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 over activity
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 maybe helpful.
enerGY Generation
If kundalini starts and you really don’t want it then cut all carbohydrates from
your diet for 2 weeks, and this should suspend the rapid 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
“glycolysis” 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 cells, 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