Extra kidney stones, likely from the extra calcium.[13]
[13] Guess what most kidney stones are made of?
Most kidney stones are made out of calcium oxalate, which is a salt with a very low solubility.
However, the relationship between calcium and kidney stones is far from straightforward.
You consume oxalates in your food. If you are prone to kidney stones, the best thing you can do is to keep them in your digestive track rather than taking it up in your bloodstream (from where it will have to be excreted through the kidneys later). A good way to do that is to bind them into a salt with low solubility. Enter calcium oxalate, again.
So calcium in your digestive tract can reduce the risk of kidney stones: your body is still excreting the oxalates as calcium oxalate, but in the intestines there is no chance for crystals to grow over months, and your intestines have a much larger diameter than your ureters.
Still, a higher blood calcium level should lead to a higher risk of kidney stones. What is regulating the uptake of calcium again? As I learned from your article, the active vitamin D, metabolized out of the storage variant by the kidneys.
Now, it could be that the kidneys regulate the active variant in a perfect control circuit which does not depend on the blood level of the precursor (as long as it is high enough). But given that we are talking about messy biological systems, I think it is plausible that a higher supply of storage D will result in a higher level of blood calcium in equilibrium. (If you are on the brink of storage D deficiency, the proteins which produce the active form would not have to be inhibited by calcium very much. If storage D is plentiful, the mass action law (or whatever the protein equivalent is called) suggests that you will need a higher level of calcium to shut them off.)
The firstpaper I found on this topic suggests that there is some evidence that vitamin D supplements as well as calcium supplements taken between meals (when the calcium can’t protect you from the oxalates you ate with your food) increases the risk of kidney stones.
My intention was that, “likely from the extra calcium” would be read somewhat ambiguously in terms of if it was extra calcium supplemented in the WHI trial, or extra calcium absorbed from food as a result of active vitamin D getting to the guts. So I don’t necessarily disagree with the possibility that it could be due to the vitamin D itself. That said, I want to protest that calcium levels in the blood do seem to be very tightly regulated. But I don’t think you need to assume that blood calcium levels vary? If you absorb extra calcium (either because you eat/supplement more or because you absorb more) then your kidneys need to excrete it. That seems like the most likely explanation to me.
Most kidney stones are made out of calcium oxalate, which is a salt with a very low solubility.
However, the relationship between calcium and kidney stones is far from straightforward.
You consume oxalates in your food. If you are prone to kidney stones, the best thing you can do is to keep them in your digestive track rather than taking it up in your bloodstream (from where it will have to be excreted through the kidneys later). A good way to do that is to bind them into a salt with low solubility. Enter calcium oxalate, again.
So calcium in your digestive tract can reduce the risk of kidney stones: your body is still excreting the oxalates as calcium oxalate, but in the intestines there is no chance for crystals to grow over months, and your intestines have a much larger diameter than your ureters.
Still, a higher blood calcium level should lead to a higher risk of kidney stones. What is regulating the uptake of calcium again? As I learned from your article, the active vitamin D, metabolized out of the storage variant by the kidneys.
Now, it could be that the kidneys regulate the active variant in a perfect control circuit which does not depend on the blood level of the precursor (as long as it is high enough). But given that we are talking about messy biological systems, I think it is plausible that a higher supply of storage D will result in a higher level of blood calcium in equilibrium. (If you are on the brink of storage D deficiency, the proteins which produce the active form would not have to be inhibited by calcium very much. If storage D is plentiful, the mass action law (or whatever the protein equivalent is called) suggests that you will need a higher level of calcium to shut them off.)
The firstpaper I found on this topic suggests that there is some evidence that vitamin D supplements as well as calcium supplements taken between meals (when the calcium can’t protect you from the oxalates you ate with your food) increases the risk of kidney stones.
My intention was that, “likely from the extra calcium” would be read somewhat ambiguously in terms of if it was extra calcium supplemented in the WHI trial, or extra calcium absorbed from food as a result of active vitamin D getting to the guts. So I don’t necessarily disagree with the possibility that it could be due to the vitamin D itself. That said, I want to protest that calcium levels in the blood do seem to be very tightly regulated. But I don’t think you need to assume that blood calcium levels vary? If you absorb extra calcium (either because you eat/supplement more or because you absorb more) then your kidneys need to excrete it. That seems like the most likely explanation to me.