Strontium for Bones - What is it?

• A mineral. Some research suggests that it may be essential.

How does Strontium work?

• Bone-anabolic and anti-resorptive. Both reduces the excessive teardown of old bone, and increases the formation of new bone tissue.

How has it affected bone mineral density (BMD) in clinical trials?

• Significantly increases.

How does it affect bone “quality”?

• Maintains.

How has it affected fracture risk in clinical trials?

• Reduces by ~40%.

What are the side-effects?

• None reported.

Who might benefit the most?

• Appears to be appropriate for all states of bone health.

---

Questions and Answers about Strontium Supplements

Since we introduced you to the health benefits of stable Strontium in Advances 2(3), we’ve been inundated with questions about this radical new bone health mineral. We’re taking the opportunity to lay out the facts as we know them here.

Q* The Strontium supplements I have found are either Strontium citrate or Strontium carbonate. But I keep hearing about Strontium ranelate in the news. Am I getting the wrong kind of Strontium?

A* The reason for all the press stories on Strontium ranelate is because a major internatioinal drug company is now moving this salt of Strontium through the clinical trial process in hopes of marketing it as a drug. So it should come as no surprise if the most recent, most lavishly-funded, and most well-publicized studies in recent years have been the ones performed using this form of Strontium. However, there is nothing “magical” about this particular Strontium form. Independent studies have used many different forms of Strontium, including Strontium lactate, gluconate, carbonate, chloride, acetate, and still other forms of the mineral. Guess what? They all work.

So why is the drug company using the ranelic acid salt? Some of the reasons are revealed in a review of the science on Strontium written by Dr. Jean-Yves Reginster, an investigator with the World Health Organization (WHO) Collaborating Center for Public Health Aspects of Rheumatic Diseases, and with the Bone and Cartilage Metabolism Unit of the University of Liège. Dr. Reginster is the author of fourteen peer-reviewed scientific journal articles on the role of Strontium in bone health, and was a principal investigator on three of the largest and best-designed trials.

On the other hand, you can get an even higher elemental yield from some other forms of Strontium. Strontium carbonate, for instance, has 593 mg of Strontium per gram of the compound. But many of these forms of Strontium have poor “gastric tolerance” – in other words, they’re more likely to causes upset stomach or diarrhea. The ranelic acid salt has good gastric tolerance.

Dr. Reginster also notes that Strontium ranelic acid salt has good bioavailability – about 27%.9 However, this really doesn’t make much of a difference in the case of Strontium: all forms of Strontium have bioavailabilities in the 25-30% range. But there is likely another reason why the pharmaceutical company that is now pushing the ranelic acid salt of Strontium through the “drug” development pipeline:
patent control. Strontium lactate, citrate, gluconate, and carbonate are all natural, unpatentable forms of Strontium – whereas ranelic acid is a purely synthetic molecule that does not occur in nature. By using the ranelic acid salt, Big Pharma may be hoping to shore up its market protection and regulatory exclusivity on the “drug” market for what is, fundamentally, a dietary supplement: Strontium, a naturally-occurring trace mineral in the diet.

Certainly, the ranelic acid part of the Strontium ranelate compound contributes nothing to the effects of Strontium on your bones. When you swallow Strontium bound to ranelic acid, the compound splits apart into two Strontium ions and a molecule of ranelic acid. The two are then taken up into the body separately, and while the body absorbs 27% of the Strontium in a pill, it absorbs less than a tenth as much (2.5%) of the ranelic acid. And of the ranelic acid that is absorbed, 93 to 99% is excreted within 7 days without being metabolized by the body.

Molecular and animal studies have also shown that the effects of the ranelic acid salt of Strontium are due to the Strontium. In a study on the use of Strontium ranelate on bone formation in bone tissue culture, it was seen that Strontium bound to ranelic acid enhanced the replication. Independent studies have used many different forms of Strontium. They all work.

Strontium citrate enjoys the advantages of a relatively high elemental yield (about 300 milligrams elemental Sr2+ per gram of compound), so you won’t be popping fistfuls of pills to get your daily dose, and of being very soluble, giving it good gastric tolerance and bioavailability compared to many other forms (such as the carbonate). Citric acid is also a natural ligand, and is available as a dietary supplement.

Q* What do you think about all these new supplements which contain a full day’s dose of Strontium along with calcium, magnesium, and other key nutrients all in one convenient bottle?

A* They’re a disaster. In his review, Dr. Reginster specifically notes (pg. 1914) that “The simultaneous intake of [Strontium] and calcium remarkably reduces the bioavailability of [Strontium]. This is probably due to competition at the sites of active absorption. Simultaneous food intake also has a negative influence on the bioavailability of [Strontium]”. Based on this critical factor, Dr. Reginster recommends that high-dose Strontium should not be taken “concomitantly with a meal or a calcium intake.”

The competition between Strontium and calcium for absorption has long been known, and is the basis for the fact that all of the trials using strontium with major bone-health outcomes have carefully ensured that the supplement is taken on an empty stomach, away from calcium in food or in supplements. In the largest and best-designed trials, 10-13 women have taken their Strontium first thing in the morning, half an hour to an hour before breakfast, and/or three hours after dinner in the evening; they took their calcium supplements separately, with a meal.

This is the protocol supported by pharmacology and by clinical trials, and it is the one that we recommend unless your doctor specifies otherwise. It is obviously impossible to follow this protocol if you’re taking a supplement that combines calcium and Strontium in the same pill or powder! Such formulations are, therefore, not the “convenient,” “inexpensive” deals they initially seem, but are ill-designed
and likely ineffective “kitchen sink” hodgepodges. Persons taking these supplements will not reap the full benefits of Strontium documented in the clinical trials. This is a major health issue, especially for people with advanced osteoporosis. If they and their physicians are taking these combination supplements instead of a reliable, separate supplement, or instead of an established drug therapy, the results could be ruinous.

Note that these problems do not hold if there is only a small, nutritional amount of Strontium in a core bone health supplement– doses in the range of 500 micrograms to 5 milligrams, which are typical of human dietary intakes. Such doses are appropriate, as they preserve the ratio of calcium and Strontium present naturally in whole-food diets. In fact, all natural calcium sources also have a small
amount of Strontium in them, because of the similar metabolism of the two nutrients in living beings. The presence of calcium with no Strontium in calcium supplements might be expected to upset this natural
balance, leading to suppression of whatever Strontium is in your diet, ultimately perturbing the natural balance of minerals in your bone.

Indeed, some evidence already exists that, over a lifetime, these low, nutritional doses of Strontium do have a role to play in your health. For example, it was discovered in the 1960s that areas with more Strontium in the water have a lower incidence of dental caries14,15 – a finding which was to be reinforced by the findings of at least eight more studies over the course of the next few decades.

Some of these Strontium-calcium combination products further shoot their users in the foot by using poor forms of key ingredients. Some, for instance, use poor forms of calcium, such as cheap calcium carbonate (which has low gastric tolerance and which reduces your absorption of other nutrients by neutralizing stomach acid) and synthetic calcium hydroxyapatite (an extremely poorly-absorbed synthetic calcium phosphate salt, not to be confused with ossein microcrystalline hydroxyapatite complex (MCHC), an extract of bone-health nutrients contained in an intact calcium crystalline matrix). Others use
magnesium carbonate as a magnesium source; this is another antacid, and like calcium carbonate is poorly absorbed. Likewise, one of these products is even trading off of the research on Menatetrenone (MK-4) – the mammalian form of vitamin K2 and the one used in all of the “vitamin K2” clinical trials – to sell another “vitamin K2:” the unproven, bacterial menaquinones.

Q* The articles in Advances say that most trials have used dosages of Strontium in the 600-700 milligram range. But I keep hearing stories about trials using one or two grams of Strontium!

A* This comes down to the question of elemental yield: the amount of Strontium itself that is present in a given amount of an Strontium compound. Strontium, like other minerals, does not come “naked,” but as part of a compound – a salt or chelate form of the mineral. And different forms of the mineral are more or less mineral-dense. For instance, one gram (1 000 mg) of calcium carbonate contains 400
mg of elemental calcium, while the same amount of calcium citrate contains just 210 mg of elemental calcium. Similarly, to get 420 mg of elemental magnesium takes 600 mg of true, fully-reacted
magnesium aspartate, because this superior form of the mineral is only 7.5% elemental  magnesium by weight. By contrast, to get the same amount of elemental magnesium from cheap, dense,
low-bioavailability magnesium oxide requires just 696 mg of the compound, because magnesium oxide is over 60% elemental magnesium by weight.

To understand the difference on a supplement label, understand that “Calcium citrate … 1 000 mg” means 1000 mg of calcium citrate compound (yielding 210 mg of elemental calcium). By contrast, “Calcium (from calcium citrate) 1 000 mg” or “Calcium (citrate) 1 000 mg” both mean 1 000 mg of elemental calcium is present in the number of capsules or tablets listed, in the form of calcium citrate.

So when you hear that (for instance) some recent trials have used two grams (2 000 mg) of Strontium ranelate, they are telling you the amount of the compound they used – not the amount of elemental Strontium. Two grams of Strontium ranelate yield 680 mg of elemental Strontium.

Q* Can I combine Strontium supplements with a bisphosphonate drug, such as alendronate (Fosamax®)?
A* That’s an important question. Strontium is a nutrient, not a drug: you get it in your food, and it may be an essential mineral like calcium, magnesium, or zinc. At high doses, studies show that has the power to help your body to create new bone. Bisphosphonates, by contrast, are drugs – purely synthetic molecules, designed explicitly to treat a disease (osteoporosis). These drugs don’t actually build
bone – they work by merely slowing down the rate at which it is torn down (resorbed). That’s why bisphosphonates are called “antiresorptive” drugs.

But that isn’t the only effect of bisphosphonates on bone. Within weeks after you start taking a bisphosphonate, it also begins to impair your body’s formation of new bone. Because the rate at which old bone is torn down is reduced by much more than the bone-building activity osteoblasts is hampered when you take a bisphosphonate, the total mass of bone slowly increases. But by allowing old bone tissue to hang around longer without speeding its replacement, bisphosphonate use results in bone tissue that is, on average, older – and thus, of poorer quality. Because this older bone tends to be more brittle, the
overall architectural quality of the bone is decreased. The resulting bone is less prone to fracture, but is not the same as youthful, healthy bone. So the idea of combining a bone-building nutrient like Strontium
with an antiresorptive drug seems to offer a great way to get the best of both worlds. But does it actually work? 

The quick answer is: the trials haven’t been done, so we don’t know. However, two recent trials published in the New England Journal of Medicine may give us some hint as to the most likely impact of a Strontium/bisphosphonate combination. These trials did not involve Strontium; instead, they were designed to test the effects of combining a bisphosphonate with teriparatide (Forteo®), a snipped-down version of human parathyroid hormone (PTH) that has been modified using biotechnology to include only the biologically active “business end.” But teriparatide, like Strontium, works by increasing the
formation of new bone. So they probably give a good picture of the results that we can expect from taking Strontium along with a bisphosphonate drug. Although the two studies had slightly different
methodologies and the results were not exactly the same, the overall picture is this. BMD of the spine clearly increased more in women taking teriparatide only than it did in the combination-therapy group, who in turn seem to have done somewhat better than the women taking Fosamax® alone. Things were a little more complex at the femoral neck – the actual site of most so-called “hip fractures,” where the tapered area of bone at the top of the thigh that connects the main length of the thigh bone to the “ball” that fits into the “socket” of the hip. In the relatively short term (a year20 to a year and a half,21
the femoral neck BMD was unchanged in the teriparatide-only groups, or may have been slightly decreased, and any such decrease was prevented by combining teriparatide with the bisphosphonate. But in the longer term (30 months), BMD of the femoral neck was definitely highest in women taking the bone-building agent only, with no bisphosphonate drug. Meanwhile, the bone size at the femoral neck was increased by teriparatide – and Fosamax® impaired the effect. Taken together, the trials give the pretty clear picture that antiresorptive drugs, in the long term, wind up reducing the effectiveness of teriparatide. The most likely reason for this is that, as we’ve noted, bisphosphonates don’t just slow down the resorption of bone, but also reduce the overall “turnover” of bone by impairing the bone-forming activity of osteoblasts. But it’s just these bone-building cells that teriparatide depends work, by helping them mature more quickly, boosting their activity, and allowing them to live a little longer on average. So ultimately, teriparatide’s full bone-building potential is straightjacketed by bisphosphonate use. There is some direct molecular evidence that this is the case: one of the two studies measured markers of the rate at which new bone was being laid down, and found that only people taking teriperatide without Fosamax® showed evidence of increased bone formation.

While we can’t say for sure, it seems very likely that the same thing would apply with Strontium. Overall, then, the results seem to suggest that Strontium supplementation will be much less effective if it is combined with bisphosphonate use.

While you’ll have to consult with your doctor to decide what these data means for you as an individual (and certainly, you should not discontinue taking a bisphosphonate drug without your physician’s full understanding and consent), these studies do not necessarily mean that a person using Strontium should never use a bisphosphonate – or vice-versa. For one thing, it bears repeating that these studies were not performed with Strontium, and it is possible that future studies will show that bisphosphonates do not have the same restraining effect on Strontium that they do on teriparatide. Alternatively, you may decide in consultation with your doctor do adapt a protocol in which you take either Strontium or a bisphosphonate drug for a period of two to three years, and then to switch over to the other. In fact, there are already some preliminary data for just such a protocol, in osteoporotic women taking teriparatide for two years and then switching over to alendronate.

We sometimes think of our bones as being like the columns of an ancient Greek building: rigid “pillars of strength” that are built in our youth but are then slowly worn away by the forces of time. But in fact, bone is a dynamic, living tissue, like any other tissue in your body. While they seem unchanging, healthy bones are actually in a continuous process of remodeling and renewal. Old bone is torn down (resorbed) by one class of specialized cells (osteoclasts), while another kind of bone cell (osteoblasts) is responsible for building up new bone tissue to replace it. The constant balance of resorption and new bone formation allows for the replacement of old, stressed, damaged tissue with healthy new bone, and also lets the body adjust its skeletal structure when it is subjected to new or changing stresses.
But as we age, the creative equilibrium which governs the forces of remodeling becomes disrupted. In women, this is most obvious at menopause. Because the hormone estrogen suppresses the tearing down of bone by osteoclasts, the sudden reduction in the body’s estrogen production causes a dramatic increase in bone loss. But while the process of bone loss accelerates suddenly in women at menopause, it actually begins when we’re still seemingly in our physical prime. While menopause brings with it a ravaging increase in bone resorption, there is also a much less obvious slowdown in the formation of new bone which starts to take hold much earlier, in men as well as women – in our twenties, in fact.1 At this time, while bone formation is reduced, bone resorption is still under control, so the result is a gradual, almost imperceptible loss of bone mass over the course of the following decades. When the menopausal surge in bone resorption kicks in on top of decades of reduced bone formation, you get the ruinous
degradation of bone that we call osteoporosis. All of the existing, approved drugs on which mainstream medicine relies to treat osteoporosis – including bisphosphonates like alendronate (Fosamax®), hormone replacement therapy, selective estrogen receptor modulators (SERMs, such as raloxifene (Evista®)), and calcitonin (Calcimar ® or Miacalcin ®) – are “antiresorptive agents.” That is, they are all substances that work by slowing down runaway bone resorption.2-5 Even calcium and vitamin D supplements have an antiresorptive mechanism of action, keeping the body’s stores of calcium at levels high
enough to keep calcium from being leeched out of your bones by parathyroid hormone. They don’t actually increase the body’s ability to build new bone. In other words, these drugs – as well as calcium and
vitamin D – don’t actually build bone at all. They just keep old bone from being destroyed. And not only that. Believe it or not, recent research has shown that, despite what your bone mineral density (BMD) reading might say, real bone mass continues to fall while you take Fosamax® and other antiresorptive drugs. When you take antiresorptive drugs, the increase in BMD reported by DEXA machines is
not caused by an increase in true bone tissue, but by increased mineralization of the tissue you’re left with … even as the amount of tissue continues to decline. There are two problems with this approach.

The first is the issue of bone “quality.” All existing osteoporosis drugs result in bone which is, on average, made up of older, poorer-quality material. Because this older bone tends to be more brittle, the overall architectural integrity of the bone is decreased. But there’s an even more fundamental issue at stake. Conventional osteoporosis treatments are one-sided, halfway measures. That is, while bisphosphonates, HRT, SERMs, and the like are effective in treating one part of the osteoporosis problem (excessive bone resorption), they fail to address the other underlying factor in the disease
process: the age-related decline in bone formation. A doctor who treats osteoporosis with an antiresorptive drug is like a sports coach so obsessed with defensive strategy that he has his team spend all of their time learning to keep their opponents from scoring, without ever helping them learn to score goals of their own. To fully address the underlying causes of low bone mass, then, we need an agent which will not just prevent bone resorption, but also boost the body’s ability to create new bone tissue. In fact, pharmaceutical companies have been working for some time to develop new drugs that can correct the weakening of the body’s bone-building capacity. The first fruits of their labors – a drug made by modifying the structure of a fragment of the body’s parathyroid hormone (brand name Forteo®) – is expected to hit North American drug stores within a year.

But Nature already has an effective combination bone anti-resorption nutrient in her medicine chest. In fact, she’s had one since time immemorial, and it’s been known to support the health of the skeletal system for over fifty years. But until recently the research supporting its powers was incomplete, and its mechanism of supporting bone health was not understood – so its enormous importance as a bone health nutrient was overlooked. But all of that has changed in the last decade. Today, in the opening years of the twenty-first century, this nutrient is about to create a revolution in our ability to preserve – and
even to restore – the youthful structure and function of bone tissue. That nutrient is the mineral Strontium.

Two Centuries of Obscurity

Strontium was first discovered in 1790, when the Scots-Irish chemist Adair Crawford discovered a distinct mineral species mixed in with the barium crystals commonly found in ore around the Scottish town of Strontian. While some patent medicines using Strontium were sold from the late nineteenth century until the mid-50s, none of them was used for bone health, and none was ever supported by hard scientific evidence. Strontium was also used in making fireworks, paints, and TV picture tubes … a radioactive form of Strontium (90Sr) gained a certain notoriety because it was contained in nuclear fallout … and strontium was used as a delivery vehicle in some cancer treatments. But outside of these narrow fields, Strontium seemed doomed to obscurity. Certainly, few suspected that the mineral was important to human health as a nutrient, in the same sense as calcium, iron, iodine, or other essential minerals. That began to change in the 1940s, when research began to suggest that Strontium was in fact vital to the
development of a healthy skeletal system. One hint was the finding that the human body actually contains a fair amount of the mineral – and that 99% of it is concentrated in the skeleton. Scientists found that giving animals Strontium in their diets increases the buildup of bony dentin tissue in their teeth,11 and that healthy human teeth contain more Strontium than do teeth with cavities.12 In fact, areas with
more Strontium in the water were later found to have a lower incidence of dental caries13 – a finding which was to be reinforced by the findings of at least eight more studies over the course of the next few decades. More significantly, a French researcher reported that a lack of Strontium in the diet causes defective mineralization of the bones and teeth in rats and guinea pigs. This suggests that mammals need Strontium for normal development, and suffer from Strontium deficiency if they don’t get the mineral in their diets – just as they would if their diets lacked calcium, magnesium, or zinc.

Indeed, calcium and Strontium are almost always found together in natural foods, because plants, animals, and people absorb and store the two minerals in similar ways. Therefore, when studies find that calcium-rich foods support bone health, they may actually be revealing the bone-health properties of getting both minerals in the diet. The First Clinical Trials Even in those early days, some scientists were convinced that there was enough evidence for Strontium as a bone health nutrient to start doing some small-scale trials in people with osteoporosis. In fact, doctors Ephraim Shorr and Anne Carter at the Russell Sage Institute of Pathology began an open trial of Strontium for osteoporosis as early as 1942, citing as their inspiration the even earlier clinical experience of a German physician, who had used
Strontium to restore mineralization of the bones in children with bone loss caused by calcium deficiency. In the Russel Sage Institute study, people with osteoporosis took a 1700 milligram (elemental) Strontium supplement daily (in the form of Strontium lactate), usually for three to four months but sometimes for as much as four years, along with a diet carefully controlled for its calcium, protein, and phosphorus content. Several important observations were made in this study. The first was that Strontium supplements improve the retention of calcium, phosphorus, and protein in women with menopausal osteoporosis, as well as in people with osteoporosis resulting from other causes. In fact, these scientists found that when intake of calcium got high enough that retention plateaued (so that eating more calcium
resulted in no more calcium being retained by the body), adding a Strontium supplement could break the glass ceiling, causing a further increase in calcium retention. More important were the observations they made of Strontium’s effects on the disease. In the 1940s, the diagnostic technology we use today to test bone mineral density, bone formation, bone resorption, or bone quality didn’t exist. But Shorr and Carter’s studies20 revealed that subjective symptoms and objective performance tests all improved when people with osteoporosis took Strontium supplements. Women and men experienced relief from
their bone pain, and began taking up more physical activity – and their progress more strongly reflected the total retention of calcium and Strontium combined than their retention of calcium alone.
It was clear that Strontium’s effects on calcium absorption and retention alone weren’t enough to explain why the Russel Sage Institute patients were improving so much. But what could underlie the Strontium effect? One attendee at a scientific conference raised the possibility that the results meant “that strontium stimulates osteoblastic activity.” As a careful scientist, Dr. Shorr refused to engage in wild
speculation; none the less, he responded that while “We have to remain uncertain for the present as to the mechanisms … Osteoblastic activity might be stimulated”.

But it would be fifty years before science would have the tools to test this guess – and as we shall see, to prove it right. In the meantime, a second human trial using Strontium supplements in men and women with osteoporosis was performed by physicians at the Mayo clinic. Over the course of five years,  a number of their patients with osteoporosis took supplemental Strontium (again as the lactate, and again at a 1700 milligram elemental daily dose), this time for periods of three months to three years. A consistent pattern emerged in the 28 women and four men who fully completed the study. Whether they had begun the study only mildly affected by osteoporosis, or severely affected but mobile, or completely bedridden, all people suffering with osteoporosis experienced improvements in their mobility after taking Strontium supplements. “Marked” improvements in subjective symptoms were experienced by 84% of Strontium supplement users, with the remaining people still obtaining moderate improvements. “No patient failed to improve subjectively” on Strontium, the investigators reported. The effect of Strontium was also evaluated using X-rays; unfortunately, technical factors surrounding early X-ray methodology and equipment, combined with the relatively subjective nature of evaluating them, resulted in their being no consensus among the six evaluators as to whether most X-rays showed improvement.23 Indeed, it was exactly these kinds of difficulties with simple X-rays that created the push for clearer, less subjective, and much more precise results – a demand that ultimately drove the development of DEXA technology. But based on their clinical results, the Mayo Clinic physicians concluded that “the therapeutic value of [Strontium] appears to be established.” Yet, like Shorr and Carter before them, they couldn’t say just what it was about the supplement that caused the results experienced by their patients.

It would again be decades before more human research on Strontium’s role in bone health would be tested – this time, in the early 1980s, by McGill University’s Dr. Stanley Skoryna. Providing Strontium supplements (both Strontium carbonate and Strontium gluconate)) to 142 people with a range of bone health issues (including people with osteoporosis, bone loss due to not disease-related weight loss, nutrient malabsorption from liver disease, and cancer victims whose disease had spread to their skeletons), Skoryna showed that “patients treated with SST [stable Strontium therapy] have less disability than they would have had they been untreated” as judged “from radiologic findings and physical examination”. Combined with the slow trickle of animal studies which had continued to document the nutrient’s skeleton-strengthening powers over the ensuing years, these results gave Skoryna the ammunition he needed to spearhead a new human study of Strontium’s potential in osteoporosis. In a small pilot study involving just six people diagnosed with osteoporosis, his team of researchers found that, using Strontium carbonate at a dose of 600 to 700 mg daily for six months, Strontium supplementation increased the parameters of bone formation in osteoporosis patients: the surface covered by osteoblasts increased by 120.8%, and the rate of new bone formation jumped by an astounding 172.4%!

This result was unheard-of. Could Strontium actually be increasing the formation of new bone in these patients?
Skoryna’s results were not “gold standard” proof – there were too few patients, and no control group was used for comparison – but with these new findings the scientific community was forced to take notice of Strontium’s potential. Finally, then, European scientists launched the first rigorously scientific studies to evaluate Strontium’s bone-building abilities.27,28 Moving beyond the animal studies and small, uncontrolled pilot trials, these researchers initiated the large-scale, double-blind, randomized, placebo-controlled human studies that have today conclusively demonstrated the safety and effectiveness of Strontium as a mineral to build bones.

To put this result in perspective, the most powerful of the bisphosphonate drugs (alendronate/Fosamax®) increases BMD at this site by no more than 5.5%, even when combined with other therapies.

The Only True Bone-Builder

With the new wave of research into Strontium, new techniques of molecular investigation have begun to shed light on the mysteries of the mineral’s effects on bone. And this new research has confirmed what Dr. Shorr had merely guessed in 1950, and what Skoryna’s research had appeared to show in the early 1980s: namely, that Strontium not only inhibits the excessive breakdown of existing bone, but also powerfully boosts the body’s ability to build new bone.

One basis for this conclusion has been studies in experimental animals, which have shown that the actual volume of their bones increases when they are given Strontium supplemented diets. In one especially revealing study, scientists removed the ovaries of three groups of laboratory animals, as a way to simulate menopause’s low-estrogen hormonal environment. The researchers then measured the ability of estrogen replacement therapy or a Strontium-supplemented diet to prevent the loss of bone volume in their tibias (the bone that runs from the knee to the ankle). They found that, while estrogen replacement prevents the loss of bone volume caused by ovariectomy, Strontium supplements actually boost bone volume to a level 30 to 36% greater than it is before the onset of “menopause”! The loss of bone ash and bone mineral content caused by the mock-menopause was also prevented by Strontium.

These same studies have revealed the underlying reasons for Strontium’s powerful effects on bone volume. Strontium supplements cause an increase in the area of bone covered by bone-building osteoblasts, along with decreases in the number of bone-dissolving osteoclasts in bone tissue and the amount of surface that they occupy. Chemical and physiological signs of new bone formation are also boosted by Strontium supplements. The pseudo-menopause created by the removal of the ovaries in adult mice causes an increase in the rate of bone resorption and a decrease in the rate of new bone formation; Strontium prevents these changes. Parallel effects have been observed in monkeys given a Strontium-supplemented diet. More precise details have emerged from looking at Strontium’s effects on cultured bone tissue – a model that lets researchers directly study the growth, development, and activity of osteoblasts. Using this model, scientists have found that Strontium causes “baby” osteoblasts to multiply more quickly.43 An increase in the synthesis of DNA is also seen in these cells, underlying the increased growth which Strontium stimulates.  With all of these new osteoblast recruits on hand, bone tissue cultures which are exposed to Strontium synthesize more bone matrix – the mineral-enriched collagen that forms the bedrock of bone tissue. A similar model suggests that this is due to a direct increase in the formation of new bone collagen in Strontium-fortified bone tissue. The possibility that Strontium might merely be stepping in for calcium (which is in many ways metabolized very similarly to Strontium) can be ruled out, because the same amount of calcium has no effect on these parameters.

In fact, recent research appears to show that there is a receptor in the osteoblast which responds specifically to Strontium, and which is unaffected by calcium, aluminum, or other metallic elements.50 This is consistent with the fact that, while calcium is needed for the building of new bone, it does not stimulate it (although an abundance of calcium does help to suppress bone teardown). It also confirms the many other studies showing that conventional calcium supplements slow – but do not reverse – the age-related loss of bone mass (see “Bone Building Basics” in this issue of Advances).

Yet even at preventing resorption, Strontium’s powers appear to outshine calcium’s. Similar organ culture studies have found that Strontium reduces bone resorption at concentrations at which calcium has no effect. Strontium also prevents the resorption caused by excessive parathyroid hormone in this model. And unlike bisphosphonate drugs, Strontium doesn’t kill existing osteoclasts; instead, it slows the rate at which immature osteoclasts develop. This one-two punch – the coming together, in one supplement, of strong bone antiresorptive powers (see Figure 1) – creates the best of all worlds for total bone health. And – unlike what’s seen in the case of the lopsided approach of bisphosphonates and other exclusively antiresorptive drugs.

The animal evidence of increased formation of new bone is consistent with Dr. Shorr’s early speculations about osteoblast activity, and with the preliminary results seen in Dr. Skoryna’s pilot study. The bone-building activity of osteoblasts can  be measured using bone-specific alkaline phosphatase, while crosslinked N-telopeptide (NTx) and C-telopeptide (CTx) mark the degradation of bone collagen by ravaging osteoclasts. By contrast, these same tests reveal that, while bisphosphonates, HRT, and other conventional treatments for osteoporosis do inhibit resorption, the activity of women’s osteoblasts continues to fall when they take Fosamax.

Beyond “Osteoporosis”

Most of the human research on Strontium’s effects on bone structure and function has focused on women with a disease: postmenopausal osteoporosis. But unlike a drug, which would treat a “disease” as such, Strontium’s effects on bone health do not involve an alien molecule imposing itself on normal metabolic processes: instead, Strontium’s effects are the results of its natural place in bone cell metabolism,
as a nutrient in the diet. In fact, it now appears that there is even a specific receptor in osteoblastic cells that responds to strontium, and not to other minerals (such as calcium) or toxic metals (such as aluminum).

Human studies have confirmed that the benefits of Strontium on bone health are not confined to people with some specific disease state: in addition to women with postmenopausal osteoporosis, Strontium has also been found to benefit bone structure and function in bone lesions from metastatic bone carcinoma, degenerative weight loss, or liver disease, “Morquio’s disease” (also called mucopolysaccharidosis type IV, a genetic disorder which leads to a buildup of keratin sulfate in the bones, deforming them and leading to breaks in the vertebrae), “Milkman’s disease” (osteomalacia marked by multiple pseudofractures resulting from either the remodeling of previously-normal bone, or the repair of microscopic stress fractures, with osteomalacic bone tissue), Cushing’s syndrome, nutritional osteoporosis, childhood rachitic bone deformities caused by rickets, and male senile osteoporosis – and indeed, Similarly, while many recent animal experiments used experimental animal models of menopausal osteoporosis, studies performed on healthy animals with no bone disease – whether they are still developing or mature – have also confirmed the positive metabolic influence of high-dose Strontium supplementation on bone development when dietary calcium is adequate.

Calcium and Strontium: the Creative Tension

Calcium and Strontium can both play key roles in the health of your bones – if you use them properly. On the one hand, animal studies suggest that Strontium is not effective, and may even be counterproductive, if your calcium intake is not adequate. Current “official” recommendations suggest an intake of 1000 milligrams of calcium for younger adults, and 1200 milligrams for people over the age of 50. Some evidence suggests that a still higher intake (1300-1600 milligrams) of calcium is more effective for lowering fracture risk in the elderly. But remember that these numbers are your total calcium need. The more calcium you get in your diet, the less you need from supplements. At the same time, however, it’s important not to take your Strontium supplement at the same time as your calcium supplements. This is because calcium and Strontium use the same pathways for absorption in the intestinal tract, so that swallowing a calcium supplement along with your Strontium can dramatically reduce absorption. So obviously, putting Strontium and calcium in the same pill is a recipe for bone health disaster, in which you don’t get the benefits of either nutrient! As well – and surprisingly – food intake has recently been shown to reduce Strontium absorption.

The best protocol – and the one used in the most recent clinical trials – is to take your Strontium either three hours after your last meal of the day, or one hour before breakfast in the morning, or both. Because studies suggest that one last dose of calcium just before retiring can help prevent excessive resorption of bone overnight, it may be best to take all of your Strontium before breakfast, leaving you free to take a calcium supplement just before you go to bed.

Tomorrow’s Solution – Today

Until recently, all that the drug companies had to offer osteoporotic women and others concerned about their bone health was a “choice” among several drugs that slow down resorption of bone, but which do nothing to restore youthful bone formation. This has recently changed: as we mentioned before, pharmaceutical multinationals are beginning to release new drugs with bone-anabolic effects, starting with teriparatide (Forteo®), a snipped-down version of human parathyroid hormone (PTH) that has been modified using biotechnology to include only the biologically active “business end.”

But Strontium supplements are available here and now – Indeed, as far back as the early studies at the Russell Sage institute, people experienced no symptomatic or chemical or physiological signs of toxicity after taking Strontium supplements for as long as four years, at two and a half times the dose of elemental Strontium that’s used in today’s trials. That’s doubly good news to anyone waiting, with hunger and a touch of nausea, for the Fosamax® to get clear of her stomach, so that she can safely sit down to breakfast.