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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