Pulling it all Together With Dr. Batmanghelidj
The work I am drawing from for this is largely from Dr. Batmanghelidj and his water-cure books and articles. www.watercure.com Here I am attempting to pull kundalini theory together around the subject of water. Fire and water see, that is Taoist justice. The Justice of the Tao is the intercourse of opposites.
"When blood becomes concentrated, it draws water from the cells around it." Dr Batmanghelidj
Water is not only the solute in which all chemistry in life occurs, it also acts as a structural and binding material through which the body attains its form. Since water is bound into the structural components of the cell, dehydration causes a disintegration of the cell framework. 60% of cell water is bound to molecules within the cell--that means only 40% of the water in the body is "free water." In dehydration when viscosity is higher proteins and enzymes become less efficient. Dr. Batmanghelidj goes as far to say that chronic unintentional dehydration is the origin of most pain and degenerative diseases in the human body. "Chronic cellular dehydration painfully and prematurely kills. Its initial outward manifestations have until now been labeled as diseases of unknown origin."
Here is the short list of things dehydration creates: Constipation, bad digestion, ulcers, GI tract problems, heart burn, allergies, asthma, high cholesterol, high blood pressure, heart disease, kidney failure, cancer, arthritis, multiple sclerosis, obesity, diabetes, sugar/carbo craving, depression, reduced intelligence and brain function, emotional and social problems, poor eyesight etc. Since I have upped my water intake I have less appetite, less brownspot pigmentation, less pain, less depression, more energy, less ama discharge from skin, lowered blood pressure, easier breathing, better sleep, better digestion, brighter skin, and reduced sugar craving etc...
The osmotic forces that maintain extra cellular fluid volume are regulated primarily by salt, and also by sugar and uric acid concentrations. Water management systems in the body make sure that the more vital organs get preferential water rations when water intake is deficient and when under stress. Hence water management is tied into the fight-flight response to ensure priority regulation in times of danger.
Stress to the human body can be caused by dehydration, trauma, anxiety, fear, anger, infections, surgery and even exercise. General Adaptation Syndrome is a cascade of biochemical responses set off to reinstate adaptive homeostatis in response to stress. Stress, both physical and emotional, evokes release of the stress hormones: catecholamines and corticosteroids, which mediate release and utilization of substrates for energy production and for improved skeletal and cardiac muscle performance. It must be remembered also that the auto-oxidation of catecholamines yields free radicals. So stress is a factor in hypertension and in the glycation and free radical decay of metabolites and tissues.
Kundalini activation is interpreted by the body as an autogenous crisis and thus it initiates a prolonged fight or flight response and "emergency" energy production. As a consequence a cascade of hormones are released: noreadrenaline, endorphins, cortisone release hormone (CRH), prolactin, vasopressin and renin-angiotensin. These agents are produced to mobilize primary raw materials from body reserves to fight stress and repair possible damages caused by possible exposure to injury. Fat is broken down into fatty acids to be converted into an energy source during stress, through lipolysis induced by beta-catecholamines.
Thus during an awakening the body feeds off itself to make building blocks available for their emergency resuse. Under such stress some of the available water is used for the breakdown of stored materials such as proteins, starch (glycogen) and fat. To compensate for the lost water the renin-angiotension (RA) system in the kidneys is activated to hold back more water and make urine more concentrated. The RA system works in coordination with vasopressin, histamine and other hormones to conserve water during stress.
While metabolism is up and the body is catabolically "reusing" its reserves and tissues, it is apparent for the duration of a kundalini awakening the demand for water intake is increased. Dehydration creates stress--inadequate hydration will cause further stress, and stress will cause further dehydration. Prompting the body's many water management systems to come into effect to prioritize water use. The regulating neurotransmitter systems, including histamine and its agents, become increasingly active during water deficient conditions. We can see that many of the classic kundalini symptoms are various cries for more water by the different areas of functions of the body and acute prolonged stress: itching, thirst, high blood pressure, faintness, racing heart, insomnia, hypervigilence.
If concentrated blood reaches the lungs local histamine production increases. Since kundalini increases water demand, a shortness of breath similar to asthma may occur, because histamine initiates bronchial muscle contraction in an effort to reduce water evaporation from the lungs. Increased water intake may be the only sound method of dealing with the over-production of histamine due to dehydration. That is an obvious statement if ever I heard one.
Pain is the body's crisis call for water. Pain means there is a build up of toxic waste and that the body is demanding water to wash the toxins out of the body. Dr. Batmanghelidj points out that one should first assume that dehydration is the cause of any pain we might have, and the cure for dehydration of course is water.
As I mentioned 60% of cell water is bound to molecules within the cell, thus 40% of the water in the body is "free water". Besides nerve energy we also need adequate free water for all processes in the body including DNA repair, protein synthesis, metabolite and toxin removal, bile and digestion, bone marrow and immune cell proliferation, steroid production etc...
Proteins and nucleic acids (DNA/RNA) are linear polymers that fold
themselves into 3D structures. It is the specialized structure which
determines the viability of the molecule for biological processes. To
undergo this conformational rotation to facilitate this folding
adequate "free water" is needed in order to float and maneuver into the
correct shape. Ageing is determined by the rate at which DNA damage
occurs compared to the rate at which it is repaired. For correct
folding and repair DNA must be flexible--with decreased cellular free
water the activities of the DNA repair enzymes are inhibited, and
protein folding is restricted. Water management and mobilization of
free water is one of the major contributing factors in the
stabilization of protein-DNA-RNA complexes. Also the tendency of water
to form hydrogen bonded networks is also important in the self-assembly
of complex proteins.
Alterations in the intracellular environment and consequent metabolic changes can be brought about by modification of the selective permeability of the cell membrane. As with other cation pumps, the intracellular pH buffering Na+/H+ pump is driven by free water. Tryptophan has a role in controlling the free water content of the cell--evidence shows that sodium uptake might be affected by tryptophan levels and is directly involved in controlling membrane permeability. Cholesterol and Essential Fatty Acids are also moderators of membrane fluidity. Acetylcholine alters cell membrane permeability via the acetylcholine receptor; a neurotransmitter gated ion channel.
Cerebrospinal Fluid is very salty, and this salt is responsible for removing acids out of the brain cells. If we are short on salt then the acidity of excess hydrogen ions will interfere with brain cell metabolism. The more dehydrated the body becomes the higher the injection pressure has to be for injection of water into the cells...this injection pressure is called "hypertension." If however we take adequate water and salt, cells can be sufficiently hydrated without producing this high blood pressure. During dehydration the body retains salt in order to hold more water in the body.
Salt is a natural antihistamine and the sodium in salt makes mucus more fluid. During dehydration the lungs produce more mucus to protect the air passages from drying out. Plentiful water and ½ teaspoon of salt a day will prevent sinus and lung congestion. Buying the powdered form of Celtic sea salt or Redmond's Real Salt is cheaper than liquid ionic minerals...then you can just dissolve it in water and put it in a squeegee bottle for easy spiking of your water bottles.
"The cellular hydration state is dynamic and changes within minutes under the influence of aniso-osmolarity, hormones, nutrients and oxidative stress. This occurs despite the activity of potent mechanisms for cell volume regulation, which have been observed in virtually all cell types studied so far. These volume-regulatory mechanisms are apparently not designed to maintain absolute cell volume constancy; rather, they act as dampeners in order to prevent excessive cell volume deviations, which would otherwise result from cumulative substrate uptake. On the other hand, these volume-regulatory mechanisms can even be activated in the resting state by hormones, and by this means changes in cell hydration are created. Most importantly, small fluctuations of cell hydration, i.e. of cell volume, act as a separate and potent signal for cellular metabolism and gene expression. Accordingly, a simple but elegant method is created for the adaptation of cell function to environmental challenges. In liver, cell swelling and shrinkage lead to certain opposite patterns of cellular metabolic function. Apparently, hormones and amino acids can trigger these patterns by altering cell volume. Thus cell volume homeostasis does not simply mean volume constancy, but rather the integration of events which allow cell hydration to play its physiological role as a regulator of cell function." (Source)
This article by Dieter Haussinger speaks volumes about how cellular hydration affects metabolic processes and function. Whether particular chemistry is catabolic with water exiting the cell, or anabolic with water entering to swell the cell is determined by the particular molecular agents involved. For example:
Hyperosmolarity-Catabolic signal and cell shinkage agents are: Glucagon, cAMP, Adenosine, 5-HT, Hydroperoxides, Urea, Extracellular ATP, Benzylamine.
Hypo-osmolarity-Anabolic signal and cell swelling agents are: Amino acids, Conjugated bile acids, Insulin IGF-1, Phorbol ester, Phenylephrine, Bradykinin, K+channel blockers, Ouabain.
Recent evidence suggests that the state of cellular hydration is an important determining factor of cell function and that hormones, oxidative stress and nutrients exert their effects on metabolism and gene expression in part by modification of cell volume. Cell water volume determines the effectiveness of antioxidants glutathione and catalase to remove hydrogen peroxide, thus well-hydrated cells are more resistant free radical induced cellular damage. Whereas oxidative stress may lead to cell shrinkage.
Amino acids with nonpolar components are said to be hydrophobic (water-hating). Amino acids with polar R groups that form hydrogen bonds to water are classified as hydrophilic (water-loving). The remaining amino acids carry either negative or positive charges in aqueous solution at neutral pH and are therefore strongly hydrophilic.
Cellular hydration is an important determinant of protein turnover. Not only are amino acids potent modulators of cell volume, but cell volume can exert control over amino acid synthesis, transport and breakdown. Cell shrinkage inhibits protein synthesis, while cell swelling stimulates it. The mechanisms through which cell hydration determines organized protein breakdown (proteolysis) is not known, but intact microtubular structures are required. Microtubules act as transport pipes and apparently play an important role in facilitating some metabolic alterations in response to changes in cellular hydration.
Part of the metabolic effects induced by hormones and amino acids are due to their cell swelling potency. For example insulin-induced cell swelling is counteracted by glucagon--a hormone produced by the alpha cells in the islet of Langerhans of the pancreas. Glucagon causes a rise in the blood glucose level by releasing glucose from liver and muscle cells. Glucagon induces cell shrinkage and simultaneously swells the mitochondria as well as stimulating the breakdown of glycogen stored in the liver.
Kundalini, during the peak phase in particular might put such a demand on the energy production in the body that protein reserves are broken down in a pathway that is called gluconeogenesis. This is the conversion of amino acids and glycerol to "new" glucose. Glycerol is present in the form of its esters (glycerides) when fats and oils are hydrolyzed to yield fatty acids.
Gluconeogenesis 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. Under conditions of high demand the lactate produced in the muscle is returned to the liver to be recycled back to glucose, using the energy from oxidation of a fraction of the lactate. Resting muscles mainly use fats (fatty acids) for producing energy but as exercise begins, the muscles begin to use glucose as well. This glucose comes from both the blood and stores of glucose in muscle (muscle glycogen). Skeletal muscle undergoes gluconeogenesis as a mechanism to generate glucose for storage as glycogen. Glycogen is a polysaccharide that is the principal storage form of glucose in animal cells. Glycogen is found in the form of granules in the cytosol in many cell types. Up to 8% of the fresh weight of liver cells are glycogen.
The generation of glucose from amino acids and fats is more energy intensive that glycolysis, that is it uses more energy and needs more water. All amino acids except lysine and leucine are precursors to glucose via gluconeogenesis. Lysine and leucine are the only amino acids that are solely ketogenic, giving rise only to acetylCoA or acetoacetylCoA, neither of which can bring about net glucose production. A small group of amino acids comprised of isoleucine, phenylalanine, threonine, tryptophan, and tyrosine give rise to both glucose and fatty acid precursors and are thus characterized as being glucogenic and ketogenic. The rate of gluconeogenesis from various substrates is sensitive to small changes in the pH, and pH is governed largely by free water and sodium (salt) availability.
During fasting, gluconeogenesis is the main process of glucose production in the liver. In many respects the body in peak kundalini with the HPA axis firing away may be similar to the fasting body in its need for alternative glucose sources. The key that triggers this extra gluconeogenesis in the liver might be that which occurs during diabetes. Excessive production of glucose in the liver is a major contributor to hyperglycemia in both type1 and type 2 diabetes. Hepatic gluconeogenesis is tightly regulated by hormones mainly through transcriptional regulation of the rate-limiting enzymes, e.g. PEPCK and G-6-Pase. PEPCK expression is inappropriately up-regulated in diabetes resulting in excessive gluconeogenesis.
Gluconeogenesis during peak kundalini may stimulated by changes in the amino acid balance and from the drop in pH due to the acids released from lyosomes during apoptosis, and through acids produced from hyperadrenalization. Since there is intense catabolic activity during the peak with both apoptosis and gluconeogenesis, the acidic chemistry means that our demand for extra water intake during this time is crucial to help prevent oxidation damage and immune challenges like Candida, fungi, viruses and cancer. The higher blood sugar levels during an awakening could ultimately lead to insulin resistance, pancreatic necrosis, pre-diabetes and loss of calcium from the bones, so careful attention is necessary to the maintenance of a low glycemic diet to avoid blood sugar spiking.
Cell swelling in response to insulin may be a consequence rather than a cause of insulin action. The anti-proteolytic (protein conserving) effect of insulin and some amino acids is partly due to their cell-swelling effect. Whereas stimulation of proteolysis (protein degradation) by glucagons is apparently mediated by cell shrinkage. The hormone glucagon activates gluconeogenesis in the liver; this is the pathway by which non-sugar substrates such as amino acids are converted into glucose. Glucagon also enhances lipoysis, or the utilization of fats for energy, thereby conserving blood glucose by providing fatty acid fuel to the cells.
Liver cell swelling stimulates glycogen synthesis and lipogenesis; the stimulatory effect of glutamine and other amino acids on glycogen synthesis and lipogenesis is due to amino acid-induced cell swelling. Glutamine is the most plentiful nonessential amino acid in the body, the most plentiful protein in blood and is involved in more metabolic processes than any other amino acid. In the kidney, Glutamine also regulates hydration, electrolyte balance and the acid/base balance which affects muscle response. Low glutamine reserves result in excessive excretion of calcium, magnesium, potassium, phosphorus and shifts pH to an acid balance, with the resulting loss of physical energy. Large amounts of glutamine are used for glutathione, the body's most powerful, abundant, water-soluble antioxidant.
In many tissues, including the brain, some processes such as protein catabolism (nucleotide degradation) generate free ammonia. Mitochondria in liver cells contain enzymes that allow them to detoxify ammonia, a waste product of protein metabolism. Glutamate and glutamine play critical roles in nitrogen metabolism, acting as a kind of general collection point for amino groups. Glutamine has a very important role in nitrogen metabolism because of its two nitrogen atoms. It is utilized as a fuel, in protein synthesis, and to produce other important compounds and amino acids. Glutamine is also an essential nitrogen transporter, allowing ammonia to be removed from areas of the body like the brain and lungs and deposit into the intestines and kidneys.
Glutamine passes freely across the blood brain barrier and once in the brain it is converted to glutamic acid and GABA. Depletion of glutamate in the glutamine synthetase reaction may have additional effects, for glutamate and its derivative g-aminobutyrate (GABA) are important neurotransmitters. The main by-product of glucose metabolism in the brain is water itself.
Speculation on the cause of head pressure in kundalini centers on a potential depletion of ATP in brain cells through the swelling of glial cells and their consequent reduction in glucose supply to neurons. High levels of NH4+ lead to increased levels of glutamine, which acts as an osmotically active solute in brain. Brain swelling is mediated in part through an increase in the osmolyte glutamine in the brain, thus headaches or pressure in the head may occur through glutamine's cell volumizing effect. Glutamine accumulation in astrocyctes (glial cells) creates ammonia induced glial swelling and intra-cranial pressure. Excess glutamine is a by-product of high ammonia levels in the blood, which occur if the liver cannot adequately process ammonia.
This ammonia induced glutamate toxicity and astrocycte swelling might be the main cause of head pressure associated with kundalini, if the liver and kidneys are overloaded and not adequately dealing with the extra ammonia that is produced during the hypermetabolic state of kundalini arousal. Glial swelling means the astrocyctes cannot attend to the neurons as well, thereby explaining one of the reasons for reduced mental function during kundalini. Evidence suggests that glutamine forms in astrocytes and as it accumulates water also accumulates causing the cells to swell. Both ammonia toxicity and swelling is reduced by inhibitors of the enzyme glutamine synthetase, which obviously reduces glutamine production.
Inhibition of gluconeogenesis from glutamine is accompanied by a reduction in ammonia production. Gluconeogenesis occurs in acidic pH conditions thereby raising ammonia levels. Hyperammonia results in a rise in glutamine with a reduction in myo-inositol and taurine. [Inositol, also known as myo-inositol, functions closely with choline. Inositol is a carbohydrate that closely resembles glucose in structure. The body and intestinal bacteria make inositol from glucose. Inositol functions similarly to choline in helping move fats out of the liver. It functions in nerve transmission and makes up an important part of phospholipids.]
Ammonia exists as two different forms, NH3 and NF4+. NH3 is a small lipophylic molecule that is readily permeable across the phospholipid bilayer of cell membranes. In contrast, NH4+ a monovalent cation, does not passively diffuse cell membrane but only passes through cation channels. Ammonia can be a weak acid or a weak base, depending on what type of chemical it is suspended in. Ammonia is toxic for an organism even in small amounts can induce apoptosis.
In skeletal muscle, excess amino groups are generally transferred to pyruvate to form alanine, for transport to the liver. The energetic burden of gluconeogenesis is thus imposed on the liver rather than the muscle, and all available ATP in muscle is devoted to muscle contraction. Liver tissue is the site of gluconeogenesis in higher vertebrates and, during this process, amino acids are deaminated, forming ammonia. Extrahepatic tissues, especially working muscle, form ammonia which must be returned to the liver for detoxification. Working muscle also forms glutamine, which is deamidated in the liver forming additional ammonia. In mammals, the site of detoxication is the mitochondrial matrix of hepatocytes.
The classical pathway for ammonia detoxification in mammals is the urea cycle, the first two enzymes of which, are localized exclusively in the mitochondrial matrix. They convert ammonia to citrulline, which then exits to the cytosol for conversion to urea for excretion. Glutaminase is an important kidney tubule enzyme, somewhat present in many other tissues as well. It is involved in converting glutamine (from liver and from other tissue) to glutamate and NH3+, with the NH3+ being excreted in the urine. Glutamate and aspartate are important in collecting and eliminating amino nitrogen via glutamine synthetase and the urea cycle, respectively.
In the cytosol of hepatocytes, amino groups from most amino acids are transferred to a-ketoglutarate to form glutamate, which enters mitochondria and gives up its amino group to form NH4+. Mitochondria behave as perfect osmometers; they respond to changes in osmotic pressure of the suspending medium by shrinking (or swelling) as water flows across the membrane to compensate for the difference in activity when the osmolytes are added to (or removed from) the external medium. The mitochondrial membrane is permeable to NH3, which are neutral small molecules. Ammonium salts added to isolated rat liver mitochondria deviate alpha-ketoglutarate to glutamate synthesis, thus decreasing its availability as respiratory substrate. As a consequence a decrease of respiratory rate is observed which is paralleled by progressive mitochondrial swelling. It was demonstrated that L-carnitine may abolish this swelling thus improving structural and metabolic state of mitochondria.
Apoptosis, or programmed cell death, is the mechanism by which the body rids itself of damaged cells. It plays a prominent role in protection against cancer. Over the last few years, it has become apparent that mitochondria are of critical importance in the apoptosis process. Proteins that control the survival or death of cells are specifically associated with the mitochondrial outer membrane, and permeability changes across the mitochondrial inner membrane, probably associated with Ca2+ transport and mitochondrial swelling, and the release of proteins, particularly cytochrome-c, from the inter-membrane space, play an early role in the deciding the fate of the cell. The outer mitochondrial membrane is composed of about 50% phospholipids by weight and contains a variety of enzymes involved in such diverse activities as the elongation of fatty acids, oxidation of epinephrine (adrenaline), and the degradation of tryptophan.
Histamine Release Factor (HRF) promotes fluid flow and hydroelectric energy generation, water intake, blood flow regulation and inhibition of water elimination. H1 receptor activation lowers core temperature to reduce water loss, and H2 activation induces heat loss mechanisms. Regulation of wakefulness and appetite by histamine has long been suggested by observations that substances that block H1 receptors are not only sedating but also increase appetite and weight gain.
Histamine by itself is anabolic, or a promotor of growth. As a pro-adaptation hormone, histamine releases extra energy within the cell, locking it into an amplification of stimuli, leading to various changes such as increased cell division, increased acid production, and changes in energy-dependent cation exchange through the cell membrane.
Besides being a neurotransmitter in charge of water regulation, histamine also manages the immune responsibilities of defense against antibacterial, antiviral and other foreign agents. In dehydration, histamine suppresses its own activity on the immune system, otherwise dehydration would constantly activate the immune system. Histamine can inhibit the immune system through reducing interleukin, interferon, increasing cAMP, cAMP produced by the action of histamine suppresses function within cells that generate it possibly leading to depression.
Adequate hydration reduces exaggerated histamine activity. In drought management, under histamines direction, subordinate systems become active in prioritizing water distribution. These include vasopressin, renin-angiotension, prostaglandins and kinins. Kinins are blood plasma proteins that influence smooth muscle contractions, affect blood pressure, increase blood flow throughout the body, increase the permeability of small capillaries, stimulate pain receptors and promote saliva formation.
In stress the body assumes a crisis situation and will begin to mobilize for fight/flight by producing: endorphins, cortisone releasing factor, prolactin, vasopressin and renin-angiotensin. When under stress the brain has to process more information than usual. Histamine allows the blood vessels in the brain to dilate improving mental efficiency during stress or danger. With dehydration the level of energy generation in the brain is decreased leading to depression and chronic fatigue.
Excess histamine can amplify cell division, increase acid production (H+), suppress the immune system and inhibit bone marrow. According to Dr. Batmanghelidj stress/dehydration can turn T cell lymphocytes into functioning as killer cells on bone marrow. Histamine (H2) also increases killer cell activity along with serotonin. Lymphocyte proliferation is reduced when histamine induced suppressor factors cause monocytes to produce prostaglandins.
The serotonergic neuronal system regulates histamine activity through stabilization of the calcium current across the cell membrane. Serotonin also inhibits histamines acid secretory capacity in the stomach. Histamines primary function in the gut appears to be the regulation of cation exchange and the regulation of water absorption.
H3 receptors are expressed in the central nervous system and, to a lesser extent, the peripheral nervous system, where they act as feedback inhibition of histamine synthesis and release. Adequate free water to promote cell hydration makes this feedback inhibition more effective. The H3 also been shown to presynaptically inhibit the release of a number of other neurotransmitters including, but probably not limited to dopamine, GABA, acetylcholine, noradrenaline, and serotonin.
Vasopressin is released into the brain in a circadian rhythm by neurons of the suprachiasmatic nucleus of the hypothalamus. Vasopressin is an antidiuretic hormone that is mainly released when the body is low on water, where upon it causes the kidneys to conserve water by concentrating the urine and reducing urine volume. As its name implies "vaso-pressin" stimulates the contraction of the smooth muscular tissue of the capillaries and arterioles (vasoconstriction), thereby raising the blood pressure. It promotes contraction of the intestinal musculature, increases peristalsis.
Vasopressin is one of two octapeptide hormones formed by the neuronal cells of the hypothalamus and stored in the posterior lobe of the pituitary gland, the other being oxytocin. The structure of oxytocin is very similar to that of the vasopressins and its amino acid sequence differs at only two positions. The neurons that make vasopressin are adjacent to the neurons that make oxytocin. The similarity of the two peptides can cause some cross-reactions: oxytocin has a slight antidiuretic function, and like oxytocin high levels of vasopressin can cause uterine contractions.
Most of it is stored in the posterior pituitary gland to be released into the blood stream; some of it is also released directly into the brain. Vasopressin is secreted in response to reductions in blood plasma volume and in response to increases in the plasma osmotic pressure (ie: thickening of the blood), by pressure receptors in the veins, atria, and arterioles. Secretion in response to increases in plasma osmotic pressure is mediated by osmoreceptors in the hypothalamus. The neurons that make vasopressin, in the supraoptic nucleus and paraventricular nucleus, are themselves osmoreceptors, but they also receive synaptic input from other osmoreceptors located in regions adjacent to the anterior wall of the third ventricle.
In the kidneys vasopressin has a specific effect on augmenting resorption of water independently of solutes, resulting in concentration of urine and dilution of blood serum. Its rate of secretion is regulated chiefly by the osmotic concentration of the plasma. Many factors influence the secretion of vasopressin; for instance, alcohol and caffeine reduce vasopressin secretion. The resulting decrease in water reabsorption by the kidneys leads to a higher urine output.
Vasopressin acts on three different receptors: V1a, V1b and V2. The receptors are differently expressed in different tissues, and exert different actions:
V1a - vasoconstriction, gluconeogenesis in the liver, platelet aggregation and release of blood clotting factors.
V1b - corticotropin secretion from the pituitary gland. Vasopressin is secreted from the hypothalamus and transported directly to the anterior pituitary gland, where it is an important releasing factor for ACTH, acting in conjunction with CRH.
V2 - control of free water reabsorption in the collecting ducts of the kidney to influence the body's electrolyte and fluid balance. In times of extreme dehydration, over 24% of the filtered water may be reabsorbed in the collecting duct system.
Through an unknown mechanism vasopressin release within the brain has been implicated in memory formation, including delayed reflexes, image, short and long-term memory. Vasopressin is involved in blood pressure and temperature regulation and in aggression and territorialism. It is thought that vasopressin, released into the brain during sexual activity, initiates and sustains patterns of activity that supports pair bonding between the sexual partners. Studies support the hypothesis that vasopressin is involved in male aggression towards other males. Vasopressin might also be tied into aggression to ensure that during times of acute environmental water shortage, at least the most aggressive members of a population will survive by eliminating competitors for the water. Thus well-hydrated populations will tend to be less aggressive and territorial.
High levels of vasopressin secretion can occur with increased opiates, this may cause mild deficiency of sodium in the blood for several days. This is obviously an important consideration during kundalini when opiate levels are very high. It is essential to add that touch of salt to our drinking water to adjust to increased vasopression levels during high endorphin production.
The stress, or "death," hormone cortisol, can seriously damage your brain and circulatory system. Modern life probably gives many of us generally higher cortisol levels...especially since we have become cognizant of our negative impact on the planet as a species, and since we don't seem to be moving in any "benign" collective condition. This deprives us of the sense of an open-ended future and reverts our energy into present survival mode. Once we can move in a direction of high integrity and possibility, chronic stress and excess cortisol will abate.
The prolonged activation of the sympathetic nervous system that occurs during awakening leads to chronic overproduction of cortisol and an eventual reduction in anabolic steroids such as testosterone. One can see the effects of this in the feminization of advanced Gurus...note their fat faces, and enlarged bellies and breasts. Enlightenment practice has traditionally produced individuals which nature is basically saying are unsuitable to reproduce...hence the loss of sexual characteristics normally associated with attracting the opposite sex. Men lose their "cut" facial lines, their broad shoulders and narrow waists, and become more like obese women. Socially though, these enlightened types still manage to attract females and breed because of their social status and siddha power.
But we can have our cake and eat it too. One can have fully activated enlightenment chemistry in the body, and as long as one keeps up a steady strength training, and stress relief program, coupled with a heavy antioxidant regime...then you can be an advanced Guru and be a manly man also. Normally we think of Jesus as being the perfect example of the alchemical marriage between male and female but (hypothetically) he still looked very much like a male. For he came from the Essene tradition of health in which sexual characteristics are maintained at peak for the lifespan of the individual due to the dietary and living practices.
A "balance" of the sexes is not a denial or negation or a fusion of the sexes...for this would lead to an absexual or asexual effect and a diminishment of Eros. The point is the polar play...it's the play of the poles, hemispheres and sexes in their most actualized function that constitutes enlightenment...or "unity" consciousness. To have a manly man be soft and hard, now that is an exciting thing. That a man can fully embody his femininity means that he is so strong he can be soft. He doesn't look less of a man for it, but simply that he no longer holds his masculinity as a power tool.
Integral spirituality would ensure that the enlightened male would not be turned into a woman and would remain true to form. Firstly through adequate muscle building exercise to maintain testosterone levels. Also through taking antioxidants to counter the increase in free radicals that occurs with hyperactivation of the nervous system. And by taking cortisol reducing supplements as well as those that build up the sex and growth hormones.
Remember energy follows the Tao...years of stilling the nervous system with meditation and other quietening practices will allow it to flip into extreme activation. However someone who constantly autostimulates themselves with their emotions, habits or stimulants won't have the energy reserves for a full-on blasterama.
Any increase in spiritual energy/kundalini/presence is the activation of both sympathetic and parasympathetic. So this is going to increase our cortisol levels. Obviously all the nerve calming techniques in the spiritual bag of tricks will help to reduce the raw fear/danger bandwidth of sympathetic activation. But there will still be hyperactivation of brain and nerves throughout an entire awakening and beyond.
With awakening there are acute events and phases involving consecutive activation of the on and off switches...and other periods in which both on and off switches are on full-blast at the same time. Note that when you are in love there is a similar rise in nerve activity, which promotes both deeper relaxation and opening (parasympathetic), and heightened alertness and energy (sympathetic). The most impactful "practice" for reducing cortisol levels must be "loving relationship." Even loving relationship with a pet will reduce stress hormone release. Laughter, intimacy and acceptance are fundamental to our health.
Cortisol is an anti-inflammatory glucocorticoid steroid hormone arising from the adrenal glands that among other things, regulates water retention and blood pressure. Cortisol is necessary to maintain the full response of processes in times of prolonged stress. It is a major agent in the death and resurrection process, where the body is catabolically broken down and reassembled to a form that is more efficient at conveying higher levels of consciousness and sensitivity. Cortisol initiates the self-digestion and remobilization of stored energies and raw materials. Fat is broken down into fatty acids to be converted into energy (lipolysis). Proteins are broken down to amino acids to build neurotransmitters, new proteins and special aminos to be burned as fuel by muscle.
The major ergotropic (catabolic) effects of cortisol involve its facilitating gluconeogenesis and the conversion of protein in muscles and connective tissue into glucose and glycogen; and consequent increase liver glycogen stores. Gluconeogenesis involves both the increased degradation of protein already formed and the decreased synthesis of new protein. The prolonged HPA axis activation of chronic stress can create amino acid imbalances due to certain proteins being used up in the energy generating gluconeogenesis. Central to gluconeogenesis is the metabolism of glutamate (glutamine and GABA) and proline and a decrease in cysteine and methionine. There is a loss of serum tryptophan and tyrosine due to their breakdown in the liver and an increase in glutamate and arginine.
Cortisol can also decrease the utilization of glucose by cells by directly inhibiting glucose transport into the cells. An excess of cortisol can also lead to a decrease in insulin sensitivity, most likely due to blockage of insulin receptors. Cortisol also reduces the utilization of amino acids for protein formation in muscle cells, leading to a progressive loss of protein, muscle weakness and atrophy, increased protein breakdown by 5% to 20%. Loss of bone mass also occurs through increased calcium excretion and less calcium absorption. Excess cortisol can cause programmed cell death (apoptosis) in the thymus leading to thymic involution. Thus prolonged high levels of cortisol can throw the immune system into chaos and catabolically ravage the body.
Hyper-cortisol production may be central to depressive symptoms and cognitive deficits, arising from the neurocytotoxic effects of raised cortisol levels. As well as the fight-flight response, sustained freeze response and dissociation also increases blood cortisol and promotes depression. Chronic high cortisol significantly increases learning and memory impairment, as well as atrophying neurons in the hippocampus. The frontal lobes are also particularly sensitive to the neurodegenerative effects of cortisol. Prolonged high cortisol levels may also lead to hypertension because it causes sodium retention (bloating) and potassium excretion.
Even mild elevations in serum cortisol can increase plasma glucose concentration and protein catabolism within a few hours in healthy individuals. Cortisol can increase body fat levels especially when it's increased dramatically in the body. Cortisol can inhibit growth-hormone and testosterone and can directly inhibit pituitary gonadotropin and TSH (thyroid stimulating hormone). It may also interfere with the conversion of thyroid hormone T4 to the active T3, thereby decreasing metabolic rate and making it harder to lose body fat.
Studies show that restricting normal caloric intake by 50% can lead to a subsequent increase in cortisol levels by 38%. To help control cortisol levels maintain a highly nutritious diet, do not overtrain, maintain quality downtime, get 8 hours sleep a night, and consume a high-glycemic carbohydrate to increase insulin levels directly after an intense workout, for insulin interferes with cortisol. Also cultivate a nurturing social circle. During one stage of sleep cortisol levels are elevated because protein is being re-cycled. Cortisol-suppressing supplements can be taken before bedtime to help minimize excess cortisol production during sleep.
Supplements to reduce cortisol levels include Vitamin A, Zinc, and acetyl l-carnitine, DHEA, Phosphatidylserine, L-Glutamine, Zinc. Studies also showed that the individuals taking Vitamin C improved their testosterone:cortisol ratio by over 20%.
All the adaptogenic herbs will aid this transmutation process while protecting the tissues from damage by free radicals, heavy metals, metabolites and toxins: Foti, garlic, ginkgo biloba, goats rue, gotu kola, olive leaf, rhodiola rosa, rosemary, basil, wild yam, devils claw, dong quai, astragulus. The adaptogen Siberian Ginseng is a body balancer that halts the overproduction of cortisol.Exhaustion Phase: Towards the end of an awakening we might need to enhance the adrenal glands and cortisol metabolism in the body with a small amount of licorice root. I assume that licorice root is important during the exhaustion phase for returning the adrenal glands to full health. However during the peak it might amplify the effects of already high levels of adrenaline and cortisol. Licorice root extends the lifetime of cortisol in the kidney.
Glycrrhetinic acid, the steroidlike constituent of glycyrrhizic acid in licorice, inhibits an enzyme responsible for inactivating cortisol in the kidney. Licorice is useful for "deficient" adrenals, because glycyrrhizic acid allows cortisol to stick around in the distal tubules of the kidney. Cortisol binds to a protein that causes the kidney to retain sodium longer than it normally would, increasing blood pressure, possibly contributing to include water retention, headaches, lethargy and heart failure. So large amounts of licorice should not be taken if one tends towards these conditions.
Licorice helps heal ulcers by inactivating 15-hydroxyprostaglandin dehydrogenase in the stomach lining. Licorice also extends the life of prostaglandins that protect the stomach wall. The effect of licorice on the prostaglandins that release mucous may also explain why licorice helps soothe a cough.
"Prolonged periods of exposure to elevated levels of cortisol (such as occurs during chronic stress) cause a number of adverse effects in the body. These include elevation of blood sugar (diabetes), sodium retention (resulting in hypertension), suppression of immunity, gastric ulcers, headaches, loss of bone density (osteoporosis), heart attacks, loss of even more hypothalamic glucocorticoid (cortisol) receptors (creating a "vicious cycle"), and increased neuronal cell death in the brain." See the following for receptor sensitivity recovery: Neuroendocrine Theory Of Aging, Part II: Adaptive Homeostat Dysfunction, Ward Dean, M.D. http://vrp.com/art/1666.asp
White blood cells (leukocyctes) are immune cells that are produced in the bone marrow. They consist of a variety of types: neutrophils, eosinophil, basophils, monocyces, macrophages and lymphocytes-(B-cells, T-cells and Natural Killer). Although all lymphocyces originate from progenitor cells in the bone marrow, they take different paths toward becoming mature immune fighters. For example T-cells migrate to the thymus gland where they learn their role as killer cells; B-cells, which make antibodies, mature in the bone marrow; while Natural Killer cells (NK) accumulate and mature in tonsils, lymph nodes and the spleen. NK cells are the first to respond to a challenge to the immune system and burst forth from lymphoid tissue while the T & B cells are still mobilizing.
The stem cells of bone marrow produce white and red blood cells. The growth of stem cells depends on the availability of free water and on the heat of activation generated by free-osmotically active water for their maturation. If someone is so dehydrated that they have arthritis, you can be sure that their bone marrow is getting inadequate water for healthy immune cell production.
Dysregulation of the mechanisms of autonomic homeostasis associated with dehydration, stress, kundalini and depression include: the generation of imbalance in amino acids, immune suppression, excess or deficient levels of certain neurotransmitters and hormones coupled with the down-regulation of receptors.
Corticotrophin Releasing Hormone (CRH) is hypersecreted and its receptors are down regulated during depression. CRH appears to act on the immune system directly, as well as causing HPA axis activation which then has adrenal and cortisol consequences on immunosuppression. Beta-Endorphin is an opiate neuropeptide which is synthesized from the same precursor as ACTH. Which means that its production is increased along with ACTH in response to CRH release. Endorphins also have water intake regulatory properties and are involved in stress regulation. The direct action of opiates on ACTH seems to be inhibitory. Endorphins manipulate the serotonergic neural system possibly negatively affecting the delayed feedback component of the ACTH release in stress. Similarly the opiates that are generated from sustained periods of kundalini activation could bring about immunosuppression due to their effect on the serotonergic systems and ACTH release.
Unabating secretion of CRH and ACTH would create hypervigilence, suppress normal sexual activity, create immune deficiency and delayed maturity. ACTH inhibits synthesis of lymphocytes especially in response to proteins, while it amplifies the proliferation of B cells--raising levels of neutrophils the phagocytic cells that normally represent 70% of the population of white blood cells. Neutrophils can only execute one phagocytic event, because they expend all their glucose reserves in the one respiratory blast which releases NADPH oxidase enzyme, which produces large quantities of superoxide free radicals which end up killing the cell.
Depression of the immune system can occur with prolonged stress, dehydration and depression due to an amino acid imbalance generated from incessant cortisol, CRH and vasopressin secretion. This immunosuppression is characterized by an amino acid imbalance that shows an increase in glutamate and arginine and a decrease in tryptophan, cysteine and methionine.
Major depression is associated with the increased secretion of beta-endorphins and enkephalins, which act on the immune system through opiate receptors on the cells. Depression thus reduces the number of natural killer cells and monocytes and inhibits the ingestion capacity of phagocytic immune cells.
Dehydration causes histamine to bring on prostaglandin release, which in turn causes the dissolution or degeneration of bone tissue (osteolysis). Osteolysis and excess calcium release brought about by prostaglandin release (PGE2) raises cytosolic calcium which can deplete ATP reserves and bring about cell death (apoptosis). PGE2 raises transglutaminase (TGE) levels; and enzyme that is strongly anti-inflammatory and immune supressive. It induces apoptosis especially in the thymus gland and liver, through rigidifying the cell membrane. Prostaglandins in the bone marrow are reputed to produce osteolysis, thus raising Ca2+ availability to promote repair or the growth of new blood vessels from pre-existing vessels.
Cytokines are a unique family of growth factors secreted primarily from leukocytes. Many of the lymphokines are also known as interleukins (ILs); specifically, interleukins are growth factors targeted to cells of blood origin. Cytokines bind to a specific cell-surface receptor, initiating intracellular signaling cascades that then alter cell functions. This may include the upregulation and/or downregulation of several genes and their transcription factors that results in production of other cytokines, or increase in the number of surface receptors for other molecules, or suppress their own effect by feedback inhibition. Interleukins have many functions on many different cells and are secreted by a number of cells including monocytes and dendritic cells.
Interleukin-1 (IL-1) is cytokine that acts as a neurotransmitter to stimulate the HPA axis and activate the immune system. Binding sites for interleukins have been found within the HPA axis. IL-1 is also produced by macrophages of the immune system in response to infection. Originally IL-1 was described as T cell activation factor and it also helps promote the maturation and clonal expansion of B cells. Another way it facilitates the immune system is by increasing the expression of cell adhesion molecules on endothelial cells of the blood vessels which allows transmigration of leukocytes, immune cells that fight pathogens, to sites of infection
One action of IL-1 is its action on the hypothalamus. Here IL-1, and some other cytokines (including IL-6), bind to receptors on the endothelial cells within the hypothalamus and appear to reset the thermoregulatory centre increasing the core body temperature causing fever. In the muscle and fatty tissue IL-6 stimulates energy mobilization which leads to increased body temperature. Interleukins are able to trigger oxidative stress as well as general stress mechanisms. High levels are associated with an acute phase of inflammation, including alteration in liver and brain functions.
Interleukin 1-alpha (IL-1) directly inhibits insulin secretion; that is it prevents the glucose-activated increase in insulin secretion and chemical breakdown of glucose via oxidation in the pancreas. It has been found that IL-6 destroys the structure of DNA in insulin producing cells. Cortisol releasing mechanisms promote the secretion of the neurotransmitter interleukin-1 (IL-1) and IL-6, which in turn can increase Cortisol Releasing Hormone (CRH). This means that the cortisol released during stress and dehydration can cause the atrophication of the pancreas and bring about diabetic conditions. Along with lysine, tryptophan is a prominent amino acid employed in the correction of errors during DNA production. Dr. Batmanghelidj says that the cortisol releasing mechanism can result in cell nucleus breakdown and DNA fragmentation. And that the amino acid cysteine forms a type of scaffold with zinc hooks that keep the DNA segments in position.
The autoimmune nature of multiple sclerosis reveals cytokine accumulations in Cerebrospinal Fluid. In multiple sclerosis patients there is a frequent detection of interleukin-1 and tumor necrosis factor but not interleukin-6. Apparently when macrophages release IL-1 it signals more macrophages to invade damaged tissue. The initial burst of IL-1 causes more IL-1 to be released, which amplifies the injury response. This causes a runaway inflammation in the brain where you don't want it. This inflammation adds to the damage caused by the initial injury and destroys more healthy neurons, and since the brain is non-regenerating this leads to irreversible consequences for brain function. Taking substances that reduce IL-1 release reduces damage in multiple sclerosis, Alzheimer's Disease and Downs Syndrome and also reduces neuronal death after stroke.
Another cytokine called transforming growth factor (TGF) is involved in remodeling and repair of tissue after trauma. There is a strong pack relationship between the interleukins, tumor necrosis factor and TGF, which must be activated by the "trauma" of dehydration.
(For all your biochemistry needs Prof. Michael King of Indiana State University School Of Medicine is your man.)
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