Psychedelics and Intelligence

What first captured my curiosity about the relationship between psychedelics and intelligence was an interesting correlation found with psychedelics and openness to experience. It turns out, psilocybin produced long-term increases in the personality trait known as openness to experience (MacLean, Johnson, & Griffiths 2011). Interestingly, out of all the personality traits studied in the five-factor model for personality, it is openness to experience that is most strongly linked to intelligence (Ashton, Lee, Vernon, & Jang 2000). More specifically, crystallized intelligence, although there is a small correlation to fluid intelligence as well. Openness to experience is a necessary quality for making the choice to engage in a more diverse range of experiences, and so you will build a larger library of experiences and notice more patterns in the world because you have actually observed more of the world in general. This could also provide behavioral changes that lead to self-stimulating of one’s intellect, a sort of constant training of your mind due to being more willing to engage in potentially challenging unknowns in the world, confronting novelty, which should aide in learning of new information. Beyond this, a possible mechanism for cognitive disruption is explored as a new study has found psychedelics to attenuate this mechanism which is involved in various forms of cognitive dysfunction such as age-related cognitive decline, stress induced cognitive impairment, depression related symptoms, and alcohol-induced cognitive impairment.

So is there anything to this?

Do psychedelics increase intelligence?

It’s possible.

Psychedelics appear to help with PTSD (Feduccia & Mithoefer 2018). PTSD has been associated negatively with IQ (Saltzman, Weems, & Carrion 2006), something which I have explored thoroughly in my post Dynorphin Theory.

Dynorphin may help to explain the reduced IQ observed in PTSD. PTSD is associated with dynorphin (Bailey, Cordell, Sobin, & Neumeister 2013). Stress and depression have also been linked to dynorphin (Knoll, & Carlezon Jr. 2010).

The research linked here has noted that premorbid IQ being lower might make PTSD worse, but even if lower premorbid IQ were found, this may be due to early life stress or prior trauma limiting IQ and even promoting more severe stress reactions in adulthood. It was found that exposure to domestic violence suppressed IQ (Koenen, Moffitt, Caspi et al 2003) and recently traumatized individuals showed cognitive impairment (Brandes, Ben-Schachar, Gilboa et al 2002). Prior trauma is a risk factor for experiencing further trauma. So it seems likely that prior trauma may be at play here with premorbid IQ scores.

A study on cops found that their openness to experience was reduced after experiencing a traumatic event (Leigh Wills, & Schuldberg 2016), which is significant because openness to experience is the only Big 5 trait linked to intelligence (Schretlen, van der Hulst, Pearlson, & Gordon 2010). I’ve explained before that negative experiences seem to reduce openness in a way that becomes obvious in context. Imagine that you experience an abusive relationship. You will become more aversive towards potential abusive relationships, which fall under the umbrella of “relationships”. You may become less willing to expose your vulnerable side in relationships and essentially this is one of the many issues with PTSD, an unwillingness to be vulnerable, to take risks. It’s really worth reading the full post on this concept. The relevance here is that openness may be a promoter for engagement with novel (and potentially risky/unknown) experiences. Novel experiences promote learning because these are the very situations needing to be learned (you don’t learn the already learned stuff).

Dynorphin mediates alcohol-related spatial learning and memory impairment (Kuzmin, Chefer, Bazov et al 2013). This occurs by disrupting glutamate neurotransmission in the hippocampus. Another study found stress-induced learning and memory impairment was mediated by dynorphin (Carey, Lyons, Shay et al 2009). This one is interesting because it is not limited to spatial cognition. Occlusal disharmony, a jaw problem that can cause neck stiffness and psychiatric depression, was shown to cause memory and learning impairments mediated by dynorphin activity in the amygdala (Yamada, Ono, Kubo et al 2013). It may be that pain aversion is mediated by dynorphin as well (Massaly, Copits, Wilson-Poe et al 2019), which would explain this effect of the occlusal disharmony on learning and memory. Stress was negatively correlated to academic performance in high IQ students (Malik & Balda 2006). There is also research showing up to 14 points IQ reduction during periods of scarcity and stress (Mullainathan 2014). There is also evidence that age-related cognitive decline involves dynorphin as well (Ménard, Herzog, Schwarzer, & Quirion 2014).

Dynorphin is known to impair plasticity in the hippocampus (Wagner, Terman & Chavkin 1993) and psychedelics have been shown to induce plasticity (Ly, Greb, Cameron et al 2018) and neurogenesis (Catlow, Jalloh, & Sanchez-Ramos 2016).

Here’s where it gets interesting.

A study from 2019 found that psychedelics attenuate kappa-opioid receptor (KOR)-mediated depressant effects (Sakloth, Leggett, Moerke et al 2019). This could mean that psychedelics attenuate reduced plasticity induced by dynorphin, correcting glutamate neurotransmission, and restoring cognitive ability. 

UPDATE: 8 months after this post, researchers posed this very same question! Can Psychedelic Drugs Attenuate Age-Related Changes
in Cognition and Affect? (Aday, Bloesch, & Davoli 2019). The arguments are mostly similar, referencing research on neuroplasticity.

This may also help explain the various problems that psychedelics are proposed to fix, such as addiction, depression, anxiety, and PTSD.

This is likely part of the mechanism for how psychedelics attenuate addiction rapidly. This study suggests that psychedelics do not attenuate the abuse potential of methamphetamine, but only the dynorphinergic problems of stimulant use. Psilocybin has been shown to ‘cure’ tobacco addiction with one dose in 80% of subjects (Johnson, Garcia-Romeu, Cosimano, & Griffiths 2014). This is exciting because another study found nicotine to upregulate dynorphin/kappa-opioid receptor (KOR) system  (Tejeda, Natividad, Orfila et al 2012) and dynorphin has been proposed as a core element to models of addictions to many drugs (Shippenberg, Zapata, & Chefer 2007). The attenuation of KOR-mediated activity by psychedelics found in the 2019 study may reveal a core mechanism to this attenuation of addiction. I’ve explored the relationship between nicotine and dynorphin in more depth in my article Nicotine Disorder.

My understanding of addiction is as follows:

The research seems to indicate that dynorphin may mediate the experience of dysphoria in stress (Land, Bruchas, Lemos et al 2008), cannabis (Valverdre & Maldonado 2001), physical pain and injury (Massaly, Copits, Wilson-Poe et al 2019). So here we begin at trauma but it quickly becomes clear how suffering in general will trap your behavior into security-seeking and low openness to experience. The result? The drug of choice is the only secure space left after raising the threshold for suffering so high. No longer can you take uncomfortable risks or try new things.

“Traumatic experiences may reduce the range of experiences a person is willing to engage with when the expectation is that these experiences would be potentially negative or risky. Prior to the trauma, experiences would have been good-good-good and there isn’t a clear reason to be cautious if bad things don’t seem to happen. This unwillingness to engage in unpredictable and novel situations might lead to a decline in cognition simply due to cognitive neglect. It also seems to be the case that the more negative someone is feeling, the more they would desire a reward that is highly predictable because they care more about ending the suffering than they would about exploring new things. Suffering adds a dimension of motivating one towards seeking distraction, in which we must quell the pain and boredom is of less priority than security. So not only would dynorphin promote specific aversions in the case of PTSD, but it would also invoke general malaise that becomes a high priority issue, detracting from one’s curiosity and reprioritizing our behavioral biases towards security. In this case, people may favor their comfort foods, as opposed to trying a new food that is potentially dislikable. The disappointment of disliked novel food would only stack with the prior stressors and make things worse so it is good to ensure successful reward acquisition rather than take a risk. For those who’s lives are generally good, they will build a tolerance towards repetitious rewards and begin to desire something more fulfilling: novel rewards for which we have no tolerance built towards.

This may be the role dynorphin plays in addiction. The benefits of the drug become the most predictable reward that is capable of attenuating suffering. Alongside that, dynorphin is generally upregulated by elevated dopamine levels which are involved in most, if not all, addictive drugs. Eventually your willingness to seek rewards other than the drug shrink down as suffering becomes more ubiquitous.”

So in essence it could be that psychedelics would decrease cognitive issues mediated by dynorphin activity. Psychedelics would relieve the depressed state, enhance neurogenesis, enhance openness, and broaden access to previously inhibited memories that had reduced access due to dynorphin and thus expanding crystallized intelligence. In some sense dynorphin may function to sculpt relevance and priority in a way that reduces our choices and thoughts to simple compulsions and linear thinking.

Psychedelics may not necessarily boost you beyond your natural genetic cognitive limitations, but instead function to erase the limiting factors like compulsive neurotic ruminations and distracting concerns as well as abolish the state of hopelessness we acquire throughout our lives. I suspect that in a post-scarcity utopian society we would never experience the “fall back to reality” while dosed on psychedelic drugs but instead remain elated in that state. For children, their security that is provided by parents combined with their naivety about the nature of reality can act as a sort of post-scarcity utopian simulation. A care free existence before the ubiquitous background suffering that emanates from our dystopian capitalistic world kicks in and the ignorance of naivety fades into oblivion. Serotonin signals resource security which I have written about in Serotonism, which may provide some obscure level of evidence towards this notion about post-scarcity utopias and the psychedelic state.

In some sense dynorphin may signal how bad living circumstances are, where a pool of dynorphin is inhibiting the less powerful motivations. Dynorphin may inhibit the motivations that are considered wasteful to resources. The more survivalist the situation, the more you must reduce extraneous behaviors, limiting creativity and cognitive flexibility, thus Pavlovian states like addiction and PTSD become dominant. Imagine that there is pool of dynorphin liquid and motivations can become actions or at the very least considerations when they surface above the pool. More dynorphin means less and less considerations can be made, a loss of openness. With addiction we find excessive rewards to increase the volume of this dynorphin pool by upregulating it. With stimulants you are increasing all motivations, and many now surface above the dynorphin pool. But as you fail to reach goals and rewards are not granted, the pool rises to stop these failing motivations. When you stop the stimulant you are severely inhibited and depressed.

Each person and their individual lives had built up pools of dynorphin that inhibit their dreams and ambitions. Sometimes life changes but we are stuck with mentalities that source from troubled childhoods or poor living conditions in the past. For these people psychedelics can simulate a sudden surge of security that drains this pool of dynorphin. As the drug wears off the environmental circumstances bring the pool back up to match. But perhaps we can escape the childhood echoes that restrain our dreams, enhancing our proneness to becoming a dreamer again. To become hopeful, to see all the possibilities updated to our most current circumstance.

With this, maybe psychedelics can help us remove the blockades that our dystopian society pushes into our minds, so that we may someday experience some kind of true utopia.

. . .

Special thanks to the three patrons: Morgan Catha, Abhishaike Mahajan and Charles Wright! Abhi is also the artist who created the cover image for Most Relevant. Please support him on instagram, he is an amazing artist! I’d also like to thank Annie Vu, Chris Byrd, and Kettner Griswold for your kindness and making these projects and the podcast possible.

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7 thoughts on “Psychedelics and Intelligence

  1. Fascinating post. What are your thoughts on this study ( showing that “Mice lacking dynorphin showed an enhanced cue-dependent fear conditioning, as well as delayed extinction in contextual conditioning/extinction paradigms.”? It seems it may be much more complex than dynorphin promoting fear conditioning directly.

    Liked by 1 person

    1. Yes! Actually I’ve seen this study and it has me totally perplexed. I’ve been discussing this with a few people trying to understand the implications. I’m not entirely sure yet to be honest.

      This reminds me of how DRD4 7r has associations with enhanced trauma and also fear extinction. It seems to promote change and learning.

      With dynorphin it doesn’t seem to do this, BUT, I wonder if these mice don’t entirely lack dynorphin and maybe there is some interplay where fear learning and some other dynamic both sensitize each other. I’ll respond more on this once I’m off. It may have to do with AMPAr or something like this where dynorphin causes aversion learning through modulating something common.


  2. On the last paragraph, how would you go about explaining higher prevalence of psychosis during manic rather than depressive ones? If I had to guess I’d think that the hyperdopaminergia in mania would upregulate dynorphin, and by your dynorphin hypothesis, this could increase the chance of psychotic symptoms appearing. Does that all make sense?

    Liked by 1 person

    1. Yes! This is what I suspect, and possibly that serotonin is canceling out negative symptoms but I think it’s a bit tricky. Dynorphin mimetic susbstances can treat mania and do not induce psychotomimesis. Then there is the strange issue of cannabis enhancing cognitive function for bipolar individuals while worsening cognitive function in schizophrenic patients.

      I wonder though, if positive symptoms might arise from D2 related mechanisms which serotonin can induce through 5HT2a-D2 heteromers while dynorphin also enhances D2 activity but while blocking glutamate. Mania may by a hyperglutamtergic state while psychosis is hypoglutamatergic. Perhaps the cognitive function is mostly dependent on glutamatergic functioning.

      I really want to understand why mania is different. It seems heavily different compared to psychosis in some regards. It seems bipolar also have a different functioning of amygdala and prefrontal cortex functioning and the opposite relationship for schizophrenia.

      I’d also like to mention that these diagnoses may be absurd. In one way, both may originate from a sort of enhanced cognitive state that schizo is unable to maintain due to external stressors or social defeat.

      Imagine that the manic becomes quite socially successful during their manic phases and crashes once this unravels due to their intense risk taking traits. While the schizo is like the failure subtype in some regards. Mania may precipitate failure scenarios due to immense risk taking.

      The schizophrenic seems risk aversive and traumatized. Trauma is linked to low IQ, low openness. But the openness genes are actually linked to schizophrenia.

      I suspect this might critical to the subjective narrative of these disorders. While there may also be other factors that influence tendency to crash under pressure or more rapidly decline to traumatized and failing states of mind.

      Many schizophrenics have ideas that would seemingly require openness to acquire, such as conspiracies or other absurd counter cultural notions. Once they are mocked, traumatized socially, they may recluse and then fall apart in a sort of anhedonic learned helplessness state. Whereas bipolar would seem to turn aggressive or better persuade people and start cults or something like that.

      There is evidence that deviation from norms occurs before any symptoms of schizophrenia are apparent. Also the dopaminergic state seems to precede schizophrenic symptoms as well. I believe that constant engagement with novelty that occurs with openness may cause the hyperdopaminergia. It may signify intense prefrontal activity and problem solving. I’ve personally noticed after doing mathematics tests I will leave the classroom with dissociative symptoms and visual distortions. I believe the intense dopamine stimulation is combined with antidopaminergic stimulation from dynorphin in problem solving abilities. These contrast each other to sculpt solution recognition processes. Eventually this would be the basis for operant conditioning as well. In problem solving it may start with a dissociation of failing solutions and an enhancement of successful solutions.

      The creativity in bipolar disorder is likely related to reward sensitivity and a lack of dissociation and inhibition that may normally occur with dynorphin. In contrast to manic individuals, Euthymic individuals may all be more traumatized and unable to cope with reality and show reduced creativity due to their thought blocking. Then the schizophrenic would be the even lesser creative due to more intense trauma states.

      In problem solving you may succeed and it leads to more security, more serotonin, more resources, more euphoria until you become manic. If you fail, your fear of failing further would be enhanced, resources may be wasted, and you may develop an increasing anhedonic tone. Eventually you will be quite disconnected from reality, perhaps in denial of theories that caused social rejection such as conspiracy. Clinging on and eventually manifesting hallucinations due to dynorphin induced problems.

      For the manic, perhaps they begin to make mistakes due to a lack of inhibition. If they experience significant loss and trauma I think they will crush under the pressure and perhaps because of the avoidance of dynorphin that has occurred, you could have more extreme sensitivity once it starts to seep in. A lack of tolerance perhaps? Although this clearly isn’t the case since kappa agonists can treat mania and do not cause psychotomimesis for these individuals.

      Personally I believe I would fall under the category of bipolar disorder. In my experience, mania doesn’t really cause me to hallucinate directly. Instead I get visuals that resemble psychedelics. Enhanced colors, breathing walls, but when I am depressed I experience symptoms more similar to cannabis intoxication or anticholinergic even. I will feel bug crawling sensations at times, a phenomena known as formication. This has been linked to dynorphin activity.

      Even just last night I dosed myself with calcium and I’ve been on vitamin D lately which enhances calcium supplementation. This presumably would enhance NMDAr activity and it seemed to cause more mania and a purple aura effect and some breathing walls. I’ve explored the mechanisms of illusions a bit in my post The Sanity Illusion if you are curious about that. Although warning, it is an outdated article and I no longer believe schizophrenia works as I suggest in that article.


      1. I looked a little bit more into the KOR amygdala interaction and it seems that KOR agonism turns off LTP and reduces synaptic neurotransmission which would presumably over time end up decreasing amygdala volume while enhancement and reinforcement of activity should hypothetically increase amygdala volume. This should be more evidence that mania is often reduced dynorphin while schizophrenic states are enhanced dynorphin.


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