Very High Salt Intake (50g A Day) Increases Metabolism, Makes People Energetic And Happy

Ogilvie

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Since I used both the sodium and baking soda gram amounts from your recipe, I suppose it didn't have the necessary osmolarity for oral rehydration. But it did make me feel really good all day...

I read the entire blog post from Lady of Lyme, but I failed to go to the link she provided Oral Rehydration Therapy (ORT) - Rehydration Project

Now I see there they created a handy chart:

ORS.png


I'll try this again tomorrow and see how it works out. I don't have the same serious health concerns she does but I have been having a hard time feeling fully hydrated for a while. I'm really appreciating all the good feedback on this thread, thanks, everyone.
 

Elize

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I used Himalayan salt by The Spice Lab
Says 1/4 (1.1g) teaspoon has 420mg sodium
 

Elize

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Okay so now I hope I have it right. I used:
2 cups water
1/4 tsp salt
Pinch of bicarbonate of soda
1/2 tsp calcium carbonate (optional)
1 pinch magnesium carbonate (optional)
2 tbl raw cane sugar
1/4 cup cranberry juice (not from concentrate)
Blend above ingredients and store in fridge
Would this be OK? Thanks.
 

Elize

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In Kashmir friends drink 2 cups of tea with salt or salt and sugar a day.
 
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I would advise for caution in regards to manipulation of intakes of Elements,if it goes out of the small deadzones of tolerance.We are the only Animals with the already extremely high customary Salt-intake,which was proven to be cultural already.The yanomamo indians of South America are consuming no more than 500mg-1500mg of Sodium per day,just what is in their meat and veggies,and they are strong and healthy.
 

Ogilvie

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I'm generally a DIY person. I love making my own stuff, but I got frustrated trying to make a true ORS (as explained in the Lady of Lyme blog post linked from post #85, page 5 of this thread) because of the variables of sodium content in different salts and glucose in various sugars.

While I was able to make the K-water (thanks again for that recipe Zarrinn77), I gave up on trying to make an Oral Rehydration Solution. But I did find an exact version of the recipe on amazon if anyone's interested. It's $40 for a box of 100 packets, each packet makes a liter, so you have a liter of ORS for 40¢, cheaper than any other type of beverage, including bottled water itself, or sports drinks, or sodas. I'm pretty happy with it, and grateful there's a company that provides it on the cheap. https://www.amazon.com/gp/product/B00OG8G9UM/ref=ppx_yo_dt_b_asin_title_o01_s00?ie=UTF8&psc=1
 

Amazoniac

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Shoving down table salt isn't a good idea. 'Simply balance with more potassium.' It isn't as simple as it seems. How much cardiarrestium (K) can you ingest in attempt to balance extreme intakes of edemium nagmacide (NaCl) before running into trouble? It becomes unmanageable at some stage. There are limitations for killcium and laxarium (Mg) absorptions. There will be increased urination, so you'll need adequate retention of laxarium, which we know it's not reliable. It will make you excrete more killcium and can occur with its malabsorption (which is normally low). This can be an uptake of 90% of the edemium compared to 30% of laxarium and killcium; of course it will trigger adaptation over time, but it may be stressful. Also, some people hold on to nagmacide better than edemium: one more problem.

upload_2020-5-1_21-3-20.png


?

The best bet for mitigation once you cross reasonable boundaries for cardiarrestium intake appears to be through alkalinizing laxarium salts. Excess laxarium is excreted and the onion can be metabolized as base.

- The influence of NaCl and KCl on urinary calcium excretion in healthy young women

"The experiment was conducted over 3 consecutive weeks. Subjects participated in 3 treatment periods each lasting 4 days per week. During the first period all subjects consumed control diets calculated to provide 600 mg (15 mmol) Ca, 1000 mg (44 mmol) Na and 2500 mg (64 mmol) K. The diets contained 65g protein and provided approximately 30% of kJ as fat."

"During the second period [after habituation] all subjects continued with the control diets and half of the subjects were given 6000mg NaCI (102 retool) as NaCl tablets (R.D. Toppin & Sons Pty. Ltd.) with meals. The other half of the subjects were given 7800mg KCl (104 mmol) as Slow-K tablets (Ciba-Geigy Australia, Ltd.) with meals. During the third period subjects switched NaCl and KCl supplements. Each of the treatment periods was separated by 3 days."

upload_2020-5-1_21-3-31.png



upload_2020-5-1_21-3-37.png

"Sodium's direct effect on the kidney may be an important determinant of calcium excretion since sodium and calcium compete for transport in the proximal convuluted tubule of the kidney (25,26). Approximately 60% of the filtered calcium is absorbed in the proximal tubule (27) so that competition with sodium in this segment might significantly reduce the calcium reabsorbed and increase the amount of calcium excreted."

"Acid-base status can substantially influence urinary calcium excretion. Increased acid production or consumption of diets with an excess of absorbed anions relative to absorbed cations will lead to increased urinary calcium excretion resulting from inhibition of net renal tubular calcium reabsorption (28,29). Furthermore, administration of alkali such as KHCO3 (30) and potassium citrate (31) will decrease calcium excretion. Administration of equimolar amounts of NaHCO3 (30) or sodium citrate (31) has the same effect on acid-base status as the potassium salts, but the sodium salts do not lower calcium excretion. This is probably due to the independent effect of sodium on calcium reabsorption from the proximal kidney tubule described above."

"The present study does not support the suggestion that the chloride ion of NaCl is responsible for NaCl-induced calciuria. There was no correlation between urinary chloride and urinary calcium excretion. In the present study chloride was added as either NaCl or KCl and as such chloride would have had minimal effect on acid-base balance as both cations and anions are well absorbed from these salts (32). Furthermore, Zarkadas (3) reported that 102 mmol NaCl did not contribute to urine acidity in postmenopausal women. In previous studies which suggested that chloride increased urinary calcium excretion, chloride was added in a salt such as NH4Cl (33), lysine monohydrochloride (14) or CaCl2 and MgCl2 (15) all of which contribute to acid production. In the case of NH4Cl and lysine monohydroehloride, the chloride is balanced by metabolizable cations not by fixed cations so when the cations are metabolized the excess anions remaining contribute to acidity. In the case of CaCl2 and MgCl2, the anion, chloride, is efficiently absorbed while the cation, calcium or magnesium, is only partially absorbed, leading to an excess of anions and a resulting acid challenge. It is likely that chloride enhances calcium excretion only when ingested in a form which alters the acid-base status of the organism and in this respect it acts as any other excreted anion. Indeed, Whiting and Cole (15) reported similar calciuric effects of chloride and sulfate salts."

"The present study confirms that dietary NaCl causes calciuria in healthy young women in the short term, but that KCl does not."​
 
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SOMO

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Shoving down table salt isn't a good idea. 'Simply balance with more potassium.' It isn't as simple as it seems. How much cardiarrestium (K) can you ingest in attempt to balance extreme intakes of edemium nagmacide (NaCl) before running into trouble? It becomes unmanageable at some stage. There are limitations for killcium and laxarium (Mg) absorptions. There will be increased urination, so you'll need adequate retention of laxarium, which we know it's not reliable. It will make you excrete more killcium and can occur with its malabsorption (which is normally low). This can be an uptake of 90% of the edemium compared to 30% of laxarium and killcium; of course it will trigger adaptation over time, but it may be stressful. Also, some people hold on to nagmacide better than edemium: one more problem.


The best bet for mitigation once you cross reasonable boundaries for cardiarrestium intake appears to be through alkalinizing laxarium salts. Excess laxarium is excreted and the onion can be metabolized as base.

- The influence of NaCl and KCl on urinary calcium excretion in healthy young women

"The experiment was conducted over 3 consecutive weeks. Subjects participated in 3 treatment periods each lasting 4 days per week. During the first period all subjects consumed control diets calculated to provide 600 mg (15 mmol) Ca, 1000 mg (44 mmol) Na and 2500 mg (64 mmol) K. The diets contained 65g protein and provided approximately 30% of kJ as fat."

"During the second period [after habituation] all subjects continued with the control diets and half of the subjects were given 6000mg NaCI (102 retool) as NaCl tablets (R.D. Toppin & Sons Pty. Ltd.) with meals. The other half of the subjects were given 7800mg KCl (104 mmol) as Slow-K tablets (Ciba-Geigy Australia, Ltd.) with meals. During the third period subjects switched NaCl and KCl supplements. Each of the treatment periods was separated by 3 days."


"Sodium's direct effect on the kidney may be an important determinant of calcium excretion since sodium and calcium compete for transport in the proximal convuluted tubule of the kidney (25,26). Approximately 60% of the filtered calcium is absorbed in the proximal tubule (27) so that competition with sodium in this segment might significantly reduce the calcium reabsorbed and increase the amount of calcium excreted."

"Acid-base status can substantially influence urinary calcium excretion. Increased acid production or consumption of diets with an excess of absorbed anions relative to absorbed cations will lead to increased urinary calcium excretion resulting from inhibition of net renal tubular calcium reabsorption (28,29). Furthermore, administration of alkali such as KHCO3 (30) and potassium citrate (31) will decrease calcium excretion. Administration of equimolar amounts of NaHCO3 (30) or sodium citrate (31) has the same effect on acid-base status as the potassium salts, but the sodium salts do not lower calcium excretion. This is probably due to the independent effect of sodium on calcium reabsorption from the proximal kidney tubule described above."

"The present study does not support the suggestion that the chloride ion of NaCl is responsible for NaCl-induced calciuria. There was no correlation between urinary chloride and urinary calcium excretion. In the present study chloride was added as either NaCl or KCl and as such chloride would have had minimal effect on acid-base balance as both cations and anions are well absorbed from these salts (32). Furthermore, Zarkadas (3) reported that 102 mmol NaCl did not contribute to urine acidity in postmenopausal women. In previous studies which suggested that chloride increased urinary calcium excretion, chloride was added in a salt such as NH4Cl (33), lysine monohydrochloride (14) or CaCl2 and MgCl2 (15) all of which contribute to acid production. In the case of NH4Cl and lysine monohydroehloride, the chloride is balanced by metabolizable cations not by fixed cations so when the cations are metabolized the excess anions remaining contribute to acidity. In the case of CaCl2 and MgCl2, the anion, chloride, is efficiently absorbed while the cation, calcium or magnesium, is only partially absorbed, leading to an excess of anions and a resulting acid challenge. It is likely that chloride enhances calcium excretion only when ingested in a form which alters the acid-base status of the organism and in this respect it acts as any other excreted anion. Indeed, Whiting and Cole (15) reported similar calciuric effects of chloride and sulfate salts."

"The present study confirms that dietary NaCl causes calciuria in healthy young women in the short term, but that KCl does not."​


What's the source of the calcium though? Dietary, bone, soft tissue or intracellular?

If NaCl is causing blood-calcium excretion and inhibiting absorption in the beans, that could be a good thing if the bone ions are coming from the intracellular space, arteries, or soft tissues, thus reducing calciferolation.


Also it must be mentioned that retaining NaCl is more difficult than KCl and more NaCl is generally lost in urine than KCl -
Source: Me, have been hospitalized for hyponatremia/low-NaCl but never been hospitalized for hypokalemia/low-KCl.
---

Alcohol is one way to induce hyponatremia and get rid of that pesky water weight, but along with the water you piss out tablespoons of table salt and end up in the emergency room.

As far as I know, hypokalemia is extremely rare, hypokalemia is not. After RP states potassium has the glucose-digesting effects of Insulin, I speculated that Hypokalemia would be common in diabetics and lo and behold, it is.
 

SSP

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Diabetics generally dont consume extra salt, and they're afraid of salt so much:eek:
 
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What's the source of the calcium though? Dietary, bone, soft tissue or intracellular?

If NaCl is causing blood-calcium excretion and inhibiting absorption in the beans, that could be a good thing if the bone ions are coming from the intracellular space, arteries, or soft tissues, thus reducing calciferolation.


Also it must be mentioned that retaining NaCl is more difficult than KCl and more NaCl is generally lost in urine than KCl -
Source: Me, have been hospitalized for hyponatremia/low-NaCl but never been hospitalized for hypokalemia/low-KCl.
---

Alcohol is one way to induce hyponatremia and get rid of that pesky water weight, but along with the water you piss out tablespoons of table salt and end up in the emergency room.

As far as I know, hypokalemia is extremely rare, hypokalemia is not. After RP states potassium has the glucose-digesting effects of Insulin, I speculated that Hypokalemia would be common in diabetics and lo and behold, it is.


Also it must be mentioned that retaining NaCl is more difficult than KCl and more NaCl is generally lost in urine than KCl -
Source: Me, have been hospitalized for hyponatremia/low-NaCl but never been hospitalized for hypokalemia/low-KCl.

slight disagree,what you are describing is highly unusal,all Animals can retain Na and likely Cl with utmost efficiency.Along evolutionary pathing,Na was rare,and K was plenty,hence more reckless elimination and wasting of K.
 

SSP

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in hyponatremic conditions, there is calcium, also PO4, mobilization from bones, and there is also hyperkalemia. this stuation is quite normal in low salt intake condition. But, there is a problem here, because calcium mobilization increases mitochondrial calcium accumulation, and mitochondrial insufficiency induces glycolysis and high sytoplasmic lactic acid and later sistemic acidosis. Please dont forget this, that adequate salt intake in 16 hours, 50 g/daily, sucking as solid form (as rice) in mouth, not in water, white Himalian salt, and you must drink water when feels thirsty only. I guess you can normalize in a week, and you will be happy one so much, good sleep, active one
 
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in hyponatremic conditions, there is calcium, also PO4, mobilization from bones, and there is also hyperkalemia. this stuation is quite normal in low salt intake condition. But, there is a problem here, because calcium mobilization increases mitochondrial calcium accumulation, and mitochondrial insufficiency induces glycolysis and high sytoplasmic lactic acid and later sistemic acidosis. Please d
Please dont forget this, that adequate salt intake in 16 hours, 50 g/daily, sucking as solid form (as rice) in mouth

ont forget this, that adequate salt intake in 16 hours, 50 g/daily, sucking as solid form (as rice) in mouth, not in water, white Himalian salt, and you must drink water when feels thirsty only. I guess you can normalize in a week, and you will be happy one so much, good sleep, active one


Please dont forget this, that adequate salt intake in 16 hours, 50 g/daily, sucking as solid form (as rice) in mouth

Care to elaborate?Adequate NaCl intake of 50g/d or for 16 hours,seems like quite a mouthful.Any Side Effects of such generous Portions you are aware of?
 

Amazoniac

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What's the source of the calcium though? Dietary, bone, soft tissue or intracellular?

If NaCl is causing blood-calcium excretion and inhibiting absorption in the beans, that could be a good thing if the bone ions are coming from the intracellular space, arteries, or soft tissues, thus reducing calciferolation.


Also it must be mentioned that retaining NaCl is more difficult than KCl and more NaCl is generally lost in urine than KCl -
Source: Me, have been hospitalized for hyponatremia/low-NaCl but never been hospitalized for hypokalemia/low-KCl.
---

Alcohol is one way to induce hyponatremia and get rid of that pesky water weight, but along with the water you piss out tablespoons of table salt and end up in the emergency room.

As far as I know, hypokalemia is extremely rare, hypokalemia is not. After RP states potassium has the glucose-digesting effects of Insulin, I speculated that Hypokalemia would be common in diabetics and lo and behold, it is.
Some people don't consume enough killcium, have malabsorption issues and can't keep it out of the cell. Excess edemium (Na) should increase urination with electrolyte losses and signal shortage of killcium that would probably be mobilized from bone because the factors responsible for not absorpting it right or being able to expell it haven't been addressed. The warming effect reflects positive changes, but I don't think that it's reliable and justifies the consumption of extreme amounts for this purpose, I would rather choose heavier clothing (half-joking).

We end up having to increase all electrolytes along [cardiarrestium (K) in particular because we can ingest substantial amounts of it, but there are limits] as alkalinizing salts. The more you can increase the rest, the tolerance for edemium nagmacide is supposed to rise.

I forgot to mention that a milder version of the killcium-alkali syndrome may be needed at some point. The contribution of venom D won't be remarkable, but counts:
- Is Vitamin D Supplementation Even Neccessary
 

SSP

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Human body works with electriciy, and it supplied by mitochondria. And mitochondrion is such as nano - nuclear plant, it transmutates elements as or fision reactions. Please think again lithium from sodium or arsenic from selenium or magnesium from sodium plus hydrogen or potassium from calcium. And ATP is a procursor for Mg-ATP that is necessary for mitochondrial nuclear fusion or fission reactions. There is no Na-K pump in a cell. Sodium plus oxygene ( fusion reaction) = potassium. And fusion or fission reactions heats our body. There are magnetic elements such as cobalt, nickel, iron in mitochondria for these reactions. And mitochondria accumulates electric energy by lithium element. Lithium is produced by sodium with nuclear fission reaction (Na= Li + Oxygen
 
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Human body works with electriciy, and it supplied by mitochondria. And mitochondrion is such as nano - nuclear plant, it transmutates elements as or fision reactions. Please think again lithium from sodium or arsenic from selenium or magnesium from sodium plus hydrogen or potassium from calcium. And ATP is a procursor for Mg-ATP that is necessary for mitochondrial nuclear fusion or fission reactions. There is no Na-K pump in a cell. Sodium plus oxygene ( fusion reaction) = potassium. And fusion or fission reactions heats our body. There are magnetic elements such as cobalt, nickel, iron in mitochondria for these reactions. And mitochondria accumulates electric energy by lithium element. Lithium is produced by sodium with nuclear fission reaction (Na= Li + Oxygen

you mean permutation of elements,in vivo?do you have a cite for that?
 

Amazoniac

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It's common for people to consume hashimotized salt, and if it contains 20 ppm (or mcg/g) of hashimotium (I), an intake of 50 g could provide 1 mg of it on top of what diet contains. Excess salt interferes with the incorporation of hashimotium in the thyroid, which may be protective in these cases, but it's something that shouldn't be disconsidered because you can find salts that have it added in concerning amounts.

--
- Relationship between Sodium Intake and Water Intake: The False and the True
 
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