This is an archive version of 'Psychedelic Information Theory' Alpha chapters. The final version of this text can be found at:

psychedelic-information-theory.com

Chapter 14 : Psychedelic Information Theory

Before settling into a complete and exhaustive deconstruction of psychedelic phenomena, I would like to briefly summarize some of the more popular proposed models of psychedelic mind states and look at their pros and cons. I do this so that I can compress the totality of modern thought on psychedelic pharmacology in one chapter and refer to it later during more detailed analysis. I will also add the bulk of my own personal speculation to these theories in the hopes that we can "tie them all together" into one comprehensive model of psychedelic action that not only makes sense from a neurological point of view, but also accurately predicts the subjective phenomenological effects, whatever they may be. Within this chapter are all the kernels of psychedelic theory that will be addressed within the following sections of this book, so if you were looking for all the answers in one chapter, this is as close as you will get. The remainder of the text will be a closer look of how these various models might interact to produce the unique and profound states of consciousness encountered during the psychedelic experience, but for your reference, all in one place, I give you the Neural Models of Altered Perception.

Holisitic Brain State Remodulation : Excitation, Tranquilization, & Interruption

As we have discussed in great detail up to this point, the overall activity and excitation in the brain - as defined in terms of number of active firing neurons and frequency of neural firing - is controlled by a set of chemical neuromodulators which are produced (primarily) in the brainstem and project upward into many areas of the brain to modulate holistic shifts in mood, alertness, wakefulness, and general brain activity. Although there are many primary and secondary chemical messengers within the neural mix, the major work-horse neuromodulators are serotonin, dopamine, norepinephrine, adrenaline, and acetylcholine, not to mention the basic messengers GABA and glutamate. Drugs which mimic, aid, or block the functioning of these major transmitters and modulators will produce a corollary excitation, interruption, or tranquilization of basic neural activity on a global level. The term I use to describe this kind of holistic interaction across the entire brain is remodualtion.

In this model, the chemically remodulated mind may react in three distinct ways. In the case of global excitation, the holistic activity and firing-rate of neurons increase, thus creating a faster processing speed and generating higher signal throughput or information bandwidth in the neocortex. The result of this type of activity would be an amplification of signal sensation and a corollary increase in focus and clarity. Drugs which classically act in an excitatory capacity include amphetamine stimulants, tryptamine psychedelics in low doses, and phenethylamine entactogens in low to moderate doses. In the case of global interruption, the activity and firing-rate of neurons becomes chaotic and asynchronous, causing misfires, lags, emergent signal noise, and signal disruption. Holistic modulatory interruption would lead to an augmentation or distortion of signal in the brain, causing dissociation, perceptual aberrations, and a corollary decrease in focus and increase in confusion. The classic interrupters are the tryptamine and phenethylamine psychedelics in moderate-to-high doses, NMDA antagonist dissociatives in moderate-to-high doses, and the anticholinergic delirients in moderate-to-high doses. Finally, there are the tranquilizers which act to decrease overall brain activity and signal firing rate, causing a corollary decrease in focus and alertness with an increase in lethargy and relaxation. Classic tranquilizers are CNS depressants like alcohol; benzodiazepines like valium; all forms of opiates; GHB; Kava; and a whole pantheon of plant and chemical downers, antipsychotics, antihistamines, narcotics, and drowsing agents.

It is important to note that some drugs, like psychedelics, can act as an excitatory agent at one dose range, but then suddenly become an interrupter at a higher dose range. This is an essential point to understand about psychedelics, and one that is often poorly understood. To crudely illustrate this point, I find it helpful to use the following metaphor based in the terminology of industry and economics.

Imagine that each neuron is like an industrial logic-processing assembly room in a city-sized "Logic Mill" (otherwise known as the brain) which refines "contextual meaning" (awareness of self and environment) from raw sensory noise. Raw information (sense data) pours into the mill and rolls down many conveyer belts all at once. All of this information must be weeded, aggregated, and packaged for transport before it can be sent down the correct conveyor belt to the next assembly room for further processing; until it is ultimately packaged into "meaning" (an accurate representation of reality) at the end of the line (which would be the prefrontal cortex). If you give the assembly-room workers a stimulant, you will increase their focus and reaction time, thus you can speed up the conveyer belts, increase logic productivity, reduce errors, and create more high-quality "meaning". If you give the workers a low dose of psychedelics, you may see the same benefits as the stimulant, but now the workers may begin finding more creative and efficient ways to reduce workflow, thus the conveyor belts can be sped up and productivity increases. However, error rates will also begin to climb as new "trial-and-error" logic-processing techniques are attempted "on the fly" and fail to bear fruit. In this scenario more "meaning" is produced as logic "tweaks" are employed to maximize workflow, but the quality of the "meaning" may suffer, making the need for oversight and review of new methods essential for reducing future errors and maximizing performance over the long-term (integration). Finally, if you give the Logic Mill assembly line workers a high dose of psychedelics, they will begin to take raw information off the conveyer belts and wander around the room with it; studying it; grokking it; ripping it up; sticking pieces of it together in illogical but aesthetically pleasing ways; packaging it incorrectly; and sending it down whichever conveyor belts happen to be nearest. The same worker may unpack, inspect, package, and pass the same piece of information down a revolving conveyor belt a dozen times without even realizing he is stuck in a recursive loop. Meanwhile, raw information is spewing off the conveyor belts at high speed, flooding the room, overwhelming workers, and overflowing into adjacent rooms with no logical oversight at all. In a pure economic sense, logic productivity has been completely interrupted and drops to zero, while the rate of error nears one hundred percent. Although the "creative activity" and "processing power" of the assembly workers has been increased due to the hyper-stimulant effect, the actual logic processing has been almost completely interrupted.

I should point out that in this metaphor I use the word "meaning" as a shorthand for "an accurate and reliable picture of self within reality," or contextual meaning. The parsing of accurate contextual meaning is the benchmark by which we measure sound minds. Looking at a toaster and thinking, "I can use this device to toast bread," is an example of high-quality parsing of meaning from the given stimulus. Looking at a toaster and thinking, "I could use this device as an inter-dimensional portal," is an example of dubious meaning extrapolated solely from the viewer's imagination, not representative of the actual given stimulus, and would be considered very low quality overall (other than as a humorous anecdote). I should point out that contextual meaning should not be confused with "emotional impact," as in, "It was a very meaningful experience." That is a different sort of meaning altogether - sometimes referred to as emotional salience - and is grounded primarily in emotional response to new sensations. Emotional salience is not dependent on the reliability of actual sensory processing itself, which is why even absurd and paradoxical thoughts can be "meaningful" even though their contextual or applied value is quite low. Also, contextual meaning should not be confused with existential meaning, as in "What is the meaning of life?" or "What does it all mean?" Existential meaning is a meta-form of contextual meaning that is influenced by our cultural values and life experiences. Existential meaning is the kind of meaning which shapes our paradigms and worldviews, but does not necessarily reflect an accurate picture of contextual reality. Emotional salience and existential meaning are subjective methodologies we use to integrate sensory data into our own personal world-views, but contextual meaning is the benchmark of how accurately and appropriately we perceive and respond to reality at any given moment.

So going back to our psychedelic Logic Mill experiment, we can see that the end result is a massive gush of chaotic, beautiful, and horrific contextual meaning overflowing at the end of the line, but all of the meaning that is being created is of very dubious quality in terms of contextual accuracy. I want to repeat this because some people will be offended that I make this point, but it is an important one. In my crude estimation, there is almost an inverse proportion between the quantity of psychedelic dose and the quality of contextual meaning produced as a result. In other words: as the dose goes up, the quality of the contextual meaning produced goes down. This does not mean that all contextual meaning produced in the psychedelic experience is junk, just that the great percentage of it is totally illogical and defies rationality. You can flip my Logic Mill metaphor and say, "No, the brain is a Creativity Engine, and with the psychedelic I am increasing both artistic productivity and aesthetic meaning." Or you can apply the religious metaphor and claim the brain is a Spirituality Mill, and argue that psychedelics increase both productivity and existential meaning in that regard as well. I would argue that both of these metaphors have their merits, but even art and mysticism require a basic logical framework (language, syntax, parsing and processing centers, etc.) to even be conceived of in the first place. You may counter me by saying that "Faith is illogical" or "Art is illogical" but I disagree. As organisms we rely on logic and the reliability of our senses first and foremost above everything else. Even the "ephemeral" concepts like faith at art rely on proper sensory, emotional, and language parsing (logic) for us to even "recognize" and "define" something as artistic or spiritual and remember it as such; otherwise our experiences are limited to fleeting vagaries and transient emotional whims that cannot be articulated. And while a complete breakdown of all rational logic processing can be a very "meaningful" experience, what you take away from it largely depends on how much of the experience you successfully remember and integrate into language and memory, and how much of it vanishes in the moment and is simply forgotten the next day.

For those of you still offended by my Logic Mill reduction, I am willing to concede that no matter how "interrupted" or "inefficient" the production of "meaning" becomes under the influence of psychedelics, a small percentage of it (probably less than one percent) is genuinely brilliant beyond brilliant; truly revelatory in form and purpose; life-changing and beautiful; and just completely mind-blowing. However, I would like to re-iterate that the vast majority of the "meaning" produced by high-dose psychedelic sessions is nothing more than a big swirling mess of random, illogical, and semi-coherent ideas poured through the kaleidoscope of the misfiring mind at high speeds. It may be pretty to look at, but what are we supposed to do with this huge mass of beautiful, entangled, high-density, questionable-quality "meaning" that rolls out of our psychedelic Logic Mill? The psychedelic mind may look at a grain of sand and see infinity, but what is that meaning worth? Is it of value to anyone beyond the viewer? Is it of value at any time beyond that moment? Could this paradoxical extrapolation of contextual meaning (grain of sand = infinity) produce a lasting existential meaning that changes the user's life in some small way? That is the question which confounds rational analysis of psychedelics to this day, but these questions are essentially what integration is all about. We will discuss these concepts in some detail later when looking at the cognitive effects of psychedelics and the use of psychedelics in therapy.

Asynchronous Synaptic Transmission & The Neural Echo Effect

One of the interesting details discovered about 5-HT2A agonists is that they can have different effects when applied to different areas of the same neuron. So far we have discussed 5-HT2A receptor agonism in terms of uptake, or a kind of excitation of action that occurs at post-synaptic 5-HT (serotonin) receptor sites. But laboratory research (in rats at least) has shown that 5-HT2A agonists also have an affect on the release of messenger chemicals in the pre-synaptic axon terminals, via a totally different mechanism: the blocking of messengers that inhibit presynaptic transmission. The pioneering research team of GK Aghajanian and GJ Marek have spent decades in the lab trying to sort this one out, but their most recent work on the subject indicates that hallucinogens most likely produce their perceptual effects via an increase in asynchronous synaptic transmission, or synaptic signal transmission that occurs out of time with the actual firing pattern of the neuron. Although the name may be misleading, it should not be inferred that there are "extra" synaptic firings happening between regular action potentials (that is improbable, if not impossible). But what it does mean is that for every neural firing in the cortex (action potential), there is a corollary low-grade signal leakage or echo into the synapse that persists for a few milliseconds to nearly a second after the original firing.

Now, if you have worked with sound effects boxes and analog synthesizers - or at least know what a analog delay is - you may be putting two-and-two together right now and envisioning something that looks like a wiring diagram for a neural echo/delay/phaser box. In this "asynchronous" circuit, all signal which flows out of the pre-synaptic neuron hits the receptors on the post-synaptic neuron with a diminished, short-duration chemical echo. Presumably (and this is speculative, but it makes sense) the duration of the chemical echo could be mediated by the quantity of hallucinogenic molecules acting at the presynaptic site; which is a fancy way of saying the depth of the neural echo effect would be mediated by dose of psychedelic: the higher the dose, the longer the duration of asynchronous transmission, the deeper and more pronounced the hallucinogenic echo effect. Okay, that is step one, but there is more. Now imagine this neural delay box is wired into millions more just like it - all tweaked to the same duration of neural echo effect - each one feeding and feedbacking into the next with a constant low-grade increase in signal strength. Within this model, we would expect to see an excitatory effect in the cortex rising gradually in pitch and intensity over time, with more distortion, echo, and feedback creeping into the mix as the strength of the signal grows.

Although the phenomena of asynchronous synaptic transmission has been demonstrated only recently in individual rat neurons, the discovery does go a long way towards explaining how 5-HT2A agonists can amplify signal strength in the cortex without directly generating extra action potentials. And even though the amplification may be subtle, when applied to the entire networked cortex at regular rhythmic intervals over time, the asynchronous "noise" will serve to amplify global signal strength, which will in turn lead to an overall increase in brain activity and frequency of action potentials. The whole process, when looked at from a wiring standpoint, seems destined to feedback on itself until it overloads and explodes. Fortunately, our metabolism works as a constant on-duty filter to regulate the amount of active amines in our brain, and our neurons are smart enough to know when they are getting hammered, and can down-regulate their reaction to specific messengers (like hallucinogenic amines) to keep from becoming over-stimulated over time. This down-regulation of 5-HT2A receptor activity sets in only after many hours of hallucinogenic activity, and is presumably responsible for the temporary tolerance the nervous system builds in response to frequent repeat use of hallucinogens.

We will look a little more at asynchronous echo effects later when talking about audio and visual hallucinations, and discuss how the varying durations of chemical echo could effect perceptual processing at various points in any given trip.

Thalamic Interaction & Sensorimotor Gating

Since the thalamus is considered the primary "router" and "filter" for all incoming sense data (except for smell), it is only natural to speculate that psychedelics are active here, and that the psychedelic trip is like having "all of the filters removed" from our senses. It is true that the thalamus is essential in buffering "irrelevant" background data, ensuring that "noise" is reduced and our cortex is receiving only the most relevant sense data needed for immediate processing. And while it is tempting to speculate that psychedelics have a direct action on the thalamus, there is no hard scientific evidence to demonstrate this theory. Since the most current thinking links the hallucinogenic effects of psychedelics to 5-HT2A receptor agonism in the cortical layers, models which rely on disruption of thalamic sensory screening are no longer in vogue. However, I personally feel there is a strong case to be made for an indirect action on the thalamus that can result in more "background noise" creeping into the system, and there are two ways in which this might happen. First of all, the neurons in the thalamus have their fair share of 5-HT2A receptors, but they are distributed at roughly one-quarter the density of the neurons in the cortical layers. So we can assume that psychedelics may have some kind of direct interaction with thalamic processing, but not quite as intense as those we find in the cortex. It is also safe to assume that "lesser effects" on the thalamus could vary depending on dose levels.

As for the second speculation I'll put forward on psychedelic action at the thalamus: Even if it is demonstrated that there is no direct action of psychedelics on the functioning of the thalamus, I would still make a case that the downstream excitation of cortical signal processing would necessarily demand an upstream relaxation of thalamic screening in order to "feed" the excited cortical process with more data. In other words, when the neurons in the cortex become stimulated due to psychedelic 5-HT2A receptor agonism, there is a corollary "chain-reaction" of neural feedback messengers that order the thalamus to "open all gates" so that the excited cortex can get as much raw signal as possible. Though I can't (yet) identify the direct neural trigger and pathway through which the cortex sends this particular "open all gates" feedback signal, there are obvious evolutionary advantages to having such a signal mechanism in place. Arguably the "fight/flight" instinct mediated by adrenaline has exactly this effect on the thalamus, and people who are in traumatic shock often report that little details seem to stand out more, everything seems clearer, even faraway sounds seem louder, colors seem more vibrant, etc. All of these reports synch with a very specific aspect of the psychedelic state, and would indicate that the brain has temporarily diminished the intensity of thalamic filtering via some very basic brainstem or cortical feedback mechanisms. Incidentally, Layer V pyramid cells of the cortex - which have the highest density of 5-HT2A receptors, and feed cortical signal back down into the thalamus - would be the perfect pathway for such a signal to be sent.

Signal Theory: Filtering, Circular Logic & Sensory Feedback Loops

While it is fun and informative to talk about brain states in terms of global excitation or amplification of sensory processing, it is also important to look at the specific ways signals are routed and filtered through the brain. The neuro-mechanical filtering or gating of incoming stimulus is mediated by inhibitory feedback mechanisms which are - for the most part - involuntary reflexes of our perceptual systems. For instance: voluntary focus on one stimulus (signal) causes involuntary inhibition (gating) of all extraneous stimuli (noise) also happening at that moment. But beyond the "global" gating of noise that can be achieved via feedback interaction with the cortex and the thalamus, there are also many other localized forms of feedback inhibition and signal gating happening both at the neural level (via intra-neural feedback inhibition); and at the organ level (via intra-cortical, thalamocortical, or brainstem modulated feedback inhibition). To bring this down to a common-moment level: while your visual and prefrontal cortex interface with Weirnicke's area and Broca's area to parse and internalize the words written in this sentence, those areas are simultaneously inhibiting (gating) activity in other areas of your brain so your attention doesn't wander before hitting the period at the end of this sentence. Without the inhibition of extraneous signal noise, signal tangents of marginal relevance would be sprouting into your brain at a rate beyond your ability to control. You would be overwhelmed with hyper-referential noise and surrealist-tangential trains of thought that would swirl from concept to concept without resolution, until you shook yourself out of the reverie (minutes later) and returned to your original task, which was finishing the sentence. But that would only be the result of one kind of interruption of signal gating - localized inhibition. The brain is full of little feedback diagrams like this, so understanding the concept of signal and noise filtering and gating is essential to understanding the effects of psychedelics.

The concept of a signal filter is fairly universal, and can be applied to both light and sound as well as touch, taste, smell, and any other sense we have. In terms of consciousness alteration, it has often been stated that psychedelics are like "Photoshop filters" for the brain; they contain embedded routines that can alter the color, texture, shape, and intensity of what we see or hear. While this statement is experientially accurate (psychedelics can make reality seem like it has been twisted and warped through a Photoshop filter or computer screen saver), the Photoshop metaphor is not a very good one in terms of a technical description of a neurological filter. Photoshop filters are algorithms that tweak digital data to enhance or change a single aspect or set of aspects of a visual image, while the filters we are discussing in the brain are more akin to analog signal processing filters found in wiring diagrams and sound engineering. Any musician who works with electric sound processing is familiar with amplification, feedback loops, delay, echo, chorus, flange, phase, reverb, overdrive, distortion, compression, attack, cutoff, release, and the infinite array of unique combinations all these simple signal-shaping effects can produce. These sound-FX devices are nothing more than a series of circuits wired to amplify, reproduce, and shape incoming signal through a series of feedback-controlled gates and delays.

We could spend a couple chapters going into detail about the functions of capacitors, resistors, transistors, etc., but the primary notion I want to emphasize here is this simple dynamic: amplifiers make the incoming signal stronger; filters selectively squelch specific properties of that signal. Amplifiers and effects boxes use feedback loops to "boost" a signal by feeding a tiny percentage of it directly back into itself. If you do the same thing with a slight delay you get an echo; pile up the echoes at tiny intervals and you get flanging and phasing effects; increase the level of signal feedback and you get distortion; if the signal is too intense then you can drop the high-end and bring it down; if the low end sounds muddy than isolate the frequency and turn it up. I could be talking about a sound mixing board or your audio cortex on psychedelics, but either way if you run a beat through it, put an envelope on it (a curve of action that changes intensity, like the turning of a knob), then you wind up with the backbone of what people all over the world now call "House music." And to be clear, House music did not come from nowhere, it came from musicians, DJs, and producers taking a lot of LSD.

House music was originally called "Acid House," and was created specifically to mimic and intensify the kind of internal signal effecting that happens in the brain under the influence of LSD and/or mushrooms and/or MDMA. I think everyone who hears and listens to House music knows on an intuitive level that it is "drug" music, even if they don't understand why. But clearly, the people who make House music are trying to reproduce some of the unusual audio effects experienced under the influence of psychedelics, and they reproduce these psychedelic effects with signal gates and filters. Even if House musicians don't completely understand the wiring in the brain, they have found very clever ways to reproduce psychedelic "noise" with simple FX boxes. House musicians and DJs did not need to crack textbooks, spend time in an MRI machine, or sit down at a lab bench with a microscope and some Petri dishes to try and figure out how all the neural gating worked, or how all the neural filter envelopes are controlled, etc. That's all advanced neuro-sci wet-ware junk, right? Even without knowing these details, people attempting to reproduce the effects intuitively knew that the process of feedback amplification and gating was involved somehow, even if there was little hope anyone would ever figure it all out. I mean, c'mon, the brain is like a billion times more complex then a mixing board or FX box, right? Well, no, not really.

I mean, the brain is obviously more complex than a mixing board in that it is wired with holistic signal-processing redundancy, advanced interpretation of signal meaning, signal memory and recall, etc. But in terms of feedback gating and amplification of signal, the two models (neural circuits/analog circuits) function basically the same, and the same techniques can be applied (by different means) to both mediums to achieve the same range of effects. Even though the cortex is organic and plastic, it still seeks to employ efficient parallel and serial associative feedback mechanisms between processing areas for modulating intensity of focus, maintaining signal fidelity, and employing advanced signal comprehension. We'll be drawing some wiring diagrams between various areas of the brain to illustrate this concept in detail later, but the targeted control and disruption of various neural feedback mechanisms is what I refer to as the signal theory of psychedelic action, which shapes most of the underlying assumptions of this book. We will see how it applies to various mind states when discussing individual psychedelic phenomena in detail in later chapters.

Stochastic Resonance & Stochastic Signal Disruption

So far, most of our discussion has focused on the smooth flow of signal through the cortex, and how psychedelics may enhance our signal processing capabilities, but we must also take into account the fact that not all hallucinogenic or psychedelic activity is due to neural excitation, some of it is caused by neural interruption and/or signal disruption. The classic case of signal interruption occurs with anesthetics or dissociatives, but classic psychedelics may also directly disrupt neural firing patterns at higher dose ranges. While it is convenient within the context of cognitive theory to talk about neural interruption in terms of areas of the brain "malfunctioning" or "going offline," there is actually a grey area between "functioning" and "interrupted" that often gets overlooked, and I refer to this state as semi-interrupted functioning. Semi-interrupted functioning comprises the border-lands between "functioning at normal capacity" and "out of it." Being tipsy on alcohol, for instance, is a state of semi-interrupted functioning. But alcohol causes signal interruption via a depressant effect; psychedelics cause interruption via an excitatory effect. In both cases (alcohol and psychedelics) the level of interruption increases with dosage until, at high doses, full cortical interruption will cause the user to "black out." But in the semi-interrupted state - where the brain is beginning to misfire, but is not fully malfunctioning - a lot of interesting things can happen.

First of all, when talking about psychoactive drugs being introduced into the neural mix, one assumes a smooth metabolic response for the drug to come on, take effect, reach full effect, metabolize, and leave the system; and all of this is highly predictable within the confines of receptor affinity, receptor density, amount of psychoactive substance taken, metabolic rates, etc. However, what this "big picture" assumption misses is that the actual flow of psychoactive molecules through the bloodstream and into the brain is disorderly and somewhat random, and it is impossible to tell which batch of neurons will be hit with how much psychoactive substance and in what order, or how the brain will react to that specific random cascade of pharmacological events as it unfolds. What I am referring to here is the somewhat unpredictable chain of individual molecular events which lead up to and produce the holistically predictable psychedelic state. I refer to the unpredictability of specific neural events arising within the psychedelic state as stochastic signal disruption, which is just a fancy way of saying "random noise messing up the signal processing mix."

I want to clarify that when I say random, I mean unpredictable, and when I mean unpredictable I mean just that, impossible to predict. The chemical events which happen in your brain are controlled by mood, heart-rate, respiration, cranial blood flow, supply of oxygen, and more importantly, conscious will of the individual. However, the specific landing places of each psychedelic molecule ingested cannot be predicted, and while conscious "intent" of the user may be able to move blood around the head, it cannot force a ligand (such as a psychedelic molecule) to join to the specific receptor it chooses. The psychedelic molecule is thus distributed randomly around the brain and body at a more-or-less uniform density until it sticks wherever it sticks and/or is eventually metabolized. This stochastic distribution of psychedelic molecules - and consequent excitation and interruption of neural functioning - can account not only for a wide variety of different "types" of psychedelic experiences, but can also account for the seemingly random and unexpected presentation of ideas, sounds, or images that may pop into your consciousness while under the influence.

For most drugs that you might take, stochastic distribution would not factor into the tone or quality of the experience; as long as the distribution of the drug is uniform (more or less), the effects we expect to happen will happen. However, since psychedelics have such extreme and varied effects, and can act as "non-specific amplifiers" of brain functioning, the "non-specific" part of that equation can play a very weighty role in the experience. For those of you who follow trendy comparisons between quantum mechanics, complexity theory, the occult, Buddhism, and other forms of Eastern philosophy, you may have already been exposed to the notion that everything "random" is not really random at all, but is actually a smaller part of a larger pattern that we cannot fully see or comprehend. Another tenet of complexity theory is that within seemingly random interactions (such as vibrations in the sand) complex patterns (such as mandalas) can spontaneously emerge. Both of these notions speak to the implicit fact that "random" is only as random as context allows, and within seemingly random events a larger pattern of "meaning" can emerge. We will talk about both of these notions later when discussing spontaneous perceptual activity in early-stage psychedelic trips.

One more thing about random noise I want to touch on is the notion of stochastic resonance, a fairly new principle in signal transmission that is proving to have profound impact in a number of signal detection and imaging disciplines, including high-energy physics. To explain stochastic resonance, I will quote from an abstract by Thomas Wellens of the Institut Nonlinéaire, published in the 2004 edition of the Reports on Progress in Physics:

"We are taught by conventional wisdom that the transmission and detection of signals is hindered by noise. However, during the last two decades, the paradigm of stochastic resonance (SR) proved this assertion wrong: indeed, addition of the appropriate amount of noise can boost a signal and hence facilitate its detection in a noisy environment."

So here we have what appears to be a fundamental principle in the making, the notion that a certain amount of noise can boost the fidelity of a specific signal within an already noisy environment. The key words in the above description are "an appropriate amount of noise", and the successful application of stochastic resonance relies on finding the "appropriate" amount of noise to boost a specific signal. This principle is germane to our discussion in two ways: First of all, the more scientists learn about SR, the more probable it is that our brains may use some form of internal SR to "boost" signals in darkened or obscured environments; Secondly, SR gives us a working model which states that an "appropriate" amount of signal noise added to the perceptual system may actually boost our perceptual capacities. Of course, finding the "appropriate" amount of noise to amplify the specific capacities of your brain is the trick here, but if the "appropriate noise" levels of specific excitatory substances could be found, the boost in signal strength (perception) could be significant.

Hippocampus Stimulation and Spontaneous Memory Recall

Another area where noise may creep into the perceptual system is through a stimulation of the hippocampus and/or other brain areas associated with memory and recall. The act of recalling a memory is actually an electro-chemical trick you play on yourself, an illusion you re-create in your mind from tiny associative pieces stored in various forms of connective memory. When you attempt to conjure the face of a loved one or the scent of a rose in your mind, you are actually pulling out bits and pieces of these experiences from memory, and the hippocampus is essential to storing, recalling, and reassembling these little pieces into a full picture in your head. Not only can we perform this memory trick at will (such as recalling memories from your childhood), it can also be fired spontaneously in response to totally unrelated stimuli, like the scent of a rose from the flower shop on the corner recalling memories of your own rose garden, or of that woman who always wears too much rose perfume. When spontaneous recall is triggered, internal imagery is generated by a chemical impulse beyond your voluntary control; it just happens whether you want it to or not. A little neurochemical hit; we get an associative memory recall.

Now let's say this little chemical trick was artificially simulated, triggered by a substance which made the organs responsible for this recall trick hypersensitive to all incoming stimuli. The hippocampus is not the only area needed for memory recall, but it is the most important one, and we are presuming a cross-activation between the hippocampus and the many areas of the cortex needed for detailed memory recall and reassembly. In the case of hypersensitive memory recall, even the most insignificant stimulus could make the mind go Technicolor with a cascade of distinct memories. In a hyper-excited state, each memory would feedback upon itself, pulling up similar memories as fast as they could be recalled, each image piling onto the next until you think, "my life is flashing before my eyes" in the kind of nicely edited montage you'd only expect to see when facing imminent death. While still very poorly defined, this hyper-memory recall state - or having one's "life flash before the eyes" - is a very good example of a traditionally defined "paranormal experience" which can ultimately be reduced to the excited chemical triggering of a natural biological process, presumably easily reproducible with the proper chemical stimulation.

The psychedelic literature is full of information on spontaneous memory recall under the influence of LSD, so there is little question in my mind that the hippocampus and other memory-recall organs are somehow involved in a very explicit way when this type of event occurs. The memories which are accessible in this hyper-excited state both theoretically and experientially go all the way back to the womb, and it is not uncommon for a user under a high dose of psychedelics to "re-live" their birth experience and/or other early formative memories. Exploring birth regression and early-life memory is one of the central pillars of Stan Grof's work with LSD in classic Freudian psychotherapy. From the perspective of classic Freudian psychotherapy, the ability to access a multitude of birth and early-life memories is essential to understanding the root "neurosis" and "pathos" of the individual. Indeed, the ability to recall repressed or traumatic memory is a large part of the allure of using psychedelics in classic psychotherapy, but it should really be considered only one of many potential uses for psychedelics in therapy. Spontaneous memory recall is just one little part of the overall psychedelic package, and the totality of the experience is vast, messy, and must be appreciated for what it is, not viewed simply as a tool for quick access to buried memories.

Signal Noise Generated through Synesthesia

Of all the sensory distortions reported while under the influence of psychedelics, synethesia is probably the most alluring because it is the easiest to describe in concrete detail. In simple terms, synesthesia is described as a mixing of the senses, a condition which causes a person to see music, taste color, etc.. More specifically, synethesia may be defined as sensory stimuli from one sense organ (signal) affecting two or more sensory processing centers simultaneously. Synesthesia is a classically reported psychological disorder which affects many people who have never taken psychedelics, and is generally explained in terms of "cross wiring" or, more accurately, "cross activation" of specific sensory processing areas of the brain. From a recent article in Scientific American:

"Although we initially thought in terms of physical cross wiring, we have come to realize that the same effect could occur if the wiring - the number of connections between regions - was fine but the balance of chemicals traveling between regions was skewed. So we now speak in terms of cross activation. For instance, neighboring brain regions often inhibit one another's activity, which serves to minimize cross talk. A chemical imbalance of some kind that reduces such inhibition - for example, by blocking the action of an inhibitory neurotransmitter or failing to produce an inhibitor - would also cause activity in one area to elicit activity in a neighbor."
V.S. Ramachandran and E. Hubbard, "Hearing Colors, Tasting Shapes"; Scientific American, May 2003, Volume 288 Number 5, p.55.

I will dig out the meat of this quote for you here again: "Any chemical imbalance that reduces the amount of cross talk inhibition between brain regions would ultimately cause brain activity in one area to elicit spontaneous activity in a neighboring area." So for our purposes the "chemical imbalance" would be a tiny pinch of psychedelic alkaloids, and the spontaneous cross activation of sensory processing centers is dramatic. Being able to "see music" is possibly one of the most widely reported side effects of psychedelics (right after seeing "trails," which I will discuss a little later), but it is by no means the only form of synesthesia produced by psychedelics. While the exact chemical mechanism by which psychedelics produce synethesia is still unknown (i.e. specific receptor blockage, specific receptor affinity, location of signal "leakage" between areas, etc.), I would be willing to speculate that it would be achieved either through a reduction of cross talk inhibition as explained above; through a general cross excitation of multiple sensory processing centers at once; or a combination of both of these factors. We'll take a closer look at some indicated brain areas in later chapters on visual and audio phenomena in detail.

Cranial Blood Flow, Respiration, & Targeted Effect Amplification

While it is widely accepted that psychedelics act as non-specific amplifiers of mental activity, one of the greatest mysteries of psychedelic action is how psychedelics do this. We know set and setting play an important role in shaping the content and tone of the psychedelic trip, but why is this? What is the physical interaction between drug, brain, and environment that creates this non-specific, context-dependent dynamic? We've already discussed psychedelic action at the locus coeruleus (LC) and the contrasting effects 5-HT2A agonists can have on the production of norepinephrine, but that only explains one range of dynamic perceptual effects. It does not explain, for instance, why someone can spend one part of a trip in obsessive depression - perhaps locked in a very dim and dark perceptual space - then at the slightest perturbation become suddenly overwhelmed with happiness and hilarity, immersed in visions of the absurd and surreal. The obvious answer would be, "It's the music," or whatever happens to be forming the user's sensory context at that time. But what if the user is alone and in silence? If there is no external stimuli to react to, what determines the flow of effect from one area of the brain to the other?

I have thought about this question for a long time, and while it remained a mystery for many years, the obvious answer now (in retrospect), is that it all comes down to cranial blood flow. The blood carries the drug through the brain; the blood flows to wherever the brain is currently active; the drug follows with the blood; If activity and blood concentration in a specific area is high enough, the drug begins sticking to receptors, thus hyper-activating that specific area; when an area of the brain becomes hyper-activated, messengers from that area begin to bleed over into neighboring areas, thus synesthesia and tangential thoughts arise; the activation centers shift, and blood moves on to newly activated areas; the drug goes along with the blood, and the cycle repeats. That is the theory of cranial blood flow and targeted effect amplification in a nutshell.

If this targeted effect model is actually true, it would mean that psychedelic action in the brain can be directly controlled by the will and intent of the user, at any time. By consciously changing what they are thinking about at any one moment, the psychedelic user can consciously move blood from one brain area to another, and thus move the concentration of psychedelic activity from one spot to the next. And if a user is able to maintain concentration and focus on a particular thought, stimulus, or set of stimuli for a long enough period, the object of user's focus will continue to cycle, echo, feedback, and amplify within the user's mind until the notion entirely consumes and overwhelms them. This is true no matter what the notion may be: heaven, hell, or anything in between.

Now as far as I know, I am the first person to suggest this "targeted activity" theory via movement of the drug within the user's cranial blood flow, so it is pure speculation on my part. But I don't think it would be very difficult to test this theory with all the modern scanning machinery we have today. However, experiential tests on my own part (i.e., ingesting the drugs and testing the results of this theory) have led me to believe there is something to this. The psychedelic activity within the brain definitely follows the focus of the user around the brain from place to place, and when the intent of the user is shut down (intentionally or unintentionally), the action of the drug flows more-or-less in a random roller-coaster style from one area to the next, depending on (get this) the orientation of the user's head and body. Yes, I am postulating that the position you are in will directly effect how blood pools in your cranium (to the left, right, back, etc.), and will directly effect the intensity of psychedelic action in those areas. And so (follow me here), when you lie back with your head on the floor, the blood pools to the back of the head (otherwise known as the occipital lobe, or the visual cortex) and boom: the visuals instantly become more intense, immersive, and dream-like. If you sit up the blood pools down into the basal forebrain and temporal lobe, thus audio and "mystical" phenomena suddenly become more intense. Weird, but true.

I know it sounds extremely reductionist and rudimentary, but experientially psychedelic action follows all the predictions that the cranial blood flow theory would suggest. Of course, different drugs have different "lag times" in transitioning from activity in one area to another - due to varying receptor affinities - but in practical terms it is a good working model for any psychedelic experience. Yoga and mediation are nothing if not techniques for controlling respiration and flow of "energy" (blood, oxygen, glucose, etc.) through the body, and the techniques of yoga and mediation all come down to fine, targeted control over respiration and body position, the two major factors which mediate the distribution of blood in your body (and brain). So - if there is any credence to this theory at all - one would assume that a person with training in yoga and meditation might derive more benefit from psychedelics than someone without such training. Conversely, one might assume that a person who has no meditative training - but who has become casually interested in psychedelics - will naturally be drawn to the disciplines of Buddhism, meditation, yoga, Chinese medicine, etc., in order to integrate their own experiences and gain a greater sense of focus and control within the psychedelic trip. I am not just wildly speculating here; among modern users the "progression" from psychedelics to mystical arts (or vice versa) is extremely common. It is my belief that this is not coincidence. There are many mystical arts which are directly related to cranial blood flow - trepanation probably being the most extreme (which is the drilling of a hole through the skull to lower cranial pressure and increase blood flow) - but the most popular is probably kundalini yoga. The mystical arts offer techniques which are directly beneficial to psychedelic experimentation, namely the ability to control respiration and blood flow via body position, breathing techniques, focus of attention, and other voluntary biofeedback mechanisms. We will be discussing cranial blood flow and advantages of specific mystical techniques in further detail in later chapters of this book. But keep in mind that these concepts are the cornerstone of any practical psychedelic use, and the overlap between science and mysticism vanishes when it comes to things like voluntary biofeedback and user targeted brain states. In other words: it's not magic, it's technology!

<< Previous | Index | Next >>