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

[olivier24445]

On 3/8/2020 at 4:26 AM, Fawkinchit said:

Important Please Read: 

I've been reading a lot and I think that there may be a possibility and link to a nutritional deficiency in HPPD, which realistically would assess the strange variable nature of this condition. If you at immediate glance question the severity of nutritional deficiencies just look up Pellagra and Scurvy, they eventually die if its not corrected. Most vitamins are antioxidants and neutralize free radicals, and hallucinogens stimulate neuronal metabolism leading to excess free radicals. When free radicals are excessive and deficiencies have occurred of said nutrients, the free radicals can no longer be controlled and spiral out of control, damaging surrounding tissues. These tissues in turn become inflamed and even due to their neuronal nature start becoming demyelinated, this is the explanation for the very mild incidence rate of white matter hyperintensities in HPPD MRIs, however not in all. These demyelinations under the given uncorrected circumstances cannot or very difficulty be repaired, unless the deficiency is corrected. The deficiency would also explain why some people never get HPPD, even with extreme doses of LSD use, they have plenty of reserves of the free radical neutralizing vitamin necessary.  It would also explain why some people only get it after multiple uses of hallucinogens, eventually they deplete the vitamin, whichever it may be. It would also explain the relationship with alcohol initiating HPPD in people who did hallucinogens a month or two beforehand, alcohol also may variably deplete the vitamin. It also could explain the spontaneous recovery of some few individuals that have reported it. It would also explain why multiple different drugs initiate HPPD, from alcohol, to weed, to hallucinogens, they all stimulate neuronal metabolism by excitation and or drain certain vitamins that are vital to neuronal functioning and maintenance, hence the symptoms. Also some of these vitamins are absolutely crucial to proper neuronal function and a deficiency only of some, like Vitamin B3 can lead to psychosis. I could elaborate further on this but will refrain for the sake of brevity. 

If anyone in the slightest bit thinks this to be a complete impossibility, like i said look up pellagra and the mental health issues they have, and even vitamin b12 deficiencies cause demyelination of axons. And even some may argue that the nutritional RDA is met by common foods, this assuredly isn't true, and proven not to be true, especially in the cases of drug use and alcoholism, there are definitely related deficiencies common with these habits.

I think that this possibility has some of the most merit than any of my other ideas, so if anyone would like to try and experiment as to whether a treatment will work, then they should get a full spectrum b vitamin complex(All B-vitamins known). and also Vitamin C. The B complex should be higher than the average listed RDA, as typically it wouldn't be enough. And the vitamin C needs to be at the very least 1000mg a day. Treatment should be carried out for 6 months.

I wont get in to all the details as to everything correlative with vitamins, their deficiencies, and their importance, but if anyone cares to know more, they can read "How to Feel Better and Live Longer" by Linus Pauling, two time Nobel Prize winner and profession chemist. Even if the treatments don't work, at the very least it will certainly improve the health of the person taking these vitamins.

If its not that then we may have some genetic defect.

If you do try this treatment please report that you are trying it, and also please absolutely follow up with your results in the future. Thank you!

Edit: I also forgot to add that I read that taking large doses of vitamin B3 will end an LSD trip within roughly 30 minutes, which shows a specific relationship with it and hallucinations, but not however with LSD diectly as far as I can conjecture, as LSD usually is metabolized within 30 minutes of hitting the blood stream. However the hallucinations continue for hours, which shows that the actual cause of hallucinations are downstream from LSD metabolism, and have a direct correlation with Niacin(b3) if thats true. I didn't read it from what I would consider an absolute reliable source, but there very well may be some merit and truth to the statement, as it wasn't an unreputable source either. If anyone else knows more feel free to share.

Very interesting theory.

I was actully having a lifetime food dysfunction from 0 to 18 yo when i had my hppd onset.

Turns out, there is something to dig here.

I made 2 polls over the nutrition problem : 

For hppd : https://www.reddit.com/r/HPPD/comments/fgfbva/preexisting_your_hppd_food_disorder_malnutrition/

 

For VSS : https://www.reddit.com/r/visualsnow/comments/fhdp2y/preexisting_your_vss_food_disorder_malnutrition/

 

[Fawkinchit]

The relation between migraine, typical migraine aura and "visual snow".

Schankin CJ¹, Maniyar FH, Sprenger T, Chou DE, Eller M, Goadsby PJ.

Author information

Erratum in

• Headache. 2015 Apr;55(4):592. 

Abstract

OBJECTIVE: 

To assess the relationship between the phenotype of the "visual snow" syndrome, comorbid migraine, and typical migraine aura on a clinical basis and using functional brain imaging.

BACKGROUND: 

Patients with "visual snow" suffer from continuous TV-static-like tiny flickering dots in the entire visual field. Most patients describe a syndrome with additional visual symptoms of the following categories: palinopsia ("afterimages" and "trailing"), entopic phenomena arising from the optic apparatus itself (floaters, blue field entoptic phenomenon, photopsia, self-light of the eye), photophobia, nyctalopia (impaired night vision), as well as the non-visual symptom tinnitus. The high prevalence of migraine and typical migraine aura in this population has led to the assumption that "visual snow" is caused by persistent migraine aura. Due to the lack of objective measures, alternative diagnoses are malingering or a psychogenic disorder.

METHODS: 

(1) The prevalence of additional visual symptoms, tinnitus, and comorbid migraine as well as typical migraine aura was assessed in a prospective semi-structured telephone interview of patients with "visual snow." Correlations were calculated using standard statistics with P < .05 being considered statistically significant. (2) Areas with increased brain metabolism in a group of "visual snow" patients in comparison to healthy controls were identified using [(18) F]-2-fluoro-2-deoxy-D-glucose positron emission tomography and statistical parametric mapping (SPM8 with whole brain analysis; statistical significance was defined by P < .001 uncorrected for multiple comparisons).

RESULTS: 

(1) Of 120 patients with "visual snow," 70 patients also had migraine and 37 had typical migraine aura. Having comorbid migraine was associated with an increased likelihood of having palinopsia (odds ratio [OR] 2.8; P = .04 for "afterimages" and OR 2.6; P = .01 for "trailing"), spontaneous photopsia (OR 2.9; P = .004), photophobia (OR 3.2; P = .005), nyctalopia (OR 2.7; P = .01), and tinnitus (OR 2.9; P = .006). Typical migraine aura was associated with an increased likelihood of spontaneous photopsia (OR 2.4; P = .04). (2) After adjusting for typical migraine aura, comparison of 17 "visual snow" patients with 17 age and gender matched controls showed brain hypermetabolism in the right lingual gyrus (Montreal Neurological Institute coordinates 16-78-5; kE  = 101; ZE  = 3.41; P < .001) and the left cerebellar anterior lobe adjacent to the left lingual gyrus (Montreal Neurological Institute coordinates -12-62-9; kE  = 152; ZE  = 3.28; P = .001).

CONCLUSIONS: 

-Comorbid migraine aggravates the clinical phenotype of the "visual snow" syndrome by worsening some of the additional visual symptoms and tinnitus. This might bias studies on "visual snow" by migraineurs offering study participation more likely than non-migraineurs due to a more severe clinical presentation. The independence of entoptic phenomena from comorbid migraine indicates "visual snow" is the main determinant. The hypermetabolic lingual gyrus confirms a brain dysfunction in patients with "visual snow." The metabolic pattern differs from interictal migraine with some similarities to migrainous photophobia. The findings support the view that "visual snow," migraine, and typical migraine aura are distinct syndromes with shared pathophysiological mechanisms that need to be addressed in order to develop rational treatment strategies for this disabling condition.

[Fawkinchit]

https://www.tapatalk.com/groups/thosewithvisualsnow/a-discussion-with-dr-weatherall-the-leading-visual-t7745.html
 

found these people talking about their visual snow and found it interesting their non drug use sudden onsets...

[Tom]

I have just read the first couple of pages of this forum. I believe I have HPPD after a bad trip in December 2019. Onset January 2020.

I had a GI Map test in 2019 due to stomach issues. The results showed that I had a bacteria overgrowth of staph Auerus, Baccilis SPP and Morganella SPP. I wanted to share this as it correlated with your research. I’m currently seeing a Chinese practitioner who is treating me for the bacteria overgrowth and he suspects that I also have Lyme disease. 
 

 

[Guest]

Meet Wei!

Wei is one of the researchers working on Dr. McConnell’s team who wants to pinpoint exactly where the damage has been done to the HPPD brain.

How is her progress going?

Not well, in fact not at all due to COVID and that fact that she’s just returning to work from maternity leave but even after she returns, no research will begin as there’s no money to pay her to do any work. This is why I implore the tens of thousands of HPPDers on this site to donate. Let family and friends know that there is a dedicated team with the best credentials working in one of the most prestigious universities around the world. The NRF is real and as a patient I want to go back to a pre HPPD state ASAP. Funding her work will take us there.
 

PLEASE DONATE!

www.neurogroup.org

CV.WEIHE_SHORT_2018_12_16.pdf

[mgrade]

....hi....

Edited December 12, 2020 by mgrade
privacy, mistake for posting

[Fawkinchit]

On 6/18/2020 at 5:05 AM, mgrade said:

I've been a supporter of this site for 10 years.    I'm virtually disabled at this point. 

[Removed links, by request -jay1]

Whats up mgrade long time no see how have you been? Looks like you been doing some writing?

Also to everyone: I just linked up with Oliver on Whatsapp, if anyone would like to join a group chat just send me your information for whatsapp and I will add you to the chat!

Also for an update I am still doing a lot of work on trying to find something relevant for this disorder, after the long years of working on it though I'm extremely exhausted, and there have been so many other things in life that I have been trying to accomplish and keep together as well. I am still trying to make progress though and have been looking in to some interesting and relevant information involving other conditions that develop like symptoms and also hallucinations. Its become apparent that there are a lot of conditions of the body that are linked to healthy brain function, and when there are issues with these sections of the body, the brain does not function as it should, it isn't then per say, a requisite that the disorder lies solely in the brain, but could be elsewhere. I will try to share relevant information when I have time. I apologize to everyone that I haven't been as busy with this as usual. I do genuinely hope that we all end in a happy place and get a second chance, and I thank everyone that has posted here and talked with me and shared their information, it has been really encouraging and uplifting to continue trying. Thanks for everyone too that has been kind to me and reached out, I apologize also to anyone that I have not been able to help significantly, or have been rude to in the past, as I was under a lot of stress, and didn't have the best functioning brain for proper emotional handling. 

 

Also, Hope, the website looks good!

[Aangtheairbender]

From what I’ve gathered I feel like the most probable cause of hppd is excessive serotonin 5ht2a up-regulation resulting in neuronal toxicity and subsequent neuronal death. The running theory is that hppd is caused by 5ht receptor death over time. I think that what’s causing the 5ht death is overexcited / overstimulated 5ht2a receptors following drug use. These neurons are connected to vision because lsd and pcp (leading causes of hppd) affect the visual cortex primarily. I think this because all of the things that seem to make hppd “better” stimulate gaba receptors which are function to calm overexcited neurons. (Valerian root, magnesium, klonopin, benzos they all stimulate gaba receptors). When a neuron is overexcited that means it’s firing too often-wouldn’t that mean that 5ht2a is firing too often?- and gaba makes neurons fire less often, thus quelling hppd symptoms. That’s just a hypothesis though. That’s why I feel like ssri’s make hppd worse. They must up-regulate 5ht2a because ssri boost serotonin. Moreover, we know anti psychotics don’t work either. Maybe this is because when serotonin levels are too low they induce psychosis symptoms. So maybe the cure is down-regulating 5ht2a but not fully  blocking it? Just a theory again what do you guys think? 

[p3rs0n]

It also seems like there was a pattern of anxiety that occurred, sometimes very extreme anxiety, upon withdrawal which may have been a precursor to these changes.  Or was just a coincidence. 

 

Edited October 31, 2020 by p3rs0n

[Fawkinchit]

After more research I wanted to post this, as I have been postulating that there could be adrenal dysfunction involved in HPPD. But there would likely have to be clear evidence that hallucinogens have impacts on the adrenals in the first place. So here I'm presenting this study. So it shows there could be some sort of adrenal dysfunction involved, which seems a bit misguided, but Dr. Royal Lee talks about caused hallucinations and their involvements with the adrenals, and I even found a case report of a man who was hallucinating badly, and it was eventually found that for some reason his adrenals weren't producing cortisol, on administration of synthetic cortisol there was a remission of the hallucinations. 

https://pubmed.ncbi.nlm.nih.gov/26849997/

Acute Effects of Lysergic Acid Diethylamide on Circulating Steroid Levels in Healthy Subjects

P Strajhar ¹, Y Schmid ², E Liakoni ², P C Dolder ^2 3, K M Rentsch ³, D V Kratschmar ¹, A Odermatt ¹, M E Liechti ²

Affiliations expand

• PMID: 26849997
•  
• DOI: 10.1111/jne.12374

Abstract

Lysergic acid diethylamide (LSD) is a serotonin 5-hydroxytryptamine-2A (5-HT2A ) receptor agonist that is used recreationally worldwide. Interest in LSD research in humans waned after the 1970s, although the use of LSD in psychiatric research and practice has recently gained increasing attention. LSD produces pronounced acute psychedelic effects, although its influence on plasma steroid levels over time has not yet been characterised in humans. The effects of LSD (200 μg) or placebo on plasma steroid levels were investigated in 16 healthy subjects using a randomised, double-blind, placebo-controlled, cross-over study design. Plasma concentration-time profiles were determined for 15 steroids using liquid-chromatography tandem mass-spectrometry. LSD increased plasma concentrations of the glucocorticoids cortisol, cortisone, corticosterone and 11-dehydrocorticosterone compared to placebo. The mean maximum concentration of LSD was reached at 1.7 h. Mean peak psychedelic effects were reached at 2.4 h, with significant alterations in mental state from 0.5 h to > 10 h. Mean maximal concentrations of cortisol and corticosterone were reached at 2.5 h and 1.9 h, and significant elevations were observed 1.5-6 h and 1-3 h after drug administration, respectively. LSD also significantly increased plasma concentrations of the androgen dehydroepiandrosterone but not other androgens, progestogens or mineralocorticoids compared to placebo. A close relationship was found between plasma LSD concentrations and changes in plasma cortisol and corticosterone and the psychotropic response to LSD, and no clockwise hysteresis was observed. In conclusion, LSD produces significant acute effects on circulating steroids, especially glucocorticoids. LSD-induced changes in circulating glucocorticoids were associated with plasma LSD concentrations over time and showed no acute pharmacological tolerance.

 

Edited July 17, 2020 by Fawkinchit

[Aangtheairbender]

13 hours ago, Fawkinchit said:

After more research I wanted to post this, as I have been postulating that there could be adrenal dysfunction involved in HPPD. But there would likely have to be clear evidence that hallucinogens have impacts on the adrenals in the first place. So here I'm presenting this study. So it shows there could be some sort of adrenal dysfunction involved, which seems a bit misguided, but Dr. Royal Lee talks about caused hallucinations and their involvements with the adrenals, and I even found a case report of a man who was hallucinating badly, and it was eventually found that for some reason his adrenals weren't producing cortisol, on administration of synthetic cortisol there was a remission of the hallucinations. 

https://pubmed.ncbi.nlm.nih.gov/26849997/.

 

Hey how's it going. I think you're onto something here. In the DSM it says that HPPD is often misdiagnosed as panic disorder. In addition, we know from individual accounts that HPPD can sometimes mimic PTSD symptoms and severe anxiety/ panic attacks. All of these symptoms are directly connected to the adrenal response. This explains why gaba agonists like Klonopin and Valerian reduce HPPD symptoms. Because gaba functions to calm down the fear center in the brain aka the adrenal response (fight or flight). I was actually diagnosed with b12 deficiency a year after getting HPPD. Your body needs vitamin b12 to create cortisol, which means my cortisol levels were low. After taking b-12 supplements my panic symptoms reduced but I still have hppd. 

[Fawkinchit]

8 hours ago, Aangtheairbender said:

Hey how's it going. I think you're onto something here. In the DSM it says that HPPD is often misdiagnosed as panic disorder. In addition, we know from individual accounts that HPPD can sometimes mimic PTSD symptoms and severe anxiety/ panic attacks. All of these symptoms are directly connected to the adrenal response. This explains why gaba agonists like Klonopin and Valerian reduce HPPD symptoms. Because gaba functions to calm down the fear center in the brain aka the adrenal response (fight or flight). I was actually diagnosed with b12 deficiency a year after getting HPPD. Your body needs vitamin b12 to create cortisol, which means my cortisol levels were low. After taking b-12 supplements my panic symptoms reduced but I still have hppd. 

Completely agree, actually my HPPD no longer has symptoms revolving around the more recognized symptoms, it just seems to manifest in severe anxiety some times, like it literally feels like my entire nervous system is on fire. and it goes away after a couple hours. I rarely have issue anymore but sometimes it does flare up. I used to have a lot of the typical symptoms when I first got it and it was full blast.

Anyways  I want to post this write up by Dr. Royal Lee, from all the doctors I've seen I haven't seen many a greater, if any at all, and he does explain that brain dysfunction can stem from liver issues, and plainly states that narcotics can disrupt the urea(carbamide) production, which is specifically in the liver, so we may just have a liver issue.

 

What I'm wondering is maybe there is a correlation, and in HPPD the narcotic induces long term change in the liver, or the livers function in metabolizing urea/carbamide.

Edited July 18, 2020 by Fawkinchit

[Fawkinchit]

https://www.sciencedirect.com/science/article/pii/0041008X66901281

adding this for later

 

[Fawkinchit]

Mitochondria dysfunction in neurons could have a possible role. Obviously the article is geared more towards depression and suicide, but they mention PTSD as well, and I'm sure that the problems caused by mitochondrial dysfunctions could be expanded to HPPD as well.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4417658/

The Role of Nutrients in Protecting Mitochondrial Function and Neurotransmitter Signaling: Implications for the Treatment of Depression, PTSD, and Suicidal Behaviors

Jing Du,^1,3,*# Ming Zhu,^1,* Hongkun Bao,¹ Bai Li,¹ Yilong Dong,¹ Chunjie Xiao,¹ Grace Y. Zhang,³ Ioline Henter,⁴ Matthew Rudorfer,² and Benedetto Vitiello²

Author information Copyright and License information Disclaimer

 

The publisher's final edited version of this article is available at Crit Rev Food Sci Nutr

See other articles in PMC that cite the published article.

 

Go to:

Abstract

Numerous studies have linked severe stress to the development of major depressive disorder (MDD), and suicidal behaviors. Furthermore, recent preclinical studies from our laboratory and others have demonstrated that in rodents, chronic stress and the stress hormone cortisol has caused oxidative damage to mitochondrial function and membrane lipids in the brain. Mitochondria play a key role in synaptic neurotransmitter signaling by providing adenosine triphosphate (ATP), mediating lipid and protein synthesis, buffering intracellular calcium, and regulating apoptotic and resilience pathways. Membrane lipids are similarly essential to central nervous system (CNS) function, because cholesterol, polyunsaturated fatty acids, and sphingolipids form a lipid raft region, a special lipid region on the membrane that mediates neurotransmitter signaling through G-protein coupled receptors and ion channels. Low serum cholesterol levels, low antioxidant capacity, and abnormal early morning cortisol levels are biomarkers consistently associated with both depression and suicidal behaviors. In this review, we summarize the manner in which nutrients can protect against oxidative damage to mitochondria and lipids in the neuronal circuits associated with cognitive and affective behaviors. These nutrients include ω3 fatty acids, antioxidants (vitamin C and zinc), members of the vitamin B family (Vitamin B12 and folic acid) and magnesium. Accumulating data have shown that these nutrients can enhance neurocognitive function, and may have therapeutic benefits for depression and suicidal behaviors. A growing body of studies suggests the intriguing possibility that regular consumption of these nutrients may help prevent the onset of mood disorders and suicidal behaviors in vulnerable individuals, or significantly augment the therapeutic effect of available antidepressants. These findings have important implications for the health of both military and civilian populations.

Keywords: vitamin, oxidative stress, synaptic plasticity, lipid, suicide, zinc

Edited August 13, 2020 by Fawkinchit

[Fawkinchit]

So, I've been here, working on this, for 8 years now, and I think I have a conclusion. The main thing that I have noticed about HPPD, is that it is quite similar in presentation, though not so much in symptoms, to other mental health conditions, mainly epilepsy, and migraines. I have also found some convincing evidence that it is even somewhat similar in fashion to PTSD. Now, I believe its been quite discussed that as far as significant neuronal loss is concerned, it doesn't appear to be quite the case in HPPD, though I can't argue that some aren't lost, it doesn't appear to be the main driving factor involved. So, from there going on we have to look beyond the organ itself, the brain, and beyond the cell itself, the neuron, to the intricacies thereof involved within the structure, and within the metabolism. Given lack of studies this is a difficult thing, but if we take in to consideration the presentation of other similar conditions there is a common factor involved, this factor appears to be mitochondrial dysfunction. We can easily assert and know for certain that it is a definite and common finding within the investigations of epilepsy, and even in migraines as well, this is a proven fact. My idea is simple, that these are all the same conditions, effecting different areas of the brain, or possibly even different aspects of the mitochondrion. Now, this may all seem complicated, but there's no need to bewail over this matter, as I have found multiple ways of reversing mitochondrial dysfunction, some out of pure common sense, and others by proven scientific research. As for example the matter of migraines, it was shown in studies to be ameliorated by long term use of 400mg of riboflavin/vitamin b2, and reverse the condition of migraines all together. This is a great hope, and opportunity. 

Now, this isn't all, based on a lot of my reading, and findings, which I will not go in to depth about as to how I came to this conclusion, or that conclusion, there are other methods as well of achieving this outcome, which is very exciting, and may yield very positive and beneficial results. So, what I recommend also, is grape seed extract, because of the high content of proanthocyanins, which will also achieve the same goal of ameliorating mitochondrial dysfunction. Yet it would be better if you consume also a great deal of grapes with seeds in them, seedless however are rendered ineffectual, as the highest content of proanthocyanins are in the seeds. And if any are so inclined to try other things of the same magnitude, it would be wise to drink cinquefoil, and common sage as a tea, daily. All in my opinion are very fit for the amelioration of mitochondrial dysfunction, and the sage will help proliferations in the brain, and often gives a calming effect. So anyone can try this one or that one, or all together, its no matter to me. Just be safe and use increments in dosage to be sure there aren't any immediate worsening of symptoms, as some may react different than others. The time it should take for resolution is about 3-6 months. As for the dosage, grape seed extract should be minimum 8000mg, cinquefoil and sage just make a tea as anyone usually would. Good luck and if anyone is in want of a greater calming effect for their symptoms immediately, add cowslip to the tea. 

Edited September 29, 2020 by Fawkinchit

[Joseph C.]

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Edited April 23, 2022 by Joseph C.

[Fawkinchit]

On 9/30/2020 at 11:36 AM, thelostreceptor said:

I've been reading about neuronal hyperexcitability, I'm keen that HPPD could be related in some way to this.

That would mean HPPD is caused by a brain plasticity mechanism called 'homeostatic plasticity' which upregulates a neural networks output beyond their regular range, causing persistent hyperexcitability. Also there is a connection to acquired epilepsy as well as tinnitus, which are driven by excessive excitability. Tinnitus can be induced by too much noise exposure but also through brain injury which seems to be closer related to HPPD.

The homeostatic plasticity acts to stabilize neuronal activity, in an attempt to maintain a constant level of activity after an initial loss of activity. This almost immediately suggests that some sort of deficit is present. Quoted directly from this paper: "Many neurological diseases feature hyperexcitability. However, such hyperexcitability is often developed from initial loss of neurons and synapses." 

It goes along with the suggestion that visual snow involves excessive excitability of neurons in the brain's cortex.

 

Perhaps this could be a new direction to take. I'm not a scientist of any sort, nor take any scientific approach to investigate this, it is just my suggestion of this condition which sounds pretty genuine to me so far.

 

My own idea about is that the brain spontaneously healed to a certain extent after an acute insult (as seen in TBI), which was caused by the substance we took, but not a complete recovery. Then through brain plasticity it tries to achieve homeostasis and upregulates neuronal activity to compensate for deficits that could not be resolved/healed. Meaning the brain did not completely recover and there is a loss of some function. But I think this is controversial because I'm not sure if all drugs that trigger HPPD are neurotoxic.

Yah, completely agree, and this is a good study to present. There are parameters involving over excitability in traumatic brain injuries, which is mainly what this study focuses on it seems. There are other parameters involved, as not all forms of epilepsy or tinnitus appear only from blunt trauma, etc, so the findings aren't exclusive to neuronal loss. Again I'm not entirely ruling out neuronal loss, and there definitely seems to be some kind of connection involved with hyperexcitability and neuronal loss, but we do have studies that show the chemicals that cause HPPD aren't exactly proven to be neurotoxic, which begins the question of whether or not thats the case. Those studies were only done in petri dishes(in vitro) and not in living organisms, so there could be other parameters involved. But we also have cases of extremely high doses not causing HPPD, which brings the idea of neuronal loss in to question, and also low dose/micro dose also causing the condition, which also brings in to question the theory of neuronal loss. Its still not ruled out, but there do appear to be other parameters involved. As for the study though there are instances of epilepsy manifesting itself not appropriated to any form of blunt trauma, so we do have to question what the cause there is. Clearly a very difficult condition to explain.

[Fawkinchit]

On 9/29/2020 at 12:02 PM, Fawkinchit said:

So, I've been here, working on this, for 8 years now, and I think I have a conclusion. The main thing that I have noticed about HPPD, is that it is quite similar in presentation, though not so much in symptoms, to other mental health conditions, mainly epilepsy, and migraines. I have also found some convincing evidence that it is even somewhat similar in fashion to PTSD. Now, I believe its been quite discussed that as far as significant neuronal loss is concerned, it doesn't appear to be quite the case in HPPD, though I can't argue that some aren't lost, it doesn't appear to be the main driving factor involved. So, from there going on we have to look beyond the organ itself, the brain, and beyond the cell itself, the neuron, to the intricacies thereof involved within the structure, and within the metabolism. Given lack of studies this is a difficult thing, but if we take in to consideration the presentation of other similar conditions there is a common factor involved, this factor appears to be mitochondrial dysfunction. We can easily assert and know for certain that it is a definite and common finding within the investigations of epilepsy, and even in migraines as well, this is a proven fact. My idea is simple, that these are all the same conditions, effecting different areas of the brain, or possibly even different aspects of the mitochondrion. Now, this may all seem complicated, but there's no need to bewail over this matter, as I have found multiple ways of reversing mitochondrial dysfunction, some out of pure common sense, and others by proven scientific research. As for example the matter of migraines, it was shown in studies to be ameliorated by long term use of 400mg of riboflavin/vitamin b2, and reverse the condition of migraines all together. This is a great hope, and opportunity. 

 

Now, this isn't all, based on a lot of my reading, and findings, which I will not go in to depth about as to how I came to this conclusion, or that conclusion, there are other methods as well of achieving this outcome, which is very exciting, and may yield very positive and beneficial results. So, what I recommend also, is grape seed extract, because of the high content of proanthocyanins, which will also achieve the same goal of ameliorating mitochondrial dysfunction. Yet it would be better if you consume also a great deal of grapes with seeds in them, seedless however are rendered ineffectual, as the highest content of proanthocyanins are in the seeds. And if any are so inclined to try other things of the same magnitude, it would be wise to drink cinquefoil, and common sage as a tea, daily. All in my opinion are very fit for the amelioration of mitochondrial dysfunction, and the sage will help proliferations in the brain, and often gives a calming effect. So anyone can try this one or that one, or all together, its no matter to me. Just be safe and use increments in dosage to be sure there aren't any immediate worsening of symptoms, as some may react different than others. The time it should take for resolution is about 3-6 months. As for the dosage, grape seed extract should be minimum 8000mg, cinquefoil and sage just make a tea as anyone usually would. Good luck and if anyone is in want of a greater calming effect for their symptoms immediately, add cowslip to the tea. 

I want to make a small edit to this: That it would still be wise to consume seeded or seedless grapes, either or is beneficial and needs to be added to treatment, grapes at least a handful once daily, or more if desired. As for the reason for this edit I wont elaborate, but its simple and safe enough that it needs no explanation. Grapes should not be omitted from treatment.

Edited October 3, 2020 by Fawkinchit

[Joseph C.]

Victoire adjudant sciences treteaux la lointain ni eu kolbacks

Edited April 23, 2022 by Joseph C.

[Davieb123]

On 5/22/2020 at 3:56 PM, Fawkinchit said:

https://www.tapatalk.com/groups/thosewithvisualsnow/a-discussion-with-dr-weatherall-the-leading-visual-t7745.html
 

found these people talking about their visual snow and found it interesting their non drug use sudden onsets...

There was also another person who got in contact with doctor Mark Weatherall and she was able to cure her VSS using a combination of natural supplements he recommended. I will attach a link if you haven’t come across it before. 

 

https://www.google.co.uk/amp/s/overtoaila.com/2020/01/30/visual-snow-syndrome-my-journey-and-cure/amp/

[Fawkinchit]

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.

Edited November 29, 2020 by Fawkinchit

[Fawkinchit]

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. 

Edited December 1, 2020 by Fawkinchit

[SomebodySomewhere]

Hi,

I can sense your frustration.

I agree that we do need to find alternatives. SSRI's and anti-psychotics WILL make things worse, and benzos are simply an effective band-aid (I'm taking them but plan on going off of them post-Covid).

*Edit*

Shouldn't drunk post.

@Jay1Ever since the forum update we can no longer delete our own posts. Please add that back.

Edited December 1, 2020 by SomebodySomewhere

[Joseph C.]

Va survivants cimetieres as inattendus il

Edited April 23, 2022 by Joseph C.

[Fawkinchit]

On 12/1/2020 at 12:34 PM, SomebodySomewhere said:

Hi,

I can sense your frustration.

I agree that we do need to find alternatives. SSRI's and anti-psychotics WILL make things worse, and benzos are simply an effective band-aid (I'm taking them but plan on going off of them post-Covid).

*Edit*

Shouldn't drunk post.

@Jay1Ever since the forum update we can no longer delete our own posts. Please add that back.

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.

 

On 12/2/2020 at 3:26 AM, thelostreceptor said:

Thought I'd post this in case you didn't notice it, it's a recent study (Apr 2020) about visual snow.

https://pubmed.ncbi.nlm.nih.gov/32211752/
 

Structural and functional footprint of visual snow syndrome

Patients with visual snow syndrome suffer from a continuous pan-field visual disturbance, additional visual symptoms, tinnitus, and non-perceptional symptoms. The pathophysiology of visual symptoms might involve dysfunctional visual cortex. So far, the extra-visual system has not been investigated. We aimed at identifying structural and functional correlates for visual and non-visual symptoms in visual snow syndrome. Patients were compared to age- and sex-matched controls using 18F-2-fluoro-2-deoxy-d-glucose PET (n = 20 per group) and voxel-based morphometry (n = 17 per group). Guided by the PET results, region of interest analysis was done in voxel-based morphometry to identify structural-functional correspondence. Grey matter volume was assessed globally. Patients had corresponding hypermetabolism and cortical volume increase in the extrastriate visual cortex at the junction of the right lingual and fusiform gyrus. There was hypometabolism in the right superior temporal gyrus and the left inferior parietal lobule. Patients had grey matter volume increases in the temporal and limbic lobes and decrease in the superior temporal gyrus. The corresponding structural and functional alterations emphasize the relevance of the visual association cortex for visual snow syndrome. The broad structural and functional footprint, however, confirms the clinical impression that the disorder extends beyond the visual system.

So the results of this paper demonstrate grey matter volume increases and hypermetabolism. In my opinion treatment would need to be focused on regenerating the structure in the affected areas. There are not many options for that currently. It would involve methods to allow axonal regeneration to break through glial scarring, enhancing growth factors to further support growth and enhance neurogenesis, survival of newborn neurons & integration.

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.

Edited December 6, 2020 by Fawkinchit