The confounding link between Parkinson's and smoking

In the realm of medical mysteries, few are as paradoxical and thought-provoking as the link between smoking and Parkinson’s disease. This connection, one of the most robust and perplexing in neuroscience, defies conventional wisdom. Though smoking is universally known for its detrimental health effects, its association with a significantly reduced risk of Parkinson’s presents a challenging contradiction for researchers. As we delve into this odd phenomenon, we find ourselves at a crossroads of caution and curiosity, navigating the intricate interplay between a harmful habit and a potential neurological safeguard.

The relationship between smoking and a reduced risk of Parkinson’s is surprising and complex. Studies have consistently shown that smokers are less likely to develop Parkinson’s compared with non-smokers, an observation that extends to various aspects of smoking, including how many cigarettes a person smokes and for how long.

In investigations with identical twins in which one had Parkinson’s and the other did not, the twin without the disease tended to smoke more than the twin with it. Intriguingly, the risk reduction correlates with increased smoking dose and extends even to those who had smoking parents, suggesting a deep-rooted connection beyond mere coincidence.

At low concentrations, carbon monoxide demonstrates physiological functions that could hint at neuroprotection. However, protective effects of smoking are also seen when consuming smokeless tobacco (tobacco that’s chewed, sucked or sniffed), making carbon monoxide less likely to be the culprit. Monoamine oxidase-B inhibitors found in smoke have also been suggested as potentially neuroprotective because of their role in Parkinson’s treatment. These, together with the effect of smoking on the gut microbiome, are an emerging area of interest in Parkinson’s research.

At low concentrations, carbon monoxide demonstrates physiological functions that could hint at neuroprotection. However, protective effects of smoking are also seen when consuming smokeless tobacco (tobacco that’s chewed, sucked or sniffed), making carbon monoxide less likely to be the culprit. Monoamine oxidase-B inhibitors found in smoke have also been suggested as potentially neuroprotective because of their role in Parkinson’s treatment. These, together with the effect of smoking on the gut microbiome, are an emerging area of interest in Parkinson’s research.

Or should we look at this backwards?

A critical question arises: what if we have this back to front? Could it be the biology of Parkinson’s affects smoking behaviour rather than smoking influencing the risk of Parkinson’s disease? Studies suggest patients with Parkinson’s find it easier to quit smoking and need fewer nicotine substitutes to do so. This could be tied to the role of dopamine, a key neurotransmitter implicated in addiction, which is severely diminished in Parkinson’s. If this theory holds, it might explain the observed lower smoking rates among patients who have Parkinson’s.

Though the potentially positive link between smoking and a reduced risk of Parkinson’s is intriguing, we can’t avoid the overwhelming evidence of the harmful effects of smoking – it being the leading cause of numerous deadly diseases, including lung cancer, heart disease, and stroke. And then there’s the way it ages your appearance, the wrinkles, the yellow teeth, bad breath and so on.

Researchers now face the challenge of unravelling how smoking’s association with reduced Parkinson’s risk could be leveraged without endorsing smoking itself. The focus is on isolating the protective elements within tobacco smoke and understanding their mechanism of action.

Despite the undeniable harms of smoking, its strong association with a lowered risk of Parkinson’s remains a critical clue in understanding and potentially combating the disease. This paradoxical link is certainly not an endorsement of smoking, but stands as a reminder of the intricate and often unexpected ways in which lifestyle factors can intersect with disease.