I’ve held off on this posting for “a while” as events have continued to unfold. At this point, I think things have stabilized enough that I can make statements that will hold going forward.
The context is that a family member has had a kidney stone. She is a ’50 something’ and of about the age where they are more common. Her father also had a stone later in life.
First thing to note is that stones show some hereditary aspects. Partly this is genetic as some types of stones are more common in folks with particular metabolic and genetic differences. Partly it can just be “familial incidence” as families tend to eat similar foods, drink similar volumes, live in the same climates, exposed to the same water, etc.
So if you have a family history of kidney stones, “that matters”…
Before getting into the science part of this posting, a word or two on herbals.
Herbals that might help
Claims that an herb can solve stones. Adolfo in a comment also mentioned such and herb. I can’t find the comment right now to verify if they are the same, but I think they are.
BREAK-STONE, Chanca Piedra (Phyllanthus niruri)
Promotes optimal liver, kidney and gall bladder function
With the recent introduction of a very well known Amazon rainforest plant, Break-Stone (Chanca Piedra), health care practitioners have acquired a powerful plant ally in helping their patients to maintain optimal kidney, gall bladder, liver, and bladder health.
Chanca Piedra is a composite name, “chanca” meaning “to break” in Quechua and “piedra” meaning “stone” in Spanish. It is the popular name given to several small shrub-like plants in the Phyllanthus genus (botanical family Euphorbiaceae), including Phyllanthus niruri, and Phyllanthus stipulatis. These two species have the same medicinal effects and look identical, except for their seeds, by which the botanist can tell them apart. A third species, Phyllanthus amarus, has been considered identical (perhaps not a different species at all) to Phyllanthus niruri. These species of Phyllanthus have been proven in scientific research to have antihepatotoxic, antispasmodic, antiviral, bactericidal, febrifugal, and hypoglycemic activity.
Chanca Piedra got its name because one of the outstanding qualities of this herb, according to the therapeutic herbal tradition of Peru, where knowledge of rainforest remedies spread to Andean civilizations, including the Incas, is to break up and expel both kidney stones, and gall stones. It is believed to help stimulate the production of bile and to promote healthy liver and gall bladder function. The plant is shredded and boiled and then lemon juice is added as a tonic for the liver (taken in small amounts four times daily). It is also traditionally used to clear obstructions throughout the various internal organs of the body by promoting the elimination of mucous and stones.
In different areas of South America , Chanca Piedra is used to treat a wide variety of conditions. It is used to treat edema and excess uric acid, as well as to treat stones of the gall bladder, kidney, and bladder. In some areas, it is used to treat malaria, typhoid fever, flu, colds, constipation, dysentery, or stomachache. It is also used there, for inflammation of the bowels (IBS), pimples, diabetes, and ulcers.
Chanca Piedra has also traditionally been used for diabetes, prostate disorders, asthma, fever, tumors, bladder infections, as a diuretic, to remove excess uric acid (as in gout), for painful joints, jaundice, indigestion, constipation, vaginitis, viruses of the reproductive tract, proctitis, poor circulation, excessive phlegm, bronchitis, and coughs. It is also considered an anti-spasmodic and muscle relaxant, specific to the urinary tract system.
Nicole Maxwell, the author of the groundbreaking Witch Doctor’s Apprentice, first published in 1961, and based on research done in the 1950’s in the Peruvian rainforest, considers chanca piedra one of the most important healing herbs, which she encountered in the rainforest through her interactions with shamans and Amazonian Indians. She later met a German doctor who had been using chanca piedra in his medical practice in Germany who told her that 94% of all the cases he encountered among his patients of gallstones and kidney stones were “completely eliminated” within one or two weeks. For several hours during the actual process of elimination of the stones, some patients experienced stomach cramps. Another physician whom Maxwell interviewed about his use of chanca piedra for his patients said that the plant worked 100% of the time and without any side effects.
In France, Chanca Piedra has been used for some time to treat gall and kidney stones. It is part of a pharmaceutical product called Pilosuryl, which is sold as a diuretic.
The article also claims some curative properties against viruses including hepatitis-B and some activity against HIV. I don’t have the time to track down that evidence for that, but the euphorbias have a powerful collection of biochemically active agents in them. (One, a particularly nasty little spurge, sent me to the hospital with ‘eyes on fire’ just from the residue on my hands after rinsing in running water… others are known to repel gophers and to remove warts. So worth exploring, but be careful with any plant from that family…)
At any rate, I’ve not found a local source of it to evaluate, but haven’t looked that hard either. I did find many other web pages that talk about this plant. It could well be worth a “dig here”. We just ended up in the operating room before I had time to follow up on all the possibles and had the stone broken via a laser on a catheter.
One Note on Kidney Stents
After the procedure, there was a kidney stent inserted. Everything was fine for a couple of days, then the stent was removed. (It looks rather like a bent chunk of wire with a ‘curly cue’ on each end). The result was that about 7 pm we were back at the E.R. with intense pain. The doctor had said “there might be some pain” but had not bothered to mention that it might be excruciating pain. We had leapt to the conclusion that a few days after the procedure and stent out meant “done with pain”. That was “exactly wrong”.
So if you go the lithotripsy / stent route, remember to ask about pain relievers BEFORE you go home from the stent removal…
A web search of “Kidney stone stent pain” will result in more horror stories than you will want to read.
There is also a drug given that can relax the ureter and let the stone pass more easily. It’s a helpful drug to have and resulted in a reduced pain both before and after the procedures.
Given how much pain was involved, though, I think I’d be happy to try the “herbal” approach as an alternative, especially on smaller stones. (This one was just way to big to even leave the kidney on its own).
The Focus On Oxalate
I will be mostly focusing on Calcium Oxalate stones. This is for two reasons.
1) They are about 80% of all kidney stones.
2) It’s what the lab report confirmed was present.
With that said, there are two other types of stones worth mentioning.
The wiki covers them pretty well, so I’m going to quote that here:
About 10–15% of urinary calculi are composed of struvite (ammonium magnesium phosphate, NH4MgPO4·6H2O). Struvite stones (also known as “infection stones”, urease or triple-phosphate stones), are always associated with urinary tract infections. The formation of struvite stones is associated with the presence of urea-splitting bacteria, most commonly Proteus mirabilis (but also Klebsiella, Serratia, and Providencia species). Using the enzyme urease, these organisms metabolize urea into ammonia and carbon dioxide. This alkalinizes the urine, resulting in favorable conditions for the formation of struvite stones.
The key point here is that it’s a bacterial infection issue and not much you can do at home. Maybe eat more of those plants known to have antibiotic properties, but your best bet is the stuff the doctor hands out. Drink cranberry juice, that has some benefits in urinary tract infections, and perhaps acidify the urine pH a bit..
That is also why it is important to try to catch one of the stones in a filter when you pee. You need to find out if it is infection related.
Note also the reference to alkaline urine. I suspect that this gives two things you could try if stuck without access to a doctor. First off, take the urine ph. If it is consistently alkaline, you likely have an issue brewing. Secondly, if you can eat and drink things that acidify the urine, that’s a feature… Reduced protein intake would also reduce total urea production (less for the bacteria to eat), so if you are eating 4 lbs of meat a day, think about cutting back…
Uric acid stones
About 5–10% of all stones are formed from uric acid. People with certain metabolic abnormalities, including obesity, may produce uric acid stones. Uric acid stones may form in association with conditions that cause hyperuricosuria (an excessive amount of uric acid in the urine) with or without high hyperuricemia (an excessive amount of uric acid in the serum). They may also form in association with disorders of acid/base metabolism where the urine is excessively acidic (low pH), resulting in precipitation of uric acid crystals. A diagnosis of uric acid urolithiasis is supported by the presence of a radiolucent stone in the face of persistent urine acidity, in conjunction with the finding of uric acid crystals in fresh urine samples.
Another of those “doctor needed” classifications. You can, again, cut back on uric acid via a less rich diet, but the bigger problem is that “metabolic abnormalities”. Most likely you are stuck with a set of metabolic pathways that are not all that great at stopping uric acid formation. A ph test on the urine for high acidity is your major clue here (outside of labwork looking at a stone and finding uric acid in the urine).
Biggest point to make here is that in one case you want to acidify the urine and in the other you want to make it more alkaline. If you don’t know what you’ve got, you could be doing exactly the wrong thing. In an “end of the world” scenario, you could just taste your urine. ( I know, sounds gross… but for centuries tasting the urine for sugar was the diagnostic for diabetes… It takes courage to be a doctor in the dark ages ;-) so if it is sour, it is acid, if it is bitter, alkaline.) Then do what makes it the other way.
The formation of calcium phosphate stones is associated with conditions such as hyperparathyroidism and renal tubular acidosis. People with certain rare inborn errors of metabolism have a propensity to accumulate crystal-forming substances in their urine. For example, those with cystinuria, cystinosis, and Fanconi syndrome may form stones composed of cystine. People afflicted with xanthinuria often produce stones composed of xanthine. People afflicted with adenine phosphoribosyltransferase deficiency may produce 2,8-dihydroxyadenine stones, alkaptonurics produce homogentisic acid stones, and iminoglycinurics produce stones of glycine, proline and hydroxyproline. Urolithiasis has also been noted to occur in the setting of therapeutic drug use, with crystals of drug forming within the renal tract in some patients currently being treated with agents such as indinavir, sulfadiazine and triamterene.
For the catch-all “else” clause of “other types” it’s basically a metabolic “oopsy” and not much you can do about it. It’s between you, your metabolism, and the doctor. Thought notice that “Renal Tubular Acidosis”. That means that the kidneys are not dumping enough acid into the urine (so you get alkaline urine) and it results in acidosis of the blood. If you take something that causes more acid in the urine, you can have less in the blood, and diminish that particular causal factor (unless due to a cellular defect of the renal tubules).
Generic Things To Do
OK, for that “other” group and for all other kinds of stones, you are dealing with a physical precipitation process. It’s a simple chemical action. Something is precipitating from solution. What influences tendency to precipitate?
Some things precipitate at different pH levels. When in doubt, you want to be on the acid side of things, but not too far. 6 to 7 pH. But if you can find out what pH you are at, and know you have a problem at that pH, it’s likely to be helpful to move away from that pH. (Best would be to get lab results and a doctor consult, but if stuck “in the field” and you find you have persistent acid urine and are making stones, a reasonable gamble would be that alkalinizing the urine would be a good move). Alkaline urine is correlated with Calcium phosphate stones, and the Struvite stones, both fairly rare. In those cases you want to make the urine more acidic. For most folks, those who have Uric Acid stones or Calcium Oxalate stones (and similar acid urine stones) it’s best to be akalinizing the urine.
In all cases, things precipitate when their concentration gets “too high”. That “too high” is different for each thing (and varies with pH for each thing). You can find a nice chart of general solubility guidelines here:
Rule 1. All compounds of Group IA elements (the alkali metals) are soluble.
For example, NaNO3, KCl, and LiOH are all soluble compounds. This means that an aqueous solution of KCl really contains the predominant species K+ and Cl- and, because KCl is soluble, no KCl is present as a solid compound in aqueous solution:
KCl(s) => K+(aq.) + Cl-(aq.)
Rule 3. All nitrate (NO3-), chlorate (ClO3-), perchlorate (ClO4-), and acetate (CH3COO- or C2H3O2-, sometimes abbreviated as Oac-) salts are soluble.
For example, KNO3 would be classified as completely soluble by rules 1 and 3. Thus, KNO3 could be expected to dissociate completely in aqueous solution into K+ and NO3- ions: KNO3 => K+(aq.) + NO3-(aq.)
Rule 4. All chloride (Cl-), bromide (Br-), and iodide (I-) salts are soluble except for those of Ag+, Pb2+, and Hg22+.
For example, AgCl is a classic insoluble chloride salt:
AgCl(s) Ag+(aq.) + Cl-(aq.) (Ksp = 1.8 x 10-10).
Rule 5. All sulfate ( SO4=) compounds are soluble except those of Ba2+, Sr2+, Ca2+, Pb2+, Hg22+, and Hg2+, Ca2+ and Ag+ sulfates are only moderately soluble.
For example, BaSO4 is insoluble (only soluble to a very small extent):
BaSO4(s) Ba2+(aq.) + SO42-(aq.) (Ksp = 1.1 x 10-10).
Na2SO4 is completely soluble:
Na2SO4(s) => 2 Na+(aq.) + SO42-(aq.).
This matters as Calcium and Magnesium are prone to making non-soluble compounds and oxalate in particular makes a lot of insoluble compounds. So when Calcium and Oxalate are together in the urine, they tend to want to make crystals and precipitate out making stones… Your job is to replace some of that oxalate with one of the more soluble ions from above and to replace some of that Ca with some of the more soluble metals. If you cut back on the Ca and Oxalate in the urine, you get less stone formation. (For Calcium Oxalate stones… For the other stones, you need to cut back on what they are made of).
How can you do this in a generic way?
Drink a ton of water…. that makes ALL things less concentrated.
I’d shoot for one large glass of water at least 6 to 8 times a day. ( 2 to 3 quarts or liters of water per day).
As the ion concentration in the urine drops, the existing crystals and stones will start to lose ions into solution. (Even an insoluble substance has some solubility constant. The key is a thing called “Ksp” in chem class.) So, if you are not peeing at least 4 times a day with a very low ‘coloration’, your urine is too concentrated. It ought to look like clear water as much as possible.
Learn to love eating watermelon… ;-)
(At least for me, when I eat a lot of watermelon, I’m dumping that excess water ‘right quick’…)
Eat a low salt diet.
But if Na is more soluble, would you not want more of it?
In biology, there are many times that things are “inverted” as the cells take an action that is counter to what you would expect from simple inorganic chemistry. When you eat excess sodium, your body tries to stay ‘balanced’ by dumping a lot of ions, including Calcium, so you end up with MORE Ca in the urine, not less…
With a lower sodium diet, you will also dump water faster, leading to more dilute urine and lower concentrations of “stuff” in the urine.
Basically, when you pee, look at the result. If it is a dark amber, you are likely dumping too concentrated a urine. Keep drinking water until you have as light as possible and don’t add much sodium to your diet.
In the original draft of this article I wrote:
I would speculate that swapping to KCl (potassium chloride “no salt” salt) for seasoning would result in the eventual dumping of K and Cl ions into the urine, and that ought to accelerate stone dissolving. But that is just speculation and would need testing and / or confirmation from a reference. (Don’t add too much, though, as too much is lethal. For most salts and minerals, too much kills you or does other bad things. So just enough to season the food, not so much that you have kidney failure or heart failure, OK?)
I’ve now spent a bit of time looking and found two articles that lend credence to that thought. You DO want to add “no salt” KCl to your diet if you have a calcium stone “issue”.
I found one link that said that added potassium was a positive thing in stone prevention:
There is nothing wrong with KCl used as a salt substitute as long as the amount is reasonable.
As far as stones, potassium is generally helpful.
But that isn’t very helpful to a very detail oriented person… so more digging turned up:
Clinical Nephrology – Epidemiology – Clinical Trials
Kidney International (2000) 58, 748–752; doi:10.1046/j.1523-1755.2000.00221.x
Comparative effects of potassium chloride and bicarbonate on thiazide-induced reduction in urinary calcium excretion
Lynda A Frassetto, Eileen Nash, R Curtis Morris JR and Anthony Sebastian
Department of Medicine and General Clinical Research Center, University of California, San Francisco, San Francisco, California, USA
Correspondence: Anthony Sebastian, M.D., Box 0126, University of California, San Francisco, California 94143, USA. E-mail: firstname.lastname@example.org
Received 5 August 1999; Revised 7 February 2000; Accepted 21 February 2000.
Comparative effects of potassium chloride and bicarbonate on thiazide-induced reduction in urinary calcium excretion.
Background The chronic low-grade metabolic acidosis that occurs in various renal disorders and in normal people, and that is related both to dietary net acid load and age-related renal functional decline, may contribute to osteoporosis by increasing urine calcium excretion. Administration of potassium (K) alkali salts neutralizes acid and lowers urine calcium excretion. Urine calcium excretion also can be reduced by the administration of thiazide diuretics, which are often given with supplemental K to avoid hypokalemia. We determined whether the K alkali salt potassium bicarbonate (KHCO3) and the thiazide diuretic hydrochlorothiazide (HCTZ) combined is more effective in reducing urinary calcium than KHCO3 alone or HCTZ combined with the conventionally coadministered nonalkalinizing K salt potassium chloride (KCl).
Methods Thirty-one healthy men and women aged 50 or greater were recruited for a four-week, double-blind, randomized study. After a baseline period of 10 days with three 24-hour urine and arterialized blood collections, subjects were randomized to receive either HCTZ (50 mg) plus potassium (60 mmol daily) as either the chloride or bicarbonate salt. Another 19 women received potassium bicarbonate (60 mmol) alone. After two weeks, triplicate collections of 24-hour urines and arterialized bloods were repeated.
Results Urinary calcium excretion decreased significantly in all groups. KHCO3 alone and HCTZ + KCl induced similar decreases (-0.70 0.60 vs. -0.80 1.0 mmol/day, respectively). Compared with those treatments, the combination of HCTZ + KHCO3 induced more than a twofold greater decrease in urinary calcium excretion (-1.8 1.2 mmol/day, P < 0.05). Both HCTZ + KHCO3 and KHCO3 alone reduced net acid excretion significantly (P < 0.05) to values of less than zero.
Conclusions KHCO3 was superior to KCl as an adjunct to HCTZ, inducing a twofold greater reduction in urine calcium excretion, and completely neutralizing endogenous acid production so as to correct the pre-existing mild metabolic acidosis that an acid-producing diet usually induces in older people. Accordingly, for reducing urine calcium excretion in stone disease and osteoporosis, the combination of HCTZ + KHCO3 may be preferable to that of HCTZ + KCl.
Now that’s information I can use. So a short search for some potassium bicarbonate might be in order. In any case, adding some KCl “no salt” to the salt shaker is a simple and direct way to reduce the calcium load in the urine. As it’s on the grocery store shelf, that’s something of a trivially easy thing to do.
The Soda Pop Connection
I would avoid dark soda pop. Things like Coke and Pepsi have added phosphoric acid and caffeine. Notice that the Struvite stones have phosphate in them… Basically, it’s just all around a bad idea… (This was the advice of our Doctor in the initial visit) I would add to that the point that phosphoric acid will bind to Calcium and Magnesium in the gut forming insoluble salts. This matters (we will see more on this later) as we want that Ca and Mg to be binding with Oxalic Acid and making insoluble Oxalates in the gut (not in the kidney…)
This doctor says the same thing as above about avoiding soda pop:
What should I drink, you may ask? Stay clear of soft drinks as most of them, especially colas, contain phosphoric acid, a stone inducer. One study demonstrated that those who drank more than one liter per week of soft drinks that contain phosphoric acid have a 15 percent higher rate of recurrence of kidney stones at 3 years than those drinking other beverages. Grapefruit juice is another culprit and may actually enhance the risk of developing stones. Filtered water may therefore be your best bet.
On the flip side, this website claims the opposite. I’ve not had time to find the studies and try to untangle what actual details matter. Until that is sorted out, I go with the “more water less phosphate” from the guys with the MD after their names.
A Researched Remedy: Phosphoric Acid
After researchers speculated a link between soft drinks and kidney stones, researchers conducted a test on over 1000 ex-kidney stone sufferers and the recurrence of the stones. And the results might surprise you?
During the 36 month study, half of the sufferers promised to abstain from any form of carbonated beverage (soft drinks) and the other half tested would continue to drink at least 5 ounces of their preferred soft drink of choice. After the 3 year trial, drinkers of soft drinks were one-third less likely to experience a recurrence of kidney stones. And the men who completely stopped drinking soft drinks were one-third more likely to relapse with kidney stones.
The researchers thought just the opposite and were puzzled. Could something be naturally dissolving kidney stones in soft drinks?
Is phosphoric acid a natural dissolvent of calcium?
The Remedy Tested!
Research leads to proven remedy! Can phosphoric acid dissolve calcium build up? Many researchers also experimented with a natural remedy (phosphoric acid) to dissolve and pass kidney stones. Again, researchers were baffled because it worked!
I think the wiki may actually give some idea of why both ideas can be found; and a clue as to what is actually happening. It’s all in the details, IMHO.
Biological effects on bone calcium and kidney health
Phosphoric acid, used in many soft drinks (primarily cola), has been linked to lower bone density in epidemiological studies. For example, a study using dual-energy X-ray absorptiometry rather than a questionnaire about breakage, provides reasonable evidence to support the theory that drinking cola results in lower bone density. This study was published in the American Journal of Clinical Nutrition. A total of 1672 women and 1148 men were studied between 1996 and 2001. Dietary information was collected using a food frequency questionnaire that had specific questions about the number of servings of cola and other carbonated beverages and that also made a differentiation between regular, caffeine-free, and diet drinks. The paper cites significant statistical evidence to show that women who consume cola daily have lower bone density. Total phosphorus intake was not significantly higher in daily cola consumers than in nonconsumers; however, the calcium-to-phosphorus ratios were lower.
On the other hand, a study funded by Pepsi suggests that insufficient intake of phosphorus leads to lower bone density. The study does not examine the effect of phosphoric acid, which binds with magnesium and calcium in the digestive tract to form salts that are not absorbed, but rather studies general phosphorus intake.
However, a well-controlled clinical study by Heaney and Rafferty using calcium-balance methods found no impact of carbonated soft drinks containing phosphoric acid on calcium excretion. The study compared the impact of water, milk, and various soft drinks (two with caffeine and two without; two with phosphoric acid and two with citric acid) on the calcium balance of 20- to 40-year-old women who customarily consumed ~3 or more cups (680 mL) of a carbonated soft drink per day. They found that, relative to water, only milk and the two caffeine-containing soft drinks increased urinary calcium, and that the calcium loss associated with the caffeinated soft drink consumption was about equal to that previously found for caffeine alone. Phosphoric acid without caffeine had no impact on urine calcium, nor did it augment the urinary calcium loss related to caffeine. Because studies have shown that the effect of caffeine is compensated for by reduced calcium losses later in the day, Heaney and Rafferty concluded that the net effect of carbonated beverages—including those with caffeine and phosphoric acid—is negligible, and that the skeletal effects of carbonated soft drink consumption are likely due primarily to milk displacement.
Other chemicals such as caffeine (also a significant component of popular common cola drinks) were also suspected as possible contributors to low bone density, due to the known effect of caffeine on calciuria. One other study, involving 30 women over the course of a week, suggests that phosphoric acid in colas has no such effect, and postulates that caffeine has only a temporary effect, which is later reversed. The authors of this study conclude that the skeletal effects of carbonated beverage consumption are likely due primarily to milk displacement (another possible confounding factor may be an association between high soft drink consumption and sedentary lifestyle).
Cola consumption has also been associated with chronic kidney disease and kidney stones through medical research. The preliminary results suggest that cola consumption may increase the risk of chronic kidney disease.
What I think we see going on here is the same thing we will see again about calcium consumption. One would tend to think that if it’s CaOxalate in the urine that’s the problem you would cut back on Ca in the diet. Not so. There is a large self regulating buffering system between mouth and urine so what gets dumped may not be directly related to what goes in the mouth.
In particular, excess Calcium in the gut binds to oxalic acid from food in the gut, forming, you guessed it, insoluble CaOxalate that “goes right on out”… never presenting that oxalate to the kidneys for disposal after absorption. Cut back on calcium in the diet, more oxalic acid is absorbed (it does not get metabolized away after absorption) and thus more is dumped in the urine. It can now bind with the Ca in the urine that is being regulated by the metabolism via bone deposition / loss.
It is VERY important to watch for those “self regulation” driven and “gut vs urine” driven inversions of cause and effect from what you would expect from a simple solution model…
So, back at sodas:
First off, we have the complication of “what was NOT drunk instead?”. So you let folks choose the OTHER drinks, but add or remove soda. Guess what, you now have no idea what’s happening. Was it a caffeine effect? A Calcium effect? A total liquid volume effect? An acid / base effect? (i.e. did they drink citrus juice loaded with citric acid). Etc.
A truly “controlled” study needs to be, well, controlled!
So some speculation from “first principles”.
Added phosphoric acid in the gut with meals will tend to bind with the calcium and magnesium in those meals and prevent them from binding with oxalic acid. That would contribute to higher oxalic acid in the urine and greater stone formation.
Added phosphoric acid in the gut between meals has nothing with which to bind. It gets absorbed, some stored in the bones, and the excess dumped, where it can help dissolve CaOxalate stones. That is, it would break up the existing stone but not be concentrated enough to form a new CaPO4 deposit.
So I’d avoid soda pop with meals, but go ahead and have them between meals.
That the caffeine has a significant impact implies the need to avoid it. I’ll look at that more below too. But you might want to look for soda pop without caffeine in it.
The Caffeine Connection
Describe the caffeine connection as:
Background: Intake of carbonated beverages has been associated with increased fracture risk in observational studies. The usual explanation given is that one or more of the beverage constituents increase urinary calcium.
Objective: We assessed the short-term effects on urinary calcium excretion of carbonated beverages of various compositions.
Design: An incomplete random block design was used to study 20–40-y-old women who customarily consumed ≥680 mL carbonated beverages daily. Four carbonated beverages were tested: 2 with caffeine and 2 without. Two contained phosphoric acid as the acidulant and 2 contained citric acid. The study included one neutral control (water) and one positive control (skim or chocolate milk). Serving size was 567 mL for the carbonated beverages and water and 340 mL for the milks. Beverages were consumed with a light breakfast after an overnight fast; no other foods were ingested until urine collection was complete. pH, titratable and total acidity, sodium, creatinine, and calcium were measured in 2-h (morning) fasting and 5-h postbeverage urine specimens.
Results: Relative to water, urinary calcium rose significantly only with the milks and the 2 caffeine-containing beverages. The excess calciuria was ≈0.25 mmol, about the same as previously reported for caffeine alone. Phosphoric acid without caffeine produced no excess calciuria; nor did it augment the calciuria of caffeine.
Conclusions: The excess calciuria associated with consumption of carbonated beverages is confined to caffeinated beverages. Acidulant type has no acute effect. Because the caffeine effect is known to be compensated for by reduced calciuria later in the day, we conclude that the net effect of carbonated beverage constituents on calcium economy is negligible. The skeletal effects of carbonated beverage consumption are likely due primarily to milk displacement.
Which is fine for total bone calcium, but not so fine if you deposit stone for a while then stop, but do not reach the low levels needed to then dissolve the stones…
So a prudent behaviour would be to avoid the caffeine in sodas and go for the non-caffeinated.
It also looks to me like you would want to reduce milk consumption as it was clearly shown to put more calcium into the urine. (OTOH, milk with a meal full of oxalic acid is likely to bind that oxalic acid and prevent absorption, so if you do drink milk, do it with meals.)
These folks fed rats a load of caffeine without the soda and milk confounders and also found more calcium being dumped:
Effect of Dietary Caffeine and Theophylline on urinary Calcium Excretion in the Adult Rat (Citations: 3)
SUSAN J. WHITING
The chronic effects of dietary caffeine or theophylline on urinary calcium excretion were investigated in the adult male rat. When caffeine was added at two concentrations, 0.75 and 1.50 g/kg diet, 24-h urinary calcium excretion rose 300 and 450% on d 7, and 200 and 330% on d 14, respectively. There were no changes in the 24-h urinary excretion of phosphate, sulfate, sodium and cAMP nor did urine volume change. The high dose of caffeine was compared to an equimolar dose of theophylline ( 1.39 g/kg diet) in both Wistar and Sprague-Dawley rats. Urinary calcium excretion in theophylline-treated rats was significantly greater than in caffeine-treated rats on all sampling days and in both strains of rat; the calciuric effect lasted at least 22 d. When rats were given indomethacin (3.3 mg/kg diet) the calciuria induced by caffeine and theophylline was abolished, and sodium excretion in all groups was reduced by 35-50%, but urine volume was unchanged. The calciuria of methylxanthine feeding may result from a prostaglandin-mediated process distinct from diuresis. J. Fiutr. 117: 1224-1228, 1987.
So as a “probably a good thing to do” step, I’d cut back on the coffee latte all day long… Though the wiki does note that actual popoulation studies indicate a slight protective effect to coffee drinkers, so it may be that the added calcium dump is offset by some other effects even if just the added liquid volumes.
At this point, we’re looking at a Lemon Lime or Rootbeer type soda, between meals, as the optimal. It avoids the caffeine (for most of them anyway… watch the Mountain Dew and some rootbeers) and for some of them will have some phosphoric acid in them; which by itself can be a good thing.
But is there even more detail to be explored here?
The Citric Acid Connection
At several places I ran into the idea of raising the citric acid levels in the diet. (For unknown reasons, grapefruit are associated with stone forming, so avoid the grapefruit and stick with the lemons and oranges…) Citric acid in excess tends to be dumped in the urine, and Calcium Citrate is far more soluble than Calcium Oxalate or Calcium Phosphate… I might also speculate that the citrate might screw up the crystal lattice as it tries to form. There are many opportunities for “mechanism” including things like impact on the production of bio-inhibitors of calcium oxalate formation (there is such a chemical in the urine).
From the wiki http://en.wikipedia.org/wiki/Kidney_stone
Crystallization of calcium oxalate appears to be reduced by substances in the urine that retard the formation, growth, aggregation, and adherence of calcium oxalate crystals to renal cells. By purifying urine using salt precipitation, isoelectric focusing, and size-exclusion chromatography, some researchers have found that calgranulin, a protein formed in the kidney, is able to inhibit the in vivo formation of calcium oxalate crystals. Given the large amounts of calcium oxalate in the urine, and considering its potency, calgranulin might be an important intrinsic factor in the inhibition of the formation and aggregation of urinary crystals. It may also eventually become a useful pharmacologic agent in the prevention of kidney stones.
There were many references to ‘excess citrate in the urine’ being correlated with lower levels of stone formation. You want to add citrate to your diet, one way or another. It also tends to make the urine more alkaline, and oxalate stoned form in acid urine, so that’s a feature right there.
As many lemon lime sodas have added Citric Acid, they are the best bet for getting some stone dissolving action in the urine. No caffeine and with an acid component that gets dumped. (Assuming you have the most common Calcium Oxalate or other alkaline urine stone). Become a fan of lemon-lime soda between meals… Even better is drinking a load of lemonade.
I also found sodium citrate in some ‘upset stomach’ preparations. There are also magnesium supplements that are magnesium citrate, so they would give the citrate you want, along with magnesium. The magnesium would tend to bind with oxalic acid in the gut (reducing absorption). What Mg does get absorbed, when dumped in the urine, ought to tend to leach oxalic acid from the stones in passing. Magnesium oxalate is much more soluble than Calcium oxalate (about 600 times more soluble), so a few atoms at a time, the MgOxalate would tend to wash away a bit of the stone.
(This happens because solution / precipitate are in equilibrium. If you reduce the Ca and raise the Mg in the urine, some of the Ca ions will tend to come out of the stone. As it has near zero Mg in it, a bit of Mg will tend to go in. The resultant local bit of MgOxalate can then more easily be washed off by passing excess water. The CaCitrate is soluble so it too tends to be peed out. Basically, you are presenting the stone surface with disequilibrium conditions and it responds with some ion movement into solution. It may be slow, but it happens.)
A web search of “kidney stone citric acid” will turn up a load of pages / links with various ideas, tests, recommendations, etc. I’ll put a semi-random sample of them here. The “bottom line” of it is a lot of places said to drink a glass or two of lemonade a day (basically forever) to prevent kidney stones and many of them suggested up to 3 quarts / liters a day for a few days to dissolve stones. (I’d be worried about dissolving my teeth at that level, if done for any length of time…) That citric acid results in a more alkaline urine is of benefit to oxalate stone formers.
Of Vegetarians, Citrate, and pH adjustment
GENERIC NAME: CITRIC ACID/POTASSIUM CITRATE – ORAL
USES: This medication is used to make the urine less acidic. This effect helps the kidneys get rid of uric acid, thereby helping to prevent gout and kidney stones. This medication can also prevent and treat certain metabolic problems (acidosis) caused by kidney disease.Citric acid and citrate salts (which contain potassium and sodium) belong to a class of drugs known as urinary alkalinizers.
It is interesting to me that potassium citrate and citric acid are claimed as making the urine LESS acidic. But it does not say “compared to what’? If you have highly acid urine to begin with, buffering to a lower acid level can still be very acid. I also note that it says these drugs will reduce “acidosis” caused by the kidneys. But we’ve just seen that acidosis from that front is due to alkaline urine as the body is not dumping enough acid. To me, it looks like something doesn’t add up.
At any rate, I found many other references to potassium citrate as a urine alkalinizer (along with bicarbonate of soda), so there are options for “urine alkalinizers”.
A potential connection to vegetarian diet
Is a paper about urine acidifiers and alkalinizers. It has an interesting note about a herbivorous diet…
The urine of herbivora is normally alkaline, and an exclusively vegetable diet will tend to lead to a less acid urine. While human urine, when freshly passed, is usually acid, on standing and when contaminated with bacteria, it frequently becomes alkaline owing to bacterial action.
As our stone forming “subject” had converted to a vegetarian diet about a year ago, that may have been a contributory factor. Though this shows that the pH factor goes in the desired direction, so I’m most suspicious of the added oxalate foods in the diet. Spinach, nuts, beans, etc.
Adjusting urine pH
However, in persons with a persistently slightly alkaline urine, with a tendency to the precipitation of the phosphates of calcium and magnesium, the administration of 40 grains of acid sodium phosphate thrice daily will, as a rule, but not always, produce a urine of about normal acidity.
Sodii Phosphatis Acidi 3 sa
Syrupi Limonis (Aurantii) 3 i
Aquae ad 3 ii
Dilute when taken.
It is best not to add hexamine to such a solution.
I’m not sure what the units of “sa” and “i or ii” might be, but assume they are from an old system like drams and grains. The paper is dated 1931. It looks to me like they are making a citric acid phosphate solution. I find this an interesting paper precisely because it is old. They often have ingredients found ‘in nature’ and / or easily made from natural things if needed.
In many cases acid phosphate is of little value, but ammonium benzoate which is converted in the body into urea and hippuric acid, leads to an increase in the proportion of acid sodium phosphate excreted and may prove of more value than acid sodium phosphate as an acidifier, and a little of the benzoic acid may be excreted unchanged after a person has taken 20 grains three times a day for some days, and will have a slight effect on bacterial growth. Ammonium benzoate is a most unpleasant drug, and hard to cover, but if the following preparation be taken, diluted four to eight times with water, little of the disagreeable tickling flavour is noticed:-
Rx: Ammonii Benzoatis – gr xx
Syrupi Sarsee Compositi (U.S.P.) 3 ii
Aqu ad 3 as
or fifteen minims of the Liquid Extract of Liquorice and a drachm of Syrup may be substituted for the Syrup of Sarsa.
It has been found by many experiments on patients with infection of the urinary tract that ammonium benzoate will decrease the Ph, 4nd make the urine more acid, even when the acid sodium phosphate is without effect. But even more effective is the administration of ammonium chloride. This is absorbed as such, but the ammonia is converted into urea, the chlor-ion becomes free to neutralize base, and hence makes the urine more acid. Ammonium chloride can, of course, be given with hexamine.
Rx: Ammonii Chloridi gr. xx
Hexamine gr. xx
Extracti Glycyrrhizte Liquidi mm. x
Aquie ad 3 ii
To be diluted.
Unfortunately, in many cases of cystitis, a definitely acid urine may cause an undue amount of pain and hence the urine must be kept more alkaline than usual. Sodium bicarbonate has been used for this purpose, but the employment of a citrate or an acetate is much better. Large doses of citrates are frequently necessary. Hexamine is of no value, but boric acid may be of some value in decreasing bacterial growth.
Rx: Acidi Borici gr. xv
Potassii Citratis gr. xx
Glyeerini 3 i
Syrupi Aurantii ad 3 88
To be diluted 4 times.
Further, it is often found that the patient is more comfortable when hyoseyamus is given with the citrates, as in the following prescription:
Rx: Potassii Citratis gr. xlv
Tincturva Hyoseyami mm. xlv
Syrupi 3 88
Aquea Cinnamomi ad 3 ii
It looks like roman numerals for the xx and xlv quantities. Simple active minerals and syrups to mask the flavor.
In any case, we have the clue that Ammonium Chloride is a urinary acidifier. This article confirms that and includes ascorbic acid as well. We also have over the counter sodium citrate for ‘upset stomachs” so one of the better alkalinizers is also easy to get (as are magnesium and calcium citrate tablets).
C. Urinary Acidifiers and Alkalinizers
FDA is also aware of OTC drug products that have been marketed as urinary acidifiers and urinary alkalinizers. Ammonium chloride and ascorbic acid have been used as OTC urinary acidifiers, and sodium bicarbonate has been used as an OTC urinary alkalinizer. These products have not been included in any previous call-for-data notices as part of the OTC drug review. Therefore, at this time FDA invites interested persons to submit data or information on these and any other ingredients for use as OTC urinary acidifiers and alkalinizers.
So it may even be in the drug store (if the FDA have not banned it by now…) At the least, you can get ascorbic acid (vitamin C); though it can be metabolized to oxalic acid if taken in excess, so don’t go over 2 to 4 grams. (No, that’s not a typo. That’s about where it starts being metabolized on. Before that the excess gets dumped, mostly.) Then again, for folks who want the more acidic urine ( struvate formers) they are not worried so much about oxalic acid levels.
In passing, this article:
in talking about another drug mentions urinary acidifiers that might have an impact on that drug:
or urinary acidifiers (e.g., methionine, ammonium chloride, or certain diets formulated to prevent or remove bladder stones)
So we find that methionine can be a urinary acidifier (though I’ve got no clue about sources or dosing). Elsewhere we find cranberry juice described as a urinary acidifier, but a mild one.
So for folks who need the acidification (struvite, calcium phosphate) it’s a feature.
This site has a nice list of the different stone types, with photos, and a description of their conditions of formation:
Citrate plays a big part in calcium stone formation. It forms a soluble salt with calcium and inhibits the formation of calcium oxalate and calcium phosphate crystals. Anything that leads to hypocitrauria or low levels of urinary citrate increases the chance of developing stones. Chronic diarrhea, renal tubular acidosis (RTA), diets high in protein and salt, low levels of blood potassium often associated with thiazide diuretics are all associated with hypocitrauria.
Oxalate forms an insoluble complex with calcium to develop a calcium oxalate stone. High levels of oxalate in the urine, or hyperoxaluria, is even more important to stone formation than high levels of calcium or hypercalciuria. Excessive intake of food and drink containing oxalate leads to calcium oxalate stones. Also, excessive intake of Vitamin C which is metabolized to oxalate may lead to hyperoxaluria and an increase in stone formation.
That comment about Vit-C is often heard, yet the studies done of what actually happen have not shown such an effect. Then again, it may depend on just how much is meant by “excessive”…
In any case, controlling oxalate intake and keeping urine pH out of the very acid range seem to be key factors to oxalate stones.
What can we learn from the Cranberry?
The major clinical use for cranberry is to prevent recurrent urinary tract infections. Initially its benefits were attributed to acidification of the urine and then to its hippuric acid content, but more recent studies indicate that proanthocyanidins and other high molecular weight compounds found in cranberries interfere with the adhesion of uropathogenic bacteria to bladder mucosa.
Cranberry is also used as a home remedy for renal stones.
c. Urine acidifier
i. In vitro data: none
ii. Animal data: none
iii. Human data: In an early case series, adults who consumed large amounts of cranberries were noted to have acidic urine. In normal subjects in one study, drinking cranberry juice with meals significantly reduced urinary pH for a few hours after the meal. Urinary acidification effects appear to be transient. A patient would need to drink approximately a quart or more (1500 ml) of cranberry juice daily to have a significant long-term impact on urinary acidity
So it looks like there are a fair number of choices for urinary acidification including cranberry juice with meals. I do have to note that what is a “significant impact” on acidity for antibacterial properties may be far different from what is needed to shift pH enough to avoid stone deposition. There are a huge number of references to using cranberry extract, powders, and concentrates in cats and dogs to prevent kidney stones so I think there is something to it. (So many that it was hard to find articles about people without the -cat -dog etc. tags.) For folks with the calcium oxalate and phosphate stones, you want added alkalinity, so the acidification is not a feature.
Yet, for Oxalate stones in particular, there is this cautionary note from other sources:
The main causes of kidney stones are from calcium and oxalate in the urine. People with a history of having oxalate kidney stones are at an increased risk of getting them again. Oxalate kidney stones are the most common form of kidney stones. Cranberry juice drinks contain high concentration levels of oxalate, which increases the risk for getting the stones. Oxalate is the most common component in kidney stone formation.
Cranberry juice contains many risk factors for creating kidney stones. Recent studies have shown that consuming cranberry juice alters the components of urine. Cranberry juice increases magnesium and calcium levels in the urine. Cranberry juice also raises levels of calcium present in urine. Cranberry converts calcium and vitamin C into oxalate, increasing the risk for kidney stones. The juice contains the same minerals as other foods that are known to cause kidney stones. These foods include: coffee, chocolate, nuts, spinach, wheat, and bran.
Although cranberry juice has shown to be effective in preventing brushite kidney stones, these are very rare and unlikely to occur. Although the juice will reduce the risk for these kidney stones there is little chance the will ever form anyway. It’s in people’s best benefit not to drink cranberry juice in large quantities because it will raise their chances of getting the most common form of kidney stones, oxalate kidney stones.
So it may be that it is of limited use in oxalate stones and best for the non-oxalate Struvite type. (Personally, I’d likely go for the ammonium chloride as it’s simple and direct.) What bothers me about this particular article is that it is yet another of those “measure a few details but don’t look at the total impact” articles you frequently see in the medical field. It has oxalate in it and “that’s bad” so it can’t work… yet depending on other factors it may be that something else is working so well that it doesn’t matter that some oxalate is brought along for the ride. I’d rather see a direct clinical trial (though even there you have to watch for things like ‘what food was not consumed instead’… as confounders). I’ve found one other reference to the study behind the idea that cranberry can increase stone formation. It talks about the 24 patients in the study. That is just way too few to say anything statistically. You need about 1000 more to have a really clean “sample”. This leads me to believe they were not looking at statistics on stone formation, but just a simple “goes in – comes out” physical study of ions present. Not very definitive way to do things. Gives good clues, but not actual answers.
Is interesting as it brings in other fruits too.
Effects of Juice on Kidney Stone Formation
Reviewed: Kessler T, Jansen B, Hesse A. Effect of black currant-, cranberry- and plum juice. European Journal of Clinical Nutrition 2002;36:1020-1023.
High fluid intake is widely regarded as the most important preventive treatment for kidney stones, reducing the concentration of constituent ions and saturation of stone-forming salts. The most suitable fluids for this purpose are mineral water, orange juice, apple juice, and fruit and herbal teas. Patients with a history of kidney stones should avoid fluids that contain stone-forming agents and promoters; these include coffee, black tea, alcohol, and cola soft drinks. Cranberry juice has been used extensively to prevent and treat urinary tract infections, and small studies on the effects of ingestion of black currant juice and prunes (dried plums) have shown an acidifying effect on urine in humans. Various shortcomings in these studies and a lack of scientific evidence have led these researchers to evaluate the influence of these three juices on urinary composition and kidney stone formation.
Changes were noted in several urinary parameters following consumption of each juice. Black currant juice significantly alkalized the urine (P < 0.01), increased citric acid excretion (P < 0.01), and oxalic acid excretion (P < 0.05). Cranberry juice significantly acidified the urine (P < 0.05) and showed a small, not statistically significant decrease in citric acid excretion. Oxalic acid excretion was significantly increased after ingestion of cranberry juice (P < 0.05). Black currant juice did not significantly affect the relative supersaturation for calcium oxalate, uric acid, brushite, and struvite, but cranberry juice significantly increased the relative supersaturation of uric acid (P < 0.05) and decreased the relative supersaturation of struvite and brushite. Plum juice had no statistically significant effect on any of the urinary parameters measured. Excretion of calcium, magnesium, and uric acid were not significantly changed by any of the experimental juices.
The decrease in pH with cranberry juice was expected and Is associated with increased risk of uric acid stone formation; however, the relative supersaturation for struvite and brushite were slightly decreased. The authors speculate that the effect of cranberry juice might be larger if more juice was ingested.
The authors conclude that black currant juice could be used as a preventive and treatment for uric acid stones due to its alkalizing effect on the urine. Cranberry juice could be of use when acidification of the urine is indicated, as with apatite, brushite, and struvite stones as well as with urinary tract infection.
So if you are in the particular groups listed, Cranberry is your thing. For oxalate, not so much… look for that sodium citrate digestion tablet or potasium citrate pill at the pharmacy. For Uric Acid stones and Oxalate stones, we have a nice direct “drink black currant juice” result too.
Then, just to make things even less clear, we have this study:
Influence of cranberry juice on the urinary risk factors for calcium oxalate kidney stone formation.
McHarg T, Rodgers A, Charlton K.
Department of Medicine, University of Cape Town, Cape Town, South Africa.
To investigate the potential influence of cranberry juice on urinary biochemical and physicochemical risk factors associated with the formation of calcium oxalate kidney stones, as this product might affect the chemical composition of urine.
SUBJECTS AND METHODS:
Urinary variables were assessed in a randomized cross-over trial in 20 South African men (students) with no previous history of kidney stones. The first group of 10 subjects drank 500 mL of cranberry juice diluted with 1500 mL tap water for 2 weeks, while the second group drank 2000 mL of tap water for the same period. This was followed by a 2-week ‘washout’ period before the two groups crossed over. During the experimental phase subjects kept a 3-day food diary to assess their dietary and fluid intakes; 24-h urine samples were collected at baseline and on day 14 of the trial periods, and analysed using modern laboratory techniques. Urine analysis data were used to calculate the relative urinary supersaturations of calcium oxalate, uric acid and calcium phosphate. Data were assessed statistically by analysis of variance.
The ingestion of cranberry juice significantly and uniquely altered three key urinary risk factors. Oxalate and phosphate excretion decreased while citrate excretion increased. In addition, there was a decrease in the relative supersaturation of calcium oxalate, which tended to be significantly lower than that induced by water alone.
Cranberry juice has antilithogenic properties and, as such, deserves consideration as a conservative therapeutic protocol in managing calcium oxalate urolithiasis.
So maybe all those folks feeding cranberry concentrate to their dogs and cats are on to something after all..
These folks have some other speculation about “why”:
Previous studies had shown high concentrations of oxalate and calcium oxalate in the urine to contribute to crystal formation. It was also shown that citrate inhibits the formation of crystals – therefore the higher the citrate concentration in the urine, the better.
The Cape Town results add to studies published in the Journal of the American Medical Association and the New England Journal of Medicine. They found that cranberry juice had some anti- bacterial properties, which is important because it has recently been suggested that calcium-based stones may have an infectious origin. The results also state that some components occurring naturally in the berries may prevent the attachment of calcium oxalate crystals and stone-promoting bacteria to the epithelial cells in the renal tubes.
It seems there is some speculation that even the non-struvite stones might have a minor bacterial component and that the cranberry juice impact on those little buggers might be part of the effect. I also note the statement about an effect on “attachment of calcium oxalate crystals”. Even in non-stone formers we get some CaOxalate formed. But the crystals do not stick to each other and form stones. There is a compound our kidneys make that blocks that adhesion. So maybe it isn’t just about the ion concentration, but there is a ‘lubricant’ feature to cranberry juice as well?
My opinion is that it probably also depends on WHEN the cranberry juice was consumed. With a meal? The calcium in the meal can bind with the oxalate in the cranberry juice and remove it from the equation. NOT with a meal? Then you get the oxalate in / peed out effect.
Managing Oxalic Acid Absorption
For my money, it’s all mostly about managing the calcium / magnesium / oxalic acid ratio in the gut during consumption. You want excess magnesium (assuming Calcium Oxalate stones are the most common issue) with the meal so that MgOxalate is pooed out. As long as you do that, the cranberry benefits are present with low risk.
Another clue comes from this article. It may be just high doses of a concentrate that are the issue. (Perhaps as then there is not enough calcium to bind and excrete the oxalic acid?)
Controversy exists over cranberry as a risk factor for the formation of calcium oxalate kidney stones. A case report suggested that concentrated cranberry tablets caused urinary tract stones in a man with a history of nephrolithiasis. 37 However, a randomized, crossover trial conducted among healthy adults found reduced oxalate and phosphate excretion, and increased urinary citrate excretion conditions unfavorable for calcium oxalate stone formation. 38 The amount of oxalate ingested daily from cranberry juice was approximately equivalent to 86 mg/L in the crossover trial, compared with delivery of approximately 363 mg from the concentrated cranberry tablet. 38 , 39 Bioavailability of oxalate from the food source may be limited. 38 , 39
Why so much emphasis on Cranberry Juice? Because it is widely available, widely advised, and does acidify the urine while helping reduce urinary track infections. Plus, when you get conflicting results in trials, it usually indicates something ELSE that’s important is going on. Something you ought to ‘figure out’ for best results. IMHO, that something is the gut concentration of metal ions that bind to oxalic acid.
And, in particular, having high Mg levels would help to eliminate the problem of taking in excess Ca (that, when dumped, raises the saturation of ions leading to stone formation…)
One simple “test” would be to take the ‘mild laxative dose’ of MgSO4 (Epsom Salt) and divide it into 3 portions. Mix each in a glass of water drunk with each meal. That ought to result in excess Mg to bind to any oxalate in the meals and result in a big drop of oxalate load. (Be careful doing this, though. I tested it on one food and felt a slightly gritty film of MgOxalate deposit on my teeth as soon as the Epsom water hit the spinach remnants in my mouth… Best used after a ‘plain water rinse’ after high oxalate foods have been chewed… It is also possible to just drink a mineral water, like Dasani, that has added Mg salts.
There are 4 ingredients in Dasani bottled water:
water, magnesium sulfate, potassium chloride, salt
You want that MgSO4 and the KCl.
For Epsom Salt, the “dose” on the package is 1/2 to 1 teaspoon in a glass of water. 2.5 to 5 cc. So I’d make that about 1-2 cc per glass of water with each meal. (1/6 to 1/3 tsp per meal). Not much at all, really.
OK, I think that’s enough on the “output side”. Next we’ll look at the “input side”
The Low Oxalate Diet
At this point we’re just talking Oxalate stones. The others are either a “doctor only” deal due to medical metabolic issues or infection, or at best you can do small things with your urine pH (or in the case of Uric Acid stones, just cut way back on the meat).
The harder one is the oxalates. Why? Because it is something few people think about, and fewer still care about. Also because you get “advice” that’s all over the board. Why? Because a lot of folks just measure total oxalic acid and oxalates. That’s rather useless as many oxalates are just not digested and “pass on through”. It has to be absorbed into the blood to make it to the kidneys. That means only “soluble oxalate” matters. THEN you have the fact that by simply adding calcium and magnesium to the meal proper you can cause even the “soluble oxalate” to become insoluble. So “what is cooked with who” tends to change what happens in your body. “Spinach” is bad as the raw stuff in salads, but ‘creamed spinach’ has a load of calcium in that cream binding to that oxalate and “taking it on through’…
So what’s the “mantra”?
My simplest way of looking at it is “The stuff they said is good for vegetarians, don’t eat. The bad stuff? That you eat.”
So meats and animal products in general have nearly no oxalic acid or oxalates that matter. Meat, eggs, fish, dairy. Go for it. (It’s those poor sots with uric acid stones that have to avoid them and “go vegetarian” as much as possible ;-)
Things like “whole wheat” where the bran has oxalates in it? Bad. The oxalate stone former needs that “foamy white bread”… go figure…
Peanut butter and other nut butters and nuts are out. Common beans are out. (But lentils and lima beans can be used instead!).
Spinach is way out, as are beets and chards.
Mustard greens and collards are out too.
(As is okra… a vegetable that some folks love but I think is just glue in a pod…)
Potatoes and canned tomatoes need to be cut back some..
But you can have all the peas and onions you like along with cauliflower and broccoli and asparagus. Avocado, artichokes, corn, brussels sprouts, chili peppers and chives, coleslaw, cucumbers, garlic and green peppers. Lettuce too. Squash, pumpkins, sauerkraut and canned string beans.
Chocolate is out, but so are sesame seeds and rhubarb, so maybe that’s a wash ;-) (I’m not fond of sesame seeds…)
Coconut is allowed (it isn’t really in the same category as other nuts as an overall plant). So yes, that white sugary foamy coconut cake is just the ticket! Flax seeds and sunflower seeds are OK (so dump the peanuts and cashews and get sunflower seeds). Also OK are pumpkin and squash seeds.
Oatmeal is in but All Bran is out (there is a God!) while Cheerios, Corn Flakes, and Rice Crispi’s are in.
Fats and oils have no oxalic acid in them. Yes, that’s right. Butter. Olive oil. Lard. Blue Cheese dressing and French, Italian, Caesar or Ranch dressing. Go for it. Sour Cream too…
Fruits are generally fine (just avoid figs, kiwi fruit, and dried apricots (fresh or canned are OK as you can’t eat as much!).
All those starchy flour based products like pancakes, muffins, cakes, pies, crackers, tortillas, cooked rice, pasta noodles, pastries, Danish or Bagle as you like it. Cornbread too. Just no “whole grain”. You are supposed to dodge the bran…
(If this is sounding just about exactly like what we’ve all been told is a ‘bad diet’, then you are understanding clearly… Meat, fats, cakes, pies, breads, pasta. Yup, you got it. Fish too. Salmon with creamy sauces or as sushi. Tuna sandwich on white bread with tuna and mayo galore. Cottage cheese, regular cheese, cream cheese, custard, custard pies, flan. Ice Cream! “You gotta eat Ice Cream!”… Eggs…)
Corn chips, “Cheese puffs”, popcorn, tortilla chips. Even an occasional small bag of potato chips. Jelly beans, cookies, sugar and syrups galore, pudding and Angle Food Cake.
IMHO, these folks do a very good job of making a list of low oxalate foods. (It is intended for a group of folks with a specific metabolic disorder that makes them particularly prone to oxalate problems, so the list does include coffee with the caffeine “issue”, but as long as you know to reduce the caffeine a bit for reduction of calcium loss, it’s a decent list for stone formers too)
From this other site we find that eating extra fruit helps:
Clinical Nephrology – Epidemiology – Clinical Trials
Kidney International (2004) 66, 2402–2410; doi:10.1111/j.1523-1755.2004.66029.x
The effect of fruits and vegetables on urinary stone risk factors
TIZIANA MESCHI, UMBERTO MAGGIORE, ENRICO FIACCADORI, TANIA SCHIANCHI, SIMONE BOSI, GIUDITTA ADORNI, ERMINIA RIDOLO, ANGELA GUERRA, FRANCA ALLEGRI, ALMERICO NOVARINI and LORIS BORGHI
Department of Clinical Sciences, University of Parma, Italy; and Department of Clinical Medicine, Nephrology and Prevention Sciences, University of Parma, Italy
Correspondence: Prof Loris Borghi, Dipartimento di Scienze Cliniche, Università di Parma, Via Gramsci, 14 – 43100 Parma, Italy. E-mail:email@example.com
Received 2 March 2004; Revised 1 June 2004; Re-revised 21 June 2004; Accepted 30 June 2004.
The effect of fruits and vegetables on urinary stone risk factors.
Background The overall effect of fruit and vegetable intake on urinary stone risk profile is not yet known.
Methods We studied the effect of a two-week period of fruit and vegetable elimination on urinary stone risk profile in 12 normal adults, and of supplementing the diet with a fair quantity of low-oxalate fruits and vegetables in 26 idiopathic calcium stone formers characterized by hypocitraturia and a very low fruit and vegetable intake in their usual diet.
Results In the normal subjects, the elimination of fruits and vegetables from the diet decreased the urinary excretion of potassium (-62%), magnesium (-26%), citrate (-44%) and oxalate (-31%), and increased that of calcium (+49%) and ammonium (+12%) (P < 0.05 for all). The relative saturation for calcium oxalate and calcium phosphate increased from 6.33 to 8.24 (P = 0.028), and from 0.68 to 1.58 (P = 0.050), respectively.
In the hypocitraturic stone formers, the introduction of these foods in the diet increased urinary volume (+64%), pH (from 5.84 to 6.19), excretion of potassium (+68%), magnesium (+23%), and citrate (+68%), while it decreased the excretion of ammonium (-18%) (P < 0.05 for all). The relative saturation for calcium oxalate and uric acid fell from 10.17 to 4.96 (P < 0.001), and from 2.78 to 1.12 (P = 0.003), respectively.
Conclusion The total elimination of fruits and vegetables in normal subjects brings about adverse changes in the urinary stone risk profile that are only partially counterbalanced by a reduction in oxalate. In contrast, the addition of these foods to the diet of hypocitraturic stone formers not used to eating them not only significantly increases citrate excretion without affecting oxalate excretion, but also decreases calcium oxalate and uric acid relative saturation.
So eat your fruits…
Also remember that some kinds of processing bind the oxalate so it is not absorbed. If you just can’t STAND the idea of not having that Peanut Butter and Jelly Sandwich, eat it with a glass of milk to bind the oxalate. Cook your spinach in a cream sauce and wash down those french fried potatoes with a Dasani Water… Think in terms of creamed this and cheese sauce that… or even just doing things like draining the water from the can, then warming your canned beans in a pot of water with some added Mg or Ca in the water to bind the oxalate in the food. I found a couple of references to “white crystals” in canned spinach and “what to do about it” that pointed out they were just CaOxalate and to ignore them. This implies to me that cooking or canning your own spinach in calcium rich water (such as the lime treatment used to turn corn into hominy) would be a viable way to bind and remove the oxalic acid.
Similarly, while ‘black tea’ is on the “avoid” list: drunk “English style” with a generous mix of milk in it, the oxalic acid will all be turned into calcium oxalate and not absorbed. Perhaps that is why milk in tea is so common in Europe…
It is also worth note that how a vegetable was raised will change the oxalic acid levels. Part of why different lists include different plants on the good or bad list is that one batch of spinach can have a very different oxalate level from the next due to the effects of heat or water stress or the particular fertilizer used. Folks who REALLY want to go to town on that can spend the time to learn what cultural practices lead to the lowest oxalate levels in each plant. This posting is already too long to include that here.
I would also add just two minor notes in conclusion. MgSO4 tends to just “pass on through”. Because of this, the Mg ions tend not to be absorbed but end up sticking with the sulphate. That’s why Epsom Salt acts as a laxative. That sulphate doesn’t get absorbed well, so holds water in the gut along with the Mg. But if you soak in MgSO4, it is significantly absorbed into the skin. This means that a very nice way to raise the Mg levels in what you pee out is to soak in a bath of Epsom Salt. It also gives sulphate ions to be dumped as well and might lead to a more acid balance in the urine. It has helped the “subject” in several trials so far… We covered that point in another posting here:
It is also worth it to remember that Vitamin D helps to hold calcium in the bones. If it is being used in the body, it’s not being dumped in the urine and can not participate in stone forming. So get some “sun time” or buy a “lizard lamp” to keep your vitamin D levels up in the winter. (Yeah, you could just eat cod liver oil or take a vit-D pill, but where’s the adventure in that? ;-)
Now put it all together and it’s an interesting thing to realize… one of the better treatments would be:
Fire up the BBQ, slap some meat on the grill and have some boiling water for corn on the cob with loads of butter. Have a nice big angel food cake (coconut prefered) and don’t forget to have a fruit salad. Stand around in the sun while you are doing all this, and it’s best if done at the beach so you can get some “soak time” in that big puddle of naturally Ca and Mg rich water in the ocean. If not, schedule some time at the local “mineral water spa”… Oh, and don’t forget the peppers and onions on that steak and the Texas Toast to go with it…
Remember, you are doing this for your health. No sacrifice is too great ;-)
Some Final Notes:
While I don’t have a link for it, once long ago I was given some wisdom by an old guy in a bar in New Mexico or maybe Texas. There was someone moaning in the “little room”. Me, being about 21 then (or close enough to ‘pass’) but still not familiar with such things asked “Is something wrong with him?” The Old Guy said, roughly “Nope, that’s just old Joe. He’s pass’n a kidney stone. He gets ’em ’cause he’s a whisky drinker. Down here in the south, we call it the kidney stone belt of the desert, if you get dried out, you get stones. Them whiskey guys get dried out. Now you will never find a beer drinker doing that. They pee so much they never get a stone… ” So if that Old Guy is right, make sure to have enough beer (or lemonade if a tea totaler) to avoid getting dried out. It’s for the medicinal value, after all …
(Sidebar on “beer stone”: I found a site that told how to remove ‘beer stone’ from a brew kettle. Turns out that in the process of making wort, the oxalate in the grain tends to ‘plate out’ on the equipment as insoluble deposits. What works best to remove these? An alternation of acid and base conditions. First one wash, then the other. This lead to 2 understandings.
First that the idea that a load of oxalate ends up in beer; well, that must get past that fact that a lot is falling out of solution in the making. So I think beer is naturally depleted some in oxalates … but more research is needed on that… anyone wishing to fund the research need only tell me what brewpub to attend ;-) It also says that it’s darned hard to dissolve CaOxalate once deposited. I “cooked up a process” for the “subject” to try that had lemonade by the quart for 2 days, then a day of rest. When the ‘laser stone breaker” was done, the doctor said, twice, it was a “very soft stone”. I think that process was softening the stone in preparation for it to break up on its own.)
OK, the “bottom line” is that you need to know what kind of stone you are making to know what is the best approach to a cure or preventative. There are some broad things you can do in any case, but the more specific things depend on exactly what the chemical composition of the stones might be. Diet can help, but mostly it’s drinking a lot of water. That there is a band of excess kidney stones across the desert southwest speaks volumes. Still, if you tend toward stones, it’s well worth the effort to try some simple changes of diet and habit to see if you can reduce or avoid ‘the issues’. If all else fails, the traditional medical approach is far better than it was just 40 years ago. But if you go that route, expect a load of pain and ask for drugs up front. Me? I’m raising the fluid intake and dropping some “health food” from my diet as a precaution. I’ve seen what this looks like and I’m not interested in being on the other side of it… I’ll take my spinach creamed, have the lettuce salad, keep that lamb chop on the plate, and think a beer sounds just great, thank you very much… And I have a new found appreciation for “mineral baths” and “mineral waters” in the diet. The things I have to put up with “for good health” ;-)