Syntheso

Actually, the claims you pasted from that Longecity member about fasting got me thinking about what sensory deprivation could do for HPPD - would it allow the brain to rewire itself in the same way that that person claimed fasting causes your brain to rewire itself. I haven't looked into it, but the first thing that came to mind was Charles Bonnet Syndrome, whereby blind people begin to experience visual hallucinations. It is theorized that the brain does this to make up for the lack of visual stimuli. So, potentially, sensory deprivation could worsen things. Maybe it could make things better - the brain is funny. The thread about temporary visual snow treatment seems to indicate that more excitable visual stimuli, in correspondence with our visual distortions, is more efficient at ameliorating symptoms. (Edit: lol... http://www.wired.com/2009/10/hallucinations/ ) I generally agree with the OP's theory, and I quite like the analogy. In my vision therapy classes, when I am not able to complete an exercise ('perceiving incorrectly' - my term), my teacher will prompt me to relax, or breathe properly; this often allows for the correct perception. It is something that is reiterated throughout vision therapy training. How do we relax? Meditation... yoga (studies show it releases up to 30% more GABA), listen to music. I quite like herbal teas to relax. I recommend the Yogi Tea Calming/Relaxed Mind teas (also their super antioxidant tea). They have lots of good ingredients with studies behind them. Baths (with epsom salts/magnesium flakes if you can), candles, incense, all dat hippy shit. Second edit: From the article above... Interesting!

Some treat schizophrenia with megadose glycine.. like 50-60g/day IIRC. I think this is for theorised glutamatergic hypofunction, but I could be incorrect. I tried it a while back for HPPD but didn't get passed the first day as I couldn't be bothered with those doses. There should be some discussion about glycine in the 'Why NMDA antagonism' thread. Edit: http://www.ncbi.nlm.nih.gov/pubmed/9892253 Given your thoughts on your personal pathology, might be worth a trial for you. I have loads of powdered glycine I don't need if you want it.

If you haven't read this already, give it a read. I've read it a couple of times in the past, but the following caught my eye this time: Two positive sounding actions to me... Look at the profile of LY354740 a.k.a Eglumegad: A concern is that they appear to reduce dopamine. AMPA or kainate glutamate antagonist also block 5-HT2a-induced release of glutamate. Thoughts?

Really happy to hear of your recovery, well done! So have you recovered fully? Thanks for sharing.

I know you did, I felt it warranted it's own thread, but then again, perhaps not..!

Visual, sorry I did not reply to your PM. I'll get back to you this evening. Didn't look into that any more.. am reading about other things at the moment. I'll get around to it. So it seems that the COMT gene is not a hugely determinative factor in HPPD... Back to me and Sinemet.. have been on it at <2 pills/day for the last couple of weeks. Not really getting the success that I initially had, although things are okay. I am not getting consistent results. Some days I will drink a cup of coffee with the Sinemet and be good for the whole day. Other days, I am still fairly unmotivated.. which manifests itself in laziness (going to sleep.. although I am not sure I would call it lethargy, just anhedonia). I am going to try what you recommended to me privately. I added in Gabapentin 300mg before bed recently, just to take the edge off things. It's my last month of studies (exams etc.) so want to be on good form. Once completed I will do a washout, including supps, for 1-2 months, let the body do a bit of its own healing. Then I have plans to try some other things.

Soothe the brain on fire... Anti-inflammatories will not cure HPPD but might provide a useful adjunct to treatment. Soothing neuroinflammation might even be a required part of healing. I've copied and pasted relevant information, with sources below. Please add information. Key concepts related to brain inflammation: • Your brain is saturated with immune cells called microglia cells. • The microglia cells perform many important functions under normal conditions to help transmission between neurons, such as removal of dead neurons and plaques. • In a heightened state of activation, microglia create a persistent, self-perpetuating state of neuroinflammation. • Microglia cells can become activated and promote neuroinflammation in response to inflammatory diets, head trauma, lack of oxygen, diabetes, environmental toxins, autoimmunity, and systemic inflammation. • Neuroinflammation decreases the speed of neuron responses and leads to symptoms such as brain fog and depression. Chronic neuroinflammation leads to neuron death and neurodegenerative changes. [Kharrazian, Datis (2013-05-01). Why Isn't My Brain Working? ] Summary of potentially useful agents: Fish Oil/DHA Apigenin Baicalein Resveratrol Rutin Catechins Curcumin Aspirin Estrogens N-acetylcysteine (NAC) Astaxanthin Tips: Go easy on meat and egg yolks, which contain pro-inflammatory arachidonic fatty acids, and eat more fish—nature’s best source of anti-inflammatory omega-3 fats. Studies show that people who eat fish just once a week reduce their risk of Alzheimer’s by 60 percent. In addition to eating fish, recommend taking 2–4 grams of high-quality fish oil daily. Low levels of the omega-3 fat DHA have been linked with Alzheimer’s as well as other types of dementia and mood disorders. One of the most abundant fats in the brain, DHA helps construct robust cellular membranes and protective myelin sheaths. It also turns on genes for brain-derived neurotrophic factor (BDNF), which makes neurons more resistant to injury and free-radical damage. [The Alzheimer’s Disease Neuroimaging Initiative (ADNI), a large, multicenter study funded by the National Institutes of Health, also found that long-term use of fish oil supplements was associated with reduced age-related shrinkage of the brain and better cognitive function in older adults identified as having “normal cognition” at the start of the three year study. http://www.drwhitaker.com/protect-your-brain-with-natural-anti-inflammatories] Apigenin (flavonoid) Apigenin is a bioflavonoid found in parsley, artichoke, basil, and celery. It has very powerful neuroinflammation quenching and neuroprotective properties. Research has demonstrated the compound can modulate activation of the microglia cells during neuroinflammatory processes. Apigenin has demonstrated the ability to inhibit microglial proliferation. Apigenin has also demonstrated the ability to protect neuronal cells from artery occlusion that may occur after stroke. 50 51 52 53 Luteolin Luteolin is a bioflavonoid found in celery and green peppers and has been shown to block inflammatory responses in the brain by inhibiting microglia activation. Luteolin has been shown to inhibit several different microglial activating pathways and demonstrated the ability to protect neurons from inflammation-induced injury in research studies. 54 55 56 57 Baicalein (flavonoid) Baicalein is a flavonoid that has been shown to exert anti-inflammatory and antioxidant properties on the brain microglia system. 58 It has a long history of safe administration to humans and has been found to easily cross the gastrointestinal tract and the blood-brain barrier by membrane permeability assays. 59 Baicalein has demonstrated neuroprotective properties to dopaminergic neurons implicated in the pathogenesis of Parkinson’s disease. Animal subjects given MPTP (a dopamine neurotoxin) in combination with Baicalein demonstrated decreased neuronal damage and microglia activation. 60 61 62 63 Baicalein has been reported to protect cortical neurons from beta-amyloid, the protein involved in Alzheimer’s disease. 64 It has demonstrated to ameliorate inflammatory processes of diabetic retinopathy and have inhibitory activity against neuron loss in diabetic retinas. 65 Baicalein has been found to protect neurons from decreased blood flow to the brain. 66 67 Traumatic brain injury triggers a complex series of inflammatory responses that contribute to secondary damage. Research has found that post-injury treatment with baicalein improved functional outcomes and reduced pro-inflammatory activity in traumatic brain injury. 68 Resveratrol (flavonoid) Resveratrol, a flavonoid found in grapes and wine, has been reported to reduce the activation of microglia in numerous studies. Activated microglia produce excessive nitric oxide, which leads to neuronal inflammation. Resveratrol has demonstrated nitric oxide attenuating properties on microglia cells. 69 70 Resveratrol has potent antioxidant effects on oxidative stress activity derived from microglia cell activation. 71 72 Resveratrol reduces activated microglia cell activity and may reduce neuroinflammation. 73 74 Resveratrol has demonstrated the ability to protect against microglia-dependant amyloid-beta toxicity through inhibiting NF-kappaB signaling and may provide a novel compound to be considered for Alzheimer’s disease. 75 Research on resveratrol has found it inhibits LPS-induced nitric oxide and TNF-alpha production in microglia by blocking phosphorylation, and is suggested as potential support compound for neurodegenerative conditions. 76 77 Rutin (flavonoid) Rutin, a citrus flavonoid found in plants, acts as a powerful antioxidant. It attaches to the iron ion Fe2 +, preventing it from binding to hydrogen peroxide and allowing it to become a free radical. Rutin has demonstrated the ability to quench lipid peroxidation. 78 It has demonstrated the ability to modulate microglia inflammatory mediators TNF-alpha and nitric oxide. 79 It has been found to protect against toxicant-induced hippocampal injury by suppression of microglia activation of inflammatory cytokines. 80 Catechins (found in teas) Catechins are polyphenolic antioxidant plant metabolites abundant in various tea leaves. They have been shown to protect microglia cells and neurons from DNA damage by oxidative stress by increasing their expression of DNA repair by the enzyme poly( ADP-ribose) polymerase and by translocation of NF-kappaB. 81 82 Catechins have been reported to possess divalent metal chelating, antioxidant, and anti-inflammatory activities, to penetrate the brain barrier, and to protect neuronal death in a wide array of cellular and animal models of neurological disorders. They appear to have both an iron chelating and antioxidant effect. 83 84 One study demonstrated catechin is a potent inhibitor of microglia activation and thus is a useful candidate for alleviating microglia-mediated neuronal injury. 85 Curcumin Curcumin are antioxidant compounds found in the Indian curry spice of turmeric that have been found to modulate microglia neuroinflammation. Curcumin has demonstrated the ability to protect dopaminergic neurons against LPS-induced neurotoxicity in animal neuronal/ glia culture. 86 Curcumin has been found to have neuroprotective effects by blocking the production of pro-inflammatory and cytotoxic mediators such as nitric oxide, TNF-alpha, IL-1 alpha, IL-6, and NF-kappaB by activated microglia. 87 88 89 90 91 Curcumin has been found to inhibit amyloid peptide-induced chemokine gene expression and may represent a potential therapeutic aid to ameliorate the inflammation and progression of Alzheimer’s disease. Increase your intake of curry, a staple in India, where there is a low incidence of Alzheimer’s. Turmeric, the spice that gives curry its color, is an excellent source of curcumin, one of the most powerful, natural anti-inflammatories (and antioxidants). Animal studies show that curcumin lowers levels of inflammation in the brain and reduces beta-amyloid plaque by up to 50 percent. A human study also revealed that people who ate curry had significantly better scores on tests of cognitive function than those who never ate it. If you can’t tolerate the taste of curry, you can also supplement with curcumin. The suggested daily dose is 1,000–2,000 mg of regular curcumin or 500–1,000 mg of curcumin phytosome. [Kharrazian, Datis (2013-05-01). Why Isn't My Brain Working? (pp. 214-215). Elephant Press. Kindle Edition. ] - - The following three show significant effects in the schizophrenia study below: Aspirin Can cause stomach to bleed with chronic usage. Finding a low effective dose can avoid this. []http://www.ncbi.nlm.nih.gov/pubmed/20981485] Estrogens []http://www.ncbi.nlm.nih.gov/pubmed/21774811] NAC []http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3044191/] Astaxanthin is now thought to be the most powerful antioxidant found in nature. Astaxanthin is by far the most powerful carotenoid antioxidant when it comes to free radical scavenging: astaxanthin is 65 times more powerful than vitamin C, 54 times more powerful than beta-carotene, and 14 times more powerful than vitamin E. Astaxanthin is far more effective than other carotenoids at "singlet oxygen quenching," which is a particular type of oxidation. The damaging effects of sunlight and various organic materials are caused by this less-stable form of oxygen. Astaxanthin is 550 times more powerful than vitamin E and 11 times more powerful than beta-carotene at neutralizing singlet oxygen. Astaxanthin crosses the blood-brain barrier AND the blood-retinal barrier, which brings antioxidant and anti-inflammatory protection to your eyes, brain and central nervous system and reducing your risk for cataracts, macular degeneration, blindness, dementia and Alzheimer's disease. Astaxanthin is soluble in lipids, so it incorporates into cell membranes. It's a potent UVB absorber and reduces DNA damage. It's a very potent natural anti-inflammatory. Sources: http://www.drwhitaker.com/protect-your-brain-with-natural-anti-inflammatories http://www.ncbi.nlm.nih.gov/pubmed/21143138 http://www.dana.org/News/Details.aspx?id=43258 http://articles.mercola.com/sites/articles/archive/2011/07/12/astaxanthin-the-antiinflammatory-nutrient.aspx Kharrazian, Datis (2013-05-01). Why Isn't My Brain Working? Elephant Press.

Minocycline Minocycline is traditionally an antibiotic for acne treatment, but it can modulate glutamate-induced excitotoxicity, and has antioxidant, anti-inflammatory and neuroprotective effects. [http://www.ncbi.nlm.nih.gov/pubmed/22486246] It is said to synergise with N-acetylcysteine (an amino acid antioxidant at the NMDA receptor which many HPPD sufferers report amelioration of symptoms with); [http://www.ncbi.nlm.nih.gov/pubmed/20824218] Neurodegenerative diseases such as Huntington's disease and Parkinson's disease have shown a particularly beneficial response to minocycline in research studies, and an antipsychotic benefit has been found in people with schizophrenia and minocycline is proposed as a possible addon therapy for some schizophrenics. It is worrying that Minocycline, but not other tetracyclines, can cause vestibular disturbances with dizziness, ataxia, vertigo and tinnitus. This user report from the board is worrying; It seems to have potential, but there are some worrying factors, particularly the user report above.

Only had two responses.. there must be some more creatives on this board.. get in touch !

http://www.ncbi.nlm.nih.gov/pubmed/17971830

Really impressive how long you've gone for.. I hope it's not for nothing. Not long till your target now (is it 20 days)!

In correlation with the birth of the Society for the Study of Perception Disorders, I would like to host an exhibition / event to promote awareness and evoke the issues involved in HPPD and other perception disorders. I am putting the feelers out there for all creative types with ideas to exhibit work in a space.. I will not set any limitations as to what it can be. If you have any ideas, please propose them to me by PM or ask me for my email. If you have documentation of previous work, please send that to me also. Thanks.

This sounds really good. What would you say you were on before you started?

Interesting! See this. This concurs with your experience LaizzesFaire; Young, C. R. (1997). Sertraline treatment of hallucinogen persisting perception disorder. Journal of Clinical Psychiatry, 58(2), 85-85.

Could you recommend some reading on ketogenic diets?

lol Thanks for the report. By scale rating I just mean, for example, out of 10. 10 could be symptoms at their most aggressive, 0 as no symptoms. Do this everyday for each symptom (e.g anxiety / visuals / concentration / lethargy are ones I use) and afterwards it is easier to pick up on trends.

Bump. Started supplementing this. Phosphatidylserine inhibits the effects of IL-6, a cytokine that spikes in response to emotional, chemical, or physical stress, saturating IL-6 receptors in the midbrain. This in turn stimulates the IML, generating a sympathetic response. Paraphrased from Datis Kharrazian's book Why Isn't My Brain Working?.

I have tried the text feature twice with no response from the system. On a UK phone.

It would be quite useful for you to keep a more detailed log of your symptoms and give each day a scale rating. Post it here for us if you'd like.

I agree with Society for the Study of Perception Disorders.

I agree with you, somewhat, but I find it hard to believe that 'everyone can see visual snow'. This is my issue.. I am sure you could convince anyone of minor perceptual distortions if you place a thought in their head before. I think that is more likely the suggestibility of the mind.

Can they ?

Following this with great interest. Wishing you all the best!

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