dasitmane

Bit of an idea for possible CURE. Has some weight to it.

601 posts in this topic

lol.....hahahhahahahahahhaha..........wait qaiphyx, i got some drugs for you to check out tell me what you think of these drugs, ptsd drugs: Minipress and propranonol. And also~ Nootropics (don't know much about them).

***I just looked it up----wow thats a lot of them lol------i'm on like 10 of them if you count nicotine lol

What? Im pretty sure youre reading my posts wrong...

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No, i was just throwing some ideas up........Listen with science, you can be wrong and you back track and start again......We are all looking for the same truth, and i am sure we will find it if we continue to work together. I learned something today that i was dead wrong about (regen./recycle receptors). ....It's good to know.

Now to the Ambien-stuff, we both know it's a sleeping pill. People get terrible hypnopompic hallucinations when trying to stay awake on this drug. (And also supposedly the dreams are wild, and people sometimes can get into the state of mind between sleep and consciousness and sleep paralysis, i believe.) Certainly, no driving.

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I know it is hard to find any emotion sometimes and it's ok; i totally feel that sometimes but i think you all should watch this it will lighten things up and clear the mind some. (you probably have seen it ):

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No, i was just throwing some ideas up........Listen with science, you can be wrong and you back track and start again......We are all looking for the same truth, and i am sure we will find it if we continue to work together. I learned something today that i was dead wrong about (regen./recycle receptors). ....It's good to know.

Now to the Ambien-stuff, we both know it's a sleeping pill. People get terrible hypnopompic hallucinations when trying to stay awake on this drug. (And also supposedly the dreams are wild, and people sometimes can get into the state of mind between sleep and consciousness and sleep paralysis, i believe.) Certainly, no driving.


asdf
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ok what were the first drugs you were mentioning on this post?; a few were i thought could be golden. (****not sure about the antihistamines though: little sketchy) On further review of an old drug, seriously tell me if propranolol is possibly helpful.

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ok what were the first drugs you were mentioning on this post?; the first few were golden. On further review of an old drug, seriously tell me if propranolol is possibly helpful.

Its just a beta blocker, it MAY treat symptoms.

5htp2a receptor Inverse agonists

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Wheres visual at when u need him

Hahaha exactly my thought as well! :D

But anyway, i may try betablockers, they are easy to get prescribed and nothing points toward worsening of hppd.

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Well.....in about a week i am going to a world-renown Neuropsychiatrist: who wrote books with the man that basically discovered antipyschotic meds. He is one of the leading experts in drug-induced mental disorders. And I would say he knows neurochemistry pretty well. Organize a list of questions that you are confused about and i'll ask him. Thanx.

***Oh....and also get Visual to enter the post***

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I think to understand HPPD you have to recognize the idea of phenomenology in brain disorders. As far as i know there are not many (if any) cures of brain disorders aside from eliminating the cause (or self-limit). Our cause is ingestion of psychedelics, dissociatives, etc. Basically what you are doing is treating the brain (and/or psychological) disorder by eliminating symptoms. I would assume you are looking for some sort of "vaccination" and taken-one-time antidote, i would suppose. People with anxiety/disorders don't have cures, they treat with benz. and ADs. Bipolar, schizophrenia, ADD, panic episodes, borderline personality, etc: there are no cures; simply most effective ways to eliminate symptoms. I wouldn't classify HPPD, medically, as an infection.

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Please provide the evidence of claims, I have seen absolutely no usage of inverse 5HT2A agonists for the treatment of hppd. Nor have I seen that gene mutation is negligible.

Again, can someone confirm that? I thought we had already tried those. If we didnt we should.

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The uses of 5HT2A agonists would only be viable it seems in low doses, unless you plan on sleeping for 20 hours a day. Gene mutation perhaps maybe a reality from taking LSD, but what about HPPD caused by non-lethal amphetamine overdoses, pcp overdoses, RC chemicals, and all the other drugs. ................. Can it be proven that HPPD, caused by some of these other drugs, is a symptom of genetic mutations?

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There may be something to genes and our ability to metabolize drugs; and perhaps there are gene-types that all HPPD sufferers carry. ......You have to decide whether the genetic damage is caused from the drug, the phenomenal existence of HPPD, or just the nature of HPPD sufferers. Here is a study from the National Institute of Health:

Science. 1971 Apr 30;172(3982):431-40.

LSD and genetic damage.

Dishotsky NI, Loughman WD, Mogar RE, Lipscomb WR.

Abstract

Of nine studies in vitro, six have indicated some degree of induced chromosomal breakage after exposure to LSD; three failed to confirm these results. The damage, when found, was generally of the chromatid type, arising during or after DNA synthesis. This damage, with one exception, was the result of concentrations of drug and durations of exposure which could not be achieved in humans with reasonable dosages. There did not appear to be a dose-response relation. The magnitude of damage, when found, was in the range encompassing the effects of many commonly used substances. The absence in vitro of excretory and detoxifying systems present in vivo, as well as several negative reports, cast doubt on the relevance of in vitro results. In 21 chromosomal studies in vivo, 310 subjects were examined. Of these, 126 were treated with pure LSD; the other 184 were exposed to illicit, "alleged" LSD. A maximum of only 18 of 126 (14.29 percent) of the subjects in the group exposed to pure LSD showed higher frequency of chromosome aberration than the controls. In contrast, a maximum of 90 of 184 (48.91 percent) of the subjects taking illicit LSD showed an increase in frequency of aberrations. Of all the subjects reported to have chromosome damage, only 18 of the 108 (16.67 percent) were exposed to pure LSD. The frequency of individuals with chromosomal damage reported among illicit drug users was more than triple that associated with the use of pharmacologically pure LSD. We conclude that chromosome damage, when found, was related to the effects of drug abuse in general and not, as initially reported, to LSD alone. We believe that pure LSD ingested in moderate dosages does not produce chromosome damage detectable by available methods. No significant work on carcinogenic potential of LSD has been reported so far. No cause-and-effect relation and no increase in the incidence of neoplasia among LSD users have been demonstrated. Case reports (three in 4.0 years) of leukemia and other neoplasia in this population are rare. The results of early chromosome studies suggested that true genetic damage might be a consequence of LSD exposure. The comprehensive evidence from studies on drosophila indicates no mutagenic effect from 0.28 to 500 microg of LSD per milliliter and a definite mutagenic effect from 2,000 to 10,000 microg/ml; this is consistent with a threshold response or a sigmoid dose-effect relation. We believe that LSD is, in fact, a weak mutagen, effective only in extremely high doses; it is unlikely to be mutagenic in any concentration used by human subjects. Circular dichroism experiments suggested that the specific mechanism of action of LSD on DNA may be a direct interaction resulting in conformational changes in the DNA helix. These changes are unlikely to result in a decrease of internal stability sufficient to cause breakage of chromosomes, but they may be the physical basis of the weak mutagenicity. Early chromosomal studies implicated LSD as a potential cause of congenital malformations, fetal wastage, and germinal chromosome damage. First reports of a teratogenic effect in hamsters and rats have not been confirmed. A review of 15 rodent studies indicated a wide range of individual, strain, and species susceptibility to the effects of LSD. The applicability of such investigations to man is doubtful. In a study of human pregnancies, those exposed to illicit LSD had an elevated rate of spontaneous abortions. There is no reported instance of a malformed child born to a woman who ingested pure LSD; there are six cases of malformation associated with exposure to illicit LSD, four of which have similar limb defects. Given, however, the high frequency of unexplained "spontaneous" birth defects, the rare occurrence of malformed infants born to women who used illicit LSD may be coincidental. While there is no evidence that pure LSD is teratogenic in man, the use of any drug during pregnancy requires that its potential benefits significantly outweigh its potential hazards. From our own work and from a review of the literature, we believe that pure LSD ingested in moderate doses does not damage chromosomes in vivo, does not cause detectable genetic damage, and is not a teratogen or a carcinogen in man. Within these bounds, therefore, we suggest that, other than during pregnancy, there is no present contraindication to the continued controlled experimental use of pure LSD. Note added in proof: A brief review has been brought to our attention. Although based on a sample of only 15 studies the author reached conclusions similar to our own (92).

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This shows evidence that many antipsychotics use today act as 5HT2a inverse agonists already (though we do know that antipsychotics definitely have their place in the treatment of HPPD; the side effects are often enough for discontinued use):

5-hydroxytryptamine2A receptor inverse agonists as antipsychotics

by

Weiner DM, Burstein ES, Nash N, Croston GE, Currier EA,

Vanover KE, Harvey SC, Donohue E, Hansen HC, Andersson CM,

Spalding TA, Gibson DF, Krebs-Thomson K,

Powell SB, Geyer MA, Hacksell U, Brann MR.

ACADIA Pharmaceuticals Inc.,

San Diego, California 92121, USA.

dweiner@acadia-pharm.com

J Pharmacol Exp Ther 2001 Oct;299(1):268-76

ABSTRACT

We have used a cell-based functional assay to define the pharmacological profiles of a wide range of central nervous system active compounds as agonists, competitive antagonists, and inverse agonists at almost all known monoaminergic G-protein-coupled receptor (GPCR) subtypes. Detailed profiling of 40 antipsychotics confirmed that as expected, most of these agents are potent competitive antagonists of the dopamine D2 receptor. Surprisingly, this analysis also revealed that most are potent and fully efficacious 5-hydroxytryptamine (5-HT)2A receptor inverse agonists. No other molecular property was shared as universally by this class of compounds. Furthermore, comparisons of receptor potencies revealed that antipsychotics with the highest extrapyramidal side effects (EPS) liability are significantly more potent at D2 receptors, the EPS-sparing atypical agents had relatively higher potencies at 5-HT2A receptors, while three were significantly more potent at 5-HT2A receptors. Functional high-throughput screening of a diverse chemical library identified 530 ligands with inverse agonist activity at 5-HT2A receptors, including several series of compounds related to known antipsychotics, as well as a number of novel chemistries. An analog of one of the novel chemical series, AC-90179, was pharmacologically profiled against the remaining monoaminergic GPCRs and found to be a highly selective 5-HT2A receptor inverse agonist. The behavioral pharmacology of AC-90179 is characteristic of an atypical antipsychotic agent.

~~It seems to say that there may be something to inverse agonist because the APs that effect the receptors as inverse agonists more than dopamine antagonists had less side effects. So they may be promising.

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qaiphyx and mgrade: this is the most interesting post I've read in a while. I really appreciate the effort, information and knowledge you sharing.

So far, we have spoken mainly of visual phenomena of the disorder, but what do you think of the related disorders as DP-DR, tinnitus, muscle tension, OCD ... etc? Some people claim to experience a decrease in symptoms under the influence of opiates, so perhaps the kappa opiod receptor is also linked.

Something I would like to add: regardless of my emotional states HPPD-dpdr started after taking 20mg of paxil for about a week. When i cutt of the paxil some visual distorsions dissapear.

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Esp. w/ HPPD (but not exclusive to), SSRIs like Paxil can cause migraine-like symptoms (certainly at high doses) and dissociation (possibly). I have heard horror stories about Paxil but I am on an SSRI but i have never been on Paxil so I can not tell you first hand if these things are true with myself.

I have tinnitus and i have had it for 15 years. The anxiety that came with the hearing loss was a significant reason (as well as an early case of persistent flashbacks) for me to initially go on SSRIs about 12 years ago. My tinnitus was a result of loud music; nevertheless it coincided with drug use (mainly marijuana and LSD).

While i have not experienced OCD, in terms being neurotic with cleaning and tidiness, my own OCD-like behavior could be seen with taking in a much information as I can because I feel that i am losing my mind (so constant check and rechecking of yahoo posts, email, certain books, etc). But this is really far from real OCD, by a long shot. With OCD, people do things like: check to see if the front door is locked like exactly 114 times every time, they wash there hands 77 times every time, they comb their hair 43 times to the left and 44 times to the right, before sitting down for dinner they circle the chair 19 times pat their heads 5 times rub their stomach 17 times and sit down and shake their hair out (all as a ritual), etc.

A lot of what maybe people are seeing with HPPD and "OCD" is just neurosis, which in my mind would certainly seem better the psychosis. But i could see that how your brain could be beaten down that you are reduced to do things that (let's say) i did at the age of 11, count passing cars on the highway or jumping over cracks on tiles floors.

DP/DR or dissociation seems to be a common symptom of HPPD. I have had it a lot, lot, lot, lot (still do) and i don't know a cure yet. For me, you can breathe into a paper bag, benzos, NSAIDS, stay hydrated , biofeedback, no smoking, no drugs/alcohol, get proper sleep, proper circadian rhythms, SSRIs, Wellbutrin, supplements, etc. I am not totally sure on this one i will look it up more.

Muscle tension is a real issue. For the last 6 months, I have been a tightened knot (esp. my neck and back, and really really bad at the base of the skull). I get bad regular headaches, and also migraine-headaches too. Headache: around ears, temples, back of the head, forehead, etc. Right now NSAIDs are the answer. But i have taken very small dose Vicodin maybe 3 or 4 times in the 6 months. It made me feel pretty good and took away the pain some. So i think is has some potential to help and not make HPP worse at very low dose. One time it made my stomach a little weird not terrible, and made me feel slightly dizzy but most of the other symptoms actually went away. Of course i took it before i went to sleep so i can only give you part of the experience. It may have a part in HPPD treatment.

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Hallucinogens; especially LSD, release glutamate. Excess glutamate kills neurons; and/or causes synaptic changes. Either way, seems irreversible. Matches my experience anyway....

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qaiphix>> I really hope you are here for the long run, i do not understand all of it but you seem to be very driven and possess a lot of knowledge about neurology.

About sleeping pills, when i was admitted to the hospital before getting my meds, when i got my zopiclone/zolpidem (ambien etc) all of my symptoms vanished in 15 minutes and i forced myself to stay awake just to be free from HPPD for a while. I talked about this at the time but no one really looked in to it.

in the US ambien is prescribed pretty frequently for sleeping problems, so you should try to get a script! It's great that something cures all your symptoms, if only for 15 minutes. I've also heard some pretty crazy stories about ambien hallucinations too, so I wonder what effect it'll have on someone's hppd if they trip on ambien...

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Thank you very much for your answer mgrade. It's true what you say about OCD, obvious for someone with DP- HPPD any neurosis its like a gigantic wave.

I dont know if you experience a kind of fluctuation in your dp-dr, as your memory comes and goes, or suddenly your vision becomes clearer. I'm trying to define which of the supplements I am taking is one that gives me such mental states.

PD: Visual come back!!

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qaiphyx----i found some interesting inverse agonist info <it's only an abstract though>:

http://www.ncbi.nlm....pubmed/21921840

****A thing that needs to be considered is post-synaptic density. (this involves the proteins near the membrane) -----Also receptor density. -------maybe Raphe Neurons as well...

Then Ion channels: Na, K, Ca2, et al

I know that disrupting the K+ channel is the action used by drugs used for arrhythmia and atrial fibrillation: getting the heart back in normal sinus rhythm.

Calcium Channel Blockers are used for hypertension and epilepsy.

I believe that the inherent conductance of each of these ions are as follows (from least conductive to most conductive): K, Na, Ca

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inverse 5ht2a agonists to accomplish the rebalancing of our receptors. unfortunately these dont exist that are on the market today, only in clinical trials, for the treatment of insomnia. Anyone have any ideas?

Imovane works partially..!

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