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Hallucinogen Persisting Perception Disorder (HPPD) Support Forum
dasitmane

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

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Qaiphyx brought to my attention 5ht2a inverse agonists.  It was a great success in FDA trials.  And because of his ideas i invested in a stock that went up 1000%.  

Thank you!  ....but ofc the money is not as important as something that will help us and other people with nerve based problems.  

 

This is what I have been interested in now:  a treatment for MDD and stem cells.  The treatment for MDD is a drug called NSI-189.   I'm not sure we have mentioned it before  but there are official trials being performed as we speak.  And i found a site where people were getting the drug from chemical companies and this is some of their "opinions":  http://208.71.46.190/search/srpcache?ei=UTF-8&p=longecity+nsi-189&fr=yfp-t-140&rs=0&u=http://cc.bingj.com/cache.aspx?q=longecity+nsi-189&d=4573935196046048&mkt=en-US&setlang=en-US&w=y653-FeiyYof_A2CyQ0KTNLrnI9JNkzn&icp=1&.intl=us&sig=VNrvcJFPLC2J_zIR6jbtCw--

 

The company behind these therapies is neuralstem. 

 

Wow! Thats great Mg. Ha.

 

Just wanted to check up and see how everyone is doing. Been a while since I have been here. Hope you're all doing well.

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Correct me if I'm wrong but if there were ever an approach and modality to help us, wouldn't this be it?
Someone able to speak science needs to get in touch with these doctors, inform them of this condition and explain how and why their research could probably help us. I could think of you, Qaiphyx, Visual and of course David but there are plenty of others who could articulate the theory behind our problem and perhaps pose a challenge to these scientists that will entice them to solve. Will someone with the smarts contact them please???

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-This is the part that I found relevant to HPPD and as a modality to a potential cure.

“Interestingly, the reactive astroglial cells were reprogrammed into excitatory neurons, whereas the NG2 cells were reprogrammed into both excitatory and inhibitory neurons, making it possible to achieve an excitation-inhibition balance in the brain after reprogramming,” Chen said.

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Some of us are not as fortunate and functional as u

We are all on a spectrum, and it changes over time.  If you can, grit your teeth and move forward a little bit at a time, a day at a time.  All you have to do is cope for the next five minutes.  Don't think past that.  Or today.  Today you will do something to make an improvement.  Do one thing you enjoy, and one thing that may be difficult but good for you.  Call that a good day.  Repeat.

 

My guess is that the chemical reaction we all experienced, and the effect it had on our neurochemistry and patterns of signal firing, is not going to respond to a single, simple approach to a cure.  Think "whole body, mind" healing and do what you can.

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Ok here is the full laid out explanation of HPPD
 
The Cerebellum Connection
 
In the rat cerebellum, 5ht2a receptors have been found in the Golgi cells of the granular layer, and in the Purkinje cells. This shows that the cerebellum will be effect in specific cells under the influence of hallucinogens.
 
Purkinje cells are a class of GABAergic neurons located in the cerebellar cortex. 
 
People with cerebellar ataxia may initially present with poor balance, which could be demonstrated as an inability to stand on one leg or perform tandem gait. As the condition progresses, walking is characterized by a widened base and high stepping, as well as staggering and lurching from side to side. People with damage to the cerebellum from strokes also have vertigo and other similar balance disorders and problems have been reported with anxiety I believe as well.
 
Symptoms of HPPD have been known to exhibit balance disorders. This gives an obvious full line of connections for the cerebellum being a critical center that is effected by HPPD.
 
Now on to golgi cells in the cerebellum
 
Golgi cells are inhibitory interneurons found within the granular layer of the cerebellum. 
 
This ties in with the inhibitory feedback that I was talking about in the beginning of this thread(push pull idea), that there may have been damage to these inhibitory cells, and the brain now lacks the ability to modulate anxiety!
 
That sums up most of the cerebellum
 
Lets take a look at other areas in the brain affected.
 
Newer findings reveal that psychoactive effects of classic psychedelics are mediated by the receptor heterodimer 5-HT2A–mGlu2 and not by monomeric 5-HT2A receptors.
 
The mGluRs perform a variety of functions in the central and peripheral nervous systems: For example, they are involved in learning, memory, anxiety, and the perception of pain. They are found in pre- and postsynaptic neurons in synapses of the hippocampus, cerebellum, and the cerebral cortex, as well as other parts of the brain and in peripheral tissues.
 
This shows other areas in the brain that are going to be negatively affected by hallucinogens. The hipp, cere, cere cortext, and other parts, most likely visual related. 
 
So, now we know all the areas of the brain being affected by hallucinogens. 
 
Lets take an even closer looks at where and what the 5ht2a receptors do.
 
5-HT2A is expressed widely throughout the central nervous system. It is expressed near most of the serotoninergic terminal rich areas, including neocortex(mainly prefrontal, parietal, and somatosensory cortex) and the olfactory tubercle. Especially high concentrations of this receptor on the apical dendrites of pyramidal cells in layer V of the cortex may modulate cognitive processes, by enhancing glutamate release followed by a complex range of interactions with the 5-HT1A, GABAA, adenosine A1, AMPA, mGluR2/3, mGlu5, and OX2 receptors. In the rat cerebellum, the protein has also been found in the Golgi cells of the granular layer, and in the Purkinje cells. In the periphery, it is highly expressed in platelets and many cell types of the cardiovascular system, in fibroblasts, and in neurons of the peripheral nervous system. Additionally, 5-HT2A mRNA expression has been observed in human monocytes.
 
I bolded the parts that are the more important keys to showing what causes HPPD. Not also that the golgi and purkinje cells are brought up again. Also note that one of the main functions of the 5ht2a receptor when activated is to enhance the release of glutamate, and effects the AMPA receptor.
 
Lets tie it all up now.
 
Excitotoxicity is the pathological process by which nerve cells are damaged and killed by excessive stimulation by neurotransmitters such as glutamate and similar substances. This occurs when receptors for the excitatory neurotransmitter glutamate such as the NMDA receptor and AMPA receptor are overactivated by glutamatergic Storm.
 
So, hallucinogens extremely high agonist(push) affinity for 5ht2a receptors will overstimulate the receptor, causing a higher than normal release of glutamate, leading to a glutamatergeic storm of all the areas listed above, thus leading to excitotoxicity of those areas, and causing apoptosis to occur to specific sites in the brain. The brain then no longer has the ability to regulate certain stimuli and electromagnetism. Hence, the symptoms of HPPD.
 
That should clear it all up for you guys.

 

 

I think there are some excellent kernels of value and interest in what you say, though the question I have about all this is the failure of any MRI, CAT (I've had both) and possibly PET scans (can someone check?) to detect any cell death.  So I am not sold on neurotoxicity and neuron death as primary factors in HPPD.

 

BUT:  you bring to mind another possible avenue of research with excellent bona fides: deep brain stimulation, and trans-cranial stimulation.  Both are vetted, with published and verified results in the areas where they have been applied.

 

For example, 100,000 Parkinsons patients are running experimental devices that SHUT OFF their tremors by stimulating the clusters of neurons responsible for the out-of-whack firing patterns.

 

What if, instead of cell death, a "malformed" but resonant pattern of firing has been set up amongst groups of neurons, causing the responses that developed during intoxication to return and persist - and what if electrical stimulation would disrupt the resonant pattern and extinguish the misfirings, hence the symptoms?

 

I have to say, my HPPD has been much less an issue for me since my breakdown and subsequent electro-shock.

 

Think about it.

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Mind/Body, Inhibition/Disinhibition; we can as a group postulate wtf is going wrong and ruinning lives until the day we die. It won't make one bit of difference unless we have someone with influence, credentials and resources to fast track research into this dreadful condition. We need publicity like that DANA or New Yorker article multiplied by a factor of 1000 in order to inspire a group of reserachers that want to tackle the challenge of HPPD and put an end to our misery. There is a cure, has to be and with all that is going on in science, all the discoveries and breakthroughs, why should we be left behind? This board is great but it's not enough. We need a formulated plan to get HPPD on talk shows, scientific conferences, publised in the news and eventually scientific journals. Dr. Abraham is great but honestly one guy leading the way yelling "CHARGE" with nobody behind him isn't working. If there is a cure and if we ever to expect to see one in this lifetime, it's not going to happen by a bunch of us throwing theories at one another. Granted there are some brilliant posts here and I understand sometimes it takes a community of people who share a common affliction to operate as their own advocates but we've reached a threshold that we cannot pass. We need to break this threshold and get people to notice US to fully appreciate our SUFFERING and inspire gifted minds to HELP.

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I think there are some excellent kernels of value and interest in what you say, though the question I have about all this is the failure of any MRI, CAT (I've had both) and possibly PET scans (can someone check?) to detect any cell death.  So I am not sold on neurotoxicity and neuron death as primary factors in HPPD.

 

BUT:  you bring to mind another possible avenue of research with excellent bona fides: deep brain stimulation, and trans-cranial stimulation.  Both are vetted, with published and verified results in the areas where they have been applied.

 

For example, 100,000 Parkinsons patients are running experimental devices that SHUT OFF their tremors by stimulating the clusters of neurons responsible for the out-of-whack firing patterns.

 

What if, instead of cell death, a "malformed" but resonant pattern of firing has been set up amongst groups of neurons, causing the responses that developed during intoxication to return and persist - and what if electrical stimulation would disrupt the resonant pattern and extinguish the misfirings, hence the symptoms?

 

I have to say, my HPPD has been much less an issue for me since my breakdown and subsequent electro-shock.

 

Think about it.

 

This actually isnt a bad probabillity, its definitely possible that instead of apoptosis is caused some malfunction in neuronal resonance, maybe there is some sort of scarring involved. Hard to say. Mainly the post was to make the connections of how the problem most probably occurs. Its definitely open to enterperit the end result. Apoptosis was the best I could come up with, though it definitely could be some other form of damage. Also would MRIs pick up scattered apoptosis? I think they are generally only capable of showing large clusters of the brain tissue death. But I could be wrong about this.

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Correct me if I'm wrong but if there were ever an approach and modality to help us, wouldn't this be it?

Someone able to speak science needs to get in touch with these doctors, inform them of this condition and explain how and why their research could probably help us. I could think of you, Qaiphyx, Visual and of course David but there are plenty of others who could articulate the theory behind our problem and perhaps pose a challenge to these scientists that will entice them to solve. Will someone with the smarts contact them please???

 

Um, yah, this would be a great thing to inform them of. Basically is all you would need to do is copy and paste the information that I posted to them. Couple problems there though are that, honestly, most modern day scientists are just mainstream method followers, they generally are most likely to be about getting funding, they dont want to do research that may tarnish their reputation, and, youll need to make sure that it was already made public information what you;re sending them so they dont try say they came up with the idea lol. :lol: Seriously though I wouldnt be surprised hahaha. This system really is a failure.

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This is the first time I've posted an idea, so I hope this is this right place for it and that I'm not just repeating something that's already well known.

 

Going back to -mg's post about PTSD and cortisol, I assume most people on this forum have some pre-existing anxiety issues, or at least ones which stem directly from their HPPD symptoms.

 

I have a history of cumulative stress from various concrete unfortunate issues from age 8! And I'm pretty sure that the result, (what I can really only think of as PTSD), is what primed me for HPPD, from just one single bad trip. 

 

I also have ADD (type 5/7, self-diagnosed from Dr Amen's website: http://www.amenclinics.com/conditions/adhd-add (bottom of page). He recommends 'Relora' for the anxiety-related issues specifically related to this. Relora reduces cortisol: http://www.ncbi.nlm.nih.gov/pubmed/23924268

Hey, I thought, something that will treat my ADD and anxiety all in one! So, I ordered some. Like most of us here, I am petrified of taking anything that may worsen my HPPD symptoms, so before taking it, I googled 'Cortisol and PTSD'.

 

What came up was a real surprise. I always thought stress releases cortisol. It does under moderate stress but severe stress (PTSD) often reduces cortisol levels. It turns out that PSTD dysregulates the basal cortisol level so that it can go either way. One of many studies out there: http://www.med.navy.mil/sites/nmcsd/nccosc/healthProfessionalsV2/reports/Documents/ptsd-and-cortisol-051413.pdf

 

I know that raised cortisol levels cause cells in the hippocampus to shrink, but what about lowered levels?

 

This is all way over my head. I am only 16 and struggling. I know there are various ways of measuring cortisol: blood, brain etc. I am just trying to work out whether I should take this Relora or not, but I thought maybe one of you out there who is really qualified to understand this stuff could maybe consider this cortisol issue and come up with a theory about why so many of us suffer such high anxiety!

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This is all way over my head. I am only 16 and struggling. I know there are various ways of measuring cortisol: blood, brain etc. I am just trying to work out whether I should take this Relora or not, but I thought maybe one of you out there who is really qualified to understand this stuff could maybe consider this cortisol issue and come up with a theory about why so many of us suffer such high anxiety!

Relora is a mixture of Magnolia Officinalis bark, and Phellodendron Amurense bark. I forgot most about it, but from a quick glance it doesn't seem all that dangerous, especially if you don't take anything else with it. I've taken it myself for a while, but it did nothing for me; neither good nor bad. I don't see any reason why not to try it if you already have it.

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Yes, it can't do much harm, can it, a bit of plant bark? I'm having great difficulty (given my age and conservative German doctors) getting a script for ANY anti-depressants.

 

Fluoxetine screwed me: (looking back, pre-HPPD, I realise it was already giving me double vision and Strattera made bits of the wall disappear).

Prescribed mirtazapine made my visuals worse and since then, as the docs know nothing about HPPD, they only trust themselves to hand out neurexan (diddly squat) and now relora.

 

I've been trying for months now to convince somebody to prescribe Tianeptine but Emanupil sounds awesome. Looks like the wait for that will be longer, hey?

So it's tree bark for the time being.

 

Thanks for your reply.

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Qaiphyx-How on Earth will we ever get help for this condition if we don't ask for it and spread awareness?
Science is slowly emerging where within a 5-10 year window we could see some type of therapy or cure applicable to HPPD but only if we act as our own advocates. Talking theories is great but at the end of the day, nobody here has a PhD or a doctorate to their name.

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i had mentioned this one drug on this thread, post #181

 

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

default_large.png Posted by -mg on 27 September 2012 - 09:43 PM in MAIN AND GENERAL FORUM

Qaiphix---Check out this drug: Retigabine.
 
 
------------------------
 
 
IDK if this guy i am about to show you is any good or is no good.  But here he is:
 
Phil Corlett Ph.D., winner of a 2013 IMHRO/Janssen Rising Star Research Award, explains the basis for his proposal to test the drug Retigabine as a potential therapy for schizophrenia's delusional and anhedonic symptoms.
 
 
*Note the dates LOL

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i had mentioned this one drug on this thread, post #181

 

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

default_large.png Posted by -mg on 27 September 2012 - 09:43 PM in MAIN AND GENERAL FORUM

Qaiphix---Check out this drug: Retigabine.
 
 
------------------------
 
 
IDK if this guy i am about to show you is any good or is no good.  But here he is:
 
Phil Corlett Ph.D., winner of a 2013 IMHRO/Janssen Rising Star Research Award, explains the basis for his proposal to test the drug Retigabine as a potential therapy for schizophrenia's delusional and anhedonic symptoms.
 
 
*Note the dates LOL

 

 

I will check it out when I have time. Thanks Mg. Btw I sent you a PM.

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I've been looking into other phenomena mostly visual:

1. Amblyopia. W. Or w/o tobacco

2. Crowding

And interesting causes/ideas/odd relations:

1. B12 deficiency

This is what b12 is:

Vitamin B12 consists of a class of chemically related compounds (vitamers), all of which have vitamin activity. It contains the biochemically rare element cobalt sitting in the center of planar tetra-pyrrole ring called a Corrin ring. Biosynthesis of the basic structure of the vitamin is accomplished only by bacteria and archaea (which usually produce hydroxocobalamin), but conversion between different forms of the vitamin can be accomplished in the human body. A common semi-synthetic form of the vitamin, cyanocobalamin, does not occur in nature, but is produced from bacterial hydroxocobalamin and then used in many pharmaceuticals and supplements, and as a food additive, because of its stability and lower production cost. In the body it is converted to the human physiological forms methylcobalamin and 5'-deoxyadenosylcobalamin, leaving behind the cyanide, albeit in minimal concentration. More recently, hydroxocobalamin, methylcobalamin, and adenosylcobalamin can be found in more expensive pharmacological products and food supplements. The extra utility of these is currently debated.

Vitamin B12 was discovered from its relationship to disease pernicious anemia, which is an autoimmune disease in which parietal cells of the stomach responsible for secreting intrinsic factor are destroyed; the same cells are responsible for secreting acid in the stomach. Intrinsic factor is crucial for the normal absorption of B12, so a lack of intrinsic factor, as seen in pernicious anemia, causes a vitamin B12 deficiency. Many other subtler kinds of vitamin B12 deficiency and their biochemical effects have since been elucidated.[2]

The names vitamin B12, vitamin B12, or vitamin B-12, and the alternative name cobalamin, generally refer to all forms of the vitamin. Some medical practitioners have suggested that its use be split into two categories.

In a broad sense, B12 refers to a group of cobalt-containing vitamer compounds known as cobalamins: these include cyanocobalamin (an artifact formed from using activated charcoal, which always contains trace cyanide, to purify hydroxycobalamin), hydroxocobalamin (another medicinal form, produced by bacteria), and finally, the two naturally occurring cofactor forms of B12 in the human body: 5'-deoxyadenosylcobalamin (adenosylcobalamin—AdoB12), the cofactor of Methylmalonyl Coenzyme A mutase (MUT), and methylcobalamin (MeB12), the cofactor of enzyme Methionine synthase, which is responsible for conversion of homocysteine to methionine and of 5-methyltetrahydrofolate to tetrahydrofolate.

The term B12 may be properly used to refer to cyanocobalamin, the principal B12 form used for foods and in nutritional supplements. This ordinarily creates no problem, except perhaps in rare cases of eye nerve damage, where the body is only marginally able to use this form due to high cyanide levels in the blood due to cigarette smoking; it thus requires cessation of smoking or B12 given in another form, for the optic symptoms to abate.[citation needed] However, tobacco amblyopia is a rare condition, and it is yet unclear whether it represents a peculiar B12 deficiency that is resistant to treatment with cyanocobalamin.

It is cobalt containing. Cyan- blue. Though b12 is a red colored.

http://en.m.wikipedia.org/wiki/File:B12_methylcobalamin.jpg

Halides

Cobalt(II) chloride hexahydrate

Four dihalides of cobalt(II) are known: cobalt(II) fluoride (CoF2, pink), cobalt(II) chloride (CoCl2, blue), cobalt(II) bromide (CoBr2, green), cobalt(II) iodide (CoI2, blue-black). These halides exist in anhydrous and hydrated forms. Whereas the anhydrous dichloride is blue, the hydrate is red.[12]

The reduction potential for the reaction

Co3+

+ e- → Co2+

is +1.92 V, beyond that for chlorine to chloride, +1.36 V. As a consequence cobalt(III) and chloride would result in the cobalt(III) being reduced to cobalt(II). Because the reduction potential for fluorine to fluoride is so high, +2.87 V, cobalt(III) fluoride is one of the few simple stable cobalt(III) compounds. Cobalt(III) fluoride, which is used in some fluorination reactions, reacts vigorously with water.[8]http://en.m.wikipedia.org/wiki/File:Cobalt(II)-chloride-hexahydrate-sample.jpg

Vitamin B12 (see below) is an organometallic compound found in nature and is the only vitamin to contain a metal atom.[17]

Idk just found this interesting. : /

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Cobalt-60 (Co-60 or 60Co) is a radioactive metal that is used in radiotherapy. It produces two gamma rays with energies of 1.17 MeV and 1.33 MeV. The 60Co source is about 2 cm in diameter and as a result produces a geometric penumbra, making the edge of the radiation field fuzzy. The metal has the unfortunate habit of producing a fine dust, causing problems with radiation protection. Cobalt machines have fallen from favor in the Western world where linacs are common.

Cobalt-57 (Co-57 or 57Co) is a radioactive metal that is used in medical tests; it is used as a radiolabel for vitamin B12 uptake. It is useful for the Schilling test.[2]

Industrial uses for radioactive isotopesEdit

Cobalt-60 (Co-60 or 60Co) is useful as a gamma ray source because it can be produced—in predictable quantity, and high activity—by simply exposing natural cobalt to neutrons in a reactor for a given time. It is used for

sterilization of medical supplies, and medical waste;

radiation treatment of foods for sterilization (cold pasteurization);

industrial radiography (e.g., weld integrity radiographs);

density measurements (e.g., concrete density measurements); and

tank fill height switches.

Cobalt-57 is used as a source in Mössbauer spectroscopy of iron-containing samples. The electron capture decay of the 57Co forms an excited state of the 57Fe nucleus, which in turn decays to the ground state with emission of a gamma ray. Measurement of the gamma ray spectrum provides information about the chemical state of the iron atom in the sample.

The primary decay products before 59Co are iron isotopes and the primary products after are nickel isotopes.

Radioactive isotopes can be produced by various nuclear reactions. For example, the isotope 57Co is produced by cyclotron irradiation of iron. The principal reaction involved is the (d,n) reaction 56Fe + 2H → n + 57Co.[1]

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Today is Wed. Sept. 17, 2014

 

        I've been thinking about a few things:  

 

1.  Sensory Loss and Mental Illness

2.  Head Injury and Parkinson's 

 

 

and 

3.  Head injury, Seizures, Tremors, Restless Leg Syndrome,  and ADD

 

(Somewhat of a word association, but i see the link.)

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I've been thinking this one lately and hopefully somebody can give his/her opinion. Well, how probable is it - after all this we know so far about, that drugs have kind of "blown up" our receptors by overloading serotonin into them, so they cannot function properly anymore at all? Are those receptors like dead now? If it is the chemical imbalance of the brain, why is it so difficult to fix? I just cannot understand that. Why can't we just eat a single pill that rebalances the brain, could it ever be so simple?

My 3 year mark will be in the next month and not a single symptom has faded so far. All the best to you!

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I've been thinking this one lately and hopefully somebody can give his/her opinion. Well, how probable is it - after all this we know so far about, that drugs have kind of "blown up" our receptors by overloading serotonin into them, so they cannot function properly anymore at all? Are those receptors like dead now? If it is the chemical imbalance of the brain, why is it so difficult to fix? I just cannot understand that. Why can't we just eat a single pill that rebalances the brain, could it ever be so simple?

My 3 year mark will be in the next month and not a single symptom has faded so far. All the best to you!

 

Basically thats the assumption that I have come to, not that the receptors are gone, but that specific cells in the brain are gone, its like if you were to damage the visual section of the brain, the eye, though in perfect condition, would become very blurred, such is the same sense I assume in perception of other senses, they are more or less blurred and or uninhibited now. So we have certain symptoms such as vertigo, dp/dr, imbalance, severe anxiety, etc. Hence, no pill will alleviate the symptoms, but only hinder them to so speak. Someone on here once gave a good analogy, is like a siren going off in the head, blaring, and the meds, such as sedatives, only dull the sound of the siren, but its still there. No chemical rearrangement in the brain can bring back the lost brain cells, hence the reason that people with cerebral stroke are in vertigo the rest of their lives till they die. Some puking 3 times a day from it. That I assume, would be a nightmare somewhat comparable to ours.

 

Btw if you find the page that I mention in my first post in this thread, you can go to it and read how its shown that the cells are damaged through hallucinogen usage. It goes through the whole process and is better explained in later pages.

 

Basically, brain cells commit suicide when overly stimulated, in which hallucinogens do.

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