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

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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/


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

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Erratum in

  • Headache. 2015 Apr;55(4):592. 



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.


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.


(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).


(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).


-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.

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