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Fawkinchit

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Everything posted by Fawkinchit

  1. God damn 6 year bump. Slightly curious what the "other plants" were, but as far as ayahuasca, they are morons IMO. These shamans are most likely unknowledgeable, but theres a 1% chance of one being a master, then he would know.
  2. No, not particularly, but its not to far fetched. I've mainly derived the idea of the possibility of the thing mainly from observing the reports and symptoms that people have mentioned with HPPD, and also common symptoms of synonymous conditions of the sort.
  3. No offense but I scarcely doubt a virus similar to the flu would cause this. @Stve It sounds like maybe you might have something going on aside with HPPD, possibly. I think something may be causing the increase in symptoms that may not necessarily be from the sudafed specifically, hard to say though.
  4. I do not, I did take it a couple times, but the routine didn't last more than a few days. I fell more energy though. But as for HPPD I can't say anything. What dose?
  5. I would like to correct my statement here, that CoQ10 is an amazing supplement for the mitochondria, and if you read in my thread on the subject I theorize the main issue here is a form of mitochondrial dysfunction. CoQ10 accelerates electron chain transfer and makes it very efficient in the mitochondria, which at proper dosage and duration of time can definitely ameliorate mitochondrial dysfunction. Personally I feel Niacin is way better at this and less expensive, but the two can even be combo'd. And you could even add antioxidants Rutin, and Resveratrol, which will help as well. It can take months to alleviate mitochondrial dysfunction, but in most conditions its worth the wait. Also Vitamin D is a good supplement as well and I have seen it do amazing things in calcium metabolism and inflammation. So it could be good as well. I would assume in the persons report that was provided, that it was more so the CoQ10 that was of assistance to him.
  6. Are you on any other medications? Have there been any other changes in your life or medical treatment? Did you get vaccinated?(not recommending it by the way). Heart rate in the 100s is quite high if that's sedentary readings, mine was only that high for a few weeks after getting the condition. Do you have any other medical conditions? What's your diet like? Do you have any palpitations/skipped heart beats?
  7. In a few weeks is possible, but it could take longer, the only reason I say that is the duration since you last took sudafed. Interestingly enough the OCD may even be a manifestation of the HPPD. HPPD appears to be somewhat similar in fashion with other mental disorders and derangements. Some HPPD patients suffer from what I would call pseudo schizophrenic related issues like paranoia, it even appears to blunt social behaviors as well, a lot of symptoms that though mild, still appear, and seem to be relatively unnoticed by usual HPPD patients. It is very difficult to relax with HPPD, for sure, sometimes the anxiety that is HPPD driven, is quite overwhelming. Some people may think the anxiety is driven by the visuals, etc, however it appears to be a symptom direct from HPPD itself. Definitely though negative thoughts can accelerate other symptoms, not that they are the cause, but rather can invoke bodily survival reactions, which definitely can make symptoms worse, then sufferers can soon find themselves in a cascading spiral of anxiety, fear, and dread as you put it.
  8. Nah, pseudoephedrine may exasperate the symptoms of HPPD, but it cant cause them, so you're safe there. HPPD is really sensitive though. Hang in there and give it time, and I'm sure you'll return to baseline, just give it time man. Its hard though I understand, even when my HPPD gets bad for a day its overwhelming, we definitely understand.
  9. Definitely, its possible. Anxiety has really fine lines, I'm not saying its mental, cause I've heard that and I know HPPD isn't mental, but our thoughts can exasperate HPPD, its true. People still dont understand that its unnatural anxiety. Two months is longer than I would expect for returning to baselines. Are you still drinking the green tea everyday? Have you changed anything in your normal routine? Honestly your doctor is probably a dipshit, but I will agree its unlikely that sudafed has had this dramatic and long term of and effect. Its not impossible, just, improbable.
  10. Technically Sudafed is nothing like MDMA, its active ingredient is pseudoephedrine, and its chemically similar to ephedrine I suppose. What I would personally guess is you have jarred your neurons so to speak, so they will probably be on high alert for a while, but I would assume its more than likely with a little time they will calm back down again. Also quit doing fucking drugs, jesus christ what is wrong with people that get HPPD. Its nature literally screaming in your face "dont do drugs" Calming down is the best way to start the process, maybe try some chamomile tea to help relax. I'd say in a couple weeks should be fine. When did you last take sudafed?
  11. So after more reading today, the difference may lie in the metabolites of hallucinogens, and their interactions with the brain. Where as it can be found that some chemicals in vivo are neurotoxic, but in vitro not so much the case, however if neuronal cultures are grown with liver cell culture, that chemical then becomes neurotoxic in vitro. So essentially a study needs to be done with a mix of rat embryo neuronal cultures combined with rat liver cell cultures, and then dosed with hallucinogens, and then an assessment done to gather cell counts of neurons to establish and evidence of neurotoxicity. It would be feasible to be done at home, however, likely expensive, and there may be restrictions on obtaining cell cultures and embryonic neurons obviously have to be taken from the fetuses of a dead rat mother. Anyways this is a study that critically needs to be done to distinguish between seemingly contrasting results of in vivo vs in vitro neurotoxicity. Also for anyone not aware In vivo = Living organism In vitro(Latin for "Within the glass) = Petri dish cell cultures
  12. I'm wondering if it might even be possible to replicate the labelled ligand study, its really a novel idea for understanding neuronal changes. https://www.labome.com/method/Receptor-Ligand-Binding-Assays.html I'm also wondering if hallucinogens cause a marked vasoconstrictive effect leading to neuronal loss, which would explain why neurons in vitro survive fine, and why outcomes in vivo differ in said studies. As this study below shows that not only cause 5htp activation cause vasoconstriction in higher doses, but it also appears to be an effect specific to 5-ht2a receptors, which if I remember correct are the specific ones for hallucinogens. https://pubmed.ncbi.nlm.nih.gov/12122496/ Its likely improbably however, since from what I am reading, the vasoconstrictive effects of 5ht2a receptors are relatively low.
  13. https://journals.sagepub.com/doi/10.1177/0957154X16629902 Abstract LSD was introduced in psychiatry in the 1950s. Between 1960 and 1973, nearly 400 patients were treated with LSD in Denmark. By 1964, one homicide, two suicides and four suicide attempts had been reported. In 1986 the Danish LSD Damages Law was passed after complaints by only one patient. According to the Law, all 154 applicants received financial compensation for LSD-inflicted harm. The Danish State Archives has preserved the case material of 151 of the 154 applicants. Most of the patients suffered from severe side effects of the LSD treatment many years afterwards. In particular, two-thirds of the patients had flashbacks. With the recent interest in LSD therapy, we should consider the neurotoxic potential of LSD.
  14. So there is evidence for possibility of neurotoxicity in vivo for LSD, and likely to be the same for any other hallucinogen. However I have seen conflicting studies of neurotoxicity that I posted in my previous thread. So I'm not entirely sure what is going on here. I was going to contact the physician that did the study, Gaylord Ellison, unfortunately he passed away in 2003 though. basically in this study there is a long term decrease in labeled ligand binding, which as far as I understand could indicate neuronal loss. However as far as I do understand I also think there are other possibilities for the reason. Its to be noted as well that its most evident in limbic regions of the brain, which deal a lot with emotions etc. https://pubmed.ncbi.nlm.nih.gov/2780790/ Abstract Groups of rats were administered either 80 micrograms LSD-25 continuously over seven days using subcutaneous minipumps, or were given the same total amount of drug in seven daily injections, or were administered vehicle. When tested long after cessation of drug administration, persisting alterations in behavior and brain were found in the continuous LSD groups. In social open-field tests, this consisted of decreased social distance between animals; this effect increased upon repeated testing. In uptake of labeled ligands, this was reflected predominantly by decreased 3H-LSD binding in several limbic regions. LSD appears to have especially persisting neurotoxic effects when administered in a continuous, low-level fashion. https://pubmed.ncbi.nlm.nih.gov/8558166/ Abstract The ontogeny of serotonin receptors in the human brainstem is largely unknown, despite the putative roles of serotonin in neural development, synaptic transmission, brainstem modulation of vegetative functions, and clinical disorders of serotonergic function. This study provides baseline information about the quantitative distribution of [3H]LSD binding to serotonergic receptors (5-HT1A-1D, 5-HT2) in the human brainstem, from midgestation through maturity, with a focus upon early infancy. Brainstems were analyzed from 5 fetuses (19-25.5 weeks postconception), 5 infants (42-55.5 weeks postconception), and 3 mature individuals (4, 20, and 52 years). Tissue autoradiography was used with [3H]LSD for total serotonergic receptor binding and [3H]LSD and serotonin for nonspecific binding; computer-based quantitation was applied. The highest levels of [3H]LSD binding occurred prenatally throughout the brainstem. At all ages, the highest relative binding localized to the rostral raphe. A marked decline in [3H]LSD binding occurred between the midgestation and infancy in brainstem regions involved in control of cardiovascular function, respiration, and pain. The fetal peak in [3H]LSD binding to 5-HT receptors is consistent with a trophic role of serotonin in immature human brainstem, and a decrease, between midgestation and infancy, in serotonergic modulation of vegetative functions controlled by the brainstem.
  15. I don't think that I had any actual change in appearance immediately from HPPD, although I did have a lot of hair falling out in the shower immediately after from the stress of my brain being entirely fucked, but as far as appearance nothing change. I did however notice, or in retrospect, do notice that I had an increase of insecurity, it was strange, as though when i looked in the mirror I would only see flaws, pre HPPD I was pretty confident about how I looked. After HPPD it took me a long time to build confidence, it was really hard too. I think there are definitely social impacts of HPPD for sure, its generally the case with most mental disorders. Anyways what I am saying is I think maybe you might be perceiving yourself differently than you used to, even though you actually look the same. If that makes sense.
  16. Crazy. Lol, it appears I was quoted in the original post, hopefully I didn't offend.
  17. Most of the members here are non drug users and prefer to avoid drugs altogether, so you may get better reception on reddit forums for what it seems like you're trying to find out. However, on a purely research basis it is something to question if it has no causative effects for HPPD, as it would be somewhat contradictory to what anyone would expect.
  18. Interestingly enough the research that has already been done on other disorders could technically be used synonymously with HPPD.
  19. Thats awesome, at the time do you or they have the study summary or objective? Essentially an outline of the idea of what they are looking for? Or what specifically they will be studying? Edit: Nvm found your other post.
  20. Never will I understand why so many people want to do hallucinogens after getting HPPD.
  21. I've looked through the article some, they do appear to be promoting the use of psychedelics, granted in restricted doses I would assume, either way I still dont agree with their use, as some people who have microdosed even got HPPD. However, as you mentioned there is some interesting information in there for sure, and the actions and effects of some of these compounds which helps to give further insight in to their effects, and some appear to have some beneficial effects, granted though it needs to be further researched what the mechansims are for HPPD before they continue. I saw some parts where they mentioned reactive oxygen species and glutamate excitotoxicity, and I cant quite tell whether they are saying it is beneficial in preventing these or if it causes these, so I will have to do some more reading.
  22. Oh my bad, I misunderstood, I'll definitely have to check out the article, and I apologize, Ive been really limited for time lately. Thanks for posting it! Thats even more interesting because both immune and mitochondrial dysfunction are quite often linked. I've actually reversed a condition for someone that is technically classified as an immune disorder, and manifests as skin rashes, they no long have it though, and it took about 6 months to reverse. So could be the same case with this, and neuronal inflammation is a real thing.
  23. 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!
  24. 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.
  25. 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
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