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

[Lokzo]

I feel awesome using copious amounts of salt on my foods.

 

[Amazoniac]

- Salt sensitivity and insulin resistance: Is there a link?

Salt sensitivity is not only found in patients with essential hypertension but also in normotensive individuals. These salt-sensitive normotensives are believed to be genetically predisposed to the development of hypertension. In this paper we present data from our studies in such normotensive salt-sensitive individuals, thereby focusing on the relationship between salt sensitivity and familial history of hypertension and on insulin sensitivity. Salt-sensitivity was associated with a positive familial history of hypertension, a finding that supports the hypothesis that salt sensitivity in normotensive individuals points to a genetic predisposition for the development of hypertension. Also, salt-sensitive subjects displayed a hyperinsulinaemic response to an oral glucose load and a decreased insulin-mediated glucose disposal, as assessed by the insulin suppression test. The latter finding implies that insulin resistance is present in otherwise healthy, hypertension-prone individuals before overt hypertension develops. Assuming that there is a pathophysiological relationship between insulin resistance and salt sensitivity, our findings suggest that early recognition of insulin resistance and the implementation of measures aimed at improving insulin sensitivity could contribute to the prevention of cardiovascular disease in these individuals.

- Subtle Acquired Renal Injury as a Mechanism of Salt-Sensitive Hypertension

Salt sensitivity is present in about half of people with essential hypertension; decreasing salt intake ameliorates the hypertension. This review provides an explanation of how initially subtle renal injury promotes a tendency toward hypertension. The kidneys, initially normal in many persons with early primary hypertension, sustain subclinical injury over time, resulting in arteriolosclerosis and tubulointerstitial disease that lead to established hypertension.

- Changing views on the common physiologic abnormality that mediates salt sensitivity and initiation of salt-induced hypertension: Japanese research underpinning the vasodysfunction theory of salt sensitivity

High-salt intake is one of the major dietary determinants of increased blood pressure and cardiovascular disease. Thus, there is scientific and medical interest in understanding the mechanistic abnormalities mediating the pressor effects of salt (salt sensitivity). According to historical theory, salt sensitivity stems from an impairment in renal function (referred to as “abnormal pressure natriuresis” or a “natriuretic handicap”), which causes salt-sensitive subjects to excrete a sodium load more slowly, and retain more of it than salt-resistant normotensive controls. However, this historical view has come under intense scrutiny because of growing awareness that in salt-sensitive subjects, acute salt loading does not usually induce greater increases in sodium balance and cardiac output than those induced by salt loading in salt-resistant normotensive controls. Here we highlight pioneering studies from Japan that challenge the historical thinking and provide insights into a contemporary theory of salt sensitivity termed the “vasodysfunction theory.” According to this theory, initiation of salt-induced hypertension usually involves abnormal vascular resistance responses to increased salt intake, not greater renal retention of a salt load in salt-sensitive subjects than in normal subjects. By shifting the focus from the historical theory to a contemporary final common pathway for the pathogenesis of salt sensitivity, research from Japan is building the scientific foundation for more effective approaches to the prevention and treatment of salt-induced hypertension. Among the most promising approaches are dietary strategies for reducing the risk for salt-induced hypertension that do not depend on reducing salt consumption in the population.

- Hypertension as an autoimmune and inflammatory disease

Hypertension that is considered idiopathic is called essential hypertension and accordingly has no clear culprit for its cause. However, basic research and clinical studies in recent years have expanded our understanding of the mechanisms underlying the development of essential hypertension. Of these, increased oxidative stress, both in the kidney and arterial wall, closely coupled with inflammatory infiltration now appear to have a prominent role. Discovery of regulatory and interleukin-17-producing T cells has enabled us to better understand the mechanism by which inflammation and autoimmunity, or autoinflammation, lead to the development of hypertension. Despite achieving considerable progress, the intricate interactions between oxidative stress, the immune system and the development of hypertension remain to be fully elucidated. In this review, we summarize recent developments in the pathophysiology of hypertension with a focus on the oxidant stress-autoimmunity-inflammation interaction.

 

[Mauritio]

Salt Might Be 'Nature's Antidepressant'

The article is full of bs and fear mongering . But some passages are pretty telling . For example that salt deficiency makes rats depressed . What a coincidence that salt lowers serotonin . And high serotonin is the major cause for depression .
Yet they still are able to turn it around and call salt an addictive substance...
Also interesting: worldwide intake of salt is 10g !! Much more than I would have thought.

" Sodium restriction also increases serotonin, activity of the sympathetic nervous system, and plasminogen activator inhibitor type-1 (PAI-1), which contributes to the accumulation of clots and is associated with breast and prostate cancer. "
Ray Peat.

 

[Rafael Lao Wai]

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.

​

Spoiler

View attachment 17691​

​

?​

​

​

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."​

​

​

Spoiler: Urinary consequences

View attachment 17692​

​

​

View attachment 17693​

​

​

​

"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."​

It's interesting that simply adding cardioarrestium chloride caused the subjects to excrete a lot more edemium than the NaCl group( nearly 3 times as much), and even more than the control group( 10 times as much). I would expect aldosterone to increase in the cardioarrestium group, making them excrete less edemium, but the opposite happened( with regards to excretion). I wonder what the mechanism for that is.

 

[David90]

Very cool study done in the 50’s.

https://www.jstage.jst.go.jp/article/jjphysiol1950/2/0/2_0_303/_pdf

View attachment 17453

Interesting Study.

I use Personally around 8-10g of Salt per Day. It Definently warms you up for sure. But i should Limit my Liquid Intake a Little Bit, behause i think it could be too much. Also my Potassium Intake is around 4500-5000mg per Day.

Also don‘t Forget That certain Fruits have also Water in them....

 

[Nomane Euger]

Nice find! Must have been pretty disgusting though to eat 50g salt daily.

when i went out a fruitarian style of eating,where i was not using salt,i started to add salt to my water,redmond real salt,it you left it long enough to disolveit switch from a salty taste to a sugary cholate type like taste,and it was fueling me crazy to the point where i did not eat for 2 days,not hungry,just wated more salt,i was averaging 30 grammes of salt daily

 

[TheBeard]

Personally, I rely more on whole and dried fruits than fruit juice.

I never understood the focus here on fruit juice instead of whole fruits. The literature strongly suggests better health with whole fruits, the polyphenol content is much higher, which protects from endotoxin and helps gut health. Sure, they have some fiber, not anything like wheat bran or something, but the fiber in fruits tends to positively modulate our microbiome so that there is less inflammation present.

Not for me.

Good if it works for you

 

[David90]

Personally, I rely more on whole and dried fruits than fruit juice.

I never understood the focus here on fruit juice instead of whole fruits. The literature strongly suggests better health with whole fruits, the polyphenol content is much higher, which protects from endotoxin and helps gut health. Sure, they have some fiber, not anything like wheat bran or something, but the fiber in fruits tends to positively modulate our microbiome so that there is less inflammation present.

Feel also better on Whole and/or Dried Fruits.

Sure they have Fiber. By i would not Worry too much about the Fiber in Fruit.
I would not go higher then 25g per Day though in Terms of Hormones and SHBG. At the Moment i'm Around 15-20g of fiber per Day.

 

[Rafael Lao Wai]

Feel also better on Whole and/or Dried Fruits.

Sure they have Fiber. By i would not Worry too much about the Fiber in Fruit.
I would not go higher then 25g per Day though in Terms of Hormones and SHBG. At the Moment i'm Around 15-20g of fiber per Day.

Fiber gives me way too much pain now. I can only drink filtered juice, or else my gut( especially my lower gut) hurts a lot. I must have a really messed up intestine. Before using doxycycline, I would get constipation from fiber, now the fiber goes through me much faster, making it apparent that my gut isn't in a condition to handle roughage, even soft fibers like from fruits. But, at least right now, I feel better in general when I eat fiber. The main problem is really the pain when the fiber is getting to the end of the small intestine I think.

 

[TheBeard]

Lean meat, organs, salt, milk and fruit juice gives you a pretty well rounded nutrition profile.

 

[Rafael Lao Wai]

Lean meat, organs, salt, milk and fruit juice gives you a pretty well rounded nutrition profile.

Oh yeah, I agree, nutrition-wise, fruit and meat is great. It just kinda sucks to not be able to eat some ripe, juicy fruits and have to juice them instead.

 

[TheBeard]

Oh yeah, I agree, nutrition-wise, fruit and meat is great. It just kinda sucks to not be able to eat some ripe, juicy fruits and have to juice them instead.

I miss biting in a mango so bad.
But the 20 seconds of pleasure won't be worth the bloating and the trips to the bathroom, so I'm overall happier without.

 

[Rafael Lao Wai]

I miss biting in a mango so bad.
But the 20 seconds of pleasure won't be worth the bloating and the trips to the bathroom, so I'm overall happier without.

Completely agree.

 

[Daniil]

И тонкий, и толстый кишечник каким-то образом не усваивают эту соль. В вашем теле должен быть встроенный механизм, который не позволяет вам принимать больше соли. Возможно, у вас мало калия. Даже если вы потребляете большое количество калия, он будет выводиться из организма только в том случае, если у вас недостаточно запасов магния.

Я думаю, что у большинства людей, даже на этом форуме, мало магния в магазинах. Причина:

1. Большинство людей не получают достаточного количества магния в течение жизни.
2. Люди здесь надеются, что у них достаточно запасов магния, но они никогда по-настоящему не проверяют (тест дорогостоящий; есть дешевый тест, который я опубликовал, но никого, ни одного не заинтересовал), если в них мало магния. Поэтому они просто надеются, но на самом деле у них мало магния.
3. Люди опасаются, что без проверки на магний и начала терапевтических добавок магния они могут перегрузиться и убить себя. Таким образом, они осторожны и в конечном итоге потребляют слишком мало добавок, чтобы изменить ситуацию и восполнить запасы магния в достаточном количестве. Таким образом, им по-прежнему не хватает магния.

Я принимал 600 мг магния (элементаль) в течение года. И этого было недостаточно. Недавно я возобновил прием добавок. Потом у меня началась диарея. Даже если каждая доза была низкой. Это знак, который мне нужен. Тело говорит мне, что больше не может принимать магний. Теперь я знаю, что в моем теле достаточно магния.

При пероральном приеме добавок магния смертельного отравления магнием не произойдет. До того, как это случится, у вас будет понос.

Следующий проект - терапевтическая добавка калия, теперь мое тело будет легко принимать калий и накапливать запасы калия. Как только это будет сделано, я могу начать принимать небольшое количество соли.

Could you please provide a link to the magnesium test? It is very interesting. I don't really trust the usual blood mineral tests.

My high salt intake seems to have caused metabolic alkalosis. Is it possible due to depletion of magnesium reserves? In general, I did a blood sodium test and it showed an upper limit of normal. Also now my palms are sweating and sometimes my appetite is missing. However, the pulse did drop.

 

[yerrag]

A

Could you please provide a link to the magnesium test? It is very interesting. I don't really trust the usual blood mineral tests.

My high salt intake seems to have caused metabolic alkalosis. Is it possible due to depletion of magnesium reserves? In general, I did a blood sodium test and it showed an upper limit of normal. Also now my palms are sweating and sometimes my appetite is missing. However, the pulse did drop.

I don't know what I was saying translated in Greek, but I think you were referring to a magnesium test involving injecting magnesium sulfate and testing before and after it for magnesium in urine. We're you referring to that?

 

[Daniil]

A

I don't know what I was saying translated in Greek, but I think you were referring to a magnesium test involving injecting magnesium sulfate and testing before and after it for magnesium in urine. We're you referring to that?

It is Russian . Forum is buggy) You talked about a cheap test that lets you know your magnesium levels.

 

[yerrag]

It is Russian . Forum is buggy) You talked about a cheap test that lets you know your magnesium levels.

Sorry about that. They are both Greek to me, in a manner of speaking

You can find the reference here: Magnesium deficiency: a cause of heterogeneous disease in humans - PubMed

You'd have a hard time reading the test procedure in the article, but this is basically what it is:

A test for magnesium deficiency is to inject 2.4 milligrams of magnesium per kilogram of body weight over 4 hours and urine collected for 24 hours. If 25% of the magnesium is retained a deficiency is probable. If 50% of the magnesium is retained a deficiency is certain.

It's also called a magnesium loading test.

 

[Rafael Lao Wai]

My high salt intake seems to have caused metabolic alkalosis. Is it possible due to depletion of magnesium reserves? In general, I did a blood sodium test and it showed an upper limit of normal. Also now my palms are sweating and sometimes my appetite is missing. However, the pulse did drop.

How are your blood chloride levels?

 

[Daniil]

How are your blood chloride levels?

Almost the lower limit of the norm.

 

[Daniil]

Apparently, I messed up the interpretation of the tests and I have metabolic acidosis, not alkalosis. I tried taking magnesium and it seems to aggravate the symptoms. It makes me want to breathe slowly and deeply, and it's very strange. I only feel normal when I don't take any electrolytes, and that's weird. I would like to understand why this is so. Tomorrow I think to pass the test for lactate.