Obesity and inflammation linked to early lung ageing and higher COPD risk
Obesity and chronic low-grade inflammation may accelerate lung ageing and increase the risk of chronic obstructive pulmonary disease (COPD), according to new research from Brazil. While smoking remains the strongest driver of lung function decline, the study suggests that excess body weight and systemic inflammation can independently damage the lungs, even in younger adults.
The findings come from a long-running population study involving nearly 900 adults under the age of 40. Researchers found that obesity and elevated levels of inflammation were associated with measurable losses in lung function over time, raising concerns about future COPD risk among people who have never smoked.
COPD, often described as a “smoker’s disease”, is a progressive and irreversible condition marked by chronic airway inflammation, breathlessness and reduced airflow. However, the new evidence reinforces growing recognition that COPD has multiple causes beyond tobacco exposure.
Over a 12-year period, smoking was linked to the largest decline in lung function, with an average reduction of 1.95 per cent. But systemic inflammation, measured using C-reactive protein (CRP) in the blood, also had a significant effect: each one milligram per decilitre increase in CRP was associated with a 0.76 per cent decline in lung function. Obesity further compounded the risk, with each one kilogram per square metre increase in body mass index (BMI) linked to an additional 0.28 per cent loss.
The study analysed data from 895 participants in the Ribeirão Preto Birth Cohort, which tracks individuals born between 1978 and 1979. Lung function was assessed in early adulthood, between the ages of 23 and 25, and again in late thirties, at 37 to 38 years of age.
Professor Elcio Oliveira Vianna, coordinator of the study at the University of São Paulo’s Ribeirão Preto School of Medicine, said the results highlight the role of metabolic health in respiratory ageing.
“Our findings reinforce what smaller studies have already suggested: beyond smoking, systemic metabolic and inflammatory processes can significantly contribute to lung deterioration, even in younger people without diagnosed respiratory disease,” he said.
Vianna explained that inflammation originating in fat tissue may play a key role. “Low-grade systemic inflammation, already known to increase cardiovascular risk, also affects the lungs. In obesity, this constant inflammatory stimulus can damage lung tissue over time and accelerate premature lung ageing.”
Although participants were below the usual age for a COPD diagnosis, early signs of lung impairment were already detectable. This allowed researchers to infer that obesity and inflammation may increase the likelihood of developing COPD later in life.
“Because the participants were young, we were able to identify changes in lung function before clinical disease became apparent,” Vianna said.
Traditionally, COPD has not been associated with obesity, as advanced disease is often accompanied by weight loss and muscle wasting due to the high energy demands of breathing. However, the researchers argue that this perception may overlook the role of obesity earlier in the disease process.
Ana Carolina Cunha, a pulmonologist and first author of the study, said the findings underscore the complexity of COPD. “The disease is multifactorial and far more complex than previously thought. Alongside smoking-related inflammation, some individuals may have a systemic inflammatory profile, linked to obesity or metabolic factors — that increases their vulnerability.”
The study, published in BMC Pulmonary Medicine and supported by FAPESP, adds to growing evidence that obesity is not only a cardiometabolic risk factor, but may also have long-term consequences for respiratory health.