bone health

Your bone health: A guide through menopause and beyond

Bone health is often described as a “silent” aspect of women’s health, yet the underlying tissue is far from static. Bone is a dynamic, living organ that constantly breaks down and rebuilds itself. During the menopausal transition, the delicate balance between bone breakdown and formation undergoes a profound shift, making perimenopause and menopause critical windows for proactive protection.

What happens to your skeleton at menopause?

Oestrogen plays a primary role in maintaining skeletal strength by acting as an environmental brake on osteoclasts (cells that break down bone) while supporting osteoblasts (cells that build bone). During menopause, falling oestrogen levels remove this protective brake, causing bone resorption to outpace bone formation. Women can lose up to 10% to 20% of their total bone density during the 5 to 7 years spanning perimenopause and early postmenopause. After this rapid phase, bone loss continues steadily with age.

The timing of this transition matters significantly. Women who experience Premature Ovarian Insufficiency (POI, loss of ovarian function before age 40) or early menopause (between ages 40 and 45) stop producing protective oestrogen years earlier than average (age 51). Without hormonal intervention, these women face a substantially higher lifetime risk of severe osteoporosis and early fragility fractures. Beyond natural hormonal shifts, other clinical risk factors accelerate bone loss, including a family history of hip fractures, a low body mass index (BMI under 20), smoking, heavy alcohol intake (more than two standard drinks daily), prolonged glucocorticoid steroid use, and malabsorptive conditions like unmanaged Coeliac disease.

Understanding osteoporosis, T-scores, DEXA, and biomarkers

Osteoporosis is a systemic skeletal disease characterized by low bone mass and microarchitectural deterioration of bone tissue, leading to enhanced bone fragility and increased fracture risk. It is a common misconception that osteoporosis is defined solely by a scan. While a Dual-energy X-ray Absorptiometry (DEXA) scan diagnoses osteoporosis with a T-score of -2.5 or lower at the lumbar spine or hip, a clinical diagnosis is also made whenever a minimal trauma fracture occurs (a fragility fracture resulting from a fall from standing height or less, such as slipping on a rug), regardless of the DEXA result.

When you receive a DEXA scan, your bone density is expressed as a T-score, which compares your bone mineral density (BMD) directly to the peak bone mass of a healthy 30-year-old adult of the same sex. Because maximum bone density is reached around age 30, this standard serves as the benchmark for peak structural strength. A T-score of 0 means your bone density matches that young adult reference average. Scores between +1.0 and -1.0 are considered normal. As density drops, scores fall into negative numbers, with each negative whole number representing a standard deviation below peak density. A T-score between -1.0 and -2.5 indicates osteopenia (mildly reduced density), while a score of -2.5 or lower meets the diagnostic criteria for osteoporosis. It is also compared against a Z-score, which compares your bone density to age-matched peers; a significantly low Z-score (below -2.0) alerts clinicians to look for secondary causes of rapid bone loss beyond natural ageing, such as thyroid disorders, vitamin deficiencies, or coeliac disease.

For those diagnosed with osteopenia, progression to osteoporosis is not inevitable. Osteopenia is simply a warning sign of lower-than-average bone mass, and targeted lifestyle and medical strategies can successfully stabilise density.

To evaluate risk before or alongside screening, clinical assessment tools like FRAX® (which calculates 10-year fracture probability based on clinical factors) and Australia’s Know Your Bones tool (developed with the Garvan Institute) provide tailored risk profiles. A DEXA scan is indicated if you are 70 or older, over 50 with a prior fragility fracture, have POI/early menopause, or take long-term oral steroids. In Australia, Medicare provides a rebate (MBS item numbers) for DEXA scans meeting these specific clinical criteria, while non-qualifying baseline scans can be accessed privately via a GP referral.

Beyond DEXA, doctors can evaluate dynamic bone activity using Bone Turnover Markers (BTMs) via a routine blood test. While DEXA provides a static snapshot of density accumulated over years, BTMs measure real-time skeletal metabolism. Fasting blood tests look at markers like P1NP (procollagen type 1 N-terminal propeptide, which reflects rate of bone formation) and CTX (carboxy-terminal cross-linking telopeptide, which measures rate of bone breakdown). High CTX levels indicate rapid bone resorption, allowing clinicians to identify fast bone losers, monitor compliance, and evaluate how quickly MHT or osteoporosis medications are actively protecting the skeleton—months before changes appear on a DEXA scan.

The role of menopausal hormone therapy (MHT)

Menopausal Hormone Therapy (MHT) is a primary, evidence-based strategy for preventing postmenopausal bone loss and osteoporotic fractures. By directly suppressing hyperactive osteoclast activity, systemic oestrogen restores balance to the bone remodeling cycle, reducing fracture risk at all skeletal sites by 30% to 50%.

Dosing depends on your age and health history. For women reaching menopause at the average age (around 51), even low to ultra-low doses of systemic transdermal oestrogen (such as a 25–37.5 mcg patch or low-dose gel) provide significant bone-preserving benefits and slow postmenopausal bone loss. For women with POI or early menopause, standard to higher replacement doses (such as a 50–100 mcg patch or equivalent) are required until at least age 51 to replicate natural physiological exposure. For women with an intact uterus, a progestogen (such as daily or cyclical micronised progesterone) is added alongside oestrogen to protect the endometrial lining.

Prescription medications for osteoporosis in Australia

Beyond MHT, several subsidised prescription medications are available on the Australian Pharmaceutical Benefits Scheme (PBS) for individuals diagnosed with osteoporosis or who have sustained a minimal trauma fracture. These fall primarily into two categories: antiresorptive therapies (which slow bone breakdown) and anabolic therapies (which actively build new bone).

• Bisphosphonates: Available as oral tablets (such as weekly alendronate or risedronate) or an annual intravenous infusion (zoledronic acid). They bind to bone matrix to suppress osteoclasts, reducing spine and hip fracture risk by roughly 40–50%. Side effects can include reflux with oral forms or flu-like symptoms after infusions. After 3–5 years of continuous use, clinicians often evaluate a “drug holiday” because bisphosphonates remain bound in bone tissue for years, allowing protection to persist even after stopping.
• Denosumab (Prolia): A subcutaneous injection administered strictly every six months. It is a monoclonal antibody that targets RANK-L (a protein vital for osteoclast survival), rapidly turning off bone breakdown and significantly boosting density. However, denosumab must never be stopped without an immediate transition plan. Unlike bisphosphonates, its effects reverse quickly upon discontinuation; missing or stopping a dose causes a rapid rebound in bone turnover, exposing patients to accelerated bone loss and a surge in multiple vertebral fractures. If stopped, patients must immediately transition to a bisphosphonate to lock in the density gains.
• Anabolic agents (Romosozumab & Teriparatide): Reserved for severe, high-risk cases (such as multiple fractures or extremely low T-scores), these agents actively stimulate new bone formation rather than just slowing breakdown. Romosozumab (Evenity) is a dual-action monoclonal antibody targeting sclerostin that simultaneously ramps up bone formation and reduces resorption. It is administered as two monthly subcutaneous injections for a strict 12-month course. Because its bone-building effect wanes after one year, patients must immediately transition to an antiresorptive agent (like a bisphosphonate or denosumab) to lock in the newly gained bone matrix. Note: Romosozumab is contraindicated in patients with a history of heart attack or stroke in the preceding year.

Rare complications for long-term antiresorptive therapies include atypical femur fractures and osteonecrosis of the jaw (ONJ), though their incidence is extremely low compared to the number of fractures these medications prevent.

Nutrition: Building blocks for bone matrix

A strong skeleton requires adequate structural raw materials, starting with calcium, vitamin D, and protein.

• Calcium: Women over 50 require 1,300 mg of calcium daily. Food sources are strongly preferred over supplements due to better absorption and fewer gastrointestinal side effects. You can achieve 1,300 mg through 3–4 daily servings of calcium-rich foods:

• 1 cup (250 ml) cow’s milk or fortified plant milk (~300 mg)
• 200 g tub of Greek yoghurt (~240–300 mg)
• 40 g hard cheese like cheddar (~300 mg)
• 100 g firm tofu prepared with calcium (~250–350 mg)
• 100 g canned salmon with soft bones (~200 mg)
• 1/2 cup cooked dark leafy greens or 30 g almonds (~75–100 mg)

• Vitamin D: Essential for unlocking calcium absorption in the gut, with a target blood level of ≥ 50 nmol/L year-round. While safe sunlight exposure is the primary source, many women require an 800–1,000 IU daily Vitamin D3 supplement during winter or if sun exposure is limited.
• Protein: Bone tissue is approximately 50% protein by volume, forming a flexible collagen matrix that prevents bones from becoming brittle. Consuming 1.2–1.6 grams of protein per kilogram of body weight daily supports both bone matrix synthesis and muscle mass, reducing fall risk.

Targeted exercise sessions for bone stimulation

Not all exercise builds bone. While walking, swimming, and cycling benefit cardiovascular health, they lack the mechanical strain required to trigger osteoblasts to lay down new bone tissue. To stimulate density at vulnerable sites—such as the hip, femoral neck, and lumbar spine—exercise must combine Progressive Resistance Training (PRT) and high-impact movements such as in a validated program (eg ONERO) or as included in the sample program below which you can do at home, or preferably in a gym.

• Monday (Resistance A + brief impact): Compound lower-body lifting focusing on squats or box squats (3 sets of 5–8 heavy reps), trap-bar deadlifts (3 sets of 5–8 reps), and overhead dumbbell presses to load the axial spine. Finish with 3 sets of 10 firm ground stomps or heel drops.
• Tuesday (Dynamic impact & balance): 3 sets of 10 hard stomps, 3 sets of 5–8 countermovement vertical jumps or low-box drop jumps, and 3 sets of 15 seconds of skipping. Follow with 3 sets of 30-second single-leg balance holds to build joint stability and prevent falls.
• Wednesday (Active recovery): Casual walking, light stretching, or mobility work.
• Thursday (Resistance B + brief impact): Weighted step-ups (3 sets of 6–8 reps per leg), barbell bench press or push-ups, and heavy dumbbell rows to pull on spinal muscle attachments. Finish with 3 sets of 10 bounding strides.
• Friday (Dynamic impact & balance): 3 sets of single-leg hops, multidirectional star jumps, and high-challenge balance drills (e.g., standing on a foam pad or tandem foot stance).
• Weekend: Rest and active recovery.

By combining targeted strength and impact training, optimizing daily dietary intake, monitoring dynamic blood markers alongside DEXA scans, and considering tailored MHT or prescription therapies when indicated, women can actively protect their skeletal strength and maintain lifelong mobility.

References

• Australasian Menopause Society (AMS). (2023). Menopausal Hormone Therapy (MHT) and bone health. AMS Fact Sheet.
• Healthy Bones Australia. (2023). Bone Health, Risk Factors and Prevention Guidelines. Healthy Bones Australia.
• Royal Australian College of General Practitioners (RACGP) & Healthy Bones Australia. (2024). Management of osteoporosis and fracture prevention in postmenopausal women and men over 50 years of age (3rd ed.). RACGP Clinical Guidelines.