Women's Bone Health: Preventing Osteoporosis

Osteoporosis is disproportionately a women's condition, for reasons that are structural rather than behavioural. Women reach a lower peak bone mass than men, and they lose it faster. Estrogen restrains osteoclasts — the cells that break bone down — so when estrogen falls away at menopause, resorption accelerates while formation does not keep pace. The steepest loss happens in the five to seven years surrounding the final period. There are additional women-specific risks that often go unrecognised: • Prolonged amenorrhea at any age. If your periods stopped in your twenties or thirties from under-fuelling or over-training, you were losing bone during years when you should have been building it — and that bone is difficult to recover. • Repeated pregnancy and extended breastfeeding without adequate calcium and vitamin D. • Restrictive dieting histories, which frequently mean years of inadequate protein and calcium. • Chronically low body weight. The condition is silent. There are no symptoms until something breaks. Height loss and a forward curve of the upper back are late signs, often indicating vertebral fractures that already happened.

A DEXA scan measures bone mineral density and returns a T-score. Above −1.0 is normal, −1.0 to −2.5 is osteopenia, and −2.5 or below is osteoporosis. Screening is generally recommended from age 65, or earlier with risk factors such as early menopause, long-term corticosteroid use, prolonged amenorrhea, a family history of hip fracture, low body weight or a prior fragility fracture. Beyond density, it is worth looking for correctable drivers, because bone loss frequently has a treatable cause hiding behind it: • 25-hydroxy vitamin D — commonly low, and a genuine cause of impaired calcium absorption. • Calcium and parathyroid hormone — to identify hyperparathyroidism. • Thyroid function — hyperthyroidism accelerates bone loss, and so does an over-replaced levothyroxine dose, which is a common and easily corrected finding. • Coeliac screening where malabsorption is plausible. Undiagnosed coeliac disease is a recognised cause of unexplained bone loss. • Medication review — long-term corticosteroids, some proton pump inhibitors and SSRIs all contribute. Bone turnover markers can show whether resorption is currently active, which is useful because it gives feedback in months rather than waiting two years for the next scan.

Bone responds to load. That is the central principle, and it explains why most general exercise advice fails to protect the skeleton. • Progressive resistance training with meaningful weight. This is the highest-yield intervention. Intensity and progression matter more than duration. • Impact loading — stepping, hopping, jumping — where joints permit. • Swimming and cycling are excellent for cardiovascular health and do essentially nothing for bone, because the skeleton is unloaded. • Walking alone is only mildly protective. Nutrition supports the process but does not substitute for load: • Protein is frequently the missing piece. The bone matrix is collagen, and older women commonly under-consume protein. Adequate intake is necessary for both bone and the muscle that loads it. • Calcium from food where possible. High-dose calcium supplementation has an uncertain risk profile, so intake is assessed first and only the shortfall supplemented. • Vitamin D dosed to a measured blood level rather than a guess, since it governs calcium absorption. • Vitamin K2 directs calcium into bone rather than soft tissue. • Magnesium supports the mineral matrix. And the endpoint that actually matters is a fracture prevented — so fall risk is addressed directly: balance work, vision, medication review and home hazards.

Nutrition and exercise are considerably better at preserving bone than at reversing established osteoporosis. Progressive resistance and impact training can produce small but real gains in bone mineral density. Correcting a vitamin D deficiency, fixing inadequate protein intake, treating undiagnosed coeliac disease or reducing an over-replaced thyroid dose can stop active loss. Those are meaningful outcomes. What they generally will not do is rebuild a skeleton that is well into the osteoporotic range. If you have already had a fragility fracture, or your T-score is significantly below −2.5, medication is usually the right call — bisphosphonates and anabolic agents have strong fracture-reduction evidence, and declining them on principle carries real risk. Naturopathic care still matters in that situation, because it addresses what the drugs do not: nutrient status, muscle mass, protein adequacy and fall risk. Dr. Sanika co-manages with prescribing physicians rather than positioning natural care as an alternative to treatment in high-risk patients. The best moment to act is osteopenia, before the loss is established. That is where the leverage is.