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The Link Between Smoking, Coffee Drinking and Parkinson’s Disease

Shubhi Pal

Parkinson’s disease is a progressive neurodegenerative disorder that is the second highest in prevalence after Alzheimer’s disease. Typical features of the disease include motor symptoms, such as ‘resting tremors’ and ‘rigidity in movements’ (Butcher et al., 2021). It is also characterized by ‘non-motor symptoms’ including psychological symptoms such as anxiety, depression, sleep dysfunction, and cognitive deficits, some of which manifest years before the motor symptoms become apparent (Butcher et al., 2021; Mappin-Kasirer et al., 2020).

In a 1968 study, a group of researchers noted a surprising observation: there was lower prevalence of Parkinson’s disease among smokers than non-smokers (Nefzger et al., 1968, as cited in Gale & Martyn, 2003). Similar observations have been made for coffee-drinkers. These findings have been confirmed by numerous epidemiological studies, as demonstrated by Hernán et al. (2002) in their systematic review and meta-analysis of such studies (Gale & Martyn, 2003). Their meta-analysis revealed that current smoking behavior was associated with 60% less risk of developing Parkinson’s disease (compared to non-smokers), and coffee-drinking behavior was linked with 30% less risk of developing Parkinson’s disease (as compared to individuals who don’t) (Hernán et al., 2002). These results were found to be stable across various geographical and study contexts. This finding was also accompanied by secondary findings indicating an inverse relationship between the amount of coffee consumed in a day, and the risk of Parkinson’s disease, although this relationship was moderated by gender (Hernán et al., 2002). Analogously, an inverse relationship was reported between the number of cigarettes smoked regularly, and the risk of developing Parkinson’s (Mappin-Kasirer et al., 2020).

This striking apparent correlation has raised important questions regarding the possible reasons for such a phenomenon, especially since habits such as coffee-drinking and smoking have usually been as having a detrimental impact on one’s health. This has led to an upsurge in research on this particular question, which even after 50 years, remains contentious and unanswered, although great progress has been achieved in terms of some plausible explanations for this phenomenon.

We have all heard the phrase: ‘Correlation doesn’t imply causation,’ and hence a healthy amount of skepticism should be present regarding broad claims on the beneficial impact of these (often) addictive substances. With that in mind, we can begin an examination of the several reasons proposed for this phenomenon, with a keen eye on the evidence that supports each.

Several scholars have proposed alternate explanations for this phenomenon. Hernán et al. (2002) discussed the three most prominent explanations discussed in literature: ‘information bias,’ ‘selection bias,’ and ‘confounding as a result of a common cause.’ The first two explanations attribute this phenomenon to a potential increase in omission of Parkinson’s diagnoses from the death records of high-frequency smokers, and relatively lesser survival rates among high-frequency smokers before late adulthood and old age due to other diseases and health problems (Gale & Martyn, 2003; Hernán et al. 2002). However, Hernán et al. (2002) mentions them to be unlikely, given that this phenomenon has been established not only through retrospective studies – which look back at the factors that could have influenced the development of the disease, but also in several prospective studies – which follow individuals as they develop the disease, and look at the various factors that could be implicated. Another prominent potential confound suggested is the presence of an external common cause for both the low risk for the disease, and increased smoking and coffee-drinking behaviors. This cause could be environmental or genetic in nature, such as a genetic linkage between the gene influencing the risk of Parkinson’s and the gene influencing vulnerability to indulge such behaviors. However, by demonstrating that even after accounting for the presence of a hypothetical haplotype which could increase the risk of developing Parkinson’s by five times, and simultaneously decrease the likelihood of indulging in smoking, 30% of the reduction in risk associated with smoking would still be unaccounted for, the implausibility of such an explanation was shown (Hernán et al. 2002).

Given the unlikelihood of alternate explanations as discussed above, primarily two kinds of hypotheses have been suggested and examined in literature. One set of hypotheses suggest that Parkinson’s disease leads to lesser likelihood to indulge in smoking and coffee-drinking behaviors. These hypotheses are grounded on studies that have shown greater prevalence of personality traits such as ‘cautiousness’ and ‘less interest in novelty seeking’ even before motor symptoms start to manifest (Evans et al., 2003, as cited in Derkinderen et al., 2014). However, proving this has been especially difficult given the large time distance between the current understanding of the onset of Parkinson’s (usually post middle adulthood) and the development of smoking and coffee-drinking behaviors (usually early adulthood). Thus, an acceptance of this hypothesis would require extending the “subclinical phase” of this disease by a large extent (Gale & Martyn, 2003, p. 561).

A second set of hypotheses emphasize the ‘neuroprotective effects’ rendered by the substances present in tobacco and coffee: nicotine and caffeine (Gale & Martyn, 2003). Several studies on animal models, particularly mice have provided some support to this explanation. One study for example demonstrated that exposure to caffeine in mouse models of Parkinson’s was associated with lesser damage and degeneration of dopaminergic systems in response to neurotoxins such as MPTP (Chen et al., 2001, as cited in Ren & Chen, 2020). Despite strong evidence, such studies suffer from challenges regarding the representativeness of such animal models for human progressive diseases such as Parkinson’s (Derkinderen et al., 2014). Other emerging lines of research emphasize the influence of caffeine and nicotine on gut microbiota and the gut-brain connection (Derkinderen et al., 2014; Ren & Chen, 2020).

            A further question that arises is whether these findings can point to possible ways of prevention and treatment of Parkinson’s disease? While research on this field is still ongoing, with a consensus yet to be reached, these findings may provide clues regarding methods of prevention, rather than providing relief from symptoms or offering methods of treatment. Several clinical trials have found no clinically significant difference in the progression of the disease or change in symptoms post administration of nicotine and caffeine (Kandinov et al., 2007; Wood, 2017).

While the biological mechanisms mediating such effects are still being studied actively, a more interesting and perhaps alarming question, is whether public knowledge of such findings may promote greater indulgence in smoking and coffee-drinking behaviors? And whether, a lay man reader like me, can take this as an excuse to engage in these behaviors? Research is emphatically clear on this issue: the risks outweigh the benefits when it comes to smoking behaviors, with smoking linked to increased risk of cancer, cardiovascular and respiratory diseases among other health problems (Hernán et al., 2002; Mappin-Kasirer et al., 2020).


References

Butcher, J. N., Mineka, S., & Hooley, J. M. (2021) Abnormal Psychology (18th ed.). Pearson Education Limited.

Derkinderen, P., Shannon, K. M., & Brundin, P. (2014). Gut feelings about smoking and coffee in Parkinson's disease. Movement Disorders, 29(8), 976–979. https://doi.org/10.1002/mds.25882

Gale, C., & Martyn, C. (2003). Tobacco, coffee, and Parkinson's disease. BMJ (Clinical research ed.), 326(7389), 561–562. https://doi.org/10.1136/bmj.326.7389.561

Hernán, M. A., Takkouche, B., Caamaño‐Isorna, F., & Gestal‐Otero, J. J. (2002). A meta‐analysis of coffee drinking, cigarette smoking, and the risk of Parkinson's disease. Annals of neurology, 52(3), 276-284. https://doi.org/10.1002/ana.10277

Kandinov, B., Giladi, N., & Korczyn, A. D. (2007). The effect of cigarette smoking, tea, and coffee consumption on the progression of Parkinson's disease. Parkinsonism & related disorders, 13(4), 243-245. https://doi.org/10.1016/j.parkreldis.2006.11.004

Mappin-Kasirer, B., Pan, H., Lewington, S., Kizza, J., Gray, R., Clarke, R., & Peto, R. (2020). Tobacco smoking and the risk of Parkinson disease: A 65-year follow-up of 30,000 male British doctors. Neurology, 94(20), e2132-e2138. https://doi.org/10.1212/WNL.0000000000009437

Ren, X., & Chen, J. F. (2020). Caffeine and Parkinson’s disease: multiple benefits and emerging mechanisms. Frontiers in Neuroscience, 1334. https://doi.org/10.3389/fnins.2020.602697

Wood, H. (2017). Caffeine and nicotine do not provide symptomatic relief in Parkinson disease. Nature Reviews Neurology, 13(12), 707. https://doi.org/10.1038/nrneurol.2017.155 


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