More Dietary Salt Increases Urea Synthesis And Energy Requirements

[Runenight201]

Matt stone writes a little on this and unfortunately I don’t have any scientific studies to back up, all just conjecture, but how about adjusting salt intake relative to urine frequency?

On a high liquid peat diet, which is apparently most optimal due to the intake of primarily sugar as fuel accompanied with the minerals found in milk + oj, I find that I pee... a lot. I know this can’t be good, and I’ll often also start feeling weak and sometimes nauseous or have gastrointestinal distress.

However, by correspondingly eating very salty foods, such as heavily salting meat and veggies, I find I feel much better. The more OJ I drink the clearer and more frequent my urine, so I think something is very off with my body’s ability to regulate sodium.

I don’t think it’s smart to hit a set salt goal per se, but go based on how frequently urination occurs, the color of urine, and overall body sentiment. I think the more spaced the urination events (every 2-3 hours or so) and the darker the urine (to an extent) the better.

Consuming sugar with salt I think might be the winner here. You get the lower aldosterone, increased energy needs, and then the sugar blunts the corresponding rise in cortisol. I know for me, when I have a heavily salted meal with eggs, cheese, veggies, and salsa, and then chase with OJ, my brain starts to tingle, as if everything “right” is occurring metabolically.

 

[BeHealthy]

I don't think 10g is that much. Up until the early 1960s the average salt intake for an adult in the US was about 12g-15g daily. These days, with everything being made "low sodium" by default, those 10g probably bring you closer to normality and not anywhere in danger-zone. But I think salt should be eaten to taste, not so much based on set daily goals.

Thank you so much for your response and for your help. I will apply your insight and eat salt to taste. Knowing that 10 grams is fine is important for me because this way I have an upper limit in mind while salting to taste.

 

[tankasnowgod]

Of note to this thread, Ray Peat cited the following study in the article Salt, energy, metabolic rate, and longevity.

The study is https://www.sciencedirect.com/science/article/pii/S0939475305001705

"
Design and methods
Rats were fed a low (LSD), normal (NSD), or high (HSD) salt diet. In a first set, body weight, tail-cuff blood pressure, fasting plasma thyroid-stimulating hormone, triiodothyronine, l-thyroxine, glucose, insulin, and angiotensin II were measured. Angiotensin II content was determined in white and brown adipose tissues. Uncoupling protein 1 expression was measured in brown adipose tissue. In a second set, body weight, food intake, energy balance, and plasma leptin were determined. In a third set of rats, motor activity and body weight were evaluated.

Results
Blood pressure increased on HSD. Body weight was similar among groups at weaning, but during adulthood it was lower on HSD and higher on LSD. Food intake, l-thyroxine concentration, uncoupling protein 1 expression and energy expenditure were higher in HSD rats, while non-fasting leptin concentration was lower in these groups compared to NSD and LSD animals. Plasma thyroid-stimulating hormone decreased on both HSD and LSD while plasma glucose and insulin were elevated only on LSD. A decrease in plasma angiotensin II was observed in HSD rats. On LSD, an increase in brown adipose tissue angiotensin II content was associated to decreased uncoupling protein 1 expression and energy expenditure. In this group, a low angiotensin II content in white adipose tissue was also found. Motor activity was not influenced by the dietary salt content.

 

[ecstatichamster]

Thanks @tankasnowgod

People wanting to lose weight might want to increase salt intake.

 

[tankasnowgod]

However, the higher the salt intake the higher the glucocorticoid release was in those same subjects. I think the increase in urea and energy requirements (metabolism) would be solid reasons to increase salt intake as per Peat's recommendations. However, the high cortisol release is potentially bothersome and may explain some negative effects of higher salt intake in sick people

if high salt increases the energy requirements

could this lead to low blood sugar and consequently to higher cortisol?

That's certainly a possibility. Another one is that aldosterone and cortisol may have an inverse relationship since they both bind to the same "receptors" and when aldosterone is lowered by the high salt then cortisol rises to compensate. But I like the energetic deficit explanation more.

In regards to the potential cortisol issue, I found this study on Salt Loading that measured both plasma cortisol and urine cortisol metabolites during a week of higher salt loading, in both normal and salt sensitive individuals- Salt Loading Affects Cortisol Metabolism in Normotensive Subjects: Relationships with Salt Sensitivity

It seems this study found that plasma cortisol was lowered in normal individuals. The higher amount of urinary cortisol metabolites would be the body eliminating excess cortisol-

" This study clearly demonstrates changes in cortisol metabolism in response to dietary sodium in normotensive subjects. Interestingly, the sum of urinary cortisol metabolites, which can be considered as an estimate of cortisol elimination, was on average increased in sr, but decreased in ss subjects after salt loading. Likewise, the excretion of UFF, UFE, and each of the individual cortisol metabolites (THF, allo-THF, and THE) was higher after salt loading in sr subjects but was unaltered or lower in ss subjects. Of note, these changes in cortisol metabolite excretion after salt loading were accompanied by a decrease in plasma cortisol concentration, particularly in sr individuals. Taken together, it can be envisaged from these data that salt loading induces an increase in cortisol elimination and hence a decrease in circulating cortisol in sr subjects, whereas these effects of salt loading on cortisol metabolism are blunted in ss individuals."

"In agreement with a primary enhancing effect of sodium loading on cortisol elimination, the changes in plasma cortisol were negatively correlated with the changes in urinary cortisol metabolite excretion in the whole group. In ss subjects, the change in plasma cortisol was not significant, whereas urinary cortisol metabolite excretion tended to decrease. In this respect, the aforementioned inverse relationship between the sum of cortisol metabolites and the percentage change in plasma cortisol is of relevance. It suggests that the reciprocal relationship between changes in urinary cortisol metabolite excretion and plasma cortisol can be regarded as a continuum rather than as a qualitatively different response to salt loading in ss subjects."

So it seems that in most individuals, increased salt intake would tend to lower plasma cortisol. Caution might be warranted in individuals with known salt sensitivities, and also to be sure to be getting enough sugar to meet increased metabolic demands when consuming extra salt.

As you can see from the study, plasma aldosterone was absolutely crushed in both groups after one week of salt loading.

 

[haidut]

In regards to the potential cortisol issue, I found this study on Salt Loading that measured both plasma cortisol and urine cortisol metabolites during a week of higher salt loading, in both normal and salt sensitive individuals- Salt Loading Affects Cortisol Metabolism in Normotensive Subjects: Relationships with Salt Sensitivity

It seems this study found that plasma cortisol was lowered in normal individuals. The higher amount of urinary cortisol metabolites would be the body eliminating excess cortisol-

" This study clearly demonstrates changes in cortisol metabolism in response to dietary sodium in normotensive subjects. Interestingly, the sum of urinary cortisol metabolites, which can be considered as an estimate of cortisol elimination, was on average increased in sr, but decreased in ss subjects after salt loading. Likewise, the excretion of UFF, UFE, and each of the individual cortisol metabolites (THF, allo-THF, and THE) was higher after salt loading in sr subjects but was unaltered or lower in ss subjects. Of note, these changes in cortisol metabolite excretion after salt loading were accompanied by a decrease in plasma cortisol concentration, particularly in sr individuals. Taken together, it can be envisaged from these data that salt loading induces an increase in cortisol elimination and hence a decrease in circulating cortisol in sr subjects, whereas these effects of salt loading on cortisol metabolism are blunted in ss individuals."

"In agreement with a primary enhancing effect of sodium loading on cortisol elimination, the changes in plasma cortisol were negatively correlated with the changes in urinary cortisol metabolite excretion in the whole group. In ss subjects, the change in plasma cortisol was not significant, whereas urinary cortisol metabolite excretion tended to decrease. In this respect, the aforementioned inverse relationship between the sum of cortisol metabolites and the percentage change in plasma cortisol is of relevance. It suggests that the reciprocal relationship between changes in urinary cortisol metabolite excretion and plasma cortisol can be regarded as a continuum rather than as a qualitatively different response to salt loading in ss subjects."

So it seems that in most individuals, increased salt intake would tend to lower plasma cortisol. Caution might be warranted in individuals with known salt sensitivities, and also to be sure to be getting enough sugar to meet increased metabolic demands when consuming extra salt.

As you can see from the study, plasma aldosterone was absolutely crushed in both groups after one week of salt loading.

Thanks. That last part about lower aldosterone should be rubbed into the faces of ALL cardiologists who relentlessly prescribe salt restriction for people with heart problems, and in more severe cases even dole out aldosterone antagonists like spironolactone.
Spironolactone - Wikipedia

All this fraud and money wasted on drugs when the solution is simply...eat more salt (to taste).

 

[magnesiumania]

A 3 page thread about salt and ive need seen magnesium mentioned. To my knowlegde electrolyte balance is the key, but also kinda tricky. Salt and potassium is what fuel the adrenals and the sodium to magnesium ratio is regulates the Na/K pump.

 

[tankasnowgod]

A 3 page thread about salt and ive need seen magnesium mentioned. To my knowlegde electrolyte balance is the key, but also kinda tricky. Salt and potassium is what fuel the adrenals and the sodium to magnesium ratio is regulates the Na/K pump.

Not much to say about it, nor is it that tricky. High aldosterone levels will encourage the excretion of magnesium, so the body can preserve sodium. Eating more salt will lower aldosterone levels, which lead to improved magnesium retention. If you want to improve Mag levels, you can either supplement directly and/or start eating more salt.

 

[Cirion]

So since I have some massive bloating going on, I guess that means I need to push my salt intake ever higher?

 

[GreekDemiGod]

@Cirion Hmm, I too been dealing with chronic bloating past 2 years.
Since peating, it has reduced.
Gonna up my salt intake.
On Carnivore, I was intaking up to 8g of Sodium / day.

 

[Tristan Loscha]

Not much to say about it, nor is it that tricky. High aldosterone levels will encourage the excretion of magnesium, so the body can preserve sodium. Eating more salt will lower aldosterone levels, which lead to improved magnesium retention. If you want to improve Mag levels, you can either supplement directly and/or start eating more salt.

The Aldosterone lowering effect of Salt is a illusionary one.
Aldosterone amount in blood decreases,hence lowerered Aldosterone-levels.
But sensitivity increases,and and it increases above the threshold that they deemed normal and viable compared to baseline for their study.
Normal to High Sodium increases true Aldosterone activity potently,with all side effects.

 

[tankasnowgod]

The Aldosterone lowering effect of Salt is a illusionary one.
Aldosterone amount in blood decreases,hence lowerered Aldosterone-levels.
But sensitivity increases,and and it increases above the threshold that they deemed normal and viable compared to baseline for their study.
Normal to High Sodium increases true Aldosterone activity potently,with all side effects.

I've seen nothing to support this claim. Sure sounds like one of those "Rube Goldberg" claims to justify a failing hypothesis.

 

[Tristan Loscha]

One high-impact cause of higher Aldosterone is also metabolic acidosis,Chlorine component of salt can effect this.

 

[Tristan Loscha]

I've seen nothing to support this claim. Sure sounds like one of those "Rube Goldberg" claims to justify a failing hypothesis.

Anti-Peat - High-Salt Augments Aldosterone Toxicity Despite Lowered Plasma-Readings

High-Salt Augments Aldosterone Toxicity Despite Lowered Plasma-Readings

Effect of aldosterone and mineralocorticoid receptor blockade on vascular inflammation
Hylton V Joffe, Gail K Adler
Heart failure reviews 10 (1), 31-37, 2005
Aldosterone, the final product of the renin-angiotensin-aldosterone system, is classically viewed as a regulator of renal sodium and potassium handling, blood volume, and blood pressure. Recent studies suggest that aldosterone can cause microvascular damage, vascular inflammation, oxidative stress and endothelial dysfunction. In animal models, aldosterone-mediated vascular injury in the brain, heart, and kidneys leads to stroke, myocardial injury, and proteinuria. These effects may be modified by dietary salt intake; aldosterone-mediated vascular damage is increased in susceptible animals fed a high-salt diet compared to a low-salt diet despite lower plasma aldosterone levels on the high-salt diet. In humans, there is a growing literature supporting the adverse effects of aldosterone in heart failure, hypertension, left ventricular hypertrophy, and renal disease. Aldosterone receptor antagonists are beneficial even in patients on angiotensin converting enzyme inhibitors and attenuate aldosterone-mediated vascular injury by mechanisms that appear to be independent of changes in systolic blood pressure. This review focuses on the adverse effects of aldosterone on the vascular system and describes our current understanding of the underlying mechanisms for this injury.

also "haha" at rube goldberg.he is a genuine guy,and a creative thinker.

 

[rei]

what does "in susceptible animals" mean?

 

[tankasnowgod]

Anti-Peat - High-Salt Augments Aldosterone Toxicity Despite Lowered Plasma-Readings

High-Salt Augments Aldosterone Toxicity Despite Lowered Plasma-Readings

Effect of aldosterone and mineralocorticoid receptor blockade on vascular inflammation
Hylton V Joffe, Gail K Adler
Heart failure reviews 10 (1), 31-37, 2005
Aldosterone, the final product of the renin-angiotensin-aldosterone system, is classically viewed as a regulator of renal sodium and potassium handling, blood volume, and blood pressure. Recent studies suggest that aldosterone can cause microvascular damage, vascular inflammation, oxidative stress and endothelial dysfunction. In animal models, aldosterone-mediated vascular injury in the brain, heart, and kidneys leads to stroke, myocardial injury, and proteinuria. These effects may be modified by dietary salt intake; aldosterone-mediated vascular damage is increased in susceptible animals fed a high-salt diet compared to a low-salt diet despite lower plasma aldosterone levels on the high-salt diet. In humans, there is a growing literature supporting the adverse effects of aldosterone in heart failure, hypertension, left ventricular hypertrophy, and renal disease. Aldosterone receptor antagonists are beneficial even in patients on angiotensin converting enzyme inhibitors and attenuate aldosterone-mediated vascular injury by mechanisms that appear to be independent of changes in systolic blood pressure. This review focuses on the adverse effects of aldosterone on the vascular system and describes our current understanding of the underlying mechanisms for this injury.

also "haha" at rube goldberg.he is a genuine guy,and a creative thinker.

A single sentence in the abstract of a meta-analysis is hardly proof of anything, especially when that sentence is qualified to "susceptible animals." Did you track down the full text of the study to which this is referring to?

 

[Tristan Loscha]

In susceptible Animals means that the conductors made the rodent hypertensive to study effects
of Aldosterone Levels along this model of hypertension.


"It is currently
unknown whether there are additional direct
effects of aldosterone on target organs. The
primary insult caused by aldosterone in susceptible
individuals and animals has not been identified,
and the mechanism by which high salt
intake contributes to this injury is unknown.
Furthermore, the relative importance of circulating
aldosterone levels, local cardiovascular aldosterone
production, and aldosterone uptake from
the circulation remains to be determined."

They havent figured it out how this part of the system operates,but they recognize that High-Salt amplifies damage
mediated by Aldosterone,despite lowered readings of blood-level.An important finding,in that low Aldosterone
blood-lvl-readings arent indicative of true ,low-Aldosterone-activity,but to the contrary.If we base future risks
on bloodwork,it means there is a high possibility for a wrong outcome if,in this case,low lvl does not mean low lvl,
but in vivo high lvl-activity.
If im feeling calm,secure and sedated with my low,Hi-Salt induced Aldosterone machine-printout,
and this thing is actually up-side-down,i have to adapt to reach a favorable outcome.

 

[Tristan Loscha]

Furthermore,the study was a review of the available literature,the uncontrolled for,population-based
meta-analyses are a problem,there we are on the same page,but for an author of an review of controlled models
it is just like using his footnotes,like anyone else imo.

 

[tankasnowgod]

In susceptible Animals means that the conductors made the rodent hypertensive to study effects
of Aldosterone Levels along this model of hypertension.


"It is currently
unknown whether there are additional direct
effects of aldosterone on target organs. The
primary insult caused by aldosterone in susceptible
individuals and animals has not been identified,
and the mechanism by which high salt
intake contributes to this injury is unknown.
Furthermore, the relative importance of circulating
aldosterone levels, local cardiovascular aldosterone
production, and aldosterone uptake from
the circulation remains to be determined."

They havent figured it out how this part of the system operates,but they recognize that High-Salt amplifies damage
mediated by Aldosterone,despite lowered readings of blood-level.An important finding,in that low Aldosterone
blood-lvl-readings arent indicative of true ,low-Aldosterone-activity,but to the contrary.If we base future risks
on bloodwork,it means there is a high possibility for a wrong outcome if,in this case,low lvl does not mean low lvl,
but in vivo high lvl-activity.
If im feeling calm,secure and sedated with my low,Hi-Salt induced Aldosterone machine-printout,
and this thing is actually up-side-down,i have to adapt to reach a favorable outcome.

Oh, so in other words, they decided that high salt intake was a problem, despite no evidence, and now they are trying to prove it. I'm still not buying it, especially since it's a third hand interpretation.

Furthermore,the study was a review of the available literature,the uncontrolled for,population-based
meta-analyses are a problem,there we are on the same page,but for an author of an review of controlled models
it is just like using his footnotes,like anyone else imo.

Reviews of "available literature" can be just as problematic. Again, if you really think this is something worth investigating (I personally don't), then you should track down the original study and review it.

 

[Braveheart]

A salt lover....