Osteoporosis: Bad Aim

An Essay on Bones, Bricks, and the Wrong Measure

An elderly woman was wheeled into the emergency room from a nursing home. She had stood up from her bed — not fallen, not stumbled — and fractured both hips simultaneously. Bilateral femoral neck fractures without trauma. The X-ray told the expected story at first glance: her bones were so demineralised you could barely see them, just faint outlines where the femurs should have been.

But the X-ray also told an unexpected story. Running alongside each nearly invisible femur, about a quarter of an inch to the outside, were two bright white crystalline pipes. Dense, vivid, unmistakable on the film. The emergency physician, a young Dr. Tom Cowan, asked the orthopaedic surgeon what they were.

Her calcified femoral arteries.¹

The woman did not lack calcium. She did not lack phosphorus. She did not lack the minerals that would mineralise a bone. She had plenty. Her body had simply deposited them a quarter of an inch from where they were supposed to go. “She doesn’t have osteoporosis,” Cowan told the surgeon. “She has bad aim.”¹

That observation — made over forty years ago in a small New Hampshire hospital — contains the seed of everything mainstream osteoporosis medicine gets wrong. The entire diagnostic and treatment apparatus is built around measuring mineral density: how much calcium is in the bone. The DEXA scan quantifies it. The bisphosphonate drugs try to increase it. The supplement regimens of vitamin D3 and calcium try to supply it. None of them address the question that X-ray raised: what determines where the minerals go?

When Cowan put this question to visiting osteoporosis specialists from Harvard — holding up a copy of that X-ray — the answer was always the same: we have no idea.¹

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The Baby’s Bones

Around the same time, possibly even the same day, a baby arrived in Cowan’s ER with suspected pneumonia. The chest X-ray captured most of the infant’s skeleton. What struck Cowan was something he had never noticed before: the bone density of the baby’s skeleton was almost identical to that of the elderly woman who had just broken both hips.¹

On the standard model, this makes no sense. If low bone density causes fractures, babies should be the most fracture-prone humans alive. They are the opposite. Babies almost never fracture bones. When subjected to forces that would snap an adult bone, a baby’s bone bends. You can break a baby’s bone, but it takes extraordinary force, and even then the break is typically a greenstick fracture — the bone splinters on one side while bending on the other, like a green twig.

Both the elderly woman and the baby had low mineral density. One broke both hips standing up. The other could be dropped, squeezed, and jostled without a fracture. The difference was not in the minerals. It was in what the minerals were deposited on.

Bones are two things. They are a proteinaceous matrix — a gel-like scaffolding made primarily of collagen — and they are minerals (calcium, phosphorus, and others) laid down on top of that matrix. The relationship is architectural. The collagen matrix is the wooden frame of a house. The minerals are the bricks.¹ A baby has a strong, supple, intact collagen matrix with relatively few minerals on it. The frame is excellent; there just aren’t many bricks yet. An elderly woman with osteoporosis may have a degraded, weakened matrix — the frame is rotting — and the minerals have nowhere reliable to deposit even if they’re available.

This distinction — matrix versus mineral — reframes the entire condition. Osteoporosis is not a mineral deficiency. It is a scaffolding problem. And everything in the mainstream treatment paradigm, from the diagnostic test to the drugs to the supplement protocols, is fixated on the bricks while ignoring the frame.

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Measuring the Wrong Thing

The DEXA scan measures bone mineral density. That is all it measures. It cannot assess the collagen matrix. It cannot tell you whether the scaffolding onto which those minerals are deposited is strong, supple, and intact or degraded and crumbling. It measures the bricks and says nothing about the frame.

The clinical justification for DEXA scanning rests on a specific claim: that low bone mineral density causes fractures, and that the correlation between DEXA scores and fracture incidence is tight enough to make the scan predictive. Cowan went looking for evidence that this had been proven — that low bone density was the direct cause of, or was exactly correlated with, fracture rates, particularly hip fractures. He found no such evidence.¹

There is some statistical correlation between low DEXA scores and fracture risk. But correlation across populations is not the same as causation in individuals, and the relationship is far looser than the diagnostic apparatus implies. Many people with low DEXA scores never fracture. Many people with normal DEXA scores do. The scan creates a number. The number creates anxiety. The anxiety creates a prescription. None of this addresses why bones actually break.

What the baby’s X-ray reveals — and what the DEXA scan cannot capture — is that fracture resistance comes from the integrity of the collagen matrix. A bone with a healthy matrix and low mineral density bends. A bone with a degraded matrix and low mineral density snaps. The measurement that would actually predict fractures would assess the protein scaffolding, not the mineral content. No such scan is in routine clinical use, because the entire paradigm has been built around the wrong variable.

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Heavy Bricks on a Weak Frame

The treatment that follows from measuring the wrong thing is predictably destructive.

Bisphosphonate drugs — Fosamax, Boniva, Actonel, and their successors — work by driving calcium into bone. They increase mineral density. DEXA scores improve. On paper, the treatment is working. In the body, something else is happening.

These drugs force heavy minerals onto whatever matrix exists, regardless of its condition. If the scaffolding is degraded — and in the patients being prescribed these drugs, it usually is — the result is equivalent to piling heavy bricks onto a rotting wooden frame. The structure becomes denser but more brittle. It does not become stronger. It becomes more likely to crumble.¹

The main side effect of bisphosphonates confirms this analysis exactly: pathological fractures. Bones that simply crumble without injury. Not the clean breaks of trauma — the disintegration of a structure that has been overloaded beyond what its scaffolding can bear.¹ Bisphosphonates do not prevent fractures. That has never been shown. They change the kind of fracture. Instead of a break from a fall, you get a crumbling from standing, from walking, from nothing at all.

There is a second confirmation. Bisphosphonates cause osteonecrosis of the jaw — the jawbone dies and crumbles.² The drug that is supposed to strengthen bones destroys them in the one location where mechanical stress is constant and intense. Dr. Carolyn Dean documents this as part of a broader pattern: osteoporosis drugs causing the very bone destruction they claim to prevent.³

The side effects are not a paradox. They are a prediction. If osteoporosis is a matrix problem and you treat it as a mineral problem, you will make the structure worse. The side effect profile of bisphosphonates is the clearest available evidence that the mainstream model has the mechanism backwards.

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Where Does the Calcium Go?

Cowan’s “aim” question — what directs calcium to bones rather than arteries — has an answer. It just isn’t the one mainstream medicine is looking for.

Barbara O’Neill, the Australian natural health practitioner, describes what she calls the calcium cascade.⁴ The mechanism runs as follows.

Chronic acidity — from stimulants, refined sugar, high-carbohydrate diets, stress, dehydration — pushes blood pH downward. The body’s tolerance for this is extremely narrow: blood pH below approximately 7.22 is fatal. As a last-resort buffering strategy, the body pulls calcium phosphate out of the bones to alkalise the blood. The blood pH returns to safe range. But now free calcium is circulating in the bloodstream with nowhere specific to go.⁴

The body dumps this excess calcium wherever it can. On the bones — producing bone spurs, which are calcium deposited on bones rather than in the matrix structure. In the kidneys — producing kidney stones. In the gallbladder — producing gallstones. On the eyes — producing cataracts. In the arteries — producing the calcification that Cowan saw on that X-ray forty years ago.⁴

The elderly woman didn’t lack calcium. Her body had mobilised it from her bones to buffer chronic acidity, and it landed in her femoral arteries because there was no functioning pathway to direct it back into the bone matrix.

That pathway depends on vitamin D. O’Neill describes calcium as unable to enter the cell or the bone without vitamin D, which is produced when sunlight hits the skin.⁵ Block that pathway — through indoor lifestyles, sun avoidance driven by skin cancer fears, or simple vitamin D deficiency — and calcium has no route back into the bones even when it’s abundant in the bloodstream. It circulates and deposits wherever it can.⁵

This is the answer to the “aim” question. The body does have a guidance system. It has been disabled by the conditions of modern life: chronic acidity mobilises calcium out of bones, vitamin D deficiency prevents calcium from returning to bones, and the surplus deposits in arteries, kidneys, and joints. The mainstream response — prescribing more calcium and vitamin D3 supplements — ignores the acidity that is driving the mobilisation in the first place and risks accelerating arterial calcification. Research confirms that high-dose vitamin D3 and calcium supplementation accelerates calcification of arteries,¹ which is precisely what Cowan observed on that X-ray.

The drug manufacturers know this, even if they won’t frame it this way. Osteoporosis tablet manufacturers expressly indicate patients should avoid phosphate and foods containing oxalic acids — specifically meat, sausages, soft drinks, cocoa, and chocolate — which they describe as “calcium robbers.”⁶ The manufacturers of the drugs designed to treat calcium deficiency are telling patients to stop eating the foods that create the acidity driving calcium out of their bones. They have the mechanism in their own brochures. They just haven’t followed it to its conclusion.

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What Actually Depletes Bones

If osteoporosis is a matrix problem compounded by misdirected minerals, the question becomes: what degrades the matrix and what drives the misdirection?

The matrix degrades from protein deficiency — specifically, from lack of the collagen and gelatin that form the scaffolding. Bone broth, made from simmering animal bones and cartilage, is essentially melted collagen.⁷ The gelatin it contains is the direct dietary precursor to the protein matrix of bone. A diet devoid of bone broth, gelatin, and adequate protein starves the scaffolding. The frame rots. Minerals have nothing solid to deposit on.

The misdirection — calcium leaving bones and landing in the wrong places — is driven by anything that creates chronic acidity. O’Neill and others catalogue the specific agents.

Caffeine strips calcium and magnesium from the body. O’Neill states directly: “Caffeine takes the minerals out, especially calcium and magnesium, and bones and teeth are deteriorating far too young today.”⁸

Refined sugar is an acid that enters the body with no minerals attached. It leaves the body having taken minerals with it. As O’Neill describes it: “Sugar leaves the body better dressed than when it went in. What did it go in as? Naked. Nothing. No minerals at all. It’s a pure acid.” Test the urine afterward and you find calcium and magnesium.⁸ Dr. Nancy Appleton’s research documents that sugar interferes with calcium and magnesium absorption, contributes to osteoporosis, upsets mineral relationships, and produces oxidative stress.⁹

Magnesium deficiency prevents calcium from being absorbed into bone even when calcium is present. Dr. Carolyn Dean documents that adequate magnesium is essential for calcium metabolism, yet mainstream health advice consistently recommends calcium and vitamin D for bone health while omitting magnesium entirely.¹⁰ High calcium intake without sufficient magnesium produces exactly the calcium misdirection that Cowan observed: buildup in the blood, deposition in arteries and kidneys rather than bones.

Immobility removes the mechanical stimulus that drives bone remodelling. This is not a subtle factor. Professor Ute Knierim of the University of Kassel documented that caged laying hens — unable to walk, run, flutter, or fly — develop osteoporosis, skeletal anomalies, and painful broken bones.⁶ Not from mineral deficiency. From immobility. The parallel to sedentary modern humans confined to desks and cars is direct. Cultures documented in the Blue Zone research — the Okinawans, the Sardinians, the Seventh-day Adventists of Loma Linda — live past 100 without osteoporosis. Three common denominators: very active, eating food in its natural state, and highly social.¹¹ Osteoporosis is not an inevitable consequence of aging. It is a consequence of how modern populations age.

Impoverished soils compound everything. Eighty years ago, soil contained approximately 80% more mineral content than it does today.¹² A conventionally grown tomato provides one-ninth the iron of an organic one.¹² Plants grown in depleted soil produce depleted food. Humans eating depleted food develop depleted bones. Synthetic mineral supplements do not solve this. Herbert Shelton documented that humans cannot digest rock minerals — only minerals that have passed through plants are bioavailable.¹³ Synthetic supplements are industrial chemicals produced by processing rocks with acids.¹⁴ The body treats them accordingly.

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The Woman Whose Body Was Smarter Than Her Doctor

A woman came to Cowan’s practice for help with osteoporosis, recently diagnosed on a DEXA scan. He asked for the story.¹

It started a few years earlier. Her husband told her she was getting heavier and that he liked thin women. She adopted a starvation-level vegan diet — low food overall, not just low calorie. She became tired, lethargic, and generally miserable. But she didn’t lose weight.

She went to her doctor. Blood tests. The diagnosis: Hashimoto’s hypothyroidism, an autoimmune condition of the thyroid. Low thyroid function explained the fatigue and the inability to lose weight. The treatment was straightforward. Synthroid — synthetic thyroid hormone. She took it. Her energy returned. Her thyroid numbers normalised. She lost weight. Her husband was presumably pleased.

Then a routine DEXA scan showed accelerated osteoporosis — bone loss that had developed rapidly over the previous six months, corresponding exactly to when she started the Synthroid.¹

Her doctor recommended bisphosphonates. She came to Cowan instead.

Cowan read the sequence differently. The woman had been starving herself on a vegan diet that contained no bone broth, no gelatin, no collagen-rich foods. Her protein matrix — the scaffolding of her bones — was degrading. Her body recognised this. It also recognised that the mechanical pressure of body weight on bones is one of the forces that maintains bone integrity. Losing weight while the matrix was already weakening would accelerate bone deterioration.¹

So her body did what intelligent systems do: it adapted. It slowed her thyroid function to reduce her metabolic rate, prevent weight loss, and maintain the mechanical pressure on her compromised bones. She felt tired and lethargic. She couldn’t lose weight. These were not symptoms of disease. They were symptoms of protection.¹

The doctor, seeing low thyroid numbers, diagnosed Hashimoto’s and prescribed Synthroid. The drug overrode the protective mechanism. Her metabolism increased. She lost weight. The mechanical pressure on her bones decreased. Her already-degraded matrix, now bearing less weight and still receiving no collagen from her diet, deteriorated rapidly. The DEXA scan confirmed what the body had been trying to prevent.¹

Cowan’s prescription addressed the actual causes. Eat real food, particularly bone broth — nourish the matrix. Stop the Synthroid — let the body’s protective mechanism operate. Build muscle through weight-bearing exercise — restore mechanical pressure on bones. Take Quinton plasma for minerals in bioavailable form. And get rid of the husband.¹

She came back in six months. Her osteoporosis had resolved. Her bones were back to normal. Her Hashimoto’s had resolved — she no longer had hypothyroidism because her body no longer needed the protective downregulation. She did get rid of the husband.¹

O’Neill’s framework adds a hormonal layer to this case. She teaches that high estrogen opposes thyroid function — a connection that means estrogen dominance can produce the hypothyroid picture independently.¹⁵ She also documents that progesterone directly boosts osteoblast cells — the bone-building cells — and that progesterone deficiency weakens the body’s capacity to build new bone.¹⁵ A woman under stress, eating poorly, with disrupted hormonal balance would have both the estrogen-driven thyroid suppression and the progesterone-driven osteoblast weakness operating simultaneously. The conventional intervention — synthetic thyroid hormone — addresses neither.

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The Body Is Not Failing

The pattern that runs through every element of this story is the same one that runs through most of modern medicine’s encounters with chronic disease. The body does something. Medicine calls it a malfunction. A drug overrides it. The underlying condition worsens.

The elderly woman’s body deposited calcium in her arteries because chronic acidity had mobilised it from her bones and vitamin D deficiency had closed the pathway back. The baby’s body maintained flexible, resilient bones with minimal mineralisation because its collagen matrix was intact and supple. The Hashimoto’s patient’s body slowed her thyroid to preserve the mechanical pressure protecting her compromised bones.

None of these were failures. All of them were responses — intelligent, purposeful adaptations to the conditions the body faced. The DEXA scan cannot detect this intelligence. It sees a number. The number is low. The protocol says: intervene. Drive the number up. Add minerals. Force calcium into bone. Override the thyroid. The number improves. The patient deteriorates.

Osteoporosis, read through this lens, is not a disease of calcium deficiency. It is a condition of degraded infrastructure — a weakened collagen matrix caused by inadequate protein (particularly gelatin from bone broth), compounded by chronic acidity stripping minerals from bones, vitamin D deficiency preventing their return, magnesium deficiency blocking absorption, immobility removing the mechanical stimulus for remodelling, and impoverished diets failing to supply raw materials.

The resolution is not pharmaceutical. It is architectural. Rebuild the scaffolding. Stop the processes that strip it. Restore the conditions under which the body maintains its own bones: real food, bone broth, sunlight, movement, adequate body weight, minerals in bioavailable form, and the removal of whatever chronic stressors — dietary, chemical, emotional — created the conditions in the first place.

The body is not stupid. When it slows metabolism, deposits weight, or redirects calcium, it is responding to conditions. The question is not how to override these responses. The question is what created the conditions that made them necessary.

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References

1. Cowan, T. Webinar, 4 March 2026. Clinical observations from ER practice (~40 years prior) and patient case (~20 years prior), recounted in detail.

2. Dean, C. Death by Modern Medicine (2008). Cited in Lester, D. & Parker, D. What Really Makes You Ill? (2019). Documents bisphosphonate-induced osteonecrosis of the jaw.

3. Dean, C. Death by Modern Medicine (2008). On the pattern of osteoporosis drugs causing bone destruction.

4. O’Neill, B. “Food — How It Affects You” (~19:44–21:12); Self Heal By Design, chapter on pH. The calcium cascade mechanism: chronic acidity → calcium phosphate mobilisation from bones → misplaced deposition.

5. O’Neill, B. “The Use of Water” (~41:21–44:17); “Salt & Water” (~10:18–13:40). Vitamin D as the gateway for calcium entry into cells and bones.

6. Engelbrecht, T. et al. Virus Mania, 3rd ed. (2021). Professor Ute Knierim, University of Kassel, on immobility-induced osteoporosis in caged poultry. Osteoporosis drug manufacturer (Osteplus/Merckle Arzneimittel) brochure on “calcium robbers.”

7. Cowan, T. The Contagion Myth (2020), Chapters 7–9. Bone broth as melted collagen; bones as a denser type of gel within the structured water framework.

8. O’Neill, B. “Discovering the Hidden Cause of Ailments Part 1” (~22:03–25:16); Self Heal By Design. Caffeine and refined sugar as mineral thieves.

9. Appleton, N. “141 Reasons Sugar Ruins Your Health.” Cited in Lester, D. & Parker, D. What Really Makes You Ill? (2019).

10. Dean, C. The Magnesium Miracle. Cited in Lester, D. & Parker, D. What Really Makes You Ill? (2019). “Adequate levels of magnesium are essential for the absorption and metabolism of calcium.”

11. O’Neill, B. “Discovering the Hidden Cause of Ailments Part 1” (~25:16–26:16). Blue Zone populations and absence of osteoporosis.

12. Thompson, R. The Calcium Lie. Cited in O’Neill, B. “Discovering the Hidden Cause of Ailments Part 1” (~19:56–21:49).

13. Shelton, H. Cited in Lester, D. & Parker, D. What Really Makes You Ill? (2019). “We have to draw our mineral nutrients exclusively from the plant kingdom and not from the soil.”

14. Thiel, R. “The Truth About Minerals in Nutritional Supplements.” On synthetic supplements as industrial chemicals produced by processing rocks with acids.

15. O’Neill, B. “Balancing Your Hormones” (~41:53–42:14); “How to Balance Male and Female Hormones” (2018). High estrogen opposes thyroid function; progesterone boosts osteoblast (bone-building) cells.

16. Campenhausen, J. Stern 49/1999. “According to new research, the cause of bone loss is not calcium deficiency but a diet-related over-acidification of the body.”

17. Sellmeyer, D. American Journal of Clinical Nutrition, March 2001. High ratio of dietary animal to vegetable protein increases the rate of bone loss and fracture risk in postmenopausal women.

18. Roytas, D. Can You Catch a Cold? (2024). Low-grade metabolic acidosis mechanism and acid-alkaline balance.

19. Terrain Therapy (~1940s, reprinted 2022). “The Calcium Thieves” — acid residue from sugar and starch metabolism requires calcium for elimination; when dietary supply is inadequate, the body draws from teeth and bones.

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