Sostenibilidad y calidad de vida

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 maybe 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 maybe 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 membrane

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.

sPleen recYcles BoDY

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.

mitocHonDria’s role in cell DeatH

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 increased Ca2+ levels 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