From the Townsend Letter
Green Smoothie Bliss:
Was Popeye Secretly on Dialysis?
by Thomas Lodi, MD, MD(H)
J Urol. 2003 Aug;170(2 Pt 1):384-8.
Gender differences in seasonal variation of urine stone risk factors.
Parks JH1, Barsky R, Coe FL.
Nephrology Section, University of Chicago, Illinois, USA.
Overall the sexes differ markedly in the timing of stone risk. Men show a dual summer calcium oxalate and uric acid high risk, while women show a high early winter calcium oxalate high risk.
I don't see any indication that that particular SNP has any impact. Also, both alleles are extremely common, so a great many people (20-25%) would be homozygous for either version.Here's what I found and I'm homozygous. It's gene SLC13A1 and the allele (?) is rs7780966. This is just what I found as one of my variants and it says it (the gene) can cause osteochondrodysplasia and hyperoxyluria. I don't know if it's with this particular snp or not.
I don't see any indication that that particular SNP has any impact. Also, both alleles are extremely common, so a great many people (20-25%) would be homozygous for either version.
After a recent adverse event I am thanking my eye improvement to the milk riboflavin. And the worsening to excess boron / sulfites which deplete B2.After my 1st dose of milk my corneal "herpes" bothered me horribly. Then 24h later it just all of a sudden stopped hurting. I think the big oxalate crystal that was deposited in my scratched cornea has been disposed of by the K2. Also I had a curve of worsening and then improving joint pain that I think is from the K2 action in my body. I think soon I might try a small dose of K2-MK4 supp again
Blood results of vitamins D2 and D3 are useful in this instance.@Gondwanaland , I think I may need to build my vit. D back up a little first before I try the K2, as per a post I just saw on possibly needing calcium supplements that you posted. I've been a little lax on my vit. D intake, and calcium won't absorb without the D, or so I've heard.
@Asklipia @aquariusgirl @prioris @Violeta @picante @LolindaOptimizing Kidney Stone Management Using Metallomics and Metabolomics
Kidney stone disease affects nearly 10% of the US population and adds $5 billion in financial burden to the US healthcare system annually. Great strides have been made in the physical removal of urinary stones, yet little progress has been made in treating or preventing stone pathogenesis.
Patient stone and urine samples are routinely sent for chemical analysis, yet these data often have little impact on clinical decision making. Techniques for stone analysis have not advanced in many years and are often rudimentary, unreliable, and unreproducible. In addition, traditional 24-hour urine testing does not strongly predict future stone events and thus has limited utility in preventing stone recurrence.
The most common (~85%) type of kidney stones are calcium-based, typically composed of calcium oxalate and/or calcium phosphate. Monitoring urinary calcium can be useful, but does not provide a complete indication of risk. Moreover, modifying calcium intake to change systemic calcium homeostasis does not have a significant impact on stone formation.
New biomarkers of kidney stone disease are needed to improve pathophysyiological insight and the clinical management of kidney stone disease. Our previous Developmental Center for Interdisciplinary Research in Benign Urology work has shown that metals other than calcium, including zinc and strontium, play important roles in nephrolithiasis in an invertebrate model of stone formation.
For example, increasing dietary zinc strongly promotes stone formation, while chelating zinc or inhibiting zinc transport dramatically reduces the amount of stones.
To translate these findings to human kidney stone disease, this proposal to renew funding for our Center is focused on confirming the importance of trace metals in stone formation in a cohort of patients and demonstrating the value of comprehensive metallomic and targeted metabolomics analysis for predicting symptomatic stone episodes.
We will follow a group of patients with calcium-based stones associated with hyperuricosuria and/or hypocitraturia in our urinary stone clinic at the University of California San Francisco. Stone and urine samples will be collected and tested with extensive metallomic and metabolomic analysis at our Analytic Core Facility.
Combining the profiles from both metallomics and metabolomics of human stones and urine will allow us to create new diagnostic and therapeutic algorithms to augment or replace the relatively ineffective testing method currently in practice.
Our goal is to identify the compositional patterns of metal and metabolite biomarkers to reveal new aspects of urinary stone pathophysiology. This work will culminate in a novel resource that will be made available to the urology community and will provide the necessary scientific platform to launch a large intervention study in patients with recurrent kidney stone disease.
J Urol. 2017 May;197(5):1342-1348. doi: 10.1016/j.juro.2016.11.096. Epub 2016 Nov 23.
Dietary Zinc and Incident Calcium Kidney Stones in Adolescence.
Tasian GE1, Ross ME2, Song L3, Grundmeier RW4, Massey J5, Denburg MR6, Copelovitch L7, Warner S8, Chi T9, Killilea DW10, Stoller ML9, Furth SL6.
We determined the association between dietary zinc intake and incident calcium kidney stones in adolescents. We also examined the relationship between dietary zinc intake and urinary zinc excretion between cases and controls.
MATERIALS AND METHODS:
We conducted a nested case-control study within a large pediatric health care system. Three 24-hour dietary recalls and spot urine chemistry analyses were obtained for 30 participants 12 to 18 years old with a first idiopathic calcium based kidney stone and 30 healthy controls matched for age, sex, race and month of enrollment. Conditional logistic regression models were used to estimate the association between daily zinc intake and incident calcium kidney stones, adjusting for dietary phytate, protein, calcium, sodium and oxalate. Multivariable linear regression was used to estimate the association between dietary and urine zinc, adjusting for urine creatinine and dietary phytate and calcium.
Cases had lower daily zinc intake (8.1 mg) than controls (10 mg, p = 0.029). Daily zinc intake of boys and girls with calcium stones was 2 mg and 1.2 mg less, respectively, than the daily intake recommended by the Institute of Medicine. Odds of incident stones were reduced by 13% for every 1 mg increase in daily zinc intake (OR 0.87, 95% CI 0.75-0.99). There was an estimated 4.5 μg/dl increase in urine zinc for every 1 mg increase in dietary zinc (p = 0.009), with weak evidence of a smaller increase in urine zinc in cases than in controls (interaction p = 0.08).
Decreased dietary zinc intake was independently associated with incident calcium nephrolithiasis in this population of adolescents.