My grandchildren are given 9% cottage cheese. That's for two reasons. One, it's the only cottage cheese not laced with extra calcium, and two, because my daughter and I don't see the natural milkfat as unhealthy. It's certainly healthier to have 9% cottage and not eat yellow or processed cheese. Also the natural milkfat helps in the digestion of the milk protein.
More and more, actually, an uncontrollable, for the consumer that is, amount and varieties of foods nowadays have added calcium.
The little red light and siren screaming added-calcium went off in my head when I read this article, actually first in the International Herald Tribune. It's all about how common it now is for children as young as five or six to suffer from kidney stones, "once considered a disorder of middle age."
The article blames salt and processed foods.
Forty to 65 percent of kidney stones are formed when oxalate, a byproduct of certain foods, binds to calcium in the urine. (Other common types include calcium phosphate stones and uric acid stones.) And the two biggest risk factors for this binding process are not drinking enough fluids and eating too much salt; both increase the amount of calcium and oxalate in the urine.
Excess salt has to be excreted through the kidneys, but salt binds to calcium on its way out, creating a greater concentration of calcium in the urine and the kidneys.
I don't understand why they ignore the fact that there is a lot of added calcium in foods kids eat, like breakfast cereals and dairy products. I'm not saying that salt is "innocent," but it does take two to tango.
11 comments:
Interesting post. I always buy calcium fortified orange juice. Maybe I will rethink that...
Google the problems with calcium. A lot of the "osteoperosis" medications are problematic. Some cause serious conditions.
One problem with the fats from milk and meat is dioxins, which come from pesticides in animal feed. It stays in the body's fat and is only excreted through the uterus to the fetus, and less so, through breast milk. Men have no way of excreting it. It is more of a problem in human milk than in cow's milk because we are at the top of the food chain.
Needless to say this is a problem with pollution, not breast milk itself, and the risks of cow's or soy milk outweigh any risks from dioxins (this has been shown conclusively in various studies).
Still, it's good to limit the amount of animal fat one eats, especially children, teenage girls and women.
I'm confused. Where does that article say fortified-calcium is problematic? It seems to say drink more water, eat less salt.
And the problem with fats in milk and meat sounds like a separate issue.
?
I'm so confused...I just try to balance my diet and eat healthy foods...
It was interesting to hear about the problems with chickens raised without anti-biotics...
leora, the quoted section states that the salt combines with the calcium, but it only blames the salt.
t, yes, it's confusing. Read labels, and you'll see that there are all sorts of pitfalls.
mii, soy dependence can cause other problems.
Maybe I wasn't clear. I meant that for babies,dioxins in breast milk cause many fewer problems than cow's or soy milk. As for soy, I hardly have it in the house.
If you study the peer-reviewed research, scientists discovered years ago that ADDED calcium in the diet is PROTECTIVE against calcium oxalate stones, and reduced calcium in the diet increases the risks of calcium oxalate stones. That was backwards from what they expected, but there was a reason for it.
Calcium that stays in the gut (and 80% of it typically does) is available to bind oxalate in the gut and that keeps us from absorbing a good bit of the oxalate that comes from our food. When the oxalate (not bound to calcium) is instead absorbed into the blood, it will travel to tissues where it will then react to calcium that is local in those tissues, and that is what will form the calcium oxalate crystals. In the kidney this may start to form calcium oxalate stones but only in genetically or otherwise at risk individuals. The risks come from lack of protective molecules in the kidney that help the stones not form.
So eliminating calcium in foods is a way to INCREASE your risks of forming calcium oxalate stones.
For more information, please see www.lowoxalate.info and its associated yahoogroup or just look for relevant articles in PUBMED.
J Am Diet Assoc. 1993 Aug;93(8):901-6.Click here to read Links
Effect of dietary oxalate and calcium on urinary oxalate and risk of formation of calcium oxalate kidney stones.
Massey LK, Roman-Smith H, Sutton RA.
Washington State University, Spokane 99204-0399.
Dietary restriction of oxalate intake has been used as therapy to reduce the risk of recurrence of calcium oxalate kidney stones. Although urinary oxalate is derived predominantly from endogenous synthesis, it may also be affected by dietary intake of oxalate and calcium. The risk of increasing urinary oxalate excretion by excessive consumption of dietary oxalate is greatest in individuals with a high rate of oxalate absorption, both with and without overt intestinal disease. Although oxalate-rich foods enhanced excretion of urinary oxalate in normal volunteers, the increase was not proportional to the oxalate content of the food. Only eight foods--spinach, rhubarb, beets, nuts, chocolate, tea, wheat bran, and strawberries--caused a significant increase in urinary oxalate excretion. Restriction of dietary calcium enhances oxalate absorption and excretion, whereas an increase in calcium intake may reduce urinary oxalate excretion by binding more oxalate in the gut. This review of the literature indicates that initial dietary therapy for stone-forming individuals can be limited to the restriction of foods definitely shown to increase urinary oxalate. The effects of oxalate-restricted diets on urinary oxalate should be evaluated by means of laboratory analyses of urine composition. Subsequent long-term therapy can be recommended if beneficial results are obtained from oxalate restriction at an appropriate calcium intake.
PMID: 8335871 [PubMed - indexed for MEDLINE]
Rev Urol. 2002 Spring;4(2):53-60.Click here to read Links
Reconsideration of the 1988 NIH Consensus Statement on Prevention and Treatment of Kidney Stones: Are the Recommendations Out of Date?
Goldfarb DS.
In 1988, a consensus conference was held at the National Institutes of Health to develop guidelines for prevention and treatment of kidney stones. The recommendations regarding the medical evaluation of stone formers and treatment directed at stone prevention are reviewed. The relevance of those 1988 guidelines is evaluated for continued pertinence. Most of the recommendations promulgated in the consensus statement remain useful today. One significant change is the current consensus that dietary calcium restriction is no longer considered appropriate therapy, as there is no evidence that it actually prevents stones and has as a consequence the potential to worsen bone demineralization.
PMID: 16985656 [PubMed - in process]
Southeast Asian J Trop Med Public Health. 2004 Dec;35(4):1028-33.Links
Effects of calcium supplements on the risk of renal stone formation in a population with low oxalate intake.
Stitchantrakul W, Sopassathit W, Prapaipanich S, Domrongkitchaiporn S.
research Center, Mahidol University, Bangkok.
It has been speculated that calcium supplement in subjects with low oxalate intake might increase the risk of calcium stone formation due to an increase in calcium absorption without a significant reduction in oxalate absorption. There have been no human studies addressing specifically the effects of taking calcium supplements in populations whose dietary oxalate is low. This study was conducted to determine the effects of calcium supplements on the risk of calcium stone formation in a population with low oxalate intake. Thirty-two healthy male navy privates, 22.7 +/- 1.9 (mean +/- SD) years old, who had oxalate intake of less than 1 mmol/day, a serum creatinine of less than 150 micromol/l, and no history of renal stones, participated in the study. Dietary oxalate was controlled to be under 1 mmol/day throughout the study. Twenty-four hour urine collections for the determination of urinary constituents were obtained at baseline and after taking calcium supplements. Detection of calcium oxalate was performed to assess the risk of calcium oxalate stone formation. The urinary excretion of calcium was significantly elevated above baseline values while taking the calcium supplements (3.48 +/- 2.13 vs 5.17 +/- 2.61 mmol/d, p < 0.05) and urinary oxalate was significantly decreased when the subjects took calcium supplements compared to the corresponding baseline value (0.13 +/- 0.05 vs 0.17 +/- 0.07 mmol/d, p = 0.01). Urinary citrate was significantly elevated when the subjects took calcium supplements compared to the baseline (0.83 +/- 0.57 vs 0.64 +/- 0.39 mmol/d, p = 0.03). There was no significant alteration in the activity products of calcium oxalate while taking the calcium supplements (0.54 +/- 0.25 vs 0.57 +/- 0.22, p = 0.54). The effect of calcium supplements with meals, for the reduction of the risk of calcium stone formation, was unchanged, even in a population whose oxalate intake is rather low. Taking calcium supplements resulted in a reduction in urinary oxalates and an elevation in urinary citrates. Both alterations in urinary constituents counterbalanced the elevation in urinary calcium which resulted from the calcium supplements.
PMID: 15916110 [PubMed - indexed for MEDLINE]
Susan Owens
webmaster: lowoxalate.info
listowner: Trying_Low_Oxalates@yahoogroups.com
Head of the Autism Oxalate Project
at the Autism Research Institute
Susan, some of your surveys and studies are much too old to be relevant. In recent years many foods have added calcium which never had before. We're talking about children born after those studies who have been eating foods unlike the ones from 20 years ago.
Why do five year olds develop conditions once exclusively found in middle-age? Yes, being sedentary is one factor, but I'm sure that if you check their diets, besides the salt you'll find all sorts of mineral additives rarely used twenty years ago, like calcium.
Hi,
There are newer studies. I just posted the ones I like the best.
Here are two new ones. The second article was written by a wonderful and distinguished oriental oxalate professor who sat next to me at the FASEB Summer research symposium on oxalate three years ago where I attended along with about sixty oxalate scientists from around the world.
I'm going to another oxalate conference at the NIH in a few weeks. I stay at the cutting edge of this research, I promise!
Also, there are a series of studies looking at the neurotoxicity of oxalate that comes from a cancer drug called oxaliplatin. Calcium and magnesium infusions before and after the oxalate infusion protected the brain and nervous system from serious damage from oxalate.
G Ital Nefrol. 2007 Nov-Dec;24(6):535-46.Links
[Calcium kidney stones. Diagnostic and preventive prospects]
[Article in Italian]
Arcidiacono T, Terranegra A, Biasion R, Soldati L, Vezzoli G.
Unità di Nefrologia e Dialisi, Istituto Scientifico San Raffaele, Università Vita Salute, Milano, Italy.
Kidney stone disease is one of the main causes of hospitalization in Italy. Its prevalence increased in the last century and is probably still increasing. The pathogenesis of the disease is not known, although two main theories have been elaborated. The first hypothesizes that hydroxyapatite deposition in the interstitium of the renal papillae (Randall's plaque) precedes urinary calcium oxalate precipitation on the ulcered surface of the papilla to form a stone. The second presumes the tubular lumen of Bellini's duct to be the site where calcium-oxalate salts precipitate to form the nucleus for stone formation within the urinary tract. These pathogenetic processes may be favored by different dietary and genetic factors. The genes involved are not known, although many studies have been performed. Polymorphisms of genes coding for the vitamin D receptor, calcium-sensing receptor, interleukin-1 receptor antagonist, and urokinase were found to be associated with kidney stones, but these results have not been replicated. Different nutrients are suspected to predispose patients to calcium kidney stone disease. A high intake of animal proteins, sodium, vitamin C and oxalate has been implicated in stone formation, whereas calcium, alkalis and phytate may have a protective effect. The prevention of calcium stone formation is based on the recognition of risk factors like those already mentioned here. Furthermore, a family history of kidney stones may be useful in identifying subjects predisposed to become calcium stone formers. However, the expectations of the scientific community are turned to the advances in genetics and to the findings of genetic studies, which may provide diagnostic tools and criteria to define the risk profile of the single individual.
PMID: 18278757 [PubMed - indexed for MEDLI
Urol Res. 2006 Jun;34(3):168-72. Epub 2006 Jan 28.[] Links
Gastrointestinal oxalic acid absorption in calcium-treated rats.
Morozumi M, Hossain RZ, Yamakawa K, Hokama S, Nishijima S, Oshiro Y, Uchida A, Sugaya K, Ogawa Y.
Department of Urology, Faculty of Medicine, University of the Ryukyus, 207 Uehara, Nishihara, 903-0215, Okinawa, Japan. ma-morozm@umin.ac.jp
We studied whether urinary oxalate excretion after an acute oral load of oxalic acid is influenced by concomitant administration of calcium in rats. Male Wistar rats weighing approximately 180 g were divided into six groups of five animals each. After inducing anesthesia, the animals were orally (via a gastrostomy) given 110 micromol of oxalic acid along with 0, 27.5, 55, 110, or 220 micromol of calcium (0, 27.5, 55, 110, or 220 micromol Ca group, respectively). Saline was given to the control group instead of oxalic acid. Urine specimens were collected before administration and then at hourly intervals up to 5 h afterward. Urinary oxalate and citrate levels were measured by capillary electrophoresis, while urinary calcium, magnesium, and phosphorus levels were measured by ICP spectrophotometry. Urinary oxalate excretion peaked at 1 h after administration and was higher in the 0, 27.5, and 55 micromol Ca groups than in the control group. The urinary recovery of oxalate in these groups was 10-15%, while the recovery rate was less than 3% in other groups. Urinary Ca excretion showed no significant changes, either over time or between groups. Free oxalic acid is absorbed more readily from the gastrointestinal tract than calcium oxalate, while simultaneous administration of calcium appears to block intestinal oxalic acid absorption in a dose-dependent manner.
PMID: 16705467 [PubMed - indexed for MEDLINE
thanks
It would be interesting then to check how much salt is in the processed foods which also have added calcium.
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