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Personal Hypotheses surrounding HPPD


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The following is a message I wrote to a user. Please excuse any misspelling or grammatical errors; I wrote this on mobile.

 

——-

 

— the pathogenic hypothesis.

 

only recently there was a study done on pigs that showed psilocybin altered many of their neuro immune genes; some for a few days and others persistently. 

 

usually, infections of the pns stay there and are fiercely deterred from entering the cns. When they do, however, they can cause a symptom set that is not only different than that of a patient suffering from a pns infection, but much more severe.

 

an example of this is mononucleosis. In children, there have been reports that it can get into the cns. Imo, the reason this doesn’t happen often in adults vs children is children have different immune systems. Once it does, it can create a syndrome called Alice in wonderland syndrome, which is characterized by the growing and shrinking of objects. I have had Alice in wonderland syndrome, and I can tell you it is indistinguishable from hppd visuals from psilocybin (growing/shrinking). It is interesting to see non drug induced hppd symptoms. 

 

so, when a person takes any hallucinogen there is a change in pns and cns immune functioning just due to its effects on the 5ht2a system. They are powerful immune suppressants and immune modulators. Lsd even causes a 50% decrease in 5ht2a function after its initial agonization in the days following. 

 

why is this so interesting? Well Abraham did some studies interested in why it is patients can do hallucinogens dozens of times and not get hppd and that others can do it once and get it. He discovered that there were thresholds— if you do it 10 times you breach a threshold and increase the likelihood after that. 20 times. 50 times. 

 

when you apply that to the idea that one must have an active infection and do the hallucinogen at the same time to get hppd, it really becomes interesting. One could do it many times and still not get it. But one time, unbeknownst to them, they had an EBV infection, or a few others I will get to, that was only loosely controlled, like all opportunistic viruses, bacterias, and fungi, spread and even get into the cns. This could happen during the trip or even in the days after— which helps explain some of the sudden onset in the days to weeks following the trip. The immune system is not functioning correctly to fight the pathogens. The hose is unaware that they are biologically different than the other times they tripped and don’t know it.

 

wouldn’t someone know they are sick? You would be surprised. Many people get mono and don’t know it. I have extremely bad lymes disease and I don’t have the physical symptoms that are traditional in lymes. I have plenty of neurological symptoms however. Same with bartonella— primarily neurological. 

 

now, there are no studies on this. But I just talked to someone on Reddit who got hppd by taking psilocybin during their active bartonella infection. They had a bad time and got hppd. They also had a terrible reaction to cannabis with bartonella, which I have also experienced.  

 

what’s so special about bartonella? Well for one it is exceedingly prevalent in populations and people have no idea. 30% of cats have it. It likely can be transmitted sexually (officially you will read this doesn’t happen however, through asking to experts, I was told that patients who were sexually active and both test positive have more similar bacterial strains on average than they would simply by traversing the same physical environment). Ticks also carry it along with most mammals. Most people get it and can get the infection in check within 4 months but a subset of the population cannot and it takes them years to get it under control without therapy if ever. 

 

in terms of what bartonella does to the brain, it seems to be extremely excitatory. Or rather, it removes the brakes to stop excitatory activity from going unfettered. Bartonella patients require high doses of benzodiazepines— like really high— to become sedated. I was able to drink 24 beers on 6 mg of clonazepam when bartonella was in my system and I woke up 6 hours later fully conciousness with working memory. A feet even the most rambunctious of fraternity mates couldn’t achieve. It is simply not neurologically possible. I was told by a psychiatrist who works specifically with bartonella patients that the highest dose he has seen to achieve symptom relief was 20mg of clonazepam. Amazing. Now if this doesn’t directly cause hppd it would severely exacerbate it and increase the progression through further increasing excitatory tone in the brain. 


not all people with hppd have bartonella, I would think. It just would make getting hppd much more likely due to its disinhibition of brain chemistry. This same level of disinhibition could be achieved through other measures and would similarly increase the rate of hppd, imo, but not many as badly as this one as it also brings in the immune system and messes around with it. This effects the neuro immune system too— which is a much longer conversation and I have written about it this past year on this website. The interplay between neurological function and cytokines is fascinating — particularly interleukin-1b which can alter the brain into an increased excitatory tone via cb1 and gaba a. One thing this leads to panic attacks if it get bad enough, basically.

 

—-the excitatory hypothesis:

 

ampa, sv2a, neurological rewiring, excitatory tone of the pfc, and mtorc1.

 

it has recently been shown that psilocybin requires the pfc and creates an increase in excitatory activity (glutamate). This is one of the proposed mechanisms that it helps with depression. And it makes sense. But glutamate is a double edged sword and must be kept in check with gaba— some of the first info solo and educated neuro buffs learn. 

 

additinally, there was a pig study that showed an increase in sv2a activity— which is connected to gaba a activity and is what one of the most totable drugs to help patients with hppd take— levetiracetam. Increased sv2a is implicated in excitatory neurotransmittion in epilepsy.

 

https://pubmed.ncbi.nlm.nih.gov/33467676/

 

in terms of ampa— see my most recent posts that talks about them and how various hallucinogens such as lsd, ketamine, and psilocybin effect this receptor system and how the typical drugs that help or exacerbate fit into ampa—

 

—and try, at the same time, to connect the dots between an increased excitatory tone, ampa agonization, increased sv2a activity, increased mtorc1, and pathogenic infections that can increase mast cell activation and thus increased glutamate release. Do you see the perfect storm? 

 

There is hope though. Even if we have lost ampa function there may be a road to salvation. I have only recently started to research ways to control, improve, and create ampa receptors. This is the first thing I have found that may help us: 

 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4201273/

 

it should be noted I believe one must have control over everything I have said may be increasing excitatory tone before establishing new neurons or bringing about new neuronal excitatory capabilities. Hypothetically, one would just be creating new ampa receptors that would be out of control. I couldn’t say. I am not versed well enough in this to know and tbh— I don’t think anyone is in the context of everything I have written here.

 

—-the immune component: mast cells

 

in patients with pathogenic infection, we see an increase in mast cell activation. Even without it, from speaking to the foremost minds the subject, they say mast cell activation syndrome is a spectrum disorder that effects up to 18% of the population. It is not a question of if people with hppd have mcas— it’s how many do if not all.

 

how does this relate to neurological symptoms? Especially the excitatory hypothesis? Well that gets us into the world of mast cell mediators— histamine being the most noteable.

 

usually, people associate histamine with just allergies. But it is also a neurotransmitter that can elicit the release of glutamate— and this is the step by step process.

 

neuronal mast cells release histamine that then activated microglia/astrocytes to release glutamate at an uncontrolled rate. This release damages the microglia/astrocytes and damages nearby neurons as well. In patients that have their mast cells stuck in the on position— whether from pathogenic infection or mast cell activation syndrome, or both—will see their brains are stuck in a hyper-excitable state. In that case, drugs such as lamotrigine and Keppra can seem to be helpful for their microglial, glutamate reducing effects, and mast cell stabilizing effects, respectively. 

 

there is already a post hypothesizing that microglia activation plays a role in the etiology of hppd written by user fawkinchit. This activation of microglia by neuronal mast cells fits into his hypothesis as well. 

 

please refer to my mast cell posts for more information. 
 

the mtor mast cell connection: 

I have written extensively about mtor and mast cells on this site and they can be found by searching. It is incredibly complex literature and not even fully studied— but there are links between mast cells, mtor, ampa functioning, and hallucinogens. 

 

Mold: the most complex  

 

mycotoxic mold is extremely detrimental to the immune system, the brain, the pns, and basically every function in the body. More and more I’ve been seeing a subset of people who arrive at the forums, and I tell them to check their environment for mold, tell me immediately they have mold in their environment and near their sleeping areas. This is interesting to me as many people with hppd sleep and then the symptoms start. 

 

mycotixins in the system could cause other pathogens to come forth and when combined with a hallucinogen create a perfect scenario for hppd. 

 

according to the expert I spoke with about mycotoxic mold, he said that it is the most common driver of mast cell activation he sees in new patients. It is incredibly prevalent, and it is highly likely that some people have mcas genetically, environmentally, and have bartonella who take hallucinogens and find themselves in an excitatory/immune clusterfuck  

 

interesting anecdotal info:

 

I have been increasingly perusing the lyme/bartonella, hppd, candida, vs, Epstein bad virus, and vaccine long haulers Reddits and have found an amazing commonality between the symptoms of them as it relates to hppd. Sometimes it’s been eary— like the person I told you about who had the bad reaction to mushroom/weed while in a state of active bartonella infection. Other anecdotes have been the remission of visuals and vs by treating SIBO or small intestinal bacterial overgrowth. Active candida infections can cause every symptom  Killing candida can cause every emotional symptom of hppd and hallucinations too, as, apart from the other ways it does, the body creates antibodies to it that can cross the bbb and antagonize serotonin receptors (this plays into the loss of serotonin receptors in the visual cortex hypothesis— which can be found in this website and is quite old. I do believe this scenario is possible as a factor in hppd but not the direct cause of the insult). If hppd doesn’t involve the immune system directly, the hampering of it may allow fungi to grow in the gut along with other viral and bacteria to come out of dormancy and start to proliferate unchecked. 

 

another interesting fact is hppd isnt even always caused by traditional drugs. Antibiotics and ssris have been implicated. Even a heavy night of drinking I see occasionally. Some people say they were born with and have never even smoked weed. 

 

—-Oh boy… the vaccine (don’t shoot me!):

 

This is a highly politicized topic so I hope you believe me when I am completely uninterested in that side of this and am a person of science. I hesitate to even bring it up in fear that one may discredit everything else written here just based on me talking about it. But I don’t believe politics or societal views have a place in science and the influence they exert upon the scientific process is negative. Science needs to be practiced unfettered, within ethical guidelines, to work properly. I hope that you and anyone else who reads this understands that I am removing myself from any sentiment or views on vaccination and am simply trying to report what I have experienced and what I have read or heard from medical experts. 

 

there have been anecdotal reports of worsening of hppd symptoms— some just temporary and other for longer— due to vaccination of the Covid-19 vaccine. 

 

Now, that being said, I have learned from talking to both infectious disease experts and mcas experts that both their patient populations have individuals who have had negative and long lasting effects from the vaccine— and believe this is in direct effect from the vaccine.

 

Additionally, there are just now reports and literature being written about the sudden onset/worsening of autoimmune conditions in the days post vaccination. This is particularly interesting to me in respects to those who have had worsening of hppd with the vaccine, as it may indicate and point towards the immune hypothesis for hppd. Could we have an autoimmune condition? It seems plausible— considering the changes in immune functioning we have brought upon ourselves and through the agency of other actors such as pathogens (long lasting increases in immune function is correlated with development of autoimmune disorders). Additionally, there huuave been case studies about the sudden remission of autoimmune conditions through the use of hallucinogens. Most notably rheumatoid arthritis and it has been known to help treat conditions such as cluster headaches 

 

https://pubmed.ncbi.nlm.nih.gov/35378658/

 

https://pubmed.ncbi.nlm.nih.gov/34957554/

 

when I got the vaccine I had been exposed to the most mycotoxic mold varieties— penicillin, aspergillus, stachybatrus— I had an active Epstein Barr infection— and I had been using cannabinoids as my hppd was largely in remission after 7 years. 

 

I. Went. Insane. 

 

it was like hppd on crack. X1000. The only way I got it under control was prednisone and other drugs that are effective in autoimmune encephalitis (which I didn’t have but the therapy for autoimmune disorders and that are the same).

 

I still encourage that everyone gets the vaccine. In light of there very preliminary studies, one should consult with their doctors if they have an autoimmune condition. 

——

 

as you can see, there seems to be many many paths to Rome. This is likely, imo, why responses to treatment is so varied. What helps one hurts another. This was a lot to digest I’m sure and it’s all a bit all over the place, but once you get it and start researching, the connections become so apparent it’s difficult to unsee them. 

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