Minerals and bone

The control system, and the sensor that runs it

Four glands the size of grains of rice sit behind the thyroid, and their only job is watching the calcium concentration in your blood.

They watch it through a receptor sitting on their surface called the calcium-sensing receptor, which does something unusual. It detects an ion directly rather than a hormone. Calcium binding to it is the signal. When blood calcium falls, less of the receptor is occupied, and the gland releases parathyroid hormone in response.

Parathyroid hormone then does three things at once. It pulls calcium out of bone. It tells the kidney to hold on to calcium rather than lose it in urine. And it tells the kidney to activate more vitamin D, which increases how much calcium the gut absorbs from food.

Between them those three levers hold blood calcium within a very narrow band almost regardless of intake. Eat more calcium and a healthy body absorbs less of it. Eat less and it absorbs more, and borrows from bone if it has to.

Two consequences follow, and both matter for reading a result. A normal calcium tells you the system is compensating, not that intake is adequate. The compensation can be running hard and still hold the number steady. And a genuinely abnormal calcium is a significant finding precisely because it means the system has stopped managing.

The sensor is also the reason for one of the better-known traps in this area. People who inherit a less sensitive version of the calcium-sensing receptor have parathyroid glands that read calcium as lower than it is, so they run a mildly raised calcium and a parathyroid hormone that is unhelpfully normal, for life and without harm. That picture is nearly indistinguishable from an overactive parathyroid gland on blood tests alone, and the two are separated by measuring how much calcium is being lost in the urine rather than by repeating the blood test.

This is also where ALP from the Liver section reappears. Alkaline phosphatase comes from bile ducts and from bone, and the bone fraction rises when bone is being remodelled rapidly. That is why it is higher in adolescents, and why a raised ALP with a normal GGT points away from the liver and towards bone.

What the profile looks at

Adjusted calcium exists because only about half the calcium circulating in your blood is free and active. Roughly 40% is stuck to proteins, and albumin carries about four fifths of that. The last tenth or so is bound up with small anions like citrate and lactate. So the number on your report is a total, and the part doing any work is around half of it. Someone with a low albumin will therefore show a low total calcium while their active calcium is entirely normal, and the adjustment is an attempt to estimate the active fraction from the total.

It works less well than its universal use suggests, and that matters because it is on almost every report in the country. The adjustment assumes calcium and albumin move together in a fixed straight line. They do not, particularly once albumin is low, which is exactly the situation the adjustment exists for. So the correction overshoots.

Measured against directly measured free calcium, which is the actual reference method, adjusted calcium generally performs no better than the plain uncorrected total, and in several comparisons worse. It tends to read a genuinely low calcium as higher than it is and a genuinely high calcium as lower than it is. The equation in widest use was never validated against free calcium at all. The standing recommendation in lab medicine is that each lab derives its own equation locally rather than borrowing a published one, and where it matters the answer is a directly measured free calcium, which is a hospital test and not one we offer.

None of that makes the adjusted figure useless. It is the conventional way to read calcium where albumin is abnormal, and bodies now disagree about whether it should be reported at all. In April 2026 a joint group from the International Osteoporosis Foundation, the International Federation of Clinical Chemistry and the European Federation of Clinical Chemistry said adjusted calcium should no longer be reported, that the plain total should be given instead, and that a directly measured free calcium should be used where the answer matters. The UK position, set out in 2015 by the Association for Clinical Biochemistry, is the opposite, that every UK lab providing a total calcium should report an adjusted calcium alongside it. UK labs follow the UK position. It does mean reading it as an estimate with known limits, and it means noticing a low albumin on its own account rather than trusting the arithmetic to have dealt with it.

The bigger gap is that the hormone running all of this is not on the panel. Everything above describes parathyroid hormone deciding what calcium does. A calcium result on its own tells you where the number landed. It cannot tell you whether the glands are straining to keep it there, which is usually the question that matters.

Parathyroid hormone is a standard blood test and we do not sell it. A GP will request it where a calcium is abnormal, and private labs have it. The 2 get read together, because a raised calcium with a raised or inappropriately normal parathyroid hormone points somewhere completely different from a raised calcium with a suppressed one. On its own, either number is half a sentence.

Magnesium has the opposite problem to calcium. Less than 1% of the magnesium in your body is in blood. The rest is in bone and inside cells, and the body holds the blood concentration steady by moving magnesium in and out of those stores.

Which means serum magnesium can sit comfortably in range while tissue stores are depleted. A low result is meaningful and worth acting on. A normal result does not rule depletion out. Saying so is more useful than implying the number settles the question.

Red cell magnesium is what people reach for next, and it is sold widely. It measures magnesium inside red blood cells rather than in the fluid around them, which sounds like it ought to solve the problem. The evidence that it reflects magnesium in muscle and other tissue any better is weak, the ranges labs quote are not agreed between them, and we are not aware of any guideline that uses it. It is not something we sell and it is available privately. Just do not treat it as the answer serum magnesium failed to give, because it probably is not.

Magnesium turning up in hundreds of reactions sounds like supplement marketing, but it is not. ATP, the molecule every cell uses to spend energy, is not biologically active on its own. It works as a complex with magnesium. Functionally, the currency of cellular energy is magnesium-ATP. So every reaction that spends ATP is a reaction that needs magnesium, which is why the list is as long as it is.

There is one more link. Magnesium is required both for parathyroid hormone to be released and for it to act once it arrives. Severe magnesium depletion therefore produces a low calcium that will not correct however much calcium is given, until the magnesium is replaced first. The 2 travel together more often than either is looked at alone.

Zinc is required for immune function, wound healing, protein synthesis, taste and smell, and testosterone production. It also falls during inflammation and acute illness independently of how much zinc is in the body, which is one of the reasons it is read alongside hs-CRP rather than alone.

More zinc is not better, and the mechanism explains why the damage creeps up rather than announcing itself. Zinc and copper compete for absorption, but not by simply blocking each other. High zinc intake causes the cells lining the gut to produce more of a protein called metallothionein. That protein binds copper considerably more tightly than it binds zinc, so copper arriving in those cells is captured and held. The lining cells are shed and replaced every few days, and the trapped copper leaves with them rather than entering the blood.

So sustained high-dose zinc supplementation quietly reduces copper absorption over weeks, and copper deficiency produces its own anaemia and, if it runs long enough, nerve damage that is not always reversible. It is one of the most common self-inflicted deficiencies in people who supplement heavily, and it is entirely avoidable.

And you can check. Serum copper, and caeruloplasmin, which is the protein carrying most of it, are both ordinary tests. Neither is something we sell. A GP will arrange them where there is a reason to, and private labs have both. Months or years of high-dose zinc is a reason.

Albumin is doing three different jobs

Albumin appears on three separate parts of a report meaning three different things, and nothing else on your results does that. So it is worth gathering in one place.

On the liver profile it is a measure of synthetic function. The liver makes it, so a falling albumin can mean the liver's capacity to do its work is reduced.

In adjusted calcium it is a carrier. Here nobody cares whether the liver is making enough of it. What matters is how much calcium it is holding, so that the active fraction can be estimated.

And in calculated free testosterone it is a carrier again, this time for a hormone, and it is one of the three numbers that calculation is built from.

The same protein, measured once, read three ways. It is also why a low albumin quietly shifts two other numbers on the same report without anything having changed about calcium or testosterone at all.

What changes when this is disturbed

A persistently raised adjusted calcium most often means the parathyroid glands have become overactive and stopped listening to the feedback. It is always followed up, because the causes are treatable and because sustained high calcium affects the kidneys, the bones and, at higher levels, alertness and mood.

A low adjusted calcium is most often the downstream consequence of vitamin D deficiency. Less vitamin D, less calcium absorbed, and eventually the compensation runs out. At lower levels it causes muscle cramps, tingling around the mouth and fingers, and in severe cases spasm.

Low magnesium causes muscle cramps and twitching, fatigue, and disturbances of heart rhythm, as well as the calcium interaction described above.

Low zinc affects taste and smell, wound healing and immune function, and shows up in skin and hair before most people connect it to a mineral.

Bone itself, notably, produces no symptoms at all until something breaks. Osteoporosis is silent by definition. Nothing on this page measures bone strength, and nobody selling blood tests can tell you otherwise.

What does measure it is a DEXA scan. Ten minutes lying on a table under a low-dose X-ray arm, no dye and no needle, and it returns bone density at your hip and spine against a reference. On the NHS it needs a referral and there are criteria for getting one. Privately you can book it yourself and it is among the cheaper scans available.

And before you get that far there is a free tool, the same way there is for heart risk. FRAX estimates your 10-year risk of breaking a hip, and your 10-year risk of a major osteoporotic fracture, which means the hip, spine, wrist or shoulder. It is free, it is public, and it runs without a bone density result at all. Age, height, weight, and a handful of yes-or-no questions about previous fractures, family history, smoking, steroids and alcohol. A high score is a reason to go and ask for the scan rather than wonder about it.

Best done early, because every osteoporosis treatment is better at preventing a first fracture than at fixing the position after one.