chalk up to coincidence. It is important to note that I have genetically EXTREMELY HIGH dopamine levels (current baseline dopamine activity is another story) . I metabolize it very slowly. It may seem ironic that I take dopamine inducing drugs as part of my protocol, but there are realistic reasons why I do that aren’t pertinent to this conversation and require their own lengthy post. I only relate this genetic information because when I accrued hppd, I was not taking dopaminergic drugs but I might as well have been since my brain state is similar to someone on a 5mg dose of adderal (I’m guessing, I’ve never taken adderal without these genes, using this example for others reference. When I was prescribed it my reaction to amphetamines was more on par with what I understand the potency of methamphetamine is. But to be frank, at least one of my hyper dopamine genes is exceedingly rare with under 1% reported (as much as this disorder go figure...). I also have naturally high levels of glutamate and low gaba. This is due to a gene mutation that effects the enzyme that converts glutamate to gaba, resulting in a double whammy of high glutamate low gaba. With less being converted over time than someone without the mutation, any drug that increases glutamate is liable to push the limits of those glutamate receptors faster than someone without the mutation taking an equivalent dosage. If I am correct, part of what can induce hallucinogenic panic, and possibly hppd through out of control glutamate via agonization of 5ht2a receptors (downstream effect), is a combination of low gaba, high glutamate, high dopamine, and a hallucinogenic drug. If I had the ability to do experiments without ethical limitations, I would induce this state in subjects and give them dopamine antagonist drugs, nmda blockers, and possibly MAYBE something to increase gaba BUT NOT by allosteric modulation. Maybe not at all, as gaba can be strangely hallucinogenic in its own right. I suspect through anectodal reports of concurrent affliction of hppd through the use of hallucinogens in the same period as benzodiazepine drugs that the mechanisms in place on these receptor do not always respond well to change in this highly malleable brain state. Obviously though, that is impossible and I would never ever conduct such experimentation and neither do I endorse anyone trying this on themselves. It is only through my mistake that I even stumbled across this possibility. I reiterate that I was really on the fence for about 30 min and believe that had I tripped over, I would have difficulty erasing the profoundly deep long term neural pathways such a state might result in. Now, weeks after this event, I experienced the “negative event” that I referred to in my other post in the discussion forum. What was interesting is, in that brain state, I was unable to take selegiline at all without inducing panic. I stopped taking it and did not experience any withdrawals as I usually do if I stop suddenly (excessive sleep, depression). I theorize that part of what causes the emotional discomfort of hppd may be excess dopamine (at least in certain brain regions if not all, possibly high in places and low in others), and my brief brush with it again cause my brain to temporarily enter a hyper dopaminergic state. Once the negative event passed (took about a week of no use age of delta 8 or any cannabinoid), I was able to restart my selegiline protocol and responded favorably. Now, why traditional dopamine antagonist tend to worsen hppd symptoms in many remains a mystery to me. This may be because, while high dopamine may be bad in hppd, something else is broken that causes those drugs to have a bad reaction in patients. Or that, as I mentioned earlier, there may be a combination of low and high dopamine in different brain regions. It is important to note that while rare, some people with hppd do respond positively to antipsychotics and I have had discussions with some. I imagine symptoms and treatments outcomes for this disorder are HIGHLY genetically predisposed and are combination of unique brain insult, genetic propensity for imballances in neurotransmitter and receptor function, and (see post in discussion) possibly altered Endocannabinoid functioning. Part of the reason I am posting this is so other who know they have these gene mutations can understand their reactions. But most importantly, if you take anything away from this post it is this— I am WELL on my way to “recovery” from this disease. It has been 7 and a half years since my last dose of traditional psychedelic. While my experience with delta 8 has been positive, I do not believe anyone who is still in the early stages of hppd will respond favorably to it. In fact, I believe quite the oppsite. This belief is due to my theory that hppd manifests itself as brain injury and other some other dysfunction with the Endocannabinoid system. Delta 8 may help with the other dysfunction in the Endocannabinoid system but may be contraindicated for the brain insult. I imagine it would be very uncomfortable at the very least if what I have written here is even partly true. While I could be wrong on this, the ability to tolerate d8 early after hppd onset, I can only go off of what I know and can theorize. Luckily, there is a huge community of people out there ingesting this substance as we speak, many of which are poly drug users and no strangers to hallucinogens. We may see anecdotal reports similar to mine (I have already seen one post of someone stopping habitual daily heroin and benzodiazepine use cold turkey through D8 without discomfort) so I ask you all to keep your eyes out. If I was to guess based off my own experience, a good indicator for if you can tolerate D8 might be if you still have a positive, or at least not horribly negative, response to CBG/delta-9-thc and CBD in that order. I experienced several levels of hppd 7 years ago, before the final wham bam full fledged hppd that I was left with. My response to cannabinoids went from positive to negative as I went deeper down that hole. Like many I didn’t even know what hppd was until too late. I wish I knew whether people would respond positively to delta-8 early on in this disease, as I and you all know how horrible it is. I would give anything to help those poor souls. But we, I, must endeavor to do no harm, and can only suggest that those well on their journey with hppd, and are suffering in the “chronic” phase to try this drug. Lastly, if I am correct about my theories on the cannabinoid system, then it is also possible that my positive reaction to D8 may just as well be a negative reaction in others. (THEORETICAL) This would depend on the specificity of ones cannabinoid dysfunction (quite literally the shape of my receptors may be disfigured in a different way than yours). The only other cannabinoid I was taking that I still cannot tolerate now, in addition to d8, is CBG where before my reactions to it were overwhelmingly positive—if short lived. While this is not a concrete jump based off of any evidence but my own subjective experience, if you respond well to CBG you may respond well to D8. On a personal note, I would prefer to not have to use delta 8 again, especially since I do not know how long I must abstain from it before it will be tolerable again. However, it is the only substance I know of that helps me with the muscle spasticity I was left with after my first brush with hppd (pregabalin requires long abstinence periods for me). At times, this spasticity can be so great that it pushes my bones out of alignment, and the pain can overwhelm my logical reasoning. I might feel forced to try it again. I will admire too—D8 is pleasurable. It would be nice from a social and relaxation standpoint to be able to use it in reasonable amounts. So far, for the time being, I wish to find other modalities to treat my spasticity and other less risky substances for relaxation. Had I not consumed D8 in excess, I do not believe I would be forced to make this choice, but I cannot say that for certain this reaction would not have happened over time even with a reduced dosage. The same way I believe if I had just used hallucinogens responsibly they could have potentially benefited me over the course of my life but may have still resulted in hppd even if micro dosed. Abrahams data on onset after x trips comes to mind....although I consider that data to be more indicative of the role of other variable environmental/neurological factors not yet understood than the idea that hppd is magically random and one can accrue it for no reason on the 50th trip. In my first post in this thread, I tried to conceal my intense joy at this return in brain functioning as to not cause false hope in others. It is my hope that this effect persists over time. I will endeavor to continue to update this thread as time goes on and update the community as the the permanence of these positive effects. I had never gotten used to living without my full depth of emotion. I’ve tried so so many different chemicals to try and bring back this ability to feel. I had gotten close, maybe 90% there, but I honestly had come to the conclusion that brain damage was the only possible explanation, as even when I was able to induce my most positive emotional state post HPPD through those chemicals, I found there was something distinctly missing. Something that I do feel now. Something beautifully human. There is so much we do not know about HPPD; do not give up hope, brothers and sisters. All my love, oms

If you are interested in raising your dopamine levels, I recommend selegiline for that. It is much gentler.

Your response to sinemet will largely depend on your genetics and if there is an increased need for dopamine because of your specific hppd. Especially if you are talking about how it might make you "feel". Sinemet improved my symptoms a lot but tolerance accrued rapidly and it gave me a (not the fatal kind) skin rash that took quite some time to resolve.

Hey there! Good to hear from you again. My experience has been similar. I decided to go full stoner for 4 months though haha. Honestly I don't recommend it if only because it makes the memory so much worse even for those without HPPD! If you try a chemical and react okay, just monitor yourself and don't increase dosage :), take breaks and use infrequently. But most of all remember what all of us have learnt the hard way--- I've missed the world and the little things the most. Not drugs. I've missed the pleasant feeling of walking through the park on a sunny day, or enjoying my favorite meal with friends, or being captivated by a subject or art form. Those are the things I yearned for in the throes of HPPD, not the drugs haha. Enjoy your new lease on life brother. Take it all in :')

The Epigenetics of the Endocannabinoid System "Recent evidence has revealed that ES undergoes epigenetic modulation by alcohol, diet, stress, smoking, exercise, or drugs [44,45,46,47,48,49,50,51,52,53,54,55]. The main targets appear to be the genes encoding for cannabinoid receptors, especially CNR1 which encodes for CB1, and the hydrolysing enzyme FAAH, with subsequent alteration of endocannabinoid signalling or tone. The detected epigenetic mechanisms involve changes in DNA methylation (both global and gene-specific), histone tail modifications such as acetylation, deacetylation, or methylation, and the production of specific miRNAs in different brain regions, peripheral tissues, and cell lines. Of note, epigenetic changes in the ES have been detected in several pathological situations such as Alzheimer’s disease, glioblastoma, and colorectal cancer (CRC), and the ES is the target of several ncRNAs [56,57,58,59,60,61,62,63,64], (details in Table 1)." https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7037698/ As I mentioned before, I have a gene mutation that increases the "digestion" of my endogenous endocannabinoid--The hydrolysing enzyme FAAH is controlled by that gene.

NAC may bind to Methyl-b12 rendering it useless. Its pretty complicated but interesting stuff. If you have problems with creating methylb12 from regular b12, NAC may make that issue worse. It can for me if I'm not careful. This is from a guy I followed in treating my own genetic issues: Fred: "Now that might depend on how one defines “B12 deficiency”. NAC is a precursor to glutathione. It appears by pragmatic trial that if NAC is the limiting factor in making more glutathione, it can temporarily cause temporarily more glutathione. A popular belief in “detox” symptoms; “NAC detox” symptoms and/or “glutathione detox” symptoms, which are the same, are a percentage of people that respond that way. This time of the trial was 10–11 years before my micronutrient lithium trial. It was at the time of recovering from the glutathione damage that I developed damage from copper deficiency and could no longer have the 5 minute mecbl startup., I still had some nerve healing startup from 10mg injection, but not like before. The N=10 glutathione trial we all decided to try to find the clearly missing something. All 10 were at least a year into intense Active B12 healing. The reasons we were each deficient all were varied, from vegan to genetic polymorphisms. We had all been pursuing something that would heal us for years or mostly decades. One person said she was one of the Incline Village CSF folks. All 10 had “return of symptoms” that are popularly called “glutathione detox” that had been previously present when they started MeCbl, AdoCbl, L-methylfolate and L-carnitine, 1 or more years before. I will describe my experience. I had previously done a serious of injections and the colorimetry of urine at concentration in urine from 1 to 100 mg, and another with 3 injections per day up to 60mg for each of 3 injections, 180 mg/day. Another man did a series of IV infusions to 500 mg of MeCbl. His statement was that it gave him “lurid” urine for several days. In our experiences there is a maximum kidney excretion rate somewhere between 5 to 10 mg/hour or perhaps more. I was stunned with the first dose of glutathione and a 10mg injection. In an hour the B12 was making my urine “lurid”, like 60 mg subcutaneous injection of MeCbl. Instead of making an orange shade, it was intense red. A 2011 review of CBL-C disease it was stated that a characteristic symptom was that glutathione caused “catastrophic b12 deficiency. As the ongoing glutathione kept the B12 pouring out it turned out that active b12s disappeared from somewhere to be excreted and about 3 weeks in I started having a demyelination damage. By 6 weeks all 10 were having demyelination and everybody stopped. I had stopped glutathione precursors as soon as I recognized demyelination and other methyltrap symptoms and told the other 9 all about it. They all had the symptoms to some degree up to demyelination. So more glutathione can be made by starting various singular precursor or precursors and it may be the quantity being made beyond what can be used by the body in normaL ways. Methyltrap occurs when either no mecbl or cob[ii] i s in a place for starting the cell and there is cell making failure with l-methylfolate deficiency symptoms as it is flushed from the cell if there is no active B12 at the moment needed. So for the l-methylfolate lacking symptoms is usually caused by a bottleneck caused by a bottleneck in MeCbl or COB[II] lack becasue that all becomes glutathionylcobalamin and that is not reactive." --- No you're not being a jerk. A lot of these things I take could be considered highly risky and dangerous. I encourage everyone to always do thorough research on a drug before ingesting it. Pramipexole can lead to daws, Kava can lead to liver damage i guess if you really fuck up your sourcing... I get my liver tested frequently enough and there has been no change since kava use... However I should note that early on in my hppd, within the first year that is, kava would cause an increase in anxiety if consumed for more than three days in a row. I did not consume it again until many years later and it was very beneficial to my mental health and, I suspect but cannot prove, brain healing. Kavalactones are fascinating chemicals and can provide a large array of benefits to the brain. It has comparable effects on glutamate receptors as memantine, which really says something to the potency of it as a medication. Trust me if the alternative wasn't lay down and die I wouldn't have trialed any of these things. Severe HPPD can certainly push a person to try things they never would... Do I have other genetic disorders? I guess that depends on what you consider a disorder. I have low glutamate decarboxylase activity (decreased gaba production), increased enzyme activity metabolizing my endogenous cannabinoids, and some pretty high tyrosine hydroxylase activity (dopamine production). These aren't considered disorders in of themselves... but they can certainly lead to negative feeling. low GAD activity can lead to PTSD, sleep disorders, and other issues. It also will make one think faster as ones brain would lean towards glutamate dominance. ...Those are just two off the top of my head. Some people have too much of these enzymes and that comes with its own array of pros and cons. What I would love to know is if there is a genetic component to HPPD and if so is it one gene? or many? I suspect this is a spectrum disorder that includes input from many genetic and environmental factors. But what do i know hehe Intranasal insulin has a wide array of positive brain effects and relatively good safety profile with long term use AFAIK. I haven't read up on it since I started taking it but there was a long term study called the "sniff study" or something in which it was used for over a year daily: https://www.lostfalco.com/intranasal-insulin/ oh and as for the piracetam thing-- there is some evidence for oxidative stress to the hypothalamus. I lost all sex drive, hunger, thirst, and ability to have normal sleep for quite some time after usage. Negative reactions to racetams such as piracetam seem to be exeedingly rare. Back when I was burned, I could only find about 100 reports of it and millions and millions of people take it. But let me tell you I have never experienced such pure terror for so long.. years. Anyhoos HPPD is so individualized in its symptoms and reactions to medications. Theres a lot of trial and error that goes on. And a lot of your responses can change over time. I'm simply suggesting things that have worked for me in the hopes maybe they will help someone else. They also may hurt someone. But if we don't suggest that which has helped what are we doing here?

The following is a message between myself and a member of the forum. Its pretty free train of thought in its organization but they is the first time I've actually written this down. Its all just theories, but it makes one think... If anyone has anything to share related to these topics please don't hesitate Boy I wish we all had access to our genetics... https://selfdecode.com currently $387 for lifetime membership and dna test kit for anyone that is interested. I have made great strides in my wellbeing using the knowledge about how my body works one can only attain through this type of testing. ******__________________________________________________________***** hey ive had some interesting ideas about how our CB1 receptors might play into the etiology of HPPD. Apparently they are malleable. My reaction to cannabis and other cannabinoids has led me to feel like my receptors are more like clay than rubber. Apparently cb1 knockout mice show decreased gaba a and b levels in the brain. https://pubmed.ncbi.nlm.nih.gov/20142297/ Its just a theory, but I imagine if you had an incident in which you somehow decreased cb1 activity to almost none even for a few moments you might suffer a widespread excitotoxic event. This helps me understand why HPPD symptoms are so incredibly varied. Mine came with visual, cognitive, and physical symptoms. It did feel as if my entire brain took an insult. I recently had a negative experience with a cannabinoid called Delta-8-thc. Initially, it removed the latent feeling of "crazy" thats been with me since i got hppd. This effect continued after stopping the D8. It was really a godsend until very suddenly, it turned on me. Suddenly developed a headache and strong return of HPPD symptoms including visuals. Its taken about a week of stopping D8 for things to calm down. I imagine if I push it more, as I did with traditional hallucinogens, the effects will become permanent. Up until this point, I considered myself as healed from HPPD as I was going to get (I could somewhat tolerate cannabis again without the PANIC that it used to cause after the final HPPD onset 7 years ago, still haven't recovered the iq or memory however.) Now i cannot tolerate d8 anymore. Each time i've taken it, and accidentally taken too much not realizing my reaction to it was changing, the threshold for how much is too much became less and less. I imagine my receptor is already been pushed into a shape that accommodates d8 and not my natural endocannabinoid anandamide which might lead to poor binding. Changing a receptor shape isn't a novel concept,,, the change in receptor shape on gaba-a receptors during benzodiazepines withdrawal, and subsequent poor binding of endogenous gaba, is what causes the negative symptoms. Every attempt to take d8 has started fine, but then when I past the threshold it resulted in rapid tbi symptoms including, most alarmingly, forgetting how to trill up and down the piano which learnt years ago. These symptoms have responded very favorably to my TBI protocol (high dose epa/dha, memantine, naltrexone, bps-157, nsi-189). So the symptoms of this type of HPPD would be two fold-- 1) Diffuse Brain insult 2) change in receptor shape and subsequent poor binding of endogenous cannabinoids leading to varied cognitive and physical changes. Plus a feeling of being permanently tripping... . Over time the cb1 receptor partially returns to its prior state but never completely. This leads to less gaba in the brain and an almost pre-seizure brain state. (I also have poor glutamate decarboxylase activity (enzyme that produces gaba) genetically which adds to my propensity to acquire hppd imo) Ive been looking at my genetics as it relates to cannabis-- apparently the enzyme that metabolizes anandamide, the body's main endocannabinoid, is overactive in me. I wonder if this might play into a hypo-cannabinoid state --> decreased gaba a+b --> propensity for acquiring HPPD symptoms. As HPPD can be caused by so many different things, I imagine there may be many ways to arrive at the same end result. Symptoms would depend on the specificity of the negative neurological event in different brain regions. This helps me understand why the symptom set for hppd is varied and responses to drugs are even more so. There doesnt seem to be much rhyme or reason to this beyond "avoid stimulants". I theorize that D8 nudged a part of my cb1 receptor back into its proper shape. I have experienced a return of emotions that I have not experienced since the onset of HPPD. Mostly relating to decreased dissociation and increased empathy. This was something I had only been able to achieve with drugs such as baclofen before. ______ I am also starting to research the interplay between methylated vitamins and the cannabinoid receptors. Apparently they interact in some way. I had one neurological event that was quite similar to this one I am experiencing now 2 years ago when I became rapidly b12 deficient. I suspected minor demyelination. Visuals worsened and I felt on the verge of a psychotic state I associate with psilocybin. The striking resemblance to how that felt and this leads me to believe it may be possible that over agonization of cb1 receptors, in a specific way, may reduce the body's capacity to utilize methyfolate and b12. Apparently, Methylfolate increases the activity of cannabinoids at cb1 receptors. I have a gene mutation that inhibits my ability to produce methylfolate. This, Im theorizing, would encourage, even more, the "hypo-cannabinoid state". But its all just bioscience theory rn. Not sure how to even test it tbh. _____ All the progress I have made so far has been focused on taking things that help brain injury. They have been the only things that have made lasting reasonable differences. High dose fish oil, nsi-189, naltrexone, memantine, etc etc. While I have made amazing progress in that direction, it still didn't help support the return of a function endocannabinoid system.... --- I am having the D8 I bought tested for toxins etc. I expect it to be clean as I've had this reaction to many different brands. There may be other cannabinoids present in the d8 though that I am reaction to. ____ This post is really to help identify a possible role cannabinoids may play in the etiology of HPPD. Many of us have used them during out trips and, while it may not be of sole responsibility, it's good that we don't forget that. Another substance many of us used within a few days of acquiring hppd--- benzodiazepines. I've always wondered how the brain comprehends homeostasis under the influence of hallucinogens and weather a combination of drugs and them could screw with that... thats for another day though. ___ Since acquiring HPPD I developed what appears to be some sort of variant of stiff person syndrome. This is a brain state associated with very low levels of gaba. My symptoms would be considered mild for stiff person syndrome, as the full blown one involves tightening of the muscles that is so intense it can fracture bone. I just have insanely tight muscles and fascia that is pulling my spine and ribs out of alignment. I am meeting with a myofascial therapist soon and will be taking tests for glutamate decarboxylase antibodies soon. I do not suspect I have them however, as that is only one way to arrive at the brain state necessary for the symptoms of SPS. I suspect all you need is severely hampered gaba a and b production, both of which I may have from the theories I've listed earlier. god glad I wrote that down. Its just been swimming in my head for the last three weeks. Im running on almost no sleep from the stiff person bullshit so excuse the rambling nature of the post. Some light reading: The dynamic nature of type 1 cannabinoid receptor (CB1) gene transcription https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3525862/

Hi Bill! A lot, in fact all of the ones I have taken, have come with their ups and downs for me. I feel like it is helpful for now to write briefly as it would take more time than I have at the moment to go into depth on why I personally believe any item is "good" or "bad". So heres that and some more-- NNE: No Noticeable Effect NA Semax Amidate: NA Piracetam: BAD BAD. There is a very small chance this stuff will melt your brain. Of course my hubris didn't allow me the foresight to understand that could happen to me (the irony being AGAIN duh)... If it helps you it can be a wonder drug. If it melts your brain well.... suicide becomes a very real and probable option in a way I never understood during even the worst of my hppd from LSD. Aniracetam: BAD BAD Fasoracetam: NA Oxiracetam: BAD BAD Phenylpiracetam: BAD BAD NSI-189: GREAT BPC-157: GREAT, currently I only know of 4 people with hppd who have tried this--Myself and three others. Three had extrememly positive reactions and one had an extremely negative reaction that improved over time. This must be carefully sourced ESPECIALLY if injected. Forskolin: NA, good for increasing cyclic AMP. Alpha GPC: NNE Uridine MPS/Triacetyluridine: GOOD, i must watch mood for excess choline symptoms Vinpocetine: NA Bromantane: NA Agmatine Sulfate: GOOD, may enhance a lot of other drugs Sulbutiamine: GOOD, bad for people with severe methylation issues ALCAR: GOOD, bad for people with severe methylation issues NAC: GOOD, bad for people with severe methylation issues L-Theanine: YMMV Lion's Mane Mushroom: GOOD (If used chronically causes sever depression for me. Stops upon taking it after 1-2 days) Ashwagandha: GOOD CBD Oil: GOOD Bacopa: GOOD Rhodiola: NNE Ginkgo: GOOD Phosphatedyl-Serine: NNE Resveratol: NNE Pterostilbene: NA I also currently use many of these • Selegiline • High dose EPA/DHA • • Pramipexole (can cause DAWS in roughly 50% of users) • CBG (cannabinoid, use with caution preferably well into recovery) • CBN (cannabinoid, use with caution preferably well into recovery) • Delta-8-THC (cannabinoid, use with caution preferably well into recovery. If tolerated only use smallest dose possible with break periods) • Memantine • Naltrexone • Selank • Kava (source this well and get your liver enzyme levels checked regularly) •Intranasal Insulin (highly recommend) • Frequent Aerobic Exercise • I purify all my air with hepa or hyperhepa air filters • I keep my carbon dioxide levels in good range where I sleep. • I keep my spine straight including neck (its amazing what proper posture will do for mood and anxiety) • I treat my genetic mutations that result in negative physical and mood effects as to encourage a more stable system in which healing can occur.

How are you feeling? Are you saying that you u ate a non hallucinogenic mushroom and are experiencing cognitive symptoms? Dude that sounds like you got poisoned go to the hospital. Neurotoxins are real things... I don’t eat mushrooms people pick in the wild unless they are very experienced and even then I eat at my own risk. Very sorry you are experiencing this.

Hello everyone! I want to start off with thanking this community for being there for me for the past 7 years. I could not have made it without all of you.... ...but I am still suffering. And many of you are too. how do we fix this issue? first, we need to analyze why we haven’t found a solution yet. Because that is the real problem—not what is wrong with us- but why can’t we find the answer? Why won’t anyone help? i believe the answer to that question is two fold: 1) lack of interest due to “Rarity” of this disorder (in reality I think we are just the worst on the spectrum that is this negative neurological event) 2) lack of data so how do we spark people’s interest? Because it’s all about finding how to get the people we need to feel like they want to be engaged. We solve both problems by solving just #2. Like most things in our digital age I believe the answer is DATA. If we can harness the tech at our disposal now, which was unavailable even a few years ago, we can start to garner more interest in this condition. We have the platform and user base already to drive engagement from scientific communities. Usually you have to FIND these people out in the world if you want to study something. Genetic testing has become readily available to the public. Companies are starting to amass a large enough data set that we can use it to our advantage. We need to start compiling our genetic info and comparing it to each other. This will enable us to find commonalities in systems in which our brains and bodies operate. Once we can find a commonality, we can garner interest from the scientific community better. I personally think we should use Self Decode platforms, as I have found their tech to be suited for this. ———— So where do we go from here? What can you, the unlucky soul reading this post, do to help? 1) get your genes analyzed. You only need genetics NOT ancestry. 2) upload the data into self decode. 3) share data with each other. 4) Find genetic commonalities between each other’s genes 5) compile data, push to research systems around the country to garner interest. COSTS cost per user: roughly $350 one time fee. $100 for genetic raw data and $250 for lifetime membership to self decode (I think this is still offered; this is what I paid total). It feels like a lot of money. And it is. Especially for those of us who are struggling to hold down jobs and make ends meet because of this horrific disorder. But think of it this way—this would have cost millions of dollars to do just 20 years ago. It wasn’t possible at all then. We have been given an enormous opportunity today. I hope this post helps encourage dialogue and action. No one is going to save us; We must be the catalyst for healing. If not, this idea is at least here forever should someone one day be brave enough to pick up the torch. Love, OMS

Jay I think you are on the money with your thought process. 2mg clearly is bringing some brain function into normalcy but adversely effecting other regions. As we get better at targeting these brain systems for therapies I imagine we will have better options.

About a week ago I began supplementation with Delta-8-thc. I can not recommend this to anyone based off of scientific fact or knowledge as there is a severe dearth of research on it. I have never been able to handle the anxiety caused by cannabis but have always been drawn to it. When I heard of an anxiolytics cannabinoid that was 60% as potent and great for pain, I hopped on board. I will say that the most unexpected thing is within a few hours the underlying feeling of psychosis that has been with me since acquiring hppd severely lessened. It felt like... a key was put into the right spot. I’m posting this here mostly as a record. I really cannot say whether this is a good or bad thing for people with hppd as ymmv and I believe responses to drugs differ depending on what stage of recovery you are in. I have no idea if I would have had this Positive experience with D8-thc if I experimented with it in the first year of this condition. I will say, however, that it is an incredibly relaxing form of cannabis and feels very much like it effecting GABA B (and a) in some sort of fashion but not increasing concentrations of glutamate the way delta9 does. Anyway, hope this helps someone down the road looking for an answer to something.

I’ve tried a lot of these and I can say kava can be good. But a lot of these will downregulate your receptors over time. Fasoracetam may be different. But I don’t touch racetams... exercise or yoga are your best bet. Yoga has been shown to increase gaba by a lot. Exercise decreases gaba while you are doing it which causes the receptors to upregulates and be more active when you aren’t exercising. This isn’t something you’ll gain tolerance to as well which is great. meditation has also been proven to increase gaba. i wish I could find a good medication for this but I haven’t yet.... except kava I take quite a bit of it. Only issue is it’s a pain in the ass to prepare and tastes absolutely horrible. You’re supposed to fast etc etc... I like to eat a small meal and then take this: https://www.amazon.com/Polynesian-GoldTM-70-CO2-Extract/dp/B06VX3SKNF/ref=mp_s_a_1_1_sspa?dchild=1&keywords=kava+10g&qid=1588131615&sr=8-1-spons&psc=1&spLa=ZW5jcnlwdGVkUXVhbGlmaWVyPUEzT0xQRjlVSlhINldLJmVuY3J5cHRlZElkPUEwODc5MDc4M0FOTTZKUVhNWDAxNyZlbmNyeXB0ZWRBZElkPUEwMjg3NjQ2UFRMRlNXVk9NQkVIJndpZGdldE5hbWU9c3BfcGhvbmVfc2VhcmNoX2F0ZiZhY3Rpb249Y2xpY2tSZWRpcmVjdCZkb05vdExvZ0NsaWNrPXRydWU= It’s much smoother than traditional brew. You can also put it in capsules for easy use.

Yes you can.

Hey there!! i can confirm that when I was earlier in my recovery that I had to do no fap to feel well enough to be functional. If I masturbated I would feel bad for about a week before things got better again. In fact I had to abstain from orgasm during sex as well. I don’t think it had anything to do with porn or the method of orgasm and more to do with hormones and hypothalamic activity. I’ve had a feeling for a while that many of us have issues concerning the hypothalamus. Many of us share symptoms that point to uniquely and severely messed up circadian rhythms. i unfortunately saw no changes in visual snow from no fap. I think the longest I went was 40 days or so. I think that visual snow does not share the same etiology or brain region activity as the rest of the symptoms of hppd. I don’t consider myself to have active hppd anymore after 6 years (although it can re trigger and has recently for three days from flexeril) and I still have visual snow. It’s just a persistent part of life now. Perhaps one day it will recede but the healing schedule for it seems to be far longer than the mental symptoms I had.

The capsules tend to be in effective and sometimes dangerous. It’s important to get a good supplier who only uses roots or “noble” kava. Extracts and pills often contain “Tudei” or “two day” kava which is made from the leaves and plant above ground. These parts of the plant contain toxic chemicals to the liver. that being said I’ve tried the pills and teas and they were very ineffective. The teas especially don’t work as kava is not water solvable and must me kneaded by hand to release the active ingredients called kavalactones. I usually take 2-4 tablespoons and knead it in a mesh bad in warm water for 15 min. I mix in coconut milk, cinnamon, vanilla extract, and stevia to mine and it makes it much more palatable. I should mention that I’ve tried kava twice—once a year after getting hppd and once again 6 years after. The first time if I drank it three days in a row I would get a strange type of Constant anxiety so I stopped. 6 years later I noticed that one month into drinking it I got the same anxiety but as an attack that would last for thirty minutes the day after drinking it. This time I pushed through it because the benefits were so profound on my psyche I didn’t mind. The anxiety stopped after about two weeks. What I’m saying is I think there can be some rebound anxiety with it but it’s transient and will abate after continuous use. kava should be cycled though I think. I did better with it when I did 1-2 days on and 1-2 days off. Once I used it everyday then tolerance set in and eventually I got little immediate effects from it... however the next day antidepressant effects remained so I continued to drink it for some time until I began a new medication that interacted with it (extreme nausea and vomiting ) and now I can no longer tolerate it. shame to hear about the naltrexone! It’s a very safe and benign drug. You may be able to find it on the internet but I don’t know the legality of that where you are. In the United States, it’s technically considered over the counter and legal to sell without a prescription.

I like to vape hemp flower. I find it very relaxing and much better than taking oral cbd. It’s cheap online too.

5ht2a—> glutamate excitotoxic event time and healing my dude