Fawkinchit

Didn't watch the video but I assume its someone who thinks the symptoms are fake, left a nice comment for them lol. Doesn't matter anyways this guy probably wont ever have much traction. Edit: What a fucking idiot lmao. Imagine having to be this stupid, every day.

I know I haven't been posting much lately, this condition is very troubling for everyone, I understand. I want to let everyone know that I am dedicated to furthering the research, understanding, and treatment for this condition, fully and to complete resolution as long as the physics of the universe will allow it. I am trying very diligently to find a way to accumulate funds for further research, because I believe its at that point. I do genuinely believe that this condition is mitochondrial in origin and damaging to neurons, whether it be microstructure or apoptosis. We need ways to do extensive research to facilitate real and known ways for resolving this. Please do not excuse my lack of posting as surrender, or any form of relinquishment. As long as I live on this earth, I will continue to find a way to resolve this. Thanks to everyone that follows my posts and supports me, and I thank everyone for their kind words.

Found some extremely interesting studies today that show that hallucinogens increase over excitation in the prefrontal cortex specifically of the pyramidal cells, and another study showing that there is an interaction linking these pyramidal cells along with inhibitory neurons to anxiety, which is a commonly reported symptoms of HPPD as everyone knows. It talks about a ratio in certain cases between the types of cells becoming imbalanced, though the reason cause seemingly is untraced. I find it interesting because its likely that in HPPD these may be the specific cells that are damaged, it could also be the loss of the inhibitory cells that allow for HPPD symptoms via the pyramidal cell dysregulation. https://journals.sagepub.com/doi/full/10.1177/0269881121991569 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6345483/

Wait so.... it was caused from drugs, or had a completely spontaneous random onset? I cant really tell

Wow holy shit, great find, not entirely sure what they mean by the terminology, but it sounds like a very reserved way of saying its bad. I think we all kind of knew that though lol. Fuck. Well at least its a move in the right direction. I'll see what I can find by what they mean by "microstructure" unless someone already knows. Edit: "The aim of microstructural imaging is to quantify the properties of tissue components, such as myelin, axons, dendrites, glia, and to characterise pathological features such as demyelination, inflammation, axonal loss." They say that there is no change in morphometry, so it would appear that maybe there is no actual structural damage, aka neuronal loss, at least not enough to change shape/size of the brain structure. Thats good. They list axonal loss in microstructure, but as far as I have understood, once the axon is lost the neuron goes? Maybe someone can correct me on this?

Still waiting for updates on this....

Mitochondrial dysfunction can certainly be organ specific for various reasons. The predisposition is likely just vitamin deficiencies during the time of hallucinogenic ingestion, or some sort of metabolic disorder. I would lean more strongly towards specific deficiencies during time of ingestion. Vitamin c and various b vitamins are likely culprits, but there could be others.

I can sympathize with this, I also became more or less introvert after getting HPPD. I spend a LOT of time alone, rarely do socializing etc. Granted however there are also some variables about humans that I learned when I got HPPD that attributed to that learning curve.

Please definitely keep us updated! This could be very interesting. Thanks!

Are there any routines or medications that you have changed recently in your life? Any changes at all?

These are very crude methods for sustaining mitochondria metabolism. Gross methods rather, even if they do work to some degree. It would be much easier to get better and safer results with say CoQ10. There is quite a list of safe alternatives than what the study listed.

I am unfortunately at this time uncertain of the availability of these techniques.

I wanted to start a new topic in attempt to find willing participants for a new strategy in MRI techniques that I have found. I haven't had time to review all the information as thoroughly as I would like, however, what I have found seems very promising. In short it seems that one of my old theories about MRI and its shortcomings for detecting mild diffuse neuronal loss was accurate, and that new techniques are being used to overcome these shortcomings. In the two articles that I will post it should be a apparent to everyone that these techniques are far more accurate in accessing neuronal loss, and neuronal density. These types of MRIs are called T1p MRI, and R2t MRI, no RTD2 lol. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2637389/ https://medicine.wustl.edu/news/background-signal-in-mri-scans-reveals-how-brain-cells-develop-and-die/ Just read the articles and I believe everyone will see for themselves as to why nothing is being found in our MRIs, its specifically due to the fact that MRIs are not effective techniques for accessing mild diffuse neuronal loss, but rather only effective in detecting gross neuronal loss. If anyone would be willing to do one of these types of MRIs and could find a doctor that knows how to administer the techniques then I think that we very well could find the final accurate diagnosis to HPPD, and at the very least understand its cause, which would open up the field to more accurately accessing treatment options, and also removing lack luster prescriptions and bogus attempts at treatment that we are all very well aware of. I really do hope that we can find some people willing to seek this out and do the MRIs, I genuinely do believe they will give us far more insight in to the condition than just a general normal MRI. Please let me know what all of your thoughts are on this. Thank you so much! Edit: I would just like add the following, which basically is, that given all of this information and some information that was posted by @MentholFlavoring that just as he states and as I have theorized in the past and present, that this is definitely a condition of a case of neuronal loss. I think the evidence couldn't be more clear. The only reason that people were doubting that it was neuronal loss was because the MRIs were "normal", but this information proves that my theory about MRIs were accurate, and that there is still the definite possibility of it being neuronal loss. And ill also post some information that was brought to my attention by Menthol, which is basically just a wiki link https://en.wikipedia.org/wiki/Depersonalization-derealization_disorder#Neurobiology But it explains that these people with DPDR have atrophied regions of the brain even in normal MRIs, so their cases are likely more severe, but it also mentions the hypothalamic-pituitary-adrenal axis being disrupted, which explains the massive anxiety that a lot of sufferers experience due to it activating the fight of flight response, also they even have increase cortisol levels, which should be expected from the massive stress that is put on the organism from DPDR, but also even HPPD. Its basically the same stuff, probably affected in the same areas for the most part. It clearly doesn't affect motor neurons, so Dr. Abrahams idea that it only affects interneurons is most likely accurate.

Neuronal damage as far as modern medicine goes is entirely reversable. They would technically heal/repair on their own accord with do time, as far as we understand the nervous system. No deep brain stimulation required.

So they don't share the dose given, and also focused on only one area of the brain. Its more than likely if you are going to see neuronal loss it will be in the limbic or stem areas. Also, dosage will cause significant variations on effects. Maybe I just missed the section that talks about dosage though?

My thoughts are agreeable with MadDoc's, infections put a lot of stress on the body, so it may wind up symptoms, and could take a few weeks to even a month to wind down.

Sounds more like you have certain degenerative issues going on with the eye, its unlikely to be caused by drug use. Granted, drug use could increase susceptibility possibly. It may be beneficial to take 2g of vitamin c a day, and take vitamin a as well, normal dose. Could possibly stop or slow the progression. I havent read enough on macular or other eye issues to say for sure though.

T. gondii is an intracellular parasite that has a tropism for the CNS. Although it is generally asymptomatic in immunocompetent hosts, it can lead to severe psychiatric, neurological disorders. Several studies have shown that T. gondii affects the synthesis of neurotransmitters, particularly DOPA, in infected individuals, which could lead to personality changes, psychotic symptoms, and in some cases, neurological and psychiatric disorders. The results of this study show that T. gondii appears to be an etiological factor of schizophrenia. https://bmcpsychiatry.biomedcentral.com/articles/10.1186/s12888-020-02683-0 Pretty interesting stuff. Not making any claims that HPPD is a parasite, but its clearly shown to not be impossible. and more... Some cases of acute toxoplasmosis in adults are associated with psychiatric symptoms such as delusions and hallucinations. A review of 114 cases of acquired toxoplasmosis noted that “psychiatric disturbances were very frequent” in 24 of the case-patients (10). Case reports describe a 22-year-old woman who exhibited paranoid and bizarre delusions (“she said she had no veins in her arms and legs”), disorganized speech, and flattened affect; a 32-year-old woman who had auditory and visual hallucinations; and a 34-year-old woman who experienced auditory hallucinations and a thought disorder (11). Schizophrenia was first diagnosed in all three patients, but later neurologic symptoms developed, which led to the correct diagnosis of Toxoplasma encephalitis. Tachyzoites may invade different types of nervous cells, such as neurons, astrocytes and microglial cells in the brain, and Purkinje cells in cerebellum. Intracellular tachyzoites manipulate several signs for transduction mechanisms involved in apoptosis, antimicrobial effectors functions, and immune cell maturation. Dopamine levels are 14% higher in mice with chronic infections. These neurochemical changes may be factors contributing to mental and motor abnormalities that accompany or follow toxoplasmosis in rodents and possibly in humans. Moreover, the antipsychotic haloperidol and the mood stabilizer valproic acid most effectively inhibit Toxoplasma growth in vitro with synergistic activity.

Welcome back!

If this were the case wouldn’t just taking an anti histamine relieve symptoms to some degree?

My take personally is that it shows more prominence of reactive oxygen species(ROS) in people with mental disease, which is absolutely no surprise there. Its pretty clear that high kynurenic acid is just an end result of increased ROS, treating the ROS therefore would be more suitable. Its something I talk about in my threads, and there are various ways of reducing these problems. "Kynurenic acid (KYNA) synthesis along the kynurenine pathway and its mode of action. The catabolism of TRP by the enzymes TDO or IDO represents the rate-limiting step in KYNA synthesis. The intermediate metabolite kynurenine can be further processed through three distinct pathways to form KYNA, 3-hydroxykynurenine, and anthranilic acid. KYNA is formed by the irreversible transamination of KYN either via kynurenine aminotransferases (KAT I–IV) or through the action of reactive oxygen species (ROS)."

Riboflavin Has Neuroprotective Potential: Focus on Parkinson’s Disease and Migraine Eyad T. Marashly* and Saeed A. Bohlega Department of Neurosciences, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia With the huge negative impact of neurological disorders on patient’s life and society resources, the discovery of neuroprotective agents is critical and cost-effective. Neuroprotective agents can prevent and/or modify the course of neurological disorders. Despite being underestimated, riboflavin offers neuroprotective mechanisms. Significant pathogenesis-related mechanisms are shared by, but not restricted to, Parkinson’s disease (PD) and migraine headache. Those pathogenesis-related mechanisms can be tackled through riboflavin proposed neuroprotective mechanisms. In fact, it has been found that riboflavin ameliorates oxidative stress, mitochondrial dysfunction, neuroinflammation, and glutamate excitotoxicity; all of which take part in the pathogenesis of PD, migraine headache, and other neurological disorders. In addition, riboflavin-dependent enzymes have essential roles in pyridoxine activation, tryptophan-kynurenine pathway, and homocysteine metabolism. Indeed, pyridoxal phosphate, the active form of pyridoxine, has been found to have independent neuroprotective potential. Also, the produced kynurenines influence glutamate receptors and its consequent excitotoxicity. In addition, methylenetetrahydrofolate reductase requires riboflavin to ensure normal folate cycle influencing the methylation cycle and consequently homocysteine levels which have its own negative neurovascular consequences if accumulated. In conclusion, riboflavin is a potential neuroprotective agent affecting a wide range of neurological disorders exemplified by PD, a disorder of neurodegeneration, and migraine headache, a disorder of pain. In this article, we will emphasize the role of riboflavin in neuroprotection elaborating on its proposed neuroprotective mechanisms in opposite to the pathogenesis-related mechanisms involved in two common neurological disorders, PD and migraine headache, as well as, we encourage the clinical evaluation of riboflavin in PD and migraine headache patients in the future. Introduction With the huge burden of neurological diseases on patient’s life and society resources, the need of finding and having neuroprotective agents is critical and cost-effective. In fact, the advances in medical research have found up to date multiple agents having unique proposed neuroprotective mechanisms and influencing different neurologic disease processes. Riboflavin is one of those proposed neuroprotective agents; however, its neuroprotective abilities have been underestimated in comparison to other known neuroprotective agents. Our focus in this article is to shed light on riboflavin neuroprotective characteristics, encouraging more research to be done in the future in this regard. Riboflavin, a water-soluble vitamin, is part of the B complex vitamins, known as vitamin B-2. It is characterized by its unique bright yellow coloration of urine when taken in large amounts. Riboflavin plays a role in a wide range of metabolic pathways and processes, serving as a coenzyme for a variety of flavoprotein enzyme reactions. Riboflavin active forms are flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD). Importantly, 10–15% of global population have an inherited condition of limited riboflavin absorption and utilization; leading to a potential biochemical riboflavin deficiency worldwide (1). In fact, based on erythrocyte glutathione reductase activation coefficient test (EGRAC), 54% of British non-elderly adult population was at least having borderline riboflavin deficiency (1). Indeed, riboflavin deficiency across European countries ranges between 7 and 20% (2). As a matter of fact, neural tissue has a higher susceptibility to oxidative stress. Oxidative stress, a term refers to the injurious results in living organisms due to an imbalance favoring oxidants over antioxidants (3), has been implicated in multiple disease processes and aging. Oxidants are the normal results of in vivo interactions between oxygen and organic molecules. Concerning the brain, it forms 2% of total body weight with high levels of fatty acids, uses 20% of total body oxygen, and has lower antioxidant activity than other tissues. This gives the neural tissue a higher susceptibility to peroxidation (4) and oxidative damage in comparison to other tissues. In fact, oxidative stress has been implicated in multiple neurodegenerative disorder pathogenesis (4). https://www.frontiersin.org/articles/10.3389/fneur.2017.00333/full

https://www.frontiersin.org/articles/10.3389/fphys.2020.00598/full More valuable information

How long did you take the vitamin d for?