A simple model for kidney stones

The master equation is:

local toxins + local deficiencies = {local medical conditions}

In the generation of kidney stones, among other things, toxins include microbial waste products (examples include ammonia for sure and possibly oxalate) that are added to our waste products in the kidneys (or bladder in the case of bladder stones), then concentrated as water is removed from the filtrate.

For example, in struvite stones, microbes digest our waste product urea and make ammonia, which when combined with our waste products of excess un-chelated magnesium and excess phosphate yields insoluble magnesium ammonium phosphate. Some ammonia is present in everyone’s urine, but here an amount is needed that can only be being produced locally and in large quantities. Since the magnesium must be un-chelated or under-chelated to form a struvite stone, we may deduce that citrate, vitamin C, glutamate and other metal binding anions are deficient in this glomerular filtrate.

The majority of oxalate in oxalate stones is not coming from tea or food or the breakdown of vitamin C – that oxalate has already been used or metabolized into other waste products long ago, provided there are no major nutrient deficiencies. The majority of the oxalate in stones is being produced either locally as a waste product by microbes [including microbial production of oxalate from our excess vitamin C waste product] where it can precipitate with our excess un-chelated or under-chelated calcium and the small amount of oxalate coming from us. Alternatively, due to deficiencies (such as vitamin B6), oxalate accumulates as a metabolic intermediate at high enough levels to create calcium oxalate stones with un-chelated or under-chelated calcium during the production of urine.

All of the calcium in calcium oxalate stones is coming from us. The problem is more often that due to over-supplementation with calcium, or due to toxins and to various deficiencies (like magnesium from a poor diet and possibly secondary to calcium over-supplementation), the kidneys are excreting too much calcium by not re-absorbing what they should. This over-excretion of calcium results oddly enough in a slight hypocalcemia in a calcium oxalate kidney stone former. In most if not all cases of stone formation, due to dehydration, the kidneys are forced to over-concentrate the filtrate. Again, generally not as much of a problem without the contribution of microbial wastes to our wastes, and not a problem without multiple nutrient deficiencies.

If most of the oxalate in stones were coming from our diet and vitamin C supplementation, we would expect a much higher frequency of kidney stones in the general population. Only 5-10% of people ever have a stone. Thus, either the toxins or the deficiencies or both must be rare. The toxic effects of sufficient microbial growth in the kidneys is rare; the principal deficiency (water) in urine is not rare, but perhaps the sheer magnitude of the water deficiency in people who develop stones is rather rare. B vitamin deficiencies are common in those who do not supplement. Dietary deficiencies of magnesium and potassium are fairly common.

Deficiencies that contribute to stones include water (dehydration), whose deficiency in the final mixture concentrates all of the reactants, and at the very least makes the stones bigger than they would be with proper hydration.

Deficiencies in B vitamins, which produce major metabolic disturbances, are strongly correlated to kidney stone formation, especially vitamin B6.

Ideally, urine is roughly neutral in pH. Overly acidic urine promotes the formation of calcium urate crystals. Overly basic urine promotes the formation of calcium phosphate stones. Neither pH deviation CAUSES the stones.

Deficiencies that contribute to stone formation also include deficiencies in lots of substances that alter the solubility of the other salts, and deficiencies in substances that prevent or limit the size of the crystals that form. For example a deficiency in urinary citrate (common in stone formers, and probably due to blood pH problems secondary to major mineral deficiencies). When citrate is present in sufficient concentration in urine, it probably chelates enough calcium, forming a soluble well-hydrated calcium citrate chelate, to limit the size of calcium oxalate crystals as they are forming, allowing the small crystals to pass easily into the bladder soon after their formation in the kidneys.

Deficiencies in vitamin C probably also increase the risk of calcium oxalate stones. Like citrate, vitamin C also binds metal ions and forms water soluble complexes, leaving fewer calcium and magnesium ions to form precipitates.

Other critical deficiencies involved in the process of stone formation include deficiencies in potassium, calcium, and magnesium. These deficiencies stem from both dietary deficiencies, and in some cases unbalanced supplementation, and major regulatory deficiencies, because blood levels of calcium, magnesium, potassium (and sodium, which, unlike the others, is rarely deficient in Western diets) are carefully regulated to keep the heart beat in rhythm.

Deficiencies that contribute to stones also include deficiencies in our defenses against microbes. In some cases, microbes can help; ex. a microbe that breaks down oxalate produced by other microbes or that accumulated due to a nutrient deficiency.

To increase vitamin C, citrate, and potassium, – eat citrus fruit each and every day.

For extra magnesium, I recommend a supplement of potassium magnesium citrate (if not eating citrus daily) or cheap magnesium sulfate (Epsom salts) if already consuming citrus every day. Or possibly magnesium malate – the malate might increase the concentration of malate in cells, enabling the malate-succinate shuttle to operate faster, improving ATP production from cytosolic NADH. I need to research this idea further.

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