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  by STAFF - Matheus
 
			May 23, 2013 
			from
			
			DrSircus Website 
			
			
			Spanish 
			version
 
			  
			  
			  
			
			 Mitochondria 
			Inside
 
 
 
			  
			Dr. Terry Wahls 
			learned how to reverse accelerating multiple sclerosis using an 
			evidence-based, functional medical approach focusing on 
			orthomolecular nutrients and nutrition.  
			  
			Using the lessons she 
			learned at the sub-cellular level, she used diet to cure 
			
			her MS and 
			get out of her wheelchair.  
			  
			Her TED talk is quite 
			convincing:
 
			  
			  
			  
			 
			  
			Contemporary medicine has not understood the basics of mitochondrial 
			physiology.
 
			  
			Most doctors have no idea why, 
				
					
					
					magnesium
					
					bicarbonate
					
					selenium
					
					
					sulfur, 
			...are important to the 
			
			mitochondria.  
			  
			But basic science knows 
			this so it is a wonder that information does not get out about what 
			to do to repair and fire up the mitochondrial energy factories of 
			the cells.
 
			If too many 
			mitochondria fail, there is nothing that can be
 done to prevent death. Any successful treatment can
 only be to prevent too many mitochondria from failing.
 
 
			The mitochondria are the power stations of our cells.
 
			  
			They are as important to 
			our lives and health as electrical power stations are to modern 
			civilization. We just cannot get along without them. If mitochondria 
			get severely damaged, they die. If cells lose their mitochondria, 
			they lose their power source, and they die. When enough cells die, 
			we die.
 Mitochondria disease is not usually life threatening in an emergency 
			sense.
 
			  
			There are few infections that attack the mitochondria though 
			there are poisons like cyanide which will wipe out our energy 
			stations and kill us without much fanfare. The mitochondria are 
			extremely sensitive to heavy metals and general chemical insults.
			 
			  
			If the mitochondria are 
			denied the basic nutrition they need to function, they cease to 
			function normally.
 Dr. Majid Ali says,
 
				
				“Injured 
				mitochondria mutate at much higher rates. Damaged mitochondria 
				are exhausted mitochondria. Exhausted mitochondria cannot 
				produce sufficient ATP molecules. An insufficient supply of ATP 
				molecules means insufficient energy. Insufficient molecular 
				energy means clinical chronic fatigue.” 
			These organelles are the 
			power generators of the cell, converting oxygen and nutrients into 
			ATP (adenosine triphosphate).  
			  
			ATP is the chemical 
			energy "currency" of the cell that powers the cell’s metabolic 
			activities. This process is called aerobic respiration and is the 
			reason animals breathe oxygen.
 
			Mitochondria work 
			by generating an electrical
 potential and a pH gradient across that inner membrane.
 
 
			The mitochondrion is different from other organelles [1] 
			because it has its own DNA and reproduces independently of the cell 
			in which it is found; an apparent case of endosymbiosis.[2]
 
			  
			They really are not 
			quite us in the sense that their genetic pool is outside of our own 
			DNA that make us uniquely us. Unlike nuclear DNA, mitochondrial DNA 
			doesn’t get shuffled every generation, so it is presumed to change 
			at a slower rate.
 
			  
			
			
			 
			Mitochondria Image
 
			Recent breakthroughs in our understanding of autism and other 
			neurological diseases are coming through mitochondrial research and 
			it is important to note that pharmaceutical drugs are mostly 
			mitochondrial poisons.
 
			  
			Mercury is a 
			mitochondrial poison.  
			  
			Data suggest that 
			moderate levels of mercury administered over an 8 week period can 
			affect adversely the integrity of mitochondrial membranes.[3] 
			The field of pediatrics has been perverted by the vaccines and 
			endless antibiotics they have administered to their patients.  
			  
			Pediatricians do the 
			unforgiveable when they inject mercury directly into children’s 
			veins and that is why I wrote and have always given away The Terror 
			of Pediatric Medicine. 
			  
			The German cancer 
			researcher Dr. Paul Gerhard Seeger [4] 
			demonstrated in 1938 that in most cases cancer starts in the 
			cytoplasm, the jelly-like outer part of the cell, and especially in 
			the energy-producing mitochondria.    
			Here food fragments are 
			normally oxidized in a series of enzymatic steps called the 
			‘respiratory chain’. Seeger showed that in cancer cells this 
			respiratory chain was more or less blocked, especially at the site 
			of the important enzyme cytochrome oxidase.    
			Without it the cell can 
			produce energy only anaerobically like a fungal cell. This is very 
			inefficient and the resulting overproduction of lactic acid makes 
			the cell and the whole body overly acidic.
 Seeger and others found that cancer cells utilize only between 5 and 
			50% of the oxygen of normal cells. The virulence of cancer cells is 
			directly proportional to their loss of oxygen utilization, and with 
			this to the degree of blockage of the respiratory chain. In 1957 
			Seeger successfully transformed normal cells into cancer cells 
			within a few days by introducing chemicals that blocked the 
			respiratory chain.
 
 Seeger’s most important discovery was the certainty that that 
			certain nutrients, mainly from the vegetable kingdom, could restore 
			cellular respiration in low-virulence cancer cells and, with this, 
			transform them back into normal cells.
 
 Seeger’s finding that cancer originates in the cytoplasm and not in 
			the nucleus was confirmed by other researchers.
   
			Between 1975 and 1977 
			they repeated an experiment 93 times in which they replaced the 
			nucleus of a fertilized mouse egg with the nucleus of a cancer cell. 
			In each case the egg developed into a healthy, cancer-free mouse and 
			even the offspring remained cancer-free. Similar results were 
			achieved with frog eggs.
 There is increasing evidence that impairment of mitochondrial 
			function, oxidative damage, and inflammation are contributing 
			factors in the pathogenesis of Parkinson’s disease (PD).
   
			There is substantial 
			evidence that there is a deficiency of activity of the mitochondrial 
			electron transport chain in PD. Impaired mitochondrial function and 
			activated microglia may both contribute to oxidative damage in PD.[5]
 Multiple Sclerosis is the most common inflammatory 
			
			demyelinating 
			disease of the central nervous system and is the leading cause of 
			non-traumatic neurological disability in young adults.
   
			Researchers believe that 
			mitochondria play a key role in chronic axonal loss in this disease. 
			The mitochondria present within the chronically demyelinated axons 
			will be functioning at full capacity for many years but eventually, 
			despite antioxidant defenses, free radical damage will accumulate 
			and mitochondrial function will become compromised.    
			ATP concentration within 
			the axon will decrease and the effect on axonal function will be 
			profound.[6]
 Tissue damage in 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced 
			colitis is accompanied by the arrest of mitochondrial respiration, 
			loss of mitochondrial DNA, and the expression of nuclear-encoded 
			mitochondrial proteins. Selenium effectively protects colon 
			mitochondria prevented inflammatory and necrotic changes.
   
			Selenium in a high dose 
			is therefore a potential therapeutic agent in inflammatory bowel 
			disease.[7]
 Nearly a century of scientific research has revealed that 
			mitochondrial dysfunction is one of the most common and consistent 
			phenotypes of cancer cells. A number of differences in the 
			mitochondria of normal and cancer cells include differences in 
			mitochondrial metabolic activity, molecular composition of 
			mitochondria and mtDNA sequence, as well as in alteration of nuclear 
			genes encoding mitochondrial proteins.
   
			Mitochondria and Cancer, 
			edited by Keshav K. Singh and Leslie C. Costello, 
			presents thorough analyses of mitochondrial dysfunction as one of 
			the hallmarks of cancer.
   
			
			 
			Mitochondrial 
			Electron Transport Chain 
			
 
			Dr. Michael R. Eades 
			says,  
				
				“As the high-energy 
				electrons are passed along down the inner mitochondrial membrane 
				they occasionally break free. When they break free, they become 
				free radicals. These rogue free radicals can then attack other 
				molecules and damage them.    
				Because these free 
				radicals are loosed within the mitochondria, the closest 
				molecules for them to attack are the fats in the mitochondrial 
				membranes.   
				If enough of these 
				fats are damaged, the membrane ceases to work properly. If 
				enough of the membrane doesn’t work, the entire mitochodrium is 
				compromised and ceases functioning. If enough mitochondria bite 
				the dust, the cell doesn’t work and undergo apoptosis, a kind of 
				cellular suicide.    
				This chronic damage 
				and loss of cells is the basic definition of aging.” 
			  
			Sulfur is one of the 
			basic elements of life. In fact, sulfuris the fourth most abundant mineral in the body. The proper
 acid alkaline balance of the body cannot be maintained without it.
 
 
			Sulfur is a main source of antioxidants in the mitochondria. Sulfur 
			has a vital relationship with protein, since sulfur is found in the 
			amino acids,
 
				
					
					
					methionine
					
					cystine
					
					cysteine 
			Thus, these amino acids 
			are known as the sulfur bearing amino acids which are considered the 
			building blocks of protein.
 
			  
			  
			Magnesium 
			Bicarbonate
 
 Magnesium functions as a bicarbonate co-transporter into cells. And 
			
			bicarbonate acts as a transporter of magnesium into the 
			mitochondria.
 
			  
			Magnesium influx is 
			linked with bicarbonate transport according to the Dietary Reference 
			Intakes guide from the Institute of Medicine. Magnesium transport 
			into or out of cells requires the presence of carrier-mediated 
			transport systems.  
			  
			ATPase reaction has a 
			broad pH optimum centering on neutral pH, with little significant 
			activity above pH 9.0 or below pH 5.5.  
			  
			Thus anything that moves 
			us from overall acid conditions toward alkaline that recover the 
			neutral zone is going to enhance cell metabolism via mitochondrial 
			optimization.
 If cancer is a mitochondrial disease it can be treated directly with 
			a cocktail of magnesium bicarbonate, sulfur and selenium and it 
			would probably be a good idea to supplement strongly with iodine as 
			well.
 
			  
			All of these basic cellular substances will work together to 
			repair damaged cells and their mitochondria and fire them up for 
			full activity.
 In the near future it will be magnesium bicarbonate available in 
			concentrated form that is going to turn the world of oncology upside 
			down. It may be a year before production can make this compound in 
			concentrated form widely available to the public.
 
			  
			Presently it is 
			available to only a precious few but magnesium bicarbonate water is 
			available in a few bottled waters like 
			
			Noah’s in California and 
			
			Unique Water in Australia.  
			  
			Within a few weeks I 
			will be introducing a gravity fed Berkey-type of water filter, which 
			will be the first in the world to produce magnesium bicarbonate 
			water in peoples’ homes.
 
 
			  
			  
			References 
				
				[1] ORGANELLES mean 
				little organs. Basically this means that organelles have 
				specific roles to play in how cells Gunther, 1003; Romani et 
				al., 1993work just like organs help the body to function 
				properly as a whole. Some organelles are separated from the rest 
				of the cell by lipid bi-layers similar in structure to the cell 
				membrane.
 [2] The endosymbiotic theory concerns the origins of 
				mitochondria and plastids (e.g. chloroplasts), which are 
				organelles of eukaryotic cells. According to this theory, these 
				organelles originated as separate prokaryotic organisms which 
				were taken inside the cell as endosymbionts. Mitochondria 
				developed from proteobacteria (in particular, Rickettsiales or 
				close relatives) and chloroplasts from cyanobacteria.
 
 [3] The effects of mercury ingestion on hepatic mitochondrial 
				membranes of chicks. Poult Sci. 1976 Nov;55(6):2280-4.
 
 [4] The only book available in English is Seeger, P.G. and S. 
				Wolz: Successful biological control of cancer by combat against 
				the causes. Neuwieder Verlagsgesellschaft, Neuwied, Germany 
				1990. The most important book is Seeger, P.G: Krebs – Problem 
				ohne Ausweg? (“Cancer – Problem without Solution?”) Verl. f. 
				Medizin Fischer, Heidelberg, Germany 1974, 2nd ed 1988
 
 [5] http://www.ncbi.nlm.nih.gov/pubmed/12846981
 
 [6] Mitochondrial dysfunction plays a key role in progressive 
				axonal loss in Multiple Sclerosis. Medical Hypotheses, Volume 
				64, Issue 4, Pages 669-677 H.Andrews, P.Nichols, D.Bates, 
				D.Turnbull
 
 [7] High selenium diet protects against tnbs-induced acute 
				inflammation, mitochondrial dysfunction, and secondary necrosis 
				in rat colon. TIROSH Oren ; LEVY Eran; REIFEN Ram; Hebrew 
				University of Jerusalem. ISSN 0899-9007 2007, vol. 23, no11-12, 
				pp. 878-886
 
 [8] Gunther, 1003; Romani et al., 1993
 
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