Did you know that those with schizophrenia tend to have a reduction in illusion perception? One study showed two different perceptions of a mask, one facing towards the subject and one with facing away from the subject so that the inside, or inverted side of the mask, is facing the subject. Normally this causes an illusion where the inverted side appears as if it’s facing towards you rather than away. This is known as the inverted mask illusion, or depth inversion illusion. Shockingly, the individuals with schizophrenia tend not to experience the illusion. This non-responsiveness to illusions that occurs in those with schizophrenia has been found to occur with other illusions as well.
This brings up the question,
Is sanity itself an illusion?
One of the physiological mechanisms that occurs in those with schizophrenia is low activity at the NMDA glutamate receptor. Drugs that block NMDA receptors also produce psychotic effects and are commonly used in lab experiments to reproduce the psychological symptoms of schizophrenia. These drugs are commonly referred to as psychotomimetics, meaning they mimic/induce the effects of psychosis. NMDA receptor blockers produce sensory loss, amnesia, and eventually loss of consciousness at higher doses. Because of this, they are used as anesthetics in clinical settings, and also they are used as hallucinogens in experimental cultures. NMDA receptor blockers include ketamine and PCP for example.
On the other hand, psychedelic drugs such as LSD-25 or psilocin from magic mushrooms have an effect that increases glutamate release from neurons, promoting NMDA receptor stimulation. These drugs cause visual effects that seem to be optical illusions. For example, one such effect is the melting walls visual which seems to be an accelerated form of the motion after-effect illusion.
! ! ! Seizure Warning ! ! !
The motion-after effect illusion can be observed after the video.
It is known that many (if not all) illusions are learned and even culturally dependent in many cases. It is also known that NMDA receptors are very important for learning and perception. NMDA receptor blockers are capable of preventing the encoding process, and thus preventing the formation of new memories. They are also capable of preventing recall of already formed memories, producing amnesiac effects.
We know that repeated exposure to a stimuli reinforces memory of that stimuli, which is why we use flash cards and repetition as a study tool. Optical illusions seem to be an effect of repeated exposure to visual stimuli, where a generalization is made and a visual type of memory is formed. In the case of the inverted mask illusion, it is that we see faces so frequently that we recall memory to assume the 3 dimensional depth data of the object (the mask). This is so that we don’t have to process the sensory data through conscious (or maybe even unconscious) analysis each time. After seeing an object multiple times, we no longer have to analyze what it appears like, we seem to just ‘know’. This likely occurs through recognition of cues, a list of sensory information we check for and then assume the rest of the information that was not yet observed. For example, a few cues may signal that we are observing a face, and the depth information isn’t processed, but instead assumed to be true based on repeating patterns of observation in the past.
We generalize that the mask is almost certainly not inverted. Also, when we look at the motion after-effect illusion we can see that watching a moving image that is repetitious forms a sort of memory that is then applied to perception even when the motion is no longer persisting. It is your brain predicting motion based on the assumption that motion was persisting and so it is likely still persisting. This could save energy, where our brain checks for motion less frequently as the repetition of motion becomes more frequent and then assumed to be persisting. This form of illusion seems to be based on short term memory, while the inverted mask illusion is based on long term memory, revealing that this may be an inherent trend to memory in all forms. Perhaps something that is inherent to learning itself.
Exercise In Illusions
Here are some ways to try out illusion induction at home. Go out into the grass and find a comfortable place to sit. Find some distinct object that contrasts against the grass such as a brown leaf or a rock. Place it somewhere in front of you and stare at the rock and try not to blink or move your head much. Keep your eyes on one single spot as to allow your vision and memory to saturate with exposure to the stimuli of the grass. If you spend 10 minutes doing this, you may notice geometry emerging similarly to the photo below.
This staring technique has also been tried with staring at faces in the past. When I’ve attempted the face-staring technique, I find that my vision fades out as I stare, which reminds of what occurs when I rub my arm repetitiously: numbness like anesthesia. It seems that increasingly sustained stimuli tends to fade out into the background, while probably illusions tend to occur with strong stimuli that is frequent, but not perfectly sustained. Sustained stimulation likely gets phased out as background information. Both of these staring techniques, the grass and the face, seem to result in eventual decrease in the quality of perception, with details in both cases being reduced for a more simplified perception.
Illusions seem to be an auto correct feature of our perception and also our cognition. The auto corrections simply predict what is the most likely interpretation. Most likely, is not inherently most true. Many times our auto-correction technology inputs wrong suggestions, and likewise, we notice wrong predictive perceptions and recognize the as illusions. It makes sense that illusions are the highest layer of our perception (essentially learned perception) and then meaningless pixels of visual data are the lowest layer of our perception (essentially unlearned perception). The decrease of illusions seen in individuals with schizophrenia (who have low NMDA receptor activity) and the increase of illusions in those on psychedelic drugs (who have high NMDA receptor activity) seems to show that illusions might be dependent on NMDA receptor activity, which makes sense as NMDA is involved with both learning, recall, and perception. Psychedelics may accelerate learning, which makes sense with the current research.
Another interesting symptom that those with schizophrenia commonly face is hallucinations. One common hallucinations that these individuals experience is the sensation that bugs are crawling on them. This is known as formication. It could be that the individual’s own body hair and clothes actually causes the sensations they perceive to be bugs. Typically, we are exposed to our own body hair and clothing so much that we have tuned this experience out. I would suggest that the most frequent stimuli eventually begin to get ignored altogether in favor of more novel stimuli which are experienced as more sensitive and stimulating, because very persistent stimuli is useless without the contrast that non-persistence provides, and the information does not have utility if it is hyper-persistent. Novel stimuli stick out, while familiar information is often less exciting to us. An example of this is that we typically cannot tickle ourselves but when others touch us in the same manner we can be tickled. We take this into account when interpreting our senses. When an individual with schizophrenia no longer has the attentional numbness to their own body, self-tickling becomes possible, but our mind assumes it is not self-tickling because it expects that we would filter this out as is almost always the case, so the most likely explanation of the sensation of body hair tickling is that it is not your self, but instead insects or something similar. It is actually more rational to conclude this if you do not have awareness of your internal illusions or filters being changed.
It is likely that illusions serve as a way of reducing information and sculpting our perception by using generalizations based on memory so that many perceptions don’t consume our consciousness. This may explain why those with schizophrenia suffer from working memory problems. They may not be filtering and generalizing information via illusions and so they struggle to process and interpret conscious experience. In some sense it is increased conscious experience. This seems to be a model that is consistent with a concept known as latent inhibition, which essentially is about how we filter information. It is thought that those with low latent inhibition would be prone to psychosis, but also creativity and an increased amount of sensory and cognitive information.
In some sense, it could be that illusions represent the box in the ‘thinking outside the box’ concept. In essence the box is the assumptions we have, the expectations of meaning and understanding that we apply to the world, and those without these assumptions and filters can see more of their incoming sensory and cognitive data, allowing them to utilize it towards ends that others simply can’t reach due to the limitations that illusions cause them. What we know as creativity may just be alternative ideas that others have not yet come to, and having extra perceptual data would allow you to make judgments that others dont have sufficient information to make. Of course the rate of error would increase as the amount of information coming into consideration is increased because it isn’t that those with less filters also gain extra ability to process the information. It is also known that working memory is heavily correlated to reasoning ability, which likely reflects in the situation of high quantities of information being processed in working memory that doesn’t have the capacity to handle the extra information, resulting in reasoning ability issues.
It may be that hallucinations involve more conscious interaction than illusions do, as in the individuals with schizophrenia are rationalizing and theorizing about their perceptual data to form predictions and expectations whereas illusions seem to be automatic and based on exposure to repetitious stimuli and much less consciously directed. In some sense, illusions are Pavlovian in nature, while hallucinations may be rational.
The Ego As An Illusion
The ego develops at an early age. We aren’t born with it. It is a metacognitive sense of self. It is a generalization of your own observations of your self and your behaviors. This generalization becomes a factor in your decisions. Then you generalize the new set of behaviors that are based on these metacognitive generalizations of your self. This pattern continues until you are left with a hyper-generalized state that is based on recursive generalizations of your self, until your behavior becomes a very predictable and patterned existence. This is what psychedelics undo.
Furthermore, society expresses archetypal generalizations of individual’s egos. This occurs through media, especially television and movies where archetypes are displayed and characterized via a lens of value judgment. The superego is how we generalize other’s generalizations of our own behaviors and apply this perception to ourselves.
Assuming the ego is an illusion, it is likely that the ego death that occurs with psychedelic drug use could be caused by neurotransmitters that release to counteract high levels of glutamate to prevent what is known as glutamate-induced excitotoxicity. One such neurotransmitter that may release under circumstances of high glutamate activity is agmatine, which has NMDA receptor blocking effects. This response may be similar to the mechanism of near death experiences, including out of body experiences and the commonly reported “life flashing before one’s eyes” phenomenon. Here is my post that explains how this may work.
The Infant Mind
It is likely that the effects of psychedelics is a mix of increased and decreased illusions, depending on the dose especially. Higher doses likely cause agmatine release or some other anti-NMDA-receptor neurotransmitter (for example dynorphin or anandamide might be capable of reducing NMDA receptor activity). Many effects that occur on the higher doses of psychedelics drugs resemble the effects of NMDA receptor blockers as well. Another possibility is that some NMDA receptor blocker in our body functions to reduce persistent stimulation of NMDA receptors, while frequent but not persistent NMDA receptor binding causes learning, and not as much blocking. Another possibility is that short term memories remain and are even enhanced while under the effects of psychedelics but long-term illusions are removed.
This link gives some evidence of this short-term vs long-term illusion concept and shows that LSD enhances response to familiarity and decreases response to novelty. “The main take home message of the study is that we found that in our study LSD altered the way in which the brain processes familiar and surprising stimuli,” Timmermann told PsyPost. “Surprising stimuli was processed as being more familiar, and familiar stimuli was processed as more surprising.” It could be that novelty is much more rapidly assimilated into short-term and long-term, but that long-term predictions are being shut down so that it doesn’t interfere with processing of sensory information. In some sense, it is learning new information, but not using learned information, except short-term learned information, which likely forms faster, causing a reduced response, as if it were familiar faster. This falls in line with the idea that the psychedelic state resembles the state of mind that infants exist in, because assuming too much based on predictions very early would halt further awareness and possibly cause you to have an inferior understanding of the world based on assumptions that are too conclusive, too soon. This could also explain why people tend to experience a more expansive understanding of things after using psychedelics, mainly due to the effect of slowing the formation of conclusions as to allow further observation to take precedence.
Here is where things get interesting. For some reason, psychedelics do not pose the same risk of excitotoxicity that is seen with NMDA receptor agonists. There is also further evidence for glutamate as a mechanism for illusions with migraines being linked to increased motion after effect illusions. Migraine auras and also migraine pain have been stopped by NMDA receptor blockers, and also epilepsy and migraine both share glutamatergic mechanisms and both epilepsy and migraine produce visual effects. Psychedelics have been used to treat migraines, despite the seeming visual effects and stimulation of glutamate, further suggesting there may be another mechanism that reduces glutamate receptor stimulation as well. This paper proposes that the mechanism of psychedelics may actually be a cause of migraines, so it may be that the rebound and downregulation of the psychedelic mechanism that leads to benefits for migraine sufferers. Perhaps the downregulation also decreases glutamate release long-term as well, producing some of the psychotic symptoms that occurs for users of psychedelics.
This paper suggests its a partial agonist effect mediated by the mechanisms of psychedelics, which means it can induce both boosting and decrease of NMDA receptor activity. Perhaps this alone can explain the distinction of long-term and short-term illusion effects, where short-term memories can still form under the limitations that partial agonists induce. This can also make sense of how responsiveness to novel (highly stimulating) stimuli would be reduced while responsiveness to familiar (under stimulating) stimuli would be increased. This seems to be the most likely neurobiological explanation for the mixed increased/decreased NMDA effects that seem to exist with psychedelics.
In another sense it seems that what psychedelics do is to boost saturation levels for stimuli and allow for more rapid formation of illusions to form. Even colors and emotions appear to be highly saturated. Many NMDA receptor blocking effects occur as the brain attempts to counteract this high saturation. This also makes sense since NMDA receptor blockers reduce sensations and even shut them down entirely. The reason psychedelics could possibly worsen psychotic symptoms is probably due to provoking further reactionary hypoactivity of glutamate afterwards or probably even during the experience. This explanation doesn’t solve any functional reason for the existence of this spectrum of psychedelic effects though, but it may also exist simultaneously with the other notions presented above, they do not appear to be exclusive.
Illusions allow us to recognize a glitch in our perceptual matrix, while individuals with schizophrenia are living much less in the perceptual matrix altogether, making it less likely for them to converge on the same perceptions. This divergence is valuable to society, despite the errors that these individuals experience (delusions and hallucinations). We often know optical illusions to reveal our own errors, and it is likely that both those without and those with schizophrenia both experience a similar rate of error, but that there are more people with converging errors in those without schizophrenia simply because there are more people without schizophrenia. We can see that many individual’s with schizophrenia converge on their delusions as well, for example conspiracy theories. Our fear and mistreatment of those who have schizophrenia is based on xenophobia on some level. We should work to find roles and places for the those with schizophrenia to flourish and be valuable to society rather than always taking the path chemical and physiological interventions that aim to make them convergent with those without schizophrenia. We could design novel environments that allow schizophrenics to flourish in what their psychology is useful for, rather than dismiss non-similarity as problematic inherently. It is likely that the stigma on schizophrenia accounts for many of the symptoms of the condition.
Many of the symptoms of schizophrenia can be explained by environmental circumstance as I’ve shown in this post (grandiosity vs paranoia) and this post (theory of creativity), and so we should find ways to treat the problems that those with schizophrenia face through environmental intervention.
If those with schizophrenia do not experience optical illusions, then perhaps we could classify sanity itself as an illusion.
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2 thoughts on “The Sanity Illusion”
“We could design novel environments that allow schizophrenics to flourish in what their psychology is useful for, rather than dismiss non-similarity as problematic inherently.”
Schizos are frankly crazy. And while we want them as people to thrive, to be safe, and content, we certainly don’t want the genetic contributors of a disease like schizophrenia to flourish. Schizophrenia is something we want less of, not more. Any mode of “ending the stigma” needs comport with this reality.
You must be cautious! You are suggesting we purge genes linked to intellectual functioning, creativity, and basically progress and instead live repetitiously without growth and only security. Actually it’s the kind of security that could end the world as well. Deciding not to take care of climate change for example.
This article is outdated and so I need to be more forgiving here. It’s worth checking out my newer articles where I’ve rationalized what schizophrenia actually is.
In these cases, I would agree. We don’t need schizophrenia, as we know it, to occur or exist. Much like we don’t need PTSD to exist. But the solution isn’t to kill off or sterilize people with PTSD or schizophrenia. That actually wouldn’t prevent them from still occurring. These can happen to almost anyone but there is enhanced potential with certain genes. And not purely because of a sensitivity. But also because of behaviors.
For example, PTSD and schizophrenia are partially due to learning and some of the genes accelerate learning and make it so you get worse. This is also true of addiction. Another thing is that it’s specifically learning of negative things that leads to PTSD and schizophrenia whereas addiction is pleasure based as well.
Having novel ideas like let’s say atheism among peoples of a church might turn you schizophrenic as everyone is put against you. This naturally induces paranoia and eventually you will be traumatized by the experience and no one will even understand why you feel like that. Schizophrenia is often a condition where you label the atheist under serious pressure a crazy person for believing something else.
Now many people think religion is psychotic. But in this case it’s actually atheism that would likely lead to mental problems.
The pressure and negative experience can generate hallucinations. The dysphoria neurotransmitter binds at the same receptor as the drug salvia and effects like this and also similarly PCP or ketamine have similar effects. You dissociate and hallucinate. It is also the neurotransmitter involved in all forms of suffering and is the main mechanism for learning to avoid and protect yourself against suffering. Under extreme suffering you will manifest the symptoms of psychosis. This is the mechanism. Read my article Dynorphin I just published.
The genes are not making the neurotransmitter over produced. Rather it makes you behave in ways, such as exploratory or discovery behaviors that would make you oppose other members of society who resist change and resist novelty. There are even correlations to political affiliation and some of these genes. It fits quite well. Liberals and progressives would be more schizo in this sense. And so one might come out of the closet as homosexual or any number of deviant tendencies and get deeply traumatized and manifest psychotic symptoms from all the constant stressors they must face.
Check out the articles Dynorphin (this explains how the neurotransmitter works and leads to psychosis and decreased intelligence), Nexus (this one explains how it manifests from social problems and all the evidence), and Xenotypy (this one gets into the political correlations).
I hope I have helped and you may find yourself closer to enlightenment!
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