Upgraded cognition will tend to cascade down and cause a revolution in the limbic and autonomic system. This is perhaps why significant growth is followed by a period of "regression." I use the word dissolution instead of regression, because it is a contemporary temporary disorganisation/breakdown of patterns of function, to make way for a higher, more complex patterning to form. If there is one thing I am hoping to install in the Global Brain, it's the idea that metamorphosis is a very real and common process that is occurring within us humans. The most obvious examples of this are the huge losses of neurons during various growth periods in childhood and the die-offs in kundalini awakenings.
Apoptosis is word of Greek origin, meaning "falling off or dropping off." Apoptosis is controlled programmed cell death. Cell death plays a considerable role during physiological processes of multicellular organisms, particularly during embryogenesis and metamorphosis. For example in the development of the brain, half of the neurons that are initially created will die in later stages as the adult brain is formed. In the adult human body several hundred thousand cells are produced every second by mitosis, and a similar number die by apoptosis for the maintenance of homeostasis and for specific tasks such as the regulation of immune cell selection and activity.
Apoptosis proceeds thus: the cell shrinks, shows deformation and looses contact with neighbouring cells. Its chromatin condenses and marginates at the nuclear membrane, the plasma membrane undergoes blebbing or budding, and finally the cell is fragmented into compact membrane-enclosed structures, called 'apoptotic bodies' which contain the contents of the cell. These apoptotic bodies are then engulfed by macrophages and thus are removed from the tissue without causing an inflammatory response, or damage to surrounding tissue. Apoptosis is programmed and "tidy" compared to the messy mode of necrotic cell-death, in which the cells suffer a major insult, resulting in a loss of membrane integrity, swelling and disrupture of the cells. During necrosis, the cellular contents are released uncontrolled into the cell's environment damaging nearby cells and producing a strong inflammatory response.
Other than infection the two main modes of cell death are apoptosis (programmed) or necrosis (uncontrolled traumatic). Since a metamorphic die-off is certainly not an infection and does not appear to create inflammation in the tissues, it is apparent that the catabolic breakdown during a die-off is orchestrated by apoptosis. With the cells being recycled through phagocyctosis by the macrophages and turned into building blocks for the regenerating body. As I have said elsewhere the main phase of this "self digesting" event is three days in which bed rest is imperative. Since the HPA axis reduces immunity to conserve energy for fight/flight, die-offs occur months after the hyperaroused peak, after the intense activity of the HPA axis has dropped off somewhat. As soon as there is adequate energy for immune activation made available a die-off will occur. The intervening period reflects the intensity of the hyperaroused nervous system. That is if the hyperactivation is extreme the die-off might come 6 months after the influx-peak, or 3 months after a less intense arousal. For example for a full-on awakening following the normal annual cycle the peak HPA activation occurs in July and the corresponding die-off occurs in November.
It appears that the key player in switching into this die-off mode is the mitochondria of our cells. In fact we must look to mitochondria as being the chief orchestrators of the entire kundalini alchemy. Mitochondria play a central role in apoptosis by amplifying and mediating extrinsic apoptotic pathways, and in the integration and propagation of death signals originating from inside the cell such as DNA damage, oxidative stress, starvation. Apoptosis is most often induced through the disruption of the mitochondrial inner transmembrane potential and through a sudden increase in the permeability of the inner mitochondrial membrane. This causes an influx of water by osmosis into the mitochondria with the eventual rupture of the outer mitochondrial membrane, resulting in the release of pro-apoptotic proteins from the mitochondrial intermembrane space into the cytoplasm. Proteins released start a apoptosic cascade, ATP synthesis is stopped and free radical generation exceeds the cells antioxidant capacities leading to the oxidation of lipids, proteins, and nucleic acids.
The apoptosis signalling pathways in viable cells are kept in an inactive state and are only turned on in response to a death stimulus. It is thought that all cells of a multicellular animal might be intrinsically programmed to self-destruct and would die instantaneously unless cell death is continuously repressed by survival signals from growth factors, antioxidants, hormones, nutrients. These anti-apoptotic regulatory molecules keep in check the activation of pro-apoptotic factors. During a die-off however the pro-apoptotic factors become dominant and an exquisite cascade of cell death and self-digestion is set in motion.
Free radicals are generated in the mitochondrial electron transport system. Mitochondria are the source of 80% or more of the oxyradicals generated in the neuron. Reactive oxygen species were shown to cause neuronal degeneration by activation of ionotropic glutamate receptors. Ca2+ dysregulation causes excessive activation of glutamate ionotropic receptors, disrupting the mitochondrial electron transport system.
Mitochondrial glutathione peroxidase (GSH) depletion and subsequent oxidant induced loss of mitochondrial function was shown to precipitate programmed cell death or apoptosis, since GSH is the major defense against the endogenously produced free radicals. Seizures/kindling may result from glutathione peroxidase deficiency. Selenium is necessary to the formation of GSH, and so selenium deficiency may be an important factor in the promotion of seizures and subsequent neuronal damage.
The 5-carbon sugarD-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. So D-Ribose may be an essential supplement to take especially during the down-cycles to prevent enervation and excessive apoptosis.
Creatine is synthesized in the body from three amino acids: glycine, arginine, and methionine. It is involved in energy metabolism as a muscle fuel through its role of regenerating ATP from ADP. Creatine phosphate serves as a reservoir of high-energy phosphate bonds required to rephosphorylate ADP into ATP. The resynthesize ATP at required rate improves endurance and available energy during exercise or excessive expenditure like kundalini awakenings. To prevent fatigue and excessive catabolic breakdown from lack of ATP production ribose and creatine should be taken around the clock during awakening.
Aging appears to be in good part due to the oxidants produced as by-products of normal metabolism by mitochondria. Age related decline in the function of mitochondria is relieved by the supplementation of alpha lipoic acid and L-carnitine. Research found that the enzyme carnitine acetyltransferase is less active in old rats. Supplementation with a combination of acetyl-L-carnitine and alpha-lipoic acid restored the enzyme's activity nearly to that found in young rats. The acetyl-L-carnitine protects the enzyme and the higher levels are enabling the protein to work, while alpha-lipoic acid reduces free radicals. The two together reverse the effects of aging on mitochondria. Carnitine also helps protect the mitochondria membranes and assists in the transport of fatty acids into the mitochondria. Since the mitochondrion provide the energy source (ATP) for cell function, through mitochondrial oxidative metabolism of glucose, interference with the mitochondrial electron transport system can have fatal consequences to the cell. The high free radical load during metamorphosis may put such a high demand on the body's glutathione production that there is insufficient to protect against apoptosis. Alpha Lipoic Acid may be more effective than NAC in preventing apoptosis.
Charged phospholipids in the cell membranes play a crucial role in apoptosis. There is increasing evidence that the arrangement of polar lipids in the membraine phospholipids matrix is an important factor in apoptosis; along with homeostatic mechanism responsible for preserving membrane lipid composition and asymmetry. Early apoptotic events are associated with disturbances in the lipid bilayer matrix generating changes in membrane permeability of mitochondrial membrane in particular.
The body recycles the cellular materials from cell death by the process of autolysis, also called self-digestion. It is kind of obvious what happens to the macrophages that "eat" the body during a die-off and how they recycle resources to the body. Calculation of the influx of monocytes into the spleen and of the local production of macrophages showed that under steady-state conditions, 55% of the spleen macrophage population is supplied by monocyte influx and 45% by local production. This means that there is a dual origin of spleen macrophages. The mean turnover time calculated with the value for the efflux of spleen macrophages is 6.0 days. Since worn out red blood cells are ingested by phagocytic cells in the liver and spleen, I suspect that macrophages are also absorbed back into the system in this way. Perhaps they too undergo apoptosis and are taken up by phagocytic cells in the liver and spleen. Both the liver and spleen are capable of generating ecstasy, quite possibly when there is a fresh supply of extra ATP recycled from an increase in the breakdown of cells.
Apoptosis is a normal function of the immune system. It is apparent in metamorphosis that the body cannibalizes itself by cell death through oxidation leading to apoptosis and immune phagocytosis. Recycling the constituents of cells is probably a far more energy efficient form of nutrition than the digestion of food. And considering that the digestive system is disrupted with the hyper-SNS, it makes sense that during metamorphosis the body transforms itself through self-digestion. The macrophages eat inferior cells and scavenger enzymes breakdown used and damaged proteins into their component parts for reuse by the cell. Since the energy of the body has shifted toward self-digestion, this is the primary reason why our diet during metamorphosis needs to be light and nutrient, rather than complex and hard to digest. Digestion of food will take energy away from the self-catabolic digestive process.
The most important point I can emphasize is to not presume the catabolic breakdown of cells, and the increased free radical load during metamorphosis as pathological, for this will only increase our stress level. We cannot regenerate without going through the dissolution. Since metamorphosis is a natural process which is "self-governing," our job in working-with what is happening is to first not increase the free radical burden on the body with harmful substances and secondly to increase our antioxidant intake and distressing techniques. We all know the most harmful free radical inducers by now, they are: smoking, pollution, alcohol, charred meat, hydrogenated oils, aged cheeses, rancid fats, sugar and stress.
Found in all cells, mitochondria provide cellular energy in their role as the body's power generators. In addition, mitochondria are intricately involved in a process called apoptosis, or programmed cell death, which is the body's normal method of disposing of damaged, unwanted or unneeded cells. Apoptosis can be defined as a cell death process in which activation of catabolic processes and enzymes occurs prior to the bursting of the cell (cytolysis), thereby facilitating the recognition, uptake, and digestion of the apoptotic cell by dying neighboring cells. Cytolysis occurs in a hypotonic environment, where due to the lower osmotic pressure, water diffuses into the cell until there is more solutes within the cell. If too much water enters the cell will eventually burst, releasing cell contents.
The central role of mitochondria in neurodegenerative disorders has become apparent. Mitochondria appear to be most susceptible in glutathione-depleted tissues because of the high flux of oxygen radicals from the mitochondria's OxPhos activities. Because the mitochondria assume the bulk of the endogenous oxygen radical burden, yet are unable to make their own GSH, so they must import it from the cell cytosol. As oxidative phosphorylation proceeds in the mitochondria, invariably single electrons escape, leaking out to react with ambient oxygen and generate oxygen free radicals. An estimated 2-5% of the electrons that pass through the OxPhos system become free radicals and since OxPhos processes at least 95 percent of all the oxygen used by the body, this flux of wayward oxygen free radicals poses a potential toxic risk to the organism.
Mitochondria exhibit major changes in their structure and function during apoptosis and are now considered major players in the apoptotic process of mammalian cells. Mitochondria have been implicated in the maintenance of the calcium (Ca2+) "set-point" in cells, where control of Ca2+ levels plays a significant role in enzymatic regulation and energy production. Pathological conditions that result in increased tissue Ca2+ concentrations include ischemia, oxidative stress, and excito- and neurotoxicity. The subsequent increase in cytoplasmic Ca2+ is widely considered to be a critical initiating event in the development of damage in cells destined to die. Apoptotic and necrotic cell damage is always preceded by an increase in Ca2+. Ca2+ increase in cerebrospinal fluid was noted in connection with psychotic episodes, so I imagine that acid conditions promote cell death prior to and during psychosis.
Cell energy production is reduced by excessive free cytosolic Ca2+ leading to uncoupling of mitochondrial oxidative phosphorylation with consequently decreased ATP synthesis. The resulting inactivity of ATP-dependent pumps would lead to membrane depolarization and further exacerbating Ca2+ influx in self-reinforcing accumulative fashion. The cells then make an effort to restore the normal cytoplasmic Ca2+ concentration by removing Ca2+ to the extracellular space and/or uptake into organelles, including mitochondria.
Sodium influx into cells causes depolarization and increasing Ca2+ in the cells. In depression (down), mood shifts are accompanied by shifts in the amount of salt and fluid in and around the cells. Depressed patients have consistently shown that they retain salt and fluid only during their depressed phase. The manic (up) phase however is accompanied by increased urea in the urine, probably due to the breakdown of cells that could not handle the reduction in ATP, the increase in Ca 2+, and the excess glutamate stimulation.
Glutamate is the most prominent neurotransmitter in the body, being present in over 50% of nervous tissue. The primary glutamate receptor is specifically sensitive to N-Methyl-D-Aspartate (NMDA), which causes direct action of the receptors ion channel, to drive the neuron to depolarize. Depolarization triggers the firing, or action potential of the neuron, therefore NMDA is excitatory. Hyperactivation of glutamate receptors causes neuron programmed cell death or apoptosis through the oxidative stress of free radicals. This is because mitochondria are the source of 80% or more of the oxyradicals generated in the neuron and Ca2+ dysregulation causes excessive activation of glutamate ionotropic receptors, disrupting the mitochondrial electron transport system. Glutamate concentrations in the brain and CSF are higher in some seizure patients.
For more info read Dr. Ward Deans papers on Mitochondrial Restoration and Mitochondrial Theories of Aging
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