Fawkinchit

Its very possible, the evidence is surmounting that this is the most probably cause for our condition, and schizophrenia as well. This is true, however it does this through reducing/inhibiting mitochondrial oxidative phosphorylation, a really important pathway, I personally don't believe its even a decent treatment for type II diabetes, as other alternatives suppress glucose more efficiently, and more safely. Metformin is also the child of Phenformin, a banned drug for high risk of lactic acidosis that led to 50% mortality rates in people to developed it while on the drug. Yes! There is a lot of evidence that these conditions have a brother sister relationship. The rash from niacin is likely to be different from lamotrigine. Niacin rash isn't particularly a rash, but in not entirely familiar with lamo side effects. I truly feel that going back to compounds that brought us here, will do just that, bring us here. I do not believe cyanide to cure cyanide poisoning, thus its most inconceivable that hallucinogens cure HPPD. Your body will absorb them plenty fine, all you have to do is make sure you are getting the right ones every day. Your welcome! And thank you it has been years of work. Fruits and vegetables will always have a larger impact on health than supplements, however I do believe supplements are required for some conditions. Vitamin C should be in the range of 500mg to 1gram, but up to 27 grams is safe and has been done before, but I don't personally recommend it, Linus Pauling did take that much though. Vitamin E(not D) just however many IUs are in a capsule once a day is sufficient IMO. The niacin should be around 500mg or more a day IMO. Its in the original post. Vitamin C, Vitamin E, and Niacin. I am working more research revolving around mtDNA damage and ways to accelerate repair, as I believe this is the most crucial aspect of the condition, and has to be done precisely, I will update everyone when I have more information on the matter. I think that Niacin is amazing and one of the more critical points for DNA repair, but there are other things necessary, and beneficial. The proper cure for this condition could be very time consuming as well, it could take months, even a year. Great! Good luck. Sorry to everyone for the delayed responses, I have had a lot going on and always try to find time to make my way back here. Thanks for all the responses!

I would like to add also however, that despite current findings in the field of hallucinogens and no evidence of neuronal loss, there is still a possibility for neuronal loss in specific people that may be driven particularly by people having certain different metabolic profiles, and/or genetic metabolic mutations that predispose the person to neuronal loss under certain conditions. Its been well found out decades ago that people have certain metabolic inconsistences with the norm of others. Some inconsistencies in metabolic profiles are minor, other are more exaugurated. So a more precise test to disclose possibilities of neuronal loss would be to take neurons specifically from HPPD patients(no idea how you would do that), and then dose them with LSD or other hallucinogens that test negative for neurotoxicity and observe is the result is still the same. Basically there is a possibility that some humans may be susceptible to neuronal loss under the exposure to hallucinogens, where the relative public is immune in a sense.

I definitely believe it to be the cause of HPPD, and the mentioned treatments are all well known to alleviate mitochondrial dysfunction and assist in DNA repair, and prevent DNA and catecholamine oxidation/damage. From what I have read high dose niacin(500-1000mg I would guess) will terminate hallucinations from LSD all together. There could be linking factors to HPPD patients having certain enzyme mutations that lead to them being susceptible to HPPD whereas others are not, and these mutations typically can be recovered from proper vitamin nutrition etc. As for Niacin side effects the few were from niacinamide which is not niacin but a byproduct in niacin metabolism. Niacin is nicotinic acid and has been proven to be completely safe even in doses far above 1 gram. The studies involving any side effects from niacinimide are pretty questionable as well, and more studies should be done. As for flush its the main side effect, and its annoying, and a little scary at first, but it fades in 30 minutes and stops happening after about 1-2 weeks. I would like to post this as well in relation to mitochondria and neurons. This article explains the importance of mitochondria, not just in neurons, but in synapses, astrocytes, and oligodendrocytes as well. Note: its titled neurodegeneration, however I still do not believe LSD and most hallucinogens to be immediately neurotoxic, the article just well establishes mitochondria’s importance in relation to the brain and nervous system. Neurodegeneration Mitochondrial oxidative stress and accumulation of the mtDNA mutations are believed to be particularly devastating to post-mitotic, terminally differentiated cells such as neurons. Mitochondria are central components of synapses, where they provide the energy required for synaptic activities (97). Damage to mtDNA could potentially result in bioenergetics dysfunction and consequently aberrant nerve function. Neurodegenerative diseases are associated with a progressive loss of neurons through apoptosis and/or necrosis. An accumulation of mutations and deletions in mtDNA with corresponding defects in energy metabolism have been found in Parkinson’s disease (PD), Alzheimer’s disease (AD), amyotrophic lateral sclerosis (ALS), and Huntington’s disease (HD) (98–100). As might be expected, these mutations have been correlated with an increase in oxidative damage in the brain. Elevated levels of 8-oxoG have been found in the cortex of ALS patients (101), as well as in mitochondria in the substantia nigra of PD patients (102). Although DNA damage is elevated in both nuclear and mitochondrial DNA in AD brains, mtDNA in AD brains was shown to contain between 3- to 10-fold higher levels of oxidized bases than nDNA (103). Several studies regarding BER activity in neurodegenerative disorders showed increased expression of AP endonuclease 1 (APE1) in AD cortex extracts (104); lower activity of OGG1 in nuclear extracts from AD hippocampal gyri and parahippocampal gyri (105); and increased APE1 level in the nuclear fraction in ALS motor cortex (106). A recent publication reports significant BER deficiencies in brains of AD patients due to limited DNA base damage processing by DNA glycosylases and reduced DNA synthesis capacity by DNA polymerase β (107). Meanwhile, far less is known about how neurodegeneration is associated with alteration in the mtDNA repair pathways. Studies of whole brain regions do not differentiate between neurons and glial cells. However, evidence from studies using cells in culture suggests that there are cell-specific differences in mtDNA repair capacity between neurons and glial cells. Treating primary rat cultures of astrocytes, oligodendrocytes, and microglia with methylnitrosourea, an alkylating agent, does not alter the amount of initial mtDNA damage, but the repair efficiency was significantly decreased in oligodendrocytes and microglia compared with astrocytes (108). Moreover, the induction of apoptosis correlated with this decrease. These studies were the first to demonstrate a cell-specific difference in repair of mtDNA damage in cells from the central nervous system (CNS), and indicated that this difference correlated with the induction of programmed cell death (108). In a similar study, Hollensworth et al. showed that after exposure to oxidative DNA damage, oligodendrocytes and microglia accumulated more mtDNA damage, and they repaired the damage less efficiently than astrocytes (109). The differential susceptibility of glial cell types to oxidative damage and apoptosis did not appear related to cellular antioxidant capacity, because astrocytes had lower total glutathione content and superoxide dismutase (SOD) activity than did oligodendrocytes and microglia (109). In a subsequent study primary cerebellar granule cells were used to determine if mitochondrial DNA repair efficiencies correlated with oxidative stress-induced apoptosis in neuronal cells (110). Primary cerebellar granule cells had increased basal levels of glutathione and APE1 and were more sensitive to oxidative stress, resulting in less efficient repair of oxidative mtDNA lesions when compared with astrocytes. Of interest, however, is that the glycosylase and APE1 activities in the neurons were significantly higher with a reduction in polymerase γ activity, suggesting that the granule cells have an imbalance in the mitochondrial BER pathway. It is this imbalance which leads to the observed increase in sensitivity to oxidative stress (110). This evidence provides a link between neuronal mtDNA repair capacity and oxidative stress-related neurodegeneration. The importance of mitochondrial BER pathways in the development of neurodegenerative disorders was shown in an in vivo study examining expression of the DNA repair enzymes in transgenic mice carrying a mutant SOD1 gene, an animal model of ALS (111). The authors observed no changes in mitochondrial OGG1 activity, but down-regulated polymerase γ activity in mitochondria as well as upregulated nuclear OGG1 activity in spinal motor neurons in presymptomatic transgenic mice. They assumed that the early and selective impairment of DNA repair enzymes in mitochondria of spinal motor neurons makes them more vulnerable to oxidative stress, leading to the accumulation of DNA mutations and finally cell death in this animal model of ALS (111). Additionally, a previous report suggested the impairment of mtDNA repair enzymes in human ALS cases (112). If mitochondrial DNA repair plays a specific role in oxidative stress-induced cell death, the modulation of mtDNA repair efficiency by targeting BER enzymes to mitochondria should enhance cellular defenses of CNS cells. Indeed, targeting hOGG1 to mitochondria of oligodendrocytes enhanced mtDNA repair and protected cells against caspase 9-dependent apoptosis after menadione-induced oxidative stress (113) and cytokines-mediated damage (114). Additionally, when the yeast AP endonuclease Apn1, was expressed in mitochondria of a neuronal cell line derived from rat substantia nigra, it promoted the repair of the oxidative lesions in mtDNA and enhanced the resistance to cell death following oxidative insult (115). Thus, it can be concluded that mtDNA repair is a critical player in the response of CNS cells to genotoxic insults. Strategies to enhance the DNA repair system in mitochondria may prove useful for retarding the pathogenesis of neurodegenerative diseases

So basically if anyone doesn't understand whats happening here, mitochondria have failed, producing excess free radicals, depleting neuron and astrocyte energy, and causing excess premature oxidation of catecholamines(dopamine, noradrenaline, and adrenaline) which leads to abnormal neuronal behavior. So alleviating mitochondrial disfunction is the key to treating HPPD. Thats literally as simple as I can explain it.

What is niacin’s (B3) role in preventing symptoms of schizophrenia? Abraham Hoffer and his team theorised that in order to reduce the production of adrenochromes, a methyl acceptor such as B3 would be needed. Methyl acceptor is the name for nutrients, mainly in the B vitamin family, which each play an important role in a biochemical process known as methylation. This process is needed for a variety of biochemical reactions, such as building and breaking down neurotransmitters, supporting liver detox pathways and DNA repair, to name a few. Upon studying the pathway for adrenaline production in the brain and the cofactor nutrients supporting and inhibiting this pathway, Hoffer deduced that by giving large doses of vitamin B3, which is a methyl acceptor, this would effectively prevent the conversion of noradrenaline to adrenaline, and by limiting the amount of adrenaline, this would then prevent the build up of adrenochromes. In addition, B3 is also a precursor to nicotinamide adenine dinucleotide (NAD), a compound that is involved in redox reactions, which prevents oxidative stress caused by free radicals. These are unstable molecules that scavenge electrons from other molecules, causing a chain reaction that can eventually damage tissues in the body. NAD prevents the oxidation of adrenaline, which is what turns adrenaline into adrenochromes, therefore preventing the production of these neurotoxins that over time can damage the brain.

Edit: Evidence of everything I am saying on page 2 post #15 Ok, I’ve been working on this for years and do believe i know the exact mechanisms occurring in patients suffering from HPPD. It is quite similar to most mental derangements including epilepsy, migraines, and especially schizophrenia. Essentially what occurs is the patient uses a hallucinogen(obviously), which in turn overstimulates certain areas of the brain. Strikingly there appears to be little to no evidence for neuronal loss, so we must look deeper, where we will find the mitochondria. The mitochondria are dense in neurons and the main suppliers of energy, but also of free radicals. When the neurons become overexcited(hallucinogen use) they demand more energy, mitochondrial output is hastened and generates a far greater degree of reactive oxygen species(free radicals), which in turn depletes antioxidant and vitamin mechanisms. When the reactive oxygen species overburden the antioxidant and vitamin systems damage occurs significantly to membranes, mitochondria, and the mtDNA(mitochondrial DNA) as well, the damage results in mitochondrial dysfunction, in turn leading to multiple events likely involving neuronal dysfunction, astrocyte dysfunction, and increased catecholamine oxidation(due in part by high ROS). Neuronal dysfunction is self explanatory. Astrocyte dysfunction likely worsens neuronal dysfunction as they are regulators for glutamate. And catecholamine oxidation leads to increased adrenochrome, which in itself is known to be hallucinogenic. How then can all this be alleviated? Mitochondria are very sensitive to ROS damage and therefore the ROS must be eliminated, and mitochondrial function restored. This is done by various nutrients which will likely restore balance to the system and then supply mitochondria with the energy that they need. The patient should eat diets high in antioxidant nutrients and vitamins(fruits, veggies). Supplement vitamin C, vitamin E. Both are efficient in removing ROS. No less than a gram of vitamin C per day, natural source is better if it can be afforded. Olive leaf extract, which has extremely powerful antioxidants and will assist whole antioxidant mechanisms. High dose Niacin, up to a gram a day if the patient can tolerate the treatment. Abram Hoffer has done extensive research on niacin and the treatment of schizophrenia, I certainly believe there is a common link between HPPD and schizophrenia, and niacin will assist in restarting normal mitochondrial function by supplying a high value source for NAD, I do believe niacin will be the most important part of this treatment. Anyone can try this treatment, its accessible, safe, and affordable. Anyone doing so please report back and help others. Lets cure HPPD! Good luck and if anyone has questions I will be here to answer them all.

It is true it does contain thujone, which may make some people nervous, which I understand. However it should be noted that thujone is, if I recall properly, only neurotoxic and higher levels, and the amount in sage is very low, so nothing that I know of that can reach the threshold for neurotoxicity. I looked it up a long time ago, I believe one report even stated that some samples of sage they tested had no thujone at all. There's also a reason I recommend it. Anyways I'll make a post in the next couple of days, that outlines the most probable cause of this disease(HPPD) and what people can do for the best possible outcome. I may just simply make a new thread.

Excess fatigue is typically due to widespread mitochondrial dysfunction(cellular energy producers), try assisting them with long term use of powerful antioxidants. They take months to recover efficiency, so give it time. Also yes, most narcoleptic drugs should cause HPPD symptoms to get worse.

You definitely are having neurological disorders. You need to stop the use of any drugs/narcotics of any kind immediately and permanently. It is probably definitely possible that it was eventually brought on by a seizure. There are rare cases of people using drugs, and some other incident bringing on HPPD, even as simple as drinking alcohol, I have seen it here on this forum of one person reporting exactly that. As Jay said there does seem to be some neuro deficit associations between HPPD, epilepsy, and migraines. They are all very strange conditions that are not entirely understood yet. Some things that may help are eating a healthier diet, veges and fruits etc. Absolutely abstaining from illicit substances.

I personally dont have any visual symptoms anymore, so I cant really comment on that part, but I suppose if you are playing game that increases adrenaline, it could definitely cause symptoms to get worse, i do remember too sometimes in movie theaters my anxiety would get worse. Most of my HPPD only manifests as anxiety anymore, but I had all the typical symptoms, and my anxiety was so bad it was insane, like suicide influencing insane, not like normal anxiety, cause Ive experienced that before.

This. Sounds like you just have anxiety, and meticulously nervous behavior.

Have you tried betaine?

https://pubmed.ncbi.nlm.nih.gov/27046518/#:~:text=Glial cells such as microglia,to the extrasynaptic NMDA receptor. https://www.frontiersin.org/articles/10.3389/fnmol.2018.00414/full https://www.nature.com/articles/npp2016199 https://www.sciencedirect.com/science/article/pii/S2666354619300353 https://www.sciencedirect.com/science/article/abs/pii/S0197018613000363 https://www.mdpi.com/2073-4409/8/2/184/htm Just posting these for future reference and reading. It would appear that there is a possibility of glial cell dysfunction leading to increased levels of glutamate, which would be constant, and overstimulate the nervous system. Which would explain why some have benefited from Lamotrigine, which down regulates glutamate. So the issue could actually be dysfunction of the astrocytes and oligodendrocytes dumping too much glutamate on to neurons, or an issue with sucking it back up from the neurons, which appears to be common in neuroinflammation related conditions. Then the issue becomes finding the cause of and ameliorating the inflammation.

Most people to be completely honest, are highly unintelligent. They literally have no idea what's going on with you, they just see the surface of what you are going through. The same thing happened with me. It taught me one thing though, you can only truly rely on one person to help you, and that's what I do every day. Its harsh, but I guess that's how this place is, society focusses so much on smiling photos, fairytale movie endings, and glittering christmas lights, its hard to remember that there is a great deal of suffering on earth, and what people really should be focusing on is the remedy. No one wants to do that while they are here though, so there's a repeat of everything in every generation. HPPD is something that should be widely known, but instead scientists are doing studies on the "benefits" of hallucinogens, even recommending them for depression and learning capacity. It goes to show the deep despair society and humans really are in. So don't be too surprised when someone doesn't fully understand, or gives up, they have no idea how bad HPPD really is, and life is hard even without HPPD, people are constantly creating problems for themselves even on top of problems that are created for them, I do it even myself, its almost a subconscious thing, then next thing we know we don't have time for anything, or anyone.

Absolutely, it definitely does sound that to some degree, you have HPPD related symptoms. They aren't the most classically reported symptoms, but they are in the spectrum when considering they are the aftermath of illicit narcotic use. Not all HPPD symptoms are visual, I have no visual symptoms(Although for some time I did have visual snow). Personally I feel the visual symptoms are the more bearable symptoms. Anxiety and depersonalization IMO are the worst HPPD symptoms. My anxiety was so bad immediately after that my heart rate was 90-110 resting, dipshit doctors just thought I was on drugs, imbeciles.

I started talking the two together, for other reasons, and the first 2 days I felt a little weird in my nervous system, typically in the same areas that usually are tormenting from my anxiety from HPPD, but then my nervous system seems to have possibly calmed down. I'm not entirely sure if it has anything to do with HPPD, but if someone could try it out for a couple weeks and report back I would appreciate it. I have been taking 500mg of choline and 2 250mg of Betaine Hydrochloride, they can be purchased at any health food store.

ABSTRACT In the mid-1990s, it was proposed that quantum effects in proteins known as microtubules play a role in the nature of consciousness. The theory was largely dismissed due to the fact that quantum effects were thought unlikely to occur in biological systems, which are warm and wet and subject to decoherence. However, the development of quantum biology now suggests otherwise. Quantum effects have been implicated in photosynthesis, a process fundamental to life on earth. They are also possibly at play in other biological processes such as avian migration and olfaction. The microtubule mechanism of quantum consciousness has been joined by other theories of quantum cognition. It has been proposed that general anesthetic, which switches off consciousness, does this through quantum means, measured by changes in electron spin. The tunneling hypothesis developed in the context of olfaction has been applied to the action of neurotransmitters. A recent theory outlines how quantum entanglement between phosphorus nuclei might influence the firing of neurons. These, and other theories, have contributed to a growing field of research that investigates whether quantum effects might contribute to neural processing. This review aims to investigate the current state of this research and how fully the theory is supported by convincing experimental evidence. It also aims to clarify the biological sites of these proposed quantum effects and how progress made in the wider field of quantum biology might be relevant to the specific case of the brain. https://avs.scitation.org/doi/10.1116/1.5135170

Rat spinal cord ganglia cultures were maintained for periods of up to 19 days in a feeding solution containing LSD-25 in a concentration of 5 x 10-6. Electron microscopic examination of the nerve cells in these cultures revealed alterations in the Golgi complexes, lysosomes, mitochondria and multivesicular bodies. The changes in the membranous components of these structures were particularly prominent and resulted in organelle pleomorphism and very unusual internal membrane patterns. Variations were also noted in the fine structure of the nucleoli of some neurons. The possible relationships of the morphologic changes to disturbances of neuronal metabolism are considered. https://academic.oup.com/jnen/article-abstract/33/2/212/2612730?redirectedFrom=fulltext This article in my opinion, shows two things, that even after long durations of LSD exposure, neurons do not die, so it still appears to not be neurotoxic, and that apparent alterations in the cell bodies occur. I would like to note though there could be other physiological mechanisms that could induce neuronal loss that just neurotoxicity specifically, so its not entirely ruled out.

Strattera should never be used to treat or in conjunction with HPPD. ADD does not equal HPPD. I dont know how doctors are so stupid these days.

https://pubmed.ncbi.nlm.nih.gov/10027775/\ Conversely, immature rats can sustain major metabolic activations that lead either to a variable extent of damage, as seen at P21, or no damage, as recorded at P10. And https://watermark.silverchair.com/67-12-1205.pdf?token=AQECAHi208BE49Ooan9kkhW_Ercy7Dm3ZL_9Cf3qfKAc485ysgAAAq8wggKrBgkqhkiG9w0BBwagggKcMIICmAIBADCCApEGCSqGSIb3DQEHATAeBglghkgBZQMEAS4wEQQMYFQnE4k8JeAnLrysAgEQgIICYifamLsH4wt0PhcaiTrNAtOF6dt-jBQn6YTviY7mamU03WE6zRKh9rVTjEokSmtFRVEFga5gTkPM69GAN17GjdjZjIJHwia7qMMWoEVZ8unSvqAvJkWWDCZsd47MDzXtuOBoPLJ6loE02FREWOeXncVpnqg4_eHWJQOOEXH2exXZT3g0Ve3T9C4syIFu-S03QNNree9HsFZk9ptkOJMujuMI2xqnzapNc-JZ0DIxeSFODr6Bu3rDs4BUZ3Q3aoXYhRQLMzX427H1M28tWjREaOk-OU-HEMy5-5rR4WczoWVLoRjuQ519W53hB32XwoAtp38VLOimSFYAKMbkOCVqO3F_Plaz_KHxFAMbAY3ntXQahKxwgW0iwJyGDXE6RJSyxUzZk7MnCI2-1R4x0RHtNzDswoWa0Nilzn97rRPkQbGIr0L2OAF9kvBGZa_SevDlgHk41QQNVSGpL0TW-u5f_Rjj4Ee2VfbnTIPhunURxY7jE-aqbfoJFrWCq8Mn9bWJysiQSqlf8Fd04EkuyB_iHaDfj6jNLnaQJAScwdBjpcXZXF1UJZzePXtL696QoMopZzh4-WZjuJ-O57o4VsVpxvprt4rqGafkK0NXYkToE7Gj-LRpyG-RR6efb5dNssAsp5p-lBflfVkxvMhSDSddrBwsoa7yB9e0tjuv6rzys0UobRiJRcRTJsyFId__Ur_dm3erwb_gvSUbyS-ILI8PgA4neMWlv1LdTegpyvySag61_mdCX4msQdZO2-0UBw836km1J7Mzn2DJYIaLjMIgyoF_NtlFHhHRCLwi55a0XvWQvdo More evidence that atrophy isn't defined by neuronal loss. So this is good.

Thank you

Thanks, I completely agree. I also don't understand how everyone doesn't realize that pharmaceutical companies don't care about us at all. Even heart attacks are preventable, and they know that, I have seen the studies they have done and its easy to reverse atherosclerosis, making heart attacks a thing of the past, but they don't tell anyone because they make far more if they wait till you have a heart attack. Nice, this is interesting information for sure. Also just because there are volume increases or decreases in areas of the brain as far as I know that does not directly imply that there is neuronal loss or increase. I believe there are other reasons for volumes changes. Again for everyone that reads this thread, there will be absolutely no benefit to any of our work if no one will try anything, if anyone will just try some of the things I have lined out in this thread, there is a chance for improvement. I can't try everything. I do believe that there is just a deficiency in the neurons possibly, or some intracellular structural abnormality, that could be reversible, and yes maybe we have lost neurons too, its possible, but I dont think its the case.

I just want to say that if no one will try any alternatives to pharmacological medications we will never find an answer. I dont see anyone trying anything other than like... benzos, SSRIs, antipsychotics, etc. These medications do not heal, they just alter brain function. Modern medicine literally has zero interest in healing anyone. But there are a slew of treatments that if anyone would try, may find something. Like the whole sorts of vitamins, minerals, and other nutrients that the body needs to function, but I dont see anyone trying anything like these, or even the things that I have recommended. If no one will try any of these things, we will never find a cure.

Im considering too the possibility of calcium phosphate precipitates in the neurons or issues with the mitochondria, its actually a highly probable case. In a lot of conditions calcium phosphate precipitates are a common finding, aka chronic kidney disease, atherosclerosis, and many more. Heres an article talking about neuronal calcium precipitates. Under high loads of mitochondrial dysfunction large accumulations of calcium phosphates could theoretically be deposited in neurons, possibly even due to hallucinogenic use, which overstimulates the neurons, leading to mitochondrial dysfunction, especially more so under antioxidant deficiencies like E, C, B vitamins, etc. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2566803/ Furthermore, high-Ca precipitates were found in swollen isolated mitochondria Ca2+-overloaded in the presence of adenosine 5′-triphosphate (ATP) (Kristian et al. 2002), in swollen mitochondria of cultured hippocampal neurons exposed to toxic levels of NMDA (Pivovarova et al. 2004), and even in vivo in swollen, structurally damaged mitochondria of ischemic, Ca2+-overloaded neuronal cells (Solenski et al. 2002). I also want to add this quote, as it pertains to my previous statement of the possibility of dysregulated electrical harmonization being a cause for HPPD. "The main goal of electrical synapses is to synchronize electrical activity among populations of neurons." D. Purves; et al. (2008). Neuroscience, 4th ed. Sunderland, Massachusetts: Sinauer Associates, Inc. Here too a study on goldfish that shows junction gap calcium precipitates in goldfish under long term induced stress. https://link.springer.com/article/10.1007/s11055-005-0046-9 So theoretically it could be possible that overexcitation of our neurons has cause over precipitation of calcium in the junctions, causing long term alterations in transmissions.