Sodium Bicarbonate for issues with calcification from vitamin D? - carbon dioxide

[cs3000]

Bicarbonate-sensitive calcification and lifespan of klotho-deficient mice - PubMed

Klotho, a protein counteracting aging, is a powerful inhibitor of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] formation and regulator of mineral metabolism. In klotho hypomorphic (kl/kl) mice, excessive 1,25(OH)2D3 formation leads to hypercalcemia, hyperphosphatemia and vascular calcification, severe...

pubmed.ncbi.nlm.nih.gov

Klotho, a protein counteracting aging, is a powerful inhibitor of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] formation and regulator of mineral metabolism. In klotho hypomorphic (kl/kl) mice, excessive 1,25(OH)2D3 formation leads to hypercalcemia, hyperphosphatemia and vascular calcification, severe growth deficits, accelerated aging and early death. Kl/kl mice further suffer from extracellular volume depletion and hypotension, leading to the stimulation of antidiuretic hormone and aldosterone release.
A vitamin D-deficient diet, restriction of dietary phosphate, inhibition of mineralocorticoid receptors with spironolactone, and dietary NaCl all extend the lifespan of kl/kl mice. Kl/kl mice suffer from acidosis. The present study explored whether replacement of tap drinking water by 150 mM NaHCO3 affects the growth, tissue calcification, and lifespan of kl/kl mice. As a result, NaHCO3 administration to kl/kl mice did not reverse the growth deficit but substantially decreased tissue calcification and significantly increased the average lifespan from 78 to 127 days. NaHCO3 did not significantly affect plasma concentrations of 1,25(OH)2D3 and Ca(2+) but significantly decreased plasma phosphate concentration and plasma aldosterone concentration. The present study reveals a novel effect of bicarbonate, i.e., a favorable influence on vascular calcification and early death of klotho-deficient mice.

conflicting study outside of this model:
https://pubmed.ncbi.nlm.nih.gov/19809998/

Alkalinization increases vascular calcification in cultured cells and uremic rats.

conflicting to that one:

In contrast, the KNOW-CKD study found that lower bicarbonate concentrations were accompanied by higher arterial stiffness in patients with CKD

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I think 2g of sodium bicarbonate in water empty stomach is the only thing i've tried that helps calm my brain a bit at night without causing worse rebound. something to be aware of tho it does inhibit immune cell activity switching macrophages to repair mode (effective for inflammation / autoimmune conditions)

simple hyperventilation causes muscle spasms and paresthesia (prickling of the skin), in an experiment anyone can perform in a few minutes.​

everywhere calcium is studied, it is an activator, an excitant, a goad to activity, when it enters the cytoplasm. The evidence is that hyperventilation, which changes the serum concentration of bicarbonate, magnesium, potassium, chloride, and phosphate, does not change the serum calcium concentration, while it does increase the intracellular calcium content. (Fujimoto, et al., 1987; Stadler, et al., 1995.)

The combination of the calcium ion, Ca”, with the bicarbonate ion, HCO;, forms a very soluble complex ion with a single positive charge. In the saliva, there is more carbon dioxide than in the mouth, and this situation is believed to explain the fact that calcium which is dissolved in the saliva tends to be deposited in an insoluble form as it loses its solublizing bicarbonate, and the insoluble form contributes to dental plaque.

(Presumably, this physical principle would account for the deposition of calcium in the walls of blood vessels or in any tissue which is relatively deficient in carbon dioxide.) Simularly,
when serum bicarbonate decreases, the calcium escapes from its soluble complex, and in effect the available calclum—the forms of calcium
which are not bound to bicarbonate--has increased, exactly the opposite of what the Carlson school has argued.

Calcium, which is released into the cytoplasm by the excitotoxins, triggers the release of fatty acids, the activation of nerve and muscle, and the release of a variety of transmitter substances, in a cascade of excitatory processes, but at the same time, it tends to impair mitochondrial metabolism, and progressively tends to accumulate in mitochondria, leading to their calcification death, which is also promoted by the antirespiratory effects of the unsaturated fatty acids and the lipid peroxidation they promote. Iron and calcium both tend to accumulate with aging or stress, and both promote excitatory damage; bicarbonate contibutes to keeping iron in its inactive state, and probably has a similar effect against a broad spectrum of excitatory substances. Histamine release, nitric oxide, and carbon monoxide are broadly involved in excitotoxic damage, and carbon dioxide tends to be protective against these, too,

Besides the simple excitotoxic killing of nerve cells, the processes which impair carbon dioxide production set in motion the long degenerative process that ranges from diabetic lacticacidemi
to dementia. In Alzheimer’s disease, brain respiratory metabolism is inhibited, creating a carbon dioxide deficiency with an excess of lactic acid and ammonia.

W. F. Koch also found that excessive coagulation was produced in the toxic antirespiratory state. Carbon dioxide, probably by controlling the availability of calcium, is an important protection against abnormal clotting. The prevention of clotting by carbon dioxide is thought to be part of the explanation for its protective effect against oxygen deprivation. (Pak and Sverchkova, 1987.) Hyperventilation causes increased vascular permeability, leading to hemoconcentration when a large portion of the blood’s water escapes into the tissues. Vascular spasm, increased viscosity o the concentrated blood, and disturbed coagulation processes undoubtedly contribute to a wide range of health problems, including stroke, heart attack, and multiple sclerosis.

Since permanent high altitude residents chronically retain a larger amount of carbon dioxide in their tissue, I have looked for data on the incidence of degenerative brain disease among high altitude populations. In Kashmir, a house-to-house study of more than 66,000 people found that nearly one percent of the population suffered from some neurological impairment, such. as cerebral palsy, epilepsy, mental retardation or stroke. But no cases of Alzheimer’s disease or multiple sclerosis were found. In India, the incidence of these diseases is much lower than in the U.S., but their absence in Kashmir is remarkable.

If excess lactic acid in the brain tissue is characteristic of Alzheimer’s disease and multiple sclerosis, then the “lactate paradox” suggests that — a slightly higher retention of carbon dioxide in the brain of Kashmir residents would counteract chronic excitotoxic effects, suppressing the stress metabolism which leads to the degenerative brain diseases. Experimentally increased carbon dioxide tends to Geciense intracellular Lan ine ase of extreme “aerobic glycolysis,” is also negatively associated with increased altitude. Mortality from heart disease, too, decreases with increasing altitude, and the role of carbon dioxide in heart function is very clear.

The neuroprotective steroids, progesterone and pregnenolone, and magnesium and carbon dioxide all protect against excitoxicity and the related excess of intracellular calcium, while promoting normal calcification. The thyroid — hormone happens to promote the production of these steroids and carbon dioxide, and the retention of magnesium. By the simple process of avoiding the antithyroid substances, especially the polyunsatured fatty acids, the degenerative processes discussed here will be minimized. Cyanide, another common component of foods (usually in the bound form as cyanogenic glycosides, in seeds, sprouts, nuts, and grains), has specific antagonisms to carbon dioxide, thyroid, and respiration​

 

[GTW]

Citrate, preferably as mixed Na & K, will be easier on the stomach and produce alkaline bicarbonate after digestion. Citrate is metabolized to bicarbonate.
Cyanogen are typically inactivated at moderate elevated temps, more certainly by cooking.

 

[Highserotonin90]

@cs3000 Could boiling rice or potato water with dissolved bicarbonate help? and if we eat red meat would it significantly reduce stomach acidity and therefore protein digestion? I can't see an ideal time around a protein meal but avoiding ferrous compounds would be ideal.