Bone health and osteoporosis risk: what to measure and how to protect yourself

Vitamin D and calcium metabolism

Vitamin D is the primary regulator of calcium absorption from the gut. Without adequate vitamin D, the intestine can only absorb 10-15% of dietary calcium; with optimal vitamin D status, this rises to 30-40%. The kidneys activate vitamin D from its stored form (25-hydroxyvitamin D) into its biologically active form (1,25-dihydroxyvitamin D), which then signals intestinal cells to increase calcium uptake. When vitamin D is insufficient, parathyroid hormone (PTH) rises as a compensatory response, stimulating the body to mobilise calcium from bones to maintain blood calcium levels. This continuous low-level mobilisation of skeletal calcium is one of the primary mechanisms through which vitamin D deficiency accelerates bone loss. In the UK, vitamin D deficiency is widespread from October to March due to insufficient UV-B from sunlight, and is particularly prevalent in adults aged over 65, people with darker skin, and those with limited outdoor exposure.

Sex hormones and the menopause transition

Oestrogen plays a fundamental protective role in bone metabolism by suppressing osteoclast activity (bone breakdown) and maintaining the balance between bone formation and resorption. In the decade following the menopause, women lose on average 1-3% of bone density per year, with some individuals losing significantly more during the early postmenopausal period. This makes the perimenopause and early postmenopause the period of highest bone loss risk in a woman's lifetime. Men experience more gradual bone loss as testosterone declines with age, typically from their 60s onwards. Assessing hormonal status alongside bone-relevant biomarkers provides important context for interpreting bone density trends.

Genetic risk factors

Genetics accounts for 60-80% of the variation in peak bone mass between individuals. Several gene variants are known to influence bone density, calcium metabolism and fracture risk. Variants in the vitamin D receptor (VDR), collagen type 1 genes (COL1A1 and COL1A2), LRP5 (which regulates bone formation signalling), and genes encoding osteoblast-regulating proteins all affect how efficiently your body builds and maintains bone. A family history of osteoporosis or fragility fractures is a significant independent risk factor and indicates that genetic screening, alongside monitoring of vitamin D, calcium and bone turnover markers, is particularly valuable.

Corticosteroid use and secondary osteoporosis

Long-term corticosteroid therapy (prednisolone and related drugs) is one of the most common causes of secondary osteoporosis, suppressing bone formation by reducing osteoblast activity and increasing calcium excretion through the kidneys. Rheumatoid arthritis, coeliac disease, inflammatory bowel disease, and other chronic inflammatory conditions are independently associated with increased bone loss through sustained systemic inflammation, which activates osteoclasts. Hyperthyroidism and hyperparathyroidism both accelerate bone turnover and reduce bone density. In people with any of these conditions, bone-relevant biomarker monitoring is a clinical necessity rather than optional health optimisation.

Nutrition beyond calcium

While calcium and vitamin D receive most of the attention in bone health discussions, several other nutrients play important supporting roles. Vitamin K2 (menaquinone) activates osteocalcin, a protein essential for binding calcium to the bone matrix; deficiency impairs this process and is common in people with low intake of fermented foods and green vegetables. Magnesium is required for vitamin D activation and is a cofactor in over 300 enzymatic processes including bone mineralisation. Protein provides the collagen scaffold on which bone mineral is deposited; insufficient protein intake, particularly in older adults, is associated with reduced bone density and increased fracture risk. Alcohol and tobacco both directly impair bone formation and increase bone resorption through multiple mechanisms.

Physical activity and mechanical loading

Bone adapts to mechanical load: weight-bearing and resistance exercise stimulate osteoblast activity and increase bone mineral density over time. Sedentary behaviour, bed rest, and very low body weight all reduce mechanical loading and are associated with accelerated bone loss. High-impact activities, resistance training and balance exercises all contribute to skeletal health through different but complementary mechanisms. The benefit is dose-dependent and site-specific: resistance training increases density at loaded sites, whereas walking primarily benefits hip and lumbar density.

The gold-standard diagnostic test for osteoporosis is a DEXA (dual energy X-ray absorptiometry) scan, which measures bone mineral density at the hip and lumbar spine and produces a T-score. A T-score of -2.5 or below indicates osteoporosis; between -1 and -2.5 indicates osteopenia (reduced bone density). DEXA scans are available via GP referral when osteoporosis risk is identified through clinical assessment or the FRAX risk tool. Blood tests cannot diagnose osteoporosis or measure bone density directly, but they provide crucial information about the underlying factors driving bone loss and about any secondary causes that could be addressed.

Vitamin D (25-hydroxyvitamin D) is the most practically important biomarker for bone health in the UK population. Deficiency directly impairs calcium absorption and triggers compensatory bone mobilisation through secondary hyperparathyroidism. Identifying and correcting deficiency is one of the most evidence-based interventions for bone protection across all age groups.

Calcium (serum) measures the amount of calcium circulating in the blood. Blood calcium is tightly regulated and does not fall even when bones are being progressively demineralised; it is therefore a poor indicator of total body calcium stores. However, abnormal blood calcium can indicate hyperparathyroidism, malignancy or other conditions that cause secondary bone loss, and warrants investigation when outside the normal range.

ALP (alkaline phosphatase) reflects the activity of osteoblasts (bone-forming cells) and, at elevated levels, indicates increased bone turnover. High ALP alongside bone symptoms may indicate Paget's disease of bone or other conditions of accelerated bone metabolism.

PTH (parathyroid hormone) rises as a compensatory response to low calcium and low vitamin D, mobilising calcium from bone into the bloodstream. Elevated PTH in combination with low or borderline vitamin D indicates secondary hyperparathyroidism, a state of ongoing bone calcium mobilisation that accelerates density loss.

Ferritin is relevant to bone health through its relationship with collagen synthesis and inflammatory status; iron deficiency impairs the enzymatic processes that build the collagen scaffold of bone.

For people with confirmed risk factors (early menopause, prolonged corticosteroid use, family history of fragility fracture, or BMI below 18.5), GP referral for DEXA scanning and formal fracture risk assessment using the FRAX tool is appropriate alongside blood-based monitoring.

Vitamin D: the single most actionable bone intervention in the UK

Given the near-impossibility of achieving adequate vitamin D from sunlight alone during UK winters, supplementation during the autumn and winter months is recommended across the UK population. The standard supplementation dose is 400-1000 IU per day. However, individual response to supplementation varies substantially based on body weight, baseline status and genetic variants in vitamin D metabolism. Testing your actual vitamin D level and adjusting supplementation based on the result is more effective than blanket dosing. The target range for optimal bone protection is generally considered to be 75-150 nmol/L (30-60 ng/mL), with levels below 50 nmol/L warranting prompt supplementation.

Calcium from diet and supplementation

Dietary calcium from dairy, fortified plant milks, leafy green vegetables (kale, pak choi), and fish eaten with bones (sardines, salmon) is preferable to high-dose supplementation, as calcium from food is absorbed alongside other micronutrients that support its incorporation into bone. High-dose calcium supplementation (over 1000mg/day from supplements alone) has been associated with increased cardiovascular risk in some studies. Meeting calcium needs primarily through diet, with supplementation only when dietary intake is genuinely inadequate, is the recommended approach for most adults.

Resistance training and impact exercise

Weight-bearing and resistance exercise stimulate bone formation at the specific skeletal sites being loaded. Hip and spine, the most clinically important sites for fracture risk, respond to walking, jogging, stair climbing and lower-body resistance exercises. Upper limb and vertebral density responds to upper-body resistance training. For post-menopausal women, programmes that include both impact loading and progressive resistance training produce the most consistent bone density benefits. Balance training reduces fall risk, which is the proximal cause of most hip fractures, and should be part of any comprehensive bone health programme for adults over 60.

Reducing modifiable risk factors

Smoking cessation has a direct positive effect on bone density: smoking inhibits osteoblast activity and accelerates oestrogen metabolism, both of which increase bone loss. Reducing alcohol intake below 14 units per week reduces the hepatotoxic effects on vitamin D activation and the direct inhibitory effects of alcohol on bone formation. Maintaining a healthy body weight above BMI 18.5 ensures adequate mechanical loading of the skeleton and reduces the risk of low body mass-associated bone loss. Monitoring vitamin D, calcium metabolism and bone turnover markers over time provides objective feedback on whether these interventions are translating into measurable biological improvements.