Most people assume osteoporosis is just about getting older. But in a significant number of cases — particularly in men and younger adults — bone loss is driven by a medication or underlying condition. Secondary osteoporosis is treatable, but you have to know to look for it.
Primary osteoporosis is the age-related and postmenopausal type — the result of normal hormonal decline and cumulative wear over decades. Secondary osteoporosis has a specific, identifiable cause: a medication, a hormonal disorder, a gastrointestinal condition, or another disease. The cause isn't aging itself.
Secondary osteoporosis accounts for roughly 30–50% of osteoporosis cases in women and up to 60–80% of cases in men. In younger adults who develop osteoporosis, an underlying secondary cause is almost always present. If you or your doctor hasn't investigated why your bones are thinning, there's a meaningful chance the real culprit is being missed.
Glucocorticoids like prednisone, prednisolone, and dexamethasone are prescribed for dozens of conditions in Canada: COPD, asthma, rheumatoid arthritis, inflammatory bowel disease, lupus, allergies, and more. They're also common after organ transplantation. And they cause serious bone loss — rapidly.
Bone loss from oral steroids can begin within the first three months of use. Studies show that prednisone at 5 mg/day or more causes measurable bone density loss within 6–12 months. At higher doses (20+ mg/day), annual bone loss can reach 10–20% at the spine. This is the most preventable form of secondary osteoporosis.
Osteoporosis Canada and Health Canada recommend that anyone starting oral corticosteroids at 7.5 mg/day or more for 3 or more months should receive:
In practice, these recommendations are frequently not followed. If you're on long-term steroids and no one has mentioned a bone density scan, ask your prescribing physician directly.
PPIs — omeprazole (Losec), pantoprazole (Pantoloc/Tecta), esomeprazole (Nexium), rabeprazole (Pariet) — are among the most widely prescribed medications in Canada. They're used for acid reflux, GERD, ulcers, and stomach protection while on NSAIDs.
The mechanism of harm: PPIs reduce stomach acid, and stomach acid is required to dissolve calcium carbonate (the most common form of calcium in food and supplements). Long-term PPI use impairs calcium absorption from both food and supplements. Multiple large observational studies have found that PPI users have a 25–40% higher risk of hip fracture compared to non-users, particularly after 5+ years of use.
The fracture risk from PPIs is real but modest in any individual — not a reason to stop a PPI that's genuinely controlling serious symptoms. But it's a reason to switch to calcium citrate instead of calcium carbonate if you supplement, ensure adequate vitamin D, and discuss bone health monitoring with your doctor if you've been on PPIs for years.
Selective serotonin reuptake inhibitors (SSRIs) — fluoxetine (Prozac), sertraline (Zoloft), escitalopram (Cipralex), citalopram (Celexa) — are commonly prescribed in Canada. There's now substantial evidence that SSRIs are associated with reduced bone mineral density and increased fracture risk. The risk appears dose-dependent and increases with duration of use.
The mechanism isn't fully understood, but serotonin receptors are present on osteoblasts and osteoclasts, and disrupting serotonin signalling appears to affect bone remodelling. A 2007 Canadian study using the Canadian Multicentre Osteoporosis Study database found that daily SSRI use was associated with significantly lower bone density at multiple sites in both men and women over 50.
This doesn't mean SSRIs should be avoided — for many people they're essential. It means that long-term SSRI users should be on your doctor's radar for bone health monitoring.
Over-replacement with levothyroxine — where TSH is suppressed below normal — is a well-established cause of bone loss, particularly in postmenopausal women. TSH suppression is sometimes intentional (thyroid cancer treatment) or unintentional (dose not adjusted as weight changes). Even subclinical hyperthyroidism (low-normal TSH) has been associated with increased fracture risk.
If you take levothyroxine (Synthroid, Euthyrox), your TSH should be monitored at least annually. If your TSH is suppressed, ask your doctor whether the dose can be adjusted — and whether a bone density assessment makes sense.
Older anticonvulsants — phenytoin (Dilantin), carbamazepine (Tegretol), phenobarbital, valproate (Depakene) — accelerate the breakdown of vitamin D through liver enzyme induction, leading to functional vitamin D deficiency and consequent bone loss. People on these medications long-term often need higher vitamin D doses (2,000+ IU/day) and regular monitoring.
Long-term heparin therapy (rare now, but still used in some pregnancy contexts) causes direct bone loss. Low-molecular-weight heparins (enoxaparin/Lovenox) have less effect. Warfarin interferes with vitamin K-dependent proteins including osteocalcin; long-term warfarin use is associated with modestly lower bone density. Newer direct oral anticoagulants (DOACs like rivaroxaban/Xarelto, apixaban/Eliquis) appear to have neutral or possibly slightly positive effects on bone — better than warfarin in this respect.
Untreated or undiagnosed celiac disease causes malabsorption of calcium, vitamin D, and magnesium — the core nutrients for bone. Even treated celiac disease (strict gluten-free diet) can result in years of subclinical deficiency before diagnosis. Osteoporosis is significantly more common in celiac patients than in the general population.
If you have celiac disease, a baseline DEXA scan is standard practice. Strict gluten-free diet is the primary treatment — it can partially reverse bone loss if started before skeletal maturity, and slows further loss at any age.
Both Crohn's disease and ulcerative colitis increase osteoporosis risk through multiple mechanisms: malabsorption, chronic inflammation that activates bone-resorbing cells, and frequent corticosteroid use for flares. Patients with IBD have approximately 40% higher fracture risk than the general population.
IBD patients on steroids face compounded risk. Biologics (infliximab/Remicade, adalimumab/Humira) used in IBD management appear to be bone-neutral or modestly protective compared to steroids — but bone monitoring should still be part of IBD care.
RA causes bone loss through both the disease itself (systemic inflammation elevates osteoclast activity) and treatment (corticosteroids). Even well-controlled RA patients on disease-modifying drugs like methotrexate have higher fracture rates than matched controls. Bone protection should be a standard part of RA management in Canada.
Low sex hormones — estrogen in women, testosterone in men — are among the strongest drivers of bone loss. Causes include premature menopause (before 45), eating disorders, exercise-induced amenorrhea (female athletes losing their menstrual cycle), and testosterone deficiency from any cause in men. See our osteoporosis in men guide for the male side of this picture.
Primary hyperparathyroidism — overactivity of the parathyroid glands — causes the body to pull calcium from bones into the blood. It's common in older women and often found incidentally on blood tests showing elevated calcium. Surgical removal of the overactive gland(s) often dramatically improves bone density.
Both types of diabetes are associated with increased fracture risk, though through different mechanisms. Type 1 diabetes causes lower bone density due to impaired bone formation. Type 2 diabetes is puzzling — bone density is often normal or elevated, but fracture risk is still higher, likely because diabetes impairs bone quality and increases fall risk through neuropathy and hypoglycemic episodes.
| If you take/have... | Action to take |
|---|---|
| Oral corticosteroids ≥3 months | Ask for DEXA scan; discuss bisphosphonates; start Ca + D3 |
| Long-term PPIs (5+ years) | Switch to calcium citrate for supplements; discuss bone monitoring |
| Long-term SSRIs | Discuss bone density monitoring with your doctor after 5+ years |
| Levothyroxine with suppressed TSH | Ask about TSH adjustment; request DEXA if on high dose |
| Celiac disease | Strict GFD; baseline DEXA; optimize Ca + D3 + Mg |
| IBD (Crohn's or UC) | Baseline DEXA if on steroids; minimize steroid exposure; optimize nutrition |
| Rheumatoid arthritis | Discuss bone protection with rheumatologist; DEXA if on steroids |
| Hypogonadism (low estrogen or testosterone) | Hormone assessment; DEXA scan; consider hormone therapy or testosterone |
The most important step is treating the underlying cause. If corticosteroids can be tapered, taper them. If celiac disease is the issue, strict gluten avoidance is non-negotiable. If hyperparathyroidism is driving bone loss, surgery often reverses it.
But secondary causes often can't be eliminated — IBD, RA, and epilepsy aren't cured, just managed. In those cases, the same pharmacological treatments used for primary osteoporosis apply: bisphosphonates, denosumab (Prolia), or anabolic agents. See our osteoporosis medication guide for details on each.
Calcium and vitamin D are foundational for everyone with secondary osteoporosis risk. The specific targets (1,000–1,200 mg/day calcium; 800–2,000 IU/day vitamin D3) apply here, with the important caveat that calcium citrate is preferred over carbonate for anyone with impaired absorption (PPIs, celiac, Crohn's, elderly).