Conscious or ‘lucid’ dreaming is a fascinating aspect of the human mind - a phenomena which has received so little academic focus - despite the infintessimal nature of the source material; the intensity of the experience; and the relative ease at which any individual can train and experiment upon themselves. Lucid dreaming is most simply defined as 'self-awareness and control of dreaming', although I prefer to describe it as the closest thing to a spiritual experience or a 'trip' without the use of illegal hallucinogenic drugs or the consequent mental and physical health risks. I have never taken hallucinogenic drugs (other than two occasions, (in my teenage years) when I tried 'magic mushrooms') nor would I wish to experiment with suchlike, particularly when the experience of a lucid dream is so much more fantastical; mind-expansive and mentally rewarding, with none of the associated negative aspects, the least of which might be a criminal record!
It wasn’t until the late 1970’s that scientific evidence emerged, proving that a person could recognise and be aware they were dreaming. Research and understanding of lucid dreaming has made significant progress, largely thanks to the essential contribution of scholars such as Green; Tholey, Hearne; LaBerge; Woresly; Garfield; and Blackmore, amongst others. By far the most valued contributions have been made by Stephen LaBerge who has been active in the field of lucid dream research for nearly 30 years.
Many techniques and innovations for the induction of lucid dreaming have emerged since the 1970s, benefiting those who wish to explore their personal dream environment. Presently, the most common techniques available to prospective oneironauts (dream explorers) include: State-Testing; Intention; Reflection-Intention; Autosuggestion; MILD (Mnemonic Induction of Lucid Dreams); WBTB (Wake-Back-To-Bed); WILD (Wake Induced Lucid Dreams); CAT (Cycle Adjustment Technique) etc. These mental techniques involve training your mind to become more cognitively aware during dreaming, triggering lucidity. In addition to these entirely mental techniques, electronic techniques, in the form of dream masks, were invented. These included the DreamLight; NovaDreamer; and DreamMaker. Electronic devices are intended to cue the dreamer during REM sleep (either optically or auditory), helping them to recognise they are dreaming and induce lucidity. Mental exercise and electronic devices have been subject to various empirical tests and have proven effective, to varying degrees.
In addition to harnessing your mental powers to trigger lucid dreaming and increase dream recall, there is an increasing trend in the use of supplements and vitamins to aid dreamers seeking to enhance their dream experiences. These lucid dream supplements are also known as ‘oneirogens’. It is unwise to use oneirogens without first practicing other forms of lucid dream incubation and undertaking some degree of mental preparation. An oneirogen may jolt a novice into a lucid dream state, which may be anxiety-provoking or difficult to manage without the correct mindset. Used in conjunction with meditative and mnemonic techniques of lucid dream induction, oneirogens offer a reliable short-cut to self-awareness during dreaming and effective dream recall.
* A neurochemical approach to dreaming
The use of oneirogens is known as the neurochemical approach. Neurochemistry is a branch of neuroscience which involves the study of the chemical processes of the brain in an attempt to understand the underlying molecular bases for memory; emotions; cognition; behaviour and neurological disease, such as Alzheimer’s or Parkinson’s. Some of the neurochemicals under examination include: glutamate; histamine; GABA (gamma-amino butyric acid); acetylcholine; serotonin; dopamine; norepinephrine; and nitricoxide. The same neurochemicals which play important roles in a waking-state are also present during sleep and neuroscientific investigation allows scientists to determine what chemical processes occur in the sleeping brain. There are measurable changes in brain chemistry during sleep cycles – for example, melatonin changes during sleep are particularly significant in the regulation of circadian rhythms; and it is known that other chemicals are present, in varying amounts; during REM cycles, when lucid dreaming is most likely to occur. Of these, the neurotransmitters are the most significant as they carry neurochemical signals through the brains neural pathways.
Although there has been no empirical research on the presence and role of neurochemicals in lucid dreaming, academics such as Thomas Yuschak (2006) argue that the relationship does exist. Additional evidence for the relationship between lucid dream states and changes in neurochemical processes is provided by cross-cultural studies of persons/groups who ingest ‘oneirogens’ (i.e. herbs; roots and other organic matter; preparations etc) to induce a dream state - for example, some African tribes; shamans; and Native Americans. LaBerge has conducted some research into neurotransmitters, identifying a type of supplement that works remarkably well at boosting acetylcholine (ACh) levels by inhibiting acetylcholinesterase (an enzyme that breaks down acetylcholine into choline and acetate). The presence of an AChEI (acetylcholinesterase inhibitor) works by increasing the levels and activation of ACh. Cholinergic neurons are involved in the synthesis of ACh and believed to modulate our level of wakefulness. Taking supplements which effectively raise ACh levels affect the wakefulness of the dreaming brain and hence its ability to become more lucid. LaBerge was able to clinically show that ingesting certain AChEIs does improve the ability to become lucid whilst in a dream state. His study represents just the tip of the iceberg in our scientific understanding of LDS (lucid dream supplement) technique and underscores the fact that certain supplements favourably improve an oneironaut's chances of achieving lucidity. Many over-the-counter supplements are available that affect the various neurotransmitters; making the LDS technique fairly wide open to experimentation and refinement. As with all changes to diet or medicinal intake, anyone seeking to embark upon the use of supplements should consult a health practitioner to ensure safe dosage and expert advice is obtained regarding the risk of any potential side effects. Additionally, extreme caution must be exercised when purchasing supplements online – descriptions, ingredients and effects may not be accurately listed and there is no guarantee that such substances are fit for human consumption or indeed effective in delivering on advertising claims. Personally, I only buy supplements from reputable vendors, such as Holland & Barrett/pharmacies; or those manufactured by trusted brands. All the supplements I have researched and written about are available without prescription and where I have specifically experimented, I will outline my personal observations. As there are very many known oneirogens, I am aiming to concentrate on one per post, so please continue to check for updates on this topic thread.
* Cycles of sleep
Human sleep generally moves in cycles - first moving from wakefulness down into a deep, regenerative sleep; then coming back up toward wakefulness – a cycle which repeats itself thus. Sleepers generally move through 4 - 6 of these cycles per night, with each cycle lasting approximately between 70 and 110 minutes. Each sleep cycle is divided into two distinct phases: non-REM sleep and REM sleep. Furthermore the non-REM sleep phase is sub-divided into four stages that transition us from wakefulness (or REM) into deep sleep and then back up again. The cycles merge and transition from one to another in the smooth continuum we call sleep. During the deepening stages of non-REM sleep the body becomes increasingly relaxed with brainwaves becoming slow and regular and with blood pressure, temperature and muscle tone all decreasing. REM sleep, on the other hand, is characterised by an increase in heart and respiratory rate; rapid and irregular eye movements; increased blood pressure, as well as paralysed muscles from the chin downwards. The first cycles of the night tend to have shorter REM periods and longer periods of deep sleep. This trend reverses as the night goes on. The later cycles have longer REM periods and shorter deep sleep periods. By morning, most sleepers spend almost all of their time in stages 1, 2 and REM sleep, with very little or no deep sleep (stages 3and 4). Infants are unique in that they spend approximately 50% of their sleep time in REM sleep. The National Institute of Neurological Disorders and Stroke provides this description of the five sleep stages:
Stage 1 (Drowsiness)
We drift in and out of sleep for about 5 to 10minutes and can be awakened easily. Our eyes move very slowly and muscle activity slows.
Stage 2 (Light Sleep)
Our eye movements stop and our brainwaves (fluctuations of electrical activity, measured by electrodes) become slower, with occasional bursts of rapid waves called ‘sleep spindles’. Our heart rate slows and body temperature decreases.
Stages 3 and 4 (Deep Sleep)
Slow brain waves called delta waves begin to appear, interspersed with smaller, faster waves. By Stage 4, the brain produces delta waves almost exclusively. It is very difficult to wake someone during stages 3 and 4, which together are called deep sleep. There is no eye movement or muscle activity. People awakened during deep sleep do not adjust immediately and often feel groggy and disoriented for several minutes after they wake up.
REM Sleep
During REM sleep, our breathing becomes more rapid, irregular, and shallow; our eyes jerk rapidly in various directions; and our limb muscles become temporarily paralysed. Our heart rate increases, our blood pressure rises, and males develop penile erections. People tend to have the most vivid dreams during this stage of sleep.
LDS (lucid dream supplements) – in the form of vitamins/dietary supplements and food preparations which change the neurochemical balance of the brain, during sleep, acting as ‘triggers’ for the various stages of sleep and wakefulness.
It is an interesting fact that the human body strives to maintain a balanced sleep schedule, even when intentionally interrupted by the sleeper – i.e. by sleep deprivation or irregular sleep patterns. It is extremely difficult to deprive your body of deep or REM sleep for prolonged periods, nor should you strive to do so. Deep sleep is strongly associated with body rejuvenation and is imperative for maintaining proper mental and physical health. It is well known that during periods of sickness or injury, your sleep schedule will shift to include longer and more frequent periods of deep sleep – a form of organic healing. It is also well known that depriving your body of deep sleep can result in negative effects on both your mental and physical health, including a weakened immune system; increased levels of agitation and stress; and a generally depressed state. As a lucid dream enthusiast you must not sacrifice your deep sleep in the pursuit of higher quality lucid dreams or longer periods of REM sleep, as this approach is unsustainable at best. If you deprive your body of deep, restful sleep on one night, in addition to feeling energy deprived on the following day, you will drop into longer periods of deep sleep on the next night in order to compensate for the lost time on the previous night Any method of lucid dream enhancement must never sacrifice your quantity/quality of deep sleep if it is to enrich your overall well-being and daily functioning.
In contrast, if you suppress REM sleep for a period of time, your body will be strongly encouraged to make up for the lost time spent in this state, and therefore, the next time you fall to sleep you may experience an effect referred to as ‘REM rebound’. REM rebound can be simply defined as prolonged periods of REM sleep due to prior periods of REM suppression. This effect is commonly seen among alcohol users and cannabis smokers. Both alcohol and THC (the active chemical in cannabis) are known to suppress REM sleep. If the cannabis smoker decides to discontinue use, the individual will commonly experience several nights of increased REM sleep and accordingly, longer and more vivid dreams. Although the REM rebound effect is a somewhat indirect method to increase REM sleep time, it is still a valuable tool that the lucid dream enthusiast has at their disposal.
* Two conflicting theories of dreaming
There are two predominate theories regarding dreaming. The first theory has been referred to as the ‘REM dream theory’; the ‘brainstem dream theory’; or the ‘cholinergic dream theory’. The second theory is referred to, variously, as the ‘forebrain dream theory’; the ‘cerebral activation dream theory’; and the ‘dopaminergic dream theory’ .The first theory (hereafter referred to as the cholinergic theory) has been existent since the 1950’s when the first links between the REM sleep phase and dreaming were discovered. The theory quickly developed the concept that REM sleep is required for dreaming to occur, based on evidence that 70 - 95% of normal subjects who are awakened from the REM state report that they have been dreaming; whereas only 5 - 10% of non-REM awakenings produce similar results. In the mid 1970’s it was discovered that REM sleep was essentially controlled by various mechanisms located in the brainstem, resulting in a wide spread belief amongst the ‘dream science’ community that these same mechanisms were also responsible for dreaming. Specifically, it was determined that the cholinergic brainstem mechanism could switch on/off the REM sleep phase, and therefore dreaming, by controlling the release of specific neurotransmitters. According to this paradigm, REM sleep (and hence, dreaming) is switched on by the release of a neurotransmitter called acetylcholine (ACh) and turned off by the release of a different neurotransmitter, called serotonin. One could conclude from this model that the neurotransmitter ACh controls REM and dreaming. Probably the most disheartening aspect of this theory is that it assumes that cognition plays practically no role in dreaming, which is characterised under the model as a purely neurochemical process. The brainstem simply causes a random firing of neurons whose electrical impulses travel to the cognition centre of the brain (forebrain) where they are passively synthesised by its memory system into a ‘best fit’ for otherwise incoherent data. In other words the random impulses make it to the forebrain, which tries to ‘force’ meaning to them (and it is this ‘forced meaning’ which provides a waking memory of the dream). Although this theory explains the illogical and nonsensical dreams we sometimes experience, it doesn’t capture at all the lucid dream experience in which the dreamer directly influences and controls the dream plot and setting. In support of this theory, it has been shown that drugs/herbs that promote the release of ACh within the brainstem do not only generate REM sleep, but also dreams.
The second theory (referred to as the dopaminergic theory) is considered to be more sophisticated, elegant, and complete than the cholinergic theory and is substantiated by a strong clinical basis. It is this theory which is typically favoured by those investigating the psychological effects of dreaming and the psychical value of dream function. The dopaminergic theory tries to fill in the lacuna left by the cholinergic theory. For example, between 5 - 30% of REM awakenings do not elicit dream reports and at least 5 - 10% of non-REM awakenings do elicit dream reports (that are indistinguishable from REM dream reports). According to the dopaminergic theory, it is the forebrain that causes dreaming to occur, and not the brainstem. This assumption has a number of important consequences. It is well known that the forebrain has little, if any, effect on REM sleep and therefore the conclusion must be that REM sleep is not required for dreaming to occur. One of the clinical facts that provides the basis for this theory is that brain lesions which occur in the forebrain area can totally halt dreaming in an individual without having any affect on REM sleep. It was also noticed that the lesions which halted dreaming were located in the same region of the forebrain targeted in the prefrontal leucotomy (i.e. frontal lobotomy) operations used as a means of behaviour control. It has been confirmed that 70 - 90% of these operations yielded complete or nearly complete loss of dreaming in the subjects. It is this region of the brain that is rich with fibres connecting frontal and limbic structures with dopaminergic cells. This system was the target of the leucotomy because it is believed to control the goal seeking and pleasure seeking mechanisms. Damage along this system produces disorders characterised by substantial reductions in interest; initiative; imagination; and ability to plan ahead. These facts strongly suggest that dreaming is generated by this dopamine circuit; and furthermore, when L-dopa (a popular drug used to combat Parkinson’s disease by increasing the level of dopamine within the brain) is administered to patients during the night, dream frequency and vividness are greatly increased even though there is no corresponding increase in REM sleep. Furthermore, the dopaminergic theory suggests that dreaming is not chaotic in nature, but rather manifests from specific and highly complex cognitive processes. So if REM sleep is not responsible for dreaming, how does the dopaminergic theory address the high correlation between REM sleep and dream reports? This theory suggests that it is not REM sleep which is required for dreaming, but rather, a more general state of cerebral activation during sleep. REM sleep is often referred to ‘asparadoxical sleep’ because the brain is both asleep and simultaneously highly activated. The vast majority of dream reports that occur outside of REM sleep are associated with stage 1 or 2 sleep (i.e. very light sleep). All of these stages, including REM, line the border between deep regenerative sleep and the waking state. The fact that dreaming can be artificially generated by the administration of a variety of stimulant drugs, including both cholinergic and dopaminergic agents, is open to a similar interpretation. Of crucial theoretical significance is the fact that dopaminergic agents increase the frequency, vivacity and duration of dreaming without similarly affecting the frequency, intensity and duration of REM sleep. This observation, together with the equally important fact that damage to specific areas of the frontal lobe obliterates dreaming (but spares the REM cycle), suggests a specific dopaminergic ‘dream-on’ mechanism which is dissociable from the cholinergic ‘REM-on’ mechanism. So according to the dopaminergic theory, two independent events must occur in order to spawn the dream state – first, the subject must undergo cerebral activation during sleep (where REM initiation accounts for one form of such activation); and secondly, the dopaminergic circuits located in the forebrain must also be engaged.
Now that we have a background on the various cycles of sleep; the role of neurochemistry in sleep/dreaming, I will begin posting articles on commonly available lucid dream supplements.
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