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Mechanism of augmentation of HPPD/Psychedelia by d-amphetamine?

permastoned

permastoned

Bluelighter
Joined
Oct 10, 2008
Messages
493
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Watching the parade with pinpoint eyes, full of sm
Hello all,

I have a query for you all. I have very minor HPPD (have, NOT suffer) which consists primarily of words wriggling around on my computer screen whilst reading and some very slight warping of my general vision sometimes if I "don't concentrate".

As I have implied, these effects do not bother me. I have an extensive history of LSD use and a few random other uses of psychedelics here and there; I consider HPPD a small price to pay for the insight that I have gained through the use of these substances.

Rather, I am interested in a possible mechanism for an effect I have noticed when using d-amphetamine. I have observed that the use of d-amphetamine in average doses (25mg) when sober quite reliably and noticeably augments the severity of the pseudo-hallucinations. Warping can become VERY noticable, and letters and words wriggle away as if they were an earthworm hopped up on goof balls. Let it be known that I experience no psychotic symptoms whatsoever, just to rule that out. My dead grandmother is using bluelight to subliminally communicate with me, but for this exists an entirely logical explanation (too complicated to explain here).

In addition, I have noticed a similar effect when under the influence of a psychedelic. If I ingest d-amphetamine during the trip, the visuals are GREATLY intensified to an extreme degree. I have had morphing patterning surroundings so intense that I found it hard to discern my surroundings. Furthermore, the amphetamine was solely responsible (tested with the same batch of tabs without amphetamine) for a vastly prolonged duration of the visuals, to the extent where rather than 12 hours, the last remnants of visuals literally persisted for 72 hours! This effect has been noticed on more than one occasion (Luckily, after 12-24 hours, the remaining visuals are generally limited to sliding overlays of geometric patterns across static and monochromatic surfaces).

Does anyone have any musings on this effects/hypotheses for a mechanism? My best bet would be that it is related to the ability of the 5HT-2a receptor to evoke dopamine release. As such, during the trip, further dopamine release by amphetamine may further activate the downstream pathway that the 5HT-2a is feeding into. Regarding HPPD, increased levels of dopamine due to amphetamine use may again feed into this downstream pathway.

Regardless of the validity of the hypotheses, it is an interesting case nonetheless.
 
I don't think this has much to do with dopamine release. My guess is that since amphetamine and serotonergic psychedelics are both broken down by MAO, they are competing for that enzyme and hence the potentiation and prolonged effects. Although admittedly it does seem somewhat simplistic of an explanation and I could be way off here, but I'm sure it's at least a factor.
 
your dead grandmother is communicating with you through bluelight? Red flag right there bro.
 
ShaolinBomber said:
its hard to detect sarcasm through text when you dont use words to show it.
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Look at the coherent logic of the rest of the post. Then look at that sentence, particularly the use of italics on the word "is". Come on man...

General Patton said:
Haha, I thought it was pretty funny and playful... Usually my dead Grandma only talks to me in tongues when I smoke DiPT ;)
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Haha. I haven't smoked DiPT but you've given me cravings now. I love talking to my dead grandma.. I find it to be an extremely erotic experience.
 
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Recept said:
I don't think this has much to do with dopamine release. My guess is that since amphetamine and serotonergic psychedelics are both broken down by MAO, they are competing for that enzyme and hence the potentiation and prolonged effects. Although admittedly it does seem somewhat simplistic of an explanation and I could be way off here, but I'm sure it's at least a factor.
Click to expand...

LSD is not broken down by MAO. Amphetamine is only slightly broken don by MAO. Dopamine is broken down by MAO, however this is irrelevant, because LSD is not.

Also, that would not explain why my HPPD is augmented by d-amphetamine. But thanks for the contributions nonetheless :).
 
Hmm.. I had a feeling that my explanation was overly simplistic if not outright wrong.. Oh well, time to hit some more of those pharmacology books I s'pose! =D
 
There is still alot not understood about amphetamines. Their role in agonizing TAARs is just now coming to light. But I would have to agree that the dopamine hypothesis is a good place to start.
 
permastoned said:
LSD is not broken down by MAO. Amphetamine is only slightly broken don by MAO. Dopamine is broken down by MAO, however this is irrelevant, because LSD is not.

Also, that would not explain why my HPPD is augmented by d-amphetamine. But thanks for the contributions nonetheless :).
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amphetamines release NA and noradrenaline excites inhibitory cells. This could be why you get increased visuals with amphetamine use. But i've heard the contrary about using amphetamines with HPPD. People claim to have reduced visuals with amphetamine use.
 
Amphetamine disinhibits dopaminergic neuronal firing, so perhaps if HPPD is a disorder of disregulated inhibition as some suggest then perhaps this might partly explain why amphetamine could worsen symptoms.

That might suggest HPPD has a dopaminergic component, or that dopaminergic firing increases due to a GABAergic inhibitory interneurone problem caused by psychedelics... or even the psychedelics caused a problem even further upstream with many knock-on consequences.

It would be really interesting to see if the TAAR has any involvement in this but as theWorldWithin says, their ordinary physiological roles are not yet fully understood.

If I'm wrong please do correct me as I'm mainly speculating - am rather interested in the subject!
 
FractalDancer said:
Amphetamine disinhibits dopaminergic neuronal firing, so perhaps if HPPD is a disorder of disregulated inhibition as some suggest then perhaps this might partly explain why amphetamine could worsen symptoms.

That might suggest HPPD has a dopaminergic component, or that dopaminergic firing increases due to a GABAergic inhibitory interneurone problem caused by psychedelics... or even the psychedelics caused a problem even further upstream with many knock-on consequences.

It would be really interesting to see if the TAAR has any involvement in this but as theWorldWithin says, their ordinary physiological roles are not yet fully understood.

If I'm wrong please do correct me as I'm mainly speculating - am rather interested in the subject!
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The thing with HPPD is that anything that excites cells is going to be exaggerated even further because the current theory for HPPD is that GABA output is lowered because of a loss of 5-ht2 receptors on GABAergic neurons. Check out the negative feedback loop between the serotonergic and GABAergic system. They're also looking at the acetylcholine system. The neurotransmitter acetylcholine interacts with many cells that control the eyes, like pupil dilation, which could be part of the problem with HPPD.

But the main point i was trying to get across is the theory that "less GABA output=excessive excitation across multiple lobes of the brain located near the neocortex. the main problem is coming from the visual cortex in the back of the head but the inhibitory system is incapable of calming excitatory currents, which is what would be HPPD.

HPPD=Disinhibition in the brain. Thats pretty much it.
 
I personally think that HPPD is likely a largely psychological phenomenon, as most psych's are completely undetectable in the body after a day or three. Obviously there may be a physiological component, possibly a genetic predisposition, but i seriously doubt most psych's cause long-term changes in brain chemistry. This being said, the amphetamine come-up has a similar feel to some psych's, and if you strongly associate that feeling with visual distortions, the neural connections that have developed as a result of psychedelic use will begin to fire as if you were on a psychedelic. This combined with the pupil dilation caused by amphetamines could well cause visual distortions. Just a theory though
 
IME, if I take d-amph by itself then this effect is not present. But if I take d-amph with cannabis, then my HPPD can be aggravated drastically-- sometimes to the extent that I feel like I'm full-on tripping.
 
permastoned said:
^It is not psychological dude. I see shit warping, yes I see it very clearly warping. It is NOT psychological.
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Just because its psychological doesn't mean its not real. There are volumes of legit psych disorders, many of which have little if any effective medical treatment. Obviously all things humans experience have to have a physiological component, otherwise we wouldn't notice. But I think the cause of HPPD lies more in thought processes and our relatively malleable neural connections.
 
Roger&Me said:
IME, if I take d-amph by itself then this effect is not present. But if I take d-amph with cannabis, then my HPPD can be aggravated drastically-- sometimes to the extent that I feel like I'm full-on tripping.
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Well, there's a reason why speed and cannabis was used so frequently by the Merry Pranksters. It can extend the lifespan of an LSD trip by adding onto the manic quality an acid trip has anyways, a similar mechanism is likely at work here. It wasn't only them that noted once the mind has been sufficiently lubricated with the lysergic lubricant, the "flashback" mechanism can be triggered in various ways. Think of HST and the other speed-driven writers of the era, it was a manic bash for sure.
 
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