What Would You Suggest For BPH Prostate Trouble?

Travis

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I have some ideas. On the beach now. Getting natural E to interact with the Vit E succinate which I just started taking

It is most certainly the succinate group in particular that is responsible for this activity. This can be demonstrated in a few ways, and one being how tocopheryl succinate (left) compares to cholesteryl succinate (right):

dose response.png


This dose–response curves are nearly superimposable, something which had been observed in multiple cell lines and in multiple studies.⁽¹⁾⁽²⁾ Because cholesterol is fully saturated and thus cannot sequester free radicals, the anticancer effect of α-tocopheryl is entirely independent of its antioxidant function.

'The fact that butylated hydroxyanisole, which inhibited the proliferation of NB cells, did not affect basal or PGE₁-stimulated AC activity in NB cells, suggests that inhibition of PGE₁-stimulated adenyl cyclase by α-TS is not due to its antioxidant action.' ―Prasad⁽³⁾

Considering its mechanism of action as a calcium ionophore, and apparent lack of antioxidant activity, it is perhaps misleading to group it under vitamin E. Instead: perhaps it is best named in a way that highlights its succinate group, such as succininyl-α-tocopherol (although this would be technically incorrect because α-tocopherol should take precedence on account of its greater mass).

But stressing is function and similarity to cholesteryl succinate is not to discount it in any way. This molecule's anticancer effect is as significant as it's selective, and this is safe to use. If you scroll down to Table 1 in this⁽⁴⁾ article, I think you'd be amazed by how selective it really is.

Although safe, effective, and available, γ-tocopherol is actually more effective than succininyl-α-tocopherol at the same dose level. This may seem like an arrogant, or even blasphemous, thing to say but it's more-or-less true regardless: These two have ve been compared directly head-to-head, side-by-side, and γ-tocopherol had emerging the winner:⁽⁵⁾

toc.png


Although they hadn't been tested in combination, there is every reason to think the results would compound. Gamma-tocopherol and succinyl-α-tocopherol have different mechanisms of action, which perhaps is best illustrated by their effects on prostaglandin E activity. Gamma-tocopherol and its CEHC metabolite can lower prostaglandin E by adducting with peroxynitrite,⁽⁶⁾⁽⁷⁾ a cyclooxgenase substrate,⁽⁸⁾ while succinyl-α-tocopherol can prevent its receptor from working by inhibiting adenylate cyclase.⁽⁹⁾ [It probably doesn't inhibit adenyl cyclase directly but through the Ca²⁺ ions—which are known for this—that it's been shown to increase.]

The significant effect of γ-tocopherol is yet another thing out many that illustrates the central role reactive nitrogen species have in carcinogenesis. Heme is also illustrative, as the carcinogenicity of this most likely derives from its ability to oxidize nitric oxide (Ṅ=O) into the more carcinogenic nitrosonium ion (N≡O⁺). Free iron is less carcinogenic in the colon, although this is well-known for creating hydroxyl radicals (ȮH⁻). Vitamin C serves as a partial antidote to heme by reducing (+e⁻) nitrosylhemochrome, releasing the iron-bound nitric oxide as the less-dangerous nitroxyl ion (N=O⁻) and not nitrosonium. Phytic acid also serves to combat intestinal nitrosamine formation: Upon being attracted to heme's central iron atom phytic acid can bind it, sever the two histidine bonds, and pull it slightly out-of-plane.

[1] Djuric, Z. "Growth inhibition of MCF-7 and MCF-10A human breast cells by α-tocopheryl hemisuccinate, cholesteryl hemisuccinate and their ether analogs." Cancer letters (1997)
[2] Fariss, M. "The selective antiproliferative effects of α-tocopheryl hemisuccinate and cholesteryl hemisuccinate on murine leukemia cells result from the action of the intact compounds." Cancer research (1994)
[3] Prasad, K. "α-tocopheryl succinate, the [second] most effective form of vitamin E for adjuvant cancer treatment: a review." Journal of the American College of Nutrition (2003)
[4] Neuzil, J. "Selective cancer cell killing by α-tocopheryl succinate." British journal of cancer (2001)
[5] Galli, F. "The effect of α-and γ-tocopherol and their carboxyethyl hydroxychroman metabolites on prostate cancer cell proliferation." Archives of biochemistry and biophysics (2004)
[6] Jiang, Q. "γ-Tocopherol, but not α-tocopherol, decreases proinflammatory eicosanoids and inflammation damage in rats." The FASEB Journal (2003)
[7] Christen, S. "γ-Tocopherol traps mutagenic electrophiles such as NOx and complements α-tocopherol: physiological implications." Proceedings of the National Academy of Sciences (1997)
[8] Beharka, A. "Mechanism of vitamin E inhibition of cyclooxygenase activity in macrophages from old mice: role of peroxynitrite." Free Radical Biology and Medicine (2002)
[9] Sahu, S. "Effect of alpha tocopheryl succinate on adenylate cyclase activity in murine neuroblastoma cells in culture." Journal of the American College of Nutrition (1988)
 
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Obi-wan

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It is most certainly the succinate group in particular that is responsible for this activity. This can be demonstrated in a few ways, and one being how tocopheryl succinate (left) compares to cholesteryl succinate (right):

View attachment 9452

This dose–response curves are nearly superimposable, something which had been observed in multiple cell lines and in multiple studies.⁽¹⁾⁽²⁾ Because cholesterol is fully saturated and thus cannot sequester free radicals, the anticancer effect of α-tocopheryl is entirely independent of its antioxidant function.

'The fact that butylated hydroxyanisole, which inhibited the proliferation of NB cells, did not affect basal or PGE₁-stimulated AC activity in NB cells, suggests that inhibition of PGE₁-stimulated adenyl cyclase by α-TS is not due to its antioxidant action.' ―Prasad⁽³⁾

Considering its mechanism of action as a calcium ionophore, and apparent lack of antioxidant activity, it is perhaps misleading to group it under vitamin E. Instead: perhaps it is best named in a way that highlights its succinate group, such as succininyl-α-tocopherol (although this would be technically incorrect because α-tocopherol should take precedence on account of its greater mass).

But stressing is function and similarity to cholesteryl succinate is not to discount it in any way. This molecule's anticancer effect is as significant as it's selective, and this is safe to use. If you scroll down to Table 1 in this⁽⁴⁾ article, I think you'd be amazed by how selective it really is.

Although safe, effective, and available, γ-tocopherol is actually more effective than succininyl-α-tocopherol at the same dose level. This may seem like an arrogant, or even blasphemous, thing to say but it's more-or-less true regardless: These two have ve been compared directly head-to-head, side-by-side, and γ-tocopherol had emerging the winner:⁽⁵⁾

View attachment 9454

Although they hadn't been tested in combination, there is every reason to think the results would compound. Gamma-tocopherol and succinyl-α-tocopherol have different mechanisms of action, which perhaps is best illustrated by their effects on prostaglandin E activity. Gamma-tocopherol and its CEHC metabolite can lower prostaglandin E by adducting with peroxynitrite,⁽⁶⁾⁽⁷⁾ a cyclooxgenase substrate,⁽⁸⁾ while succinyl-α-tocopherol can prevent its receptor from working by inhibiting adenylate cyclase.⁽⁹⁾ [It probably doesn't inhibit adenyl cyclase directly but through the Ca²⁺ ions—which are known for this—that it's been shown to increase.]

The significant effect of γ-tocopherol is yet another thing out many that illustrates the central role reactive nitrogen species have in carcinogenesis. Heme is also illustrative, as the carcinogenicity of this most likely derives from its ability to oxidize nitric oxide (Ṅ=O) into the more carcinogenic nitrosonium ion (N≡O⁺). Free iron is less carcinogenic in the colon, although this is well-known for creating hydroxyl radicals (ȮH⁻). Vitamin C serves as a partial antidote to heme by reducing (+e⁻) nitrosylhemochrome, releasing the iron-bound nitric oxide as the less-dangerous nitroxyl ion (N=O⁻) and not nitrosonium. Phytic acid also serves to combat intestinal nitrosamine formation: Upon being attracted to heme's central iron atom phytic acid can bind it, sever the two histidine bonds, and pull it slightly out-of-plane.

[1] Djuric, Z. "Growth inhibition of MCF-7 and MCF-10A human breast cells by α-tocopheryl hemisuccinate, cholesteryl hemisuccinate and their ether analogs." Cancer letters (1997)
[2] Fariss, M. "The selective antiproliferative effects of α-tocopheryl hemisuccinate and cholesteryl hemisuccinate on murine leukemia cells result from the action of the intact compounds." Cancer research (1994)
[3] Prasad, K. "α-tocopheryl succinate, the [second] most effective form of vitamin E for adjuvant cancer treatment: a review." Journal of the American College of Nutrition (2003)
[4] Neuzil, J. "Selective cancer cell killing by α-tocopheryl succinate." British journal of cancer (2001)
[5] Galli, F. "The effect of α-and γ-tocopherol and their carboxyethyl hydroxychroman metabolites on prostate cancer cell proliferation." Archives of biochemistry and biophysics (2004)
[6] Jiang, Q. "γ-Tocopherol, but not α-tocopherol, decreases proinflammatory eicosanoids and inflammation damage in rats." The FASEB Journal (2003)
[7] Christen, S. "γ-Tocopherol traps mutagenic electrophiles such as NOx and complements α-tocopherol: physiological implications." Proceedings of the National Academy of Sciences (1997)
[8] Beharka, A. "Mechanism of vitamin E inhibition of cyclooxygenase activity in macrophages from old mice: role of peroxynitrite." Free Radical Biology and Medicine (2002)
[9] Sahu, S. "Effect of alpha tocopheryl succinate on adenylate cyclase activity in murine neuroblastoma cells in culture." Journal of the American College of Nutrition (1988)


I meant to say above I was enjoying natural Vit D on the beach. Travis, your post is timely. When I received the Vit E succinate last week I stopped taking the High Gamma Vit E and started feeling some symptoms of my advanced prostate cancer.. Now I take both High Gamma Vit E in MCT oil and dry Vit E succinate daily. So far a good day today.
 

Travis

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I meant to say above I was enjoying natural Vit D on the beach. Travis, your post is timely. When I received the Vit E succinate last week I stopped taking the High Gamma Vit E and started feeling some symptoms of my advanced prostate cancer.. Now I take both High Gamma Vit E in MCT oil and dry Vit E succinate daily. So far a good day today.

But selenomethionine is just as good if not better, and in more than one way: Besides inhibiting polyamine synthesis it also inhibits cyclooxygenase expression. Any form of selenium will increase glutathionine peroxidase, a selenoenzyme that converts hydrogen peroxide into water. Nuclear factor-κB is a redox-sensitive transcription factor, and also happens to be the one that transcribes for cyclooxygenase-2. Upon high cytosolic H₂O₂ concentrations: NF-κB will form an internal disulfide bond, become more compact, less charged, and distribute into the nucleus where it will help create cyclooxygenase-2 mRNA. Selenium, in any form, will reduce intracellular H₂O₂ and hence prostagladin E₂. However, selenomethionine is particularly effective because it also inhibits polyamine synthesis and is preferentially absorbed by the prostate (because of high polyamine demand). This high incorporation of methionine is not just theoretical, but actually forms a practical imaging technique: Similar to how radioactive iodine is particularly useful for imaging the thyroid, radiolabeled ¹⁴C-methionine has been used to visualize the prostate . . . Scientists say ¹⁴C-Met–PET gives more reliable images that ¹⁸F-deoxyglucose–PET.
 

Obi-wan

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But selenomethionine is just as good if not better, and in more than one way: Besides inhibiting polyamine synthesis it also inhibits cyclooxygenase expression. Any form of selenium will increase glutathionine peroxidase, a selenoenzyme that converts hydrogen peroxide into water. Nuclear factor-κB is a redox-sensitive transcription factor, and also happens to be the one that transcribes for cyclooxygenase-2. Upon high cytosolic H₂O₂ concentrations: NF-κB will form an internal disulfide bond, become more compact, less charged, and distribute into the nucleus where it will help create cyclooxygenase-2 mRNA. Selenium, in any form, will reduce intracellular H₂O₂ and hence prostagladin E₂. However, selenomethionine is particularly effective because it also inhibits polyamine synthesis and is preferentially absorbed by the prostate (because of high polyamine demand). This high incorporation of methionine is not just theoretical, but actually forms a practical imaging technique: Similar to how radioactive iodine is particularly useful for imaging the thyroid, radiolabeled ¹⁴C-methionine has been used to visualize the prostate . . . Scientists say ¹⁴C-Met–PET gives more reliable images that ¹⁸F-deoxyglucose–PET.
Yes Sir, taking that also, along with L-threonine, aspirin, and Lapodin (Pau d'Arco)
 

burtlancast

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Why don't you people do like the Japanese who have some of the lowest rates of BPH and prostate cancer in the world, thanks to ingesting 60 times the usual dose of iodine (15 mg a day from algae) ?

No increased incidence of thyroid diseases or thyroid cancer in Japan either (sorry, Ray).

The prostate gland accumulates iodine.
 
B

Braveheart

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Why don't you people do like the Japanese who have some of the lowest rates of BPH and prostate cancer in the world, thanks to ingesting 60 times the usual dose of iodine (15 mg a day from algae) ?

No increased incidence of thyroid diseases or thyroid cancer in Japan either (sorry, Ray).

The prostate gland accumulates iodine.
Am awaiting my Lugols, and then will proceed...look forward to consulting you then...thanks
 

Travis

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Yes Sir, taking that also, along with L-threonine, aspirin, and Lapodin (Pau d'Arco)
Yang & Brackenbury. "Membrane potential and cancer progression." Frontiers in physiology (2013)

'In addition, the intracellular Na⁺ level is markedly higher in tumors compared to non-cancerous tissues, whereas the K⁺ level remains more stable (Smith et al., 1978; Cameron et al., 1980; Sparks et al., 1983). A similar scenario occurs in fast proliferating Chinese hamster ovary and 3T3 cells (Cone and Tongier, 1973). Thus, an increased intracellular Na⁺ concentration could be a determinant of a depolarized phenotype in rapidly cycling cancer cells.' ―Yang & Brackenbury

'Recordings from rodent and human tissues have revealed that proliferative cells, especially rapidly proliferating tumor cells, displayed depolarized Vm, whereas non-proliferating, terminally differentiated somatic cells, such as muscle cells and neurons, are characterized by their hyperpolarized Vm (Figure 1) [reviewed in Binggeli and Weinstein (1986)].' ―Yang & Brackenbury

'Stem cells and cancer cells share similar properties, such as the ability to differentiate and self-renew, increased membrane transporter activity and the ability to migrate and metastasize (Wicha et al., 2006).' ―Yang & Brackenbury

'More recently, in vivo evidence shows that membrane depolarization itself, regardless of the types of ions and ion channel/transporter proteins, is able to bring cancerous transformation (i.e., increased proliferation, change in morphology and abnormal angiogenesis) in Xenopus laevis embryos (Lobikin et al., 2012).' ―Yang & Brackenbury

'Artificially altering Vm by modulating the extracellular ionic constitution or applying the Na⁺/K⁺-ATPase inhibitor ouabain revealed interesting results: First, hyperpolarizing CHO cells to −45 mV started to induce mitotic arrest and cell division was fully blocked at −75 mV. The cell cycle was resumed by depolarizing the cells to −10 mV (Cone, 1971). Secondly, quiescent (G₀) mature chick spinal cord neurons showed mitotic activity after depolarization (Cone and Cone, 1976) (Figure 2). Recently, artificial control of Vm was accomplished in Xenopus laevis embryos by expressing glycine-gated Cl⁻ channels and applying the activator ivermectin. Depolarization (caused by lowering the Cl⁻ concentration in the extracellular medium, which caused Cl⁻ efflux) was found to be directly responsible for malignant proliferation. This proliferation was ion and ion channel non-specific, because (1) the phenotype caused by depolarization could be rescued by expressing a hyperpolarizing channel gene, and (2) the malignant phenotype could be induced or suppressed simply by adjusting extracellular Cl⁻ concentration, as predicted by Goldman–Hodgkin–Katz equation (Lobikin et al., 2012).' ―Yang & Brackenbury
 
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Obi-wan

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Yang & Brackenbury. "Membrane potential and cancer progression." Frontiers in physiology (2013)

'In addition, the intracellular Na⁺ level is markedly higher in tumors compared to non-cancerous tissues, whereas the K⁺ level remains more stable (Smith et al., 1978; Cameron et al., 1980; Sparks et al., 1983). A similar scenario occurs in fast proliferating Chinese hamster ovary and 3T3 cells (Cone and Tongier, 1973). Thus, an increased intracellular Na⁺ concentration could be a determinant of a depolarized phenotype in rapidly cycling cancer cells.' ―Yang & Brackenbury

'Recordings from rodent and human tissues have revealed that proliferative cells, especially rapidly proliferating tumor cells, displayed depolarized Vm, whereas non-proliferating, terminally differentiated somatic cells, such as muscle cells and neurons, are characterized by their hyperpolarized Vm (Figure 1) [reviewed in Binggeli and Weinstein (1986)].' ―Yang & Brackenbury

'Stem cells and cancer cells share similar properties, such as the ability to differentiate and self-renew, increased membrane transporter activity and the ability to migrate and metastasize (Wicha et al., 2006).' ―Yang & Brackenbury

'More recently, in vivo evidence shows that membrane depolarization itself, regardless of the types of ions and ion channel/transporter proteins, is able to bring cancerous transformation (i.e., increased proliferation, change in morphology and abnormal angiogenesis) in Xenopus laevis embryos (Lobikin et al., 2012).' ―Yang & Brackenbury

'Artificially altering Vm by modulating the extracellular ionic constitution or applying the Na⁺/K⁺-ATPase inhibitor ouabain revealed interesting results: First, hyperpolarizing CHO cells to −45 mV started to induce mitotic arrest and cell division was fully blocked at −75 mV. The cell cycle was resumed by depolarizing the cells to −10 mV (Cone, 1971). Secondly, quiescent (G₀) mature chick spinal cord neurons showed mitotic activity after depolarization (Cone and Cone, 1976) (Figure 2). Recently, artificial control of Vm was accomplished in Xenopus laevis embryos by expressing glycine-gated Cl⁻ channels and applying the activator ivermectin. Depolarization (caused by lowering the Cl⁻ concentration in the extracellular medium, which caused Cl⁻ efflux) was found to be directly responsible for malignant proliferation. This proliferation was ion and ion channel non-specific, because (1) the phenotype caused by depolarization could be rescued by expressing a hyperpolarizing channel gene, and (2) the malignant phenotype could be induced or suppressed simply by adjusting extracellular Cl⁻ concentration, as predicted by Goldman–Hodgkin–Katz equation (Lobikin et al., 2012).' ―Yang & Brackenbury
Can magnesium or Vit D3 adjust extracellular/intracellular Na/Cl concentration? Potassium? Prostate swells due to intake of bulk water and calcium into the cell pushing magnesium/potassium out due to constant excitation. This is after atrophy...is this voltage differential change effected by microwave radiation (cell phones)?
 
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Travis

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Can magnesium or Vit D3 adjust extracellular/intracellular Na/Cl concentration? Potassium? Prostate swells due to intake of bulk water and calcium into the cell pushing magnesium/potassium out due to constant excitation. This is after atrophy...is this voltage differential change effected by microwave radiation (cell phones)?

I think cellular sodium and potassium is under control of mineralocorticoids and the membrane pore currently known as Na⁺/K⁺-ATPase. The reason I believe this is:

(1) A membrane aldosterone receptor had actually been discovered, twice, yet if this protein had been sequenced it was never publicly reported.

(2) Molecules used to block or activate Na⁺/K⁺-ATPase, such as oubain, are all aldosterone mimetics and nearly superimposable over spironolactone.

(3) The nuclear mineralocorticoid receptor transcribes for Na⁺/K⁺-ATPase.

(4) Na⁺/K⁺-ATPase has very low kinetic rates for ATP hydrolysis and couldn't possibly work as often supposed.

Mineralocorticoid steroids and their analogues open this pore allowing passage of Na⁺, K⁺, and other monovalent cations. The is membrane pore appears to be passive, albeit selective, and it's the oppositely-charged mitochondrial membrane potential (Ψm) of around −180·mV that provides the force. The preference of the cytosol for potassium over sodium is better explained by these ions electrophoretic mobilities, a property which quantifies speed of migration towards opposite charges. Of the five common physiological cations, electrophoretic speed follows this order: NH₄⁺ > K⁺ > Na⁺ > Ca²⁺ > Mg²⁺. Ammonia will make a beeline towards the negatively-charged mitochondria, thus lowering electron flow and hence energy production. Imbalances in the Na⁺/K⁺ ratio is likewise not good, as this will effect the plasma membrane potential (Vm).

I think someone soon needs to track down the citations in the above article, those dealing with the Na⁺ and K⁺ concentrations in cancer cells. All natural foods from beef to carrots, pineapples to coconuts, and milk to strawberries have potassium far in excess of sodium. The Na⁺∶K⁺ ratios almost invariably range between 1∶5 and 1∶11, and yet some human diets can approach a 1∶1 ratio. While its true that humans drink more water than what'd they'd normally do, naturally, imbalances of the Na⁺∶K⁺ still likely occurs. Since William Koch, M.D., Ph.D., had advised against excess sodium, it might be a good idea to balance any additional NaCl consumed with an excess of KCl.
 

Obi-wan

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I think cellular sodium and potassium is under control of mineralocorticoids and the membrane pore currently known as Na⁺/K⁺-ATPase. The reason I believe this is:

(1) A membrane aldosterone receptor had actually been discovered, twice, yet if this protein had been sequenced it was never publicly reported.

(2) Molecules used to block or activate Na⁺/K⁺-ATPase, such as oubain, are all aldosterone mimetics and nearly superimposable over spironolactone.

(3) The nuclear mineralocorticoid receptor transcribes for Na⁺/K⁺-ATPase.

(4) Na⁺/K⁺-ATPase has very low kinetic rates for ATP hydrolysis and couldn't possibly work as often supposed.

Mineralocorticoid steroids and their analogues open this pore allowing passage of Na⁺, K⁺, and other monovalent cations. The is membrane pore appears to be passive, albeit selective, and it's the oppositely-charged mitochondrial membrane potential (Ψm) of around −180·mV that provides the force. The preference of the cytosol for potassium over sodium is better explained by these ions electrophoretic mobilities, a property which quantifies speed of migration towards opposite charges. Of the five common physiological cations, electrophoretic speed follows this order: NH₄⁺ > K⁺ > Na⁺ > Ca²⁺ > Mg²⁺. Ammonia will make a beeline towards the negatively-charged mitochondria, thus lowering electron flow and hence energy production. Imbalances in the Na⁺/K⁺ ratio is likewise not good, as this will effect the plasma membrane potential (Vm).

I think someone soon needs to track down the citations in the above article, those dealing with the Na⁺ and K⁺ concentrations in cancer cells. All natural foods from beef to carrots, pineapples to coconuts, and milk to strawberries have potassium far in excess of sodium. The Na⁺∶K⁺ ratios almost invariably range between 1∶5 and 1∶11, and yet some human diets can approach a 1∶1 ratio. While its true that humans drink more water than what'd they'd normally do, naturally, imbalances of the Na⁺∶K⁺ still likely occurs. Since William Koch, M.D., Ph.D., had advised against excess sodium, it might be a good idea to balance any additional NaCl consumed with an excess of KCl.
Potassium supplementation?
 

Travis

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Potassium supplementation?

It could be a good idea to replace all NaCl with a mix of both NaCl and KCl, making sure they will always be consumed in proportion. I have seen such mixes at the grocery store, yet I haven't tried them and still buy sea salt. However, I only use salt on salads which are high in potassium to begin with. Although sodium is completely safe when properly balanced, I think we should keep in mind that all other animals consume a much higher ratio of potassium.
 

Obi-wan

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It could be a good idea to replace all NaCl with a mix of both NaCl and KCl, making sure they will always be consumed in proportion. I have seen such mixes at the grocery store, yet I haven't tried them and still buy sea salt. However, I only use salt on salads which are high in potassium to begin with. Although sodium is completely safe when properly balanced, I think we should keep in mind that all other animals consume a much higher ratio of potassium.
I just had a salad. I also have potassium pills, 99 mgs each. I can start taking with every meal.
Dosen’t Apple cider vinegar have a lot of potassium?
 
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Braveheart

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I just had a salad. I also have potassium pills, 99 mgs each. I can start taking with every meal.
Dosen’t Apple cider vinegar have a lot of potassium?
Today, so far...1 oj 480 mg...plantain 877 mg...coconut water 600 mg per cup...it's noon and I'm only 600 away from 4700...will still drink another oj/coconut water and have nanner...potassium pills useless unless you a few hundred away...people often deficient big time...would have to gulp whole container...not!
 

Obi-wan

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I just had a salad. I also have potassium pills, 99 mgs each. I can start taking with every meal.
Dosen’t Apple cider vinegar have a lot of potassium?
ACV has 11 mgs per tablespoon
 

Obi-wan

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Today, so far...1 oj 480 mg...plantain 877 mg...coconut water 600 mg per cup...it's noon and I'm only 600 away from 4700...will still drink another oj/coconut water and have nanner...potassium pills useless unless you a few hundred away...people often deficient big time...would have to gulp whole container...not!
You ingest a lot of potassium. I drink oj also in the morning
 
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Braveheart

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You ingest a lot of potassium. I drink oj also in the morning
Average per day...5668 mg ...these last 2 months...Cut way back on salt since I stopped being a meat-a-holic...meat really needs salt
 

Obi-wan

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Average per day...5668 mg ...these last 2 months...Cut way back on salt since I stopped being a meat-a-holic...meat really needs salt
Smart! I am doing less meat also
 

Travis

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Smart! I am doing less meat also

Shredded coconut isn't bad, and new Microplanes™ can make quick work of them. I go to a local chain for my coconuts but they can be found at Super Wal-Mart and just about any Asian grocery store. The fatty acid profile of coconut is very good, and they have less iron than red meat.

And after reading about folate receptor autoantibodies I won't ever consume cow's milk again, but the goat sequence has less homology and doesn't bind to the human autoantibodies. Besides the reduced potency of goat casomorphins, this represents another reason to consume goat dairy (if you can find it). Although milk is indisputably the 'perfect food' for mammals, it cannot be argued that the cow is a different species and milk is purposefully resistant to digestion—two considerations prerequisite for autoantibody formation.

Folate receptor autoantibodies will make you forget all about the casomorphins, literally. The choroid plexus is where all brain folate is absorbed, and the obligatory receptors are ~88% similar to proteins found in bovine milk. This occurs because membrane folate receptors are often cleaved-off, making for a slightly-shorter yet otherwise identical version in the plasma. These are also found in milk in high concentrations, and represent the autoantigen for folate receptor autoantibodies.

These autoantibodies bind the brain folate receptor, making the primary transporter reduced in function. Brain folate is necessary for dNA synthesis, myelination, and some neurotransmitters (i.e. norepinephrine; melatonin).The antidote for these autoantibodies is simply tetrahydrofolate, 5-methylated or otherwise, and the far more common folic acid will not do. This oxidized form normally goes through the folate receptor now blocked by the autoantibody. The electronically-reduced folates are needed to counteract this by bypassing the folate receptor (FR1) though the reduced folate carrier (RFC1), also found on the choroid plexus.
 
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Obi-wan

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The AIs(adequate intake) for potassium are: 400mg of potassium for 0-6-month-old males, 700mg of potassium for 7-12-month-old males, 3,000mg of potassium for 1-3-year-old males, 3,800mg of potassium for 4-8-year-old males, 4,500mg of potassium for 9-13-year-old males, and 4,700mg of potassium for males that are 14 years old and older.

Most Americans consume only half that amount per day.

The ion transport system moves potassium across the cell membrane using two mechanisms. One is active and pumps sodium out of, and potassium into, the cell. The other is passive and allows potassium to leak out of the cell. Potassium and sodium cations influence fluid distribution between intracellular and extracellular compartments by osmotic forces. The movement of potassium and sodium through the cell membrane is mediated by the Na+/K+-ATPase pump.[62] This ion pump uses ATP to pump three sodium ions out of the cell and two potassium ions into the cell, creating an electrochemical gradient and electromotive force across the cell membrane. The highly selective potassium ion channels (which are tetramers) are crucial for hyperpolarization inside neurons after an action potential is triggered. -Wikipedia
 

Obi-wan

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Supplementation[edit]
Supplements of potassium are most widely used in conjunction with diuretics that block reabsorption of sodium and water upstream from the distal tubule (thiazides and loop diuretics), because this promotes increased distal tubular potassium secretion, with resultant increased potassium excretion. A variety of prescription and over-the counter supplements are available. Potassium chloride may be dissolved in water, but the salty/bitter taste make liquid supplements unpalatable.[84] Typical doses range from 10 mmol (400 mg), to 20 mmol (800 mg). Potassium is also available in tablets or capsules, which are formulated to allow potassium to leach slowly out of a matrix, since very high concentrations of potassium ion that occur adjacent to a solid tablet can injure the gastric or intestinal mucosa. For this reason, non-prescription potassium pills are limited by law in the US to a maximum of 99 mg of potassium. -Wikipedia
 

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