Biology of Kundalini A Science and Protocol of Spiritual Alchemy    

The Ammonia Hypothesis


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."

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

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

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