The Effects Of Vitamin A Compounds On Hyaluronic Acid Released From Cultured Rabbit Corneal Epitheli

moa

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This new paradigm, where can I find more about, or is it popular on this form lately ?

Two years ago I knew nothing about health, I've studied many theories and Ray peat was the best for me but I also have studied evolution and evolution of diet in human evolution. My conclusion is that the species specific diet of first humans or even first homo species were based on starchy roots cooked on fire directly and or in water later on with tubers raw for water and hydration like carrots or other. Potatoes and some carrots are the perfect food for humans.

There are foods that are not the initial foods of first humans that are better than the species specific good in moderate quantities (milk, fruit) and some are worse (pufa).

For me humans are designed to eat starchy foods mostly (I do agree sugar is better if you can have it but we have so much facility to process starchy foods compared to animals, i do agree starchy foods are very bad to most mammals excepting birds as pufa are for humans but not for fish).

The reason we are a starchy tubers eating species at the beginning is that the anatomy of humans, standing and walking to find this rate tubers in the Savannah, the hands are perfectly made to extract the roots using the power of the strong legs, the brain is big on other to remember what kind of plant has what kind of root and how to know if the roots are big looking at the plant, this is why the brain developed and starchy tubers do provide glucose for brain activity.

There were this monkey standing before first homo, they were small brain like apes and had a jar like apes. They invented the fire right before the first homo with big brain appeared, because of cooked starchy roots.

I do belove after agriculture was invented most territories on Earth excepting America's, people ate the tubers up to Extinction because good supply regulated population growth but when grains provided the base instead of roots, people just consumed all the good starchy roots because they were not easy to cultivate excepting carrots that are not so great. The population boom caused the disappearance of the previous staple except in Africa, some parts of Asia and America's where you can still find some starchy tubers.

Regarding salt, I think all animals use rock as salt supplementation, it can be considered as a food since in early times if was more easy to find, but it does not mean the people then used as much salt as Ray suggests it could be just very small quantities to moderate at most and not all the time.

I will maybe explain more later, but I do believe peat is right on starch in general excepting we have adapted to tolerate it. peat is right about keto diets too, but for a cat it might not matter at all.
 

moa

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For example read in ancient books about what scythians, Goths and Huns are back then 2000+years ago, this are people retaining their old diet in Europe where everyone eats cereals.

That say in books that this nomadic people diet is comprised of mainly starchy roots and some hunting or milk, it is stated in old books, roots are the base carbohydrate food, this is why thay were strong until they eaten them all (wild roots).
 
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paymanz

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Salt is Peaty,and its where he is mistaken.Most People are clinging to Sodium,its a Low-Dose but commonly encountered element in natural occuring foodchoices.
The capacity to cling to it is enormous.even advanced kidney failures can uphold Na+ even if they have only 20%
nephrons left.He sees it way too mechanistic,the old renin-angiotensin explanations.Its autoimmune-driven,Sodium is messenger for induction und maintenance of immuneanswer to severe intracellular infection.and lots of observations are toxicity symptoms,higher bodytemp is systemic
inflammation,higher Pulse also,higher energyexpenditure is due to catabolic and toxic effects.It isnt his fault though,
it is rather new,consolidated and interdisciplinary effort that yielded a new Paradigm.
Loooots of misunderstanding! He says eat salt to taste , and many people know it in emergency room just ia saline infusion is enough to recover people.

And he says keep your temp in normal range of 37 c .

And how sodium is connected to autoimmune disease?!!
 
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paymanz

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The capacity to cling to it is enormous.even advanced kidney failures can uphold Na+ even if they have only 20%
nephrons left.
The body can do lots of things but that doesn't mean its i healthy choice, yes stress hormones are released to preserve the sodium.
 
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Loooots of misunderstanding! He says eat salt to taste , and many people know it in emergency room just ia saline infusion is enough to recover people.

And he says keep your temp in normal range of 37 c .

And how sodium is connected to autoimmune disease?!!




Good Questions.
Sodium-Autoimmune Connection was linked by recognition of Sodium induced Th17 Lineage from naive T Helper-cells.



Dietary salt promotes neurovascular and cognitive dysfunction through a gut-initiated TH17 response

[URL='https://link.springer.com/article/10.1007/s00424-014-1659-z']Sodium chloride, SGK1, and Th17 activation


[URL='https://www.sciencedirect.com/science/article/pii/S001448861630053X']High salt drives Th17 responses in experimental autoimmune encephalomyelitis without impacting myeloid dendritic cells (
https://uhdspace.uhasselt.be/dspace/bitstream/1942/21526/1/accepted%20manuscript.pdf)

The plasticity of human Treg and Th17 cells and its role in autoimmunity


High salt intake reprioritizes osmolyte and energy metabolism for body fluid conservation

High salt intake causes leptin resistance and obesity in mice by stimulating endogenous fructose production and metabolism

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4932095/pdf/nihms771998.pdf


LONG-TERM BALANCE STUDIES IN HUMANS: HOW IS STEADY STATE
ORGANIZED, AND WHERE IS THE SALT?
(Peat read studies about hypothyroidism and reduced concomitant bloodlevels of Na.It isnt excreted or excessively lost.On the contrary,it gets retained.Na+ gets exchanged for intracellular Potassium.osmotically neutral sodium retention.)

Na-MRI STUDIES IN HUMANS: Na+ACCUMULATION IN MUSCLE, SKIN,AND BRAIN

ANIMAL STUDIES: ELECTROLYTE METABOLISM AND IMMUNE
FUNCTION


[/URL]


KEY POINTS

Sodium balance in human features circaseptan variations in excretion when
dietary intake is fixed, making 24-h urine collections to determine intake of
dubious value.

Total-body sodium also exhibits even longer infradian rhythms independent
of blood pressure or body weight.

Aldosterone, cortisol, and cortisone participate in this regulation controlled
by undiscovered ‘clocks.’

Sodium is stored bound to glycosaminoglycans in skin and in muscle. A
novel magnetic resonance imaging tool can assess sodium tissue storage in
humans.

Immune cells control tissue sodium storage. Associated inflammatory
responses could be of clinical relevance.


[/URL]

Because all of this is high-impact,all cutting-edge recent,i doubt Peat had time to read these Papers.
There is a new but already elucidated inflammation paradigm,and Sodium ,a key player,needs a new Angle in Health and Disease.
Th17 Cytokines and Pathways can explain an awful lot of mystery-diseases of inflammation.And this is all around the Globe,excessive and Unphysiologic Salt intake,because it is tasting good.


"Mystery-Deseases have inflammation in common,of autoimmunity appearance.
Hypa-Tension,Multiple Sclerosis,Acne,Psoriasis,Irrtable Bowel Syndrome,Colitis,Alzheimer,
Parkinsons,etcetc.all have Th17 Pathology in common,and already "Normal" to High Salt intakes are
increasing the Maturation
of these Bad Boys so badly.I believe that Sodium is a micronutrient with low
"therapeutic breadth" between 500mg-to-1500mg per day."

Th17 Lymphocytes Induce Neuronal Cell Death in a Human iPSC-Based Model of Parkinson’s Disease


"HI SODIUM shifts the specialization of naive T-Helper-Cells (Th1,Th2,Th17) to the highly inflammatory TH17
phenotype
,which produces high amounts of toxic cytokines,the whole hog,and acts potently anti-anti-inflammatory.
TH17 helper t-cells secrete IL17 which is on topic in the study.this pathway is reserved for severe intracellular infection."


High sodium intake and high dietary or metabolic acid loading have two important things in common. Both induce a so called low grade metabolic acidosis, i.e., a moderate shift of blood pH and blood bicarbonate buffer to lower levels, usually still within the “normal healthy” range [8, 9]. The high renal sodium excretion following high NaCl ingestion causes an adaptive (renal physiological) reduction in tubular reabsorption of sodium bicarbonate (NaHCO3), thus reducing our most important circulating buffer system NaHCO3. Corresponding NaHCO3 reductions also occur after dietary acid loading, i.e., through increases in potential renal acid loads (PRAL), biochemically measurable as renal NAE increases. The consequences of either form of low grade metabolic acidosis are increases in glucocorticoids, i.e., cortisol levels, as have been reported for high salt intake.


thoughts?










 
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The body can do lots of things but that doesn't mean its i healthy choice, yes stress hormones are released to preserve the sodium.


i believe the anti-inflammatory stress hormones get excreted unfairly by the Pro-inflammatory actions of HSD.
Stress Hormone sounds bad,but lots of people have signs of inflammation that are quite similar to adrenal insuffciency.
most people arent immune-deficient,they have way too high activity.Sodium is contributing.

Salt to taste is an appeal to nature also.After what i read,Salt-liking is a primitve impulse and isnt capable to
usefully gauge need at all.Bodytemperature all the same,in regards to Sodium,not the whole Hog of possibility of
thermoregulation,Sodium has the capacity to increase Pulse,Temperature and Energyconsumption through a toxic
catabolic process.inflammation after all emaciates,Cachexin is the old name of TNF-a.
Sodium is consumed in excess amounts,and we pay the Price for it.Physiologic Range 500-1500mg/d.
Consumed Range 3000-7500mg.Maybe NaCl has low therapeutic Index?

I know what Peat has to say about it,but he couldnt know of the salt-retention because radioactive labeled Na-
Balance Studies werent conducted as of late.Would be interesting what he has to say about the Sodium-SGK1-IL23-TH17
-cascade,or if he knows about osmotically neutral Na+ Retention.The idea was that Na+ and K+ Equilibrium in cellular and extracellular space was figured out.It wasnt though.


thoughts?
 
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Also:
High salt intake reprioritizes osmolyte and energy
metabolism for body fluid conservation



Natriuretic regulation of extracellular fluid volume homeostasis includes suppression of the renin-angiotensin-aldosterone
system, pressure natriuresis, and reduced renal nerve activity, actions that concomitantly increase urinary Na+
excretion and
lead to increased urine volume. The resulting natriuresis-driven diuretic water loss is assumed to control the extracellular
volume. Here, we have demonstrated that urine concentration, and therefore regulation of water conservation, is an
important control system for urine formation and extracellular volume homeostasis in mice and humans across various
levels of salt intake. We observed that the renal concentration mechanism couples natriuresis with correspondent renal
water reabsorption, limits natriuretic osmotic diuresis, and results in concurrent extracellular volume conservation
and concentration of salt excreted into urine. This water-conserving mechanism of dietary salt excretion relies on urea
transporter–driven urea recycling by the kidneys and on urea production by liver and skeletal muscle. The energy-intense
nature of hepatic and extrahepatic urea osmolyte production for renal water conservation requires reprioritization of energy
and substrate metabolism in liver and skeletal muscle, resulting in hepatic ketogenesis and glucocorticoid-driven muscle
catabolism, which are prevented by increasing food intake. This natriuretic-ureotelic, water-conserving principle relies on
metabolism-driven extracellular volume control and is regulated by concerted liver, muscle, and renal actions.

High-Salt-Diet HSD doesnt decrease Cortisol action by increasing excretion,it increases instead Cortisol-Production and liberation and Cortisol activity and action.the higher urinary output of Glucocorticoids just reflects higher Cortisol presence.HSD is driving Tissue dissolution for ableness of excretion of sodium.



Catabolic muscle wasting by experimental salt loading

Salt induces ketogenesis, reduces gluconeogenesis, and entails fatty
acid oxidation.


Energetic consequences of salt in muscle and liver.
In line with the catabolic nature of urea production and nitrogen mobilization
in muscle
, we found increased AMP and ADP levels in skeletal
muscle in HS+saline mice.


Additional pair-feeding not only induced total body
energy deficit and catabolism
(Figures 5–7), but also resulted in
a robust reduction in cardiovascular energy expenditure, with a
low heart rate, low BP, and low locomotor activity, despite massive salt intake.

We conclude that the metabolic and cardio
-vascular response to HS+saline we observed in our mice is typical
for water conservation by aestivation. (HIBERNATION)
 
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paymanz

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@Tristan Loscha thanks, im not very familiar with all of these, i will read them.

So have you reached to a conclusion on how much salt we need?

Salt induces ketogenesis, reduces gluconeogenesis, and entails fatty
acid oxidation.
We cant generalize it and say salt promote ketogenesis.

Just saying... : )
 
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@Tristan Loscha thanks, im not very familiar with all of these, i will read them.

So have you reached to a conclusion on how much salt we need?


We cant generalize it and say salt promote ketogenesis.

Just saying... : )


True.
After what i read,500mg-1500mg Na a day from all Sources is Physiologic.Sweatsystem is homeostatically able to increase or decrease Na+ concentration excreted in it.if you workout,it can be resonable to increase the amount of Na between 50% to 100% on training days. So for 500mg,750mg to 1000mg would be intake target.500mg of Sodium is contained in 800g of lean Pork,as an example.Benefit would be lowered lipid peroxidation,lower inflammation even without autoimmunity,and way better Potassium Balance.above this recommeded threshold,Potassium excretion increases 3-4fold.Im doing Low Sodium(a misnomer)
since 2 weeks and have less edema,and better muscular filling.
 

moa

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Interesting. I do high salt in the past 6 months, 5 grams a day off added salt I guess in average.

My blood pressure is 80/ 120 or 70/110, it never changes. When I drink some days 40 grams of salt, blood pressure does not change at all, always the same.

Once a took 60 mg of prednisol doctor gave me for sinus infection, my blood pressure was 80/160 that day, my blood pressure never ever was more than 130 in the past 5 years even when drinking salt excepting that day. I stopped the cortisol next day. Blood pressure as usual since even with salt intake high.
 
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Salt isnt a hypertensive agent for most it seems.Only so-called Salt-sensitive hypertensives.
I see the problem with salt not in some BP-points,but with general inflammation and autoimmune-reactivity.
 

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