The most likely explanation for the inverse association between dietary zinc and incident calcium stones is the inhibitory effect of zinc on CaP crystallization. Zinc promotes more soluble CaP phases, decreases the size of CaP crystals and inhibits the transformation of brushite to hydroxyapatite.8,17 This inhibition of CaP crystallization and transformation is important to CaP and CaOx stone formation.
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One hypothesis for the association we observed is that zinc inhibits early CaP crystallization in the kidney and this proximal inhibition prevents growth of CaP stones and the initial formation of Randall plaques.
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Prior studies have revealed conflicting results about the direction of the association between zinc and nephrolithiasis. Rapid stone formation was reported in a woman with zinc toxicity.20 Additionally
analysis of the National Health and Nutrition Examination
Survey found that adults older than 30 years with zinc intake greater than 15 mg daily (which far exceeds recommended intake for adults) had a 70% increased odds of nephrolithiasis compared to those who consumed less than 7 mg daily.9
However, among patients 18 to 29 years old daily zinc intake was 1 mg lower in those with a history of stones than in those without stones. One explanation for these discrepant results is that excess and insufficient zinc promotes stone formation.
It is also possible that the greater importance of adequate zinc intake during adolescence accounts for the different findings between younger and older patients. Multiple prior studies have found that higher zinc intake is associated with greater bone mineral content and density in children and young adults.21,22
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We also found an association between increased dietary phytate and decreased odds of incident calcium nephrolithiasis, which is consistent with findings in young women.25 Phytate, which is the principal storage form of phosphate in plants, strongly binds zinc in the gut and reduces its bioavailability. Additionally phytate inhibits
hydroxyapatite and CaOx crystallization and may have an independent inhibitory effect on stone formation.26,27
Nevertheless, our results should be considered preliminary since the association between phytate and calcium stones became statistically insignificant after excluding the participant with high dietary oxalate. We also detected an inverse relationship between dietary oxalate and calcium nephrolithiasis. This association is likely spurious since it was driven by 1 control with extremely high oxalate intake and there is no biological plausibility for this association.
I am also deficient and increasing it via food and/or supplements seems very problematic for me.I have huge oxalate problems and I'm also definitely zinc deficient so I don't think I'll be chelating zinc any time soon.
https://www.karger.com/Article/Pdf/345550
Am J Nephrol. 2012;36(6):549-53. doi: 10.1159/000345550. Epub 2012 Dec 4.
Dietary zinc intake and kidney stone formation: evaluation of NHANES III.
Abstract
AIMS:
We aimed to determine whether there is an association between dietary zinc intake (DZI) and prevalent kidney stone disease defined as self-report of any previous episode of kidney stone.
METHODS:
We examined The Third National Health and Nutrition Examination Survey (NHANES III), a large US population-based cross-sectional study, and used logistic regression analyses to determine the independent association between DZI and prevalent kidney stone disease.
RESULTS:
A total of 15,444 men and women over 18 years of age were eligible for analysis. Among them, 710 participants reported a history of kidney stones. Stone formers tended to have higher DZI than non-stone formers among NHANES III participants, though this difference did not reach statistical significance (p = 0.1). Multivariate adjusted logistic regression analysis revealed that higher DZI (log transformed) was associated with a significantly increased risk of kidney stone disease (odds ratio, OR = 1.41, 95% confidence interval, CI: 1.10-1.81, p = 0.01). After categorizing zinc intake into three groups, those with highest DZI (>15 mg/day) were also associated with a significantly increased risk of kidney stone disease, compared to those with lower DZI (<7 mg/day; OR = 1.70, 95% CI: 1.13-2.57, p = 0.01).
CONCLUSIONS:
Our study suggests that higher DZI is associated with increased risk of kidney stone disease. Future prospective studies are needed to clarify the causal relationship between zinc intake and kidney stone formation.
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We show that stone formers tend to have a higher DZI than non-stone formers. Higher DZI is associated with a significantly increased risk of prevalent kidney stone disease, especially when DZI exceeds 15 mg/day.
I have huge oxalate problems and I'm also definitely zinc deficient so I don't think I'll be chelating zinc any time soon.
same here... I took tons of zinc.. 100mg a day for a long time ... .it's still low in range on blood testing.
Been dumping oxolates for about 8 months by supplementing biotin, b6, b1 but then you run into that whole refeeding nightmare. You need cofactor magnesium....so then you supplement magnesium and your sodium goes low.
Bob Naviaux talked about refeeding IIRC at that Stanford symposium & I got the impression he thought we were screwed... and I'm thinking the same thing.
Bob Naviaux talked about refeeding IIRC at that Stanford symposium & I got the impression he thought we were screwed... and I'm thinking the same thing.
There's a possibility I might end up on TPN for a while soon and I'm kind of terrified of it given my sensitivity to any level of supplementation and the fact that the doctors who would be administering aren't very experienced with patients like me.
@Gondwanaland or someone that knows about buying the B2 and K2 supplements.....What brand would be good and how much should I take? (I'm sensitive with supplements).
I was reading about this and I think now I'm low on B2 because of the skeletal problems a deficiency can cause, and I've been meaning to get the K2. I almost bought it once but it had the mk4 and mk7 in equal amounts. I wasn't sure if that was good or a different percentage would be better.
I seem to have deficiencies in boron also, so maybe a small amt of boron and B6 (yes, now I'm low in
B6) so.....thanks if you know. I'm wondering if they would just all end up cancelling each other out?
Gut Bacteria Treatment Shows Promise for Rare Genetic Kidney Condition
The Swedish biotech Oxthera reported positive preliminary Phase II results using its gut bacteria treatment, Oxabact, in patients with a rare genetic condition that causes kidney failure.
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I think the blood serum measurement of zinc is useless. It's how much is getting in the tissues that is important. You should be getting enough sea salt in your diet. It is normal for salt and magnesium to tug at each other.
Susan Owens thinks the opposite. Biotin supplementation is highly recommended on the lo-ox site both as a counter to the detrimental effect of oxalates on biotin dependant enzymes and as a counter to the candida overgrowth which seems common in autistic children.
There is the additional wrinkle that the candida product arabinose appears to be a precursor to oxalate.
I wonder if thiamine deficiency would be an important factor with dumping oxalates.
I have recently started supplementing with TTPD (Allithiamine) and it has stopped immediately a vigorous bout of oxalate dumping dead in it tracks.
Or maybe it is the other way around and oxalate dumping induces a thiamin deficiency ?
It was something I had considered a few years ago and I had tried thiamin HCL and I found it too stressful, giving me in a manic kind of energy, so I never tried it again. But TTPD is completely different. It gives me enrgy and relaxes at the same time. Maybe I am now ready for it after all these probiotics?