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dasitmane

Back! Possible Cure Part 2 - No Guarantees But Were Here Anyways

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Like I make mention of in the second post anyone can try sage if they want, I do believe for various reasons this is a suitable treatment for this condition. How long the treatment takes on average I have no idea. Sufferers can also try cinquefoil as well as this may have long term beneficial effects on the condition as well.

Also someone could simply try a mineral supplement with ALL minerals, not just the basic minerals. Its possible that there was simply a depletion of one of the said minerals in the brain that takes a long time to build up and once depleted is in a state of deficiency causing said symptoms. There is still a lot that science doesn't know. The one that I recommend trying is colloidal minerals by NOW. If anyone does try this please report your findings. When deficiencies occur for various reason though they are rare they can be hard to bring the organ back up to the requisite levels, for example the case of zinc deficiency and the liver. So this is worth a shot or try as well. 

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Thats a report for lithium overdose and I’m just using it as an example for evidence of the possibility for neuronal loss. We still don’t have definitive evidence that it is in fact neuronal loss. Also in the case of neuronal loss neurogenesis is not a complete impossibility. It may be impossible currently in modern medical science, but it doesn't mean it cant be done. 

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So I've been doing some more reading, as per usual. Whenever I have any new ideas that I haven't checked I always google. Anyways I was reading about DMT and its effects on the brain and if there are any signs of neurotoxicity, I didn't exactly look to far in to the details but according to everything I read not only does it show limited neurotoxicity, but it doesn't even appear to be neurotoxic even when injected in large quantities, which is extremely interesting. Also, believe it or not it even showed neuroprotective abilities, very interesting. DMT is originally what triggered my HPPD, and it was bad. I also used Syrian Rue in conjunction of the DMT source, as is typical in Ayahuasca concoctions, so I also had to read up on the possibility of Harmala and related alkaloids having any neurotoxicity, which interesting enough not only do they not show any significant signs of being neurotoxic, but they have neuroprotective effects by inhibiting glutamate caused apoptosis. So absolutely remarkable, and fascinating information.

To be completely honest this is a great deal of information that I almost feel that neuronal loss in the case of HPPD as a cause, very well may at this point be removed as a possibility.

At this point its a VERY confusing subject of what causes this disease.

Edited by dasitmane

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Preclinical and clinical studies indicate that synthetic psychoactive substances, in addition to having abuse potential, may elicit toxic effects of varying severity at the peripheral and central levels. Nowadays, toxicity induced by synthetic psychoactive substances poses a serious harm for health, since recreational use of these substances is on the rise among young and adult people. The present review summarizes recent findings on the peripheral and central toxicity elicited by “old” and “new” synthetic psychoactive substances in humans and experimental animals, focusing on amphetamine derivatives, hallucinogen and dissociative drugs and synthetic cannabinoids.

Keywords: cannabinoids; dissociatives; hallucinogens; ketamine; MDMA; methamphetamine; methoxetamine; neuroinflammation; neurotoxicity; NPS

 

http://www.nrronline.org/article.asp?issn=1673-5374%3Byear%3D2020%3Bvolume%3D15%3Bissue%3D5%3Bspage%3D802%3Bepage%3D816%3Baulast%3DCosta

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Good post but it looks like most that report neurotoxicity are drugs like meth and mdma. This is what the section on hallucinogens says. The only “hallucinogens” they really list are ketamine and methoxetamine.

 

  Toxic Effects of Hallucinogen and Dissociative Drugs   Top



Preclinical studies

Studies in vitro have demonstrated that both acute and prolonged exposure to hallucinogen phenethylamines (2.4–100?μM) inhibit neuronal activity in rat primary cortical cultures (Zwartsen et al., 2018). Similarly, studies in users have demonstrated toxic effects of serotoninergic hallucinogens, including the newest ones, which have been frequently associated with acute serotonin syndrome, hyperthermia, seizures, hyponatremia and sympathomimetic toxicity (Hill and Thomas, 2011). Degree of symptoms can range from mild to severe; complications may include seizures and extensive muscle breakdown. Animal studies have described the behavioral components of the serotonin syndrome induced by hallucinogen drugs which include lateral head weaving, hind limb abduction, backward locomotion, and lower lip retraction (Halberstadt and Geyer, 2011; Gatch et al., 2017).

Ketamine is a non-competitive antagonist of glutamate N-methyl-D-aspartate (NMDA) receptors that induces dissociative anesthesia and analgesia at clinical doses; however, at recreational doses of subanesthetic levels, ketamine may produce an intense psychedelic experience. Accordingly, although present on the drug market for long time, ketamine continues to be abused worldwide, and its consumption among adolescents is particularly worrying. A study in Cynomolgus monkeys has shown that repeated parenteral administrations of a recreational dose of ketamine (1 mg/kg) induce neurotoxic effects, involving the activation of apoptotic pathways in the prefrontal cortex, that lead to irreversible deficits in brain functions (Sun et al., 2014). In line with this, repeated parenteral administrations of sub-anesthetic doses of ketamine (5–50 mg/kg) increased cell death in hippocampal cornu ammonis area 3, caused irreversible changes in both brain structure and function in young adult mice (Majewski-Tiedeken et al., 2008) and induced apoptotic and necrotic neuronal cell death in the perinatal rhesus monkey (Slikker et al., 2007).

Methoxetamine is an NPS structurally related to ketamine and phencyclidine, designed to mimic the psychotropic effects of its parent compounds (Zanda et al., 2016) and increasingly available on the Internet as ‘legal ketamine’ (EMCDDA, 2014). Methoxetamine acts as a NMDA receptor antagonist, but also potently inhibits neuronal activity and alters monoamine metabolism in in vitro models (Hondebrink et al., 2018). Moreover, acute repeated parenteral administration of methoxetamine (0.125–5 mg/kg) considerably stimulates the mesolimbic dopaminergic transmission in rats (Mutti et al., 2016), and affects brain functions and behavior in rodents (Zanda et al., 2017). A recent study in mice (Ossato et al., 2018) found that acute parenteral administration of methoxetamine (0.01–30?mg/kg) induced alterations in sensory function processing that resembled those reported by users (Kjellgren and Jonsson, 2013) and persisted for hours when methoxetamine was administered at high doses. Moreover, another recent study in rats found that repeated parenteral administrations of methoxetamine (0.1–0.5 mg/kg) induced persistent behavioral abnormalities in tests used to evaluate anxiety-like states and recognition memory (Costa et al., 2019). The same investigation also demonstrated that methoxetamine induced persistent damage of dopaminergic fibers and neurons in the nigrostriatal and mesocorticolimbic systems as well as of serotonergic fibers in the nucleus accumbens core (Costa et al., 2019). [Table 3] provides further details about the toxic effects of hallucinogen and dissociative drugs demonstrated by preclinical studies from the past 3 years.

NeuralRegenRes_2020_15_5_802_268895_t6.j Table 3: Overview of the toxic effects of hallucinogen and dissociative drugs demonstrated in studies from the past 3 years

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Human studies

In 2007, tryptamine derivatives were listed as ‘narcotics’ or ‘designated substances’ and were quickly replaced on the online drug market by cathinones, phenethylamines, and piperazines. Yet, several novel tryptamines continue to appear on the online drug market as ‘legal highs’, which include AMT, 5-MeO-AMT, 4-HO-DALT and 5-MeO-DALT [Figure 2]. In addition to visual and auditory hallucinations, these drugs may induce agitation, tachyarrhythmia, hyperthermia and death (Wood and Dargan, 2013).

NeuralRegenRes_2020_15_5_802_268895_f2.j Figure 2: Chemical structures of some hallucinogen/dissociative substances used as recreational drugs.
AMT: α-Methyltryptamine; 5-MeO-DALT: N-allyl-N-[2-(5-methoxy-1H-indol-3-yl)ethyl]prop-2-en-1-amine; 25I-NBOMe: 4-Iodo-2,5-dimethoxy-N-(2-methoxybenzyl)phenethylamine.


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According to the EMCDDA (2015), some phenethylamines with hallucinogenic properties are very popular in the current drug market, including the so-called 2C series (e.g., 2C-B/‘Nexus’) and the NBOMe series drugs (e.g., 25I-NBOMe, [Figure 2]). Their use has been associated with serotonergic and sympathomimetic toxic effects, including vomiting/diarrhea, metabolic acidosis, mydriasis, convulsions, thrombocytopenia, renal failure, hyperthermia and coma (Schifano et al., 2017). Fatalities and hospitalizations have been reported following use of 25I-NBOMe and symptoms of acute toxicity included tachycardia, hypertension, agitation/aggression and seizures, while laboratory tests detected elevated level of creatinine kinase, leukocytosis and hyperglycaemia (Suzuki et al., 2015). Rhabdomyolysis is a relatively common complication of severe NBOMe toxicity, an effect that may be linked to NBOMe-induced seizures, hyperthermia, and vasoconstriction. Slightly different from 25I-NBOMe, 25C-NBOMe was found to induce aggression, unpredictable violent episodes, dissociation and anxiety (Lawn et al., 2014). Although studies on the pharmacology of hallucinogenic phenylethylamines from the 2C series are still scarce, it has been demonstrated that they may act either as agonists or antagonists of G-protein-coupled serotonin and α-adrenergic receptors (Villalobos et al., 2004; Fantegrossi et al., 2008) and some of them (i.e., 2C-C, 2C-D, 2C-E, and 2C-I) were found to act as full agonists at 5-HT2A/2C receptors (Eshleman et al., 2014).

Use of methoxetamine by humans has been recently associated with acute neurological (Elian and Hackett, 2014; Fassette and Martinez, 2016) and cerebellar toxicity (Shields et al., 2012), including psychomotor agitation and altered motor coordination (Craig and Loeffler, 2014). Case reports described intoxicated patients with hypertension and tachycardia following use of methoxetamine (Thornton et al., 2017), ketamine (Kalsi et al., 2011), phencyclidine (Akmal et al., 1981) or methoxylated phencyclidine analogs (Bäckberg et al., 2015). Induction of gastrointestinal and urinary toxicity by ketamine have also been described (Wei et al. 2013). [Table 3] provides further details about the toxic effects of hallucinogen and dissociative drugs demonstrated by clinical studies from the past 3 years.

Due to the numerous medical issues associated with the use of new hallucinogen and dissociative drugs, being aware of the toxicity of these compounds is of primary importance for health professionals. Since it is not always possible to know the exact compound(s) consumed, management of toxicity should be based on clinical symptoms that an individual presents with and training of medical staff should focus on the management of the pattern of toxicity, rather than on the specific drug(s) used. This view is supported by a recent study revealing that physicians and nurses have less confidence in managing acute toxicity related to the use of NPS compared with classical recreational drugs (Wood et al., 2016).

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 I just found out that when I was a child, I would go to my parents room at night because I would say I couldn’t sleep because I saw things but I couldn’t say what. That’s really interesting because my hppd ongoing only really kicked off about last year and was most noticeable after I did molly and then it was nonstop after 900mg of pure dxm. I’ve also been bitten by ticks too so I find this very interesting and I also have joint pains (mostly knees, ankles, wrists and fingers, but I don’t have arthritis). I also remember seeing visuals and white snow before I ever did any drugs, especially in my early childhood. 

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No neurotoxicity.....

Behavioural and neurotoxic effects of ayahuasca infusion (Banisteriopsis caapi and Psychotria viridis) in female Wistar rat.

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Abstract

Ayahuasca, a psychoactive beverage used by indigenous and religious groups, is generally prepared by the coction of Psychotria viridis and Banisteriopsis caapi plants containing N,N-dimethyltryptamine (DMT) and β-carboline alkaloids, respectively. To investigate the acute toxicity of ayahuasca, the infusion was administered by gavage to female Wistar rats at doses of 30X and 50X the dose taken during a religious ritual, and the animals observed for 14 days. Behavioural functions were investigated one hour after dosing at 15X and 30X using the open field, elevated plus maze, and forced swimming tests. Neuronal activation (c-fos marked neurons) and toxicity (Fluoro-Jade B and Nissl/Cresyl staining) were investigated in the dorsal raphe nuclei (DRN), amygdaloid nucleus, and hippocampal formation brain areas of rats treated with a 30X ayahuasca dose. The actual lethal oral dose in female Wistar rats could not be determined in this study, but was shown to be higher than the 50X (which corresponds to 15.1mg/kg bw DMT). The ayahuasca and fluoxetine treated groups showed a significant decrease in locomotion in the open field and elevated plus-maze tests compared to controls. In the forced swimming test, ayahuasca treated animals swam more than controls, a behaviour that was not significant in the fluoxetine group. Treated animals showed higher neuronal activation in all brain areas involved in serotoninergic neurotransmission. Although this led to some brain injury, no permanent damage was detected. These results suggest that ayahuasca has antidepressant properties in Wistar female at high doses, an effect that should be further investigated.

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Broooossss, if this isn't neurotoxicity, we saved.

 

Edit: This really is one of the most profound and confusing conditions I have seen in medicine, probably only comparable with Stevens Johnson Syndrome.

 

Can someone try Cinquefoil, for 1-2 months and report their findings as far as improvement, and someone else please try zinc sulfate for about 4 months, and please report your findings, Oliver is already taking sage as far as I know to see if there is any improvement, that treatment may be shorter than I determined initially, which was 2-3 years. If you do try these please report any findings or improvements. If you take zinc please make sure it is zinc sulfate. Thank you.

Edited by dasitmane

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The weirdest thing about this condition is that it is highly related to palinopsia, and visual snow syndrome(like oliver states), however typical cases of palinopsia usually have some degree of neuronal damage done, but MRIs for most HPPD patients mainly have normal results aside from white matter lesions, which realistically could just be demyelination

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https://www.ncbi.nlm.nih.gov/pubmed/30910546

Maybe there are certain cases of hallucinogens depositing these protein in the brain, and maybe some people have a disorder that prevents the removal of them. As the link explains a person to developed visual snow before his CJD became serious.

CJD, is a type of transmissible spongiform encephalopathy (TSE), which are caused by prions.[5] Prions are proteins that occur normally in neurons of the central nervous system (CNS). These proteins, once misfolded, are thought to affect signaling processes, damaging neurons and resulting in degeneration that causes the spongiform appearance in the affected brain.[13]

The CJD prion is dangerous because it promotes refolding of native prion protein into the diseased state.[14] The number of misfolded protein molecules will increase exponentially and the process leads to a large quantity of insoluble protein in affected cells. This mass of misfolded proteins disrupts neuronal cell function and causes cell death. Mutations in the gene for the prion protein can cause a misfolding of the dominantly alpha helical regions into beta pleated sheets. This change in conformation disables the ability of the protein to undergo digestion. Once the prion is transmitted, the defective proteins invade the brain and induce other prion protein molecules to misfold in a self-sustaining feedback loop. These neurodegenerative diseases are commonly called prion diseases.

People can also develop CJD because they carry a mutation of the gene that codes for the prion protein (PRNP). This occurs in only 5–10% of all CJD cases. In sporadic cases the misfolding of the prion protein is a process which is hypothesized to occur as a result of the effects of aging on cellular machinery, explaining why the disease often appears later in life.[4][15] An EU study determined that "87% of cases were sporadic, 8% genetic, 5% iatrogenic and less than 1% variant."[16]

 

https://en.wikipedia.org/wiki/PRNP Prions protein link.

 

This is super weird condition. Its like an infection.... but its just a protein....

Edited by dasitmane

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