Must Read, Killing Cancer Cells Using Electric Potential, DMSO, Methylene Blue

Obi-wan

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IMO cells like to be at a resting potential of -40 to -80 Volts. Excitation causes the cell to depolarize (potassium leaves the interior and sodium enter it). Per Ray cancer cells develop during chronic low excitation keeping the cell depolarized. This creates a disconnect to oxidative phosphorylation.

Cancer cells go into a fermentation process producing high Lactic acid

ACV/BS connects the oxidative process through acetate causing the cell to hyperpolarize (potassium re-enters the interior and sodium leaves)

Cancer cells revert to normal when the cells return to their resting potential of -40 to -80 volts but excitation would have to be removed

Excitation could be from endotoxin, ionized radiation, etc.
 
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TreasureVibe

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There are different pathways but oxaloacetate eventually converts to acetyl-CoA also

A seminar at the physicians Conference in 2014 on Oxaloacetate supplementation in disease with studies.. He mentions that in brain tumors some tumors continued to grow despite supplementation of oxaloacetate. But it is an interesting seminar to look at. It also describes ascorbic acid funnily enough to be able to aid in the Krebs cycle in some way:

 
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TreasureVibe

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"mitochondrial respiratory capacity is maintained in cancer" I don't agree. Fermentation is maintained in Cancer...Cancer has a respiratory defect...normal cells produce oxidative phosphorylation, cancer does not. But ACV/BS allows that to happen. "Don't get caught up in the tree's. Look at the forest" -my quote
hey generally selected for during tumor evolution. In most cancers, oncogenic driver mutations, such as activation of K-ras, c-Myc, and phosphatidylinositol-3 (PI3) kinase or loss of phosphatase and tensin homolog (Pten) and p53, not mutations that inactivate mitochondrial respiration complexes, promote glycolysis (Vander Heiden et al., 2009). Moreover, most cancers still retain mitochondrial function, including respiration. Some tumors have high levels of oxidative phosphorylation, while others that are relatively glycolytic still retain mitochondrial respiration and other functions (Zu and Guppy, 2004). When quantitated by flux analysis in cultured cells, Akt transformation does not substantially impact respiration, whereas Ras transformation reduces respiration, but nevertheless a majority of ATP is still produced by oxidative phosphorylation (Fan et al., 2013; Gaglio et al., 2011; Yang et al., 2010). Functional tests for the requirement for mitochondrial activity in cancers have revealed their importance. Inactivation of the mitochondrial transcription factor Tfam, which depletes mitochondria from tumor cells, impairs K-ras lung tumor growth in autochthonous models (Weinberg et al., 2010). Depleting mtDNA from tumor cells by generating r0 cells by poisoning mtDNA replication compromises tumorigenesis (Tan et al., 2015). Moreover, selection for restoration of the growth of mtDNA-depleted r0 tumors is associated with the horizontal transfer of mitochondrial genomes from host tissue and restoration of respiration. These and other findings suggest that the role of mitochondria in cancer is not as simple as Warburg envisioned. In contrast, they point to the importance of mitochondrial function to tumor growth. Mitochondria Integrate Catabolism, Anabolism, and Signaling Mitochondria are bioenergetic and biosynthetic organelles that take up substrates from the cytoplasm and use them to drive fatty acid oxidation (FAO), the TCA cycle, the electron transport chain (ETC), and respiration, and to synthesize amino acids, lipids, nucleotides, heme, and iron sulfur clusters, as well as NADPH for their own antioxidant defense (Figure 1) (Wallace, 2012). NADH and FADH2 produced via TCA cycle turning powers the ETC, which in turn generates a proton gradient across the mitochondrial inner membrane that produces ATP through the action of the H+ -ATP synthase. Dihydroorotate dehydrogenase (DHODH), which is essential for de novo pyrimidine synthesis, requires a functional respiratory chain for activity (Khutornenko et al., 2010). The reactive oxygen species (ROS) generated in mitochondria as a byproduct of the ETC can activate signal transduction pathways such as that of MAP kinase and the HIFs (in normoxia is referred to as pseudohypoxia) (Shadel and Horvath, 2015; Sullivan and Chandel, 2014). Excess ROS production can also lead to cell death. Mitochondria sequester Ca2+, the selective release of which controls signaling and a broad array of cellular functions. Mitochondria act as signaling platforms for innate immunity (e.g., MAVS and by the release of mtDNA) (Weinberg et al., 2015; West et al., 2015). The BCL-2 family of proteins at the mitochondrial outer membrane control programmed cell death by apoptosis.

Source: https://www.cell.com/molecular-cell/pdf/S1097-2765(16)00095-2.pdf


For decades, tumor cells have been considered defective in mitochondrial respiration due to their dominant glycolytic metabolism. However, a growing body of evidence is now challenging this assumption, and also implying that tumors are metabolically less homogeneous than previously supposed. A small subpopulation of slow-cycling cells endowed with tumorigenic potential and multidrug resistance has been isolated from different tumors. Deep metabolic characterization of these tumorigenic cells revealed their dependency on mitochondrial respiration versus glycolysis, suggesting the existence of a common metabolic program active in slow-cycling cells across different tumors. These findings change our understanding of tumor metabolism and also highlight new vulnerabilities that can be exploited to eradicate cancer cells responsible for tumor relapse.


Source: Tumors and Mitochondrial Respiration: A Neglected Connection

Maybe in some types of cancer, or in cases of advanced cancer, mitochondrial respiration exists in certain cancer cells. Perhaps mitochondrial respiration is a means by which a tumor grows past a certain point. Tumors seem to have some type of intelligence or so it seems, or possess certain means to grow.
 
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TreasureVibe

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https://link.springer.com/article/10.1007/s10863-007-9070-5

This study contains a very interesting quote, something I've been saying too:

Therefore, optimistically, if we view cancerous cells as sophisticated types of “infectious-like” cells that have developed and gone awry in our own bodies, i.e., exhibit the capacity to multiply, mutate, invade, spread (metastasize), and kill, we can believe also that natural agents may already exist, or synthetic agents can be made, that will selectively and repeatedly kill the major types of cancer regardless of stage.

Official estimates state that 20% of all cancers worldwide are caused virally:

Viruses May Cause More Cancer than Previously Thought
Viruses Associated with Human Cancer

Sloane said that he estimates that 90% to 98% of cancers are caused by a virus. The rest 2 to 10% of cancers he said were caused by bacteria, fungi, or genetical caused cancers. Genetical caused cancers were very rare he said, and almost only seen in newborns.
 
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TreasureVibe

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I forgot to mention to my previous post, that parasites too are part of the 2 to 10% of cancers according to Sloane and that parasites-caused cancers are also very rare.
 
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TreasureVibe

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Nothing works without electric potential. That's what makes electrons flow just like water flows from higher potential to lower potential. Ray did not believe in ion pumps but Ray had limited knowledge in cellular electricity. Below from Wikipedia:

Membrane potential


Membrane potential (also transmembrane potential or membrane voltage) is the difference in electric potential between the interior and the exterior of a biological cell. With respect to the exterior of the cell, typical values of membrane potential range from –40 mV to –80 mV.

All animal cells are surrounded by a membrane composed of a lipid bilayer with proteins embedded in it. The membrane serves as both an insulator and a diffusion barrier to the movement of ions. Transmembrane proteins, also known as ion transporter or ion pump proteins, actively push ions across the membrane and establish concentration gradients across the membrane, and ion channels allow ions to move across the membrane down those concentration gradients. Ion pumps and ion channels are electrically equivalent to a set of batteries and resistors inserted in the membrane, and therefore create a voltage between the two sides of the membrane.

Virtually all eukaryotic cells (including cells from animals, plants, and fungi) maintain a non-zero transmembrane potential,[citation needed] usually with a negative voltage in the cell interior as compared to the cell exterior ranging from –40 mV to –80 mV. The membrane potential has two basic functions. First, it allows a cell to function as a battery, providing power to operate a variety of "molecular devices" embedded in the membrane. Second, in electrically excitable cells such as neurons and muscle cells, it is used for transmitting signals between different parts of a cell. Signals are generated by opening or closing of ion channels at one point in the membrane, producing a local change in the membrane potential. This change in the electric field can be quickly affected by either adjacent or more distant ion channels in the membrane. Those ion channels can then open or close as a result of the potential change, reproducing the signal.

In non-excitable cells, and in excitable cells in their baseline states, the membrane potential is held at a relatively stable value, called the resting potential. For neurons, typical values of the resting potential range from –70 to –80 millivolts; that is, the interior of a cell has a negative baseline voltage of a bit less than one-tenth of a volt. The opening and closing of ion channels can induce a departure from the resting potential. This is called a depolarization if the interior voltage becomes less negative (say from –70 mV to –60 mV), or a hyperpolarization if the interior voltage becomes more negative (say from –70 mV to –80 mV). In excitable cells, a sufficiently large depolarization can evoke an action potential, in which the membrane potential changes rapidly and significantly for a short time (on the order of 1 to 100 milliseconds), often reversing its polarity. Action potentials are generated by the activation of certain voltage-gated ion channels.


Ions and the forces driving their motion[edit]

Main articles: Ion, Diffusion, Electrochemical gradient, and Electrophoretic mobility

Electrical signals within biological organisms are, in general, driven by ions.[3] The most important cations for the action potential are sodium (Na+) and potassium (K+).[4] Both of these are monovalent cations that carry a single positive charge. Action potentials can also involve calcium (Ca2+),[5] which is a divalent cation that carries a double positive charge. The chloride anion (Cl−) plays a major role in the action potentials of some algae,[6] but plays a negligible role in the action potentials of most animals.[7]

Ions cross the cell membrane under two influences: diffusion and electric fields. A simple example wherein two solutions—A and B—are separated by a porous barrier illustrates that diffusion will ensure that they will eventually mix into equal solutions. This mixing occurs because of the difference in their concentrations. The region with high concentration will diffuse out toward the region with low concentration. To extend the example, let solution A have 30 sodium ions and 30 chloride ions. Also, let solution B have only 20 sodium ions and 20 chloride ions. Assuming the barrier allows both types of ions to travel through it, then a steady state will be reached whereby both solutions have 25 sodium ions and 25 chloride ions. If, however, the porous barrier is selective to which ions are let through, then diffusion alone will not determine the resulting solution. Returning to the previous example, let's now construct a barrier that is permeable only to sodium ions. Now, only sodium is allowed to diffuse cross the barrier from its higher concentration in solution A to the lower concentration in solution B. This will result in a greater accumulation of sodium ions than chloride ions in solution B and a lesser number of sodium ions than chloride ions in solution A.

This means that there is a net positive charge in solution B from the higher concentration of positively charged sodium ions than negatively charged chloride ions. Likewise, there is a net negative charge in solution A from the greater concentration of negative chloride ions than positive sodium ions. Since opposite charges attract and like charges repel, the ions are now also influenced by electrical fields as well as forces of diffusion. Therefore, positive sodium ions will be less likely to travel to the now-more-positive B solution and remain in the now-more-negative A solution. The point at which the forces of the electric fields completely counteract the force due to diffusion is called the equilibrium potential. At this point, the net flow of the specific ion (in this case sodium) is zero.


Action potential

From Wikipedia, the free encyclopedia


In physiology, an action potential occurs when the membrane potential of a specific axon location rapidly rises and falls:[1] this depolarisation then causes adjacent locations to similarly depolarise. Action potentials occur in several types of animal cells, called excitable cells, which include neurons, muscle cells, endocrine cells, and in some plant cells.

In neurons, action potentials play a central role in cell-to-cell communication by providing for—or, with regard to saltatory conduction, assisting—the propagation of signals along the neuron's axon towards synaptic boutons situated at the ends of an axon; these signals can then connect with other neurons at synapses, or to motor cells or glands. In other types of cells, their main function is to activate intracellular processes. In muscle cells, for example, an action potential is the first step in the chain of events leading to contraction. In beta cells of the pancreas, they provoke release of insulin.[a] Action potentials in neurons are also known as "nerve impulses" or "spikes", and the temporal sequence of action potentials generated by a neuron is called its "spike train". A neuron that emits an action potential, or nerve impulse, is often said to "fire".

Action potentials are generated by special types of voltage-gated ion channels embedded in a cell's plasma membrane. These channels are shut when the membrane potential is near the (negative) resting potential of the cell, but they rapidly begin to open if the membrane increases to a precisely defined threshold voltage, depolarising the transmembrane potential. When the channels open, they allow an inward flow of sodium ions, which changes the electrochemical gradient, which in turn produces a further rise in the membrane potential. This then causes more channels to open, producing a greater electric current across the cell membrane, and so on. The process proceeds explosively until all of the available ion channels are open, resulting in a large upswing in the membrane potential. The rapid influx of sodium ions causes the polarity of the plasma membrane to reverse, and the ion channels then rapidly inactivate. As the sodium channels close, sodium ions can no longer enter the neuron, and then they are actively transported back out of the plasma membrane. Potassium channels are then activated, and there is an outward current of potassium ions, returning the electrochemical gradient to the resting state. After an action potential has occurred, there is a transient negative shift, called the afterhyperpolarization.

In animal cells, there are two primary types of action potentials. One type is generated by voltage-gated sodium channels, the other by voltage-gated calcium channels. Sodium-based action potentials usually last for under one millisecond, but calcium-based action potentials may last for 100 milliseconds or longer.[2] In some types of neurons, slow calcium spikes provide the driving force for a long burst of rapidly emitted sodium spikes. In cardiac muscle cells, on the other hand, an initial fast sodium spike provides a "primer" to provoke the rapid onset of a calcium spike, which then produces muscle contractions.







Overview[edit]



Shape of a typical action potential. The membrane potential remains near a baseline level until at some point in time, it abruptly spikes upward and then rapidly falls.

Nearly all cell membranes in animals, plants and fungi maintain a voltage difference between the exterior and interior of the cell, called the membrane potential. A typical voltage across an animal cell membrane is −70 mV. This means that the interior of the cell has a negative voltage of approximately one-fifteenth of a volt relative to the exterior. In most types of cells, the membrane potential usually stays fairly constant. Some types of cells, however, are electrically active in the sense that their voltages fluctuate over time. In some types of electrically active cells, including neurons and muscle cells, the voltage fluctuations frequently take the form of a rapid upward spike followed by a rapid fall. These up-and-down cycles are known as action potentials. In some types of neurons, the entire up-and-down cycle takes place in a few thousandths of a second. In muscle cells, a typical action potential lasts about a fifth of a second. In some other types of cells, and also in plants, an action potential may last three seconds or more.

The electrical properties of a cell are determined by the structure of the membrane that surrounds it. A cell membrane consists of a lipid bilayer of molecules in which larger protein molecules are embedded. The lipid bilayer is highly resistant to movement of electrically charged ions, so it functions as an insulator. The large membrane-embedded proteins, in contrast, provide channels through which ions can pass across the membrane. Action potentials are driven by channel proteins whose configuration switches between closed and open states as a function of the voltage difference between the interior and exterior of the cell. These voltage-sensitive proteins are known as voltage-gated ion channels.

Process in a typical neuron[edit]



Approximate plot of a typical action potential shows its various phases as the action potential passes a point on a cell membrane. The membrane potential starts out at −70 mV at time zero. A stimulus is applied at time = 1 ms, which raises the membrane potential above −55 mV (the threshold potential). After the stimulus is applied, the membrane potential rapidly rises to a peak potential of +40 mV at time = 2 ms. Just as quickly, the potential then drops and overshoots to −90 mV at time = 3 ms, and finally the resting potential of −70 mV is reestablished at time = 5 ms.

All cells in animal body tissues are electrically polarized – in other words, they maintain a voltage difference across the cell's plasma membrane, known as the membrane potential. This electrical polarization results from a complex interplay between protein structures embedded in the membrane called ion pumps and ion channels. In neurons, the types of ion channels in the membrane usually vary across different parts of the cell, giving the dendrites, axon, and cell body different electrical properties. As a result, some parts of the membrane of a neuron may be excitable (capable of generating action potentials), whereas others are not. Recent studies[citation needed] have shown that the most excitable part of a neuron is the part after the axon hillock (the point where the axon leaves the cell body), which is called the initial segment, but the axon and cell body are also excitable in most cases.

Each excitable patch of membrane has two important levels of membrane potential: the resting potential, which is the value the membrane potential maintains as long as nothing perturbs the cell, and a higher value called the threshold potential. At the axon hillock of a typical neuron, the resting potential is around –70 millivolts (mV) and the threshold potential is around –55 mV. Synaptic inputs to a neuron cause the membrane to depolarize or hyperpolarize; that is, they cause the membrane potential to rise or fall. Action potentials are triggered when enough depolarization accumulates to bring the membrane potential up to threshold. When an action potential is triggered, the membrane potential abruptly shoots upward and then equally abruptly shoots back downward, often ending below the resting level, where it remains for some period of time. The shape of the action potential is stereotyped; this means that the rise and fall usually have approximately the same amplitude and time course for all action potentials in a given cell. (Exceptions are discussed later in the article). In most neurons, the entire process takes place in about a thousandth of a second. Many types of neurons emit action potentials constantly at rates of up to 10–100 per second. However, some types are much quieter, and may go for minutes or longer without emitting any action potentials.

Membrane potential and cancer Membrane potential and cancer progression

Membrane potential (Vm), the voltage across the plasma membrane, arises because of the presence of different ion channels/transporters with specific ion selectivity and permeability. Vm is a key biophysical signal in non-excitable cells, modulating important cellular activities, such as proliferation and differentiation. Therefore, the multiplicities of various ion channels/transporters expressed on different cells are finely tuned in order to regulate the Vm. It is well-established that cancer cells possess distinct bioelectrical properties. Notably, electrophysiological analyses in many cancer cell types have revealed a depolarized Vm that favors cell proliferation. Ion channels/transporters control cell volume and migration, and emerging data also suggest that the level of Vm has functional roles in cancer cell migration. In addition, hyperpolarization is necessary for stem cell differentiation. For example, both osteogenesis and adipogenesis are hindered in human mesenchymal stem cells (hMSCs) under depolarizing conditions. Therefore, in the context of cancer, membrane depolarization might be important for the emergence and maintenance of cancer stem cells (CSCs), giving rise to sustained tumor growth. This review aims to provide a broad understanding of the Vm as a bioelectrical signal in cancer cells by examining several key types of ion channels that contribute to its regulation. The mechanisms by which Vm regulates cancer cell proliferation, migration, and differentiation will be discussed. In the long term, Vm might be a valuable clinical marker for tumor detection with prognostic value, and could even be artificially modified in order to inhibit tumor growth and metastasis.

Very interesting post and chart!
 

Obi-wan

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hey generally selected for during tumor evolution. In most cancers, oncogenic driver mutations, such as activation of K-ras, c-Myc, and phosphatidylinositol-3 (PI3) kinase or loss of phosphatase and tensin homolog (Pten) and p53, not mutations that inactivate mitochondrial respiration complexes, promote glycolysis (Vander Heiden et al., 2009). Moreover, most cancers still retain mitochondrial function, including respiration. Some tumors have high levels of oxidative phosphorylation, while others that are relatively glycolytic still retain mitochondrial respiration and other functions (Zu and Guppy, 2004). When quantitated by flux analysis in cultured cells, Akt transformation does not substantially impact respiration, whereas Ras transformation reduces respiration, but nevertheless a majority of ATP is still produced by oxidative phosphorylation (Fan et al., 2013; Gaglio et al., 2011; Yang et al., 2010). Functional tests for the requirement for mitochondrial activity in cancers have revealed their importance. Inactivation of the mitochondrial transcription factor Tfam, which depletes mitochondria from tumor cells, impairs K-ras lung tumor growth in autochthonous models (Weinberg et al., 2010). Depleting mtDNA from tumor cells by generating r0 cells by poisoning mtDNA replication compromises tumorigenesis (Tan et al., 2015). Moreover, selection for restoration of the growth of mtDNA-depleted r0 tumors is associated with the horizontal transfer of mitochondrial genomes from host tissue and restoration of respiration. These and other findings suggest that the role of mitochondria in cancer is not as simple as Warburg envisioned. In contrast, they point to the importance of mitochondrial function to tumor growth. Mitochondria Integrate Catabolism, Anabolism, and Signaling Mitochondria are bioenergetic and biosynthetic organelles that take up substrates from the cytoplasm and use them to drive fatty acid oxidation (FAO), the TCA cycle, the electron transport chain (ETC), and respiration, and to synthesize amino acids, lipids, nucleotides, heme, and iron sulfur clusters, as well as NADPH for their own antioxidant defense (Figure 1) (Wallace, 2012). NADH and FADH2 produced via TCA cycle turning powers the ETC, which in turn generates a proton gradient across the mitochondrial inner membrane that produces ATP through the action of the H+ -ATP synthase. Dihydroorotate dehydrogenase (DHODH), which is essential for de novo pyrimidine synthesis, requires a functional respiratory chain for activity (Khutornenko et al., 2010). The reactive oxygen species (ROS) generated in mitochondria as a byproduct of the ETC can activate signal transduction pathways such as that of MAP kinase and the HIFs (in normoxia is referred to as pseudohypoxia) (Shadel and Horvath, 2015; Sullivan and Chandel, 2014). Excess ROS production can also lead to cell death. Mitochondria sequester Ca2+, the selective release of which controls signaling and a broad array of cellular functions. Mitochondria act as signaling platforms for innate immunity (e.g., MAVS and by the release of mtDNA) (Weinberg et al., 2015; West et al., 2015). The BCL-2 family of proteins at the mitochondrial outer membrane control programmed cell death by apoptosis.

Source: https://www.cell.com/molecular-cell/pdf/S1097-2765(16)00095-2.pdf


For decades, tumor cells have been considered defective in mitochondrial respiration due to their dominant glycolytic metabolism. However, a growing body of evidence is now challenging this assumption, and also implying that tumors are metabolically less homogeneous than previously supposed. A small subpopulation of slow-cycling cells endowed with tumorigenic potential and multidrug resistance has been isolated from different tumors. Deep metabolic characterization of these tumorigenic cells revealed their dependency on mitochondrial respiration versus glycolysis, suggesting the existence of a common metabolic program active in slow-cycling cells across different tumors. These findings change our understanding of tumor metabolism and also highlight new vulnerabilities that can be exploited to eradicate cancer cells responsible for tumor relapse.


Source: Tumors and Mitochondrial Respiration: A Neglected Connection

Maybe in some types of cancer, or in cases of advanced cancer, mitochondrial respiration exists in certain cancer cells. Perhaps mitochondrial respiration is a means by which a tumor grows past a certain point. Tumors seem to have some type of intelligence or so it seems, or possess certain means to grow.



A lot of "if's"
 

Obi-wan

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https://link.springer.com/article/10.1007/s10863-007-9070-5

This study contains a very interesting quote, something I've been saying too:

Therefore, optimistically, if we view cancerous cells as sophisticated types of “infectious-like” cells that have developed and gone awry in our own bodies, i.e., exhibit the capacity to multiply, mutate, invade, spread (metastasize), and kill, we can believe also that natural agents may already exist, or synthetic agents can be made, that will selectively and repeatedly kill the major types of cancer regardless of stage.

Official estimates state that 20% of all cancers worldwide are caused virally:

Viruses May Cause More Cancer than Previously Thought
Viruses Associated with Human Cancer

Sloane said that he estimates that 90% to 98% of cancers are caused by a virus. The rest 2 to 10% of cancers he said were caused by bacteria, fungi, or genetical caused cancers. Genetical caused cancers were very rare he said, and almost only seen in newborns.
There are a few cancers caused by virus's. Most are not. Most are caused by a steady chronic stress response...
 

Travis

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According to G Forrest... but ACV is VERY antifungal, so is plain old vinegar. I notice there are many forum members saying things that are totally wrong...

Acetic alone is antifungal, second only to lauric acid in potency. This effect is not pH-dependent and acetate is antifungal through its entire pH-range. Unpasteurized apple cider vinegar has the additional benefit of being a probiotic, a property not shared with the distilled white variety. I believe that apple cider vinegar, in particular, is unnecessarily-emphasized because the exact same species of bacteria are found also in raw wine vinegars. I cannot conceive of a significant difference between apple cider vinegar and Balsamic vinegar—now on sale for $80.01!—for instance, besides perhaps cell count: The Bragg™ brand does has have quite a bit of precipitate on the bottom, it is also aged less, so I suppose it could have more viable bacteria.
 

Obi-wan

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Bragg Organic Apple Cider Vinegar is: • USDA Certified Organic – organically grown apples follow the scientific standards used to meet organic certified food product standards. • Unfiltered – contains benefits of apple peel that’s
rich in important polyphenol antioxidants. • Raw – Not Pasteurized, recognized as a “live food”, rich in enzymes and made the best natural way. • Contains Miracle “Mother” of Vinegar, a natural cloudy substance found only in raw, unfiltered organic vinegar formed from naturally occurring strand-like chains of protein enzymes. It is highly regarded for it’s nutritional and health benefits
 
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TreasureVibe

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Bragg Organic Apple Cider Vinegar is: • USDA Certified Organic – organically grown apples follow the scientific standards used to meet organic certified food product standards. • Unfiltered – contains benefits of apple peel that’s
rich in important polyphenol antioxidants. • Raw – Not Pasteurized, recognized as a “live food”, rich in enzymes and made the best natural way. • Contains Miracle “Mother” of Vinegar, a natural cloudy substance found only in raw, unfiltered organic vinegar formed from naturally occurring strand-like chains of protein enzymes. It is highly regarded for it’s nutritional and health benefits
Talking about apples, you might want to check out modified citrus pectin - Did you get my PM on it? MCP lowered PSA in cancer patients in a study.. It chelates heavy metals.. It is one of the few if not the only substance that is able to inhibit galectin-3, a protein that is active in all cancers... It is worth investigating.
 

Travis

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Bragg Organic Apple Cider Vinegar is: • USDA Certified Organic – organically grown apples follow the scientific standards used to meet organic certified food product standards. • Unfiltered – contains benefits of apple peel that’s
rich in important polyphenol antioxidants. • Raw – Not Pasteurized, recognized as a “live food”, rich in enzymes and made the best natural way. • Contains Miracle “Mother” of Vinegar, a natural cloudy substance found only in raw, unfiltered organic vinegar formed from naturally occurring strand-like chains of protein enzymes. It is highly regarded for it’s nutritional and health benefits

I just ran out of Bragg's™ today, yet I do have another brand that I'd just taken this out from its forgotten home in the fridge. Similar to Bragg's™, this one is: organic, raw, and has a precipitate on the bottom.

I still think Bragg's™ tastes better, yet I kinda hate their label. It also bothers me that they use the term 'miracle' in their advertising, as if they didn't know how it worked.
 

Travis

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There are a few cancers caused by virus's. Most are not. Most are caused by a steady chronic stress response...

Adrenocorticoids reliably antagonize melatonin, which can lead to lower concentrations of interleukin-2 and natural killer cells—second only tumor necrosis factor (αlpha) in cancer-fighting notoriety. Natural killer cells are called 'natural' because they need neither antibodies nor complements to recognize a cell and destroy it, a property not shared with killer T cells. Natural killer cells will attack bacteria and cancerous cells just the same, so it's not surprising that their deficiency has been observed in facilitating cancerous states. Unlike immune cells that primarily rely on small reactive molecules (i.e. nitric oxide, hypochlorite, hypoiodite) to kill cells—such as macrophages and neutrophils—natural killer cells secrete a protein called perforin, which does exactly as you might imagine: Perforin perforates the cell membrane causing it to leak-out its ions, its enzyme cofactors, and its glycolytic metabolites into the extracellular space. Perforin alone is quite punishing to a cell, yet killer cells also secrete in unison proteolytic enzymes—i.e. granzyme B—that that add insult to this injury by hydrolyzing the protein matrix. The natural killer cell and neutrophil combination should be fatal for any cell, including: bacteria, yeast, fungi, and even cancer. Neutrophil myeloperoxidase works better with iodide than with chloride, and selenium is also an important mineral for these cells: A neutrophil having low glutathione peroxidase activity can actually destroy itself with self-generated reactive oxygen species, while one having the adequate selenoenzyme can maintain its destructive 'respiratory burst' for up to forty-five minutes. The selenium atom of selenomethionine can be donated to ornithine, forming selenocysteine, making this an acceptable supplemental form. So besides being an inhibitor of polyamine synthesis in more than one way, selenomethionine can also prevent neutrophils from becoming their less-effective kamikaze subtype.
 

Obi-wan

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Adrenocorticoids reliably antagonize melatonin, which can lead to lower concentrations of interleukin-2 and natural killer cells—second only tumor necrosis factor (αlpha) in cancer-fighting notoriety. Natural killer cells are called 'natural' because they need neither antibodies nor complements to recognize a cell and destroy it, a property not shared with killer T cells. Natural killer cells will attack bacteria and cancerous cells just the same, so it's not surprising that their deficiency has been observed in facilitating cancerous states. Unlike immune cells that primarily rely on small reactive molecules (i.e. nitric oxide, hypochlorite, hypoiodite) to kill cells—such as macrophages and neutrophils—natural killer cells secrete a protein called perforin, which does exactly as you might imagine: Perforin perforates the cell membrane causing it to leak-out its ions, its enzyme cofactors, and its glycolytic metabolites into the extracellular space. Perforin alone is quite punishing to a cell, yet killer cells also secrete in unison proteolytic enzymes—i.e. granzyme B—that that add insult to this injury by hydrolyzing the protein matrix. The natural killer cell and neutrophil combination should be fatal for any cell, including: bacteria, yeast, fungi, and even cancer. Neutrophil myeloperoxidase works better with iodide than with chloride, and selenium is also an important mineral for these cells: A neutrophil having low glutathione peroxidase activity can actually destroy itself with self-generated reactive oxygen species, while one having the adequate selenoenzyme can maintain its destructive 'respiratory burst' for up to forty-five minutes. The selenium atom of selenomethionine can be donated to ornithine, forming selenocysteine, making this an acceptable supplemental form. So besides being an inhibitor of polyamine synthesis in more than one way, selenomethionine can also prevent neutrophils from becoming their less-effective kamikaze subtype.

Another plus for selenomethionine. I take 400mg each day...
 

Obi-wan

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I just ran out of Bragg's™ today, yet I do have another brand that I'd just taken this out from its forgotten home in the fridge. Similar to Bragg's™, this one is: organic, raw, and has a precipitate on the bottom.

I still think Bragg's™ tastes better, yet I kinda hate their label. It also bothers me that they use the term 'miracle' in their advertising, as if they didn't know how it worked.

They have been around since 1912. "Miracle" was a cool word back then and they probably didn't exactly know how it worked...Travis was not born yet...
 

Obi-wan

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Talking about apples, you might want to check out modified citrus pectin - Did you get my PM on it? MCP lowered PSA in cancer patients in a study.. It chelates heavy metals.. It is one of the few if not the only substance that is able to inhibit galectin-3, a protein that is active in all cancers... It is worth investigating.

I would like to get a @Travis take on this...
 

Mito

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The selenium atom of selenomethionine can be donated to ornithine, forming selenocysteine, making this an acceptable supplemental form. So besides being an inhibitor of polyamine synthesis in more than one way, selenomethionine can also prevent neutrophils from becoming their less-effective kamikaze subtype.
Do you think selenium blood levels above the typical lab reference range could be a problem? I had been supplementing 200 μg of selenomethionine 3 or 4 days per week for at least a year. I tested my blood selenium and the test came back well above the reference range at 290 μg/L (lab reference range 91-198 μg/L).
 

Travis

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Do you think selenium blood levels above the typical lab reference range could be a problem? I had been supplementing 200 μg of selenomethionine 3 or 4 days per week for at least a year. I tested my blood selenium and the test came back well above the reference range at 290 μg/L (lab reference range 91-198 μg/L).

It is good to hear about the serological consequences of the standard 200·μg-sized dose because I had just found such pills at my grocery store last night, and had bought it along with aspirin: Thus far, I have taken two of them totalling 400·μg.

I think you are fine because a bit higher could very well be natural. Although most popular tables and charts declare plants to have low levels, a thorough comparison of these commonly-reported values to the respective speciated selenomethionine concentrations may lead a person to conclude that selenomethionine and selenocysteine are not routinely determined by the USDA. Some basic chemical methods that I've seen rely on: (1st) chelating the selenium, (2ndly) centrifugation–decanting of the aqueous phase, and then (3rdly) determining the concentration by IR absorbance.

I do remember reading that Americans have a tissue selenomethionine/selenocysteine concentrations in the middle range, with the Australians being considerably lower and the Japanese substantially higher. I would imagine that circulating levels as high as yours would translate into higher glutathione peroxidase & deiodinase activities. Also worth remembering is that a mere 200·μg per day selenomethionine has been shown to increase survival in thousands of humans and rodents with cancer.
 
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