Thiazide Type Diuretics Reduce Stone Formation

The common thiazide type drugs in use today are hydrochlorothiazide, chlorthalidone, and indapamide. All three have been used in stone prevention trials and shown to have beneficial effects. A nice recent review is also the source for the drug structures pictured above.

I have obtained and studied nine trials. In all nine trials, there was a comparison – untreated – group. This spreadsheet contains links to the trial documents, but you will find it not easy to obtain the original publications unless you have access to a university library system. For this reason I have copied out the key data. Briefly, there were 330 controls, of which 149 relapsed (45%), and 314 treated subjects of whom 72 relapsed (23%), a savings of about half (23%/45%). That is the bottom line for this class of drugs.

Here is a picture of the 9 studies. For each study the left panel has a bar whose height is how many control – red, and treated – blue subjects it had. The right panel shows how many of the red and blue people made new stones.

It is obvious that there were no differences in new stones between control and treated people (right panel) in studies 1 and 6. These were both brief (see the spreadsheet). In the others, the treated – blue bars – were lower than the red controls. Trial 9 had no relapses in the treated group. (Trial 5 has two drug doses and one control group so the height of the blue bar for 5 on the left panel is the average of the number of subjects in the two dose groups).

By now many of you will want some statistics. The spreadsheet depicts 9 studies each with numbers of treated and untreated people who did and did not relapse. Using ANOVA in which the numbers who relapsed is dependent, treatment or not is a categorical variable, and numbers of total subjects is a covariate, the mean number of relapse subjects adjusted for number of subjects was 16.1 in the control group and 8.3 in the treated group (p=0.008).

A simple X2 test using the four numbers from the bottom line of the spreadsheet: Treated, 72 relapse 242 no relapse; untreated 149 relapse, 181 no relapse gives a X2 of 35.2, p<0.001 (Yates’ correction is virtually identical for those who care).

I have deliberately included all studies that had a control and treatment group without fussing about the ‘quality’ of the trials. Several expert groups have reviewed these trials and a few more I omitted. Fink and colleagues in 2012 reviewed all available stone treatment trials. The same group did a similar review for the American College of Physicians which I did not think much of because of its codicils that seemed inclined to mediocrity – if not folly in practice. Escribano and colleagues authored an outstanding Cochrane review focused on thiazide.

The experts properly quibble about the intricacies of trial conduct and call for more trials. Personally I think more thiazide trials are of marginal importance and little interest. Mine is the untutored opinion of a bystander who does not perform trials as a profession. But I can count, and no one can tell me that the main fact – the pills reduce stone recurrence – will be overturned by trials of increasing ‘quality’. That is very unlikely. So, why do them?

Thiazide is Not Used Alone

Because they can reduce formation of new calcium stones, thiazide type diuretics are co-equal with potassium citrate as a medication physicians can use for stone prevention. Thiazide works differently from potassium citrate, so the two drugs can be used together with additive effects.

But more to the point, diet and lifestyle changes are crucial for stone prevention and need always put in place before writing a prescription.

The goal is to lower supersaturation. Fluids will do this. So will reduced diet oxalate, or raising urine citrate and, in uric acid stone disease, urine pH. Reduced sodium diet will lower urine calcium, and that will lower calcium salt supersaturations. So fluids and diet come first. Aspects of living that promote dehydration are serious obstacles to prevention, and to learn what they are in a given person and some to ways around them is an art of considerable passion and value. 

Trials are all about the effect of a pill, and that is a virtue. But no doctor who practices stone prevention with a mere pill can achieves the joyous satisfaction of an accomplished clinician. So all I want or need from trials is to know the pill can reduce stones – presumably by reducing urine calcium, and thereby feel justified to add it into my instruments of practice, which I had done decades ago.

Why Use Diuretics?

It is Not to Raise Urine Volume

Because of the name one might think the drugs work by increasing urine volume, and therefore prevent stones the way water or other fluids might. That is not the case. Diuretics raise urine volume only transiently. Urine volume is set by how much extra water is available for urine loss. After a short while on any diuretic, the average day’s urine volume will be no different taking a thiazide than it would be not taking it.

They Lower Urine Calcium and Urine pH

How they do this is a matter for some detailed commentary, but let us begin by saying they do indeed. When physiologists comment on how this occurs the correct answer is that they lower the urine calcium by stimulating the kidney tubule cells to reclaim back into the blood a higher than usual fraction of the calcium that the kidneys filter out of the blood in the usual course of their functioning. How they lower urine pH is not well known.

But higher calcium reabsorption, though true, could not lower urine calcium for very long any more than reducing the radius of a bathtub drain can lower the flow of water out of the tub whose faucets are open. If you did that, narrow the drain of such a tub, the water would rise until the greater weight of the water column raised outflow back to match the inflow from the faucets or the tub simply overflowed onto the bathroom floor. The amount of calcium in the urine every day is exactly the amount entering the blood from diet and bone. So thiazides have to somehow alter that inflow – either reduce diet calcium absorption or promote calcium entry into bone. It is mainly the latter they do, so they are not without some potential to maintain bone health.

They Must Lower Calcium Salt Supersaturations on Average

This is an old theme on the site. Reduction of supersaturation will lower formation of stone crystals and eventually stones. Given a random variability of urine volumes, and of other key factors that control supersaturations for calcium oxalate and calcium phosphate – eg. excretions of oxalate, phosphate, citrate, and urine pH, a fall in urine calcium from a drug will inevitably lower supersaturations on average unless that drug systematically raises urine oxalate or phosphate excretions, lowers citrate excretion, or alters pH upwards – calcium phosphate. In fact, thiazides can lower urine citrate, probably in part because they deplete body potassium stores and lower the pH inside kidney cells, but that can be corrected by potassium repletion. Lower pH from thiazide will specifically reduce calcium phosphate supersaturation.

How do Thiazides Affect the Kidneys?

Calcium and Sodium

With a brief blush and downward gaze, I choose our own publication as perhaps not unreasonable as a source. Partly I am guilty of favoritism, partly we are the only group to have studied individual stone formers before and during thiazide treatment in a clinical research setting on a constant diet. We did do this, and the results, if perhaps not exactly arising from a multitude, are secure in their precision and in their depth of insights.

revised figure one with proper units for feli and fecaFour men with calcium stones and idiopathic hypercalciuria were studied in our CRC before (gray symbols) and after 6 months (black symbols) of chlorthalidone, 25 mg daily used in treatment for stone prevention.

We have spoken of filtration and reabsorption elsewhere on this site. The drug had no effects on glomerular filtration, and therefore on the filtration of sodium and calcium. It lowered urine calcium – as expected – but did not change urine sodium excretion.

Fasting (circles) and fed (triangles) but not overnight (squares) the drug lowered urine calcium excretion (Figure to the left, upper left panel) shown here as millimoles/hour. The effect was statistically significant fed because of the large number of observations; fasting it was more marked but we had fewer measurements so formally speaking it was not significant. Overnight there was no change at all.

The fraction of the filtered calcium excreted (upper right panel) represents how the kidney tubule cells alter their reabsorption of filtered calcium – a highly regulated process. Both fasting and fed, that fraction fell markedly with chlorthalidone and both effects were statistically significant. Note that you can make these fractional excretions into percents – multiply by 100 (0.04 = 4%).

Lithium is everywhere, in our water and our food in minute concentrations. It has an odd property. Part of the kidney unit – the nephron -, that part closest to the glomeruli and therefore called the proximal tubule, handles lithium and sodium more or less equally, whereas the latter parts of the nephron do not handle them equally but let most lithium go by into the urine.

This tiny fact lets us sort out where along the nephron thiazides might have their main effects. Fasting and fed, chlorthalidone raised the fraction of filtered lithium reabsorbed in the proximal parts of the nephron so that less went forward into the later parts of the nephron (Lower left panel of the figure).

Here is a fact. Calcium and sodium and reabsorbed along the proximal nephron more or less in parallel. So by knowing the fraction of filtered lithium and therefore the fraction of filtered sodium sent forward, we also know the fraction of filtered calcium (lower right panel), That fraction falls with chlorthalidone. As a result, the early portions of the nephron conserve more calcium with the drug than without, and that is one part of why the urine calcium falls.

My article on idiopathic hypercalciuria is an excellent primer and overview of lithium clearances and proximal vs. distal nephron calcium handling.

Acidity of the Urine

Chlorthalidone, and presumably other thiazide type drugs make urine more acidic. Fasting (upper left panel of figure, circles) the effect is small: Chlorthalidone points (black circles) are just a little to the left – lower pH more acid – than without the drug. But overnight, the four black squares are far to the left meaning the urine is a lot more acidic with the drug. Fed (Upper middle panel) the same.

6 plot of sscaox sscap and urine pH fast and fedThis matters a lot for supersaturation with respect to calcium phosphate, not so much for calcium oxalate. Therefore, although the calcium oxalate supersaturations with and without the drug are barely different (right upper and lower panels) those for calcium phosphate are much lower with the drug (lower left – fasting and overnight and lower middle panel – fed).

This makes thiazide type drugs ideal for preventing calcium phosphate type stones and calcium oxalate stones. They can prevent the former because they lower calcium phosphate supersaturation via both reduction of urine calcium excretion and urine pH. Calcium phosphate stones  form on plugs of calcium phosphate in kidney tubules or perhaps just in the urine itself, driven by supersaturation.

Calcium oxalate stones are more complex. They form on the surfaces of the renal papillae over deposits of calcium phosphate in the kidney tissue (plaque). A crucial initial step in this process involves the laying down a film of calcium phosphate over plaque. Calcium oxalate then deposits from urine on top of this initial film to make the stone. So thiazide acts in two ways to reduce calcium oxalate stones: by lowering calcium phosphate supersaturation and therefore hampering formation of the calcium phosphate film needed for overgrowth of calcium oxalate on plaque, and by reducing calcium oxalate supersaturation itself.

Note that the nine trials concerned calcium stones, and did not always distinguish between those that did and those that did not contain appreciable percentages of calcium phosphate.

I have not discussed here how thiazide lowers urine pH. That would take us too far afield. The original article points to changes in intestinal uptake of alkali, which seems to be reduced by the drug.

Urine Oxalate

In our paper reviewed above we found no changes in urine oxalate with chlorthalidone, and did not therefore include oxalate data in the tables. In the past we have published a rather large group of patients who were put on thiazide and exhibited no increase whatever in urine oxalateI do not believe it is likely that thiazide treatment raises urine oxalate. 

How Do Thiazides Lower Urine Calcium?

I have said it is not just by acting on the kidneys, for that is to close down the drain – the bathtub will overflow perhaps but you cannot reduce the flow out of the drain for long that wayThis is a sometimes overlooked point when people speak about urine calcium losses.

sca ccr flca uca fourplot by food and by thiazide or notWhat happened in our patients must have been a fall in absorption of calcium from food, or an increased uptake of calcium into bone, because multiple measurements of serum calcium – the water in the bathtub – were almost unchanged despite a fall in urine calcium.

But almost is not quite unchanged.

Serum calcium – the upper left panel of the figure, rose significantly with thiazide. The amount of calcium filtered from blood into the kidney tubules (lower left panel) did not change significantly – the error bars overlap -, because filtration itself – (upper right panel) also varied. As I already showed you, urine calcium fell (lower right panel).

So the picture does have in it a bit of the bathtub with a somewhat closed drain – the water level, serum calcium, rose.

Now, I am about to leap into conjecture: Possibly, this increase in serum calcium could promote near instantaneous movement of calcium into bone by sheer physical chemistry.

A body of work that is perhaps more obscure than it should be, edges toward the idea that a portion of bone mineral, brushite in fact, may be in physical chemical equilibrium with blood so that large amounts of calcium can move in and out of bone mineral without any necessary cellular control.

This latter is critical, because bone cell process hours to change in response to hormones whereas urine calcium, as an example, can rise within a few minutes and yet serum calcium remain unchanged or even rise slightly as seen here.

This colorful picture (shown below) is similar to much of what we have often discussed on this site. To the left is diet calcium coming in and leaving, the absorbed calcium entering the ECF or extracellular fluid – we have approximated this as blood. Kidneys can release calcium, as noted.

The big addition is that a large amount of calcium may well be circulating between blood and bone – the 6,000 mg in the middle of the picture. This exchange is affected by serum phosphate, drugs like anticoagulants that alter bone mineral modifiers, and other factors. Of the 6,000 mg of calcium that enter and leave bone every day, only 400 mg go into the slowly exchangeable bone pool which is our familiar hydroxyapatite – the majority of calcium phosphate stones and the principle stiffener of bone.

calcium bone balance from Picklbauer and mayerWhat if, when kidney conservation falls – the drain opens – calcium leaves the exchangeable pool so the ‘faucet’ opens. What if, when thiazides raise conservation, the slight rise of serum calcium – from diet inflow perhaps – is just enough to nudge calcium flow into bone?

In other words, envision that bathtub. As we eat, the drain opens, the diet ‘tap’ opens, and bone comes into a kind of balancing act: If diet inflow is large enough calcium flows into the exchangeable bone mineral – brushite – pool. If not, calcium flows out. Thiazide clearly tightens the drain, the diet is the same with and without the drug, so possibly diet calcium inflow is raising blood calcium a bit and calcium is moving into bone.

If I were young I would test this idea in humans.

Effect of Thiazide on Bone Mineral Balance

All this raises an obvious question: Do thiazides improve bone health, reduce fractures, increase bone mineral content?

A recent review summarizes a large amount of evidence that they do indeed reduce fractures. The data, from the Danish population, suggest that duration of continuous treatment is more important than dosage in fracture prevention. In particular, fracture risk appeared to increase during the first year of use but then fall progressively. A Cochrane analysis concludes that all evidence to date – 2011 – supported this idea of reduced fractures, albeit there were no prospective controlled trials. Several such trials subsequently confirmed that thiazides maintain or increase bone mineral. Dalbeth and colleagues describe a link between rise of uric acid and bone mineral with thiazide implying a possible causal linkage not otherwise tested.

The overall impression is that one would not win by betting against thiazide as helpful to bone.

By now you might be asking if stone formers are at risk for bone disease. A recent long term followup of nurse and physician cohorts showed an increased risk of wrist but not hip fractures. Our article on idiopathic hypercalciuria summarizes additional information linking it and stone disease to fractures.

How About Salt?

As their prime purpose diuretics cause renal sodium wasting so that for any given intake of sodium the total body sodium stores will be less than without the drug. This is perhaps a main reason why they can reduce urine calcium via increase of proximal tubule calcium retention and also reduce blood pressure.

From this, one might think that low sodium diet might be like thiazide and help with bone mineral balance. In the one really ideal study testing this idea it was correct, and I have summarized that work in another article on this site.

Clinically, reduced salt intake is critical for successful thiazide use. From its basic physiology, high sodium intake will essentially undo the effect of the drug, and raise urine calcium. More, thiazides cause losses of potassium and lower serum potassium, and this is worsened by high salt intakes.

A caution. Thiazides can lower serum sodium levels, especially in older people, and this site advises reduced sodium intake which could increase that risk. In general diagnosis of low serum sodium was made 19 days after initiation of treatment (95% CI 8, 31 days). For this reason physicians invariably monitor serum electrolytes after a few weeks of treatment, and should do so after a few months, and at reasonable intervals, as well.

Is One Drug Better Than Another?

I think so. For example, hydrochlorothiazide has been used 2 times a day in the stone trials, whereas indapamide and chlorthalidone are long acting and needed once a day. People can forget the second dose. It is said that hydrochlorothiazide causes less of a fall in serum potassium but at least in hypertension trials it is less potent so you need more and when more is used it is the same as the other two drugs with respect to potassium, and dosed twice daily.


I like to start with lower doses than used in the trials. For chlorthalidone, 12.5 mg (1/2 of a standard 25 mg pill) is enough for most people. For hydrochlorothiazide I like the 12.5 mg pill twice a day – short acting. For indapamide I like 1.25 mg pills. Chlorthalidone and indapamide are long acting so the pill is once a day.

What Have We Learned?

Thiazide drugs can reduce stone recurrence at least in part by reducing urine calcium loss and supersaturation. They act on the kidney but also seem to improve bone mineral balance and reduce fractures. While stone prevention is certainly not accomplished by one pill, thiazide is an important part of what physicians can offer for prevention of stones.


  1. Denise

    Hi Dr Coe! What a fabulous site you have created. Thanks for your generosity! I am a 120lb female with 300 urine calcium and urine sodium at 115 and I make calcium stones. I am trying to find a general rule of thumb for how much to expect urine calcium to decrease using
    1. HCTZ 12.5 once a day
    2. HCTZ 12.5 twice a day
    3. Chlorthalidone 12.5 once a day
    4. Chlorthalidone 12.5 every other day.
    I thought I read you generally expect #3 to reduce calcium by 100 but I am wondering how these other meds/dosages might compare in your mind. I know there are no guarantees but your vast experience is appreciated. Thanks!

    • Fredric L Coe

      Hi Denise, You ask a very good question. My only data – much of it not published, some extracted from trial data – shows the 100 mg fall in urine calcium from what is expected given the urine sodium. For you, as a general rule, lowering your diet sodium from 115 to perhaps 60 or 65 will get urine calcium down by 75 to 100 mg, and chlorthalidone 12.5 mg daily will get you another 100 or so mg/day – as a rule. No two people are alike, the data spread a lot, so you will have to get 24 hour urine testing to find out. The sodium step is very powerful, and if you can do it you may not even need the drug. Regards, Fred Coe

      • Denise

        Dr Coe,
        You are a gem!! After reading your response a lightbulb went off! I finally understand the power of sodium reduction. You see, I was deluded into thinking my sodium level of 100 was good based on comments from 2 different urologists saying it was low and both explaining there would be no benefit to reducing it further. As such, I believed the 100 sodium level signified I was successfully implementing the 1500mg diet. Boy, I was fooling myself. I understand now my diet sodium was actually 100/.044 – 2300mg not 1500mg. I clearly have more work to do. Your quick analysis illustrating possible results of a low sodium 1500mg diet applied to my situation was impactful and gave me the strong motivation I needed to put in the extra work to successfully implement my low sodium diet. I have received 3 different scripts for medication and have been so close to just medicating for the rest of my life. I emphatically wish to avoid medication. I am so happy I held out and continued to educate myself on your site. I feel empowered to control my health. I am thankful you are in a position where you can not only educate other doctors at U of Chicago but also millions of people like myself who read your site. Please know, Dr Coe, you are extremely valued and the generosity of your time and talents is both admirable and remarkable. Thank you!

        • Denise

          Correction – meant to write current sodium of 115 = 2613 mg rather than the 1500mg.

        • Fredric L Coe

          Hi Denise, Thank you for your supportive remarks about the site, and also for being so preceptive about your own care. If you do achieve a lower urine – diet – sodium, urine calcium will be at that level one can reasonably attain with diet sodium management, and I presume with adequate diet calcium of 1000 mg or 1200 mg daily. At that point one can use the meds if needed. One can expect a fall of 100 mg of calcium below what diet sodium yields using either K citrate or a low dose of chlorthalidone of 12.5 mg. I said this before but here is the article showing the data. You are right about numners. About 3 million people have come to this site since I opened it in 2015, so it is hopefully helping a lot of people. If you like irony, these numbers exceed by orders of magnitude those who have read my scientific papers (300 or so published) and books, reviews, chapters etc (another 300 or so) in aggregate – probably no more than 10 thousand albeit mostly physicians and scientists – over the 50 years of my career. Regards, Fred

  2. GMP

    How long one should use this hydrochlorthalidone or diuretics after an incidence with calcium oxalate stone

  3. Lois Wag

    Hello Doctor,
    I have recurring kidney stones which started apparently from bad parathyroids (my mother also had this). I had 8 stones and 3 1/2 parathyroids removed in 2016. My doctor has had me on hydrochlorothiazide 12.5 mg ever since. Two new small stone have formed since then. I’m told to take this medication in the morning, 1 per day, but I have read some literature that says it is better to take it at bedtime. Does it matter? Is it OK to be on this medication long-term at this low dose? Thank you

    • Fredric L Coe

      Hi Lois, We have published that hypercalciuria is common after cure of hyperparathyroidism. Assuming your serum calcium is normal – meaning surgical cure – the drug is reasonable, but you have had recurrence. One possibility is that the drug and/or dose is/are less than optimal. I have always favored chlorthalidone, 12.5 mg over OHCTZ as being very long acting. But for either drug you need to control diet sodium for it to work and be sure via 24 hour urine testing that what you are taking has indeed reduced urine calcium below the risk limit of about 200 mg/d. Regards, Fred Coe

  4. Andrea

    I had Total Thyroidectomy August 2019 for Thyroid Cancer. My parathyroids were not functioning after surgery. I was given a calcium infusion while in the hospital and re-hospitized the day after requiring another calcium infusion. For 6 months after surgery I was taking up to 8000mg orally of calcium daily and my numbers were barely if in range. I now take 3600mg daily and I still have days of symptoms ie, tingling in my lips,face,feet and fingers. I did a 24 hour urine and my numbers were 468mg (100-300) range. Endocrinologist has prescribed 12.5 mg of hydrochlorothiazide once daily. I take Calcitriol 2 x daily along with potassium & magnesium. Does this sound right? I’m worried about getting stones.

    • Fredric L Coe

      Hi Andrea, You do indeed have a problem, and a famous one at that. Your bones are a taking up calcium and your kidneys are not conserving it, and stone risk is real. After a while things will get less extreme. IN the meantime high fluids – a gallon of fluid a day – is your best protection. Your physicians can consider replacement PTH but it is injected, complex, and fraught with possible risk, so that is a very complex decision. Regards, Fred Coe

  5. Anna B.

    In patients with a history of calcium-containing kidney stones who also have gout, or in patients with a mixture of calcium and uric acid containing stones, would thiazides still be beneficial? Or would you expect the benefits of reduced urinary calcium excretion to be offset by the increased uric acid?

  6. Eva Pearl

    I recently had my first kidney stone at the age of 25, which required an unpleasant procedure to break up. I had begun taking Edarbyclor 6 months ago for high blood pressure. Do you think this drug could have caused or contributed to the formation of the stone? The drug includes a diuretic (12.5 mg chlorthalidone), but not the one you recommend, should I use a different BP drug to reduce chance of more kidney stones? Thank you, Eva.

  7. Lesley P.

    I take Topamax for Epilepsy and have calcium oxalate stones. I’ve had stones for about 17 years and have passed several and currently have 6. They are relatively small-no surgeries or stents. I take potassium citrate 15 meq at least once a day, twice if I can remember. Years ago Hydrochlorothiazide may have been mentioned, but I’m not sure why it wasn’t pursued. Possibly because my blood pressure runs on the low side? Stopping the Topamax is a thought and I do take other anticonvulsant meds, but it’s a difficult decision to make. What is your opinion on Hydrochlorothiazide and patients with low blood pressure? If I follow a lower sodium diet, drink enough fluids, eat fruit and vegetables, cut down on refined sugars, is it necessary to decrease protein intake? I try to use a 30-40-30 calorie ratio- 30% protein, 40% carbs, 30% fats.

    • Fredric L Coe

      Hi Lesley, Topamax causes a form of renal tubular acidosis and stones are usually calcium phosphate. No drug really can offset stones from Topamax. Ideally you would be on another drug if possible. Potassium citrate and hydrochlorothiazide are not likely to help prevent more stones. But in the final decision, your personal physicians need to help you weight the balance between more stones and problems of changing drugs. Regards, Fred Coe

  8. Deborah Courtney

    Hello, I had calcium oxalate kidney stones that required surgery to remove. Follow up ultrasound showed calcifications of the renal papilla. I am on a low oxalate diet and drink 1.5L water daily. I have just been prescribed hydrochlorothiazide 12.5mg once daily. I don’t consume any dairy products and am confused about how much calcium to supplement my diet. Also, would the addition of potassium citrate be helpful? Thank you, Deborah

  9. Elizabeth LaBoone

    I am being prescribed hydrochlorothiazide 12.5 bc of calcium leakage in my urine. My bone density readings this year decreased significantly and the Dr. wants to try this. With the bathtub analogy above I am concerned that it might be futile. I have never had a kidney stone and am otherwise quite healthy (weight 100 lbs.) and exercise daily. Should I also reduce my sodium intake?

    • Fredric L Coe

      Hi ELizabeth, I presume you have idiopathic hypercalciuria and bone disease with it. Indeed lower diet sodium is valuable for maintaining bone balance, and allows the thiazides to work better at lower doses. The combination of low diet sodium with high diet calcium has been proven to cause positive bone mineral balance, as well. If bone mineral keeps falling your physicians should consider bone active drugs in addition to these measures. Regards, Fred Coe

      • Elizabeth LaBoone

        I have osteopeonia, and am trying to do my best not to get into full osteoporosis. I met with a dietician to increase my calcium intake without taking calcium pills and she was able to provide some ideas for higher D and calcium foods. Is it inevitable that I will develop osteoporosis?

        • Fredric L Coe

          Hi Elizabeth, High calcium with low diet sodium (1500 mg) was shown to produce positive bone mineral balance in one very well done trial, so I can recommend that combination without reservation. So it is not inevitable. The real problem is to intervene early so as to minimize need later on for more bone active drugs that all have their problems. Regards, Fred Coe


Leave a Reply