Running head: COMPARATIVE ESSAY

Comparative Essay

Abstract In this essay, we are reviewing two articles, which are devoted to the same theme revealing a relationship between the incidence of Parkinsons disease (PD) and alcohol consumption. The final aim of both investigations was to better understand the nature of low risk of PD incidence in cigarette smokers and coffee drinkers, which was revealed in other experiments.

Comparative Essay Both articles, which we are going to be reviewed, are devoted to topical issues of the influence of regular alcohol consumption on the risk of developing Parkinsons disease. This issue is debatable due to the presence of conflicting data resulting from different research studies. The first article - A Prospective Study of Alcoholism and the Risk of Parkinsons Disease was written by the following authors: Miguel A. Hernn and Giancarlo Logroscino from Department of Epidemiology of Harvard School of Public Health and Luis A. Garca Rodrguez from Spanish pharmacoepidemiological Research Center. The article was published in J Neurol (2004) 251 [Suppl 7] : VII/14VII/17. In this article, the authors conducted an indirect test of hypothesis that alcohol consumption influences the risk of Parkinsons disease development. The second article Alcohol Consumption and the Incidence of Parkinsons Disease was written by the following authors: Miguel A. Hernan, MD, DrPH, from the Departments of Epidemiology, Harvard School of Public Health; Honglei Chen, MD, PhD, from the Departments Nutrition, Harvard School of Public Health; Michael A. Schwarzschild, MD, PhD, from the department of Neurology, Massachusetts General Hospital; Alberto Ascherio, MD, DrPH - Channing Laboratory, Department of Medicine, Harvard Medical School and Brigham and Womens Hospital, Boston, MA. In this article, the authors investigated the association between consumption of alcoholic beverages and risk of PD in two large prospective cohorts Nurses Health Study, and Health Professionals Follow-up Study. They detected 415 new cases of PD during follow-up. The article was published in the journal Annals of Neurology Vol 54 No 2.

In our opinion, these articles are similar in terms of the overall theme of the study. So, we should, first of all, pay attention to differences in these articles. First and foremost, we note that the studies in articles were conducted in various groups of patients. In the first article, the authors investigated the relationship between alcoholism and the incidence of PD in a case-control study nested within a prospectively followed population: the General Practice Research Database (GPRD), which includes over 3 million Britons who are enrolled with selected general practitioners. In the second article, the authors investigated whether drinkers of alcoholic beverages faced a lower risk of PD than abstainers in two large prospective cohorts: the Nurses Health Study and the Health Professionals Follow-up Study. It is worth noting that in the first article exclusion criteria for patients in the study were carefully selected in order to exclude patients, who had the history of PD or drug use for the treatment of PD, and the history of drug use that may cause drug-induced Parkinsonism. Followup also ended in this study at the first computerized symptom (tremor, rigidity, bradykinesia, abnormal gait) or diagnosis of PD, initiation of drug use that may cause Parkinsonism, date of last data collection, death, whichever came first. The lack of such exclusion criteria in the second paper may adversely affect the accuracy of the results, leading to errors in the understanding of the Parkinsons disease causes. In the second article, the authors restricted their analysis to participants without symptoms of PD, who had not received a diagnosis of stroke or cancer (other than nonmelanoma skin cancer) before they answered the baseline questionnaire, who reported plausible energy intakes, who left fewer than 10 of 61 food items (women) or fewer than 70 of 131 food items (men) blank on the SFFQ, and who provided information on alcohol intake.

The authors of the first article used conditional logistic regression to compute odds ratios (OR) and their 95% confidence intervals adjusted for the matching factors. Alcoholism (yes or no) and smoking status (current smoker, past smoker, never smoker, missing status) were added as covariates to the model. Under their design, the OR is an unbiased estimator of the incidence rate ratio. Statements about statistical significance refer to the conventional 0.05 cutoff. In the second article, the authors used stratified (by age, smoking, and caffeine intake) Cox model to estimate adjusted incidence rate ratios (RRs) of PD and their 95% confidence intervals for each category of alcohol intake at baseline and compared with nondrinkers. Similar analyses were conducted for intake of each alcoholic beverage at baseline (less than 1 drink per week, 1 to 3 drinks per week, 1 to 4 drinks per week, and more than 5 drinks per week). The authors used the continuous variable alcohol intake (g/day) and the nine-category classification of intake of alcoholic beverages to evaluate trends. Also, the authors included analyses using the cumulative updated average of alcohol intake in which the incidence of PD during each time interval was related to the alcohol intake averaged over all the previous SFFQs. In addition, 31 Log RRs from the two studies were weighed by the inverse of their variances to obtain a pooled estimate. Such a detailed classification of the patients participating in the study allows the authors to evaluate not only the presence of good communication between alcohol consumption and risk of Parkinsons disease, but also to establish a quantitative relationship between these events (if any happens). Both articles have successfully been using classical statistical methods that are acceptable in these cases. In the first article, the authors used conditional logistic regression, while in the second one the stratified Cox model was applied.

The results of both articles were quite comparable, yet the differences are quite significant. The authors of the first article did not find a dose-response relationship between alcohol intake and PD risk in non-alcoholics (men and women). Interestingly, the authors of this article found that their findings hint that there may be qualitative differences between men and women regarding the risk of PD associated with alcoholism (slightly lower risk of PD in men, and with over a two-fold increased risk in women). The authors also examined whether the alcoholPD association in women was modified by the use of postmenopausal hormones and found no significance. According to the results of the second article, total alcohol intake was not clearly associated with a lower PD risk. The authors found that beer drinkers had a 30% lower incidence of PD than nonbeer drinkers. This interesting finding clearly demonstrates the advantage of the second article over the first one in terms of the quality of patient classification and analysis of results. The obtained data do not allow us to take up the position that low PD incidence in cigarette smokers and coffee drinkers is caused by a tendency towards avoiding addictive behaviours among future PD cases.

References Hernn, M. A., Logroscino, G., & Garca, L. A. (2004). A prospective study of alcoholism and the risk of Parkinsons disease. Schwarzschild, M. A., & Ascherio, A. (2003). Alcohol consumption and the incidence of Parkinsons disease, 2003