Calcium and Dogs - Poochie Revival

Calcium is the most common mineral in the body and an extremely important electrolyte for muscle and nerve function, while also being the main building block of the skeleton. Calcium intake is often considered the biggest problem among minerals in nutrition, although it is perhaps the easiest.

Calcium has been written about the most because it has been studied the most as the “easiest” mineral. Therefore, it has somewhat gained an overemphasized position. At the same time, the emphasis on calcium’s role in nutrition and its importance for a dog’s development and health have gone astray.

The essential thing is absolute intake, nothing else.

If raw feeding includes even a little bit of bones, or so-called dog minced meats that have ground bone, and if vitamin D intake is ensured, there is practically never a deficiency of calcium.

Calcium is the most abundant mineral in a dog’s body, stored in the bones. In the skeleton, calcium is found as hydroxyapatite Ca₁₀(PO₄)₆(OH)₂. Besides making the skeleton so hard that it keeps the body upright, it is also released from there for the body’s other needs every time, for example, when not enough calcium is obtained from food or when there is another acute need, such as after exertion. This so-called free calcium is found everywhere – in the blood, extracellular fluid, and generally in all body cells.

Ionized calcium (Ca++) is essential for all information transfer in the body, and it accounts for about half of the free calcium. The other half is bound to albumin. Without it, intracellular or intercellular signals, nor nerve signals, would not be transmitted. Gland secretion would fail without free calcium, and a significant number of enzymatic reactions would not occur. In wounds and injuries, blood would not clot. The body’s calcium level is kept almost constant within a very narrow range and is probably the most precisely regulated homeostasis, balance, in the body.

When a dog eats food containing calcium, whether it’s a chicken leg or calcium-fortified dry food, the actual absorption of calcium takes place in the intestine. The calcium in the food mixes with the calcium in the digestive juices, and the entire mixture is utilized in the small intestine either passively or actively, which also requires energy. Active absorption is the most important and efficient, and here the best companion of calcium supplements comes into play: vitamin D. Active absorption is entirely dependent on the function of 1,25-dihydroxy-D3-vitamin (1,25(OH)2D), and if there is a deficiency of vitamin D, absorption does not occur significantly. And if we want to make the matter a bit more complicated, that alone is not enough. Overall absorption is also strongly influenced by reabsorption from the intestinal fluid and the secretion that occurs.

In raw feeding, calcium is sufficient when the food contains bones at a gram per kilogram of weight, or when calcium from ground bone is about 0.5% of the food’s wet weight.

for adults 130 mg/kgME
630 mg/kgME up to three months of age
315 mg/kgME up to six months of age and from there to just under a year, the same or just slightly over the adult need
Ca/P ratio for adults 1.2:1
Ca/P ratio for puppies 1.1 – 1.4:1

The most essential thing to understand about the recommendations for puppies and adults is that despite everything, there is no difference. Everyone fits into the same range when fed according to energy needs.

Regulators

99 percent of calcium is in the skeleton, part as a structural material and part as a storage for the body. Bone tissue is the regulation center for the body’s calcium balance. Calcium is continuously released and reattached in the bone. The turnover can be up to a gram per day.

Calcium outside the skeleton is in soft tissues and extracellular fluid. It is a central messenger, for example, in enzyme activation and participates in muscle contraction, nerve impulse transmission, glycogen metabolism, and cell differentiation and division.

Metabolically, the most active is the ionized calcium in extracellular fluids. Its share of the entire body’s calcium is only about one percent, but its role is immensely important. It participates in many vital functions, such as enzyme function and the passage of muscle and nerve impulses. Therefore, vitamin D and hormones strive to keep its amount constant. When the calcium level in the blood rises, the excess is stored in the skeleton. When intake is low, the necessary calcium is taken from the skeleton, calcium excretion by the kidneys decreases, and absorption is enhanced.

When the amount of calcium in the diet decreases, the calcium level in the blood also drops somewhat. This triggers certain hormonal functions that enhance calcium absorption. If not enough calcium is obtained from the diet, or its absorption is weak, for example, due to a lack of vitamin D, the body takes the calcium it needs from the skeleton.

Factors that increase calcium absorption:

Vitamin D, which forms calcium-binding protein in the small intestine,
the body’s need and growth-promoting hormones,
stomach acidity (at low pH, calcium does not dissolve enough),
low dietary intake, and
amino acids released during protein breakdown.

Factors that decrease calcium absorption:

high fiber content,
phytates and oxalates,
excessive calcium intake, and
age.

Fat can bind calcium in an unabsorbable form in fatty diarrhea.

Calcium balance in the body is tightly regulated. The most important in this work are three hormones:

parathyroid hormone (parathormone, PTH),
thyroid hormone (calcitonin), and
calcitriol (the active form of vitamin D3, 1,25-dihydroxycholecalciferol, 1,25(OH)2D).

The skeleton was the storage, and blood was the transport route, and to keep calcium levels in cells constant, logistics must work – store when there is something to store, and put into transport when there is a need somewhere. Parathyroid hormone, thyroid hormone, and vitamin D do this by regulating the intake and release of calcium in the intestines, skeleton, and kidneys.

Vitamin D

Vitamin D is classified as a vitamin based on ancient criteria, but in behavior, it is more of a hormone. But since dogs (and we) must get vitamin D from food, it also fits the definition of vitamins. It has been said at a textbook level that its only function is to regulate calcium homeostasis with parathyroid hormone. Today, it is known that the matter is not that simple (or calcium balance is a significantly broad issue), but that task is certainly among the most important.

The amount of calcium in the blood (plasma) is constantly monitored. When the amount of calcium begins to decrease, the parathyroid glands start secreting parathyroid hormone, which in turn activates osteoclast cells in the skeleton. Osteoclasts were bone-eating cells, one of whose tasks is to remove old bone. In practice, they break down the bone structure on the command of parathyroid hormone and release calcium into the bloodstream. Parathyroid hormone also theoretically increases the kidneys’ efficiency in removing calcium, but unlike humans, dogs do not excrete much calcium in urine. At the same time, as the amount of parathyroid hormone rises, it begins to release calcitriol, or more familiarly, vitamin D, from the kidneys. It has three tasks:

it increases calcium and phosphate absorption in the small intestine mucosa,
increases the transfer of available calcium from the skeleton to the blood, and
calcium reabsorption in the kidneys.

Vitamin D thus accelerates, and effectively, the absorption of calcium from food and thereby reduces the amount of calcium taken from the skeleton.

When calcitriol has done its job, it is almost entirely excreted through bile into the feces. Vitamin D can thus be colloquially characterized as disposable. It is, of course, stored, but the stores are not eternal, whereas, for example, the body is completely self-sufficient regarding parathyroid hormone.

If the stores begin to empty, that is, there is a deficiency of vitamin D from food, and there is calcium in the food but not vitamin D, then the intestine’s ability to absorb calcium is poor or zero. Then all the calcium needed by the cells is taken from the skeleton, no matter how much feeding chalk is shoveled with a measuring cup or cartilage is given as a source of calcium when barfing. If vitamin D is forgotten, the result is bone fragility due to osteoporosis, and the yard is full of white, chalky piles of feces.

When the amount of calcium rises above normal, the thyroid gland and its secreted calcitonin are activated. There is always a force and a counterforce. In muscles, there is an influencer and a counter-influencer. Hormones have the same thing, and calcitonin is the counter-influencer of parathyroid hormone – as is calcitriol, or vitamin D. Calcitonin inhibits the breakdown of the skeleton by osteoclasts and activates osteoblasts, the cells that build new bone. And they do this by taking calcium from the blood. For the skeleton, parathyroid hormone is a catabolic, breaking down hormone, and in turn, thyroid hormone is an anabolic, building hormone.

The skeleton is not a stable, dead mineral framework. It is a living organism that continuously breaks down and rebuilds itself.

Magnesium

Although it is not a direct regulator of calcium and phosphorus metabolism, magnesium should not be forgotten. It participates to a lesser extent in calcium regulation but otherwise works together with calcium, phosphorus, and vitamin D. About half of the magnesium is stored in the skeleton, and the rest is found in muscles and soft tissues.

Magnesium is needed, for example, for muscle contraction and nerve impulse transmission (hence magnesium deficiency can cause cramps), but it also participates in the energy production of cells. So, in the same things as calcium and phosphorus, and it can, in a way, balance fluctuations in calcium or phosphorus levels.

There are different views on magnesium needs depending on what is being calculated at any given time, but one assumption is easy to remember: magnesium should be half the amount of phosphorus.

Absorption and Excretion

An adult dog can regulate calcium absorption. Depending on the dog’s current need, the dog absorbs between 0 – 80% (or 90, depending on the source) of the available calcium. Available does not always mean the same as the total calcium in the food, but if the food source of calcium, often bone, dissolves in stomach acids, then calcium is available.

If there is enough calcium in the food, calcium is absorbed passively, without needing to enhance absorption. But if there is less calcium in the food, active regulation through vitamin D starts enhanced absorption. A sufficient amount is considered 1.1% of dry matter, and less (apparently insufficient) is 0.55% of dry matter.

The relationship between the amount of calcium and passive/active regulation is considered particularly essential in dog nutrition. There are two things that cannot be avoided when discussing dog nutrition, which always focuses on the most important component, calcium: passive/active absorption and the Ca/P ratio; the role of the calcium and phosphorus ratio will be returned to later.

Dog food must therefore have 1.1% of dry matter calcium or more. It has never been clear to me what bad things happen in the world if the percentage is below that – except that the normal physiological reaction of the body, called active calcium intake, is triggered. Let’s play with numbers.

The food contains 1.1% DM calcium, and a 30 kg dog eats 500 grams of it. It then gets 3.3 grams of calcium. Of this, it absorbs passively 0 – 80%, and if we take the familiar 40% absorption limit from puppies, it gets 2.2 grams of calcium. Its need is 1.7 grams. The 1.1% recommendation is therefore not about anything other than that the dog gets the amount of calcium it needs with the 40% passive absorption borrowed from puppies. In that respect, it is a completely unnecessary emphasis in feeding.

1.1 DM is the rule of dry food manufacturers, based on two reasons. The first is that with the same recipe, every dog, regardless of its age group and breed, gets a sufficient amount of calcium, but not totally too much. The second reason is the age-old phosphorus and calcium ratio. Due to raw materials, phosphorus is always in the range of 0.8 – 1% of dry matter, and if the Ca/P ratio is to be maintained, calcium must be at least 1.1.

The rule that has guided feeding for the last few decades is not based on anything other than the recipe and the Ca/P ratio. It has no significance for calcium absorption, utilization, or intake. In wet food, there should be about 0.5% calcium to meet the calcium requirement. Assuming 65% moisture, it is about 1.5% in dry matter.

Puppies

For puppies, it is a slightly more complicated matter, but only slightly. In puppies under 5 – 6 months of age, active regulation does not work. They cannot enhance calcium absorption but always absorb 40 – 80% of the calcium in food. At the same time, their ability to excrete calcium is limited. For this reason, only balanced foods can produce a puppy with a healthy skeleton – or so it is claimed.

The lack of active regulation does not mean anything but only ensures sufficient calcium for the puppy. When the puppy’s need for calcium decreases around six months of age, active regulation starts to prevent calcium overdose. A normal physiological function has been made into one of the most important factors in puppy feeding, even though it has no significance. The essential thing is only and only that absolute real calcium grams are obtained sufficiently from food. Practically, they are obtained if the puppy gets the amount of adult food it needs.

Ca/P Ratio

Everyone knows the most important equation of the theory of relativity, energy is mass times the speed of light squared. According to Albert (if I remember correctly), during his time, there were a couple of others in the world who understood the equation – others just chanted it. Yet it runs the entire universe, whether you understand it or not. In the dog world, there is a similar equation or claim: the ratio of calcium and phosphorus must be at least 1:1 and at most 2:1 – calcium must therefore be at least as much as phosphorus, but at most double. Much of that is chanted, but heaven help you if you ask why, the reason for that ratio, the answer is: the correct Ca/P ratio prevents developmental disorders caused by calcium. Good, but the question was why, not what results from the wrong ratio. No dog book tells it, but it is self-evident – perhaps with the exception of calves, almost everyone has an optimal ratio between 1:1 – 2:1, whether it is a guinea pig, human, dog, or horse.

Explaining the matter is not easy, and I may only be able to scratch the surface, as a layman to other laymen. The difficulty is due to three reasons.

Firstly, one should understand the function of ions and their effects on each other. Most dog enthusiasts have already forgotten even elementary school chemistry.

Secondly, one must understand the function of the endocrine system and hormones – it is already a big subject and solely focused on training specialists and researchers make big dissertations on some precisely defined part.

The third reason is that no one really knows – it is known how calcium behaves and sometimes even why, but phosphorus has been forgotten. The significance of the dietary phosphorus load in food has only recently been studied.

So, the knowledge of the importance of the Ca/P ratio is based very strongly on experimental research from the early last century, and the actual theory is only being built.

Why should there be more calcium than phosphorus, and what happens if the amount of phosphorus exceeds calcium? The general perception is that phosphorus prevents calcium absorption. Sometimes it is claimed that phosphorus prevents calcium utilization. However, everyone agrees that if the dog does not die immediately, it will at least develop hip dysplasia over time. There are many views on the timeframe. Dry food purists require a daily balance, while barfers are satisfied with a three-week balance – even though they feed meaty bones daily. The truth is probably somewhere between those extremes.

It is known that if there is too much phosphorus in the blood, it prevents or weakens the absorption of ionized calcium into the skeleton. On the other hand, too high phosphorus levels in the blood weaken the release of calcium from the skeleton. When it is said that an inverted Ca/P ratio prevents calcium absorption, it is not related to digestion but to the body’s metabolism.

Phosphates increase the amount of parathyroid hormone and disrupt the entire balance, causing calcium breakdown from the skeleton to accelerate even if there is no need. If the parathyroid hormone level in the blood is constantly high due to excessive phosphate intake, the skeleton is broken down, and calcium is wasted. But if its level only increases momentarily, as it normally should, thyroid hormone actually increases bone formation. In the latter case, it has an anabolic effect. If the parathyroid hormone level in the blood is constantly low, bone metabolism slows down, which also weakens the skeleton.

When the amounts of calcium and phosphate in the diet remain correct based on their mutual relationship, both minerals support each other. And how has this mysterious range of 2:1 .. 1:1 and the optimal, depending on the source, 1.6:1 – 1.2:1 been reached? Two ways. By experimenting, and because it is the ratio of calcium and phosphorus in the body.

But as always, there is a but here too, which partly undermines the whole beautiful theory. Namely, Canadian researcher Carl F. Cramer studied whether the amount of calcium or phosphorus, the Ca/P ratio, or pH affects calcium absorption. According to his results, the Ca/P ratio did not affect the absorption of calcium or phosphorus when given “reasonable” amounts, but calcium absorption did weaken if phosphorus was not obtained (1968).

For humans, the same Ca/P ratio is recommended as for dogs, but we – especially in the Nordic countries – get a significant amount of phosphates from food, and our ratio is distorted. If the Ca/P ratio is as critically important as suggested, we should all be either dead or crippled. However, we are not. Of course, women, especially on the verge of menopause, experience osteoporosis, for which one preventive measure is to increase calcium intake, but still, the biggest culprit is considered to be hormone balance (estrogen as one) and too low vitamin D intake.

Try to make sense of this too. Who is lost? I am, and I am becoming more convinced that the emphasis on the Ca/P ratio by dry food manufacturers is just a smokescreen; attention is drawn to something irrelevant, something that just is.

Balancing the Ca/P Ratio

To get the right Ca/P ratio in your dog’s food, it may need to be balanced, usually concerning calcium. Easy as pie or child’s play. Dry food users do not need to do anything; the manufacturer has already done it, but mixed and raw feeders need to get to work. And that’s where the fun begins.

First, you need to find out how much calcium and phosphorus there is in the food overall. Mixed feeders can easily find this out for dry food. With meats, problems arise. Very few meat suppliers provide the amount of ash and the proportions of calcium and phosphorus. Fineli does not help because dog minced meats have been ground with more than just meat. Those who feed chunks of meat may find some sort of guess. Fortunately, the task is made easier by the fact that the phosphate content of vegetables, and also calcium, do not need to be considered. This is due to the phytates they contain, which effectively prevent the absorption of calcium and phosphorus. Although barfers criticize grains, those who feed porridge do not, in principle, increase the phosphate amounts in the dog’s diet.

Once you have some guess about the amounts of calcium and phosphate, the calculation of the necessary amount of calcium to add is easy. At the same time, it is good to ensure that the amount of calcium in grams is sufficient – the ratio does not take a stance on real grams. Two milligrams of calcium and one milligram of phosphorus give the same correct ratio as two kilograms against one kilogram – but in both cases, the dog may be very ill. And again, we encounter another fun fact: we have no measuring device or method to estimate the dog’s actual calcium need. Recommendations give some direction, usually based on experimentally obtained information or pure guesses about the minimum amounts a dog must get – the optimum is another matter entirely. But if you aim for at least 680 mg/kgME for puppies and 130 mg/kgME for adults (NRC 2006), you’re not far off.

We are starting to reach a situation where the term easy as pie or child’s play leads to the same outcome. Because there are no exact values, just guesses, the tools are missing. We don’t even know reasonably accurately how much the need would be. Still, milligram-level calculations and adjustments should be made. With these resources, easy pie-making ends up in a flattened field and a cut on the shin, and child-making goes awry.

But because we end up with some conclusion, some calcium supplement is used if necessary. Calcium cannot be given raw unless you want to kill the dog. Therefore, the general name is chalk, although it technically means calcium oxide (CaO). Most feed chalk mixtures state the amount of calcium, so it usually does not need to be solved through molecular masses. However, pure calcium carbonate contains about 40% calcium, i.e., 40 g/100 g. Calcium phosphate is another commonly used supplement, but it is not a sensible solution for balancing the Ca/P ratio, as it also provides phosphate. Another problem is how much of the calcium from, for example, calcium carbonate the dog can genuinely utilize, what its bioactivity is, but let’s not complicate the matter too much this time.

Sometimes it is claimed that calcium is an antagonist of iron, meaning iron cannot be utilized if there is also calcium in the food, and therefore, especially in supplements, calcium should be given at a different time than iron. I found no confirmation for that assumption. And if that were the case, dry food dogs would have succumbed to anemia long ago.

Studies have been conducted on the effects of whole meat, milk, grain, and additive phosphorus. From each food, phosphorus intake was 1500 mg. Meat increased both bone formation and breakdown but did not affect blood parathyroid hormone levels. Grain had no effect at all due to the phytate in grains. Milk’s effect was entirely different because it contains both calcium and phosphorus. Milk reduced blood PTH levels and decreased bone resorption but did not affect bone formation. So, the type of food used also has a significant impact on this palette, so the number of variables only increases.

Phosphorus

Due to calcium intake in dogs and supposedly too high phosphate intake in humans, phosphorus has somewhat become a curse word. However, it is the second most common mineral in the body, and without it, death would be knocking at the door. About 85% of the body’s phosphorus is stored in the skeleton and is one of the factors strengthening it. Phosphates (“pure” forms never occur in any mineral) participate in the same things as calcium. They are essential for, among other things, cell energy production and acid-base balance regulation, and without phosphates, enzymes could not function.

Phosphorus absorption and amount are not regulated nearly as effectively as calcium, but phosphorus absorption depends heavily on the amount in the diet. A relatively new discovery is a hormone-like compound, FGF-23, produced in bone-forming cells, osteoblasts. It regulates only phosphorus metabolism, mainly phosphorus excretion. This is the most important mechanism for regulating serum phosphorus levels.

There is practically never a deficiency of phosphorus, as it can be obtained from everywhere. The problem in feeding is never adding phosphates but rather a calcium deficiency and sometimes a rare attempt to reduce phosphates.

Calcium Deficiency

When there is a deficiency of calcium, the first symptom is seen in its role in muscles. Low calcium causes nerve signal transmission to fail and makes muscles and nerves more irritable and hypertonic. The latter can cause cramps and spasms in the muscles. Deficiency leads to bone fragility, joint problems, and directly increases the risk of injury in greyhounds.

Fortunately, acute calcium deficiency is very rare, except for a birthing and nursing female. Mild deficiency and thus some degree of bone fragility are likely very common and may be one reason for overuse fractures or more broadly involved in bringing out growth and developmental disorders.

Calcium Overdose

Although calcium overdose in adult dogs is relatively harmless, it can still weaken the absorption of other minerals, such as iron, zinc, copper, and iodine. Excessive fiber intake in the diet, in turn, weakens the absorption of calcium, magnesium, phosphorus, zinc, and iron.

Calcium Need

One thing that still puzzles me about feeding a growing puppy is that if the calcium content in the food should be about 0.5g/weight kilo and phosphorus about 80% of the calcium amount, how on earth would a puppy in nature get those amounts, not to mention barfing, where in addition to meats and bones, large amounts of everything else less important are given?!?! I don’t understand that equation, and I would be very grateful if you could explain it to me!

Let’s start with the easiest, especially since it wasn’t even asked. But let’s recap for the sake of it. The intake recommendations for calcium are (in principle):

for adults 130 mg/kgME
630 mg/kgME up to three months of age
315 mg/kgME up to six months of age and from there to just under a year, the same or just slightly over the adult need
Ca/P ratio for adults 1.2:1
Ca/P ratio for puppies 1.1 – 1.4:1

Should we complicate matters further by how recommendations change if calculated through energy consumption? Or when energy consumption does not rise, but the need still grows – e.g., sighthounds? Or what happens to pregnant females? Let’s not complicate, as the point is simple: no one actually knows exactly what any individual’s real need is; nor is there any definitive, clear recommendation that considers the dog – not the dog food industry.

Calcium needs are talked about a lot, on a milligram scale, but not even on a gram scale is it known what the intake/release ratio is for that particular dog, i.e., the net need. Meeting the need is also complicated by the fact that assessing calcium utilization is quite adrift.

It puts an interesting light on the industry’s advertising texts, where the words researched, healthy, and growth disorder preventing appear.

Which brings us indirectly and circuitously to the actual question: how do wild canids manage to meet their calcium needs, and how do barfers handle it. You’ve put me in a tough spot – because soon the most enthusiastic barfers will start looking for rope, torches, and matches.

In the very early stages of solid food, the wild puppy hardly gets any. Part of the need is covered by mother’s milk, but the actual food is received over a couple of weeks as regurgitated. If the prey situation is good, the food is half-digested meat. A lot of excellent animal protein, whose digestion has already begun, continued with some amount of fat – depending on the animal. Nothing difficult to handle. Something every breeder should keep in mind when they start extending puppy kibble with cornstarch. That is such a short time – albeit extremely important – that calcium deficiency has no significance. After that, calcium is obtained from what the mother brings along. A moose leg, a piece of rib, a crippled hare, or a game bird (yes, it’s not just a privilege for cats) and from that, they get what they get. Sometimes probably well over the intake recommendations, any of them.

The point is that they get their calcium in a form they have learned to utilize throughout their evolution. And if they don’t get it and develop osteoporosis with age… We are supposed to expire around 40-50 years, and a dog is not “supposed” to live to 15 years. A wolf lives as long as it can function as a food provider at the top of the food chain. It doesn’t matter to it whether it dies at 8 years old from a bone fracture caused by chronic calcium deficiency or from a mammary tumor – it has already done its job for the species, and external causes don’t matter when those causes don’t threaten the continuation of the species, the pack, or its own genetic line.

In barfing, I still don’t see the problem as whether dogs get enough calcium. But that they get too little animal protein as a building block and too little animal fat as fuel, and in relation to that, too much of something called calcium. Quite often, they don’t even get calcium but cartilage – which doesn’t have calcium. And then, at the stage when a barfing owner genuinely gives bones, the amount is high, and it is extended with rabbit food – avoiding constipation, which is by no means a normal state, but a disturbance – in this case, purely a feeding error. Calcium intake is not day-to-day but a self-balancing and correcting process. In this, the principle of longer-term balancing of barfers works. But somewhere along the line, it has been forgotten that at least in terms of energy nutrients, we live one day at a time. A fasting day always turns the energy balance negative, and then the body’s reserves are used – those reserves are needed if the idea from nature is mimicked all the way to famine.

In barfing, it is not essential whether dogs get 0.1, 0.5, or a gram of calcium per day – but that they get enough food: bones, cartilage, necks, and wings are not food. A 30 kg dog must be given at least 50 grams of real bone per day (to satisfy the 1.5 – 5 gram assumption). If that size eats, say, 800 g per day, most of it must be meat – not cartilage and iceberg lettuce.

And no large amount of bone is really justified. The plant world is not even worth counting in. Whether there is phosphorus or calcium in any amount calculated as a percentage of dry matter, due to the water content, they can be forgotten in the wet. Or calculate the entire portion through meat. If we still assume a 30 kg dog and an 800 g food portion (without bone), the need is 1.5 – 5 grams of calcium, and about 50 grams of bone or 1 – 3 eggshells were needed for that. 800 grams of food provides about 1.2 grams of phosphorus. No large amounts of bones are needed.

The problem with barfing is not a calcium deficiency but overfeeding bones.

This is such a wise statement that it’s good to end on it:

I’ve gradually realized that feeding isn’t as difficult as I thought. People make it difficult themselves: nitpick, count grams, argue about barfing, buy super-dry foods, lose sleep, burn ridiculous piles of money, etc… Nowadays, I feed adult dogs pretty much everything possible and impossible, but I keep the basis as cheap kibble, meat, and feeding chalk. -> the dogs thank and the wallet thanks!!!

Calcium Sources

Calcium Phosphate and Calcium Carbonate

A dog cannot utilize minerals in their pure form. Elements are the foundation of our world, but they must still be obtained as compounds from food. Different forms of calcium absorb differently, and their usability varies, just as with magnesium, for example – magnesium citrate absorbs significantly better than other forms. Not enough is known about the subject, so all research is welcome. Even from the human side.

Heaney et al. (2010) studied the differences between tricalcium phosphate and calcium carbonate in older women as a bone “hardener.” An issue that interests enthusiasts of greyhounds and other breeds.

The result was reasonably clear. The calcium supplement worked, but there were no differences between the compounds.

Fish

In developing countries, especially in overpopulated areas, mineral intake is often insufficient. “Hidden hunger” is talked about. It means that even if there is enough food otherwise, and calories are sufficient, there is still a deficiency of important protective nutrients. This is a major reason why the bioactivity and availability of zinc and calcium are being studied a lot. One reason is, of course, the increasing problem of osteoporosis. The third is the dietary supplement business’s need to find cheap raw materials for supplements; especially as there is an increasing demand for evidence that supplements also absorb. Fish processing waste is, in that respect, a valuable and desired raw material source.

Fish bones are a valuable source of calcium. Depending slightly on the type of fish, the ash content of a whole fish varies from just under a percent to slightly over two percent and is within those limits regardless of the type of fish. From that amount, about 40 mg/100 g of calcium is obtained. Regarding calcium utilization, a similar line of research includes a study on the absorption of calcium from Bangladeshi small fish eaten whole. Since similar-sized fish have about the same amount of calcium, the results can probably be safely transferred to, for example, herring and vendace.

The study was done on humans, but there is no reason to assume significant differences in dogs. Dogs might even be more efficient utilizers. From Bangladeshi small fish eaten whole, 379 mg of calcium was obtained, but it is not known from what amount. The scale suggests that it is the amount per 100 grams. The calcium was radioisotope-labeled, so the absorption amounts are reasonably reliable. According to it, 23.8% of the calcium was utilized from the fish, while 21.8% was obtained from milk giving the same amount of calcium. Considering variations, it can be said that the calcium from fish absorbs in the same amounts as from milk. Since absorption of the same scale was observed in larger fish, it can be safely stated that the bioactivity of fish bones is 21 – 24%, at least according to Malde et al. 2010:

cod 21.9%
salmon 22.5%

Studies often use calcium carbonate (CaCO₃) as a comparison, with an absorption rate of 27.4%.

Supplements

Calcium is sold in various supplements and feed additives. There are significantly more differences in them than one might initially think, both in terms of ingredients and prices. Feed chalk is definitely the cheapest, costing about ten euros for a 40-kilogram sack. However, its absorption and calcium content are low, and large amounts need to be dosed. Not everyone wants to feed such large amounts, and especially for those suffering from heartburn or other stomach issues, it can be even harmful, as a large amount of chalk effectively neutralizes stomach acids. Some calcium supplements also have a high phosphorus content, so they don’t work if you want to adjust the Ca/P ratio.

Whatever calcium supplement is used, it is important to ensure vitamin D intake, as without it, absorption and utilization are really poor.

Calcium Research

Calcium Stops Growth

Do you know what dog feeding calcium recommendations are largely based on? They are based on two studies by Herman Hazewinkel on Great Dane puppies. Of course, other studies have been done, but they are based on the basic assumptions of Hazewinkel’s work and have, in a way, been replicas of those two studies. Scientific research is based on one fundamental principle: all studies must be able to be repeated, and the same results must be obtained. If not, something is wrong somewhere. Either the research setup was wrong, or the conclusions are flawed. Both happen in the research world, but that’s why information based on only one study has always been considered unreliable. And for the same reason, no one believes homeopathy studies unless they are of a believing nature; studies proving the effectiveness of homeopathy have not been able to be repeated, and they have always been found to have flaws.

In 1999, the effects of excessive calcium and phosphorus intake on growing puppies and whether it causes long-term problems were studied. Great Dane puppies were given either a lot of calcium, a lot of calcium and phosphorus, or a normal amount of both, measured from dry matter from the third week of age to week 17.

According to the results, at 15 weeks:

those with high calcium ate less, and their weight did not grow at the same pace as the controls
those with high calcium excreted more calcium in their feces than the controls

Since calcium absorption with excessive intake was greatest at 9 weeks, but excretion through feces increased up to 15 weeks, the conclusion was clear and known: regulation starts only after the weaning age.

The slower weight gain of those with high calcium was because they ate less. The researchers believed this was due to two reasons: mineral intake was not balanced, and when phosphorus intake was insufficient, it was used for building soft tissues, not the skeleton. They also assumed this caused the puppies with high calcium and normal phosphorus to develop rickets symptoms.

Another noteworthy aspect of the experiment was that the food protein was around 22% and fat at 10%. Vitamin D intake was low, only 2.5 micrograms.

This was the easy part. The more challenging part is to assess whether we now have to accept that a triple amount of calcium up to about three months slows growth and is thus harmful to dogs. If so, then breeders and owners reducing protein to limit growth have been entirely off track – they should have just given a scoop of calcium.

But before moving on, let’s remember one thing again. Growth means weight again. At no point does growth mean the length growth of bones, i.e., the height of the dog. That is never measured, but always weight. Let’s take examples from real life with hatched weights because I can’t find real weighed ones at the moment. 12-week-old greyhound males, brothers from the same litter. Practically outcross breeding, although there is some repetition in the background. Both were the same height and weighed about the same at three months. A month later, A weighed a kilo more than B, but B was five centimeters taller. According to all researchers, A’s growth was therefore stronger than B’s because it weighed more. Wrong. B’s growth was stronger because its leg bones had grown more, and its weight was lower because, with the same portions fed, energy had not been enough to maintain fat, but all had gone to growth. This clearly erroneous perception plagues all dog nutrition studies.

In Great Dane studies, i.e., practically Hazewinkel’s work, it is always mentioned how the puppies did not stay or stayed on their growth curve. This curve is based on two older studies, Kirk’s from 1966 and Lewis’s research group’s from 1987. That’s it. It’s not about a broad sample. Has anyone at some point remembered to question the setups and results of those two studies? No, not even from the researcher side.

The research group itself admits that it is unclear why slowed growth, i.e., weight gain, i.e., weight loss, occurs. Mineral balance fluctuations were one explanation, and it is always highlighted. They themselves also threw out that one reason might have been too little energy intake. I could directly say that with any giant, which grows a meter in 10 months, 22/10 food does not meet any needs. It doesn’t suffice for any puppy at all. So, the research setup overlooked the fact that growing puppies were kept on insufficient protein intake and too low fat.

In plain language: the entire research setup collapsed because the basics of overall feeding were not in order. And again, we encounter the old problem: which factor is highlighted, and which all other factors might affect the result.

But it is still unexplained why the dogs with high calcium reduced their eating, which was, however, the biggest reason why they lost weight, i.e., did not grow. From experience (unfortunately), it is known that when a growing puppy is on too few calories and/or food amounts for a long time, they develop anorexic behavior. They stop eating, i.e., eat only what is necessary, regardless of whether suddenly there is plenty of food available.

Additionally, I am greatly bothered by the fact that in the calcium study, the dogs were kept in a vitamin D deficiency. But in 1999, vitamin D was not considered as significant a factor as it is today.

One of the study’s contributions was that the holy calcium and phosphorus ratio, the familiar abbreviation Ca/P, is not significant. It isn’t. It was known long ago, but it was raised as a health claim in the dry food market – when attention had to be turned elsewhere, and there wasn’t much else to praise about the foods.

This was a dry food study, but it dealt with calcium. So, the barfing cornerstone on which the entire feeding ideology launched by Billinghurst is based. Bones have an average of 30% calcium, and in young animals, less due to incomplete mineralization of bones, around 20%.

Let’s assume that in a typical barf diet, 60% of the food portion consists of so-called meaty bones, with half meat and half bone. Let’s play that we have a 30 kg dog that eats in a barf-like manner two percent of its weight, i.e., the food bowl weighs 600 grams. Of that 600 grams, 360 grams are meaty bones, half of which is 180 g bone, from which 54 grams of calcium is obtained. The calcium need of a 30 kg dog is at least 130 mg/MEkg, i.e., 1.6 grams, rounded to 2 grams. The typical barfer thus feeds 52 grams too much calcium with each feeding. Thank goodness for the adult dog’s ability to regulate calcium, fiber as a band-aid for such a feeding error, and the fact that most barfers don’t actually even feed bone – although they think they do.

Let’s take another calculation example. A 5 kg puppy on barfing, where meaty bones are given moderately, i.e., only half of the portion, and the puppy eats five percent of its weight – being greedy. Its food bowl holds 250 grams, of which 125 grams are meaty bones – 19 grams of calcium is obtained. The puppy’s minimum need is 680 mg/MEkg, i.e., slightly over two grams, rounded to three. The need is 3 g – 19 grams are given. That is over six times the recommendations. Hazewood did his own studies with large, triple doses calculated from the food’s kilogram weight. Think about the rest yourself.

Do you now understand why the bone amounts in barfing are concerning?

There is a bit more about the study in the Dog Nutrition Wiki

Too Much Calcium

There are two rules, or rather memes, circulating about calcium. The first is that the ratio of calcium and phosphorus must be around 1.6. No one talks about amounts because it doesn’t matter whether a dog gets 100 mg or 100 grams, as long as the ratio is correct. The second meme is that a puppy always absorbs 40% of the calcium it receives. But again, no one asks from what the 40% is calculated – a percentage alone is nothing. Let’s take an older Hazewinkel study that examined (again) calcium metabolism in Great Danes. It explains why it is said that a dog regulates calcium absorption in the range of 0-80 (or 90) percent, and puppies 40 – 80 (or 90) percent.

The study followed eight different litters. The puppies were given calcium at 0.5, 1.1, or 3% of dry matter, and the puppies were examined four times from six weeks to 26 weeks, i.e., 6.5 months of age.

The summary of the study states that except for a difference in food amount at 14 weeks, where those in the low and high calcium groups with normal phosphorus ate less, no other significant differences were found. Plasma calcium did not vary – the opposite would have been surprising to me because calcium balance, homeostasis, is perhaps the most tightly regulated in the body, and the skeleton is used as a storage if the food’s calcium is insufficient.

Calcium absorption was:

in the control group 45 -66%
with high calcium 23 – 43%
with low calcium 70 – 97%
the amount of phosphorus did not affect

In the high calcium group, more was absorbed than in the control group dogs. As a result, the dogs with high calcium accumulated more calcium in their bodies than others. There was no difference in excretion between the control dogs and those in the low calcium group.

Hazelwood’s conclusion was that if puppies are given 3.3% calcium regardless of the amount of phosphorus, calcium absorption increases, as does accumulation, so Great Dane puppies cannot protect themselves from calcium overdose – regulation does not work. They increased absorption to over 90% when the calcium amount was reduced to 0.55% (again, phosphorus did not matter), but still, low intake later led to severe osteoporosis, i.e., bone loss.

Again, that was the easy part. But the rest is more interesting – at least to me.

The composition of the food was interesting by today’s standards. Meat meal, soybean meal, corn gluten, corn and potato starch, tallow, and soybean oil. The percentages were an impressive 21% protein and 9.9% fat. I have talked enough about the low protein and fat used in these studies. I am not interested in the fact that they met the NRC’s 1974 (!) standards in 1991 – they are too low anyway. This means that the study setup, in a way, loses its foundation. It is now known that the amount and quality of protein matter in bone development. And again – all the dogs in the study suffered from vitamin D deficiency. An essential thing when considering bone mineralization and calcium behavior.

The study is based on the claim that when Great Dane puppies are fed a restricted amount, i.e., according to the energy need determined by metabolic weight, with high-protein, high-energy, and higher calcium, they develop healthier skeletons than those fed at will. This refers to Hedhammer’s et al. study on Great Danes from 1974. I would have liked to look at what was meant by high-protein and high-energy at a time when 21/10 food was considered sufficient for puppies. It was left unexamined because I couldn’t find even a summary of that study. If anyone has it, I would like to read it.

I did, however, peek at a domestic Great Dane breeder’s puppy weekly weights. I calculated the recommended energy amounts from Kempe’s book Dog Feeding and Care and compared them to the energy provided by Hazewinkel’s food portions with the same weight assumption, as Hazewinkel only mentions the energy obtained per metabolic weight kilo but forgets to mention how much the study puppies weighed. The difference was in the megajoule range, with Hazewinkel providing less, i.e., practically negligible if the weight was the same. I’m not surprised, as Kempe’s recommendations follow official truths – which are based on studies like Hazewinkel’s. We didn’t get any wiser in this side note.

Another small side note. I have sometimes mentioned that many dogs regulate their own feeding when they are at a suitable weight. Most do not eat themselves intentionally plump. This has been experimentally tested with greyhounds, which in free feeding raised their weight from tight racing weight by about three kilos and stayed there. Hazewood bypasses a similar observation with just a mention; it probably wasn’t of interest to him because it wasn’t directly related to the subject being studied. In the control group, some received a predetermined portion size, and some ate at will. There were no differences in eating amounts between these two groups.

The sad part of this study was the fate of quite a few of the Great Danes studied. Every dog in the low calcium and low phosphorus group had bone fractures. Fractures were also received by every dog in the low calcium and normal phosphorus group two, and in group one, two dogs. Every one of them had to be euthanized, and thus no blood values were obtained at 26 weeks of age. Sad for the study… or the dogs?

The timing of calcium absorption followed a familiar pattern. At 14 weeks, regulation begins to work compared to the 8-week weaning age 70% in the high calcium groups. In the low calcium groups, absorption begins to enhance at the same pace. At 20 weeks, absorption was at 40% with high calcium, while those on too low a level still absorbed as much as they could – which still wasn’t enough to harden the skeleton. At 26 weeks, regulation worked for everyone.

When it is said that a puppy always absorbs 40 – 80 or 90 percent of the calcium it receives, it actually means that:

at 8 weeks, 70% is absorbed IF calcium intake is sufficient or greater
at 8 weeks, over 80% is absorbed IF calcium intake is too low
at 14 – 20 weeks, 40% is absorbed IF calcium intake is sufficient or greater
at 14 – 20 weeks, over 80% is absorbed IF calcium intake is too low
at 26 weeks, slightly over half a year old, everyone regulates according to need

One thing is still left to mention. The calcium and phosphorus ratio. It did not play any practical role in this study either. It was found that low phosphorus intake causes phosphorus deficiency, but it is not related to the amount of calcium, but to the lack of phosphorus. So, should we now stop talking about the Ca/P ratio?

And one more time for good measure: vitamin D…

Beagle Study

Hazewinkel’s studies on calcium overdose in puppies are based on two things. They have studied a triple overdose and Great Dane puppies. That is the foundation on which modern calcium recommendations are based. In the previous sections, some effort has been made to open the nuances related to Hazewinkel’s studies. Based on the studies, the lines have been drawn according to which calcium deficiency and energy, i.e., calorie, and calcium overdose harm bone development. However, I did not find actual evidence of the harms of calcium overdose, more about deficiency.

My biggest mental problem is Hazewinkel’s breed choice. The Great Dane is certainly the most suitable subject because it grows a lot in a year, so factors affecting the skeleton are certainly visible as overemphasized. It is precisely this overemphasis that is troubling. Giants, whether they are Danes or Irish Wolfhounds, are a very small exception in the dog breed spectrum. Their size is intentionally made to be exceptional. The size of giants is just as far from “normal” as that of dwarfs. Apologies if any giant or dwarf owner now had their feelings hurt. They are certainly just as lovely pets as all others, and normal-sized ones have their own genetic problems, but it cannot be avoided that extreme structures themselves cause problems. So, we can throw out the question of how much Hazewood’s breed choice affected the results because the study was done on a naturally skeletal-sensitive breed. When he halved the calcium intake, the Danes in the experiment had to be euthanized due to bone fractures. If we forget about Italians (do they have the same problem with hereditary weakness and de facto calcium and vitamin D deficiency?), how many, for example, Jack Russells would have had fractures if calcium was halved? Not a single one, I am sure of it.

I want more on the subject, from any angle.

Around the same age is Dobenecker’s study, which examined the digestibility of calcium and phosphorus in beagles.

The study followed 20 beagle puppies from three litters, and calcium was given in the range of 15 – 300% compared to the recommendation.

And the study results were interesting, even compared to Hazewinkel’s results. Briefly quoted:

no effect on bone health was found
no clinical symptoms were observed in the bones
diet changes did not systematically affect the weight curve (note: it is specifically about the weight curve, not the growth curve)

The composition of the food was just as interesting as in feeding studies in general. 60% processed stomach, 39% cooked rice, and 1% cellulose. But unlike what the Great Dane puppies received in Hazewinkel’s study, the main indicators were at sensible levels – could the turn of the millennium have influenced… The protein from dry matter was about 31%, and fat was 29%. Well, the real grams obtained are still the most important, and even high dry matter percentages are modest in real feeding if the moisture in the portion is 80% or the portion size is significantly small. But dry matter percentages are used to compare foods, and in that, Dobenecker is at a much healthier and healthier level than Hazewinkel, even though the fat was surprisingly high.

The study confirmed the already established belief that age affects how much calcium absorption can be regulated. The amount of absorbed calcium varied greatly between different groups and only showed a tendency to decrease. The amount of absorbed phosphorus decreased in the control group, i.e., those who received the recommended calcium and phosphorus amounts, directly according to age so that the highest amounts were observed in the youngest puppies. In the age range of 6.5 – 13.5 weeks in the first feeding trial, no differences were found in calcium absorption, which confirms the knowledge that small puppies cannot regulate calcium intake.

Dobenecker found the first signs of calcium absorption regulation in the age group of 13.5 – 15.5 weeks. At that time, the 15% of the recommendation significantly increased absorption compared to those receiving a triple overdose. Even at this stage, the control group with the normal dose, a slight excess, or those with half the dose did not differ from the other groups. I would ask at this point, however, whether this means that the 50% and 100% groups did not need to enhance intake because the intake was sufficient, or that they could not enhance it. Those are two different things. In any case, the 300% group still could not reduce calcium absorption compared to the control group.

In the age range of 15.5 – 25.5 weeks, no differences in absorption were observed anymore.

Calcium absorption was affected by the food, i.e., the amount of calcium given as long as the puppies had not yet developed an intrinsic ability to regulate it. In contrast, phosphorus was affected specifically by age, so that phosphorus absorption was reduced directly as age increased. The highest phosphorus absorption was observed when there was a clear calcium deficiency (15% of the recommendation) or when the calcium and phosphorus ratio was clearly below 1:1. The poorest absorption was obtained when a triple overdose of calcium was given. The reason may be an increase in blood PTH hormone, which increases the formation of active vitamin D in the kidneys, which in turn accelerates the absorption of both minerals from the intestine. In 15.5 – 25.5-week-olds, no differences in phosphorus absorption were found anymore.

The final conclusion is the old familiar. Puppies under four or five months of age cannot regulate calcium absorption to stay within the limits offered by the intake recommendation. They cannot reduce absorption in overdose, nor enhance intake in deficiency – although the ability to enhance absorption develops earlier than the ability to reduce. Frankly, rightly so – in deficiency, all possible must be obtained quickly to provide the skeleton with even a little building material. In contrast, phosphorus regulation starts very young.

What did we get out of this study, something concrete for everyday feeding? So much that extremes are still harmful, and if there is more calcium than phosphorus, it’s good. So here, the much-advertised common sense in the dog world applies – grams do not need to be measured with three decimal precision, as long as the worst mistakes are avoided; enough food, proteins, and fat, a reasonable amount of calcium, not letting them get fat and flabby, and giving enough exercise. And even more exercise. And that vitamin D.

Barfers will genuinely like this. It still bothers me with one question. Since calcium overdose in small puppies is harmful, and since small puppies cannot protect themselves from the harms of a triple overdose, what are the harms then? Specifically? Hazewood’s experiments found one harmful effect, and it was fractures caused by calcium deficiency in Great Danes. He did not mention any concrete problem of overdose. Dobenecker found no adverse effects from anything in beagles.

Sporting Dogs

Exertion and Calcium Metabolism

Physical exertion causes a significant increase in blood calcium levels as exertion intensity exceeds 80% of maximal oxygen uptake due to increased anaerobic energy production, leading to blood acidification. The rise in blood Ca²⁺ levels may, in the long term, affect bone density reduction.

This is true for humans. The same likely applies to dogs.

It is known that exertion and the waste products it produces change the body’s acid-base balance to the acidic side, which must be neutralized. This is a fundamental reason for using electrolytes. It is also known that food itself changes the body’s acid-base balance. Foods that produce bases include fruits, vegetables, root vegetables, and nuts. On the other hand, foods that produce acid include meat, fish, poultry, and grain products, especially wheat. Animal protein is the most important acid-producing nutrient, as it ultimately produces sulfuric acid and phosphoric acid in metabolic oxidation. Plant protein, like soy, is base-producing. The composition of the diet is thus one factor that burdens the body, as homeostasis, balance, is a fundamental requirement for staying healthy and alive.

Calcium has a very important role in neutralizing acids, and the calcium store is the skeleton. When the body becomes acidic, for example, due to exertion, calcium is taken from the skeleton. Calcium obtained from food is then transferred back to the skeleton. This detachment and attachment occur in greyhounds up to a gram per day (in humans, “only” about 0.7 grams).

But calcium is also needed to neutralize the acidity raised by food. An increasing proportion of dogs are now on a meat-based raw diet, and this increases the importance of calcium. Besides the fact that meat has little calcium and a lot of phosphorus, and it sets the assumed need for the calcium and phosphorus ratio, the acidity raised by meat as food requires calcium for neutralization. Several studies have shown that metabolic acidosis caused by food causes calcium release from the bone, and in the long term, this affects bone cell function and possibly the development of osteoporosis.

Western people, however, mainly consume food that forms metabolic acids. This leads to a decrease in the body’s bicarbonate concentration and a drop in pH. Buclin et al. (2001) studied the effects of the same four-day standardized acid-producing diet and base-producing diet on calcium retention in bone in conjunction with the aforementioned pH study. According to the results, acid-producing food increased urinary calcium excretion by 74% compared to base-producing food. The aforementioned study, like several others, agrees that metabolic acidosis causes calcium release from the bone, simply due to the physiochemical dissolution of minerals. Metabolic acidosis causes a significant increase in calcium excretion in urine, but it does not affect calcium absorption in the intestine. Long-term acidosis in the body affects bone cell function.

It is still unclear whether the acid load caused by food directly or indirectly affects bone metabolism. In the indirect case, calcium balance would depend on the cations contained in the base load, such as potassium and magnesium. In most studies, magnesium and potassium have been found to have protective effects on bone. Potassium’s main sources are vegetables, fiber-rich grain products, dairy products, and potassium-containing mineral salt. Magnesium’s main sources are fiber-rich grain products.

For example, in calcium balance studies conducted by Tucker et al. (2001), it was found that potassium promotes calcium retention in bone. Adequate magnesium intake was also found to affect maintaining normal calcium metabolism and calcium balance. The study involved 615 subjects aged 69–97 years, both men and women. Bone mineral density was measured at different points on the hip and forearm. Dietary intake was assessed using food diaries. Factors affecting bone density, such as physical activity, smoking, and calcium supplement use, were considered in interpreting the results. The interval between the initial and final measurements was four years. According to the results, the intake of magnesium, potassium, fruits, and vegetables was associated with less bone loss over four years. Contrary to the hypothesis, however, high protein intake was more associated with less bone loss compared to lower protein intake.

Bushinsky (2001) compares metabolic and respiratory acidosis, and according to him, respiratory acidosis, for example, caused by intense physical exertion, affects bone mineral dissolution and reabsorption much less. In such a situation, the bone does not act as a buffer for hydrogen ions. In acute acidification cases, calcium dissolution is significantly greater in metabolic acidosis-induced acidification than in respiratory acidosis-induced acidity. Additionally, calcium has been observed to redeposit on the bone surface in acute respiratory acidosis. In chronic metabolic acidosis, net calcium removal from the bone has also been observed. In chronic respiratory acidosis, calcium dissolution has not been observed.

In greyhounds, one injury directly linked to feeding and overexertion is a hock fracture. However, they occur less frequently than would be expected. In Finland, the relationship between work and rest is not optimal or even considered for many. Additionally, calcium intake is more luck-based than knowledge-based. It is known from humans that physical activity affects the amount of calcium in the skeleton. Strength-training-type exercise or load-bearing impacts, such as running and jumping, help strengthen the skeleton. In greyhounds, one could assume that the winter base fitness and training season would strengthen not only the muscles but also the skeleton. Maximum exertion has, in turn, been found to increase the amount of ionized calcium and thus affect bone calcium metabolism negatively. Therefore, the competition season and running dogs at full speed and always to exhaustion would cause calcium loss in the skeleton, weakening it. In addition to the poor condition of the tracks, this might be one reason why stress-related fractures are practically unknown in training but familiar during the competition season.

Daily physical activity also plays an important role for calcium. Several studies on athletes and office workers have shown that exercise has a direct impact on calcium retention in bone. The bending or jarring of the bone caused by physical activity induces a change in the electrical charge of bone cells, favoring calcium deposition on the negatively charged cell edge. This piezoelectric effect also stimulates bone cells to produce cAMP and prostaglandin E2, which in turn aids in bone formation. The benefits of exercise on bone also result partly from increased blood flow to the skeleton.

The exact optimal exercise program for maintaining bone density has not yet been determined. Benefits have been obtained from exercise that produces hard impacts on the skeleton, such as running and jumping, and from strength training that loads the skeleton through strong eccentric muscle contractions. Bone density correlates positively with peak torque of the muscle, where force affects certain bones. However, bone density has little to do with the cardiovascular system.

Whatever exercise is undertaken, calcium retention in bones cannot occur unless calcium and vitamin D intake from food is sufficient.

But do you know why greyhounds don’t have hip dysplasia, nor even shoulder joint dysplasia? This is the reason, even though it’s a different issue being discussed:

Poor eating habits and low levels of physical activity combined with genetic factors are the biggest cause of osteoporosis.

And no, we cannot change the dog’s diet to make the post-meal state of the body more alkaline. We must always remember that the above discussion was about humans – not carnivores. But it is worth keeping in mind that meat also requires calcium. Not necessarily the amounts barfers use, but enough nonetheless. And the long-told advice to greyhound people – but too slowly reaching – about giving magnesium and potassium should not be shrugged off in other breeds either.

Conclusion and Final Outcome

The entire calcium and phosphorus ratio in the diet is based on assumptions and guesses, and the whole setup can change in any direction with research. For humans, it is believed that excessive phosphate intake is a problem, as is too low vitamin D intake. For dogs, phosphates are not inherently a problem, but the calcium deficiency due to meat-based feeding is. Which, contrary to beliefs, also threatens barfers if the meaty bones they use are not genuinely bone – as cartilage still has no calcium.

When you ensure that there is calcium in the food at all, and preferably more than phosphorus, and that there isn’t a ton of it, you are within the so-called safety margins. All other considerations, like playing with milligrams or worrying about whether 1.2:1 is better than 1.6:1, are purely academic musings and theorizing – a living body and real food cannot be measured with those accuracies.

Have I ever mentioned the term RARF, running and raw food? Because besides nutrition, one of the most important bone strengtheners is exercise and exertion. Muscles adapt to exertion to withstand even harder stress (supercompensation is discussed), making the muscles stronger and more robust. The same happens to the skeleton. Exertion and movement increase bone metabolism. Lack of exertion is more harmful to the skeleton than small deviations in the Ca/P ratio or amounts in milligrams. So, if balanced food is given sufficiently and dogs move at least enough to be in reasonable muscle condition, worrying about calcium balance is quite unnecessary.