Does body elevate phosphate on purpose?

[nomoreketones]

Most medical advice (even from Dr. Peat) is to reduce phosphate intake or use phosphate binders such as calcium. While this may help to improve symptoms and prognosis, it only does this in the short term and fails to fully resolve these diseases and related symptoms in the long term, and will in all cases continue to progress because the body is elevating phosphate on purpose, not as a side effect of high dietary phosphate

Reference:
Oleic Acid, Hyperphosphatemia, and Disorders of Cellular Respiration — **** Portion Control

If this guy named Nathan is correct then focusing on the calcium/phosphate ratio of foods themselves may not be as important as focusing on cellular respiration directly.

I don't know what to think of this guy's writings. What do the people on this forum think?

So oleic acid directly facilitates cellular respiration which in turn produces sufficient CO2 to relieve the body of the states of hyperphosphatemia seen in metabolic disease and aging (as well as the resultant soft tissue calcification), and thus hyperphosphatemia is essentially caused by oleic acid deficiency.

 

[Amazoniac]

Third thread about it, awaiting the fourth.

The dissociation constants in the physiological pH range for carbonic and phosphoric acids are 6.1 and 6.8. Since the extracellular pH is around 7.4, the balance is shifted with the deprotonated forms favored.

dihydrogen carbonate 1:20 hydrogen carbonate
dihydrogen phosphate 1:4 hydrogen phosphate

It's tricky to use mEq, the free spots for interaction with ions can vary.​

Therefore, not only the ratio is higher for the hydrogen ion acceptor in the case of carbonate, but its concentration is also much higher (~24 mmol/L versus <1.45 mmol/L) and the system is renewed a lot faster (primarily lungs versus kidneys.

- Hydration: Fluids for Life

Spoiler

It can be argued that phosphate assumes this role in atypical conditions. However, the most common cause of hyperphosphatemia is kidneys dysfunction, leading to undesirable retention of phosphate. Considering it an adaptive measure is questionable, it's precisely when the kidneys are burdened that you can't rely on molecules that depend on them for excretion, it could tax them further, making more sense to transfer the duty to the lungs. But this is aggravated when you factor in the risk of damage from phosphate elevation itself and the issue that the elimination rate of phosphate is relatively constant. It's a dubious trade-off.

Severe hyperphosphatemias are not common, therefore in most cases where phosphate is elevated, the levels should be below the 4.54 mmol/L cut-off, remaining a buffer of minor importance.

- Management of Secondary Hyperparathyroidism in Stages 3 and 4 Chronic Kidney Disease

Spoiler

That's beyond the high end of normal, so it's for any elevation, not just severe.

 

[Amazoniac]

The pH of urine will vary, but counting on phosphate will have the additional cost of taking out valuable cations such as edemium. In exaggeration, it would be another hit and goes against the need to make room for the carbonate buffer system (that doesn't have this problem for being eliminated mainly as carbon dioxide and leaving the pair trace behind).

I think it's recognized by anyone that measures that attempt to control phosphate directly are for management, it's justified given the risks in allowing its elevation and the fact that it's part of a multifactorial condition, usually involving disturbed bone metabolism (excess mobilization and inadequate mineralization) with kidneys not being able to keep up. You have to be a lunatic not only to believe that the cause is oleic acid deficiency, but that if it was, such simple dietary solution wouldn't have been identified by someone; quite an underestimation of people's perception.

Since Sate is into game development, he could create one named 'Gambling with Gamblegrams', where the main character has tools at disponsal to use in a renal ward, the fanciest one being a Colavita bottle that should lead to completion after normalization of the derangement.