The following ties together much of what I have
written on the possible physiology of kundalini so far and is the most
speculative piece in this book. I am pretty sure that
convulsive/seizure/kindling can actually produce ammonia, as well as be
caused by ammonia. If so this could be one of the main causes of people
running into extended periods of difficulty with kundalini. The good
news is that the problem is relatively easily addressed once we know
the mechanism. I would like to point out that I am not saying that
kundalini is epileptic seizures or is caused by ammonia. But that until
we get research done specifically for kundalini, I am using the
knowledge of various phenomena like epilepsy to arrive at a deeper
understanding of what might be happening.
Research will need to be undertaken to see how early childhood trauma
affects brain development, PTSD, spiritual emergences and the kundalini
phenomena. I have observed an interesting cyclic phenomena in my friend
Jim, whom I assume has an over active basal ganglia and limbic system
due to childhood trauma. (The striatum of the basal ganglia uses
glutamate as its excitatory neurotransmitter and GABA as its inhibitory
neurotransmitter.) In his 40's Jim had a spiritual awakening that
subsequently catalyzed ongoing spontaneous repetitive cycles of
debilitating chemistry over several years. When I met Jim the duration
of his advanced stage cycle was roughly about 4-5 days.
Simply put these cycles appear to be kicked off with HPA axis,
autonomic and limbic brain activation similar to a fight or flight
response. This first produces a sense of panic, tightness in the
diaphragm and shortness of breath. Associated with the initial phase is
an intense expansive energy in the solar plexus*, shooting jolts of
electrical nerve energy and kriya-type convulsive movements. (*Note the
enteric brain uses the major neurotransmitters: dopamine, serotonin,
acetylcholine, nitric oxide and norepinephrine. We should question
whether the enteric brain can be kindled and become hypertonal and how
this affects digestion and assimilation.) This hyperactivation of the
sympathetic nervous system seemed to precipitate the production of ammonia,
which I detected on his breath; strongly for one day and tapering off
the next. I theorized that the ammonia was probably a byproduct of glucogneogenesis as the body shifted from normal glucose energy generation (glycolysis) to the emergency mode of the breakdown of protein and fats in the skeletal muscle during fight or flight activation.
Ammonia is produced during gluconeogenesis ie: the breakdown of fats
and proteins for energy, rather than the utilization of sugar/carbs.
Gluconeogenesis is often detected by athletes when they do a hard
workout as ammonia smelling sweat, due to the catabolic breakdown of
fats and protein in the muscles. Vigorously exercised skeletal muscles
operate anaerobically, producing pyruvate and lactate from glycolysis
as well as ammonia from protein breakdown. These products must find
their way to the liver, where pyruvate and lactate are incorporated
into glucose, which is returned to the muscles. The energetic burden of
gluconeogenesis is thus imposed on the liver rather than the muscle, so
all available ATP in muscle is devoted to muscle contraction for
movement. Gluconeogenesis thus takes place in the liver and muscle
cells of the body, and for this process the cell uses many of the
enzymes of sugar burning (glycolysis), operating in the reverse
direction.
As well as gluconeogenesis, in many tissues including the brain,
some processes such as nucleotide (RNA, DNA) degradation generate free
ammonia. Most of the free urinary ammonia is produced in the kidneys by
the deamination of amino acids, particularly glutamine, and
utilized for hydrogen ion excretion as part of the pH regulatory
system. Since the body cannot obtain usable energy from the nitrogen in
amino acids, the nitrogen must be removed before the carbon skeleton
(ketoacids) can be used. Deamination involves removing the amino group
from amino acids, whereupon the nitrogen from these amino groups is
transfered to glutamate, which can then be released as ammonia in the
glutamate dehydrogenase reaction. This removed nitrogen is used to form
urea in the liver, which is sent to the kidneys to be excreted.
To illustrate the symptoms of ammonia in the body by extreme
example, the ingestion of massive doses of ammonium chloride by human
adults resulted in headache, insomnia, nausea, diarrhea, glucose
intolerance, and increased urinary output of magnesium, calcium and
phosphate. Generally a large intravenous dose of ammonia can produce
immediate hyperventilation, loss of equilibrium, convulsions, coma, and
death. Hyperammonemic disorders such as acute liver or kidney failure
are associated with hyperexcitability, seizures, brain edema and
increased extracellular brain glutamate (due to intracellular
alkalization and mobilization of intracellular Ca 2+ stores). Acute
ammonia exposure leads to activation of N-methyl-D-aspartate (NMDA)
receptors and their signal transduction pathways. In animal experiments
ammonia induced death is prevented by pretreatment with NMDA receptor
antagonists. Chronic hyperammonemia also results in increased
concentrations of neuroactive L-tryptophan metabolites including
serotonin and quinolinic acid.
Acetyl-L-Carnitine is structurally similar to acetylcholine and like
acetylcholine it stimulates brain cell production, stabilizes cell
membranes, is a powerful antioxidant and alleviates depression. What is
more, acute ammonia and glutamate toxicity can be prevented with
carnitine in animal studies. Studies show that acetyl-L-carnitine
prevents neurotoxic damage done by ammonia and glutamate. It was found
that betaine, trimethylamine-N-oxide, choline, acetylcholine, carbachol
and acetyl-L-carnitine prevent ammonia toxicity in mice. "These results support the idea that acute ammonia toxicity is mediated by activation of N-methyl-D-aspartate (NMDA) receptors
and that glutamate neurotoxicity could be prevented by activating
metabotropic glutamate receptors and/or muscarinic receptors." http://jpet.aspetjournals.org/cgi/content/abstract/279/1/194
During the time in which Jim was producing excess ammonia he
exhibited muscle weakness, a flaccid limpness, fatigue and a loss of
Presence. This extra ammonia in the blood then made his breathing even
more difficult with a burning sensation in the lungs and possible
oxygen deprivation in the tissues. Giving the sensation that no matter
how much he breathed he still could not get enough oxygen. The effect
of ammonia on the brain is loss of cognition, reduced focus and clarity
resulting in diminished motivation, loss of sense of self, diffusion of
being and heightened emotionality along with extreme fatigue--such that
these cycles would literally take over his life. He was victim to
chemical processes that seemed beyond his control.
Jim fell into this pattern of spontaneous hyperarousal in midlife
perhaps because he was given inadequate spiritual-emotional-physical
"holding" in childhood, coupled with abuse. Therefore his nervous
system didn't get the chance to develop a strong parasympathetic rest
and recovery pattern. Consequently his hypertonal nervous system led to
the slow depletion of body resources, metabolic weakness and the
propensity to kindle into the volatile repetitive cycle after his
spiritual initiation began.
Stress occurs when the body's normal homeostasis has been
disturbed and this stress produces an overabundance of chemicals that
lead to negative emotions, fear and depression, such as monoamine
oxydase (MAO), cortisol and adenosine GMP, which in turn lowers our
motivational resources and will to live. The liver and kidneys have
extra work to do to process the stress chemistry, ammonia and other
metabolites of gluconeogenesis such as lactic acid. Stress and sleep
deprivation increase epilepsy. Since the stress hormone CRH can
producing kindling itself and lower resistance to irritants efforts
need to be made to remove stress from ones lifestyle.
I advised Jim to hit the phenomena from several angles to try to
stop the cycling. This could be approached by first avoiding the
initiation of the cycles, diminishing the damage done by the byproducts
of the chemistry and rebuilding the total organism from the metabolic
exhaustion of chronic stress. Since I personally felt the raw intensity
of the energy passing through the nerves in his arms and shoulders
during the electrical convulsion phase, I suggested he build up the myelin
in his nerve sheaths with choline (B-complex), lethicin, fish oil and
DMAE. This would also help to boost levels of the calming and
inhibiting neurotransmitter acetylcholine (ACh). Also the
adaptogenic herb Ashwagandha root inhibits acetylcholinesterase, an
enzyme which breaks down acetylcholine. The neurotransmitter of the
preganglionic sympathetic neurons is acetylcholine (ACh); it stimulates
action potentials in the postganglionic neurons, affecting their
targets through adrenergic receptors. Acetylcholine is involved in
muscle contraction while glycine is the neurotransmitter for muscle
relaxation. When we overwork the other neurotransmitters we burn out
our acetylcholine as well.
Myelin is a fatty substance that includes acetylcholine. Since the
myelin sheath is what facilitates `speed' in the transmission of a
nerve impulse, the impairment of our myelin slows down our brain. Glial
cells produce this fatty insulating myelin sheath around axons to
insulate one neuron from another, forming a matrix surrounding neurons
and holding them in place. This matrix serves to isolate synapses
limiting the dispersion of transmitter substances released. Reduction
in the strength of myelin sheaths through exhaustion of acetylcholine
during a stressful life probably increases the propensity toward nerves
falling into the synchronous firing patterns of seizure and kindling.
Both dehydration and the extremes of high and low blood sugar
increase the stress hormone cortisol, which could trigger off Jim's
neurological cycle; and cortisol decreases fasting blood glucose. So
blood sugar must be carefully managed to prevent the body going into
stress/panic mode and kicking off a cycle. High blood sugar also makes
the kidneys filter too much blood and such overwork reduces their
filtering capacity. The vagus nerve of the parasympathetic nervous
system is affected by poor kidney function. Tight muscles at the base
of the skull can impinge on the vagus, and malfunction of the kidneys
can induce these neck muscles to contract. If too much potassium (K+)
is excreted blood levels of potassium are reduced creating alkaline
urine. This alkaline urine reduces the amount of ammonia that is
removed from the blood via the kidneys.
We know ammonia increases seizures and convulsions, but we also need
to find out if seizures and convulsions actually produce ammonia.
Glutamine protects the brain and body from ammonia toxicity. If serum
ammonia levels increase the body uses more glutamine to reduce
ammonia levels in the brain. High levels of NH4+ lead to increased
levels of glutamine, which serves as an osmotically active solute
swelling glial cells. Thus ammonia in the brain leads to glial cell
swelling which reduces their function and causes confusion and pressure
in the head. There are 10X more glial cells than neurons--they act like
liquid crystals resonating in harmony with the surrounding electrical
fields. They act as semiconductors, picking up faint electrical
impulses from the nervous system and the environment and amplifying
them thousands of times--tuning impulses to the proper frequency for
the neurons. Obviously glial cell swelling interferes with this tuning
process and other glial cell functions.
Fast and efficient enzyme systems usually maintain low tissue levels
of ammonia, these enzymes primarily include glutamate dehydrogenase,
glutamine synthase and carbamoyl phosphate synthetase. Magnesium
activates glutamine synthetase, a key enzyme that helps cells dispose
of ammonia. Chlorophyll is thought to act as a "body cleanser," neutralizing toxins such as ammonia and carbon monoxide by many mechanisms. Wheatgrass
is also one of the richest sources of vitamins A, B, and C. It is a
source for calcium, iron, magnesium, phosphorus, potassium, sodium,
sulfur, cobalt, zinc, and protein. Eat 3-4 stalks of celery per day for
the duration of any period of hyper-sympathetic stimulation especially
if you have high blood pressure or pressure in the head. This will help
with kidney function, electrolyte balance and celery is also a sex
tonic. Because celery removes excess uric acid from the blood, it might
also help the ammonia situation as well.
I suggested Jim supplement with Glutamine to serve as a
carrier to remove the ammonia. Peripheral tissues may also remove
ammonia from the blood by metabolically incorporating it into
glutamine. Glutamine is freely permeable and may transfer ammonia to
other tissues for nitrogen transfer reactions or for metabolic
degradation via the urea cycle. Substrates of the urea cycle, such as
arginine, citrulline and ornithine, are also reported to act as
protective agents against ammonia toxicity, possibly by stimulating
urea formation. Ornithine may help reduce elevated ammonia levels seen
after exercise, reducing fatigue. 500mg of L-Arginine or ornithine in the morning neutralizes ammonia (NH3) in the liver, the body and in urine.
Glutamine is also a precursor to the inhibitory neurotansmitter
GABA, which is the principle fast inhibitor of the forebrain and is an
anticonvulsant. (I did find one reference to ammonia actually
increasing GABA and this will change the way other neurotransmitters
are used.) It appears that seizure activity might be associated with
increased levels of GABA but less GABA receptor binding. Reduced GABA receptor binding
causes a disinhibition of action potentials leading to high voltage
synchronous firing. If it is the sensitivity of GABA receptors that we
need to enhance in order to stop excess firing in the basal ganglia and
brain stem then perhaps S-adenosylmethionine (SAMe) would help.
Long-term supplementation with SAMe repairs cell membrane fluidity and
enhances the sensitivity of prolactin receptors, as well as GABA and
beta-receptors and probably serotonin and dopamine receptors as well.
When there is excess stimulation by excitatory neurotransmitters or insufficient inhibition, excess Ca++ entry
into the neuron reduces K+ channel opening, which raises the neuronal
resting potential threshold such that 10-15 times the duration of
normal action potential occurs. This extended duration could also be a
factor in kindling seizure activity and the maintenance of "hot focal"
areas of hypertonality in the brain. Also there is the possibility that
the synchronization of discharge amplifies the power as well as the
duration of action potentials. "Synchronized and rhythmic action
potential discharge (in particular, in the 30-60 Hz band) may increase
postsynaptic impact of neurons--their punch--without necessarily
altering their average firing rate." 309, Christof Koch, The Quest For Consciousness.
Neurotransmitters that are pro-convulsant and may be involved in
epilepsy are: Corticotrophin, Thyrotropin releasing hormone (TRH),
while anti-convulsants are oxytocin, ACTH, vasopressin and especially
B-Endorphin. Other peptides that may be involved are Acetylcholine
(ACh), glutamate, aspartate and taurine. (BTW taurine helps in synaptic
recovery.)
Jim's kidney function needs to be addressed in order to
manage blood pressure, for high blood pressure will in turn reduce
kidney function. One of his symptoms is increased thirst perhaps due to
dehydration from excessive urination and increased loss of potassium in
urine (Hypokalemia). The kidneys are the chief regulators of our body
potassium, keeping the blood levels steady even with wide variation in
dietary intake.
Dr. Max Gerson the living-food cancer doctor, considered the balance
of sodium and potassium in the body to be the most important
electrolyte balance. "Between the potassium and sodium there is the
exchange, a sort of energy flow. If potassium is lost from the cell
system and sodium penetrates, you lose the energy flow." Sodium is
an enzyme inhibitor, therefore a poison. All toxins are defined as
enzyme inhibitors. Potassium is the enzyme activator or catalyst. "If
the potassium is lost from the cells and sodium penetrates, now the
enzyme inhibitor or toxin penetrates the cell and the cell doesn't
function properly." Gerson went as far to say that all chronic diseases exhibit a loss of potassium from the cells.
A high-sodium diet with low potassium (K) intake influences
vascular volume and tends to elevate the blood pressure. Foods grown on
poorly fertilized soils and cooked foods tend to have a higher
sodium-to-potassium ratio. I thus advised foods high in potassium such
as organic spinach, parsley, lettuce, broccoli, peas, lima beans,
tomatoes, and potatoes. Vegetables especially the skins all have
significant levels of potassium. Fruits high in potassium include
oranges and other citrus fruits, bananas, apples, avocados, raisins,
and apricots, particularly when dried. Those with kidney disease might
have too high levels of serum potassium, but Dr. Gerson found that
those with high serum levels of potassium still were K deficient inside
their cells. By giving them high potassium juices he found that these
patients lost the extra fluid caused by sodium retention.
I assume that a lowered stress threshold or stressful life would
cause excess potassium to be excreted through the effect of cortisol on
the kidneys. The adrenal hormone aldosterone stimulates elimination of
potassium by the kidneys. Also alcohol, coffee, sugar, and diuretic
drugs cause potassium loss, contributing to lowered blood potassium.
About 95% of the potassium in the body is stored within cells, while
sodium and chloride are predominantly located outside in the fluid that
surrounds your cells. Potassium is involved in the storage of
carbohydrates for use by muscles as fuel. It is also important in
maintaining the body's proper electrolyte and acid-base (pH) balance.
Potassium is especially important in regulating muscle contraction
and nerve transmission. The frequency and degree to which our muscles
contract, and the degree to which our nerves become excitable, both
depend heavily on the "right amount" of potassium. Many of our muscle
and nerve cells have specialized channels for moving potassium in and
out of the cell. Sometimes potassium moves freely in and out, and
sometimes a special energy-driven pump is required. When the movement
of potassium is blocked, or when potassium is deficient in the diet,
activity of both muscles and nerves can become compromised.
Through a mechanism known as the "sodium-potassium pump," sodium and
potassium work together closely to initiate muscle contraction and
nerve transmission, and to maintain the body's normal distribution of
fluid. During muscle contraction and nerve transmission, potassium
leaves the cell and sodium enters the cell via the "sodium-potassium
pump." This transfer causes a change in electrical charge within the
cell, which initiates the muscle contraction or the nerve impulse.
Because sodium attracts water, once the muscle contraction or nerve
impulse is initiated, the sodium is immediately pumped out of the cell
to prevent water from entering the cell and causing it to swell or
burst, and the potassium is pumped back into the cell.
If these ammonia/kindling cycles are due to the body running down in
resources after years of chronic stress, then the first order of
business should be to stimulate anabolic building chemistry. So I
emphasized to Jim that his protocol should focus on pulling out of the
exhaustion phase by generally building up the mineral, protein and
enzyme resources of the body with wheatgrass juice, spirulina and
sprouts. For I predicted that the body would be more likely to be able
to self-regulate normal homeostasis if given super-nutrition and
thereby stop the disturbing cascade of emergency-mode cycling. Raw
green as in wheatgrass juice is needed to build up the O2
carrying capacity of the blood. Then the electrolytes will correct
themselves and acidosis is prevented.
In an hypoxia (O2 deprivation) condition the cells are not
generating enough ATP to keep up the electrolyte gradient so there is
too much sodium in cells/neurons...leading to lack of action potential
in the nerves which leads to atrophication of cells. The breakdown
products of these dead cells then increases acidosis, hypoxia,
electrolyte imbalance, enervation...resulting in fatigue, depression.
The reduction in ATP production by the cells due to ammonia is probably
interferes with the exchange of nutrients into cells and toxins out of
cells. The fastest most balancing thing for this is wheatgrass. I
suggest starting with 1oz in the morning and other in the afternoon,
and build up to 2oz in the morning and another 2oz in the
afternoon...this is the fastest way for you to attack all bases and
balance your condition. Along with the wheatgrass juice you might also
consider taking 3 spirulina/kelp/slippery elm capsules that you make
yourself.
Jim experienced fatigue during the ammonia production phase
because ammonia interferes with mitochondrial energy production. Excess
ammonia hinders the oxidative metabolism of neurons and reduces the
production of the energy molecule ATP. Reduced levels of ATP would
contribute to fatigue and would also make the muscle tone become limp
and flaccid. In addition, ammonia gives rise to very harmful
nitrogen-based free radicals which can interrupt the electron transport
chain in the in the Krebs Cycle performed within the mitochondria. The
Krebs cycle is a system of removing H2 from foodstuffs which
are then combusted to water and the free energy obtained is used to
form ATP. Evidence points to ammonia interfering with energy metabolism
in the brain either by depletion of the Krebs cycle intermediates or by
reduction of ATP or NADH and subsequent effects on neurotransmitter
availability.
Caffeine should be generally avoided during spiritual
emergency for it leads to the exhaustion of the energy reserves of
cells by conversion of ATP to AMP and similarly aspartate converts the
energy molecule GTP to into its "ash" GMP.
One method of boosting ATP levels during down-cycle events would be to consume ribose. The 5-carbon sugar D-Ribose is
an energy producing ATP substrate formed in the body from glucose.
Ribose is a component of RNA and DNA and also necessary for the
manufacture of ATP. Mitochondria utilize two methods for building or
conserving cyclic nucleotides like ATP, ADP, and AMP. The longer
pathway where ATP is made "from scratch," starting with ribose, and
there is the faster "salvage" pathway, in which the mitochondria "pick
up the pieces" of ATP metabolites to form new ATP. Ribose enables cells
to quickly and efficiently recycle the end products formed by the
breakdown of ATP to form new ATP molecules. There are no foods able to
provide enough ribose to rapidly restore ribose levels, should the need
arise during exercising, working, or during a heart attack, stroke or
kundalini. Supplementing with D-Ribose may be essential during the
down-cycles to provide the ATP necessary for active cation exchange, in
order to prevent enervation and excessive apoptosis. Also creatine
might be another supplement to prevent extreme down-cycle chemistry for
the body replenishes ATP from creatine phosphate (CP), which provides a
replacement phosphate atom so that ADP recycles as a new ATP molecule.
It appeared that Jim's ammonia production was unaffiliated with his
immediate diet and more related to his neurological cycling. Yet to
ease up on the ammonia burden of the liver and kidney function it would
be advisable for him to reduce the possibility of ammonia being
generated from his digestive system. Besides the generation of ammonia
from the deamination of protein in gluconeogenesis, ammonia is also
produced as a result of the normal digestion of proteins, by a number
of harmful bacteria and yeasts. The absorption of ammonia occurs almost
entirely in the last (lowest) part of the small intestine. It has been
shown that whereas absorption of free ammonia from the intestine is
rapid, the cell membrane is relatively impermeable to the ammonium ion.
A high level of ammonia in the blood is a reliable indication of
liver failure. The liver receives some ammonia via the portal vein from
the intestine from the bacterial oxidation of amino acids. A healthy
liver detoxifies the ammonia from the gastrointestinal tract by turning
it into urea, which is passed out of the body in the urine. However, if
the liver is under-functioning the ammonia remains unprocessed and can
enter the bloodstream and can be toxic to the central nervous system,
even affecting the brain. The by products of unhealthy intestinal
bacteria and intestinal yeast (Candida) contribute to attention deficit
disorder. A compromised immune system might mean you have harmful
bacteria and yeast in your GI tract producing ammonia and phenols. Parasites
produce a great deal of ammonia as their waste product. Ammonia is very
toxic to the brain because the brain lacks the enzyme Ornithine
carbamoyl-transferase, which is essential for making ammonia harmless
by changing it into urea. Ornithine carbamoyl-transferase (OCT) is
located in the mitochondria and is part of the urea cycle. Amino acid
treatment to help OCT process ammonia is 500 mg Ornithine evening, 500
mg Arginine morning.
Graviola and neem leaf will reduce ammonia through
their antibacteria, blood cleansing and antiputrifaction properties.
However in order to preferably select and keep the healthy bacteria
population supported when using these strong antibacterial herbs, you
may need to take enzymes like papaya and probiotics, if you are using
these herbs in a primary treatment against a disease like cancer or
diabetes. Taking acidophilus replenishes healthy bacterial
flora, reduces overgrowth of yeast and lowers the pH level of the large
intestine, making it far more acidic. When a high level of acidity is
present, the ammonia produced by intestinal bacteria remains in its
ionized form. In this form, it is not passed on to the liver or
diffused into general circulation through the blood. Thereby lowering
the toxic load on the liver and reducing ammonia levels throughout the
body, including the brain. A study with rabbits found that both yucca root extract and probiotics reduced blood urea and ammonia. Also Larch arabinogalactan from the inner bark of the larch tree is a source of dietary fiber that offers powerful therapeutic benefit as a prebiotic
by acting as a food supply to friendly intestinal bacteria and as a
modulator of the immune system. Studies show that both yucca root and
larch AG reduce intestinal ammonia generation. Bentonite clay
exhibits excellent adsorption properties and high affinity for ammonia
ions. I have found the most palatible way to take bentonite is to mix
it with psyllium powder and put it in 000 capsules...then take 3
capsules per day along with a pint of water in the late evening.
Some intestinal bacteria produce DHPPA, a molecular mimic of
norepinephrine and dopamine. When dopamine levels are raised serotonin
levels tend to be lowered and vice versa. Another intestinal bacteria
toxin lipopolysaccharide (LPS) increases cytokine called IL-1 which can
have a profound effect on memory and learning and can also cause
central hypothyroidism. In hypothyroidism, there tends to be an
excess of serotonin, epinephrine and norepinephrine. Those in the
advanced stages of chronic stress syndrome almost certainly have an
underactive thyroid and adrenals from many years of overworking these
organs. Candida yeast burdens the liver by loading the body with
phenolics that need to be removed by the liver's sulfation pathway. Since the thyroid helps the liver work better, an exhausted thyroid possibly contributes to this condition.
Another effect of too much ammonia includes an increase in the turnover of serotonin
in the brain. Studies show there might be a disturbance in the
tryptophan-serotonin metabolism in people with ADD, for the more severe
the hyperactivity of ADD, the higher the plasma free tryptophan
(serotonin) level. Free serotonin in the plasma can be caused by
allergies, low magnesium, toxins from the gut, or free unsaturated
fatty acids. Stress, including that caused by low blood sugar, releases
fatty acids into the blood. Magnesium stabilizes platelets and
mast cells reducing their release of serotonin into the plasma. Yet
another form of attention deficit hyperactivity shows excessive
dopaminergic activity plus norepinephrine overactivity. Excessive
dopaminergic and norepinephrine overactivity can occur when the liver's
sulfation pathway is weakened by intestinal inflammation and mercury
poisoning. We have to consider that kundalini with its hyperactivated
HPA axis and consequent immune suppression may increase intestinal
inflammation. Plus the increase gluconeogenesis of fat coupled with
increased electrical flow may liberate more mercury from fat stores and
teeth fillings during kundalini.
Expired aerosols such as ammonia resemble the compounds of
extracellular epithelial lining fluid in the peripheral
broncho-alveolar system. The shortness of breath, difficulty breathing
and hypoxia that Jim experienced is probably related to changes in
firing in the brain stem (medulla). Hypoxia increases the toxic effect
of ammonia on the brain. Hypoxia induces the release of serotonin and
stimulates activity in the phrenic nerve that controls the diaphragm.
It is not known whether enhancement of phrenic output is caused by an
increase in strength of the synapses from medullary respiratory neurons
or an increase in serotonin release, or a combination of the two. But
it is easy to see that hypoxia plus hyperventilation would
automatically kick off an escalation of panic chemistry.
Activation of serotonin and glutamate receptors seems to aid
breathing and yet in Jims case the ammonia in the blood in his lungs
must have interfered with oxygen uptake--resulting in a sense of
suffocation despite the increased effort to breathe. The symptoms of
inhaling ammonia include coughing, sore throat, shortness of breath and
can cause the lungs to fill with fluid (pulmonary edema), which can
induce suffocation. Be reassured however that it is normal for ammonia
to be exhaled in reasonably large amounts and this even includes the
activity of bacterial urease enzymes on salivary urea.
Progesterone can decrease seizure activity, so pills
or alcohol-based gels of progesterone could be considered for both
sexes as a method of stopping problematic chronic kindling cycles. Some
intestinal bacteria deconjugate "detoxified" estrogens allowing them to
be reabsorbed from the colon and reenter circulation through
enterohepatic recirculation. To increase the progesterone-to-estrogen
ratio we could take a tablespoon of ground flaxseed a day and
incorporate the following in our diet: rosemary, tumeric, cruciferous
vegetables, grapeseed extract, citrus peel, green tea, B-complex,
probiotics, Calcium D-Glucarate, NAC, alpha lipoic acid, magnesium and
selenium.
Chronic stress impairs the reproductive homeostat (hypothalamo-pituitary-ovarian axis). Acetyl-l-Carnitine
(ALC ) normalizes blood testosterone levels, as well as hypothalamic
beta endorphin (BEP) and gonadotropin releasing hormone (GnRH)
concentrations from the hypothalamus, thereby restoring luteinizing
hormone (LH). ALC resensitizes cholinergic, serotonergic, and
GABA-ergic neurotransmitter systems, reduces age-related loss of
cortisol receptors normalizing the adaptive homeostat, and restores
mitochondrial membranes increasing receptor-sensitivity. . L-Carnitine
is equal to or better as a cognitive enhancer than ALC and is usually
used for its cardiovascular, performance-enhancing, and
lipid-normalizing benefits.
Inhibitory amino acids include tryptophan, taurine, GABA, and
glycine; although to stop the cycling of kindling it might be more a
case of receptor sensitivity that needs to be enhanced rather than
merely upping inhibitory aminos. If it is GABA receptors that we need
to enhance in order to stop excessive firing in the basal ganglia and
brain stem then perhaps S-adenosylmethionine (SAMe) would help.
Long-term supplementation with SAMe repairs cell membrane fluidity and
enhances the sensitivity of prolactin receptors, as well as GABA and
beta-receptors and probably serotonin and dopamine receptors as well.
Other supplements to enhance sensitivity of GABA-ergic, serotonergic
and cholinergic neurotransmitter systems include: Acetyl-l-Carnitine
(ALC), L-Carnitine (LC), Ca-2 AEP, Blueberries, Spinach and Strawberries all enhance cognitive behavior, signal
transduction (transmittal of a neurotransmitter or hormonal signal),
psychomotor performance, and muscarinic receptor sensitivity
(acetylcholine on smooth muscles and glands). Ca-2 AEP is the
calcium salt of 2-aminoethanol phosphate. It is an essential factor for
cell membrane integrity and cell sensitivity; binding fatty acids and
electrolytes to the cell membrane structure that generates the cells
electrical charge. Ca-2-AEP is essential for neurotransmission, nerve
impulse generation, and muscular contractions, is a cell membrane
sealer and protector, and increases the activity of various
neurotransmitters, improves cellular membrane signaling and receptor
sensitivity.
Besides the afore mentioned supplements, excess ammonia needs to be managed by diet and lactulose. Lactulose
is a synthetic sugar known as an "osmotic laxative," that is used to
treat constipation. Mammals and birds are not able to digest lactulose
so it passes unabsorbed from mouth all the way down to the large
intestine. When bacteria flora in the intestine produce lactic, acetic,
and formic acid and carbon dioxide gas. These acids biochemically draw
fluid into the bowel to soften the stool. The acidic bowel condition
favors the formation of the nonabsorbable NH4+ from NH3, preventing NH3
from being absorbed through the colon and effectively reducing plasma
NH3 concentrations. Lactulose is even used to reduce the amount of
ammonia in the blood of patients with liver disease, by drawing ammonia
from the blood into the colon where it is removed from the body.
To enhance the sulfation pathway in the liver use N-acetyl-cysteine.
Of the three amino acids needed to make glutathione--cysteine, glycine
and glutamic acid--cysteine is the most crucial due to its sulfur
molecule. Levels of cysteine will determine how fast we produce
glutathione and how much we make. N-acetyl-cysteine or NAC is a potent
antioxidant and immune stimulant, shown to enhance lung function. It
enhances glutathione production more than taking glutathione itself.
Protects the mitochondrial DNA from damage, and tissue free radical
damage from exercise, pollution and UV radiation. It also helps remove
mercury and other heavy metal deposits. Barley and yogurt are
particularly high cysteine foods. Suggest you eat plenty of cabbage and
broccoli family...even juicing raw cabbage juice and drinking a glass a
day with some parsley, spinach and carrot in it. This should give you
immediate relief and assist your liver.
Phosphatidylserine (PS) is a phospholipid that occurs
naturally in all cells of the body, with particularly high
concentrations in the brain. PS has cognitive-enhancing properties
probably due to its ability to sensitize acetylcholine receptors. It is
an essential cell membrane component for nerve cells; playing a key
role in communication across synapses between nerve cells, and reverses
loss of membrane fluidity associated with age-related mental decline.
PS also ameliorates elevations of stress hormones (ACTH and cortisol)
and helps prevent memory loss and other cognitive decline. PS is a
cortisol receptor sensitizer, resulting in improved levels and
efficient use of cortisol, It is also a very effective antidepressant
due to its ability to normalize the adaptive homeostat (HPA-axis). Docosahexaenoic acid (DHA)
is an omega-3 fatty acid in fish oil that controls inflammation and
decreases free radical induced levels of lipid peroxide in the
hippocampus (learning and memory). DHA also increases choline and
acetylcholine levels in the brain. The lecithin extract
phosphatidyserine supports acetylcholine and improves motivation,
initiative and socialization. Brain cell survival is highly dependent
on the availability of DHA to facilitate the incorporation of
phosphatidyserine into its membranes.
Pressure in the head occurs when ammonia swells the glial cells,
coupled with charged cerebrospinal fluid. To alleviate this try and get
at least 1/2 an hour lying down on the grass per day. Baths with
volcanic salts might help, even foot baths. Do gentle stretching and
rolling around exercises on the floor even if you don't feel like
exercising...some gentle walking would be good, and some pushing
against walls with your feet, and against door frames with your arms.
Try to get plenty of bodywork if you can, and do lots of breathing. You
will probably find fresh ginger root tea up to 6 cups a day will reduce
nausea and vertigo. Borage tea will increase wellbeing, balance and
fortitude. Some of the herbs I recommend for this cyclic condition are
Pinebark extract, Grapeseed extract, Olive Leaf extract, Ashwagandha
root, ginkgo. Ginger root tea. Peppermint tea. The rest are listed
under various areas in the herb listings at the back of the book.
Research: Besides the metabolic byproduct of ammonia
resulting from the seizure-type electrical activity of the nerves and
glyconeogenesis and ketogenesis (alternate energy generating systems)
scientists should also looking into aromatic phenyls and acetone and
their subsequent effects on metabolism. Small amounts of acetone are
metabolically produced in the body, mainly from fat. In humans, fasting
significantly increases its endogenous production via ketosis or the
breakdown of fat for energy. Acetone can also be elevated in diabetes.
More Reading:
OSMOLARITY AND GLUCONEOGENESIS in the Fire and Water section of Biology of Kundalini by Jana Dixon for more on gluconeogenesis and ammonia.
See Exhaustion Phase Profile and Recovery From the Exhaustion Phase in Biology of Kundalini, Jana Dixon
Change Your Brain Change Your Life, Daniel Amen, M.D. for how focal hot areas of the brain affect cognition and behavior.
Ammonia: assessment of its action on postsynaptic inhibition as a cause of convulsions, ILES and JACK Brain.1980; 103: 555-578
For receptor recovery see Ward Dean's articles Neuroendocrine Theory of Aging Chapter 7: Restoring Receptor Sensitivity Parts 1-V at http://vrp.com
Also useful for understanding this condition are Dr. War Deans articles Neuroendocrine Theory Of Aging, Part II: Adaptive Homeostat Dysfunction and Mitochondrial Restoration, Part II: Restoring Mitochondrial Function and Bio-Energetics
©2006
Biology of Kundalini by Jana Dixon