Evidence-based bone protection for women in perimenopause and beyond.
One in three women over 50 will suffer an osteoporotic fracture. Most of them were never told their bone density was at risk. Osteoporosis is preventable, measurable, and treatable — but only if you know what to look for and when to act.
Select a Topic
Osteoblasts build new bone — they lay down collagen matrix and mineralise it with calcium and phosphate. Osteoclasts resorb old bone — they dissolve mineral and break down collagen, releasing calcium into the bloodstream. In healthy young adults, these processes are in balance: approximately 10% of the skeleton is remodelled each year. Peak bone mass is reached between ages 25 and 30. After that, the balance tips — resorption progressively outpaces formation, and net bone loss begins.
Estrogen directly suppresses osteoclast activity — it is the primary brake on bone resorption in women. When estrogen falls at perimenopause, this brake is released. Osteoclast activity surges, resorption accelerates, and women can lose 2–3% of bone density per year in the first 5 years post-menopause. Over a decade, this compounds to 15–30% bone loss — enough to move a woman from normal bone density to osteoporosis without any other risk factors.
DEXA scans measure bone mineral density (BMD) — the amount of calcium in a given area of bone. But fracture risk is also determined by bone microarchitecture: the trabecular structure, cortical thickness, and collagen quality. A bone can have adequate mineral density but poor microarchitecture — which is why some women fracture at T-scores that are not yet in the osteoporosis range, and why building bone quality through loading and nutrition matters alongside mineral density.
The single most important modifiable determinant of fracture risk at 60 is how much bone you built before 30 and how much you protected between 35 and 55. Bone health is a lifelong investment — but the perimenopause decade is the highest-leverage window for intervention.
In the 5 years surrounding the final menstrual period, bone loss accelerates dramatically — this is the most rapid period of bone loss in a woman's life outside of early childhood. Studies using serial DEXA measurements confirm losses of 2–3% per year at the spine and hip during this window. A woman who enters perimenopause with normal bone density and receives no intervention may have osteopenia by her late 50s and osteoporosis by her mid-60s purely from hormonal bone loss.
Women who undergo bilateral oophorectomy (removal of both ovaries) before natural menopause experience an immediate, complete loss of ovarian estrogen and testosterone. This produces bone loss that is faster and more severe than natural menopause. Women who have surgical menopause before age 45 are at significantly higher lifetime fracture risk and should almost universally be offered MHT until at least the natural age of menopause.
After the initial accelerated loss phase, bone loss continues but at a slower pace (~0.5–1% per year) driven by age-related factors: declining calcium absorption, reduced vitamin D synthesis, declining physical activity, and progressive muscle loss that reduces mechanical loading on bone. This slower late-phase loss is why bone health requires attention beyond just the menopausal transition.
The best time to protect bone is before you lose it. A DEXA scan at perimenopause gives you a baseline and the ability to act. Waiting until a fracture occurs — or until a DEXA ordered after a fall shows advanced osteoporosis — is a failure of preventive care that I see too often.
— Dr KD · The Longevity ShiftThe T-score compares your bone mineral density to that of a young healthy adult at peak bone mass. Each unit (standard deviation) represents approximately 10–12% of bone density. WHO definitions:
The Z-score compares your BMD to others of the same age and sex. A Z-score below −2.0 suggests bone density is lower than expected for your age — this raises the possibility of secondary causes of bone loss (coeliac disease, steroid use, hyperparathyroidism, etc.) that require investigation. In premenopausal women and men under 50, the Z-score is more clinically relevant than the T-score.
The majority of osteoporotic fractures in absolute numbers occur in women with osteopenia — not osteoporosis — simply because osteopenia is far more prevalent. A T-score of −2.0 combined with other risk factors (age, family history, prior fractures, steroid use) can produce a clinically significant fracture risk that warrants treatment even without meeting the −2.5 osteoporosis threshold. T-score alone does not determine treatment — the FRAX score integrates multiple risk factors for a more complete fracture risk estimate.
Your T-score is a snapshot — not a sentence. An osteopenia diagnosis at 52 is an opportunity to intervene before osteoporosis develops. Most women with osteopenia who receive appropriate management (HRT, resistance training, calcium, vitamin D) will not progress to osteoporosis.
Dual-energy X-ray absorptiometry (DEXA) uses two low-dose X-ray beams to measure bone mineral density at the lumbar spine (L1–L4) and the proximal femur (hip). These are the two sites of greatest clinical importance — vertebral fractures and hip fractures cause the most morbidity and mortality from osteoporosis. The scan takes 10–20 minutes and involves minimal radiation (less than a dental X-ray).
Repeat interval depends on the initial result and clinical context. For women with normal bone density and no significant risk factors: every 5 years. For osteopenia: every 2 years if on treatment, or annually if risk is changing. For women on bone-active medications: 2-year follow-up to assess response. A single scan without follow-up is of limited clinical value — the rate of change matters as much as the absolute value.
These are total daily intakes — from food and supplements combined. Most women on a reasonable diet consume 500–700 mg/day from food; supplements should cover the gap, not replace dietary calcium entirely.
Dietary calcium is better absorbed and distributed than supplemental calcium. Dairy (milk, yoghurt, cheese), fortified plant milks, tinned fish with bones (salmon, sardines), tofu made with calcium sulfate, almonds, bok choy, and broccoli are all meaningful dietary sources. A glass of milk provides ~300mg; a pot of yoghurt ~250mg; a small tin of sardines ~350mg.
Most common and cheapest form. Requires stomach acid for absorption — take with food. Contains 40% elemental calcium by weight. Adequate for most women with normal gastric acid production.
Absorbed without stomach acid — take anytime. Better for women on proton pump inhibitors (PPIs) or with reduced gastric acid. More expensive but meaningfully better absorbed in this group.
The concern that calcium supplements increase cardiovascular event risk arose from a 2010 meta-analysis (Bolland et al.) and has been widely reported. Subsequent larger analyses, including re-analysis of the Women's Health Initiative data, have not confirmed a significant cardiovascular risk from calcium supplementation at recommended doses when vitamin D is co-administered. The current consensus: calcium supplementation at 500–600 mg/day to fill the dietary gap (not megadoses) alongside adequate vitamin D does not meaningfully increase cardiovascular risk in healthy women.
Do not exceed 500–600 mg calcium from supplements at any one time — absorption is saturated above this level. Split doses across the day. And do not take more than needed: excess supplemental calcium is associated with kidney stones and is not more protective than adequate intake.
Vitamin D (as its active form, calcitriol) is required for calcium absorption from the gut, calcium reabsorption by the kidney, and calcium deposition into bone. Without adequate vitamin D, even high dietary calcium intake is poorly absorbed. Vitamin D deficiency causes secondary hyperparathyroidism — the parathyroid gland, sensing low calcium, pulls calcium from bone to maintain blood levels. Chronic vitamin D deficiency is a direct driver of bone loss, independent of dietary calcium intake.
Vitamin K2 (menaquinone-7, MK-7) activates osteocalcin — a protein that directs calcium into bone rather than allowing it to deposit in arteries and soft tissue. K2 does not raise calcium levels — it acts as a traffic director for the calcium already in circulation. The combination of D3 + K2 is now widely recommended for bone health and may reduce vascular calcification risk from calcium supplementation. Dose: 90–180 mcg MK-7 daily alongside D3.
Bone responds to mechanical stress. When muscle pulls on bone during resistance exercise, osteocytes (bone-sensing cells) detect the strain and signal osteoblasts to lay down new bone. This is the principle of Wolff's Law: bone remodels in response to the loads placed on it. Without adequate mechanical loading, bone atrophies — which is why astronauts lose bone mass in zero gravity, and why sedentary postmenopausal women lose bone faster than active ones regardless of calcium intake.
High-impact and progressive resistance training are the two most bone-effective forms of exercise. The LIFTMOR trial (Queensland, 2017) demonstrated that high-intensity resistance training (deadlifts, overhead press, back squat at ≥85% 1RM) significantly improved bone density at the lumbar spine and femoral neck in postmenopausal women with osteopenia and osteoporosis — safely, in just 8 months. Walking, swimming, and cycling, though beneficial for cardiovascular health, do not produce sufficient bone strain to build or maintain bone density meaningfully.
Lifting heavy is not dangerous for women with osteopenia. It is protective. The fear of fracture during resistance exercise leads many women to choose only gentle exercise — which does nothing for their bones. A supervised, progressive programme starting with correct technique is safe and effective even at T-scores of −2.0 and below.
— Dr KD · The Longevity ShiftEstrogen directly suppresses osteoclast activity — replacing the brake that is lost at menopause. MHT (menopausal hormone therapy) started at or near menopause prevents the accelerated phase of bone loss entirely. Studies consistently show that MHT maintains or increases bone mineral density at the spine and hip, and reduces vertebral and non-vertebral fracture risk by 25–35%. The WHI confirmed this even with older oral preparations — the bone benefit is one of the most robust findings across all HRT trials.
The bone-protective effect of HRT is maintained while the therapy continues — and reverses when it is stopped. Bone loss resumes after HRT discontinuation, potentially at a faster rate than if HRT had never been started. This is a key consideration in the "when to stop" conversation: women who stop HRT in their late 50s may rapidly lose the bone density they protected during treatment. Sequential management (HRT in perimenopause, transitioning to bisphosphonate if ongoing pharmacological protection is needed) is increasingly the recommended approach.
Bisphosphonates (alendronate, risedronate, zoledronic acid) inhibit osteoclast activity, reducing bone resorption. They are the most widely prescribed anti-osteoporosis medications. Alendronate (70mg weekly oral) and risedronate (35mg weekly or 150mg monthly) are the standard oral options. Zoledronic acid (5mg IV annually) is an intravenous option for women who cannot tolerate oral bisphosphonates. Evidence: 40–50% reduction in vertebral fracture risk; 25–40% reduction in hip fracture risk.
Osteonecrosis of the jaw (ONJ) is a rare but serious complication of bisphosphonates. In the context of oral bisphosphonates for osteoporosis (not high-dose IV bisphosphonates for cancer treatment), the risk is estimated at less than 1 in 10,000 to 1 in 100,000 treatment-years. Good dental hygiene, informing your dentist of bisphosphonate use before invasive dental work, and completing necessary dental treatment before starting bisphosphonates significantly reduces this risk. For most women with osteoporosis, the fracture risk reduction outweighs ONJ risk by a large margin.
Denosumab (Prolia, 60mg subcutaneous injection every 6 months) is a monoclonal antibody that inhibits RANKL — a key signalling molecule for osteoclast formation. It produces greater bone density gains than bisphosphonates and is the preferred option for women with severe osteoporosis or renal impairment. Important caveat: denosumab must not be stopped abruptly — cessation causes a rebound increase in bone resorption markers and a significant risk of multiple vertebral fractures. Patients stopping denosumab must transition to a bisphosphonate to prevent rebound.
Romosozumab (Evenity) is a newer agent that both builds bone (anabolic) and reduces resorption simultaneously — a dual mechanism. It is given as monthly subcutaneous injections for 12 months and produces the largest bone density gains of any current agent. It is reserved for women with severe osteoporosis and high fracture risk. It carries a warning regarding cardiovascular risk in women with prior myocardial infarction or stroke — careful patient selection is essential.
The WHO FRAX tool calculates the 10-year probability of a major osteoporotic fracture (hip, spine, forearm, or shoulder) based on clinical risk factors with or without BMD. It integrates age, sex, BMI, prior fragility fracture, parental hip fracture, current smoking, alcohol (≥3 units/day), glucocorticoid use, rheumatoid arthritis, and secondary osteoporosis — alongside DEXA T-score if available. FRAX produces a percentage probability that guides treatment decisions more accurately than T-score alone.
Treatment thresholds vary by country and guideline. As a general principle: a 10-year probability of major osteoporotic fracture above 20% or hip fracture above 3% typically warrants pharmacological treatment discussion. FRAX is most useful in the grey zone — women with osteopenia where the decision to treat is not obvious from T-score alone. A 60-year-old woman with a T-score of −2.0 and a prior wrist fracture has a much higher FRAX score than a 60-year-old with the same T-score and no fracture history — and may warrant medication where the latter does not.
FRAX is a starting point for the conversation — not a verdict. It does not include all risk factors (falls, muscle strength, trabecular bone score) and may underestimate risk in some populations. A clinician who understands your full picture will always contextualise FRAX alongside the rest of your clinical history.
Approximately 30% of bone by weight is protein (primarily collagen type I). Adequate protein is essential for bone matrix quality, not just mineral density. Studies show that higher protein intake is associated with better bone density and lower fracture risk in postmenopausal women — the old concern that protein "acidifies" the skeleton and causes calcium loss is not supported by current evidence. Target: 1.2–1.6g/kg body weight/day.
Approximately 60% of the body's magnesium is stored in bone. Magnesium is required for vitamin D activation and for crystal structure of bone mineral. Deficiency is common — up to 50% of Western populations are suboptimal. Food sources: leafy greens, nuts, seeds, dark chocolate, legumes. Supplement: magnesium glycinate 300–400mg/day (better absorbed and less laxative effect than magnesium oxide).
Secondary osteoporosis is not rare — it is under-investigated. When I see a 45-year-old woman with a Z-score of −2.5 and no obvious risk factors, I do not accept "idiopathic osteoporosis" as the conclusion until I have checked thyroid, calcium, PTH, vitamin D, coeliac antibodies, and reviewed her medication list. There is usually an answer. Find it.
— Dr KD · The Longevity Shift