After the invasion of the smoking cranks last week into the comments of the three posts I somehow ended up doing on the topic of secondhand smoke (SHS), the health dangers it poses, and some of the deceptive quote mining used in the service of trying to discredit studies demonstrating a moderate but real risk from SHS , I was ready to move on to other topics. I’ll give these guys credit for one thing; they’re almost as persistent as the antivaccinationists. Despite my flooding this blog with fluff unrelated to smoking and the hazards it causes (or even, for that matter, medicine or surgery), both to the smokers and those unfortunate enough to be exposed to SHS, they’re still there. Just like the Energizer Bunny, they keep going and going and going and going. Naturally, they’re not happy that I haven’t answered each and every challenge they have made, but guess what? This is not Usenet. I used to be very active on Usenet; if I were still interested in getting down and dirty with the discussion in a Usenet-style forum, I wouldn’t have started a blog. I would have stayed in Usenet. Basically, this is my blog. It’s my hobby. Sometimes I’ll get heavily involved in the comments section; sometimes I don’t. Personally, I much prefer using that time to produce new material for you, my readers, to mull over, enjoy, attack me for, or whatever.
Besides, I was a bad boy this weekend. I bought the Harry Potter book and got through around 500 pages of it, even to the point of doing very little work on a paper that I need to submit next week. (Bad, bad Orac! I hope my postdoc will forgive me. Don’t worry, though, I’ll be back to my workaholic ways after I finish the book.) I don’t know about you, but I consider finishing the Harry Potter book to be far more important than sparring with smoking apologists. When I finish the book, maybe I’ll get back into it. In the meantime, though, despite my desire to move on to other topics for a while, there was one last smoking-related study that was rather unusual; consequently, I thought I’d look into it a bit before moving on to other topics. Here’s the abstract:
Pooled Analysis of Tobacco Use and Risk of Parkinson Disease. Beate Ritz, MD, PhD; Alberto Ascherio, MD, DrPH; Harvey Checkoway, PhD; Karen S. Marder, MD, MPH; Lorene M. Nelson, PhD; Walter A. Rocca, MD, MPH; G. Webster Ross, MD; Daniel Strickland, PhD; Stephen K. Van Den Eeden, PhD; Jay Gorell, MD
Arch Neurol. 2007;64:990-997.
Context: Epidemiologic studies have reported that cigarette smoking is inversely associated with Parkinson disease (PD). However, questions remain regarding the effect of age at smoking onset, time since quitting, and race/ethnicity that have not been addressed due to sample size constraints. This comprehensive assessment of the apparent reduced risk of PD associated with smoking may provide important leads for treatment and prevention.
Objective: To determine whether race/ethnicity, sex, education, age at diagnosis, and type of tobacco modify the observed effects of smoking on PD.
Design, Setting, and Participants: We conducted the first ever pooled analysis of PD combining individual-level data from 8 US case-control and 3 cohort studies (Nurses’ Health Study, Health Professionals Follow-Up Study, and Honolulu-Asia Aging Study) conducted between 1960 and 2004. Case-control studies provided data for 2328 PD cases and 4113 controls matched by age, sex, and ethnicity; cohort studies contributed 488 cases and 4880 controls selected from age- and sex-matched risk sets.
Main Outcome Measure: Incident PD.
Results: We confirmed inverse associations between PD and smoking and found these to be generally stronger in current compared with former smokers; the associations were stronger in cohort than in case-control studies. We observed inverse trends with pack-years smoked at every age at onset except the very elderly (>75 years of age), and the reduction of risk lessened with years since quitting smoking. The risk reductions we observed for white and Asian patients were not seen in Hispanic and African American patients. We also found an inverse association both for smoking cigars and/or pipes and for chewing tobacco in male subjects.
Conclusions: Our data support a dose-dependent reduction of PD risk associated with cigarette smoking and potentially with other types of tobacco use. Importantly, effects seemed not to be influenced by sex or education. Differences observed by race and age at diagnosis warrant further study.
Basically, this study is a meta-analysis of 8 case-control and 3 cohort studies looking at smoking and its effect on the risk for the development of Parkinson’s disease. Basically, if you boil the meta-analysis down, it reports that there is a protective effect of smoking tobacco when it comes to Parkinson’s disease. If I wanted to be really snarky, I could use the same rationale used by some of the smoking apologists who’ve infested my blog, and declare the study to be a pile of crap because the relative risk is less than 2 (or, more appropriately, between 0.5 and 1.0, meaning the protective effect is less than a 50% reduction). After all, as we have been told by these cranks, any relative risk less than 2 can be discounted. Obviously, by that standard, this study could easily be discounted by us “radical antismokers” (which is what the SHS apologists seem to think I am). What’s good for the goose, as they say.
Fortunately, I’m intellectually honest.
So, let’s look at the study. Here’s what is perhaps the meat of the study, a table that shows the decrease in relative risk as a function of pack-years smoked in case control studies:
Basically, the relative risk falls from 1.00 for nonsmokers to 0.52 for women and 0.64 for men who’ve smoked more than 60 pack-years. (So close to the magical decrease in relative risk by 2, but so far…) This study also looked at some subgroup analyses (although this was somewhat limited by the fact that the overwhelming majority of the subjects of the studies used in the meta-analysis were white). There was no difference in the inverse association between smoking and Parkinson’s disease based on sex or educational status. More interesting, there was even a modest reduction in relative risk (13%-32%) noted even in those who had quit smoking up to 25 years prior to a diagnosis of Parkinson’s disase. Quoth the authors: “This later observation suggests that the risk reduction is unlikely to be attributable to recent changes in smoking habits resulting from behavior modifications related to incipient disease onset.”
Given the number of studies suggesting a protective effect of smoking on Parkinson’s disease, I tend to accept the results of this meta-analysis as probably vaild. So the question is: Should you smoke up in order to avoid Parkinson’s disease?
Don’t be silly!
Given the massively increased risk of lung cancer and heart disease due to smoking, it would be foolish to take up the habit to avoid Parkinson’s disease. In any sort of risk-benefit analysis, it would be obvious that smoking causes far more harm than good. Still, this result is interesting for a number of reasons. First, it is, as we say in the biz, “hypothesis generating.” Assuming that the result is valid and smoking really does have a modest protective effect against Parkinson’s disease, then there are a number of hypotheses that can be tested that could help us understand the etiology of Parkinson’s disease better than we do now. For example, one very obvious hypothesis that comes out of this research is that perhaps nicotine (or some other substance in tobacco smoke) somehow has a protective effect on the dopamine-producing neurons whose dying off results in Parkinson’s disease, whether the mechanism is due to alterations in enzyme activity or other causes. Another hypothesis to test is based on the observation from this study that there was an inverse association between smoking and Parkinson’s disease in whites and Asians, but this association was not observed in Hispanics or or African American subjects. This sort of observation screams that there is likely a genetic component involved in any protective effect of smoking on Parkinson’s disease. Finally, as with all epidemiological research, it is not possible to rule out confounding factors, as the authors point out:
Alternatively, behavioral characteristics or personality traits of patients with PD may be confounding the observed smoking association in that the same genetic or constitutional traits that increase susceptibility to PD may also prevent subjects from smoking. Thus, these traits would be the common cause for both smoking behavior and PD. Observations that smoking and personality are associated with dopaminergic functions lend support to this argument.
Of course, the most useful aspect of this sort of work is not so much smoking itself, but rather identifying what, specifically, it is in smoking that might be causing the protective effect. If there is a compound in cigarette smoke that protects against Parkinson’s disease, it’s possible that the same coumpound, whatever it might be, could be used to reverse the disease or slow its progression. Alternatively, if it is a genetic component that leads to something in cigarette smoke having a protective effect, then that could lead to a better understanding of genetic alterations that predispose people to developing Parkinson’s disease.
Of course, if one followed the strict, dogmatic line that relative risks of less than 2 are crap, as so many of the people claiming that SHS is not harmful seem to do, this potential line of research would have to be rejected out of hand. After all, if you look at the quote that were mined out of context, you’ll see that it’s epidemiologists who are supposedly saying that relative risks of less than 2 (or of greater than 0.5 for protective effects) should be rejected out of hand in epidemiological studies like this.