means the hyper-charge is allowed to continue like wildfire 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. 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 maybe 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 an “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 over firing 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