Syntheso

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:

 

Both LY354740 and the type II/III metabotropic agonist (1S, 3S)-ACPD, which reduce the release of glutamate by acting on presynaptic inhibitory autoreceptors, are able to block excitation induced by 5-HT_2A receptors in vitro (Marek et al, 2000).

Two positive sounding actions to me...

Look at the profile of LY354740 a.k.a Eglumegad:
 

 

Mechanism of action

Eglumegad acts as a group-selective agonist for the group II metabotropic glutamate receptors (mGluR_2/3).^[4][5] It is unclear whether eglumegad directly interacts with dopamine D2 receptors.^[6][7]

Effects

In experiments on mice, eglumegad was found to be as effective as diazepam for treating anxiety symptoms in several standard tests, but without producing any of the negative side effects of diazepam such as sedation and memory impairment.^[8] Tests in humans confirmed that it produced anxiolytic effects without producing sedation.^[9][10]However it did slightly reduce cognitive performance in tests on monkeys.^[11]

Eglumegad has also been found to be effective in relieving the symptoms of withdrawal from chronic use of both nicotine^[12] and morphine in animals,^[13] as well as inhibiting the development of tolerance to morphine,^[14] raising hope that this drug may be useful for treating drug addiction in humans.

Eglumegad and related drugs are neuroprotective^[15] and are synergistic with the neuroprotection produced by N-methyl-D-aspartic acid (NMDA) antagonist drugs,^[16] which may make these drugs useful in aiding recovery from brain injury.

This class of drugs also interacts with hallucinogenic drugs, with eglumegad reducing the effects of 5HT_2A agonist hallucinogens,^[17] while conversely the mGluR_2/3 antagonist LY341495 increased the behavioural effects of these drugs.^[18] This suggests that mGluR_2/3 agonists such as eglumegad may have potential uses in the treatment of some forms of psychosis, although eglumegad had only limited effects on the action of the dissociative drug phencyclidine^[19] which is generally a better model for schizophrenia than the 5HT_2A agonist hallucinogens.^[20]

Eglumegad also interferes in the hypothalamic–pituitary–adrenal axis, with chronic oral administration of this drug leading to markedly reduced baseline cortisol levels in bonnet macaques (Macaca radiata); acute infusion of eglumedgad resulted in a marked diminution of yohimbine-induced stress response in those animals.^[21]

In human adrenocortical cells, eglumegad has been shown to down-regulate intracellular cyclic AMP (cAMP) and steroidogenesis, with a significant decrease in aldosterone and cortisol production.^[22]

 

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 posted about it in the HPPD stack thread - minocycline+aspirin seem to be useful for psychiatric purposes (more so than each individually, if I remember correctly). 

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

You're right (I was wrong) you should benefit the most from COMT inhibition.

 

Did you learn more on the methylation stuff?

 

Some of the confusion with A,C,G,T,Val and Met may because research in COMT came early in gene studies so the used Val/Met instead of A/G.  And depending on how a gene strand is read, it T is A and C is G.  Wish they would have standardized a little better.

 

So we are opposits: AA verses GG.  I respond strongly to Sinemet and you respond less so.  Am suspecting that my problem is not COMT gene related, though there are several COMT genes.  Found a list of 80+ dopamine genes ... lots of homework now...

 

But the nature of your responces seems similar.

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? ]

Inflammation is a lifesaving process used by the immune system to combat infection. But sometimes the inflammatory response is inappropriately activated. The most blatant examples are autoimmune disorders, in which the immune system ignites a full-fledged attack against the body’s own tissues,making natural anti-inflammatories necessary.
However, chronic low-level inflammation also takes its toll. It releases compounds that are toxic to neurons and unleashes a cascade of free radicals that damage and destroy brain cells.
Brain tissues affected by Alzheimer’s are rife with inflammatory chemicals. In addition, blood levels of C-reactive protein (CRP), a marker of inflammation, are linked with increased risk of the disease. Therefore, addressing inflammation with natural anti-inflammatories is critical for protecting against Alzheimer’s and its progression.

 
 
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.
 

The ability of ASA to increase anti-inflammatory LXA₄ and 15-epi-LXA₄ and reduce pro-inflammatory PGE₂ and TXB₂ suggests considering aspirin further for treating clinical neuroinflammation.

 
[]http://www.ncbi.nlm.nih.gov/pubmed/20981485]
 
Estrogens
 
 

Estrogens regulate neuroinflammatory genes via estrogen receptors α and β in the frontal cortex of middle-aged female rats.
Abstract

BACKGROUND:
Estrogens exert anti-inflammatory and neuroprotective effects in the brain mainly via estrogen receptors α (ERα) and β (ERβ). These receptors are members of the nuclear receptor superfamily of ligand-dependent transcription factors. This study was aimed at the elucidation of the effects of ERα and ERβ agonists on the expression of neuroinflammatory genes in the frontal cortex of aging female rats.
METHODS:
To identify estrogen-responsive immunity/inflammation genes, we treated middle-aged, ovariectomized rats with 17β-estradiol (E2), ERα agonist 16α-lactone-estradiol (16α-LE2) and ERβ agonist diarylpropionitrile (DPN), or vehicle by Alzet minipump delivery for 29 days. Then we compared the transcriptomes of the frontal cortex of estrogen-deprived versus ER agonist-treated animals using Affymetrix Rat230 2.0 expression arrays and TaqMan-based quantitative real-time PCR. Microarray and PCR data were evaluated by using Bioconductor packages and the RealTime StatMiner software, respectively.
RESULTS:
Microarray analysis revealed the transcriptional regulation of 21 immunity/inflammation genes by 16α-LE2. The subsequent comparative real-time PCR study analyzed the isotype specific effects of ER agonists on neuroinflammatory genes of primarily glial origin. E2 regulated the expression of sixteen genes, including down-regulation of complement C3 and C4b, Ccl2, Tgfb1, macrophage expressed gene Mpeg1, RT1-Aw2, Cx3cr1, Fcgr2b, Cd11b, Tlr4 and Tlr9, and up-regulation of defensin Np4 and RatNP-3b, IgG-2a, Il6 and ER gene Esr1. Similar to E2, both 16α-LE2 and DPN evoked up-regulation of defensins, IgG-2a and Il6, and down-regulation of C3 and its receptor Cd11b, Ccl2, RT1-Aw2 and Fcgr2b.
CONCLUSIONS:
These findings provide evidence that E2, 16α-LE2 and DPN modulate the expression of neuroinflammatory genes in the frontal cortex of middle-aged female rats via both ERα and ERβ. We propose that ERβ is a promising target to suppress regulatory functions of glial cells in the E2-deprived female brain and in various neuroinflammatory diseases.

 
[]http://www.ncbi.nlm.nih.gov/pubmed/21774811]
 
NAC
 

There is an expanding field of research investigating the benefits of alternatives to current pharmacological therapies in psychiatry. [/size]N-acetylcysteine (NAC) is emerging as a useful agent in the treatment of psychiatric disorders. Like many therapies, the clinical origins of NAC are far removed from its current use in psychiatry. Whereas the mechanisms of NAC are only beginning to be understood, it is likely that NAC is exerting benefits beyond being a precursor to the antioxidant, glutathione, modulating glutamatergic, neurotropic and inflammatory pathways. This review outlines the current literature regarding the use of NAC in disorders including addiction, compulsive and grooming disorders, schizophrenia and bipolar disorder. [/size]N-acetylcysteine has shown promising results in populations with these disorders, including those in whom treatment efficacy has previously been limited. The therapeutic potential of this acetylated amino acid is beginning to emerge in the field of psychiatric research.[/size]

 
[]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.

Efficacy of Anti-inflammatory Agents to Improve Symptoms in Patients With Schizophrenia: An Update
Abstract
Background: The inflammatory hypothesis of schizophrenia is not new, but recently it has regained interest because more data suggest a role of the immune system in the pathogenesis of schizophrenia. If increased inflammation of the brain contributes to the symptoms of schizophrenia, reduction of the inflammatory status could improve the clinical picture. Lately, several trials have been conducted investigating the potential of anti-inflammatory agents to improve symptoms of schizophrenia. This study provides an update regarding the efficacy of anti-inflammatory agents on schizophrenic symptoms in clinical studies performed so far.Methods: An electronic search was performed using PubMed, Embase, the National Institutes of Health web site http://www.clinicaltrials.gov, Cochrane Schizophrenia Group entries in PsiTri, and the Cochrane Database of Systematic Reviews. Only randomized, double-blind, placebo-controlled studies that investigated clinical outcome were included.Results: Our search yielded 26 double-blind randomized controlled trials that provided information on the efficacy on symptom severity of the following components: aspirin, celecoxib, davunetide, fatty acids such as eicosapentaenoic acids and docosahexaenoic acids, estrogens, minocycline, and N-acetylcysteine (NAC). Of these components, aspirin (mean weighted effect size [ES]: 0.3, n = 270, 95% CI: 0.06–0.537, I² = 0), estrogens (ES: 0.51, n = 262, 95% CI: 0.043–0.972, I² = 69%), and NAC (ES: 0.45, n = 140, 95% CI: 0.112–0.779) showed significant effects. Celecoxib, minocycline, davunetide, and fatty acids showed no significant effect. Conclusion: The results of aspirin addition to antipsychotic treatment seem promising, as does the addition of NAC and estrogens. These 3 agents are all very broadly active substances, and it has to be investigated if the beneficial effects on symptom severity are indeed mediated by their anti-inflammatory aspects.

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.
 

 

Minocycline: therapeutic potential in psychiatry.

Abstract

Pharmacological interventions to treat psychiatric illness have previously focused on modifying dysfunctional neurotransmitter systems to improve symptoms. However, imperfect understanding of the aetiology of these heterogeneous syndromes has been associated with poor treatment outcomes for many individuals. Growing evidence suggests that oxidative stress, inflammation, changes in glutamatergic pathways and neurotrophins play important roles in many psychiatric illnesses including mood disorders, schizophrenia and addiction. These novel insights into pathophysiology allow new treatment targets to be explored. Minocycline is an antibiotic that can modulate glutamate-induced excitotoxicity, and has antioxidant, anti-inflammatory and neuroprotective effects. Given that these mechanisms overlap with the newly understood pathophysiological pathways, minocycline has potential as an adjunctive treatment in psychiatry. To date there have been promising clinical indications that minocycline may be a useful treatment in psychiatry, albeit from small trials most of which were not placebo controlled. Case reports of individuals with schizophrenia, psychotic symptoms and bipolar depression have shown serendipitous benefits of minocycline treatment on psychiatric symptoms. Minocycline has been trialled in open-label or small randomized controlled trials in psychiatry. Results vary, with findings supporting use in schizophrenia, but showing less benefit for nicotine dependence and obsessive-compulsive disorder. Given the limited data from rigorous clinical trials, further research is required. However, taken together, the current evidence suggests minocycline may be a promising novel therapy in psychiatry.

[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);
 
 

Minocycline synergizes with N-acetylcysteine and improves cognition and memory following traumatic brain injury in rats.


Abstract


BACKGROUND:
There are no drugs presently available to treat traumatic brain injury (TBI). A variety of single drugs have failed clinical trials suggesting a role for drug combinations. Drug combinations acting synergistically often provide the greatest combination of potency and safety. The drugs examined (minocycline (MINO), N-acetylcysteine (NAC), simvastatin, cyclosporine A, and progesterone) had FDA-approval for uses other than TBI and limited brain injury in experimental TBI models.

METHODOLOGY/PRINCIPAL FINDINGS:
Drugs were dosed one hour after injury using the controlled cortical impact (CCI) TBI model in adult rats. One week later, drugs were tested for efficacy and drug combinations tested for synergy on a hierarchy of behavioral tests that included active place avoidance testing. As monotherapy, only MINO improved acquisition of the massed version of active place avoidance that required memory lasting less than two hours. MINO-treated animals, however, were impaired during the spaced version of the same avoidance task that required 24-hour memory retention. Co-administration of NAC with MINO synergistically improved spaced learning. Examination of brain histology 2 weeks after injury suggested that MINO plus NAC preserved white, but not grey matter, since lesion volume was unaffected, yet myelin loss was attenuated. When dosed 3 hours before injury, MINO plus NAC as single drugs had no effect on interleukin-1 formation; together they synergistically lowered interleukin-1 levels. This effect on interleukin-1 was not observed when the drugs were dosed one hour after injury.

CONCLUSIONS/SIGNIFICANCE:
These observations suggest a potentially valuable role for MINO plus NAC to treat TBI.

[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 !

Memantine upregulates BDNF and prevents dopamine deficits in SIV-infected macaques: a novel pharmacological action of memantine.

Abstract

N-methyl-D-aspartate (NMDA) receptor activation is involved in the pathogenetic cascades of neurodegenerative disorders including human immunodeficiency virus (HIV) dementia. Memantine, an uncompetitive NMDA receptor antagonist, which has been recently approved for the treatment of Alzheimer's disease, is being discussed as a potential adjunctive therapeutic substance for HIV dementia. We used simian immunodeficiency virus-infected rhesus macaques to assess the effects of memantine on brain dysfunction and brain pathology within 3-5 months after initial infection during early asymptomatic stage of disease. We had shown previously that within this time frame, marked changes were evident in the dopaminergic systems. Memantine was administered two weeks post infection, at peak viremia, in order to prevent early NMDA receptor activation due to immune mediators. We found that memantine prevented onset of dopamine deficits in the brains of SIV-infected macaques, without affecting early brain pathology or peripheral course of infection. Memantine specifically upregulated mRNA and protein expression of the neurotrophic factor brain-derived neurotrophic factor (BDNF), suggesting that the protective effect of memantine on dopamine function may be mechanistically remote from NMDA receptor antagonism. This novel pharmacological action of memantine may also be relevant for other neurodegenerative disorders and supports the involvement of neurotrophic factors in adult brain neuroprotection.

 

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.

Day 13: scale ratings 0-10 (0 being as close to baseline as I remember, 10 being very aggravated symptoms)

Anxiety: 3 I'm not that anxious per se, but I'm not totally zen

Visuals: 6

Concentration: 4 still a little hazy

Lethargy: 5

Memory recall: 6

I hold a very high bar for myself, so some of these ratings may be a little harsh

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. 
 

Reports the case of a 22-yr-old man who presented with hallucinogen persisting perception disorder and symptoms of mild depression 6 mo after discontinuing the use of LSD. Antidepressant treatment was begun with sertraline, until a target dose of 100 mg was reached. Mild exacerbations of the LSD-like phenomena were noted for 2-4 days after each dosage increase. Within 1 mo of reaching the target dose the perceptual disturbances decreased until they had almost completely remitted, and the depressive symptoms also improved. It is hypothesized that hallucinogen persisting perception disorder is serotonergically mediated, and that sertraline initially exacerbates the perceptual disturbances, but attenuates them after chronic administration. 

 

A lot of the benefits of fasting can actually be obtained by eating MORE, as proper oxidative metabolism, and to a degree, mitochondrial uncoupling, increases autophagy/phagocytosis; this researcher noticed rodents lived longer the less they ate, but hypothesized that this was probably from a decreased toxin load. He fed another group a calorie un-restricted diet, though depleted in metals such as iron and aluminum, and they lived just as long as calorically restricted rodents. That being said, I've been having decent results with Paul Jaminet's+Dave Asprey's take on fasting. For the past few weeks I've been completing a ketogenic intermittent fast for 16-18hrs, though eating carbs and what not throughout the rest of the day, and then completing a full-on ketogenic fast for 24-36hrs 1x/week. I feel great after this. Simply restricting very specific amino acids, for instance, methionine, increases autophagy and mitochondrial biogenesis. Yet 1x/week I'm doing more than this and completely fasting outside of some medium chain fats, coffee, mineral water, and salt. 

 

When I get KetoForce (a salt of beta-hydroxybutyrate) I may try a 7-10 day fast. Fasting has been shown to cure drug resistant forms of schizophrenia, and all that is needed to maintain the results is a whole foods diet and an occasional 3-5 day fast.  

Could you recommend some reading on ketogenic diets?

-I am more than likely skinnier than your dick

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.

It's all natural stuff, imo, we just can't filter it very well.

I agree with you, somewhat, but I find it hard to believe that 'everyone can see visual snow'. 

when you ask them to look for it

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.

I mean I can slightly see staticky stuff if I look for it, but so can everyone.

Can they ? 

Just stay away from all drugs. It's the ONLY sensible choice.

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

double post

Goldsmiths is just down the road from me 

due to structural changes to the brain (gray and white matter/cortical matter, etc). 

Is there evidence for this claim?