AbstractHumans have long been interested in the alteration of their consciousness. They have done so through a variety of means, including external chemicals, physical stressors and mental disciplines. Humans have also taken great care to pay attention to their dreams’ actions in which regularly provides an altered state in which the experience inadvertently interacts with their so called subconscious. No matter what path individuals take to reach these altered states, the states themselves bear striking similarities to one another. By understanding the baseline connections between the disassociation (change in normal consciousness) of individuals in both dreams and in the use of drugs, one may be able to understand the waking consciousness better or conscious altered type disorders. In the past, few researchers have suggested the connection between psychedelics and sleep menations but due to lack in technological they were unable to test humans for such indigenous psychoactive drugs. Theses purposed hypothesis are becoming more and more popular as new technology and further research into the reasons for sleep and its chemical relationship to our minds become supported.
The mind prepares the body for sleep about 12 hours prior to the actual initiation of sleep onset (Barrett & McNamara, 2007). This transition is controlled by what is called the circadian rhythm, a brainstem controlled mechanism for keeping time, heartbeat, heat control, and many other automatic functions (Barrett & McNamara, 2007). The one aspect of circadian rhythm that deals mainly with sleep is the temperature control (Barrett & McNamara, 2007). Temperature control during the 24 hours cycle of the circadian rhythm allows our core temperature to change from cold to hot or hot to cold depending on the phase in the 24 hour cycle (Barrett & McNamara, 2007). During sleep onset our circadian rhythm automatically lowers the body’s core temperature using the body as a radiator. This change in temperature is one of the first signs of brainstem activation which precedes further demodulation and modulation of specific brain areas during the 5 sleep stages. The decrease in body temperature is greatly supported by the production of melatonin synthesized in the pineal gland in the brain (Callaway, 1988) (Strassman, 2001) and shows that in relation to circadian rhythm, melatonin supports peak core body temperature drop at early morning hours when melatonin levels are highest (Strassman, 2001). Secretions of melatonin into the hypothalamus help in sustaining this process. Research has shown that micro injections of melatonin have the same effect as this process (Cramer, Rudolph, Consbruch, & Kendel, 1974). Supporting this transition from waking to NREM sleep, prostaglandin (PG) D2 is also secreted into the cerebrospinal fluid as an indigenous sleep aid, serving the mind in preparation for REM and recovery of fatigue (Huang, Mochizuki, Eguchi, Watanabe, Urade, & Hayaiski, 2001) (Moussard, Albert, Mozer, & Henry, 1994). Sleep modulation specifically is broken up into two categories Non-REM (NREM) and REM. NREM is broken up into 4 different stages: drowsiness, light sleep, deep sleep, and delta waves. REM represents the last of the sleep phases as stage 5 or Rapid Eye Movement (Yuschak, 2006). These phases are graphically depicted in figure 1.
Determining when these stages start and stop is an extremely difficult process since each phase transitions flawlessly into the next and sometimes seems similar to each other. One extremely complex stage of sleep, where the majority of our definition of dreaming or mentation comes from, is the REM stage. Although 80% of sleep is spent in the NREM phase (Barrett & McNamara, 2007), a particular amount of attention should be spent on the REM stage and transitional phases to REM since that is where the majority of dream like induced hallucinations occur.
Once activated by the circadian rhythm and supported by melatonin production, the brainstem starts to modulate the brain through physical activation or deactivation of specific areas. These same changes that happen during the sleep transition of NREM to REM are apparent in the onset of all forms of altered consciousness as they ultimately rely on the brainstem for any physical changes in the brain. This brainstem activation either modulates or demodulates different area of the brain depending on what type of activation signal is represented; either by external or indigenous chemical induction.
Possibly one of the most complex stages of our sleep is REM. REM is characterized by the rapid side to side movement of the eyes and the paralysis experienced by the sleeper from the chin down (Yuschak, 2006). Rapid eye movement and dreaming is not limited only to the REM stage but is also experienced during the last stages of NREM or the transitional phase between NREM and REM. The average person experiences 25% of their dreams during the transition from NREM to REM (Hobson, 2002). NREM dreams are described by patients that experience them as less vivid and shorter than those experienced during REM sleep. The differences in intensity of dreams between these stages are attributed to the amount of time spent in sleep, or the length of time the brain has had to produce dream related chemicals. The processes of activation and deactivation of specific parts of the brain during NREM and REM transitions are graphically depicted in figure 2.
Activation and Deactivation
The transition from NREM to REM is described by Allen Hobson and Robert McCarley in their proposed hypothesis of activation synthesis as a process of modulation and demodulation of specific areas of the brain in which mentations are produced (Barrett & McNamara, 2007) (Hobson, 2002). This activation synthesis hypothesis builds its foundation on the concepts produced by the REM Dream Theory. In REM Dream Theory, specific neurotransmitters acetylcholine (ACh) and histamine REM on, as well as serotonin REM off cause either modulation or demodulation of the brainstem (Hobson, 2002). The activation synthesis theory states that during the transitional phase between NREM and REM sleep, the brainstem has already systematically deactivated the aminergic systems ,which disengages the dorsolateral prefrontal cortex and blocks muscle motor function via the pontine brainstem’s deactivation of the anterior horn cells. The now deactivated aminergic system results in the loss of the ability to process new memories, cognitive functions of the ego, and the paralysis that inhibits the acting out of dreams (Hobson, 2002). This deactivation accounts for the common occurrence of amnesia that many people experience during sleep, the inability to understand self and to recognize the bizarreness of dreams, as well as the inability to move which has been experienced by some lucid dreamers, night terror patients, and narcoleptic patients (Hobson, 2002) (Lucidology, 2008) (Richard, 2006). Other areas such as the pons, the amygdala, the pariental operculum, the deep frontal white matter, and the parahippocampal cortex show evidence of having higher neuron function during NREM and REM transition as well as REM sleep phase than in waking (Barrett & McNamara, 2007). This modulation of specific areas of the brain is due to the increase in acetylcholine and results from the activation of the cholergenic REM on system (Hobson, 2002). The activation of the amygdala, due to the cholergenic system, can explain why the majority of dreams are experienced as fearful, full of emotion or nightmarish in nature due to the nature of the amygdalae in an over active state causing fearful emotions(Barrett & McNamara, 2007) (Hobson, 2002).
Using Dr. Hobson’s activation synthesis theory as a model, we can understand the reasons for the type of mentations or dreams that are experienced during NREM phase 2, and REM stage 5 of sleep. However we still have no understanding of what makes theses mentations occur. These occurrences may be explained by the remarkable correlation between the pineal gland and the synthesis of specific neurotransmitters that may contain psychoactive properties.
Mentations and the Pineal Gland
Neurotransmitters are the basis of how we perceive the world around us. They are the basic communication tool between neurons as well as activators and deactivators of multiple functions. Not one neurotransmitter completes only one function, on the contrary they sometimes complete functions that are in opposition of each other and brain function, competing for a completed task (Hobson, 2002). The more research is conducted on sleep and mentation the easier it is to understand how complex and integrated with neurotransmitter function sleep really is. In dealing with sleep and mentation we can break neurotransmitters into two basic groups - the aminergic system, comprised of the neurotransmitters dopamine, noradrenaline, and serotonin, as well as the cholinergic system, composed of the neurotransmitters acetylecholine, and histamine. The process of how the aminergic and cholinergic systems function in sleep can be described as a REM-on and REM-off type switch. Research has shown that the orexin or the hypocretines system is involved in controlling these two systems (Kaslin, Nystedt, Ostergard, Peitsaro, & Panula, 2004).
The pineal gland is a chemical production factory, either producing melatonin or serotonin depending on the presence of absence of light. In this process, light source information is relayed from the eyes via the optic nerves and results in the activation of synthesizers that either produces melatonin in the absence of light or serotonin in the presence of light, becoming the brains largest producer of serotonin. Also in the absence of light, other process are continued as melatonin is then processed into tryptamine and pinoline. Pinoline is a beta-carbolin called 6-Methoxytetrahydro-beta-carboline and acts as a monoamine oxidase-A inhibitor (MAOI) which in turn allows for the increases concentrations of serotonin (Callaway, 1988). The synthesis of tryptamines and pinoline is most dominate during the REM stage of sleep but also shows partial activation during NREM phases 2 as well as during highly stressful situations in animal and human lives (Strassman, 2001). In relation these stressful events, mentations also turn out to occur during this time. Some beta-carbolines and tryptamines have also been known to cause psychedelic hallucinations as they deal directly with brainstem modulation (Hobson, 2002) (Callaway, 1988). Melatonin has also been reported as having hallucinogenic effects on the brain; however, recent studies have shown negative evidence of such a relationship and that the further chemical breakdown of the beta-carbolines and tryptamines from melatonin are the results of these experiences (Cramer, et al., 1974) (Strassman, 2001). The buildup of these two known types of hallucinogens in the form of pinoline and tryptamines could easily explain the visual mentations experienced during specific pineal gland stimulation. “A shunt of serotonin metabolism to a pathway that occurs and leads to accumulations of abnormal amounts of such potentially pschotomimetic compounds” (Callaway, 1988) could explain many other hallucinogenic based abnormal brain dysfunctions such as schizophrenia. Blinding of the nerve fibers from cervical ganglion and the pineal causing inactivation of the melatonin process has been suggested as a way to reduced waking hallucinations in schizophrenic syndromes and shows support towards the pineal glands involvement in dream mentations (Maurizi, 1985). The processes of chemical conversion inside the pineal gland during different stages of sleep and light interaction are graphically depicted in figure 3.
Pineal Location in Relation to the Brain
The location of the pineal gland is also very important in supporting how an indigenous psychedelic excretion from this gland would cause the described effects of dreaming. The pineal gland is located directly over the colliculi and is surrounded by the limbic system (Strassman, 2001). If hallucinogenic chemicals excreted from the pineal gland, the result could be a barrage of emotional thoughts with respect to the involvement of the limbic system and a combination of audio and visual alterations in the colliculi experienced during dreaming. Due to the position of the pineal gland, blood flow is not necessary for the transfer of hallucinogens to the regions of the brain most affected. It can be assumed then, that mentations could occur at the point of death in the patient and possibly explaining out of body exerpences and other religious experiences.
The question still presents itself of what indigenous tryptamine based psychedelic would produce such mentations since beta-carboline pinoline may be psychedelic in nature but most likely not potent enough to cause full blown psychedelic experiences as experienced in dreams. It has been hypothesized that the indigenous psychedelic Di-methyle-trypamine (DMT) and LSD-25 could be the answer (Shulgin and Shulgin, 1991).
DMT, LSD-25, and Other Psychedelics
Understanding the different key precursors needed to make indigenous DMT and LSD-25 is an important part in understanding why the pineal gland has been selected as a possible production tool for tryptamine based psychedelics. The pineal gland, in addition to having its serotonin production properties also has the highest concentration of serotonin in the body (Strassman, 2001). Methyltransferases are necessary enzymes that have the ability to convert serotonin, melatonin, or tryptamine into psychedelics by methylating them (Strassman, 2001). Pinoline as well as other beta-carbolines may support this process by inhibiting the breakdown and extending the effects of tryptamine based psychedelics. With the abundance of serotonin, the transforming based methyltransferases, and the amplification ability of beta-carbolines, the pineal gland is one of the most logical places for indigenous DMT synthesis (Strassman, 2001). Also chemically similar to melatonin is LSD-25, which relates specifically to the activity on the raphe nucleus (a control center for serotonin release) (Maurizi, 1985) (Hobson, 2002). Few studies into the relationship of the formation of DMT or LSD-25 in the pineal gland have been conducted; however, indigenous DMT has been found in the lungs and brain of humans.
Though DMT, LSD-25, and other psychedelic drugs are similar in structure, the effects of these drugs are sometimes dramatically different. These differences are based on the individual as well as the environment of the individual taking the drug. A few instances have occurred where the same psychedelic trip has been described by different people taking the same drug. The amount of drug administered is also another key factor in how the effects of the drugs will be experienced. Dream mentations seem to follow the same trend as psychedelic as they are normally random and differ in intensity from dream to dream and person to person as well as setting. Vividness as well as intensity of the dream also increases with the amount of sleep the individual receives. This is due to the longer lengths of REM sleep as well as if they have a fully active pineal gland. With these common experiences, it is easy justify a relationship between dreams, psychedelic experiences, and the pineal gland.
Degrees of Disassociation
Contrary to the dream type experience, waking life, or normal consciousness, is kept in equilibrium during the day. Only with the administration of psychedelic drugs or sleep like alterations of the mind do we see a change in the consciousness or a degree of disassociation. The differences between sleep modulation and how psychedelic drug induce these changes is the speed of onset in which the mentations occur, the amount of allowed outside stimulation that can affect the patient, and the different areas of the brain affected by different types of drugs. These alterations in the consciousness seem to be in common with specific events that indicate different levels of disassociation or degrees away from the equilibrium of normal consciousness. The onset of psychedelic and dream like mentations all have in common the precursor effects of this consciousness change. Those effects are described by individuals as a feeling of heaviness, change in core body temperature, a relaxing feeling, audible buzzing sounds, and an increase in perceived bodily movement. These same events are described by patients that experience REM behavior disorder (RBD), sleep paralysis, perceived out of the body experiences, (OBE) and lucid dreaming (LD) (Yuschak, 2006) (LaBerg & Rheingold 1997) (Lucidology, 2008) (Richard, 2006).
During the transitional phase of NREM to REM, consciousness is also playing its part in changes in phase. In stage 2 of NREM sleep the thalamus becomes partially activated, allowing for conscious thinking, while in REM sleep the thalamus becomes fully activated mimicking our waking life allowing for full conscious thought (Barrett & McNamara, 2007). As we can see, the main difference in waking and REM sleep is the deactivation of the prefrontal cortex disengaging our brain from remembering the majority of our events. Individuals that practice lucid dreaming and experience out of the body type occurrences pay close attention to improving their memories of dreams as well as the transitional phase between NREM stage 2 and REM. It could be hypothesized that the techniques used to improve memory allow for the activation of the prefrontal cortex during REM sleep and allowing them to remembering these nightly events and allow for more psychedelic type of dream experiences.
Much of the information that supports the theory of activation synthesis as well as the proposed hypotheses of psychoactive drug synthesis during REM sleep is contrary to Sigmund Freud's theory of disguise censorship. Sigmund Freud used the disguised-censorship hypothesis in parallel with his practice of psychoanalysis in order to explain the aspect of sleep. In the disguised-censorship hypothesis, the brain is made up of a distinct subconscious and conscious. During sleep the left side of our brain being responsible mainly for logical thinking and ego, is less activated than our right side of our brain the side responsible for the id. Because of this the id is able to act out its wants and needs while still hidden from our ego by the amnesia felt after awakening and hidden interpretations of these signals produced into dreams. In addition to Freud’s dream hypothesis is that dreams are only produced moments before awakening (Barrett & McNamara, 2007). This difference is supported based on the concept that menations are experienced during NREM and REM and not as Freud theorized as only during the moments right before waking. Also Freud supported his theory with explaining that dreams have no randomness to them as they are childhood repressed wants and needs, and is kept in our subconscious to protect our conscious mind from damaging thoughts. As explained earlier there is evidence that dreams are sometimes random, remembered, and closely related chemically to psychedelic experiences.
Using psychedelic experiences as a model for dream mentaions we can explore the effects of altered states of mind while subjects are fully conscious. Further research into this field could give scientist a better understanding of the subconscious minds true intent in altered states as well as possibly answering the question of why dreams occur. Research into understanding the true purpose of the pineal gland and its production of indigenous tryptamine based psychedelics may also help in understanding sleep disorders such as night terrors, sleep paralysis, and narcolepsy. This type of research should be conducted in a controlled environment to increase manipulation of the dependent variables and maximizing the authority of such research. Development of more sensitive testing assay for indigenous psychedelic drugs allowing for baseline values in normal patients should be developed before future research is conducted.
Barrett, D., & McNamara, P. (2007). The New Science of Dreaming. Greenwood Publishing Group.
Callaway, J (1988).Proposed Mechanism for the Visions of Dream Sleep. Medical Hypotheses. 26, 119-124.
Hobson, A. J. (2002). The Dream Drugstore: Chemically Altered States of Consciousness. MIT Press.
Cramer, H., Rudolph, J., Consbruch, U., & Kendel, K., (1974) On the Effects of Melatonin on Sleep and Behavior in Man. Advances in Biochemical Psychopharmacology, 11.
Huang, Z.-L., Qu, W.-M., Li, W.-D., Mochizuki, T., Eguchi, N., Watanabe, T., Urade, Y., & Hayaishi, O. (2001). Arousal effect of orexin A depends on activation of the histaminergic system. Proc. Natl. Acad. Sci USA, 98, 9965-9970.
Kaslin, J., Nystedt, J. M., Ostergard, M., Peitsaro, N., & Panula, P. (2004). The orexin/hypocretin system in zebrafish is connected to the aminergic and cholinergic systems.
The Journal of Neuroscience , 2678-2689.
LaBerg, Stephen, & Rheingold, Howard (1997). Exploring the World of Lucid Dreaming.Ballantine Books.
Lucidology, (2008). Lucid Dream Forum, OBE Forum. Retrieved March 30, 2009, from Saltcube Lucid Dream and OBE Forum Web site: http://www.saltcube.com
Maurizi, C (1985).The Anatomy and Chemistry of Hallucinations and a Rational Surgical Approach to the Treatment of Some Schizophrenic Syndromes. Medical Hypotheses. 17, 227-229.
Moussard, C., Alber, D., Mozer, J. L., & Henry, J. C., (1994). Effect of Chronic REM Sleep Deprivation on Pituitary, Hypothalamus and Hippocampus PGE2 and PGD2 Biosynthesis In the Mouse. Prostaglandins Leukotrienes and Essential Fatty Acids. 51, 369-372.
Richards, David (2006). Night Terros Resource Center Forum. Retrieved March 30, 2009, from Night Terrors Resource Center Web site: http://www.nightterrors.org
Strassman, Rick (2001). DMT: Spirit Molecule. Rochester: Park Street Press.
Shulgin, Alexander, & Shulgin, Ann (1991). Pihkal .Transform Press.
Yuschak, T. (2006). Advanced Lucid Dreaming - The Power of Supplements. Lulu.com