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By Rodrigo Santos Andrade
Why do smokers get Parkinson’s less often? New evidence from half a million adults in China points to carbon monoxide, not smoking itself.
olesea vetrila/ShutterstockSmoking is one of the biggest causes of ill health and early death. Yet smokers seem to have a lower risk of developing Parkinson’s disease than non-smokers – by around half according to some studies.
This surprising link was first reported more than 50 years ago, when researchers in the UK and the US noticed that smokers were dying at much higher rates overall, but were less likely to die from Parkinson’s. Many studies since then have found the same pattern.
Why smoking is linked to a lower risk of Parkinson’s is still unclear. Researchers have proposed several explanations, but there is no definitive answer yet.
Cigarette smoke contains thousands of chemicals and gases, so researchers have looked at many of them for clues. Nicotine has attracted particular interest because it affects the brain, but trials testing nicotine in people with Parkinson’s have found no evidence that it slows the disease. The search for the molecule that appears to lower the risk of Parkinson’s in smokers continues.
Half a million adults
A study my colleagues and I recently conducted provides new evidence that carbon monoxide (CO) may play a role. Laboratory and animal studies have suggested that low doses of CO might protect the brain. Until now, though, no large-scale human study has combined measurements of people’s CO levels with information on whether they later developed Parkinson’s.
We used data from the China Kadoorie Biobank, a diverse group of half a million adults from across China, to examine disease associations of CO. At the start of the study, researchers in China measured the amount of CO in participants’ breath, which gives an indication of their recent exposure to the gas. They then followed the participants over time, recording whether they developed conditions including Parkinson’s disease.
Consistent with previous studies, we found that regular smokers had about 30% lower risk of developing Parkinson’s. Smokers were also found to have higher levels of exhaled CO.
What was interesting, though, was that among people who had never smoked, higher exhaled CO levels were associated with a lower risk of developing Parkinson’s. Exhaled CO was not, however, associated with risks of other neurodegenerative diseases such as dementia, or of lung cancer or other smoking-related diseases among these participants.
Our study challenges the idea that smoking itself has a protective effect for Parkinson’s. Instead, it suggests that CO may contribute to the lower risk of Parkinson’s seen in people who smoke and that CO may have a protective role in Parkinson’s independent of smoking. Our findings do not, therefore, support or justify starting smoking or delaying stopping smoking, which has well-established harmful effects on health.
Why do some people exhale more CO?
Some people who have never smoked still have higher carbon monoxide levels in their breath, and this can come from their surroundings. CO is released when fuels that contain carbon, such as wood, coal or petrol, don’t burn completely. So breathing polluted outdoor air, or air indoors where solid fuels are burned for cooking or heating, can raise the amount of CO in someone’s breath. Breathing in other people’s tobacco smoke can do the same.
Burning solid fuels indoors can raise exhaled CO levels.
Darcy Perkins/Shutterstock
We tried to account for these factors in our analysis. Even so, people with higher CO levels in their breath were still less likely to develop Parkinson’s disease. In other words, the link between higher exhaled CO levels and a lower risk of Parkinson’s remained even after we accounted for region, season, use of solid fuels and exposure to second-hand tobacco smoke. However, we cannot tell from our study where the other sources of CO came from.
Exhaled CO can also come from inside the body. Cells make tiny amounts of CO all the time. At high levels, CO is toxic, but at these low levels it plays a helpful role in the body. It can protect cells from damage, calm inflammation and support the immune system. These effects may help explain why people with higher CO levels have a lower risk of Parkinson’s disease.
A study like ours, which only observes people and does not intervene or change anything, can’t prove that CO protects against Parkinson’s. CO could simply be a sign of who is less likely to get the disease, rather than the cause. Even so, the findings help support the idea that CO may help protect the brain’s nerve cells from Parkinson’s.
Large, well-designed trials in humans are needed to find out whether CO could be used as a treatment for Parkinson’s. One trial of low-dose CO in people with Parkinson’s is already underway. Its results will be important for understanding how CO relates to the disease and whether it could one day be used to treat or prevent Parkinson’s.
Clara Bueno Lopez does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.
Tags: Academic Journalism, The Conversation, The Conversation Academic News