In a prospective cohort of 3,024 Swedish women aged 75–80, current smokers faced a 35% higher risk of any fracture (HR 1.35) and a striking 123% higher risk of hip fracture (HR 2.23) compared to never-smokers, even after competing mortality risk was accounted for. Mediation analyses identified two key mechanistic pathways: slower walking speed (mediating 18–28% of excess risk) and lower total volumetric BMD. Critically, each additional year of cessation conferred approximately a 1% relative reduction in both fracture and mortality risk, with women abstinent 5–10 years showing substantially lower risk than current smokers.
Hip fracture is among the most consequential injuries in older adults — carrying one-year mortality rates of 20–30% — so a doubling of risk in current smokers is clinically urgent. What elevates this study beyond standard smoking-fracture associations is its decomposition of pathways: physical function, not just bone density, is independently implicated. This reframes the clinical response: fall-prevention and strength training alongside cessation counselling are warranted, not bone protection alone. The cohort is large, prospectively followed, and uses competing-risk models that correct for the confound that heavy smokers die before fracturing. Limitations include an exclusively white, older European female sample and observational design preventing causal claims. Nevertheless, the dose-response cessation signal is convincingly precise and actionable — any age of quitting appears to yield measurable skeletal benefit.