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

[dayum_son]

This is a bit off-topic but your post made me buy Ulfkotte's book. Time to dig out my old german skills.

[LethargicAcid]

nice! I have some ideas I'm just formulating them and them I'm gonna post them such as electromagnetic shock therapy, herbal holistic remedies/medicines, and such

[Fawkinchit]

51 minutes ago, LethargicAcid said:

nice! I have some ideas I'm just formulating them and them I'm gonna post them such as electromagnetic shock therapy, herbal holistic remedies/medicines, and such

Yes please do!

7 hours ago, dayum_son said:

This is a bit off-topic but your post made me buy Ulfkotte's book. Time to dig out my old german skills.

You can read German??

[Fawkinchit]

Mgrade, nice to see you back.

[dayum_son]

5 minutes ago, dasitmane said:

You can read German??

Yeah well I grew up speaking Swiss-German so it should be possible.

[mgrade]

Thanx Kfix

 

ECT is probably THE most stupid therapy discovered by these fuckheads.  Imagine your redneck friend deciding to hook you up to his 1985 Dodge Ram battery, saying "it's all good, I got a degree from the university."

 

The Ulfkotte book now goes for $1,000 a copy on Amazon.  Fuck you Amazon. 

 

I've searched all over and can't find an English version: bootlegged or not. 

 

It's been banned in Germany and now it's banned (essentially) in the USA.   Keep in mind, this book was a bestseller in Germany. 

[dayum_son]

The book isn't banned in Germany. https://www.amazon.de/gp/aw/d/3864451434/ref=mp_s_a_1_1?__mk_de_DE=ÅMÅZÕÑ&qid=1523989205&sr=8-1&pi=AC_SX236_SY340_FMwebp_QL65&keywords=gekaufte+journalisten&dpPl=1&dpID=51VVgBaPK5L&ref=plSrch

You can buy it there and available in Switzerland too.

However I can confirm it is impossible to find an english version.

[mgrade]

Ulfkotte died suddenly in his 50s.  Shortly after whistleblowing.  When he was alive, supposedly the German government banned the German book.  

I don't speak German.  The book was prepped to be published in English. Then Udo suddenly dies. 

Fricken sow, don't know German.

[dayum_son]

As I have previously read, he already had 3 heart attacks prior to his death. So , or it was just another heart attack, or german BND decided it was time.

Who knows.

[mgrade]

Yes I know he had a history of that.  But the the BND is basically a faction of the CIA in a lot of ways. 

The whole key to the Phoenix Program and bio, EM, or chem warfare on a country's own citizens is based in broad application of gas lighting. In other words, there is a movement towards No-Touch weaponry.  The trojan horse exterior to that is "non-lethal weapons".  There are non lethal weapons in the hands of security, police, and military that would make you wish you WERE dead. 

With no touch weapons, it's extremely hard to trace and prove. 

If you want to see what this sort of thing has done to a citizen of my country, watch a man named Mr. Rush questioning Zuckerberg at the recent Congressional Facebook Investigation, recounting his experience with COINTELPRO (let the man speak for himself):

 

[Fawkinchit]

On 4/17/2018 at 8:53 AM, dayum_son said:

Yeah well I grew up speaking Swiss-German so it should be possible.

Interesting. I may have some old German manuscripts that maybe you could help me understand? Might, its been a long time since I've looked at my non english stuff.

[dayum_son]

1 minute ago, dasitmane said:

Interesting. I may have some old German manuscripts that maybe you could help me understand? Might, its been a long time since I've looked at my non english stuff.

Sure, as long as there aren't 300 pages ^^

[Fawkinchit]

25 minutes ago, dayum_son said:

Sure, as long as there aren't 300 pages ^^

Haha, no not that long. Some may be pertaining to medicine. Ill see what I have when I have time. 

[Fawkinchit]

Heres a Danish study that did tests on 400 different people, 154 complained about long term problems years later. AKA HPPD sufferers. Some even committed suicide. And they lean toward potential neurotoxicity.

"two-thirds of the patients had flashbacks."

http://journals.sagepub.com/doi/10.1177/0957154X16629902

Edited April 22, 2018 by dasitmane

[dayum_son]

Good find ! It may not be as uncommon as we (or everyone else) think.

[dayum_son]

Found something weird :

When I focus on something really hard with my eyes, everything starts to move. Now that's not the weird part.

What I noticed is that I would get "exposure" shifts, like the brightness changing randomly.

So I filmed my eyes while focusing on something, and weirdly enough, my pupils dilate and constrict randomly for no apparent reason. What the hell.

[Fawkinchit]

Shit bros the more I read and learn the more confused I am. It could be so many things that cause HPPD. Some people do so much LSD and have zero symptoms after. I think that we must have some susceptibility, it may not even be brain damage. I was thinking that other possibilities could be allergic reaction related swelling causing microvascular ischemia in the brain, starving scattered neurons(neuronal loss).

Another possibility really could be possible gene/DNA changes that create ion channel mutations, I dont know how it coiuld be that since it seems to come on over nice, but I did notice a progression in my symptoms from day one, so I dont know. But ion channel mutations could cause this.

This is an impossible disease.

 

Heres some stuff that ive found to be pretty interesting lately

Posterior visual pathway cortical lesions (tumor,^[1] abscess,^[3] hemorrhage,^[4] infarction,^[1] arteriovenous malformation,^[5]cortical dysplasia,^[6] aneurysm^[1]) and various seizure causes (hyperglycemia,^[7] ion channel mutations,^[8] Creutzfeldt–Jakob disease,^[9] idiopathic seizures,^[10] etc.) cause focal cortical hyperactivity or hyperexcitability, resulting in inappropriate, persistent activation of a visual memory circuit.

Illusory palinopsia is a dysfunction of visual perception, resulting from diffuse, persistent alterations in neuronal excitability that affect physiological mechanisms of light or motion perception. Illusory palinopsia is caused by migraines, HPPD, prescription drugs, head trauma, or may be idiopathic. Trazodone,^[11] nefazodone,^[12] mirtazepine,^[13] topiramate,^[14]clomiphene,^[15] oral contraceptives, and risperidone^[16] have been reported to cause illusory palinopsia. A patient frequently has multiple types of illusory palinopsia, which represent dysfunctions in both light and motion perception. Light and motion are processed via different pathways, suggesting diffuse or global excitability alterations.

https://en.wikipedia.org/wiki/Palinopsia

 

This information could send us in an accurate general direction of whats going on here. 

Edited May 3, 2018 by dasitmane

[dayum_son]

Interesting find. I really think there's something else than glutamate. 

How come I took Ketamine a week ago (NMDA antagonist) and it made my symptoms worse ?

I am leaning towards calcium channels. Will elaborate later.

[mgrade]

Ketomine is a dissociative drug.  Pcp is a nmda antagonist as well.  

I think what is going on in terms of me is this: you start with a fairly sensitive nervous system, you take an "over-quota" for your particular lifetime of certain chemicals, or one or two significant "ODs", ultimately (for me) the pleasure centers of the nervous system are altered, in other words this: the feeling of euphoria, wellbeing, elation, calm-happiness, anxiety-free ability to focus, the soothing assured opposite feelings to anxiety and panic and depression: all these things are absent from the psychedelic and dissociative and high-level cathionone/subcath/amphetamine/amphetamine-related drug experience: in other words, maybe at one point you smoked weed or drank or did K or LSD (and while things were "weird" and different a bit and consciousness was altered to an extent) there was an underlying feeling of tranquility or euphoria or "happiness" that ultimately made the experience enjoyable.  But after youve blown your load (or brain) or whatever, these particular drugs leave you only with the anxiety, unsettling aspects to them when these drugs are taken.  

As far as just the sensory (vision) part goes, it is important of course to explore that and discover the exact neurological reasoning of such a phenomenon. 

 

But to look at what i am discussing earlier, it is a multi-line issue: dopamine, glutamate, serotonin, etc. 

And the "semi-organic" issues should not be ruled out, as well.

Don't get me wrong though, the strictly visual issues of HPPD are important.  Because people who have had issues with any of all  the senses have been know to lose there mind in some cases and turn into psychosis.  Such is the cases sometimes with people whose eyes are failing, or hearing failing, etc.

So as far as the "anhedonic" part of all this goes, you ask yourself why does it feel good to take a klonopin or a ritalin or a lexapro or a wellbutrin.  Well these are the systems that may be damaged.  An analogy would be if you thirst and there is a spring in site, you go to the source and drink as one experiencial movement.  The dry meets the wet.  The receptor meets the ligand.  

But if you look at the drugs that i just mentioned a lot of the action/mechanism is somewhat indirect, in that they are "helpers" in double-ligand receptors or reuptake agents. 

So it seems two things are issues: 1. Low neurochem concentrations 2. Large number of receptors 

(The latter would explain our original sensitivity, perhaps for some cases/people).

A third one could be right concentrations but in the wrong places of the brain. And a fourth is right number of receptors except in certain parts of the brain. The example of this fourth one is the idea that some people have excess dopemine and/or nmda receptors in the frontal and prefrontal cortices. 

So this brings me to the opioid receptors that have fairly direct ligands and cascade into dopamine.  I always felt opiates used very sparingly are good in the treatment of anhedonia. This can sort of apply with the nicotinic system too.

 

So think if i gave you 2mg of ritalin, .5mg ativan, an 1/16 vicodin, 5mg of Lexapro, a 1/16 of a propranolol, 1mg of klonopin, an aspirin, 2 ibuprofen, half a diet coca cola, a brownie, a cheeseburger, and a cigarette.  You'd probably feel somewhat normal.  And here you can realize how it is a very multisystem issue.

Edited May 5, 2018 by mgrade

[Fawkinchit]

Well guys, I've pretty much figured it all out.

This condition is actually quite simple as to the cause. I sometimes pray for an answer as to the cause, so that we can better understand the condition. Yesterday during my usual walk, I did the same. Last night I decided to do some quick reading and found 1 thing after another within a short amount of time and everything adds up. Researchers dont have any information on what hallucinogens do to the brain seemingly, but this isn't quite the case. We know for certain that take for example LSD, acts on 5ht2a receptors, we know this for sure because 5ht2a antagonists taken before LSD ingestion, will prevent hallucinations. As to the reason for the hallucinations they aren't quite sure, but they do know that 5ht2a activation exhibits increases in glutamate. Glutamate is the most available receptor in the brain, it also is notorious for excitotoxic apoptosis. The clear answer is that LSD and other hallucinogens increase neuronal output of glutamate, the hallucinations are probably from the overly excessive production of glutamate, and its stimulant effects. This is the cascade effect leading to overexcitation of neurons, and their eventual course to apoptosis, leading to the condition of HPPD.

Now, some may argue that there are some who don't get HPPD, and that HPPD is rare. This is true, and creates a bit of elusiveness. The most possible reasons for this is that for one, many people are pretty complacent as to their actual cognitive function, and deficits created therein, this is one possible reason for less reports of HPPD. Granted however, I dont think this is the primary case for the rarity of HPPD, but rather, that glutamate requires breakdown, and utilizes P5P, or vitamin B6, for its breakdown with glutamate decarboxylase. Thus, the most probable explanation for HPPD is that the sufferers most likely have a variable amount of metabolic deficiency for the production of P5P or glutamate decarboxylase. This would explain why the condition is rare, and why some people come out seemingly unscathed by hallucinogens. I hardly doubt that they come out completely unscathed, but I am sure that their neuronal loss is most likely quite limited.

The most likely explanation for MRIs having little to no findings is most probably due to the fact that the neuronal loss is scattered. Thus it will hardly show on MRIs, if at all, and this is why a small percentage actually do seem to have some minor findings of scattered white matter micro lesions, commonly associated with migraines.

I'd like to comment too, that in my own personal case, the most likely cause for my HPPD was that I consistently, for years, would always take folinic acid, which I always noticed had a strong stimulant effect, not really knowing the reason for it however. Now I have found that folinic acid and other folate compounds are directly linked to the availability of free glutamate, hence during the use of hallucinogen use incombinate with high glutamate availability, you're going to be more prone to excitotoxicity leading to apoptosis and HPPD. Folate supplementation is also readily found in breads, and multivitamins. The cause for some people developing HPPD simply could be eating high amounts of folate in breads and grains unknowingly, and then taking hallucinogens, buffering glutamate production and excitotoxicity.

Like I said, super simple, and easily explained.

I should add too that people who experience recovery is due to neuronal plasticity. I'm not going to explain what that is here but its pretty simple to google and is pretty limited to the amount of recovery.

 

From here I will try to find out if long distance axonal tracts can be repaired, if not even with neurogenesis and even stem cell research we will be limited to recovery based on that alone. Long distance axonal tracts are very important.

As I've stated before, the Axolotl Salamander, who can regenerate large chunks of his brain, is incapable of repairing long distance axonal tracts after blunt trauma. This most certainly will inhibit functional regrowth of the brain.

Also I'd like to add that the areas of the brain effected, are the cortico limbic systems. So frontal cortex, hipp, thalamus, etc. Heres a good read for understanding the limbic system https://www.interaction-design.org/literature/article/our-three-brains-the-emotional-brain. It all pretty much makes perfect sense. Heres for frontal lobe, https://en.wikipedia.org/wiki/Frontal_lobe#Function. Just skip to function and damage. I think we all will see a lot of our symptoms correlate or fall in to place in these areas of the brain. 

Edited May 11, 2018 by dasitmane

[dayum_son]

I also had the excessive glutamate production theory in mind, and makes perfect sense to me.

However, I think the damage caused by the condition is negligible. People who had HPPD for decades aren't any dumber than a "normal" person.

Imo, the main problem we are having is brain disinhibition caused by excess glutamate. If we could stop this excess glutamate, I'm sure almost, if not all hallucinations and DP/DR will stop.

Let's not forget the brain is one tough motherfucker, it will recover to an extent.

My theory is this excess glutamate is due to messed up P and N-Type Calcium Channels.

They are responsible for many things, including neurotransmitter (Gaba, Glutamate etc) release.

I have Asperger's syndrome and so does my best friend.

Treatments for autistic people are aimed at modulating or blocking N-Type channels. Which makes me think I was predisposed to HPPD. My best friend always had VS and tracers, even before taking LSD.

Many success-story-meds like lamotrigine among others, block the N and P-Type channel.

All this makes me think that our condition is caused by many things, but the primary being calcium channels. Too high voltage for example ?

[dayum_son]

Hey, HPPD is still a great disease ! Look at all the shit we learned because of it, I'm sure we could all work as neurologists now 

[Fawkinchit]

1 hour ago, dayum_son said:

I also had the excessive glutamate production theory in mind, and makes perfect sense to me.

However, I think the damage caused by the condition is negligible. People who had HPPD for decades aren't any dumber than a "normal" person.

Imo, the main problem we are having is brain disinhibition caused by excess glutamate. If we could stop this excess glutamate, I'm sure almost, if not all hallucinations and DP/DR will stop.

Let's not forget the brain is one tough motherfucker, it will recover to an extent.

My theory is this excess glutamate is due to messed up P and N-Type Calcium Channels.

They are responsible for many things, including neurotransmitter (Gaba, Glutamate etc) release.

I have Asperger's syndrome and so does my best friend.

Treatments for autistic people are aimed at modulating or blocking N-Type channels. Which makes me think I was predisposed to HPPD. My best friend always had VS and tracers, even before taking LSD.

Many success-story-meds like lamotrigine among others, block the N and P-Type channel.

All this makes me think that our condition is caused by many things, but the primary being calcium channels. Too high voltage for example ?

They could be considered for possibility, however ion channel damage directly from hallucinogen use would be repairable by the brain. Indirect ion mutation through dna changes from hallucinogens would easily ruled out as well due to the fact that it would then be a progressive onset, not overnight like HPPD. 

[Fawkinchit]

I can add too that in the case of Risperodone, a 5ht2a inverse agonist, and other anti convulsion medications which are 5ht2a antagonists there is a correlation with palinopsia. Palinopsia being obviously common with HPPD, the most probable reason being, that the 5ht2a specific neurons that underwent glutamate excitotoxic apoptosis, are now gone, and therein laying a lack of 5ht2a input, which would be similar to that of these drugs, being inverse agonists and antagonists. So this gives even more credence that HPPD is caused by 5ht2a induced glutamate excitotoxic apoptosis.

Edited May 12, 2018 by dasitmane

[dayum_son]

Interesting.