NO operates as a neurotransmitter, vasodilator, and heart expander, so it is key to
increasing blood supply to heart and brain to “feed” the awakening, and is one of
the main neurotransmitters involved in the extreme kundalini events and strange
symptoms like itching, tingling, bubbles, gravity warping and kriyas.
Prolonged activation of glutamate receptors stimulates eNOS; NMDA receptor
activation can increase levels of nitric oxide and hydroxyl radicals. As a free radical
NO enables white blood cells (macrophages) to kill tumor cells and bacteria.
NO is also involved in apoptosis (programmed cell death), DNA breakage and
mutation. Thus it is undoubtedly involved in the catabolic breakdown of the
body especially during the Die-off. The highly liable NO might also be one of the
methods by which connective tissue in the body is “released” by kundalini, thus
dissolving the old body armor structure.
no anD neUrotoXicitY
While NO mediates normal synaptic transmission, excess levels of NO maybe
neurotoxic. One theory proposes that in the presence of high levels of glutamate,
nitric oxide producing neurons behave more like macrophages, releasing lethal
amounts of nitric oxide. The neurotoxic effects of NO include depressing
glycolysis, DNA damage, depletion of NAD(H) and ATP. The formation of
NO is implicated in cell death (apoptosis) through DNA damage, suppressed
mitochondrial respiration-(the electron transport chain in the mitochondrion or
Oxidative Phosphorylation), leading to energy depletion. Neurons are particularly
sensitive to impaired mitochondrial ATP synthesis capacity, because neurons depend
almost exclusively on the oxidative degradation of glucose and ketone bodies. The cells
energy molecule ATP is used by ion selective pumps to maintain the proper ion
gradients, for action potential generation in the nerves and neurotransmitter release
in presynaptic membranes.
If we maintain a high intensity of metamorphic fire we will simultaneously have
to work towards preventing neuron death by glutamate and NO neurotoxicity.
That is we must take antioxidants to prevent free radical and crosslinking damage
to cell membranes and DNA. In particular mitochondrial tissue needs to be
protected to preserve energy generation. Thus on the one hand we make sure the
fire doesn’t run out of fuel, or we would plunge into one of the forms of Dark
Night, and we simultaneously protect our tissues from the very metamorphic fire
we are feeding. In this way we should be able to manage a sustained accelerated
evolution and heightened creativity and productivity.
The fatigue that accompanies acute heart expansion is probably primarily due
to NO interfering with cellular respiration. While providing an intense burst of
neurological activity NO must then lead to exhaustion and energy depletion.
NO as an inhibitory effect on oxidative phosphorylation by blocking the electron
transport chain and controlling the levels of citrate in the Krebs cycle essentially
blocking the oxidative degradation of acetyl-CoA. Robert J. Marshall, PhD, in his
fabulous web article “The Overlooked Role of Chronic Infection in Neurodegeneration
and Its Reversal Using Nutraceutical Agents,” relates how oxidative stress leads