Of all the knowledge on this site, a tiny nugget of three well established facts has explosive power for patients and physicians. Put to actual use they let you prevent idiopathic calcium stones and preserve bone mineral.
If you do not want to read the article, I have made a VIDEO to tell you the story in about 13 minutes. On my iphone the video opens well and looks better horizontal. Please let me know if it does not work well for you.
I have not been shy nor secretive. Article after article speak about the three, but always in context so other facts can distract one, as can superb but unmagical paintings from a few masterpieces hung on the same wall. I know some patients, some physicians, have fully grasped the crucial importance of the three, and put them to use. From the many comments I read weekly, I know many have not. So I am taken with a passion to redress matters.
Les Demoiselles d’Avignon, Picasso, 1907, Hangs in MOMA, NY. It is my choice of masterpiece. I deliberately cropped into the center as I love the abstraction and also want metaphor for limiting attention to a few essentials in the midst of a richness of details.
Because Spring has come to cold Chicago, I used my picture from some Springs ago. Partly it is the green ivy, partly reminiscence.
This is About Idiopathic Calcium Stone Formers
Cystinuria, uric acid stones, struvite stones – all these are to one side. Calcium stones from systemic diseases likewise. Physicians detect these and manage them. My focus is on the vast mainline of patients who form calcium stones without systemic disease.
The Three Essential Facts
Diet Sodium Controls Urine Calcium
If I could I would paint this on the sky, draw it on sidewalks across the world. It has been demonstrated by scientists for at least 70 years,
and how it happens is reasonably well known. I made this picture using published data from many sources, and I placed the original data and references within this site. The blue points are from calcium stone formers, the red from normal people.
Urine sodium is diet sodium, because we absorb almost all the sodium we eat, and excrete it in the urine. Urine calcium is not diet calcium. We absorb only 18 – 35% of the calcium we eat, and that absorption is regulated by the intestines, and by hormones like vitamin D.
Stone formers absorb a higher percentage than normals, but that is not why their urine calcium is higher. It is higher because they have idiopathic hypercalciuria and their kidneys do not retain calcium as well. At the heart of idiopathic hypercalciuria is what this graph shows – urine calcium is abnormally sensitive to diet sodium. As you lower diet sodium from the average US value of 150 – 200 mEq ( 3500 – 4600 mg) to the present ideal diet sodium of 65 mEq (1500 mg), their urine calcium (blue) falls into the normal range.
Not rarely my own patients seem disappointed when I begin their treatment with lower diet sodium. It seems so mundane, so like the common nostrum that we all eat too much salt. Many have had multiple 24 hour urine tests, and I make a crude pencil graph of urine calcium vs. urine sodium and show them their own behavior. That works, sometimes. Otherwise, they agree to so alter their food lives, but – I sense this – wonder at coming all the way to a professor for a dull seeming advice. They do not sense the power sodium has, even if I show them this graph – or their own.
Diet Calcium Controls Urine Oxalate
I made this messy but remarkable graph from work other people have done and put the name of the main author below their dots. These were experiments with variations of diet calcium, on the horizontal axis, measurements of urine oxalate on the vertical axis and diet oxalate as the size of the symbols. The smallest symbol means 50 mg/day of oxalate, the largest means 200 mg/d, the middle size is 100. In the main article using this I placed links to the original data.
The data scatter but above 1,000 mg of diet calcium all four authors found only modest urine oxalate, 35 mg/d or less as mean values. Average US calcium intake is about 500 mg/d or less, which permits a much higher swing in urine oxalate.
People with idiopathic hypercalciuria, the reason for high urine calcium in idiopathic calcium stone formers, absorb diet calcium more efficiently than normal, so a higher diet calcium supply will raise urine calcium and stone risk.
But, low diet sodium will offset this, improve kidney calcium conservation, so urine calcium can stay low even though diet calcium is high enough to lower urine oxalate.
This is part of the magic and the peril. You must lower diet sodium first and show it is low by another 24 hour urine. Then you can raise diet calcium to block diet oxalate. If you do it right, and keep the diet sodium low, urine calcium will rise little if at all with a higher diet calcium.
Diet Sodium and Calcium Control Bone Mineral
Only one trial proves this, and only in one kind of person – perimenopausal women. We could use more trials. But this one was so perfectly done, and so dramatic, we can for the moment use it as out guide.
Each woman ate each of four diets, high and low sodium, high and low calcium, and in a random round robin fashion. Specifically, the sodium levels were 1600 and 4400 mg/day, and low and high calcium (518 and 1284 mg/day. On each diet, each woman participated in a full balance study so bone mineral uptake or loss could be quantitated.
The four diets are on the horizontal axis. Calcium balance of bone is the black bars scaled on the vertical axis in mg/day, and it can be negative – bones are losing – or positive – bones are gaining calcium.
Absorption is plotted upward, meaning more for bone. Urine and intestinal secretory (‘endofac’) losses downward meaning potential losses for bone,
Balance was positive only with the high calcium + low sodium diet.
The amount of calcium absorbed was higher on the two high calcium diets, of course, and the urine calcium was lower on the low than on the high sodium diets.
As I have already said, the odd term ‘endofec’ means the amount of calcium secreted from blood into the stool by the duodenum, pancreas, and small intestines. This was measured using stable isotopes. If you look close, it was a fall in urine calcium and calcium secretion, both, that created the bone mineral gain from high calcium low sodium diet vs. the high calcium high sodium diet.
Also look close at the urine calcium. The high calcium low sodium diet gave the very same urine calcium as the low calcium high sodium diet. In other words, the women could raise their diet calcium from 500 to nearly 1300 mg/day and yet by lowering diet sodium to 1600 mg/day keep urine calcium unchanged.
The Magic Works for Stones
This is the one trial of the magic formula. Low diet sodium to keep the calcium in the body and thence the bones, high diet calcium to keep oxalate out of the body and thence the urine. It works for bones. Does it work for stones?
Of course, why else would I put it here, and many other places on this site.
I made the graph very large so your could see the printing in the overlay. The patients were men forming calcium oxalate stones whose urine calcium exceeded 300 mg/d. Low calcium diet was 400 the high calcium 1200 mg/day. The low sodium diet was aimed at 1150 mg, the high at the usual level of about 4000 mg/day.
After five years, stones were fewer in the high calcium reduced sodium group – highly significant statistically.
The why of less stones is exactly what my prior graphs predict.
Of course urine sodium was lower in the low sodium diet group (2,800 vs. 4,600 mg/d, low vs. high sodium, respectively).
Urine calcium of the low and high calcium groups was virtually identical (248 vs. 236 mg/d, low vs. high diet calcium, respectively). Just like for the women in the bone study, one could triple diet calcium yet keep urine calcium the same by lowering diet sodium.
Are you not amazed by this? In two studies one can raise diet calcium three fold and urine calcium does not increase if you also lower diet sodium. Look at the power diet sodium has.
How about oxalate?
Both groups were told to avoid high oxalate foods – walnuts, spinach, rhubarb, parsley and chocolate. The high calcium diet lowered urine oxalate (333 vs. 411 umol of oxalate/d, high vs. low diet calcium, respectively). Supersaturation for calcium oxalate, the proven driver of stone risk, was 3.5 in the high calcium and 4.5 in the low calcium group.
Think about how the threefold magic formula worked. Low sodium diet permitted high diet calcium. The high calcium lowered the oxalate but could not raise urine calcium because sodium was so low.
How to Use the Three Facts
These are magical facts, but they must be used in the right order. It is exactly like casting a magic spell.
Lower Diet Sodium First
Make the change and then be sure you did it by getting a new 24 hour urine. Without the urine test you will never know if you succeeded. Ask yourself if what you did during the collection was like the usual for you and also ask if you really mean to keep the diet sodium as low as during the test. If you get tired of the low diet sodium, and urine sodium rises, all is lost.
Raise Diet Calcium Next
Once you know your diet sodium is low, raise the diet calcium and test again. Is diet sodium (urine sodium) still low? If so, is urine calcium low enough? Low enough is about 200 mg/d of calcium or less.
If so, you are done. If not, you need to keep changing diet sodium and calcium until you get there – high diet calcium, below 200 mg urine calcium.
Some people cannot make do with only diet. Their urine calcium remains too high. For them, we add thiazide to the diet, usually in a very low dose. But for most, this will do. You must keep the low diet sodium, so the thiazide works well at a low dose, and to avoid potassium loss.
Now, Consider Diet Oxalate
With high diet calcium in place, is urine oxalate high enough to raise risk of stones – above 25 – 30 mg/d. If so, it is time to get rid of the highest food oxalate sources. Not all food oxalate, but foods on the high end. I listed some just above. My site has the main ones on a graph. Work from the top down.
Diet oxalate is the last thing to worry about, never the first. One wants to remove what high diet calcium has not removed.
Of course, repeat 24 hour urines are the only way to know if success or failure has attended your efforts.
If You Have Bone Disease
If your bone mineral is deficient, these diet changes are good but you need a physician to be sure they are enough. You may also need medication. Do not rely on just diet. Repeat bone mineral measurements are essential. Be sure your physician is satisfied with your bone health.
If you do Not Have Bone Disease
You may not have looked. Get a bone mineral density. If it is normal, get another some years later. The diet is fine for you unless bone mineral declines. If it does decline your physician needs to manage things. The diet is still advisable, but may not be enough.
There is More but Focus Here, on the Big Three
Diet potassium and protein matter, the former from from fruits and veggies. Diet refined sugars matter, they raise urine calcium. Diet protein matters, too much raises urine calcium. The kidney stone diet accounts for all of these.
Fluids matter. Urine volume should be above 2 liters/d, the point at which stone risk has been reduced. But fluids are never enough.
But the three way magic spell predominates over all else: – lower diet sodium, then raise diet calcium, then consider diet oxalate.
Keep your mind on diet sodium and calcium first, and be sure they are set properly. Then go on, if you must, into the thicket and brambles of oxalate lists. Then control unhealthy sugars, excess protein, and get adequate diet potassium. They matter, I always attend to everything I can.
But always, I urge, stay on the main road. Perform the magic spell and see how far you can get.
115 Responses to “THREE ESSENTIALS TO REDUCE CALCIUM STONES AND PRESERVE BONE”
Margaret Rossi, RN
Hi Dr. Coe. Have you heard anything about abnormal gut microbiomes with stone formers? Specifically the lacking of Oxalobacter formigenes?
Fredric L Coe, MD
Hi Margaret, Many papers have presented data on OF. It correlates with stones or not but attempts to give it as a treatment have proven futile. Some new treatments have emerged using an oxalate degrading enzyme – I have not as yet worked with it. So in all, an active area of interest, not any major patient benefits thus far. Regards, Fred
Margaret Rossi, RN
Thank you for responding to my first question. I have another question: I read that calcium oxalate stone-formers should avoid soy products. Then I came across this abstract (https://pubmed.ncbi.nlm.nih.gov/15998131/) that said, while soy tends to contain a lot of oxalate that can lead to stones, it also contains phytates that inhibit stone formation. Are soy products still to be avoided by stone-formers?
Thank you for your time.
Fredric L Coe, MD
Hi Margaret, Inhibitors are a dodgy matter. Urine contains innumerable calcium crystal inhibitors but crystals still form. Adding a food with oxalate in hope another molecule will offset the increased supersaturation is just that – a benign hope. I would not desire to trust in it. Fred
I am a 72-year-old male, treated for prostate cancer in 2016 with TURP and brachytherapy. Cystoscopy in May 2020 reveled stone accumulation in the urethra just below the bladder neck, removed with lithotripsy. Recheck in June 2021 reveled even greater stone regrowth; scope could not be passed into the bladder. CT scan showed large stone accumulation in same area and all else in the area normal, again removed with lithotripsy September 2021.
September Stone analysis: 40% calcium phosphate, 30% calcium oxalate monohydrate and 30% calcium oxalate dihydrate. I have never had a kidney stone.
I’m interested in your thoughts on prevention and possible future treatments.
Fredric L Coe, MD
Hi James, a common cause of crystal formation in the bladder is incomplete drainage, perhaps present despite the TURP. A secondary cause would be 24 hour urine abnormalities that predispose to crystallization via increased supersaturation. A common other contributor is low fluid intake because of bladder drainage problems that is in fact supersaturating the urine via low volume. Perhaps your physicians might want to pursue these possibilities in hope of stopping the problem. Regards, Fred Coe
Thanks for your reply. Please allow me to add a couple of points: I have never had a kidney nor bladder stone, the stone accumulation is in the urethra just below the bladder neck. The latest was 2.7 cm craniocaudal by 2.0 cm AP by 2.8 cm transverse and took about 14 months to accumulate. This caused pain, often severe, for several months.
I’ve has numerous ultrasounds to check bladder emptying and bladder was always fully empty. These stones did not start appearing until had I had the procedure to remove the bladder neck restriction. Could they possibly be growing on scar tissue?
Fredric L Coe, MD
Hi James, Thanks for the additional information. Quite possibly. Crystals can form on tissues that lack the normal epithelial mucous layer, and become a stubborn nidus. Even so, one wants to make urine chemistries as minimal as possible with respect to the crystals in hopes of reducing growth. Regards, Fred Coe
I’ve gone on a low oxalate diet with particular elimination of spinach which was a big part of my diet previously. And a large glass of water with lemon juice in the AM. I’ll have a recheck for stone buildup in January hoping for none or, at the worst, to not let the stone get as large as before. I’ve had no pain at all since the stone removal in September.
Fredric L Coe, MD
Hi James, This article offers a lot more than you mention, and I hope you consider more than diet oxalate. As for lemons, it is merely a way to get a food version of potassium citrate. You have to ask if that is what you need – low urine citrate, too acid a urine pH, as merely adding lemons has no real basis in fact as a treatment. I do not see mention of diet sodium or calcium, so please consider if they are ideal. Regards, Fred Coe
Another update. I have had urethrla crystals (hesitant to call them stones) removed 3 times in the past year: September ’21. January ‘22 and August ’22. A recent 24-hour urine test revealed the following that were out of range: Ca24 – 433; SS CaP — 3.49; Mg24 – 147; CL 24 – 141 and Ca24/Cr24 – 268.
I’ve been on a low-oxalate diet since November and it, apparently, had no effect on the crystal growth.
I would travel the 750 miles to your clinic but my Medicare insurance does not list U of C Hospital as in-network.
Do you see any reason for this rapid crystal growth or, more importantly, are able to suggest what I may do to solve or slow this issue?
Fredric L Coe, MD
Hi James, You have very high urine calcium that is the likely cause of the crystals; the high SS CaP suggests that urine pH is also high – over 6.3, and that diet oxalate is of little consequence. So I see good reasons for the crystal formation. I imagine it is calcium phosphate crystals and they can form very rapidly. You should have the crystals analyzed. Will your insurance cover telehealth?? If you say where you live I can try to find someone for you. Regards, Fred Coe
Dr. Coe, Thank you for the wealth of information you provide. If it hadn’t been for your site, I would not have known to ask for a 24 hour urine after my ostoperosis diagnosis at age 54. I thought I was controlling things with diet, but my most recent test showed a level of 400 (I admit I had fallen off the sodium wagon). 12.5mg of Thiazide gives me constant headaches and stomach upset. I started cutting the pills in half and the side effects have vanished. Do you think a half dose could be effective? By the way, I do not have kidney stones and my osteoperosis has stayed stable for the last few years focusing on diet and exercise and high diet calcium. I wish you offered telehealth. I would sign up in a moment! Thank you again!
Fredric L Coe, MD
Hi Shelley, Idiopathic hypercalciuria (and stones, too) associate with bone mineral loss, as does menopause, so things are complex with you. Thiazide is bone sparing, and dose effects not at all clear so very little may help. It may be time to consider bone directed meds, as well. I do telehealth (though I do not advertise the fact) and my secretary can arrange things, if you like (Banita Williams – 773 702 1475; firstname.lastname@example.org). Regards, Fred Coe
I’m a 54 year old female who has been making kidney stones for 35 years. Most recent (2018) CT scan revealed at least eight stones in my left kidney 5mm or less. Recent stone analysis indicated calcium oxalate. Results from recent 24-hour urine collection tests (2.5/2.8 urine volume) and blood serum test were normal except for urine calcium was borderline elevated (214/198) and urine pH was high (7.4/7.6). Preventing new stone formation by increasing fluids and decreasing sodium is reasonable, but increasing dietary calcium is more difficult since I eat mostly vegetarian and have wheat/dairy sensitivities. To make things more complicated, I have Hashimoto’s thyroiditis (partial thyroidectomy 2012) and a recent osteoporosis diagnosis. Trying to navigate through dietary guidelines for kidney stones, osteoporosis, and thyroid disease is very challenging. Due to my recent osteoporosis diagnosis I’m very concerned about my bone health. I’m hesitant to start taking osteoporosis meds due to side effects. I prefer to try a more natural approach (diet and exercise), Since getting enough calcium from plant-based non-dairy foods is more difficult, I have been researching calcium supplements. I’ve learned traditional supplements are likely to increase new stone formation. Are plant-based calcium supplements from algae also going to increase new stone formation? Do you have any other recommendations for increasing calcium without the risk of forming new stones. Many many thanks!
Fredric L Coe, MD
Hi Lisa, with so many stones, and an alkaline urine pH you really should consider using thiazide diuretics to lower urine calcium and reduce stone production. Ask your physician about the matter. Thiazides have been tested for calcium oxalate stone prevention in three excellent trials and work. I also am suspicious that your stones may contain a high proportion of calcium phosphate crystals – high urine pH does that – and thiazide would be even more specifically valuable for prevention. As for sources of calcium, dairy products are ideal, but given thiazide and a marked reduction of diet sodium you could use calcium supplements especially taken with meals. Regards, Fred Coe
Thank you for all of your wonderful articles, Dr. Coe. They are a treasure of knowledge. I do have a question about one sentence in this article. The sentence reads: “At the heart of idiopathic hypercalciuria is what this graph shows – urine calcium is abnormally sensitive to diet calcium.” Shouldn’t the last word of the sentence be “sodium” rather than “calcium”?
Fredric L Coe, MD
Hi Michael, How good a reader! Of course, and I just changed it. Best, Fred
Hi Dr. Coe. I am an intermittent faster (IF), in which I only ingest calories in a 5 hour window, 24/7/365. Upon discovering your site in May, I modified my diet to ensure I get ~500mg of calcium in my first meal and then ~500 more in my final meal ~4.5 hour later.
1. Is it necessary for me to separate my calcium intake? Everything I’ve found on the web states, “the human body can only process around 500mg of calcium / meal.”
2. What is the minimum time gap between ingesting the 500mg of calcium that would still constitute a separate meal? Is my 4 to 4.5 hour gap enough? I can try modifying my eating window a bit, but would prefer not to.
Fredric L Coe, MD
The calcium is meant to bind oxalate, so absorption or not is irrelevant for stone prevention. Fred
Can you expand on your answer, Dr. Coe? For instance, I don’t think you’re suggesting that it’s fine to ingest 1,500+mg of calcium in one meal, in relation to stone formation, are you?
In fact, do you have an upper limit on total calcium for a day, spread out? I try to keep between 950 and 1,100 / day (separated in 2 meals), but in your above article, you indicated that, as long as we are on a low sodium diet, we can go up to 1,300. Are there any data on going higher / day?
And back to how much in a single meal, is it “safe” to have 700-800 in one meal, especially if there is oxalate intake? Or is more research needed to answer these questions? Thanks again!
Fredric L Coe, MD
Hi Brett, US recommendations are for about 1000 – 1200 mg of calcium from food daily and that is about right for stone formers. I think it ideal to put the calcium mainly in meals that contain oxalate in most abundance, as calcium will reduce oxalate absorption. I do not think it much matters for any one meal if food calcium is 1/2 of the day’s intake – absorption of calcium is at best 18-22% and as high as perhaps 30% in idiopathic hypercalciuria, and spread out over hours in food, so stone risk is mainly reduced by lowering oxalate. Refined timing studies are not available. Regards, Fred Coe
Fred, have you read the article, “damaging effects of oxalates on the human body” on the Urology of Virginia website? I found it pretty alarming. They are arguing that, oxalates are a lot more pernicious than just playing a role in kidney stone formation and can cause all types of problems They are also suggesting some radical ways of dealing with it, such as the Carnivore Diet. Is it a reputable institution, this Urology of Virginia? I have no idea as I live in the UK. Best wishes, John
Fredric L Coe, MD
Hi John, I answered you in detail in your private email. The only way oxalate can cause injury – that I know of – is by forming crystals, as the molecule itself is a metabolic end product. Regards, Fred
Dr Coe; I don’t know how I missed this article but I did. It seems I already was doing part of the magic potion (based on my 24hr collection a couple months ago). My sodium was 87 mmol, and my oxylate was 27.3 mg. However, at the time of the test, I was not getting much diet calcium (only a little from cheese, berries, brocoli, tomatoes etc) and output only 1.7 liters. I was also making no attempt to add citrate. Consequently, from the 24hr collectiion, my citrate was 556. PH was 5.5. Calcium was at 340, Potassium was 46mmol, and magnesium was 187 mg. This was a two year follow up from previous stone and surgery. Recent CT scan shows a previous 2mm stone has grown to 3mm and I have two new 1mm stones. I have now made the following changes: increased fluids to 2.5 liters a day, and I add two grams of potassium citrate powder (weighed with a scale) to my 2 liters of water each day. I also take 3 capsules a day of a potassium-magnesium bound form of HCA. Finally, I have significantly increased my dietary intake of calcium with mainly swiss cheese (less sodium) and milk to get around 1,200 to 1,400 mg a day. Whether or not it’s enough for my recently diagnosed osteoporosis, do you think it may be enough for stone prevention? I have another 24hr collection coming up in about two weeks. What numbers should I expect to see changed if I’m indeed now on the right path?
Fredric L Coe, MD
Hi Robert, I suspect you have genetic hypercalciuria and your stones are calcium oxalate. Adding citrate seems wrong as there is risk of converting to calcium phosphate stones, and your urine citrate is already far above the risk limit – high enough citrate is not posing any stone risk. Your only stone risks seem low urine volume and high urine calcium, the latter is being treated with low sodium diet is remains very high. Your bone disease may well be from the genetic hypercalciuria. Whereas you may well need more diet calcium for your bones, urine calcium will rise, and I think you are an ideal candidate for thiazide which will help protect bones and also lower urine calcium. There may be other reasons for bone disease that need evaluation – beyond the scope of this site at present. Regards, Fred Coe
Thanks Dr Coe. It’s all so confusing and complicated. I think I understand something, only to discover later that I don’t. My nephrologist doesn’t want me to eliminate all additional citrate intake so I’m stopping the potassium citrate mixed in my water (with a small amount of lime juice for flavor) and just using the potassium-magnesium hydroxycitrate (1 capsule every 8 hrs, total 1.5 grams a day). I have read a couple of studies that show hydroxycitrate (HCA) does not raise PH nearly as much as potassium citrate. She also finally talked me into a trial of thiazide at the lowest dose. I have always resisted because of it’s diuretic properties and my BPH issues and already lowish BP (typically around 115 over 60). She explained it’s a pretty weak diuretic and at the lowest dose, I might be able to tolerate it.
Fredric L Coe, MD
Hi Robert, Thiazides have multiple positive trials in calcium stone prevention, and a massive patient use over the past 5 decades. As for hydroxy citrate, it is a food additive and in health stores, and I have no evidence it does any harm. There are theoretical reasons why it might reduce stones but I have no real evidence that it does. Regards, Fred Coe
Well, it turns out I have no trouble tolerating 12.5 mg of Thiazide and I feel foolish for avoiding it all these years. No bad side effects at all. No dizziness, no effect on blood pressure, and strangely enough it seems to alleviate my most troublesome BPH symptoms. Urgency has gone way down as well as frequency. I have read studies that Thiazide can cause a decrease in PSA levels in middle aged men, they don’t apparently know why. Maybe it’s just psychological but the Thiazide seems to make me feel better overall somehow. I’m writing this for anyone else out there that has been avoiding Thiazide like I was. Just try it. You might be surprised. Added plus…$10 for a 90 day supply even without proscription drug coverage!
I really appreciated how the video explained the article and would love to see a similar video that goes with this article “DIET PROTEIN AND POTASSIUM AND KIDNEY STONE RISK”. Thanks
Fredric L Coe, MD
Hi Terry, thanks for the comment. Others have expressed a liking for the videos, and I will do one on the protein article – for you. Fred
Hi Dr. Coe,
Thank you for these thorough and clear articles. Can you please comment on the intake of sodium in the context of a very low carbohydrate diet (less than 40g/day net). I am assuming that the studies above and elsewhere on your site were done in the context of a normal American carbohydrate load of between 100-300g/day. I have heard in the context of a ketogenic diet that sodium needs actually increase some. I am curious what you may know or studies you may know of that deal with urinary calcium excretion and net acid loads in the context of low fasting blood glucose levels. My husband (57) forms calcium oxalate stones ( 3 times since 45). He has a history of high fasting blood sugars but has now turned this around with a extremely low oxalate, very low carb (40g or less), higher protein (1.2-1.5g/kg day) diet. His fasting blood sugars are down from over 109 to 88 mg/dl. We are curious what effect on his kidney stone formation his lowered blood glucose might have and how that may or may not change the sodium recommendations included above. Thank you,
Fredric L Coe, MD
Hi Amy, If the diet produces high ketone loads for excretion, the ketones can promote sodium and potassium losses being negatively charged ions. I do know know the data concerning urine calcium response to reduced diet sodium during high urine ketone losses, but suspect urine calcium will be higher from the ketones. This kind of complexity is why he needs attentive physicians, and they need 24 hour urine testing to determine what is happening. I would suggest that 24 hour stone urines be done for monitoring and that urine ketones also be measured. Day to day management has to be from his physicians because this is complex physiology, but I suspect reduced diet sodium will always be helpful. Regards, Fred Coe
Thank you Dr. Coe,
He is about to do another litholink test to see where he is in terms of urinary output of calcium, sodium, potasium, etc. I do not suspect he is actually particularly ketogenic with high urinary ketones despite the low carb intake because his protein intake is higher as opposed to his fat intake being higher as in a typical ketogenic diet. His diet is high meat(1.5kg/kg), very low carb( 40g) , high but not crazy high fat intake.
I guess I am wondering if carb intake being exceptionally low influences sodium requirements or recomendations in the absence of ketones. He has been following a 90% carnivore diet. Mostly animal meat, a bit of onion, mushroom,etc, sometimes a few teaspoons of honey and a little fruit ( one serving or less per day). So his diet is not specifically ketogenic due to high protein intake but again blood sugars have been brought into healthy fasting ranges in the 80’s. The meat offsets the typical ketone production in such a diet.
People who go on low carb diets typically feel better with additional salt intake ( especially during initial transitions).
I guess I am just curious if you have heard of carb intake and higher blood sugar being a lever that affects calcium/sodium output. It is an unusual situation as so few people follow such a low oxalate ( near none), high protein diet. It is not well studied. The best resource I could think of for further info on such low oxalate, low blood sugar situations might be you and your team since you have done so very much with regard to treating stone disease through diet. I am very grateful for this by the way as there are so few doctors who focus on the effects of and are knowledgeable about the intricacies of diet in the diseases they treat. So thank you for any additional insight you might have.
Fredric L Coe, MD
Hi Amy, the only link I know of between CHO restricted diets and sodium is via ketones – they are anions and obligate sodium and potassium loss. High protein without high fat or carbohydrate is a special case. It causes depletion of body fat stores and weight loss if CHO intake is very restricted, so ketones form from one’s own fat. Later on, it is not healthy – good reading here is what happened with Lewis and Clark, 5 pounds a day per person of Elk meat and they lost body fat and were starving. Regards, Fred Coe
Thanks Fred! Great reference. Yes absolutely high protein low fat diets would cause starvation. Completely get that. Rabbit starvation situation. Elk can be extremely lean. Good to remember the importance of fat especially once body fat percentages get really low. I would assume lewis and Clark were in single digits by the time they did all that outdoor living and traveling. Thanks for reminding me. Well if the ketones create greater excretion of salt and potassium it must be why it is suggested to supplement salt while ketogenic. Again specific case here though while trying to fix stone formation. I guess litholink should be best guide here based on mineral excretion data. He has the test on order and will be very interesting to see where he is at. Thank you again for your response.
Could you please post link to article you mentioned re: Lewis & Clark eating lots of meat but starving? I searched online, but couldn’t find it. Thank you, and thanks for creating this article and video. It was very helpful.
Fredric L Coe, MD
Hi Chantal, It was in a book on the expedition and I cannot find it on the web – with a brief attempt. I suspect it was the well described problem of eating animals with no fat and also having no available carbohydrates. This latter – usually arising from eating mainly rabbits that have very little body fat – is well known as ‘rabbit starvation‘. Of course none of this happens in cities unless one pursues a drastic kind of diet. Regards, Fred