NAC-OLEANDER PROTOCOL reply to Cypriano

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Cypriano, I don't think you read my feedback properly. I never said at any point that taking oleander and antioxidants makes the oleander less effective. In fact, I said just the opposite. The oleander plus NAC is very effective precisely because both promote the synthesization of Glutathione, the main antioxidant in the body. It is also involved with the mitochondrial production of ATP. The researchers who promote the Apoptosis/Necrosis theory advise against any substance that does that because it is the lack of ATP that initially leads to the Apoptosis or Necrosis of cancer cells.

 

I suggest you read Dr Heinrich Kremer's recently translated book "The Silent Revolution in Cancer and AIDS Medicine" where the role of Glutathione, oxidative stress and the involvement of the mitochondria in the cancer process are discussed in depth (with nearly 100 pages of references to studies that you can peruse for a year or more).

Marc Swanepoel

 

 

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Cypriano Aguerria

oleander soup

Friday, November 13, 2009 1:52 AM

RE: NAC-OLEANDER PROTOCOL questions

Thank You for your information. However, your theory is wrong. the very fact that you say that the taking of antioxidants and oleander makes the oleander in effective is nonsense.Where are you getting your information? what research supports your theory? It sounds like the nonsense that most oncologists believe that vitamins and natural supplements can make chemotherapy ineffective. PLease point me to the research that supports your theory. Sincerly Cypriano

 

oleander soup From: marcswan (AT) global (DOT) co.zaDate: Thu, 12 Nov 2009 21:47:41 +0200 NAC-OLEANDER PROTOCOL questions

 

 At least the researchers had the honesty to admit that "the mechanisms by which this effect is produced are not clear" when describing the anti-cancer effect of the oleander glycosides in the paper quoted below. Apart from not understanding the mechanisms, it is also important to realize that there are only minute quantities of the cardiac glycosides that these researchers are referring to in a properly filtered water extract of oleander. The glycosides can therefore not be the ONLY mechanism whereby oleander is effective against cancer. The main reason why the researchers consider NAC a problem, is because it increases glutathione, the main antioxidant in the body. As in the case of Paw-paw, Graviola, Cantron, Protocel and the chemotherapy drug Tarceva, the researchers rely on the possibility that oleander without NAC will also lead to either apoptosis or necrosis of cancer cells. As I have explained before, the period when the apoptosis/necrosis destruction of cancer cells is possible, is very limited and the cancer cells themselves very quickly use their own countermeasures to overcome this possibility. At that stage, it is only by taking both oleander and NAC that cancer can be reversed. The Cysteine in NAC allows the body to synthesize Glutathione which, in turn, helps the body to correct the oxidative stresses - which initially caused certain mitochondrial imbalances - which subsequently led to cancer (a self-protection mechanism of cells that are under stress).

 

For people who have not read my explanation of the apoptosis/necrosis theory, I have repeated it below.

 

Marc Swanepoel

 

 

The Apoptosis/Necrosis theory:All cells require energy in the form of Adenosine Triphosphate (ATP). This substance cannot be stored in the cells and at any stage we have enough to last for about 3 to 5 seconds. It is thus a continuous process. A few billion years ago, before there was oxygen in the atmosphere, primitive cells (eukaryotes) evolved the process of producing ATP energy without the use of oxygen by a process of glycolysis. Later on in the evolutionary process, when oxygen became part of the atmosphere, certain types of bacteria evolved a much more efficient way of producing ATP by utilizing oxygen through a process known as oxidative phosphorylation (OXPHOS). This new process was roughly 20 times more efficient than the glycolysis process. Roughly two billion years ago, these bacteria and the original eukaryotes fused into a symbiotically functioning and more complex cell system. Researchers now acknowledge that the bacterial component of cells is the cellular mitochondria. All cells, with the exclusion of red blood cells, can have thousands of the mitochondria. These new "symbionts" can switch between the two systems of ATP production, depending on the demands of the cells. During the fetal stage and repair of cell damage, it switches to the ATP production from glucose in the cytoplasm. During the cell differentiation stage, it switches to the OXPHOS system of oxidative ATP production in the cell mitochondria. The switching system itself is controlled by an intricate signaling system that depends on the permeability of the mitochondrial membrane and its influence on the Ca 2+ cycle, the electrical charge across the mitochondrial membrane and other factors. All these factors, in turn, are modulated by the so-called thiol pool of which glutathione is the most important component.When body cells are under oxidative or nitrosative stresses caused by environmental factors and/or life style, the thiol pool normally gets depleted and, with it, the ability of the mitochondria to produce ATP through the OXPHOS system. As a defensive measure, the mitochondrial switch puts the cells into the more primitive way of survival by reverting to the much less efficient enzymatic production of ATP in the cytoplasm. If the aforementioned stresses are chronic, the switch remains in this position and we call the condition "cancer" - identified by the undifferentiated division of cells.If the cut-off of ATP production by the OXPHOS system is sudden, the cells will die and the process is known as 'necrosis' or sudden cell death. If it is more gradual, the affected cells can 'commit suicide', a process know as 'apoptosis'. Treatments like the acetogenins in Paw-Paw extract, Graviola and similar plants, Cantron, Protocel as well as the chemotherapy drug Tarceva, have the effect of reducing the ATP in all cells and it is then hoped that the described 'apoptosis' of cancer cells will take place. Because of the fact that the ATP production of ALL cells is reduced, one can feel very tired when using these supplements (or chemotherapy).Another very important fact is that the apoptosis of cancer cells will only take place if the mitochondrial membrane is still permeable and the CA 2+ cycle is still working. In all advanced cancers, this permeability is blocked as part of the defense mechanism of cells and apoptosis CANNOT take place, however much Paw-Paw extract or any ATP reducing substance one takes. One can thus see that the treatment will work in some cases where the cancer is at a stage where the mitochondrial switch is still fluctuating between the two methods of ATP production. This 'window of opportunity' is relatively short and when metastases have appeared, it is normally a sign that the mitochondrial membranes are blocked. The only alternative is then to reactivate the mitochondrial switch by getting rid of the oxidative and nitrosative stresses, and by topping up the depleted glutathione. Nothing else will work.

 

The danger in using substances that will reduce ATP and/or glutathione is twofold. As the reduction of ATP and/or glutathione is not restricted to cancer cells it can (a) result in cells that are not yet cancerous becoming cancerous and (b) result in fungal and bacterial overgrowth that can be dangerous for weakened patients. If one looks up the known side-effects of Tarceva, for example, one will see that they are all associated with a reduction in energy and the inability of cells to defend themselves against internal pathogens (fatigue, rash, infection, mouth sores, etc).

 

 

 

--- On Tue, 11/10/09, fehmiunal <unal.fehmi > wrote:

fehmiunal <unal.fehmi > NAC-OLEANDER PROTOCOL questions??oleander soup Date: Tuesday, November 10, 2009, 8:24 PM

Following excerpt is from a paper studying oleander, explaining its mechanism of effect against cancer cells. It is explained here that oleander needs oxygen species for anticancer effects, and NAC inhibits formation of -oleander induced- oxygen species. that means it is not beneficial to use antioxidants during oleander treatment. NAC stops oleander killing cancer cells. it increases gluthation and serves as antioxidant. I wonder why it is favored in this group to use NAC as it interferes whith oleander? any ideas?best wishes to all,excerpt: J Exp Ther Oncol. 2006;5(3):167- 81.Oleandrin-mediated oxidative stress in human melanoma cells.Newman RA, Yang P, Hittelman WN, Lu T, Ho DH, Ni D, Chan D, Vijjeswarapu M, Cartwright C, Dixon S, Felix E, Addington C.Department of Experimental Therapeutics, Univ. Texas M. D. Anderson Cancer Center, Houston, TX 77054, USA. rnewman (AT) mdanderson (DOT) orgWhile certain cardiac glycoside compounds such as oleandrin, bufalin and digitoxin are known to be associated with potent cytotoxicity to human tumor cells, the mechanisms by which this effect is produced are not clear. We now demonstrate that incubation of human malignant melanoma BRO cells with oleandrin results in a time-dependent formation of reactive oxygen species (ROS). Use of Mito-SOX and dihydroethidine dyes revealed the presence of oleandrin-mediated superoxide anions. Formation of superoxide anions correlated with a loss in cellular viability, proliferation and cellular defense mechanisms such as GSH content. Oleandrin also resulted in an unusual time-dependent mitochondrial condensation in BRO cells that could be blocked with use of N-acetyl cysteine (NAC). NAC was also shown to block ROS formation and partially prevent oleandrin-mediated loss of cellular GSH. Taken as a whole, the data suggest that exposure of human tumor cells such as BRO to oleandrin results in the formation of superoxide anion radicals that mediate mitochondrial injury and loss of cellular GSH pools. These mechanisms play a role in cardiac glycoside mediated tumor cell injury. Conversely, incubation of NAC, a precursor to GSH, largely prevents oleandrin-mediated inhibition of proliferation and mitochondria structural changes.PMID: 16528968 [PubMed - indexed for MEDLINE]