Bliss is synonymous with kundalini
Before starting this section on bliss I wish to clarify that the experience of spiritual awakening is not "just" a bunch of chemicals. Just because a particular subjective experience can be the "cause of" or "caused by" a particular release of chemical or electrical phenomena, doesn't mean to say that the subjective experience can be reduced "down" to that physical chemistry. All manifestation has its atomic, chemical and electrical component. The apperception of "interiors" realized in the subjective experience of phenomena is what makes us human.
Normally we just hum along in our conditioned everyday consciousness, and then life seems to perturb this throwing us into heaven or hell depending on the circumstances. Hell...the death of a loved one, a breakup, losses of various kinds can be a direct route to Heaven. Any arousal of the Hypothalamic-Pituitary-Adrenal Axis will cause increased activation of the opiate systems, whether the arousal be stress, shock, trauma, freeze, sports activity or sexual attraction. Kundalini represents perhaps the greatest ongoing efflux of opiates. Sometimes the bliss is so acute that it makes rational thought all but impossible. The point is not to fight the bliss, or fall into compulsive degradation using the bliss as though it were a drug or alcohol binge. While undergoing excessive bliss there is indeed a need to rehabilitate ones faculties by pursuing challenging cognitive tasks. If this is not done chances are one could remain a spiritual bum for the rest of ones life, riding on the high of ones own internal chemistry.
Bliss might be directly associated with healing energy for it does dissolve the pain-body and impact of past trauma on the body and it does dissociate one from ones past pain, however it doesn't automatically create happiness. One can be blissed out and simultaneous be in ennui and depression due to cortisol burnout and hyper-parasympathetic activity. Kundalini can leave one both less functional and with a reduction in spiritual faculty while at the same time being blissed out of our tree. So the whole thing is very complex and to navigate such waters we need to stay focused on the creation and integration of the Whole Human.
Although there may be a deepening or change of flavor of the bliss and a rounding out of other functions to rise above the dysfunction of being blissed out, I don't think one could classify bliss in stages and lines of consciousness, other than to say that bliss affects all states, lines and stages. The good news is that when we are well into our substantiation phase we can have our bliss and our high cognitive function too.
Bliss appears to be kundalini phenomena especially related to heart expansion and is a consequence of increased energy flow in the nerves. One of the functions of spiritual bliss is to incapacitate the higher cortical functions rendering the individual "childlike" soft, maluable, changable, open and to conserve energy and internal resources for the metamorphosis of the physical body that occurs. Normally our conditioned "I" is kept so busy, hypervigilant and preoccupied by the tasks of daily life and obligations that this "fall" into the spiritually receptive state doesn't occur. Hence the preponderance of unpopped humans populating the planet, all vigilantly remembering who they are.
Memory takes tremendous energy. The energy used in an effort to maintain the sense of who we are right now prevents us from discovering what we might become. Thus the normal tight hold (neurosis) we have over who we are, our place in the world, and our past...keeps kundalini at bay. Once lit however kundalini dissolves our neurosis, our pain-body, accumulated stress and trauma, and does so by essentially flooding the limbic brain with bliss making us somatically forgetting our past. All parts of the body can experience the flow of bliss, I have had bliss move through the digestive system, spleen, liver, pelvis, lungs etc... I have experienced bliss throughout the entire body, but I don't ever remember my adrenal-kidney area being in bliss
The loss of memory and mental faculty experienced from bliss, expanded states and kundalini occurs because the body's forgetting chemicals: anandamide, enkephalins, endorphins are produced in large amounts in the hippocampus and amygdala, and hypothalamus (limbic system). The increase in charge through these areas heightens the body's cannaboid and optiate systems. This acts in a healing fashion, to help our Pavlov's dog brain to forget past trauma, but it can incapacitate one to varying degrees. Thing to do is to not get anxious on top of the loss of faculty because that will only increase the stress, thereby increasing the "numbing/forgetting" chemistry.
To balance out the bliss, overcome the diffusion and lack of focus and recover our edge we need to drink lots of water, reduce food intake, breath into the belly, jump into cold water to regain lucidity, take long walks in nature, get around falling water, take doses of spirulina and yerba mate etc... The Nootropic Formula listed in the supplement section might help with overcoming the bliss by stimulating higher cortical function. But I think that a serious attempt at addressing bliss overload requires more environmental stimulation, like radical sports, radical nature or radical social events to produce endogenous wakeup chemicals. I think there might be something in pinching the end of the nose, for during evolution the limbic system grew out of the olfactory system, giving the end of the nose a sharp pinch seems to wake the brain up a little.
There is a tendency while in ecstasy to think: "I better not meditate or I will increase the bliss and become a total basketcase." This is a very common situation with active kundalini. Whereas forms of meditation or focusing the energy in different parts of the brain and heart really helps us to cope with excessive bliss. You see the bliss can put one into a narcotic sleep--a mythic uroboric dreamland in which we are no longer functional to ourselves or others. One can also automatically resist the bliss and then it becomes just another thing to run from with our addictions or small-nature. However by drawing the energy up, maintaining a seat in the Mind's Eye and deep breathing one can essentially ride the dragon, (like riding the spice worms in Dune). Meditation while already blissed out with active kundalini is the most effective period for growth. There is a chance of regression, brain damage and resorting to addictions and distractions if we do not "actively cultivate" the Force. (See Mind's Eye in Down Is Up).
Neuroadaptation is the principle element of physical addiction and drug tolerance. When the brain is frequently exposed to a drug it adapts to compensate for the presence of the drug; so that if the drug is stopped, it leaves the brain 'overcompensating' and in disequilibrium in an unaccustomed way. Whatever pain or anxiety condition the drug was masking returns with a vengeance in a "rebound" experience. During kundalini ecstatic peak events and stages our brain would become neuroadapted to excessive levels of "up" chemicals, so that when that cycle is over and chemistry flips the other way we can go through an extreme withdrawal. Hence both the Dark Night experience and the exhaustion phase are often accompanied by withdrawal symptoms such as anxiety, depression, memory problems, lack of motivation, and feelings of emptiness. Because of both neuroadaptation and neuron damage kundalini awakenings can be just as much a downer trip as a high, especially to the uninformed.
Nathan Luno has an amazing website on the use of the drug Ecstasy; especially check out his neurotoxicity section. Kundalini researches might be interested in this as an info source. Specifically in the area of how like Ecstasy, kundalini might create excess dopamine release that could damage serotonin receptors in the brain. Kundalini is likely to increase the release of transmitters from synapses because of the increased charge in nerves, increased Ca2+, NO and ATP, heightened adrenaline and norepinehrine. The enzyme monoamine oxidase (MAO) breaks down the neurotransmitters norepinephrine, serotonin and dopamine in the brain. MAO's occur in high concentrations in the blood, liver, stomach, brain and intestines. During Kundalini or Ecstasy use however the brain may be so loaded with neurotransmitters that the available MAO may be insufficient to deal effectively with them. So during the extreme ecstasy (up) and dark night (down) events there is likely to be dopamine damage to the serotonin receptors, similar to that which occurs on the drug Ecstasy. "The dopamine, once in the serotonin cell, gets broken down by the monoamine oxidase into hydrogen peroxide which oxidizes a healthy cell into a deformed and no longer fully functioning one." ~ thedea.org/neurotoxicity.html
Kundalini can stimulate compulsivity, until we reach the
point where we can dive into the bliss and Emptiness without
resistance. It's like the blissed brain is seeking to drown itself in
more and more bliss. There is less self-control somehow, probably
through limbic override of the prefrontal cortex.
Since raised kundalini means an activation of the sympathetic nervous system the demand for energy generation goes up, just as it does with the fight flight response. Besides the use of glucose and fat for energy, Dr. Batmanghelidj says that that body uses water for the generation of hydroelectric energy, especially in the neurotransmission mechanisms. Thus the demand for water increases during kundalini. If however we do not drink extra water, we may read the cues for thirst as the desire for the energy to be obtained from sugar and carbohydrates. If we take in simple sugars instead of water, we will get a temporary energy boost, followed by a depletion of energy reserves. Plus since the immune system is compromised by hypertonal sympathetic activation, this means the sugar is likely to feed yeast and pathogen growth. The solution is to read Dr. Batmanghelidj's Your Body's Many Cries for Water...and drink 5 pints (10 cups) of water a day, and perhaps even more during peak events.
There are natural cannaboids in the brain (eg:anandamide), as part of the bliss, pleasure-reward, and anaethetizing/numbing function. I suspect the extra kundalini firing through the brainstem, limbic system, amygdala etc... turns on the bliss making chemistry pretty permanently. This has many consequences: modulating the raw, unrepressed emotionality that occurs on kundalini, giving a background of bliss to all kundalini events and phenomena. But it can also reduce motivation, make one loose one's sense of self, and could promote a false sense of security while one's life tumbles down around one. Considering the loss of normal adaptive left-brain functions that can occur with kundalini, the bliss gives a background of equanimity and grace, and helps to reduce the terror, worry and anxiety that would normally arise in association with incapacitation of our faculties. The world could be going to hell in a hand-basket, but it all looks wonderful to us.
The level of cannabinoids in the hypothalamus is controlled by a fat-regulating hormone, called leptin. This hormone keeps tabs on the energy status of the body and helps regulate body weight. Leptin is the primary signal through which the hypothalamus senses nutritional state and modulates food intake and energy balance. Leptin reduces food intake by upregulating appetite-reducing neuropeptides, and downregulating appetite-stimulating factors. When leptin levels are low, cannabinoid levels rise to stimulate appetite. Marijuana overwhelms the normal system and swamps the receptors, making pot smokers want to eat everything in sight.
There are three groups of opiate neuropeptides--Endorphins, Enkephalins and Dynorphins. It is the levels of these neurotransmitters in your brain that governs your mood and degree of compulsive behavior. Anything that disrupts their natural balance will interfere with character, will, morality and resolve. Insufficient enzymes available for the manufacture of these neurotransmitters will reduce their number in the brain. An increase in blood acidity decreases the permeability of the Blood Brain Barrier, this reduces the supply of the amino acids that are the precursors to these neurotransmitters. Remember body acidity rises with too much animal protein, fats and processed foods, too much coffee and soda, too little vegetables and alkaline mineral reserves, too little exercise and oxygen. Fear, anger and other negative emotions also increase body acidity. Positive ions (H+) in the air such as during a thunderstorm, in urban environments and in hot winds like the Santa ana or Chinook also increase body acidity, this explains the increase of violent behavior under these conditions.
Genetically obese people and binge eaters release abnormally large amounts of these opioid neurotransmitters in response to food. These opioids mediate the cravings for foods high in fats and sugars. The opioid receptors in the brains of these people are probably working overtime resulting in an artificially high need for these opioids. Like heroine these opioids are addictive. Substances which block the opioid receptors or prevent the breakdown of the opioids can help reduce the craving for foods high in fat and sugar. Very high doses of vitamin C such as 6–8 gms per day may reduce the addictive withdrawal symptoms of dieting or caffeine because it slows down the breakdown of the opioids in the brain. The amino acids D–phenylalanine and D–leucine both retard the breakdown of opioids in the brain so can be used to reduce food cravings and drug addiction.
I wish to add a caution against using cannabis while in active kundalini. Using dope on top of the huge increase in opiates would probably add to the general anaethetization. Leading to an inability to form a self-center of focused-ego and personal-drive. Personally I think there is so much unusual stuff going on in the transmuting body I would want to get a clear witness to the natural phenomena and unfoldment of symptoms. I however still drink coffee, which is grounding and helps the energy to return to the egoic-prefrontal lobe function in order to "fend" for oneself in the world. But even coffee on a nervous system that is in sublime reconstruction is not a good idea.
Until we stop resisting the Kundalini we may try to stimulate ourselves with sugar, caffeine and/or drown ourselves in fat and protein. Because we are more limbicly and sensorally activated we could have problems with run away urges. The increased compulsivity is the result of both the egoic self-seeking comfort for the loss of "self-ground" and running from the larger sense of being; but it is also caused by the changes that go on in the brain. We need to study this intently and work out what needs to be done in order to support our growth without becoming radically compulsive. Deliverance of our appetites to a higher power and purpose like the 12 step program might work. When we stop resisting we learn to thrive on the pure energy of our Self, and to clarify, purify, and deepen our experience of Being.
Endocannabinoids made by the body, extinguish the memory of adverse stimulation. Studies found that a process involving activation of endocannabinoid receptors is essential in the extinction of conditioned fear. The release of such opiates during the excessive firing of kundalini is one of the main ways that the brain is eventually rewired to a less hypertonal and less defensive (reptilian) nature. The synaptic plasticity to change fear related memories requires activation of NMDA receptors.
The 'endocannabinoid' system is involved in the extinguishing fear-related memories. The amygdala, is crucial in acquiring and, possibly, storing the memory of conditioned fear. The extinction of the memory of fear requires neurons in the basolateral amygdala, and changes in the strength of their connection with other neurons ('synaptic plasticity') that depend on the NMDA glutamate receptors. There seems little doubt that activation of these glutamate receptors in the basolateral amygdala is somehow required for extinction.
The receptors for the endocannabinoids anandamide and 2-arachidonylglycerol, are some of the most abundant neuromodulatory receptors in the central nervous system and are expressed at high levels in the limbic system, cerebellum and basal ganglia. The classical behavioral effects of exogenous cannabinoids such as sedation and memory changes have been correlated with the presence of these receptors in the limbic system and striatum. Endocannabinoid release serves to increase synaptic plasticity and inhibition of neuron firing.
The depolarization of neurons by repetitive activity led to the release of endocannabinoids, which diffused to the terminals of other neurons and inhibited neurotransmitter release. This effect was found to be transient in the hippocampus and cerebellum and long lasting in the striatum. The endocannabinoids reduce GABA release in interneurons of the basolateral amygdala, thereby helping to extinguish the fear-conditioned response. Not sure why inhibiting GABA release will reduce fear memory, although GABA which is normally inhibitory, sometimes works in cahoots with glutamate as an excitatory neurotransmitter. GABA release is active in the immobilization of the freeze mechanism, and the calming down after flight-fight, so GABA might serve to lock nerves into a certain fear conditioning and reduce synaptic plasticity.
Anandamide is a recently discovered messenger molecule that plays a role in pain, depression, appetite, memory, and fertility. Its name comes from ananda, the Sanskrit word for "bliss." Anandamide is synthesized enzymatically in areas of the brain that are important in memory and higher thought processes, and in areas that control movement. This implies that anandamide's function is not just to produce bliss.
The ability of brain tissue to enzymatically synthesize anandamide and the presence of specific receptors for it, suggest the presence of anandamide-containing neurons. Anandamide is an eicosanoid, that is it belongs to a group of substances that are derived from arachidonic acid, including leukotrienes, prostaglandins, and thromboxanes. Anandamide is basically a compound that reduces activity, such as reducing the formation of many stimulatory neurotransmitters. The human brain muscarinic acetylcholine receptor (mAChR), which is involved in memory function is inhibited by arachidonic acid and is also inhibited by anandamides.
Anandamide's long hydrocarbon tail makes it fat-soluble and allows it to easily slip across the hydrocarbon-rich blood-brain barrier. Its shape strongly resembles that of THC (tetrahydrocannibol, the active ingredient in marijuana), but unlike THC, anandamide is fragile. It breaks down very quickly in the body, which is why anandamide doesn't produce a perpetual natural 'high'. Scientists reasoned that since THC is not naturally present in the body, there must be a natural key molecule with a very similar shape that activates this receptor. The key was isolated by Israeli scientist Raphael Mechoulam in 1992 as being arachidonyl ethanolamide, later called 'anandamide':
Learning and memory is established by connections between nerve cells by either making new connections or breaking old ones. Repeated use of a connection makes it grow stronger while lack of use can cause the connection to be lost. Some biochemical evidence suggests that anandamide plays a role in the making and breaking of shortterm neural connections. Anandamide might be one of the bliss making chemicals that helps to produce a self-forgetfulness by which we can separate more fully from our past. Animal studies suggest that anandamide induces forgetfulness and calm. Animals treated with anandamide walk less and lay down more; they have reduced body temperature and slower respiration.
Three anandamide-like compounds were found in dark chocolate by Daniele Piomelli and co-workers at the Neurosciences Institute in San Diego [Piomelli, 1996]. www.nsi.edu Eating chocolate is not advisable due to the negative effects of sugar on protein structures, the feeding of candida, and fermenting GI Tract contents. However raw cacao beans might be just the thing for overcoming down-cycle blues. They can be purchased at www.rawfood.com as Cacao Nibs (peeled raw/organic cacao beans). Apparently raw cacao beans provide MAO inhibiters which increases the serotonin and other neurotransmitters circulating in the brain. Cacao beans are said to help reduce appetite, however we all know that marijuana increases appetite, so I don't know the role these endogenous cannabinoids have on appetite.
Anandamide is not the only THC-like molecule used for signalling in the brain. Piomelli's group has found a new molecular key that closely resembles anandamide [Piomelli, 1997]. Naturally produced sn-2 arachidonylglycerol (2-AG) can also lock into the bliss receptor. 2-AG is present at 170 times the concentration of anandamide in some regions of the brain. Piomelli thinks that 2-AG and anandamide perform complementary functions.
The endogenous cannabinoids anandamide and 2-arachidonylglycerol may be produced under distinct physiological conditions or in distinct brain regions. Anandamide activity was found to be highest in the hippocampus, followed by the thalamus, cortex, and striatum, and lowest in the cerebellum, pons, and medulla.
Outside the brain, anandamide acts as a chemical messenger between the embryo and uterus during implantation of the embryo in the uterine wall. Thus it's one of the first communications that occurs between mother and child. In animal studies the highest concentrations of anandamide were found not in the brain, but in the uterus just before embryo implantation. Anandamides play a survival role for young mammals in their instinctive suckling behavior and lack of anandamide levels can cause spontaneous abortions in mammals.
There areimportant functional relationships between endogenous cannabinoid and opioid systems. Levels of the endogenous opiate anandamide in the hypothalamus regulate compulsivity and appetite initiation. Research found endocannabinoids are involved in retrograde synaptic inhibition in the hippocampus, in long-term potentiation and memory, in the development of opiate dependence, and in the control of appetite and food intake. They also suggested the existence of as yet unidentified cannabinoid receptors in the cardiovascular and central nervous systems and in macrophage-mediated helper T cell activation.
A decrease in GABA inhibition both facilitates the induction of long-term potentiation (LTP), and promotes the hyperexcitability of epileptic seizure. Scientists investigated how the nervous system maintains its discriminating control on GABA's inhibitory effect, in order to promote memory by LTP and prevent seizure. They found that pyramidal cells, the ones towards which inhibition is directed, may regulate their own state of inhibition by sending a signal backwards across the synaptic junctions (retrograde synaptic inhibition) and thereby causing the inhibitory interneurons to stop releasing GABA temporarily. This signal from the pyramidal cell to the interneuron is the endocannabinoid molecule anandamide.
The cerebellum is a brain structure vital to many functions including learning and memory. These functions are controlled by ion channels in the Purkinje cells of the cerebellar cortex. This is a specific type of nerve cell with more branches than any other kind of nerve cell, which carries information output by the cerebellum and possess a great deal of control over the refinement of motor activities. It was found that Purkinje cells release endogenous cannabinoids in response to elevated calcium, thereby inhibiting presynaptic calcium entry and suppressing transmitter release.
These endogenous cannabinoids mediate retrograde signals from postsynaptic neurons to presynaptic terminals in the CNS. Endocannabinoids can be released from postsynaptic neurons following depolarization-induced elevation of intracellular Ca2+ concentration. The released endocannabinoids act retrogradely onto presynaptic cannabinoid CB1 receptors and suppress inhibitory or excitatory neurotransmitter release. This type of modulation has been termed depolarization-induced suppression of inhibition (DSI) or depolarization-induced suppression of excitation (DSE).
The endocannabinoid-mediated retrograde modulation is an important and widespread mechanism for the regulation of synaptic transmission in the CNS. Endocannabinoid release and resultant retrograde suppression of transmitter release are also triggered by activation of certain glutamate receptors (mGluRs) or acetylcholine receptors (mAChRs) in the postsynaptic neurons. This pathway can work independently or cooperatively of the depolarization-induced mechanism. It is shown that DSI is enhanced significantly when these glutamate and acetycholine receptors are activated simultaneously, and that this enhancement is much greater than expected and cannot be attributed to mere increases in Ca2+.
Nerve cells communicate by releasing special 'key' molecules that are intercepted by other nerve cells downstream. When the key molecule at right locks into the receptor on the surface of a nerve cell, it opens a door in the membrane that allows chloride ions to flood into the cell. This equalizes charges inside and outside the cell and prevents the cell from firing. The keys must be removed again from the lock somehow, or the nerve cell will be permanently prevented from firing. Certain enzymes are produced that remove (by degrading and destroying) the keys after a certain amount of time, so that the nerve cell can go back to work.
Drugs that have a powerful effect on the central nervous system often mimic natural molecular keys. For example, morphine is a potent pain killer that was found to lock into an 'opiate receptor' present on nerve cells and blocks enkephalins out. The body's key removing enzymes can't pry it from the receptors. The endogenus equivalent to morphine are enkephalins. Although morphine is just a forgery of enkephalins, it's much more powerful (and more addictive) than the enkephalins because the key-removing enzymes can't pry it from the receptors.
Christina Grof had an experience of morphine stopping kundalini during childbirth.
"During the birth of my first child, for which I had prepared with the Lamaze method of breathing (very much like yogic pranayama), this enormous spiritual force was released in me. Of course, I didn't understand it and was given morphine to stop it as soon as the baby was born.... Then the same thing happened when my second child was born. This all led to more and more experiences. I threw myself into yoga, although still not acknowledging it as a spiritual tool. My meeting with Swami Muktananda really blew the lid off everything. He served as a catalyst to awaken what I had been resisting, which was kundalini (the universal life force). I felt something snap inside me. A powerful force was unleashed in my body, and I began to shake uncontrollably. Electrical tremors ran from my toes and legs through my spine to the top of my head, where brilliant mosaics of white light exploded. A new, involuntary breathing rhythm overrode my practiced Lamaze pattern. I was excited and terrified. As soon as my son Nathaniel was born, I was given two shots of morphine, which returned me to normal. I felt fearful, and very embarrassed that I had cost control of myself. A more powerful version of the same thing happened two years later, when I delivered my daughter Sarah." ~ Christina Grof
Increase in vasopressin during the heart expansions and inner-conjunctions might be one of the factors involved in cortical shutdown during extreme kundalini events. Vasopressin (VP) is a peptide neurotransmitter in the limbic system synthesized in the medial amygdaloid nucleus in the presence of sex steroids, transported to other limbic structures such as the hippocampus and septum and secreted there by a calcium-dependent process. Its excitatory action on the inhibitory interneurons produces near-total shutdown of electrical activity of the efferent fibers of pyramidal cells, the projection neurons of the hippocampus.
During the Inner-Conjunction/silver cord when massive orgasmic energy streams through the body (what I call the peak of the influx stage), the dominant hormone might be the amphetamine-like love chemical Phenylethylamine (PEA). This neurotransmitter occurs during the infatuation state of romantic love to promote elevated mood, promotes alertness, confidence, openness to risk, essentially leading to a state of excitement. The levels of this stimulant also spike at orgasm and ovulation.
The drug Ecstasy (MDMA) is a phenylethylamine, and there are similarities in the symptoms of kundalini and use of Ecstasy: expanded heart, feeling of love, oneness with others, amplified senses and increased energy. Phenylethylamine along with dopamine no doubt propel us into the "super-sensoral realm" associated with the peak of awakening. When all senses are greatly heightened, one has transcendental vision, celestial music plays in one's head and the muse is practically sitting on one's shoulder. The incredible love and heart expansions that occur during the influx and transmutation are similar to the heart opening that happens on Ecstasy. Nitric oxide, oxytocin and vasopressin are probably key in the dilation of the vascular system that occurs during heart expansions.
Levels of PEA are increased by monoamine oxidase inhibitors. Moderate exercise raises PEA levels for most people. Interestingly PEA might be the agent of bliss associated with Eureka experiences, profound insight, thrill seeking and risk. As such geniuses and daredevils no doubt produce more than the average person.
Our bodies can convert the amino acid phenylalanine to tyrosine and PEA. Tyrosine is a precursor to norepinephrine and dopamine. D-phenylalanine, which does not normally occur in the body or in food, is metabolized to PEA. Although L-phenylalanine can be converted to PEA it is preferentially converted to L-tyrosine. Since D-phenylalanine is not widely available the mixture DL-phenylalanine is most often used as an anti-depressant. Because other amino acids compete with phenylalanine for entry into the brain it needs to be taken on an empty stomach. This shortens the time it takes for the brain to convert it to norepinephrine. (See Neurotransmitter Food Formula.)
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