A Review of the Epidemiological Literature Supporting the Association of Cigarette Smoking and PD
The relationship between cigarette smoking and Parkinson’s disease has been demonstrated by several studies. For example, Breckenridge, Berry, Chang, Sielken, and Mandel (2016) have shown that there is a reduced risk of PD in cigarette smoking compared to exposure to farm chemicals. Van Der Mark et al. (2014) show that the protective effect of cigarette smoking against PD reduces over time following smoking cessation.
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A Rationale for Such a Study on Nicotine and PD
Evidence from the literature shows that there is an inverse association between cigarette smoking and PD (Nielsen, Franklin, Longstreth, Swanson, & Checkoway, 2013). These observations are attributed to the chemical constituents of tobacco including nicotine, which is the major component of tobacco (Yuncai, Ling, Zhaomei, Furong, & Yuping, 2014). However, it is uncertain whether nicotine or other chemical constituents in cigarettes contribute to the protective effects.
Parkinson’s disease is incurable and causes irreversible damage to the nervous system (Bennouar et al., 2013). Additionally, Parkinson’s disease is associated with symptoms such as insomnia, anosmia, poor balance, anxiety, and loss of memory, which reduce the quality of the lives of the affected people significantly (Weintraub, Papay, Siderowf, & Parkinson’s Progression Markers Initiative, 2013). Therefore, given the knowledge that cigarette smoking protects against the disease (Liu et al., 2015), it is necessary to determine the validity of these observations by finding the precise relationship between nicotine and PD. Confirming that nicotine is responsible for the protective effects will guide the development of vaccines against PD.
The Design of Potential Studies to Address this Question
An Experimental Approach
An experimental approach would involve the use of mice as animal models. Mice have been used extensively in the development of therapeutics for Parkinson’s disease. Two groups of mice would be used with a minimum of 8 mice per group. The study would use a classic toxic approach to test the therapeutic effects of nicotine in counteracting PD-associated cell death (Blandini & Armentero, 2012). One group would be treated with nicotine while the other would act as the negative control. Thereafter, Parkinsonism-inducing neurotoxins such as N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine would be used to induce the disease in both groups (Le, Sayana, & Jankovic, 2014). This chemical can reproduce most of the pathological and phenotypic characteristics of Parkinson’s disease in mammals. The protective effect of nicotine would be established by observing the magnitude of the disease symptoms in both groups.
An Epidemiological Approach
An epidemiological approach would involve the recruitment of two groups of study participants: smokers and non-smokers. The appropriate age group would consist of people between the ages of 50 and 65. Though PD has been reported to affect adults above the age of 65, several cases have been diagnosed in patients around the age of 50 in what is known as young onset Parkinson’s disease (Pagano, Ferrara, Brooks, & Pavese, 2016). The study would exclude participants with a family history of PD to ensure that genetics does not interfere with the observations. Both groups of participants would be required to disclose their exposure to environmental pollutants such as farm chemicals, which are known to increase the risk of PD. The participants would be monitored for PD symptoms for a total duration of 5 years. The incidence of PD would be documented and compared between the two groups. A low incidence of PD in the smokers would corroborate the hypothesis that nicotine reduces the risk of PD.
Strengths and Limitations of Each Chosen Approach
The experimental approach helps to confirm the effect of nicotine on PD. However, the shortcoming of this method is that the development of the disease in the animal model may not follow the exact pattern in humans. Conversely, the epidemiological approach would establish the precise relationship between cigarette smoking and the development of PD. However, it would not be possible to verify whether other environmental factors contributed to the development of the disease or not.
Bennouar, K. E., Uberti, M. A., Melon, C., Bacolod, M. D., Jimenez, H. N., Cajina, M.,… & Gubellini, P. (2013). Synergy between L-DOPA and a novel positive allosteric modulator of metabotropic glutamate receptor 4: Implications for Parkinson’s disease treatment and dyskinesia. Neuropharmacology, 66, 158-169.
Blandini, F., & Armentero, M. T. (2012). Animal models of Parkinson’s disease. FEBS Journal, 279(7), 1156-1166.
Breckenridge, C. B., Berry, C., Chang, E. T., Sielken Jr, R. L., & Mandel, J. S. (2016). Association between Parkinson’s Disease and cigarette smoking, rural living, well-water consumption, farming and pesticide use: Systematic review and meta-analysis. PloS One, 11(4), e0151841.
Le, W., Sayana, P., & Jankovic, J. (2014). Animal models of Parkinson’s disease: A gateway to therapeutics? Neurotherapeutics, 11(1), 92-110.
Liu, Y., Zeng, X., Hui, Y., Zhu, C., Wu, J., Taylor, D. H.,… Hu, J. (2015). Activation of α7 nicotinic acetylcholine receptors protects astrocytes against oxidative stress-induced apoptosis: Implications for Parkinson’s disease. Neuropharmacology, 91, 87-96.
Nielsen, S. S., Franklin, G. M., Longstreth, W. T., Swanson, P. D., & Checkoway, H. (2013). Nicotine from edible Solanaceae and risk of Parkinson disease. Annals of Neurology, 74(3), 472-477.
Pagano, G., Ferrara, N., Brooks, D. J., & Pavese, N. (2016). Age at onset and Parkinson disease phenotype. Neurology, 86(15), 1400-1407.
Van Der Mark, M., Nijssen, P. C., Vlaanderen, J., Huss, A., Mulleners, W. M., Sas, A. M.,… Vermeulen, R. (2014). A case-control study of the protective effect of alcohol, coffee, and cigarette consumption on Parkinson disease risk: Time-since-cessation modifies the effect of tobacco smoking. PLoS One, 9(4), e95297.
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Weintraub, D., Papay, K., Siderowf, A., & Parkinson’s Progression Markers Initiative. (2013). Screening for impulse control symptoms in patients with de novo Parkinson disease: A case-control study. Neurology, 80(2), 176-180.
Yuncai, G. A. O., Ling, L. I. U., Zhaomei, X. U., Furong, L. I., & Yuping, W. U. (2014). Analysis of main chemical components and quality of different tobacco varieties in Yuxi. Analysis, 6, 34-39.