sensation

Psychedelics may induce the same state of mind as the childhood critical period of learning and development. The flexibility and fluidity of this state of mind may be key to the way humans develop, including with learning language and perception. We may be able to use drug-induced critical periods to accelerate language learning or promote the development of savant-like skills in adults. In this post we will explore this notion of psychedelic critical periods and the kinds of similarities and utilities of these states of consciousness.

When we think of perception, one question that comes up frequently is:

“Is your red my red?”

There may be hints to an answer to this question in an old study on LSD users who seemed to have faced permanent color-detection impairments (1). First, let’s explore psychedelics and their connection to the critical period of child development, as this is critical to understanding this puzzle.

Based on the research on childhood and neurogenesis (2), plasticity (3), increased perceptual consciousness (sensory acuity) (4), and the research on psychedelics and neurogenesis (5), plasticity (6), and increased perceptual consciousness (sensory acuity) (7), it seems that both the childhood state of mind and the psychedelic state may greatly overlap. Children are able to distinguish more phonetic sounds, an ability that is lost in adults (4). This aides in learning languages, whereas adults may struggle to learn foreign languages and end up using the wrong phonetic sounds (accents). The initial childhood sensitivity may result in distinguishing high levels of nuance in the sounds they hear, but later on this might not be as useful as one could end up struggling to interpret spoken words that are only slightly different sounding. For example, you could imagine a lisp could make one sound like an entirely different language if the auditory distinction ability persisted. So it is likely important for adults to become less conscious of distinct perceptions unless there is practical usefulness, which may be determined in the childhood critical period. Teaching perfect pitch to children may be an example of reinforcing the usefulness of specific higher consciousness to sound.

While there is no concrete evidence that psychedelics increase phonetic distinction abilities (although this is easy to test and we should), there is evidence that psychedelics induce a critical period effect, at least for social learning (8). There is also evidence of psychedelics inducing neurogenesis (5) and plasticity in the brain (6), which is character of the childhood critical period as well (3). There is also evidence of higher serotonin activity in infancy and childhood, decreasing with age (9). Aging is shown to decrease the density of 5HT2a receptors (10), which are the primary target of psychedelic drugs. Carhart-Harris, a leading expert on psychedelics, has shared the same sentiment, that psychedelia and the state of mind of children are very similar (32), based on brain scans. A developmental psychologist from UC Berkeley, Alison Gopnik, has explored this idea too (33).

This concept of psychedelic-induced recovery of the childhood critical period can be dubbed the phoenix effect. This effect is a drug-induced psychological rebirth, a destruction of the adult self and a return to the childhood state of naivety. 

As children, the psychedelic state may help one maintain an openness in perception, in order to calibrate it over a longer period of time before forming some kind of conclusive and inflexible perceptual modality. For example, if the perceptual modality of the child was too conclusive, object-permanence may never be learned and adults may still retain some perceptual conclusion that objects disappear when out of sight. You may remember as a child, opening a door and wondering whether it might lead to another faraway place, rather than the usual path that the door opens to. This could be viewed as door permanence.

This kind of magical mode of perceiving the environment is driven by uncertainty and novelty. The sense of wonder is derived from the capacity to believe in unpredictable and strange outcomes. It is an openness to perception, an openness to being wrong, it is to assume one holds insufficient information to conclude. In early childhood, we don’t actually know whether the door might lead somewhere new yet because we haven’t tested the door enough times to have solid evidence that this is the case. 

The most repetitious and consistent elements of perception may stabilize first, simply due to recurring successful predictions. Overtime, this mechanism of cognitive fluidity decreases with age, which may function to crystallize perspectives and perceptual formations. One may become quicker to conclude as they grow older, which becomes more useful after accumulating some amount of base knowledge. It is especially crucial for stressful and survivalist environments, as being quick to form judgments can be important in time-critical situations. 

The effects of psychedelics sometimes brings out mysterious sensory dimensions that often shocks users. Many struggle to explain these experiences, probably simply because qualia itself is rather difficult to explain. These experiences may be even more difficult to explain than usual because they are elements of sensory space that most adults have entirely forgotten or abandoned and as such are not even a part of our common language or thinking. It is known that some percentage of children often rely on eidetic, or photographic memory, whereas most adults lose this ability (11). This is one way in which internal cognitive systems might learn how to simplify and remove unnecessary complexity in experience, very similarly to the loss of phonetic distinction abilities in adults. The lack of usefulness or even the detrimental excessiveness of many perceptual processing strategies may lead to their abandonment in adult life and these kind of systems may reboot upon dosing with psychedelics.

Another similar phenomenon is eidetic internal experience, or what we often refer to as a visual imagination. The loss of this has been dubbed aphantasia. It may be that aphantasia develops when imagination loses its’ necessity or usefulness, when it becomes too expensive and inefficient for the adult mind, or even because of school pressuring us to focus on the environment rather than distracting inward visions. Ayahuasca has been found to restore the inner imagination ability in one case report (12). In my own personal experience, meditating for 4 hours by counting endlessly each hour and imagining each number being seen, heard, and felt as pencil motions led to enhanced inner imagination for around a week or two after the experience. This included a stronger sense of inner voice and the ability to ‘see with my mind’s eye’. 

On the other hand, dementia and age-related cognitive decline could be seen as an opposite effect of the childhood critical period, where too much of our cognitive abilities have been deemed useless, possibly because of living a life of cognitive neglect, with no reinforcement of abilities. The effect may be very hard to reverse and the person may feel stressed by tasks that go beyond their capacity, which could perpetuate their declining mental status by driving them to avoid stressful tasks. We often suggest that people engage their minds with games or other strategies to prevent cognitive decline. This may also apply to other mental health conditions as well.

This is supported by research showing that 5HT2a receptor density decreases with age (10) and is low in Alzheimer’s patients (13). Psychedelics are being researched for Alzheimer’s at Johns Hopkins (for depression) and I’ve done a post on psychedelics for Alzheimer’s and cognitive ability titled HypoCognition. This could be interpreted as reversing a kind of cognitive aging and youth restoration through psychedelics.

The way that psychedelics induce a flood of early life memories may depend on this restoration of earlier senses. Much of the memories we lose from our younger years may be contextually tied to these different modalities of perception and cognition. Some memories may be primarily eidetic, before other simplified strategies for memory formed. Once you return to these modalities of perception, you may recall memories that are more reliant on these modalities, perhaps even remembering more vividly. The effect can feel like one is awakening back to their true youthful self and it can be very shocking or even horrifying to some. In support of this, one Guardian article explores a user of LSD who noticed recall of traumatic memories from childhood that the individual had forgotten. 

In the case that one is less psychedelic than the usual child, they may come to conclusions more quickly, remaining inflexible to alternative perspectives. Both autism (14) and schizophrenia (15) are linked to reduced capacity for the 5HT2a receptor effects. This may lead one with schizophrenia or autism to form conclusions with insufficient evidence in general, causing problems with development, perception, and mental models of the world. Their errors may impede their development all throughout life, even starting early on. 

Side note: The absurdity of human politics could be a reflection of the decreasing nuance that people have the capacity for in adulthood. Humans become overly judgmental, form simplistic and inconsiderate perspectives about the perceived enemy who threatens them, perhaps similarly to a schizophrenic. 

Dissociative drugs may induce a similar kind of age-reversal and chemically-induced critical period, but the way it does so may be different. Dissociative anesthetics may induce an amnesia or cognitive numbness on many areas of the brain, so that the world appears new and unlearned. It may turn off the most current self, turning off your already developed self, forcing a state of novelty to emerge, inducing a secondary 5HT2ar effect. There is some evidence of this in research showing that 5HT2a receptor antagonists can reverse some of the effects induced by NMDAr antagonists (16). It is important to note that 5HT2a receptor agonists actually prevent NMDAr antagonist neurotoxicity (17). In the article Psychedelics and Schizophrenia I’ve clarified how psychedelics aren’t inherently psychotic and may even work as treatments for schizophrenia. 

Without tangenting too far, let’s move back to the key question,

Is your red my red?

is my red

Of course, we already know that many humans do not see colors the same, for example, the colorblind and those with tetrachromatic vision. Regardless, we may still wonder if we see the same kind of color represented as red as others see, despite subtle tuning and small differences in shade. 

Those on the psychedelic drug may re-activate the childhood flexibility, the critical period, the openness to perception, allowing them to re-calibrate their senses, which may have total disregard for many long years of repetitive reinforcement towards confirming color constancy. The user of psychedelics may re-calibrate their colors, if even by just a tiny bit, resulting in a mismatch of what they remember colors to be. The memories may be permanent scars in their mind, while their perception has refreshed to a new tuning, leaving them a bit ‘off’ from where they were before.

One might even wonder if people’s color perception fades with time and age, but our cognitive structures may adapt to mitigate the loss of colors. Age can especially decrease one’s ability to distinguish blues and greens (18). Usually, the adult mind may simply recall prior representations of color from memory, rather than intaking new information that represents the true incoming information. The adult may be living with the illusion of perceptual continuity that is useful to everyday life. We may not fully recognize the subtle changes to our perception over time because of the way that the perceptions are being represented from memory data. 

The continuity of perception would prove useful in daily life, to maintain a consistent and solid perception for easy navigation of the external world. This is much like optical illusions, which are a kind of perceptual auto-correct failure. 

The user of the psychedelic drug may override the significance of representing reality from memory data and move onto perceiving the world more in line with incoming sensory data. At the extreme end of dosing these drugs we might wonder if we entirely lose access to our memory representations database, leaving us to freely experience incoming stimuli without interpretation. 

For the child, this is the point, to make sure one is still intaking environmental stimuli and having a higher priority to factor the external stimuli, with less priority on memory-based representations. As the child experiences repetitions of the world, their models can become sharper and eventually they can rely on memory over external stimuli. To rely on it too early may produce loads of optical illusions, essentially an untrained perceptual auto-correct system. 

For the adult using a psychedelic drug, they may forgo their memory representations, tapping further into the external reality, allowing the person to accumulate more present data and form new memories that override prior information. The current data are more relevant to the sensory capabilities of your body, which in the case of a child, is extremely important, but in the case of the adult might suddenly bring awareness to faded color perceptions, dropping memory of the memory representations in favor of the newer model. 

Those who experience more HPPD might have altered/impaired visual or cognitive systems that emerged with aging or were even removed due to the lack of use and the neglect because of their heavy reliance of the memory-representations that have replaced those visual processing systems. This may unveil glitches, color problems, and other effects. This is likely not the case for all HPPD phenomenon. Much of the common effects of HPPD seem concurrent with migraine and seizure aura, which aren’t permanent visual changes. Although, this lack of permanence may be due to temporary impairment to recall for the memory-based representations, which are restored after the migraine or aura ceases. 

The next possibility is that one may re-calibrate their color perceptions ever so slightly, causing the new perceptions to solidify and become permanent as one leaves the psychedelic drug-induced critical period. The mismatch between memory and the newly crystallized color representations may lead to errors.

If this is true, it would suggest that we do not all see the same red. 

Instead, we might all see very different colors than each other, but, on the other hand, it seems highly unlikely that these post-LSD users are seeing drastically different colors from before dosing, otherwise stories of radically altered color themes would be more commonly heard of by now. Another limitation is that the subjects with altered color weren’t tested before LSD use. It may also be the case that downregulating 5HT2a receptors is linked to reduced ability to discriminate stimuli, kind of like the opposite of the childhood critical period.

While this is all interesting, it is still weak and doesn’t entirely address this question about whether we represent colors the same as each other or not.

Although, on the bright side there are a few experiments we could design to test some of these hypotheses. We could find drug-naïve individuals who appear to have lost more cones with age and give them LSD and observe if they perform worse both before and after and test whether they are more prone to these kind of aftereffects. We would expect that those who lose cones with age might have reduced color vision even without the drug, which is true (18), however, a change in the balance of cones that might produce a shift in a person’s private color spectrum may be accommodated for by memory representations that persist across time. For example, we do not really hear reports of elderly suggesting the sky is green for them, but perhaps their cone ratios should in theory produce such a sky. We could especially measure whether blue-green distinction is the primary change observed in LSD users.

Consider color constancy, which is an illusion that makes us accommodate for tinted lighting. So if our vision slowly becomes tinted by different ratios of cones with aging, there may be neural mechanisms accomodating these changes by relying on memories from childhood that signify some sort of base color set.

These strawberries are not red.

color constancy

Another possible experiment would be to simply check the cone status of people who report these visual changes and those who do not. We might expect those with new impairments in color discrimination to have an altered unusual ratio compared to normal. 

Undergoing such experiments could help us understand the nature of psychedelics, the childhood critical period, and perception. They may get us closer to bridging the qualia systems of other creatures. Perhaps in the distant future we can reach a point of technological telepathy if we continue on this path. 

An Update: In regards to the loss of acuity for foreign phonetic sounds, one might wonder if pruning of neurons is involved. It has been observed that those who are bilingual as children have increased grey matter volume in the brain compared to those who only speak one language (19). Those who are multi-lingual as children might prune less because they end up using more of the brain and more of the phonetic acuity. If pruning follows the neglect of cognitive abilities, such as phonetic acuity and eidetic memory, then these abilities may not be recoverable after pruning has taken place. I would bet that the brain is potentially more flexible than this though, perhaps one could see a partial recovery. It might be that expensive memories are lost once the new memory strategies are used in place of outdated eidetic strategies. This seems to be the case, since Taxi drivers gain brain volume in regions related to navigation (20), suggesting we can gain ability too. 

Those with autism sometimes have eidetic memory in tact (21) and also experience less pruning (22) which is thought to underlie the higher brain volume in autism (23). This lack of pruning might help explain savant-like abilities or even factor into sensory overload and other cognitive deficits seen in autism. 

In relation to plasticity, those with autism are thought to have increased dendritic spines (24), which psychedelics also increase (6). Intelligence has been negatively correlated to increased dendrites (25), but this story is a bit complicated as reduced dendrites in the prefrontal cortex (26), cerebral cortex (27), auditory cortex (28) are observed in schizophrenia, which is important because schizophrenia is associated with low intelligence as well (29). High dendrite counts might represent an unlearned state, so those with impaired learning ability might be expected have not narrowed down their neural pathways as much as those who have learned more. It would be as if the neurons did not sculpt to ‘correct’ answers to problems, as if the problems remained ignored, unsolved, and unaddressed yet. Those with a low density dendrites might have more automated and already learned cognitive abilities, narrowing down the neural activity so that the noise of bad solutions is tuned out.

Consider the phoneme acuity here. This acuity may represent a lack of synaptic pruning, which allows a lot of noise into the processing of words and sounds. The person who lacks pruning might retain their sensitivity to phonemes but also experience difficulty in detecting familiar phonemes because of mishearing sounds.

This synaptogenesis and plasticity might represent a kind of openness and naivety, reversing the solved status of previously ‘solved’ problems, allowing one to approach life with new solutions to old problems. Those with lower intelligence might have increased dendrites only as a reflection of a lack of learning, a lack of sculpting of one’s mental processes, a lack of solving the problems. They may still have a mind like the naïve child on some level. In the case of those with mental illness, addiction, schizophrenia, depression, PTSD, there may be hope in reversing these toxic developments and finding self-improvement. These may be learned or developed problems that are not useful and even detrimental. 

A final note on bad trips: One might wonder why we don’t constantly experience such highly conscious and especially emotionally sensitive states, like the ones we can observe on psychedelic drugs and the ones that some researchers believe occurs in children (35). I suspect it is the propensity for and negative impact of bad tripping that makes the state a vulnerability. This is apparent when you consider the notion of set and setting. You could imagine tripping in daily life posing major risks for a bad trip. It would be expected that one’s daily life cycle would bring one in contact with triggering events.

According to Johns Hopkins Medical Institutions, research shows that higher emotionality makes stimuli more memorable (34). Psychedelics also enhance associative learning and memory (30, 31), which might be due to the increased emotionality. While this enhanced emotionality might enhance learning of experiences by making them more intense, there may be an increasing risk of negative intensity as one ages and leaves the comfortable environmental bubble of childhood. Much of the learning that is centered around emotionality may also exist for the purpose of controlling the emotions. We learn to avoid bad feelings and we learn to seek out good feelings. 

The child lacks the burden of the chaotic sadistic world. That is why the child is free to be conscious, curious, and vulnerable. It is the accumulation of knowledge of how dark life is that keeps us demented and low consciousness. We become increasingly aware of the darkness in humanity, we realize there are so many things about people that we disagree with. We reach a status of self shame, one that may be so far away from the kind of unconditional love the child believes in. We see the world void of magic and purity. It is only with Utopia that we might find ourselves free to be vulnerable like the child.

The price one pays for consuming the fruit from the tree of knowledge of good and evil is the loss of the soul.

If you’d like to see my model for how psychedelics, dissociatives, and even childhood critical periods may produce their cognitive effects, see Cognitive Atomization, which explores the idea of reversing associative learning, essentially splitting apart associations and increasing cognitive and perceptual acuity. The atomized existence may be the unlearned cognitive state, where schizophrenics may exist in.

Special thanks to the six patrons: Melissa Bradley, Morgan Catha, Niklas Kokkola, Abhishaike Mahajan, Riley Fitzpatrick, 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 through your donations.

If you’d like to support these projects like this, check out this page.

 

If you liked this, follow me on

Twitter

You can also follow the discussion for this post on Reddit:

r/DrugNerds

r/Nootropics

r/neuro

r/SlateStarCodex

is your color

CITATIONS

  1. Abraham, H. D. (1982). A chronic impairment of colour vision in users of LSD. The British Journal of Psychiatry, 140(5), 518-520.
  2. Stiles, J., & Jernigan, T. L. (2010). The basics of brain development. Neuropsychology review, 20(4), 327-348.
  3. White, E. J., Hutka, S. A., Williams, L. J., & Moreno, S. (2013). Learning, neural plasticity and sensitive periods: implications for language acquisition, music training and transfer across the lifespan. Frontiers in systems neuroscience, 7, 90.
  4. Kuhl, P. K. (2004). Early language acquisition: cracking the speech code. Nature reviews neuroscience, 5(11), 831-843.
  5. Catlow, B. J., Jalloh, A., & Sanchez-Ramos, J. (2016). Hippocampal neurogenesis: Effects of psychedelic drugs. In Neuropathology of drug addictions and substance misuse (pp. 821-831). Academic Press.
  6. Ly, C., Greb, A. C., Cameron, L. P., Wong, J. M., Barragan, E. V., Wilson, P. C., … & Duim, W. C. (2018). Psychedelics promote structural and functional neural plasticity. Cell reports, 23(11), 3170-3182.
  7. Fischer, R. (1968). On the steady state nature of evolution, learning, perception, hallucination and dreaming. In Quantitative Biology of Metabolism (pp. 245-257). Springer, Berlin, Heidelberg.
  8. Nardou, R., Lewis, E. M., Rothhaas, R., Xu, R., Yang, A., Boyden, E., & Dölen, G. (2019). Oxytocin-dependent reopening of a social reward learning critical period with MDMA. Nature, 569(7754), 116-120.
  9. Whitaker-Azmitia, P. M. (2001). Serotonin and brain development: role in human developmental diseases. Brain research bulletin, 56(5), 479-485.
  10. Meltzer, C. C., Smith, G., Price, J. C., Reynolds III, C. F., Mathis, C. A., Greer, P., … & Cantwell, M. N. (1998). Reduced binding of [18F] altanserin to serotonin type 2A receptors in aging: persistence of effect after partial volume correction. Brain Research, 813(1), 167-171.
  11. Haber, R. N. (1979). Twenty years of haunting eidetic imagery: Where’s the ghost?. Behavioral and Brain Sciences, 2(4), 583-594.
  12. dos Santos, R. G., Enyart, S., Bouso, J. C., Pares, Ò., & Hallak, J. E. (2018). “Ayahuasca turned on my mind’s eye”: Enhanced visual imagery after ayahuasca intake in a man with “blind imagination”(aphantasia). Journal of Psychedelic Studies, 2(2), 74-77.
  13. Lorke, D. E., Lu, G., Cho, E., & Yew, D. T. (2006). Serotonin 5-HT 2A and 5-HT 6 receptors in the prefrontal cortex of Alzheimer and normal aging patients. BMC neuroscience, 7(1), 36.
  14. Cook, E. H., & Leventhal, B. L. (1996). The serotonin system in autism. Current opinion in pediatrics, 8(4), 348-354.
  15. Polesskaya, O. O., & Sokolov, B. P. (2002). Differential expression of the “C” and “T” alleles of the 5‐HT2A receptor gene in the temporal cortex of normal individuals and schizophrenics. Journal of neuroscience research, 67(6), 812-822.
  16. Carlsson, M. L., Martin, P., Nilsson, M., Sorensen, S. M., Carlsson, A., Waters, S., & Waters, N. (1999). The 5-HT2A receptor antagonist M100907 is more effective in counteracting NMDA antagonist-than dopamine agonist-induced hyperactivity in mice. Journal of neural transmission, 106(2), 123-129.
  17. Farber, N. B., Hanslick, J., Kirby, C., McWilliams, L., & Olney, J. W. (1998). Serotonergic agents that activate 5HT 2A receptors prevent NMDA antagonist neurotoxicity. Neuropsychopharmacology, 18(1), 57-62.
  18. Salvi, S. M., Akhtar, S., & Currie, Z. (2006). Ageing changes in the eye. Postgraduate medical journal, 82(971), 581-587.
  19. Olulade, O. A., Jamal, N. I., Koo, D. S., Perfetti, C. A., LaSasso, C., & Eden, G. F. (2015). Neuroanatomical evidence in support of the bilingual advantage theory. Cerebral Cortex, 26(7), 3196-3204.
  20. Maguire, E. A., Woollett, K., & Spiers, H. J. (2006). London taxi drivers and bus drivers: a structural MRI and neuropsychological analysis. Hippocampus, 16(12), 1091-1101.
  21. Cesaroni, L., & Garber, M. (1991). Exploring the experience of autism through firsthand accounts. Journal of autism and developmental disorders, 21(3), 303-313.
  22. Tang, G., Gudsnuk, K., Kuo, S. H., Cotrina, M. L., Rosoklija, G., Sosunov, A., … & Yue, Z. (2014). Loss of mTOR-dependent macroautophagy causes autistic-like synaptic pruning deficits. Neuron, 83(5), 1131-1143.
  23. Hardan, A. Y., Minshew, N. J., Mallikarjuhn, M., & Keshavan, M. S. (2001). Brain volume in autism. Journal of child neurology, 16(6), 421-424.
  24. Hutsler, J. J., & Zhang, H. (2010). Increased dendritic spine densities on cortical projection neurons in autism spectrum disorders. Brain research, 1309, 83-94.
  25. Genç, E., Fraenz, C., Schlüter, C., Friedrich, P., Hossiep, R., Voelkle, M. C., … & Jung, R. E. (2018). Diffusion markers of dendritic density and arborization in gray matter predict differences in intelligence. Nature communications, 9(1), 1-11.
  26. Glantz, L. A., & Lewis, D. A. (2000). Decreased dendritic spine density on prefrontal cortical pyramidal neurons in schizophrenia. Archives of general psychiatry, 57(1), 65-73.
  27. Garey, L. J., Ong, W. Y., Patel, T. S., Kanani, M., Davis, A., Mortimer, A. M., … & Hirsch, S. R. (1998). Reduced dendritic spine density on cerebral cortical pyramidal neurons in schizophrenia. Journal of Neurology, Neurosurgery & Psychiatry, 65(4), 446-453.
  28. Sweet, R. A., Henteleff, R. A., Zhang, W., Sampson, A. R., & Lewis, D. A. (2009). Reduced dendritic spine density in auditory cortex of subjects with schizophrenia. Neuropsychopharmacology, 34(2), 374-389.
  29. David, A. S., Malmberg, A., Brandt, L., Allebeck, P., & Lewis, G. (1997). IQ and risk for schizophrenia: a population-based cohort study. Psychological medicine, 27(6), 1311-1323.
  30. Harvey, J. A. (2003). Role of the serotonin 5-HT2A receptor in learning. Learning & Memory, 10(5), 355-362.
  31. Zhang, G., & Stackman Jr, R. W. (2015). The role of serotonin 5-HT2A receptors in memory and cognition. Frontiers in pharmacology, 6, 225.
  32. Martin, R., & Carhart-Harris, R. (2016, April 17). Your Brain On LSD Looks A Lot Like A Baby’s. NPR. Retrieved July 24, 2020, from https://www.npr.org/2016/04/17/474569125/your-brain-on-lsd-looks-a-lot-like-a-babys
  33. Gopnik, A. (2019). A Separate Kind of Intelligence. Retrieved July 24, 2020, from https://www.edge.org/conversation/alison_gopnik-a-separate-kind-of-intelligence
  34. Johns Hopkins Medical Institutions. (2007, October 07). Why Emotionally Charged Events Are So Memorable. ScienceDaily. Retrieved July 24, 2020, from https://www.sciencedaily.com/releases/2007/10/071004121045.htm
  35. Kolitz, D. (2018, September 10). Do Kids Feel Stronger Emotions Than Adults? Gizmodo. Retrieved July 24, 2020, from https://gizmodo.com/do-kids-feel-stronger-emotions-than-adults-1828933152

5 thoughts on “The Phoenix Effect

  1. Actually, that lsd user didn’t recall a “buried memory”. It probably was a case of a false memory, as the article points.

    Like

    1. In my experience, I remember more early life experiences on LSD but it might not always happen. I have never had “repressed” memories brought back. Only forgotten things that I maybe recalled 10 years ago but never since.

      What is the rationale behind false memories? Cannabis seems to allow this to occur although there are many differences between cannabis and psychedelics.

      Like

  2. The study on Hopkins is about comorbid depression in Alzheimer patients not about treatment of cognitive disfunction in Alzheimer disease.

    Like

    1. It’s so odd that I didn’t catch this. I was working on the notion of treating Alzheimer’s with psychedelics before the Johns Hopkins bit was announced and I didn’t fully check that out. Thank you for clarifying that. It’s strange as I also was showing a friend who’s at Johns Hopkins and into psychedelics and somehow I still didn’t realize this and it’s been months.

      Like

Leave a comment