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Osteoporosis

Where your DNA places you among other people, and the studies behind it.

General information

Not tailored to your result, and not medical advice

Load Your Bones With Resistance And Impact: Bone remodels in response to mechanical strain, and low-strain activity such as ordinary walking appears to do relatively little for the spine and hip. In the LIFTMOR randomised trial, postmenopausal women with low bone mass who did 30 minutes of supervised high-intensity resistance and impact training twice a week for 8 months gained 2.9% in lumbar spine bone density while the low-intensity control group lost 1.2%, with femoral neck density and cortical thickness also improving. The training was supervised throughout and reported only one minor adverse event, which is why people with already-low bone density normally work out an exercise plan with a clinician or exercise physiologist before starting heavy loading. Journal of Bone and Mineral Research (PubMed)

Train Balance To Prevent Falls: Most fragility fractures happen when someone falls, so reducing falls matters as much as bone density itself. A Cochrane review of randomised trials in community-dwelling older adults found that exercise reduced the rate of falls by about 23% on high-certainty evidence. Balance and functional training was the best-evidenced single category, cutting falls by about 24%, also on high-certainty evidence, while programs mixing balance, functional and resistance work showed a larger reduction of roughly 34% on moderate-certainty evidence. Tai Chi showed a smaller effect on low-certainty evidence. Cochrane Database of Systematic Reviews (PMC)

Quit Or Avoid Smoking: In a meta-analysis pooling ten prospective cohorts and 59,232 people, current smokers had a higher risk of any fracture than non-smokers (RR 1.25) and a substantially higher risk of hip fracture (RR 1.84). Low bone mineral density accounted for only about 23% of the smoking-related hip fracture risk, so smoking appears to act through bone quality and fall-related routes that a density scan does not capture. Having a smoking history was also associated with raised fracture risk, but with lower risk ratios than current smoking. Osteoporosis International (PubMed)

Keep Alcohol Intake Low: A pooled analysis of three prospective cohorts covering 5,939 men and 11,032 women found no significant increase in fracture risk at intakes of two units of alcohol a day or less. Above that threshold, risk rose for any fracture (RR 1.23), osteoporotic fracture (RR 1.38) and hip fracture (RR 1.68). The relationship was non-linear rather than a steady rise across all intakes, and showed no significant interaction with age or bone mineral density, which suggests alcohol affects fracture risk through more than bone density alone. Osteoporosis International (PubMed)

Be Realistic About Calcium From Diet: Dairy, tinned fish eaten with the bones, calcium-set tofu, leafy greens and fortified plant milks are the practical food sources of calcium, and adequate intake is part of normal bone maintenance. The honest reading of the evidence is that raising calcium intake does relatively little on its own: a BMJ systematic review of 59 randomised trials found that more calcium, from food or from supplements, produced small non-progressive bone density gains of roughly 0.6% to 1.8%, which the authors judged unlikely to produce a clinically significant reduction in fracture risk. Getting diet right is worthwhile, but it is not a substitute for loading the skeleton, avoiding smoking and heavy drinking, or talking to a clinician about bone health and whether bone density testing is worth discussing. BMJ (PMC)

Genetics vs Environment

How much of this is genetic?

Genetics explains 60% of why people differ in this trait. The rest is environment, daily habits and chance.

Heritability estimate: Ralston & Uitterlinden 2010, Endocrine Reviews

About Osteoporosis

Background and further reading

Osteoporosis is a systemic skeletal disease characterized by low bone mineral density (BMD) and micro-architectural deterioration of bone tissue, which increases bone fragility and the likelihood of fracture [1]. It is often called a silent disease because bone loss occurs without symptoms until a fracture happens, most commonly at the hip, spine (vertebral compression fractures), or wrist. It is a leading cause of fractures in older adults and becomes markedly more common after menopause in women, owing to the loss of estrogen's protective effect on bone. Diagnosis is typically made by measuring BMD with a DXA scan, where a T-score of -2.5 or lower defines osteoporosis [1].

Genetic Basis: Bone mineral density is strongly heritable. Twin and family studies estimate that 50 to 85 percent of the variation in peak bone mass and BMD is due to genetic factors, making it one of the most heritable common traits [2]. Osteoporosis is highly polygenic: a large genome-wide association study of heel bone density in more than 420,000 UK Biobank participants identified 518 loci influencing estimated BMD [3], building on earlier GEFOS consortium work that mapped 56 BMD loci and 14 loci linked to fracture [4]. Many implicated genes cluster in the WNT signaling pathway (LRP5, WNT16, SOST) which regulates bone formation, and in the RANK/RANKL/OPG pathway (TNFSF11, TNFRSF11A, TNFRSF11B) which governs bone resorption. The estrogen receptor gene (ESR1) and the type I collagen gene (COL1A1) also contribute.

Environmental and Lifestyle Factors: Bone strength is shaped by many modifiable factors across life. Adequate calcium and vitamin D intake, and weight-bearing and resistance exercise, help build and preserve bone, while smoking, heavy alcohol use, low body weight, and physical inactivity accelerate bone loss [1]. Sex hormones are central: the drop in estrogen at menopause is the single largest driver of accelerated bone loss in women, and low testosterone affects men. Long-term use of glucocorticoid medications, certain endocrine conditions, and low peak bone mass attained in early adulthood all raise susceptibility. Because much of adult bone mass is set by the late twenties, nutrition and activity during childhood and adolescence have lasting effects.

How this was calculated

The published research behind your score, and the variants it draws on.

Study Details

9 published scores from 5 studies

The osteoporosis score combines 9 polygenic scores drawn from 5 published studies.

Mars N (2022). Systematic comparison of family history and polygenic risk across 24 common diseases. Am J Hum Genet: 1.1M

Truong B (2024). Integrative polygenic risk score improves the prediction accuracy of complex traits and diseases. Cell Genom: 1.9M

Jung H (2024). Integration of risk factor polygenic risk score with disease polygenic risk score for disease prediction. Commun Biol: 1.1M

Privé F (2022). Portability of 245 polygenic scores when derived from the UK Biobank and applied to 9 ancestry groups from the same cohort Am J Hum Genet: 659k

Tanigawa Y (2022). Significant sparse polygenic risk scores across 813 traits in UK Biobank. PLoS Genet: 1k

Sources

Kanis JA, et al. European guidance for the diagnosis and management of osteoporosis in postmenopausal women. Osteoporosis International (2019)

Ralston SH, Uitterlinden AG. Genetics of osteoporosis. Endocrine Reviews (2010)

Morris JA, et al. An atlas of genetic influences on osteoporosis in humans and mice. Nature Genetics (2019)

Estrada K, et al. Genome-wide meta-analysis identifies 56 bone mineral density loci and reveals 14 loci associated with risk of fracture. Nature Genetics (2012)

Related Traits

These traits are influenced by some of the same genes and variants as this one

Osteoarthritis: The most common joint disease, caused by progressive cartilage degradation and joint inflammation.

Chronic Kidney Disease: Progressive loss of kidney function over months to years, affecting waste filtration and fluid balance.

Venous Thromboembolism: Blood clots that form in the deep veins and can travel to the lungs.

Back to All Traits

Content updated August 2026.

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