Some of the conditions for the initiation of kundalini appear to be:
Hyperactivation of the thyroid and parathyroids.
Hyperactivation of estrogen and testosterone (plus metabolities of T. eg: Estradiol).
Hyperactivation of the sympathetic nervous system (adrenaline, norepinephrine).Hyperactivation of the stress hormones (corticosteroids eg: cortisol, DHEA) Hyperactivation of opiate systems (endorphins, enkephalins, anandamide, phenylethylamine).
Kundalini awakenings are likely if hyper-arousal of the nervous system is kept going for several years and conditions of perpetual irritation to the brain neurons occurs. The particular blend of hormones and neurotransmitters reduces the threshold by which kundalini passes through the body. Like a river of fire, kundalini forges its own effluent cascade through the nerve tributaries and sustains itself through the changes it induces. In recent years there has been some attempt to correlate the phenomena of kindling with kundalini.
Kindling in epilepsy was first discovered accidentally by researcher Graham Goddard in 1967, while he was studying learning in rats. He found that a sustained, periodic, low-intensity stimulation of the limbic region of mammalian brains eventually sets up a cumulative resonance which increases in magnitude until the entire organism is in sympathetic resonance. Eventually these bursts of electrical activity induce similar patterns in nearby brain regions, and the seizure threshold progressively lowered. While normally the electrical stimulation he used was too low to cause any type of convulsing, he discovered that repeated exposure of brain areas to small electric shocks seem to make subsequent episodes of spontaneous seizure-like electrical events more likely to occur. After repeated stimulation at the same intensity, their brains had become sensitized to electricity, and even months later the rat would convulse when stimulated.
The name kindling was chosen because the process was likened to a log fire. While the log itself is very hard to set afire in the first place, when surrounded by smaller, pieces of wood, kindling, soon the log itself will catch fire. There is evidence that the more mood episodes a person has, the harder it is to treat each subsequent episode..." thus taking the kindling analogy one step further: that a fire which has spread is harder to put out.
The kindling sensitization hypothesis suggests that initial seizure episodes make it more likely that future seizure and depressive episodes will occur. Spontaneous kindling is more likely if there has been early damage to the brain through chemical exposure, childhood sexual or emotional abuse, or if one has inherited a sensitive nervous system. If reared in an abnormal, deprived, stressful and socially isolated environment, the limbic system neurons will atrophy and the septal nuclei, amygdala and hippocampus may develop seizure-like activity, referred to as kindling. Trauma affects our capacity for cortical control over the limbic system to regulate bodily homeostatsis. This includes unusual patterns of cortisol, norepinepherine, and dopamine metabolite excretion; the role of serotonergic and opioid systems (arousal and numbing); receptor modification by processes such as kindling; and involvement of central pathways involved in the integration of perception, memory and arousal.
Kindling can start only in the limbic brain where it progresses from the amygdala, then to the amygdala on the other side of the brain, to the hippocampus, to the occipital cortex, and finally to the frontal cortex. In fetal brain development the limbic or emotional brain predates the development of the cortex or "seat of intelligence". The brain's limbic system modulates emotions and memory organization systems, balance, gastrointestinal motility, the autonomic nervous system, and the auditory and visual integration of stimuli.
While kindling was originally thought to be a model of epilepsy, John Gaito of York University has reported that a different mechanism is apparently involved since the amino acid, taurine, which suppresses epileptic seizures in laboratory animals, does not prevent phenomena caused by kindling. Also, kindling apparently causes permanent changes in the neural circuitry.
Kundalini has elements similar to the kindling phenomena, and yet runs through a very complicated sequence of "events." The article: "Kindling, once epilepsy model, may relate to kundalini," Brain/ Mind Bulletin, Vol. 2, No.7, February 21, 1977; pp. 1-2.) reports on the convulsion-like phenomenon called kundalini. At the Max Planck Institute in Germany, subjects reported "electrical sensations, tingling, inner lights, even convulsions usually followed over a period of time by a moderation of 'symptoms' and apparent alterations in the central nervous system." This article says that the kundalini phenomena typically occurs after a period of meditation in a setting that is non-threatening. This report suggests that while meditating, the individual tries to arrest all thought or cortical activity, thus allowing the evolutionary more primitive areas of the brain to assert itself. The Kindling Model is one of the current interpretations of PTSD. The scientists concluded that those who experienced the kundalini phenomenon were actually reexperiencing primal pain laid down before the brain has completely developed (See Toxic Mind Theory).
Periods of cycling may begin with an environmental stressor, but if the cycles continue or occur unchecked, the brain becomes kindled or sensitized. With repetitive use pathways inside the central nervous system are reinforced so to speak--and future more frequent episodes of depression, hypomania, or mania will occur by themselves independent of an outside stimulus. Thus, to put it simply, brain cells that have once been involved in an seizure episode are more likely to do so again, and more cells will become sensitized over time. Goddard demonstrated that it was possible to induce kindling chemically as well through repeated small exposures to inhaled toxins; or single overwhelming exposures of chemical, visual, auditory, electrical stimulation. It has been shown that substances such as cocaine and alcohol have their own kindling effects which can contribute to bipolar kindling.
As a result of many studies involving the kindling model, many researchers now believe that kindling contributes to both rapid mood cycling and treatment-resistant bipolar disorder. This kindling model also is consistent with cases where cycling began with definite mood triggers, stressful or exciting events, and later became spontaneous. Researchers concluded that there was a need for early and aggressive treatment of bipolar disorder, to prevent the brain from becoming more and more sensitized and going into rapid cycling or manic depression.
A seizure is a sudden involuntary alteration in perception or behavior caused by an abnormal synchronized discharge of cortical neurons in the central nervous system. Epilepsy, on the other hand, refers to chronic recurrent seizures from a primary underlying brain abnormality. Seizures can be attributed to a number of causes including metabolic abnormalities, infections, nutritional deficiencies, or trauma. Emotional stress and sleep deprivation also increase the frequency of seizures, but most seizures occur due to unknown reasons. Seizures can be broadly classified into two major categories: partial, involving onset from a discrete area of the brain that may or may not secondarily generalize to the rest of the brain, and primary generalized, involving simultaneous onset from both hemispheres.
What is really interesting is that pulsed repetitions of telepathic senders have also been shown to increase the reception of telepathic messages. Thus the kindling effect apparently applies to the paranormal channel as well as to more orthodox transmission channels.
The two primary regions of the brain that are involved in epilepsy are the cerebral neocortex and the hippocampus. In the neocortex, excitatory synapses are made primarily on the dendritic spines and shaft. The release of neurotransmitters at these sites gives rise to excitatory postsynaptic potentials. The inhibitory synapses are more prominent on the soma or proximal dendrites, and give rise to inhibitory postsynaptic potentials. Abnormal neuronal excitation is thought to occur as a result of disruption of the depolarization and repolarization mechanisms of the cell. Aberrant neuronal networks develop abnormal synchronization resulting in the propagation of an epileptic seizure.
The primary excitatory neurotransmitters in the central nervous system are the amino acids glutamate and aspartate. The primary inhibitory neurotransmitters in the central nervous system are gamma-aminobutyric acid (GABA) and glycine. Excitatory neurotransmitters usually act by opening Na+ or Ca2+ channels, whereas inhibitory neurotransmitters usually open K+ or Cl- channels. Glial are mainly responsible for K+ reuptake.
It seems that one of the mechanisms of kundalini may be the overstimulation of the neuro-inhibitory glycine and GABA receptors in the spine and brainstem, during the hyper-activation of the sympathetic nervous system. This dis-inhibition means the hyper-charge is allowed to continue like wild-fire because the "off switch" has essentially been rendered ineffective. Simply upping one's glycine intake doesn't return neuron inhibition back to normal. Kundalini abates when the glycine receptors themselves become operational again, once the hyper-charge of kundalini up the spine reduces, perhaps when the fire runs out of fuel. Thus kundalini awakening ends when the "charge" reduces and the "glycine receptors" are once more fully receptive and able to do their neuro-inhibiting job.
Compounding this, it might be that when the free radical load goes up with the onset of kundalini, glycine is pulled from all readily available sources in order to make the antioxidant Glutathione (ie: glycine + glutamic acid + cysteine). The cerebrospinal fluid (CSF) would be one of those sources since it contains 100mg of glycine for 100ml of fluid. This reduction in CSF-glycine would further reduce the inhibition of nerve firing up the spine. The wild fire would thus burn until it burns itself out.
Glycine is an inhibitory neurotransmitter in the central nervous system especially in the spinal cord. The cerebrospinal fluid contains 100 mg of glycine per 100 ml. When glycine receptors are activated, chloride ions enter the neuron and the cell membrane undergoes hyperpolarization, which inhibits the neuron. In seizures the brain naturally accumulates more glycine at the seizure site in order to protect itself by inhibiting neuron firing.
It may be that during the inner-conjunction the kundalini ignition up the spine is so intense that the inhibitory neurotransmitter glycine may have failed to stop the cascade of electro-chemical reactions that constitutes the awakening. The force of the kundalini cascade may overwhelm the normal nerve inhibition of glycine by rendering the glycine receptors useless or "disinhibited." The poison strychnine causes convulsions for this reason. B-alanine and taurine also activate glycine receptors but with lower inhibitory capacity.
In the brain, glutamine is precursor to glutamate is a "on-switch" neurotransmitter, it is also the precursor to GABA which is an "off-switch" neurotransmitter. Lower GABA correspond to increased seizures and epilepsy. Anti-seizure medications work by increasing levels of the inhibitory neurotransmitter GABA in the temporal lobes, calming neuronal activity and inhibit nerve cells from overfiring or firing erratically. Glutamic acid decarboxylase (GAD) is the rate limiting enzyme responsible for conversion of glutamate to gamma-aminobutyric acid (GABA) regulating levels of glutamate and GABA in the mammalian brain. GABA can be taken as a supplement (L-Glutamine), produces a calming effect on people who struggle with temporal lobe symptoms like temper, irritability, and anxiety.
Many people with temporal lobe problems also suffer from memory problems, which can be helped with Phosphatidyl Serine (PS), Gingko Biloba and Vitamin E. Brain GABA levels depend on both zinc and vitamin B6. Consequently, zinc deficiency may increase the risk of seizures by reducing brain GABA.
Glutamate concentrations in the brain are higher in some seizure patients, and these concentrations can increase to potentially neurotoxic concentrations during seizures causing cell death. One study showed that with a higher dose of B6 (10 mg/kg), the CSF glutamic acid was normalized. It was concluded that the optimal dose of B6 for epileptics should be the dose that normalizes CSF glutamate levels, not just the control of seizures.
Glutamate is the principal excitatory neurotransmitter in the brain thus it inevitably plays a role in the initiation and spread of seizure activity. The process of "kindling" limbic seizures in rodents by repeated electrical stimulation is dependent on activation of N-methyl-D- aspartate (NMDA) receptors. The function of these receptors is enhanced in the hippocampus of kindled rats and in the cerebral cortex of patients with focal epilepsy.
It is probable that the adrenocorticotrophin releasing hormone system in the central nervous system is mainly distributed in the limbic system, and glutamate might be one of the trigger factors to induce excessive stress response in the hypothalamus-pituitary-adrenal axis. Acute mania is accompanied by elevated glutamate/glutamine levels within the left dorsolateral prefrontal cortex. Glutamate and aspartate NMDA receptor antagonists are one potential mechanism for anticonvulsants.
Psychosis could result from AMPA receptor activation caused by overactivity of the glutamatergic system, due to reduced GABAergic inhibitory control. Expression of messenger RNA for the GABA synthesizing enzyme in the prefrontal cortex and the number of GABAergic neurons in the hippocampus are reduced in schizophrenia and bipolar disorder. GABAa receptor drugs, which activate Cl-, appear more effective as anticonvulsants than GABAb receptor agents, which activate K+. Apparent the GABAa receptor is involved in epilepsy due to its role in the synchronization or desynchronization of thalamus-cortical pathways. The oscillatory and burst-firing of these circuits is attributed to neurons in the thalamus and leads to synchronization and desynchronization of the EEG.
Dr. Stephen Lasley found that brains of rats that are genetically prone to seizures also have reduced levels of taurine as well as increased levels of aspartate. Therefore, I believe that avoidance of aspartame should be a key element in an anti-seizure diet. Also, taurine, in doses of 1-3 grams per day may be helpful.
If kundalini starts and you really don't want it then cut all carbs from your diet for 2 weeks, and this should suspend the cascade of change. If stopping the consumption of carbohydrates stops or lessens the progression of kundalini metabolism, this then points to the mechanism of kundalini itself. It is therefore apparent that kundalini is fueled it seems by the burning of glucose "glycolosis" and less so or not at all by ketosis or the burning of fat. Glucose is taken up by glial cells and metabolized by glycolysis to lactate and pyruvate, which are then released as substrates for oxidative phosphorylation in the neurons. Within the brain, glycogen is primarily stored in glial cless, Glycogen stores in the brain are low compared to liver and muscle however the glycogen turnover is very rapid.
Glycolysis is the conversion of glucose to pyruvate and lactate resulting in the net production of only 2 mol of ATP. Pyruvate can enter the Krebs cycle and produce 30 mol of ATP via the mitochondrial oxidative phosphorylation cascade. Hence the energetic value of oxidative phosphorylation over glycolysis is obvious. In the early stages of activation the increased energy demand is met by glycolysis rather than oxidative phosphorylation. It was found with PET scans that glucose utilization in activated cortical areas was not matched by an equivalent increase in oxygen consumption, because Glycolysis does not require oxygen to function.
Glucose is the energy fuel for the brain and is almost entirely oxidized to CO2 and H2O. A quarter of the total body's glucose is utilized by the brain although the brain only represents 2% of the body weight. Glucose can be incorporated into lipids, proteins and glycogen, and it is also the precursor to certain neurotransmitters such as GABA, glutamate and acetylcholine. GABA and glutamate serve to regulate the excitability of virtually all neurons in the brain. GABA and glycine are the most important inhibitory neurotransmitters in the brainstem and spinal cord. The neurotransmitter glutamate is derived from glucose, and I think that glutamate is probably the primary neurotransmitter involved in the changes in the conveyance of energy through the nerves.
I propose that Nitric Oxide is produced in excess during certain hyper-kundalini events causing a hypersensitivity to glutamate NMDA receptors and this produces the most radical peak experiences and pivotal height of the awakening cycle itself. Energy metabolism may be controlled by specific neurotransmitters such as norepinephrine (NE). Cell bodies of NE-containing neurons are localized in the brainstem from which axons project to various regions of the brain including the cerebral cortex. Hence the noradrenergic system could regulate energy homeostasis globally in the brain.
Polarity is vitally important for living cells, hence they continually work to generate and maintain regions of differing electrical properties against continual leakage of charge. In fact, the ceaseless work involved in achieving and maintaining these electrical needs consumes some 50Ð60% of the metabolic activity of the cell.
"When our cells are functioning normally, a proton (H+, a hydrogen atom with its positive charge) gradient exists across the oxygen-using parts of our cells, which keep out calcium and sodium ions. But when these oxygen-using parts, the mitochondria, are unable to make ATP, they cannot keep up the gradient. Sodium and calcium ions rush into the cell in a fatal process of cell damage called necrosis. (269) If damage caused by these [oxidative] reactants is not reversed to normal, there will be decreases in the capacity to generate ATP, lower global biochemical activity, and reduced use of free energy. The oxidative poisoning can lead to cell damage or trigger the mechanism of cell self-destruction call apoptosis. (271) Levels of the intracellular antioxidant glutathione fall when ATP is not around. Lowered ATP thus reduces the cell's ability to make more of the ATP it needs more than ever." 270, Eric Schneider & Dorion Sagan, Into the Cool: Energy Flow, Thermodynamics and Life. University of Chicago, 2005
Ketogenesis is the process by which ketone bodies are produced as a result of fatty acid breakdown. Ketogenesis may or may not occur, dependent on how many carbohydrates are available. Ketone body formation occurs as an alternative energy source during times of prolonged stress e.g. starvation. The initiating event is a change in the ratio of glucagon:insulin in the blood. Insulin deficiency triggers the lipolytic process in adipose tissue with the result that free fatty acids pass into the plasma for uptake by liver and other tissues. Glucagon appears to be the primary hormone involved in the induction of fatty acid oxidation and ketogenesis in the liver. It insures that long-chain fatty acids can be transported through the inner mitochondrial membrane to the enzymes of fatty acid oxidation and ketogenesis.
Ketone bodies are produced mainly in the mitochondria of liver cells when carbohydrates are so scarce that energy must be obtained from breaking down fatty acids. Fatty acids are long chains of carbons with an acid group on one end. The body gets energy from fatty acids by breaking the carbon chain down into pieces that contain only two carbon atoms. These pieces are in the form of acetyl-CoA. When the body has no carbohydrates available, fat instead must be broken down into acetyl-CoA in order to get energy. CoA is not being recycled through the citric acid cycle: it is being attached to more and more acetyl groups. You need more CoA to keep breaking down fats, and the only place to get it is from all those acetyl-CoA molecules, by attaching them to each other to get the CoA to fall off. A large amount of energy is released during this process, which can be used for muscle contraction and all of the other activities in the cell.
L-carnitine acts to increase energy by carrying fat across the cell membrane and into the mitochondria. Energy is then stored as ATP. It reduces the metabolites of fats (ketones) in the blood from incomplete fat metabolism and reduces hyperammonemia.
Patients suffering from temporal lobe epilepsy (TLE), experienced increased extracellular glutamate levels in the hippocampus both during and after clinical seizures. These increased glutamate levels could be the result of malfunctioning and/or downregulation of glutamate transporters, indicating impaired clearance of glutamate released by neurons. Glutamate is predominantly cleared by glial cells through the excitatory amino acid transporter 2 (EAAT2) and its subsequent conversion to glutamine by the glial enzyme glutamine synthetase.
Cerebrospinal Fluid, limbic, temporal and striatum glutamine concentrations are implicated in schizophrenia, bipolar disorder and major depression. The answer, it appears, is by cleaning up their synapses. For LTP to occur, a presynaptic neuron must release the glutamate in a continuous manner. Normally, glutamate is removed from the synaptic cleft by housekeeping proteins, known as glutamate transporters, in the postsynaptic neuron. Suspecting that this glutamate-removal system might play a role in maintaining input specificity,
An increase in the extracellular concentration of glutamate and aspartate before or during seizure onset, suggesting that either enhanced amino acid release or impaired uptake contributes to seizure initiation. Glutamate antagonists are potent anticonvulsants and provide significant protection against brain damage following stroke or traumatic injury, but can have cognitive side effects. Anticonvulsant compounds which act on sodium channels and reduce ischemia-induced glutamate release, are cerebroprotective but are free from the cognitive side effects of NMDA-receptor antagonists.
In developing a supplemental protocol for kundalini we would do well to consider Ward Deans article Seizures: A Nutritional Approach at www.vrp.com/
For seizure Ward Dean M.D. suggests:
Magnesium: 500-1,000 mg/day, Selenium: 100-200 mcg/day, Taurine: 1-3 gm/day, L-carnitine: 1-3 gm/day, GABA 500-1,000 mg/day, Vitamin E: 400-800 IU/day, DMG (dimethylglycine): 50-200 mg/day, Pregnenolone: 100-500 mg/day, Kava Kava: 200-800 mg/day; Vitamin B complex, w/special emphasis on: Vitamin B1: 50-100 mg/day, Vitamin B6: 200-500 mg/day, Folic Acid: 400-1,000 mcg/day
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