Perhaps the most common abnormality among calcium stone formers, idiopathic hypercalciuria (IH) causes calcium kidney stones and can lead to bone mineral loss and fracturing bone disease. Proper treatment requires a high calcium intake, a low sodium intake, moderation of very high protein intakes, and – not rarely – use of diuretic drugs which can lower urine calcium losses, prevent stones, and protect bones.
All this requires effort and belief. I have found that patients will change their diets and take medications only if they fully understand why such measures are likely to benefit them. That is why I have written this article.
Without apologies, here is that presentation.
As I did with salt, I have added summaries in bold italics.
Why The Bathers?
I placed the bathers here because nothing seems so fit as bathing for an explication and a metaphor for IH. Not these illuminated and immortal bathers, but the simple bather in a bathtub engaging with the flow of water as, in my terms, the kidneys, bone, and gut engage each other in the flow of calcium through the body.
LIkewise, as the images of bathers capture in canvas a far larger sensibility about life, the image of a humble bather and bathtub captures – I believe – a far larger truth about our bodies.
(1884-87) of Renoir and (1900-1906) of
What is Hypercalciuria?
High urine calcium ‘clinical hypercalciuria’ is a urine calcium excretion above 200 mg/day in either sex.
Hypercalciuria is the name we give to a high urine calcium excretion, but ‘high’ must mean something more than mere quantity. I agree with Dr. Gary Curhan that urine calcium is ‘high’ when it causes disease, as blood pressure is ‘high’ when it causes disease. And his criteria for ‘high’ are acceptable to me.
Association with Kidney Stones
I have already shown you Curhan’s results linking urine calcium losses to risk of stone disease. For two cohorts of women – red – and one of men – blue – increasing levels of urine calcium – shown along the horizontal axis in six bins – go with increasing risk of becoming a kidney stone former (Relative risk, on the vertical axis). A risk of 1 means no higher than among people with urine calcium below 100 mg/day – the reference population.
The average, or mean risk for forming a stone, is at the top of each bar, which is plotted from a base of 1 (the dashed line). The lower 95th percentile of risk is at the end of the solid bars which are also plotted up from one. When the top of the solid bar reaches above one, which is the case for all bars above the 150-199 bin, increased risk is very likely to be present present; that point of increased risk begins, in both sexes, around 200 mg/day. Throughout the range of urine calcium excretions, risk rises smoothly with urine calcium, which reinforces its significance.
Given this, ‘high’ urine calcium – clinical hypercalciuria – is above 200 mg/day in men and women, because above that level begins risk of at least one disease – stones.
What Does ‘Idiopathic’ Mean?
Many diseases can raise urine calcium excretion, but among hypercalciuric stone formers the vast and overwhelming majority have no disease but rather a familial and almost certainly hereditary tendency to excrete, on average, more calcium than people who do not form stones.
It is for this reason, they are said to have ‘idiopathic’ hypercalciuria – ‘idiopathic’ meaning high of itself, or without overt cause.
Do We Need Special Diets During 24 Hour Urine Collections?
I do not believe special conditions of diet are critical for determining if someone has IH. I say this because the Curhan data were assembled as things were. Some people were no doubt eating more, some less calcium or sodium.
That is not to say diet does not matter. It does. But if one wants to determine who has IH in practice, or choose people for experiments, I think it is reasonable to collect 24 hour urines without setting any diet requirements, and that is exactly how we practice here and, incidentally, do research.
Who, Then, Has Idiopathic Hypercalciuria?
Until someone corrects me I say a stone former with urine calcium excretion above 200 mg/day, either sex, is hypercalciuric. If no disease is causing hypercalciuria that stone former has IH.
For research, I might select for higher values. For example, above 250 or even 300 mg/day is a better choice if one wants to understand how the high urine calcium comes to be and chooses subjects who will give more robust signals in a research protocol.
Calcium Excretion in Normal Women and Men
IH is not a disease; it is simply the label for someone at the high end of the normal distribution – like tallness.
You can see how a urine calcium values from normal adult men (blue) and women (red) sweep from low to high in one unbroken distribution. People whose values are in the higher registers show up among stone forming populations at a higher rate than those with lower urine calcium losses. That is what the Curhan data show us: People who became stone formers during years of observation were those with higher urine calcium excretions.
See where the Curhan demarcator – 200 mg/day – resides; it is at about the 75th percentile: 25% of people are above it. But stone formers are certainly not 25% of adults. Perhaps 7-10% or less is a reasonable estimate of who will form at least one stone in a lifetime. So high urine calcium is indeed like high blood pressure: It confers risk, but risk will not always culminate in disease.
The 95th percentiles of these distributions, conventional cut points for extreme values, are at about 275 and 325 mg/d of calcium, and once were used for the definition of ‘high’ urine calcium. But if disease causation is the criterion, as it should be, they are way too high. It is like older definitions of ‘high’ blood pressure, which greatly underestimated the risk from values within the upper mid range of values from large populations.
I renounce criteria not long ago promoted by my colleagues and I: >250 mg/day women, >300 mg/day men, >4 mg/kg body weight either sex, 140 mg of urine calcium/gm urine creatinine. No doubt they confer risk of stone, given the Curhan demarcator. But they are too high and we should abandon them.
Hypercalciuria Raises Supersaturation
Urine calcium above 200 mg/day goes with high supersaturation and stones.
Stone crystals cannot know about how much calcium is lost in the urine, they can only respond to supersaturation. High calcium excretion, however, will associate with high supersaturation given the simple logic that for any range of urine volume, and of salt ligands – divalent phosphate and oxalate – more calcium in the urine will raise calcium concentration and therefore the critical product of calcium and oxalate (calcium oxalate crystals in stones) or calcium and divalent phosphate concentrations (calcium phosphate crystals in stones).
This article is a delightful window into stone prevalence in Tennessee that I chose because it illustrates two points and because it is probably not popular and could use some readers. In a study of uranium workers the authors found that 40/208 reported kidney stones, much higher than the 7% found in the NHANES 11 survey current at the time. They reported what Curhan has yet to report: Supersaturation, the central issue in crystal formation, was a good predictor of stone formation.
Calcium oxalate supersaturation is shown here in somewhat different units than those we usually present, but as it rises (horizontal axis of the graph) probability of stones (vertical axis) increases. Family history matters: Those with it get stones with less supersaturation.
You might ask by now, what about hypercalciuria in that population?
Those with stones had a calcium excretion of 250 mg/day, those without had a value of 164 mg/day. One was above, the other below the Curhan demarcator. Urine volumes and urine oxalate excretion did not differ.
IH is Hereditary
IH is familial, breedable in animals, and a cause of stones and of hematuria (urinary bleeding) and pain in children.
I am not sure if we were the first, but here is our evidence from 1979.
The arrows point to stone formers, filled symbols are men (square) and women (circles) with IH, * are children, and dashed people are deceased. In the 9 families IH was about 50% prevalent. Many others have found IH heritable.
It is not likely to be a simple trait from one abnormal gene, but some outcome of a number of genes. As this reference mentions, urine calcium is not the only stone forming trait that appears genetic; urine citrate appears to be, as well.
Dr. David Bushinsky, in decades of outstanding research, has proven that rats can be bred for what appears to be a rather close match to human IH. His strategy was to breed rats with the highest calcium excretion, and continue doing this for generations.
What attracts my notice is the progression over the generations. For the first 40 generations, urine calcium rises almost linearly. Thereafter, it is at a near plateau, more or less.
Yet, if we think about the matter, 800 years is nothing in evolutionary time. Even his outermost generation, near 100, or 2,000 years, is nothing as against evolution. So I am satisfied that IH is breedable in animals, and could have easily arisen in us as a response to evolutionary pressures. What those pressures might have been is not a topic for here.
I cannot pass by this heroic accomplishment without a pause, and some stirring of admiration and sense of accomplishment. How brave to have started this, and how persevering and accurate to maintain these generations intact and continuing. How productive, too.
Some years ago we had the opportunity to collect 24 hour urine samples on large numbers of boys and girls who were brothers and sisters of children with kidney stones. Some of those siblings were stone formers, others were not. As a contrast, we were able to collect samples from children in families that did not harbor the stone forming trait as none of the children, their parents, or other relatives were known to form them.
Urine calcium excretion is shown in the same q plots as I have shown before.
Urine calcium excretions of siblings with more than two stones are farthest to the right – highest. Next highest – second from the far right – were siblings with 1 – 2 stones. Siblings with no stones were even lower, third from the far right.
Children from families with no kidney stone history were lowest – most leftward – and almost none had above 200 mg/day of urine calcium loss.
The four bars in the right hand graph say the very same thing. Mean values of urine calcium, shown by the top of each bar, rose progressively with stones.
Even though children are smaller than adults, we can compare amounts of daily urine calcium loss to those of adults because the values are adjusted for body surface area. Such an adjustment is widely used to compare people and even animals of varying sizes.
Hypercalciuria in children not rarely causes hematuria found on routine screening. Loin pain with hematuria is a common syndromic epithet, ascribed to crystals because IH can raise urine supersaturation and higher supersaturations promote crystals. Hematuria can be familial because it is due to IH and crystals or stones. In adults, unlike children, hematuria can be from malignancy so proper evaluation, even in stone formers, requires imaging and considerable care.
IH Is Not the Only Reason Stones Are Familial
I will not pursue the matter here, but stones themselves are familial, presumably hereditary, and not always because of IH. In fact the lovely figure from Tenessee shown above makes clear that a positive family history of stones shifts the probability of stones upward at any given level of supersaturation, and it is mainly supersaturation that IH can influence.
There is more, of course. Possibly, and we have put this idea forward, IH occurs because of altered pathways for calcium movement through the nephrons of the kidneys and it is these altered pathways that might promote crystallization and stones. All that is for a later time, as it is speculative, and a matter of ongoing research.
IH can cause bone mineral loss and bone disease, so stone formers are at risk for fractures.
There Is Bone Disease
An outstanding scientist in the kidney stone field, Dr. Khashayar Sakhaee, has authored a superb review of the bone problem of stone formers. This figure, from a prior study of people living in Rochester, Minnesota, shows the cumulative incidence of vertebral fractures among people who had a symptomatic stone (irregular line) and the expected rate of fractures based on the entire population (the smooth line) between 1950 and 1974. The excess of fractures was not observed for hip or forearm.
The review collates 20 studies that concern bone mineral density mostly in relation to idiopathic hypercalciuria in stone formers. The broad message is a reduced level of bone mineral as a general finding, observed by many independent investigators using a variety of instruments to assess the bone. One cannot escape the conclusion that among stone formers, most of whom are described as having IH, bone mineral is reduced as a rule.
The authors summarize their wide ranging literature review in a little table I find irresistible. Among 2,052 patients reviewed, between 31 and 65% (939 patients) had some reduction of bone mineral density.
Furthermore, the radius, a site not remarkable for fractures in the Rochester study, is most affected with regard to reduced bone mineral density.
We have shown that the magnitude of IH predicts future loss of bone mineral. We had occasion to measure bone mineral density in a number of stone formers with IH, collect 24 hour urine samples,
and then make a follow up measurement of bone mineral density three years later. From this, we could ask if changes in bone mineral were at all related to the urine calcium losses.
As a group, the net change in bone mineral density of femoral neck (left panel) and spine (right panel) centered around 0. You can see this because the points more or less fall equally above and below the horizontal line at 0 change.
But when the points are aligned along the initial urine calcium losses (horizontal axis), the change over time is negative: Points above the line at 0 are shifted to the left (lower urine calcium losses) than those below.
The ellipses are designed to fit around 68% of the points without any assumptions about the underlying distribution, if any, that the points reflect (like a normal distribution). For the interested, they are non parametric containment ellipses, and their tilt does
indeed reflect correlation of one axis with the other.
Using statistics not shown here, the slopes of change in bone mineral over time are significant. The higher the urine calcium, the larger the loss of bone mineral.
IH Is A Main Factor in the Bone Disease of Stone Formers
This is a bold statement but defensible.
Stone formers have a general increase of urine calcium excretion, and if risk of stones begins at about 200 mg/day, and risk of bone disease seems to follow having stones, it may well be that urine calcium levels as low as 200 mg/day are enough to promote bone disease.
Although Sakhaee is careful to point out that bone disease associates with stone disease, IH is obviously a prominent issue and many of the studies of bone disease in stone formers have centered on IH as a causal factor. I suspect the association is stronger than it might seem because IH itself has been diagnosed variably over the 20th century, often using urine calcium criteria far above those needed to increase stone risk.
I have quoted Dr. David Bushinsky elsewhere, and will repeat myself here: ‘Every stone clinic is a bone clinic, and every stone former should be evaluated for bone disease.’
The stone forming population is rife with bone disease, easily overlooked until a fracture, possibly one that could have been prevented.
Dr. Sakhaee points out that US insurance practices exclude bone evaluation in large swathes of stone forming populations. I say bone mineral scans are not very expensive compared to the eventual costs of fractures. A useful medical buying guide places the bone mineral density scan cost to uninsured people at about $200.00, and mentions that in May prices can be lower because it is national osteoporosis month. The price usually includes a simple medical interpretation.
How Does IH Raise Urine Calcium?
The extra calcium in the urine can come from bone or diet; the lower the diet calcium the more is lost from bone
The Extra Calcium Can Come From Diet
Over the whole of the 20th century it was not rare for laboratories to determine net calcium absorption in normal people and sometimes in stone formers with IH. To do this they fed subjects a fixed diet, usually in a clinical research center, and measured all food calcium eaten and all calcium lost in the stool. The difference between calcium eaten and calcium lost in the stool is net calcium absorbed into the blood.
These studies are laborious. Typically measurements are made in 6 day blocks after a few days to equilibrate with the diet, so subjects remained in the clinical research units for perhaps 8 – 10 days. But the measurements have a kind of immortality rare in science. Howsoever old, they remain usable, and can be aggregated, as I have done here, to show something important about humans.
Normal men and women absorb about 18% of diet calcium – the orange curve on the adjacent quantile plot combines adult men and women who in fact display identical behavior. People with IH – the blue curve – absorb much more calcium, about 30% median. You might ask how one gets negative absorptions – points to the left of the vertical 0 absorption line. It is because pancreas, duodenum, and perhaps ileum all can secrete calcium from blood back into the bowel lumen, so with very low calcium diets this ‘endogenous’ secretion can result in losing more calcium in the stool than is eaten.
One very early theory of IH was simply over absorption: High efficiency absorption, more calcium comes into the blood, the kidneys lose it – done. This theory led to decades of low calcium diet as a treatment. No one knew such diets might cause fractures.
The Extra Calcium Can Come From Bone
A Glucose Load Can Raise Urine Calcium
Food without calcium causes calcium loss from bone; be careful what you eat if you have IH
Years ago Dr Jack Lemann did this informative study. He gave glucose or sucrose (table sugar) to normal people, calcium stone formers, and relatives of calcium stone formers.
We know that calcium stone formers are often people with IH and that relatives of calcium stone formers have IH so this is normals and a population enriched with IH.
Look at the control calcium excretions of the two right hand groups: 5 or so of the stone patients have control values above all but the highest normals; the relatives are even higher – and this is fasting!
Each period was 20 minutes, so this experiment went on for 2 hours. The higher urine calcium with sugar must come from bone. It came from bone in normal people and in those with IH but the latter lost far more calcium than the former.
Low Calcium Diet Causes Bone Mineral Loss
We persuaded nine normal people and 27 stone formers with IH to eat a very low calcium diet – 2 mg/kg body weight – for 9 days, and on days 7-9 we collected 24 hour urine samples and measured calcium losses.
The diet went well; most people ate what we asked (middle panel). The normals lost in their urine less than 2 mg/kg of calcium daily – lower panel, to the left, so the difference each day between what they ate and lost was positive (upper panel, points above 0).
The patients with IH were different. They lost more in their urine than they ate, and did so most of the time. This was bone mineral lost in the urine.
On such a low intake surely everyone was losing bone mineral because the fraction of diet calcium that is absorbed into the blood is far below 100%. I just showed you that it is about 18% in normal people and 30% for people with IH.
But those with IH were more flagrant than the normals. Because their urine contained more calcium than they ate we could prove bone mineral was being lost. At that time in the history of this field, such a proof was not so easily accepted as now.
Bone Calcium Balance Is More Negative in IH than in Normals
I already showed you calcium absorption as determined by the difference between calcium eaten and lost in the stool. Balance – or retention – is the difference between the calcium absorbed and calcium lost in the urine during a study period, usually of over 6 days.
Here are the calcium balances – or retentions – of the same people whose absorption data I showed above plotted against calcium intake.
In this plot, IH is in red, and normals in blue. The lines running along the points, are tracking the mean – average – value from left to right, like the common trend line in spreadsheets. At diet calcium intakes above 500 mg/day, the average for normals is about 0, meaning that normals in general will have stable bone mineral stores. Higher intakes make the average rise above 0 and at about 1000 mg/day or so, a common nutritional goal, a majority of normal – blue – points are above 0.
For the IH subjects (red), the mean rises slowly with diet increase, but the average never reaches 0. Some points lie above 0 meaning that not all IH subjects will share the general high risk of bone mineral loss, just as some normal points lie below 0 even at high calcium intakes.
The message is that low calcium diet is not ideal for the normal population and a disaster for people with IH. But even with a liberal calcium diet IH makes it hard to bring bone mineral into balance which is probably why there is a bone disease.
Using sophisticated measurements of bone mineral turnover, Lieberman and his colleagues showed as early as 1965 that patients with IH had something very abnormal about bone. Low calcium diets remained a common treatment for stone disease for more than a decade later.
What Does All this Mean?
Fractures follow stones like a shadow. No doubt the fractures relate to the excessive bone mineral losses. Stone clinics are bone clinics.
Mineral Metabolism And Bathtubs
A real bathtub has two drains. The one at the bottom is the one you can open or close. The other one, up near the top, is to keep the tub from flooding your bathroom if someone inattentive leaves the faucets open. This second drain is about the level where most people would want their bath water. It has to be. To keep the water line above the open waste overflow drain would require both faucets be wide open.
Fill up a bathtub part way, with the bottom drain and both the hot and cold faucets partly open. Be careful to bring the water level to below the upper drain as we want it to be out of the picture. Wait until the water level is steady.
Call the cold tap inflow from diet, and the hot tap inflow from bone. The drain is the kidneys, the flow through the drain is the urine calcium excretion. The height of the water in the tub is the blood calcium concentration. Because the water level is steady the flow out of the drain equals the sum of water coming in from the hot and cold water taps combined.
A simple and compelling vision of IH is easy to experience. Open the cold tap. This is like diet calcium coming into the blood. As the water rises, the greater weight of water will force more water through the drain so the level will become steady. If you close the tap back to its original position, the water level will fall again.
Called absorptive hypercalciuria, this was for decades a powerful vision that affected treatment. Since calcium absorption is above normal in IH – I just showed you it is, every meal would lead to a larger swing in absorption and urine calcium loss, as in the bathtub. Bone would be unaffected – that there was a bone disease was not known decades ago. Treatment was obvious: Low calcium diet.
A More Realistic View
Plumbing analogues are helpful, but there are many details it cannot capture.
The Flows of Calcium
The gut takes in food calcium, absorbs some, back secretes some, and loses the rest in the stool (large tube at the left in this diagram). Bone perpetually take up and gives up calcium as it remodels.
So blood has two supplies: Gut and bone.
The urine calcium is the sum of the two: net gut calcium uptake + the net difference between bone resorbed and mineralized.
The kidneys take extra words because they are fancy bathtub drains.
They filter water out of the blood at a high and reasonably constant rate. The amount of calcium filtered into the nephrons of the kidneys is the product of that filtration rate and the blood concentration of filterable calcium (UF in the figure). A high percentage of that filtered is reabsorbed back into the blood – about 98%.
So the urine calcium is the amount filtered times (100 – the percent reabsorbed) and that urine calcium has to equal the net gut calcium uptake + the difference between bone resorbed and mineralized.
This system is self balancing in a way. If urine calcium is less than the gut and bone supply into the blood the calcium concentration and filtration will rise, and the reverse. The system is also regulated, because the kidney cells can vary the percent of calcium they reabsorb. They tend to act so as to keep the blood calcium steady.
How More Calcium Gets Into the Urine in IH
Put real people into a clinical research center, feed them exactly the same diets, and measure the things we have just been talking about: Urine calcium, the amount of calcium filtered, and the percent of filtered calcium reabsorbed. How do the kidneys get more calcium out in IH than in normals? Is it more filtration, less reabsorption, both?
In this figure men are on top, women on the bottom, fasting are the two left panels, fed are the right two panels. Triangles are IH circles are N. The ellipses of containment are as in the graph of bone mineral density over time. Dashed lines are IH solid lines are N.
Look at the left panels. This is before eating. The urine calcium – on the vertical axes – does bear some relationship to how much calcium is filtered – horizontal axis, especially in men and IH women. We would expect that – filter more into the nephron tubes, more comes out.
But, urine calcium is higher in IH than normal – the dashed ellipses ride higher than the solid ones, and the triangles than the circles, even though the amounts filtered overlap entirely. It is as if one balloon rose above the other over a single plot of ground.
Look at the tops of the graphs, on the borders. The pretty curves overlap – they mark out the filtered loads, IH and normal, showing how they do not differ. Look to the right sides of the graphs. The notched bars mark out the amount of calcium in the urine. They do not overlay.
No food has been eaten yet. Of course, some may be still trickling into the blood from last night’s meal, so we cannot be sure. But the IH kidney cells are not reabsorbing the same percent of filtered calcium as are the normals, that is the message. And therefore more calcium is being lost in the urine. One could say the drain is open more in IH and, of course, one or both faucets: Diet remnants or bone.
The right panels are dramatic, are they not? The normal balloons lift up in women and men: No change in filtration, but much more in the urine – lower percent reabsorbed. For IH, the same but a lot bigger. The balloons are like rockets, shaped like rockets. The tubule cells are letting what has been filtered out. The drains open wide. See where the curves on top of the graphs overlap showing how filtered loads are identical, while the bars at the right borders diverge, that for IH high above normals.
And the faucets? Of course it is partly the diet. IH raises absorption. But, with open drains, how can we know?
Proof That Bone Loses Calcium
In 1970, Jacob Lemann did this experiment. He gave glucose (no calcium, just sugar) to normal people but reduced filtration and calcium filtered load by asking them to stand quietly. If you stand that way blood pools in the legs, and filtration falls.
On the left side at the top you can see the filtered calcium fell a little. At the bottom you can see that urine calcium loss (UCaV) fell a lot.
When he did the exact same thing but gave glucose (right panels) the filtered calcium actually fell more with standing but the urine calcium rose. This is reduced tubule calcium reabsorption – opening of the drain.
The higher urine calcium could not be from diet – there was no calcium. The filterable calcium stayed steady (1.42 vs. 1.40 mmol/l) between the control and glucose periods – the water level in the bathtub was constant. The bone was giving up the extra calcium.
This was in normal people. I see no basis for arguing that the same would not occur in IH.
How IH Works
The kidneys behave like open bathtub drains, so to keep blood calcium up bone or diet or both must provide more calcium – like open faucets: Bone is at risk.
In normal people and in IH it is as if faucets open and the drain open in such perfect synchrony and quantitative coordination that blood calcium can stay remarkably constant even as calcium reabsorption falls and urine calcium rises.
In a real bathtub, coordination of faucets and drains is not a problem. You want, for example, more flow – perhaps to keep the soap flowing away, or maintain a specific warmth in a cold bathroom – but you also want the water level to stay where it is.
You open the faucets and also open the drain a bit.
But who is you in IH?
This is where we are.
I mean, we who do this kind of research.
What coordinates the faucets to the drain. Which faucet? We know bone can be lost, we know calcium is absorbed more rapidly than normal. So both play a role, but how much of one or the other we are not sure.
Why Would Patients and Physicians Care?
That should be obvious.
The drain is open in IH, more fed than fasting, but open. The serum calcium is maintained by open faucets. There are no alternatives to these statements.
If there is no calcium in the diet bone gives up some of its mineral.
I would like to think that when diet calcium is ample bone is safe, although I have no proof of that and I do not know what I mean by ample. Even at high calcium intakes people with IH can be in negative bone calcium balance.
Therefore: Low calcium diet is never a good idea in IH. Bone can suffer. Perhaps not always, perhaps not in everyone, but often enough it is not a good idea.
This is why patients and physicians should care. It is why it has been useful for you to follow along the tortuous narrow dusty road.
Even if plagued by calcium stones, do not believe that reducing diet calcium is a safe option. It might be under some circumstances but cannot be relied upon as safe. Bone is in jeopardy. Eat calcium and use other measures to control the stones: Water, reduced sodium, avoidance of excessive sugar and protein loads, and use of potassium citrate and thiazide type drugs in combinations as needed.
Stone patients are potential bone patients and we want that potential to remain a potential not a realized and completed disease.
All of these treatment measures are of importance, and I will try to discuss them in subsequent articles.
What Should Scientists Care About?
How do the faucets and drain coordinate.
They seem to do so beautifully, and mysteriously. It is almost too good – their matching, the constancy of serum calcium. If I were young and out to do new science I might ask about this linkage of the faucets and drain.
But I am not.
Is It Clear About the Picture of the Bathers?
Cheers, Fred Coe