Reacción a "Exhaled carbon monoxide has been linked to a lower risk of Parkinson’s disease"

The study by Bueno-López and colleagues provides a new insight into why smokers have a lower risk of developing Parkinson’s disease. After following more than half a million participants from the China Kadoorie Biobank for around 12 years, the authors confirm this association and present a very interesting finding: amongst people who had never smoked, those with higher levels of exhaled carbon monoxide (CO) also had a lower risk of Parkinson’s.

This result suggests that the reduced risk of Parkinson’s associated with smoking may not be due to tobacco itself, but that CO could contribute, at least in part, to explaining this relationship. This possibility is particularly interesting because for years it has been suggested that nicotine might be responsible for this effect, but clinical trials conducted to date have not demonstrated that it slows the progression of the disease.

The study stands out for its large number of participants, its long follow-up period and the control for numerous factors that could influence the results (second-hand smoke exposure, use of solid fuels in the home, physical activity and socio-economic status). Furthermore, the results are consistent with previous studies carried out on animal models, which show that, although CO is highly toxic at high concentrations, at low and carefully controlled doses it can activate antioxidant, anti-inflammatory and neuroprotective mechanisms.

In any case, and very importantly, this study does not prove that smoking protects against Parkinson’s disease and offers no reason to take up smoking or to continue smoking. In fact, the study itself confirms that smoking increases the risk of lung cancer, cardiovascular disease, stroke and premature death.

The research has some limitations: as it is observational, it shows an association but does not prove a cause-and-effect relationship; furthermore, exhaled CO was assessed only once, at the start of the study (using the average of two consecutive measurements), and its origin cannot be determined with precision. Although these results do not, for the time being, change clinical practice, they open up the possibility of exploring low-dose CO as a therapeutic strategy—an option that is already beginning to be evaluated in patients with Parkinson’s disease.