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Visual noise from smoking on dissociatives

dopamimetic

Bluelighter
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Mar 21, 2013
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What does cause this? I know it's easy to speculate 'toxicity' or 'constricted blood vessels' but I guess you don't see such toxicity 1:1 and it appears to be more specific to smoking, lesser so to nicotine in general than to be real toxicity.

Yeah, dissociatives alone give you visual noise, but smoking heavily increases it when on sub-dissociative doses. Even with just (60mg of) memantine. Also I remember similar visual noise / almost "diminished resolution" of vision while on sodium valproate + smoking (which was heavily euphoric, maybe cause of upregulated alpha7 receptors from previously cessating memantine).

A friend notices similar but describes it differently, like increased contrasts and sometimes euphoric, sometimes (while on rebound) dysphoric.
 
Just a very quick response since I'm procrastinating and have to do some fucking work but this thread caught my eye and I wanted to respond.

Nicotine is known to affect photoreceptor sensitivity, and has been measured to reduce colour perception, and night vision, albeit (mercifully) temporarily - although I cannot remember the exact mechanism right now.

Dissociatives - or at least ketamine, and presumably others - also have measurable and fairly significant effects on photoreceptors, causing both an immediate change in metabolic activity (oxygen/glycogen metabolisis, IIRC), supporting cellular structures, and a significant rebound afterwards. This effect in at least some instances seems to be neuroprotective against other forms of damage, ie, ischemic injury, and I believe certain chemical insults although I cannot remember exactly. Here is at least one paper describing some of the effects of ketamine on photoreceptors and the retina: Ketamine-induced Ultrastructural Changes in the Retina

This is a topic that I have read a lot about because I actually have a congenital degenerative retinal dystrophy - Retinitis Pigmentosa - which means essentially at this point that I have almost no functioning rod cells left. This was surprising to me because subjectively the deterioration of my night and peripheral vision has been gradual, and the brain does a very good job at compensating. But my night and low light vision is extremely poor and my peripheral vision even in daytime is reduced, obviously I have compensatory measures and again, the brain does a good job of compensating for missing data - but I do routinely trip over things, bump into people, stub my toes, and do other things that would be perceived as simply clumsiness or absurd inattentiveness for external observers who didn't know me. Anyway the point of me sharing this is that I am very very conscious of my visual function and the effects of the substances I continue to imbibe on it.

Nicotine for sure has obvious and detrimental effects on my vision, if I vape for too long I will start to develop increased cloudiness in my visual field, definite noise, etc. When i was diagnosed 5 years ago I was a causal, "social" smoker and I entirely quit this almost immediately - being told you have a non-zero risk of total blindness later in life is a pretty good motivator for changes in behaviour. Unfortunately, human habits and will being what they are, or perhaps just my own inconsistencies being what they are, as progression turned out to be very slow and I made some peace with my diagnosis as well as my controlled usage of certain things I know to be bad for me - I have smoked a few combustion cigarettes since, and periodically take up vaping.

My apologies that I'm just diverging to personal stories rather than answering your actual question. But dissociatives (at least ketamine, which I have most experience with) have significant effects of my vision - near dissociative doses rapidly constrict my visual field - which is of course a congruent and predictable result of rapid shutdown of the supporting cells that provide energy for the photoreceptors to fire (as in that study). Specifically again, the rod cells - which are prolific in the outer regions of the retina. The rods, for anyone reading who is not aware, are more sensitive to lower light levels, but also are entirely colourblind - compared to the cone-dense macula, which makes up our central vision and allows us to perceive colour as well as other fine details.

Rods are less complex structurally than the colour sensitive cones, being far more sensitive to lower light levels, as well as being faster to react, which is what allows us to detect quick movements in our periphery (for example, as someone who lacks rods, I cannot detect small fast moving objects easily - cones simply react too slowly. Sports such as tennis, squash, etc, ping pong, are impossible for me. If I drop a coin - if I do not spot it immediately, target the right area so that the object is visible and trackable with the slower-reacting cones in my maculae - I often do not even bother to look for it because while it is falling, possibly rolling, it will be essentially invisible to me and finding it will be an arduous task).

Anyway, rods require less energy to run - therefore the retinal changes preferentially switch many of the more sensitive rods "off", whereas the cones have more robust supporting circuitry and are less affected by the immediate dip that NMDA antagonism seems to induce. However they will likely not be entirely unaffected - reduction in glycogen and oxygen metabolism, again, essentially equating to a reduction in the supporting electricity, will cause changes in their reaction to light impact, essentially intermittent "outages" and chaotic instabilities in energetic outflow along the neuronal wiring which connects our visual input devices to our biological GPU, ie, the visual cortex and/or other parts of the brain.

My guess is this will manifest as visual noise, both from "source noise", ie, the raw electrical data from the photoreceptors, which has become slightly chaotic - perhaps best analogous to the fuzzy static from an analog television set with a poor signal - let's say this is "analog noise", in fact, from an actual information deficit from the photoreceptors. Imagine every rod cell as a kind of inverse lamp which is flickering because of an unreliable power supply.

Additionally there will be, how can I put, "digital noise", ie, decompression artifacts, which are generated by the brain's visual processing software as it attempts to adapt to cope with the changes in the input signal.

Again - rods will be most affected by any changes in the energy supply to the eyes because they are far more sensitive than cones, and cover the vast majority of our visual field. I will say actually I do not really get visual noise from dissociatives - rather, again, rapid induction of tunnel vision - and I would attribute this to the fact that my rods are already either entirely non-functioning or significantly reduced in function. So again - imagining our rods as a field of inverse lamps, flickering as a result of unreliable power supply - most of my lamps are already very dim or just non-functioning - so an interruption in the power supply simply turns them off.

However, again, there will be effects across all of our visual processing architecture. Cones will be less noticeably affected but can still be reduced in function, causing the diminished resolution that you mention, or indeed, reduced colour sensitivity - an affect which is more studied with nicotine, but which may be shared with NMDA antagonists in general.

I've spent way too much time writing this post so I'll try to be quick but the "rebound" increase in energy metabolism could definitely have the opposite effect, increased contrast, increased peripheral and night vision as the rods become hyper-sensitive. I haven't personally measured this - although I really, really should - but I have personally noticed on the return to baseline with ketamine that my night vision is vastly improved, sometimes, seemingly, impossibly so. It's hard to evaluate the objective reality of this effect because I typically dose in very familiar environments and alone (ie, just my flat) so I generally have a good awareness of where things are and again - the brain is remarkably good at filling in the blanks from missing visual data. But subjectively the effect is congruent with the measured "rebound" following anaesthetic-level doses of ketamine, which - at least in the paper I linked above - can last for days after, at least in rats. Personally however - less so on ketamine - but on diphenidine, interestingly, I have noticed a marked improvement in my peripheral visual field as well as general contrast and colour sensitivty which lasts for at least 24 hours after the subjective effects recede. Again, I have not measured this - and it could be attributable to a psychological "afterglow" rather than any real changes in photon-sensitivity or visual processing - but, damn, this makes me think I really should test these effects.
 
Fuck that's heavy, sounds almost like dissociatives could make you blind but again the sheer complexity of the matter protects us probably.. Really didn't expect retinal cells to be visibly altered for 3 days after dissociative anesthesia, what does this mean for power users?? Apparently the body is a miracle in self-regulating/healing stuff at cell level but still sounds scary..

Thanks for your very informative answer! I've got pretty strong myopia, depending on measure between - 9 and - 10.5 dpt. I am still scared off that old witch doctor telling me these values would cause heavy pressure on the retina and potentiate my chances to go blind. But the same doc also said that wearing contact lenses for too long would give you eye cancer (these silicon ones I have, if they'd make them individually fitting again like the old ones but with modern material, you could wear them for a month straight.) 😵🥴
 
I literally laughed out loud from reading this thread title.

I missed everything about psychedelics. It is good to be back.
 
If you smoke tobacco in the morning after using lots of alcohol last night, it does cause this same fog in your vision. I'm not sure about the reason.
 
If you smoke tobacco in the morning after using lots of alcohol last night, it does cause this same fog in your vision. I'm not sure about the reason.
Alcohol hits the same receptor as dissociatives do, the NMDA complex (and GABA of course). I still have much to read up about this subject though and am thankful for any input 🙂
 
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