The painting by van Gogh, The Sower with Setting Sun (1888) Kroller – Muller Museum, Otterlo, Netherlands, has no obvious connection to this article unless you have read Nellie Hermann’s essay on the former mining district of Belgium called the Borinage. Writing in the Paris Review, she reminds us van Gogh lived there in the 1880’s amidst active coal mines now long obliterated.

He based his painting on an earlier (1850) painting, The Sower by Jean-François Millet (1814–1875). The artist sold it in 1851 to William Morris Hunt (1824-1879), Boston, where in 1917 Quincy Adams Shaw, Jr. (who inherited it) and Mrs Marian Shaw Haughton donated it to the Boston Museum of Fine Arts where it resides. It seems unlikely van Gogh ever saw the original but only copies.

Millet painted in France, and van Gogh appropriated the lush fields into this painting that he made in a simple wood house facing an active coal mine.

There are, of course, no mines or mine shafts in either painting, nor a canary, just the brilliant yellow of the van Gogh and the place he painted it in with its dangerous and decaying mines. He wrote “This mine (Marcasse) has a bad name because so many die in it, whether going down or coming up, or by suffocation or gas exploding, or because of water in the ground, or because of old passageways caving in and so on. It’s a somber place, and at first sight everything around it has something dismal and deathly about it.” 

Why Write about Canaries, and Mines?

Canaries Signalled Danger

Mine gases – lethal from inhalation or explosion – killed caged canaries before they killed people. So the birds stood as warnings, if ill or dead. The use of canary birds may have originated from the advice of John Scott Haldane who first identified carbon monoxide as a major toxic mine gas. 

Stone Forming Seems to Signal Danger from Other Diseases

In a simpler time, when stone formers were just people who formed kidney stones, we had no need for metaphor or simile. They were what we saw them do, and we strove to stop their doing it.

We now know much more.

Stone formers are at increased risk of bone disease, hypertension, kidney disease, and vascular disease.

Almost no one, myself surely, has any reason to believe that for the most part all of this extra burden of disease arises simply from formation and passage of stones. While it is possible that inflammation and injury from stones leads to smoldering kidney disease and thence to vascular disease, even one stone raises risk for hypertension. And bone disease is often found when kidney function departs in no way from normal. Many, myself included, believe idiopathic hypercalciuria causes bone disease when diet calcium is inadequate, but there may be other reasons as well.

A Small Part is Obvious

Systemic Diseases Cause Stones

Well known systemic diseases cause stones and additional systemic diseases. Primary hyperparathyroidism is perhaps the most obvious example. It can evade detection, raise blood pressure, damage kidneys, and demineralize bones. Renal tubular acidosis, and myriads of rare hereditary kidney diseases cause stones, kidney damage, and bone disease. Varieties of bowel disease, including obesity surgery cause stones and can cause kidney disease. Cystinuria causes stones and is, like RTA, a kidney disease in that major transporters are abnormal. Hereditary hepatic enzyme defects cause primary hyperoxaluria that often leads to dialysis and transplantation. Defects of hepatic CYP24A1 can cause extreme hypercalciuria.

We have well established panels of testing for the purpose of screening, and good guidelines to proceed to diagnosis and specialized treatment of all of these important causes of stones. One might say it is unusual for any physician to miss a systemic cause of kidney stones, or to fail of proper treatment. So while systemic diseases might contribute to the linkages between stone forming and kidney, bone, and vascular disease, they are a minor part of the whole, and we have excellent means for dealing with them.

Uric Acid Stones

These occur when urine pH is too low, and very often that low pH arises from diabetes or a complex disorder of acid base balance. Patients are often obese. Older people predominate, and they suffer from the effects of age. So for many reasons, uric acid stones and vascular, kidney, and bone disease would appear to coincide. Even so, uric acid stones represent perhaps 10% of the total stone population, and are not a likely reason for the population wide linkages observed between stone formation and hypertension, and kidney, bone, and vascular disease.

Struvite Stones

Struvite stones arise from infection with urease possessing bacteria, and can injure kidneys because of their large size and the infection itself. They are a minority of stones, and like uric acid stones unlikely to have caused the disease linkages I have already mentioned.

The Large Part Is Not Obvious

It is among the majority of people who form stones, so called idiopathic calcium stone formers, that epidemiologists have discovered links to vascular, bone, and kidney disease, and their discoveries are puzzling and call for new thoughts about mechanisms and what they might mean for patient care.

Stones Seem a Biomarker for Other Disease Risks

One way to respond is surveillance. Those who form stones have called attention to their increased risks, and deserve a higher than usual surveillance for the diseases those risks represent and also whatever we can do to reduce risk. That is a proper clinical response, and I advocate for it.

Perhaps Diet Promotes Stones, and Cardiovascular, Renal, and Bone Disease

A more subtle response might concern why all these risks associate with stones, and what that association could mean. Do all the recent evidences of disease risks, though each one modest, support a new direction of thought concerning what appears to be a manifold of disease linkages?

I have written a lot on this site about how high diet sodium, low diet potassium, excess protein loads, and refined sugars can promote stone formation by raising urine calcium and reducing urine citrate. Likewise, many have put forward substantial evidence that low calcium diet can cause bone mineral loss with especial vigor in people with idiopathic hypercalciuria, a common trait among stone formers.

Other research communities have ample evidence that high diet sodium and low diet potassium contribute to hypertension.

Likewise, obesity is linked by epidemiological data to increased kidney stones, and also to cardiovascular and kidney disease, and to diabetes, itself a major cause of both. While explained by no single cause, the modern acceleration of obesity surely arises in significant measure from population wide increase in fructose consumption from common table sugar, and sweetened beverages. We also know that modern recommendations to increase diet calcium aim at reducing onset of osteoporosis. 

In other words, our modern diet predisposes to kidney stones via mechanisms specific to stone formation and to renal, vascular, and bone diseases via mechanisms specific to those diseases. This simply leads one to recommend improved diet for all US people, which is exactly the burden of our government’s message.

Perhaps Not All People are Equally Susceptible

But only some fraction of people who eat too much sodium, too little potassium and calcium, too much refined sugar, or just too much altogether develop any obvious disease. Many escape, meaning they are relatively less vulnerable to obvious risk factors that in other people cause manifest disease. For example, average diet sodium consumption is about 200 mEq/d, double the tolerable upper limit, but large numbers of people do not have hypertension. Likewise, only some people develop osteoporosis despite a population – wide calcium intake viewed as below ideal. Well known, a majority of hypercalciuric people do not form kidney stones. In fact, it is this very remarkable variability that has always made diet recommendations so difficult. If a given diet universally caused disease, diet planning would be far more simple than it is.

Could These Diet Vulnerabilities be Linked?

Presumably, stone formers are more vulnerable to diet than the average person and therefore form stones.

What if that increased vulnerability to diet is linked across stone forming, hypertension, vascular disease, kidney disease, and even diabetes?

In other words, what if stones give an obvious sign of an abnormally high diet vulnerability to more serious, if initially less obvious diseases?

Put as crudely as possible, perhaps stones are a biomarker for increased susceptibility to other far more sinister diseases from our common and unhealthy diet. 

If This Were True

Primum Non Nocere

When you combine this enduring precept with my speculation that stones mark for manifold disease susceptibilities from diet, we get a basis for action. If Improved diet for a stone former might help reduce not only stones but an abnormally high risk for a manifold of diseases, to omit efforts at diet improvement for stone formers is, so far as we can presently tell, to do harm.

Harm arises not only because of stones – we possess other treatments to prevent stones. But because we suspect stones mark abnormal vulnerabilities from diet to a wider and more dangerous group of diseases.

Therefore, safest is to alter diet in those directions that decades of research have established as reducing risks for stones and for cardiovascular, renal and bone disease. Here in the US we have remarkable amounts of research available concerning how to eat in a healthy way.

The precept to avoid harming patients is, incidentally, of unknown origin, and appears to have been promulgated mainly orally. Its use in the US originated – according to this scholarly article – in the early 19th century. It is surely not from the extant works of Hippocrates. 

Correct the Diet or Get Someone to Correct It

The kidney stone diet, my name for what is in fact the US ideal diet according to the vast assemblage of experts who create the US diet guidelines, can reverse many crucial urine stone risk factors, and has one excellent trial. It is safe, effective, and might well reduce risk for kidney, cardiovascular, and bone disease in this specially vulnerable population.

It Synergizes with Other Stone Preventions

The high diet calcium in the diet lowers urine oxalate markedly, saving patients much of the onerous bother of following oxalate lists to their final detail. The lower diet sodium reduces potassium wasting from thiazides, should they be needed, and the high potassium in fruits and veggies provides potassium repletion.

It Directly Benefits Patients and their Families

High diet calcium helps preserve bone mineral. Of course a high potassium low sodium diet is against hypertension, and the high potassium foods are a source of alkali that functions exactly as would potassium citrate supplements.

Less refined sugar will reduce spikes of calcium, and the Stanhope trial has proved that fructose – 1/2 of table sugar – causes insulin resistance in normal people in only 8 weeks and is therefore a powerful drive toward diabetes.

Moderation of protein can prevent unnecessary high urine calcium levels caused by protein mediated increases of diet calcium absorption and perhaps protein based acid loads.

Given that stone forming is strongly heritable, diet changes in one family member that spread to others around the table may help lower their risks of stones and its associated diseases. This could be especially important for children.

Four Brief Precepts

Here are some ways of making my one point within a few of the common situations we all encounter.

Change Diet First

Because to neglect diet is possibly a harm, always begin with diet change and do as much as possible. High fluids are fine, meds are fine, but to me should be on top of a proper diet, as needed. 

Shun ‘Just Drink More’ as a Sole Treatment

It will not do to just push fluids in hopes stones will stop. They may well stop, and even so the patient remains incompletely treated.

A large trial of just water seems inevitable, however odd one might think such an expense of money and spirit. It will of course reduce stones. We must not let that distract us from what else we need to do.

Shun Pills and Remedies as a Sole Treatment

LIkewise for thiazide or potassium citrate or both together. They may work well and, as with fluids alone, risk remain for other disease because we did not correct the diet. 

Multiple companies presently plan new drugs to reduce urine oxalate excretion. I hope they emerge from research into practice, and help in stone prevention. But the same for them. Lowering urine oxalate will not by itself correct the diet, and if the diet causes multiple disease it will remain a hazard.

Pills are great, new pills, too, but the diet remains an untreated potential menace the pills may not counter.

Shun Single Diet Changes as a Sole Remedy

The almost universal diet oxalate list will not do either for stones or the disease manifold. Likewise for piecewise suggestions like ‘eat less salt’. As for drinking lemon juice, and all other well intentioned nostrums, consider them just that. We need to change the diet to the US healthy people diet. To the diet we should eat, all of us.

I Know We Lack Proof

I do not write as if I knew that diet is the reason for the many increased disease risks of stone formers. I do not know this. It is speculation at this time.

But the speculation leads to a potentially useful interim approach to stone forming patients that is itself likely to do more good than harm for everyone, patient or not. While we wait on the slow progress of science, we can act toward a larger health aim than stone prevention alone by taking literally the idea of ‘Primum non nocere‘.

I am no therapeutic nihilist, in theory or practice. I do not advocate we give up what we have by way of useful treatments against stones. I merely mean to say that preventing stones per se is not a complete goal in stone formers given what we now know.

Speculation is the Forerunner of Hypothesis

The idea that stone forming marks abnormal diet based vulnerability to a manifold of diseases is speculative, and as such the earliest stage in science. But though early and prone to eventual disproof, the speculation leads to useful suggestions for physicians. 

My Speculation Fits What Has Been Observed

In the 14th century, speculate meant intelligent contemplation, a meaning consistent with its Latin root specere – to look at or view, and its Proto-Indo-European (PIE) root “spek” – to observe. Speculation as something ‘mere’ arose a century later, an idea disjunct from the root source.

If we are to remain true to the word, we have to contemplate what we have, and reason accordingly. Right now nothing obvious contradicts the speculation of diet vulnerability to a manifold of disease, so it is a basis for action until we have better.

Hypothesis Surpasses Speculation, but Time Runs On

Hypothesis, speculation’s successor, consists not only in our viewing the world intelligently but in imagining the causes of what we know and can observe and fashioning experiments to test the imagined causes. For example, the brilliant experiments of  Kimber Stanhope tested the imagined effects of fructose to cause insulin resistance and de novo increase in hepatic lipid production, two key mechanisms through which sugar can cause vascular disease, obesity, and diabetes.

We need this kind of science for diet change in stone formers, but it will take a while to get it done.

We Can Act While We Wait

Given that diet change has no harms, and lack of change has possible harms, I am opposed to waiting, perhaps for years, until – if ever – we have proof in stone formers of benefit. Decades of study point to proper diet structures, and all I call for is that we deploy them for our patients.

I Know Diet Change Is Difficult

Once people have dangerous disease, physicians expend considerable money and time on diet. For example Stage 4 CKD is a time for concern about diet potassium and phosphate. Dialysis even more so; great efforts are warranted to control excessive fluids or sodium, and especially potassium. When bones fracture from idiopathic hypercalciuria or other forms of osteoporosis, very costly drugs are appropriate, and calcium supplements. For diabetes with nephropathy and retinopathy and neuropathy we spare no amount of time and cost on expensive treatments.

But skill is late. Long before, when organs and tissues function well, that is when we can get the most benefit from diet change. If indeed stone formers have even modest excess risk for these terrible diseases, and the very same diet that can reduce their stones can reduce these other risks, how else can we better manage things than by using diet – whatever the difficulties.

Closing Repetitions for Emphasis

If it is a reasonable speculation that stones mark out those who cannot tolerate our modern diet without increased risk of serious disease, then it is harmful to elide diet efforts, to put away the trouble of diet counseling against new stones. If sensitivity to our modern diet causes stones as part of a manifold of disease, we need to assume that a diet that reduces new stones has the potential to reduce risk of the other diseases in that manifold.

I propose it is proper to use whatever we have to prevent stones, but always to correct the diet in a direction aimed at that same goal – stone prevention, because it may be that other systemic diseases may be avoided or minimized, or delayed through that one therapeutic effort.

I would deny no one my most passionate efforts to improve diet according to what we know presently as sound until science’s superb surprise enlighten us as to the final truth of the matter.

Scroll to Top