What happens to your bones around menopause

Bone is living tissue in constant turnover — old bone resorbed by osteoclasts, new bone laid down by osteoblasts. Oestrogen restrains the osteoclasts. When oestrogen falls, resorption outpaces formation.

The result is that the years immediately around the final period are the period of most rapid bone loss in a woman's life. Loss rates in that window are several times higher than the slow decline that follows.

That timing is the whole point of this article: the window where intervention has the most leverage arrives before most people are thinking about osteoporosis at all.

The scale of it

Roughly half of women over 50 will experience a fracture related to reduced bone density at some point. Hip fracture in particular carries substantial mortality in the year afterwards and a high rate of permanent loss of independence.

Osteoporosis is asymptomatic until something breaks. There is no warning sign to wait for, which is why it is managed on risk rather than on symptoms.

Who is at higher risk

Early menopause or primary ovarian insufficiency, which extends the low-oestrogen years. Prolonged amenorrhoea at any age — including from functional hypothalamic amenorrhoea, which is why missing periods in your twenties has consequences decades later (how stress affects your cycle and missing periods when you are not pregnant). A parental history of hip fracture. Low body weight. Smoking. Heavy alcohol use. Long-term corticosteroids. Coeliac disease and other malabsorption. Rheumatoid arthritis. Some cancer treatments, particularly aromatase inhibitors.

Peak bone mass is built early

Around 90 percent of peak bone mass is accrued by around age 20, and the peak is reached in the mid-to-late twenties. After that, you are managing a declining asset.

This is why the loss of periods in adolescence and early adulthood matters so much and is so often treated casually. Bone not built then is not easily built later.

What actually protects bone

Resistance training and impact loading. This is the most effective non-pharmacological intervention, and the mechanism is specific: bone responds to mechanical strain, and it responds to high strain rather than to volume. Walking is good for many things and does relatively little for bone density.

What works: progressive resistance training with meaningful loads, and impact — jumping, hopping, skipping — where joints permit. Trials of supervised high-intensity resistance and impact training in postmenopausal women have shown maintenance or improvement in bone density, which was long thought not to be achievable. Strength training does more for women than any other exercise makes the wider case.

The important corollary: lifting heavy is not dangerous for postmenopausal women. It is protective. The advice to be careful is often exactly backwards.

Adequate protein. Bone is roughly half protein by volume. Higher protein intake is associated with better bone density, and the old concern that protein leaches calcium has not held up. How much protein women need.

Calcium and vitamin D. Sufficiency matters; supplementing beyond sufficiency does not add much. Around 1,000-1,200mg of calcium daily from diet where possible, and vitamin D supplementation where sun exposure is inadequate — which at higher latitudes is most people for much of the year.

Not smoking, and moderating alcohol.

Adequate energy intake. Underfuelling suppresses bone formation directly, independent of exercise.

Hormone therapy

Oestrogen is genuinely effective at preventing bone loss and reducing fracture risk, and that effect was demonstrated even in the WHI. For women with menopausal symptoms who are also at bone risk, it addresses both.

For women with early menopause or primary ovarian insufficiency, hormone therapy until the average age of natural menopause is standard, and bone protection is a major reason. Hormone therapy: what actually changed after the WHI.

Getting assessed

A DEXA scan measures bone density. Access varies, and it is often reserved for people with risk factors or after a fracture.

Fracture risk calculators such as FRAX estimate ten-year fracture probability from clinical factors, with or without a density measurement, and are widely used to decide who needs treatment.

Worth asking for a DEXA if: you had early menopause or primary ovarian insufficiency, you had long stretches without periods, you have a parental hip fracture history, you have been on steroids long-term, or you have broken a bone from a minor fall after 50 — a "fragility fracture" is a red flag that is very often not acted on.

The window is now, not later

The frustrating structure of this problem is that the intervention window and the consequence are separated by decades. Nothing that happens in your late forties feels urgent. The fracture arrives at 72.

Two practical things. First, know your history — the years without periods, the family fractures, the steroid courses. That history determines whether you should be assessed early, and it is remarkably easy to forget.

Second, if you start resistance training, track it. Progressive loading only works if the load actually progresses, and the difference between training for two years and training with the same weights for two years is the difference between an intervention and a habit.

Naked holds the long record — cycles across decades, gaps in them, symptoms and what you have done about them — which is exactly the history this decision needs and exactly the history nobody has when they are asked for it.