How Pharma Invented a Fake Osteoporosis Diagnosis
About one in five Americans over age 65 fractures a hip. Depending on the cohort, between a quarter and more than half of those people are dead within a year
Many survivors never walk normally again and end their days in nursing homes.
As a public health problem, this dwarfs breast cancer, yet cultural attention is reversed.
Hip fractures happen mostly to women, but men are not exempt; men who break a hip die at higher rates than women.
The orthodox approach is to scan everyone, label about half of postmenopausal women with a manufactured precondition called “osteopenia,” and feed them oral or injected bone drugs that, in the populations they are mostly given to, do not prevent the fractures that matter and cause new fractures of their own.
The story of how this came to be is representative of how modern healthcare works.
The osteopenia con: a hotel meeting in Rome
In June 1992, the World Health Organization convened a small group of bone experts at a hotel near the top of the Spanish Steps in Rome. Until that meeting, osteoporosis had no numerical definition; doctors mostly diagnosed it after a bone fracture.
The funders wanted a number because it could be screened for, and a screening test could be sold alongside a drug. Merck, the maker of Fosamax (alendronate), had funded the development of inexpensive dual-energy X-ray absorptiometry (DEXA) scanners and was pushing hard to get them into doctors’ offices.
Anna Tosteson of Dartmouth, who was in the room, later told NPR what happened. After two or three days of arguing, the group settled on −2.5 standard deviations below the mean for a healthy young adult as the osteoporosis cutoff.
Anyone with a T-score of −1.0 to −2.5 was given a new label coined on the spot: osteopenia. Tosteson said the term was created mostly because public health researchers prefer clean categories.
None of them imagined it would be marketed back to patients as a disease that needed treatment.
Steven Cummings of UCSF, one of the most cited osteoporosis researchers alive, said flatly that there was “no basis, no biological, social, economic or treatment basis, no basis whatsoever” for using −1.0 as a clinical line, and that, as a consequence, “more than half of the population is told arbitrarily that they have a condition they need to worry about.” Alix Spiegel told this story for NPR in a piece you can read here.
So roughly half of postmenopausal women now wear a label that was invented off the cuff in a hotel suite during a meeting paid for by a company that needed more women on its drug. The chairman of that meeting, John Kanis, has confirmed in print that osteopenia was never meant to be a disease.
It became one because Merck and the DEXA-scanner industry needed it to be one. Once the label existed, the algorithm wrote itself: scan, label, prescribe, repeat.
Bisphosphonates: poison sold as medicine
Fosamax, Boniva (ibandronate), Actonel (risedronate), and the IV drug Reclast (zoledronate) are bisphosphonates, sold as bone-saving drugs. For the women they are mostly prescribed to, they are worse than nothing.
TheNNT.com summarizes the Cochrane data with their usual clarity: in postmenopausal women without a prior fracture, no high-quality study has shown a meaningful reduction in fractures that matter.
The drugs show a fracture benefit only in the smaller subset of women who already have osteoporosis on a scan and a previous broken bone. That is a population perhaps a tenth the size of the population being medicated.
These drugs do real damage. The Fosamax label and the post-marketing literature now document:
• Atypical femoral fractures. The thigh bone snaps with almost no force. The drugs were sold to prevent this and instead cause it. The risk rises with treatment duration beyond about three to five years.
• Osteonecrosis of the jaw. The jawbone deteriorates, sometimes after routine dental work. Merck has paid out hundreds of millions of dollars to settle these claims; in one Fosamax settlement, the company paid $28 million to dispose of about twelve hundred suits.
• Esophageal erosion and esophageal cancer. Oral bisphosphonates are sufficiently corrosive that patients are advised to remain upright for thirty minutes after dosing. Some users still develop esophageal injury, and the cancer signal has been debated for years.
• Atrial fibrillation. Multiple analyses link bisphosphonate use to higher rates of this dangerous arrhythmia.
• Bone and muscle pain, GI distress, eye inflammation, kidney injury, low calcium, hypersensitivity reactions. Lists of forty-plus reported side effects are not hard to find.
There are roughly eighty million bisphosphonate prescriptions written in this country. The financial reason is simple. Doctors who administer IV versions in their offices keep a margin on what they buy and inject; the same arrangement applies to Lupron for prostate cancer and several oncology drugs.
If a physician set up that kind of revenue split with another physician, it would be illegal fee-splitting. Routed through a corporation, it is the business model. I covered the same dynamic in the oncology section of Butchered by “Healthcare”.
Comment: If your doctor wants to put you or your spouse on a bisphosphonate and there has been no prior fragility fracture, you should walk out. If there has been a prior fracture, the conversation is more complicated, but it should still begin with the question, “What are we going to do about her hormones, vitamin D, vitamin K, magnesium, and muscle mass first?”
The newer drugs are worse
When the bisphosphonate franchise started showing wear, pharma rolled out three replacements. Each is more dangerous than the drug it was meant to improve upon.
Prolia (denosumab) is a twice-yearly injection that powerfully suppresses bone resorption while it is on board. The catch is that it does not remain in the bone the way a bisphosphonate does. When a dose is missed or the patient stops, bone turnover rebounds above pretreatment levels, and a wave of multiple spontaneous vertebral fractures can occur.
The FDA Prolia label reports that six percent of women who stopped Prolia in the pivotal trial developed new vertebral fractures, and three percent developed multiple new vertebral fractures. The Cleveland Clinic and others now describe roughly one in fourteen patients who discontinue without sequential antiresorptive coverage as suffering rebound fractures, and registry data link discontinuation to increased mortality.
Once on Prolia, a patient is effectively trapped on it, because getting off it safely requires giving another antiresorptive (often a bisphosphonate) for an extended period to mop up the rebound. Patients are rarely told this when they are signed up.
Evenity (romosozumab) is a monthly injection given for one year. It carries a black box warning for heart attack, stroke, and cardiovascular death. It is contraindicated in anyone who has had a heart attack or stroke in the prior year.
The FDA prescribing information exists because the pivotal ARCH trial showed an excess of major cardiovascular events with Evenity compared with the bisphosphonate alendronate. Some real-world studies argue that the cardiovascular signal is smaller than ARCH suggested. The black box warning remains on the label.
Forteo (teriparatide) and Tymlos (abaloparatide) Are daily injections of a parathyroid hormone fragment. They build bone, but the original Forteo label carried a black box warning for osteosarcoma based on rat studies showing dose-dependent bone cancer.
The boxed warning was removed in 2020, though the rat data did not change; the FDA simply allowed the company to stop printing the warning. Treatment is capped at two years.
The pattern across all five drug classes is the same. Each works by sledgehammering one side of the bone-remodeling system. None of them addresses why a sixty-year-old woman is losing bone in the first place, which is tied to her sex hormones, vitamin D, vitamin K, minerals, muscle mass, and mechanical loading. Charlotte does not have a bisphosphonate deficiency.
From my book Hormone Secrets
I wrote Hormone Secrets several years ago to share what I had learned with the patients I saw. The osteoporosis chapter opens with a real woman I called Hattie. The version below is lightly cleaned up and corrected; the substance is what was in the book.
Hattie is sixty-four and works as a federal prosecutor. She is small, single, and Chinese, and lives under chronic stress. Ten years ago, her physician told her she had “osteopenia” and started her on bisphosphonate injections, then followed her with DEXA scans. The scores still worsened. When she finally needed her hip replaced, the orthopedic surgeon told her the bone was “crumbly.”
Two years ago, Hattie started a comprehensive program: estrogen, progesterone, DHEA, testosterone pellets, vitamin K, selenium, and 10,000 IU of vitamin D daily. She added ipriflavone.
Since starting hormones, she has been able to handle jury trials and high-intensity legal work like an attorney half her age, and she cut her Prozac dose in half. Her repeat DEXA showed her bone density up seven percent over two years. She is starting human growth hormone and hopes to do even better.
The lesson from Hattie’s story is that treating bone disease is endocrine and nutritional, not pharmaceutical. The standard pathway treats osteoporosis as if the only issue is low bone density on a scan, then tries to push that number up with drugs that force the bone’s remodeling machinery into submission.
Real treatment restores the signals the bone is waiting for.
Conventional doctors usually start with bisphosphonates. TheNNT.com summarizes the Cochrane data and concludes that the drugs do not prevent fractures in women without a prior fracture and help only a small subset of women who have both osteoporosis on a scan and a prior broken bone. The drugs cause atypical femur fractures, jawbone rotting, esophageal injury, atrial fibrillation, and dozens of other side effects. Plaintiffs filed thousands of lawsuits against Merck over Fosamax-related jaw and femur disasters. The company paid $28 million to settle twelve hundred of them.
In contrast, hormone treatment usually makes people feel better while preventing and reversing bone loss. Estrogen, testosterone, DHEA, and vitamin D all build bone. Human growth hormone alone can increase bone density by about eight percent per year in some patients.
Non-hormonal treatments worth considering include selenium 200 mcg a day; vitamin K2, which I once described as “might be valuable” and now consider essential at doses of about 180 to 360 mcg a day of MK-7; and ipriflavone 600 mg a day, an isoflavone approved for osteoporosis in Japan and sold over the counter in the US.
The evidence on ipriflavone is mixed; some Italian and Japanese trials show benefit, while a 2001 JAMA trial of 474 white women found no fracture or bone density benefit and a signal of low lymphocyte counts. If a patient uses it, lymphocyte counts should be checked.
The natural history of bone loss
Bone is not a static structure. It is a constantly remodeled tissue, with osteoclasts dissolving old bone and osteoblasts laying down new bone. In a healthy young adult, these processes balance, and peak bone mass is reached around age thirty. After that, bone is slowly lost.
Estrogen levels fall sharply at menopause, and bone loss accelerates for roughly the next five to ten years. Trabecular bone in the spine and the hip is lost faster than cortical bone in the long bones. By the time a woman is in her sixties, she may have lost twenty to thirty percent of the bone she had at thirty-five.
The first warning is rarely a scan; it is a fracture from a minor fall or a vertebra that compresses without trauma.
Men lose bone too, but more slowly because their testosterone declines more gradually than women’s estrogen. In men, testosterone aromatizes to estrogen, and that estrogen is what protects bone.
Men who are chemically castrated with Lupron for prostate cancer lose bone quickly, which is one of many problems with it.
Risk factors for osteoporosis
• Female, postmenopausal, small-framed, of European or Asian background.
• Family history of osteoporosis or fragility fracture.
• Low body weight.
• Smoking and heavy alcohol use.
• Chronic steroid use, including inhaled steroids at high doses.
• Long-term proton pump inhibitors (Prilosec, Nexium and similar). They block the stomach acid needed to ionize calcium and other minerals.
• SSRIs and SNRIs (Prozac, Lexapro, Cymbalta and similar) have a documented association with reduced bone density and increased fracture risk.
• Chemical castration agents such as Lupron, aromatase inhibitors used after breast cancer, and methotrexate.
• Anticonvulsants and the diabetes drug class called thiazolidinediones (Actos).
• Hyperthyroidism, hyperparathyroidism, untreated celiac disease, inflammatory bowel disease.
• Sedentary life and lack of impact loading. Bone responds to mechanical stress; without it, bone goes away.
• Vitamin D deficiency, vitamin K deficiency, magnesium deficiency, and chronic low protein intake.
• Excess soda, especially cola, which is associated with lower bone density in women.
Should you get scanned?
The USPSTF currently recommends DEXA screening for all women sixty-five and older and for postmenopausal women under sixty-five with additional risk factors. The 2025 update emphasized DEXA over other modalities.
For Charlotte, the question is moot; she has fractured three times in eighteen months. She is osteoporotic by clinical criteria regardless of what the scan shows, and the only utility of a scan now is to track response to therapy.
For women over sixty without prior fractures, get one DEXA scan, mostly because the result tells you whether you are looking at maintenance or whether you need an aggressive program. Repeating scans every two years or so is reasonable for tracking.
Pay attention to the absolute T-score and the trend. Bisphosphonates are a failed medication class and should never be prescribed, but the other interventions here are reasonable. Ignore the term osteopenia, for this is a psych-op to sell more toxic medicines.
The scan is a brief, low-dose X-ray test. The radiation dose is about one-tenth of that of a chest X-ray. It is one of the few tests in conventional medicine that I think most women should undergo.
Vitamin D: the foundation
Vitamin D is a steroid hormone, not a vitamin, and it regulates thousands of genes involved in immune regulation and bone metabolism. The official US recommended daily allowance is 600 to 800 IU.
That amount is criminally low. It will prevent rickets and almost nothing else.
Three people I trust on this topic have steadily advanced my thinking: Neal Rouzier, MD, who has kept his level around 200 ng/mL for years; Henry Lahore, the retired Boeing scientist who built VitaminDWiki.com and keeps his level at 200; and the Brazilian neurologist Ciccero Coimbra, whose ultra-high-dose protocol of about 1,000 IU per kilogram per day has produced thousands of multiple sclerosis remissions.
Jeff Bowles, the polymath autodidact who wrote The Miraculous Results of Extremely High Doses of the Sunshine Hormone Vitamin D3, documents over a thousand self-experiments at doses ranging from 25,000 to 100,000 IU a day.
In my view, supported by these authorities and not by mainstream medicine, 25-hydroxyvitamin D blood levels well over 100 ng/mL are healthier than the levels most people have today.
Standard guidance calls 30 to 100 ng/mL “sufficient” and tells most people to aim for 40 to 60. I think 80 to 150 is closer to right for most adults, and that some people, including those with neurological or autoimmune disease, or active infection, do better at levels even higher.
I used this approach to address my own Parkinson’s after realizing my level of 120 was probably not high enough.
This is taken from a long document. Read the rest here substack.com
Header image: Renee Cotter MD