Random Smoking Trials

Hal Finney recently commented:

[Johnstone & Finch’s] Scientific Scandal of Antismoking … makes the case that smoking is not bad for your health. … [It has] the superficial appearance of referencing scientific studies and claiming the the mainstream misrepresents the results.

Yes, they are superficially credible.  Their New Scientist letter:

WHO … claims … “an epidemic of chronic illnesses … could be prevented through simple changes in diet, by being more active and by not smoking.” … There have been a number of such studies, with various combinations of these three lifestyle factors, including the WHO collaborative trial (60,881 subjects, 6 years), the Goteborg trial (30,022 subjects, 11.8 years) and the Multiple Risk Factor Intervention trial (12,866 subjects, 7 years).  These and another eight trials were conducted over three decades, one of the most expensive and sustained series of biological experiments in the history of medical science. … None showed any improvement in life expectancy and two showed a significant reduction in life expectancy in the test group.

So I dug further; bottom line:  Johnstone & Finch are right.  We usually see strong correlations between death and smoking, and we see those same correlations within each random arm (i.e., group) of a randomized trial.  Nevertheless, we see no significant net death differences between control arms and arms induced to smoke less.

So we don’t have clear evidence that smoking kills on net; it could be that most or all of the death-smoking correlation is due to selection effects, and not smoking causing death.  Experts say there is a substantial causal component, and for now I’m accepting that claim, but this lack of clear evidence is suspicious, and disturbing.  Now for some details.

First I know of only one randomized trial directly and only on smoking.  Of 1400 men, a random half were advised to stop smoking, and stop they did:

A randomised controlled trial of anti-smoking advice in 1445 male smokers, aged 40-59, at high risk of cardiorespiratory disease. After one year reported cigarette consumption in the intervention group (714 men) was one-quarter that of the “normal care” group (731 men); over 10 years the net reported reduction averaged 53%. The intervention group experienced less nasal obstruction, cough, dyspnoea, and loss of ventilatory function.

The results:

During the next 20 years there were 620 deaths (231 from coronary heart disease), 96 cases of lung cancer, and 159 other cancers. Comparing the intervention with the normal care group, total mortality was 7% lower, fatal coronary heart disease was 13% lower, and lung cancer (deaths+registrations) was 11% lower.

However, these differences are clearly not statistically significant.  (The death difference 320-300 = 20 is a typical deviation sqrt(320) = 18.)

All the other smoking trials are randomized comparisons of whole packages of lifestyle advice; smoking is only one part of the package.  The most recent such trial was MRFIT;

The MRFIT design called for the recruitment of at least 12,000 men aged 35 to 57 years who were at increased risk of death from CHD [heart attack], but had no clinical evidence of CHD. Persons were designated at “increased risk” if their levels of three risk factors-cigarette smoking, serum cholesterol, and blood pressure (BP)-were sufficiently high at a first screening visit to place them in the upper 15% of a risk score distribution based on data from the Framingham Heart Study.  After about one third of the screening was completed and success in recruitment had been demonstrated, the 15% was changed to 10%.

Out of 8000 smokers, a random half were advised to quit smoking, and more of them did quit:

4,103 special intervention [SI] and 4,091 usual care [UC] men … reported smoking cigarettes at the first screening visit. Among SI men, the reported cessation rate increased from 43.1% at 12 months to 48.9% at 72 months. The reported cessation rate among UC men increased from 13.5% at 12 months to 28.8% at 72 months. Among smokers who reported cessation at 72 months, 51.3% of SI men and 22.7% of UC men had quit smoking within the first year and remained abstinent thereafter. Average thiocyanate and expired-air carbon monoxide served as objective measures of smoking and were significantly lower among the special intervention men.

Within each half of the experiment, the study did see strong correlations between death and smoking:

For both SI and UC men, substantial differences in subsequent CHD (34-49%) and all-cause (35-47%) mortality were evident for men who reported cigarette smoking cessation by the end of the trial compared with those continuing to smoke.

But comparing the two halves, we find that smoking less has no observed effect on lung cancer deaths:

After 16 years of follow-up, lung cancer mortality rates were higher in the SI than in the UC group … 135 SI and 117 UC participants died from lung cancer.  … None of the hypotheses proposed to explain the unexpected higher rates of lung cancer mortality among SI as compared with UC subjects were sustained by the data.

Nor were there significant overall mortality effects from the entire package of advice:

After 16 years … 991 SI and 1050 UC men had died by the end of follow-up (relative difference, -5.7%; 95% CI, -13% to 2.8%)..

Again, those who smoked less died about 6% less (though more of lung cancer), but this difference still isn’t 5% significant.

The other studies are older, and harder to find.  (Can anyone get copies of these papers: EHJ83, Lancet86, EHJ86, AnnMed92?)   I did find this one:

In a randomized five-year multifactorial primary prevention trial of vascular diseases, hyperlipidemias, hypertension, smoking, obesity, and abnormal glucose tolerance of the high-risk test group (n=612 men) were treated with dietetic-hygienic measures and hypolipidemic (mainly probucol and clofibrate) and antihypertensive (mainly diuretics and β-blockers) agents.  [There was] a matched high-risk control group (n=610) … Despite the highly significant reduction in the risk factor level, the five-year intervention program did not reduce coronary mortality or morbidity. In fact, the number of total coronary events tended to be higher in the intervention group than in the control group (19 vs nine cases; P=.057).

Bottom line: when folks freely choose if to smoke, we see strong correlations between death and smoking.  The simple correlation is that smokers die about 60-70% more often, but after controlling for a few other factors this drops to 20-40%.   Yet when a randomized trials selects 8000 of the 10% highest risk smokers, and induces half of them to smoke less, so that 49% instead of 29% quit smoking by seven years, that half dies only 6% less over 16 years, and dies more of lung cancer.

Now if that entire 6% drop were real and due entirely to one half smoking 20% less, that would translate into a roughly 30% smoking mortality effect.  So if we assume high risk smokers aren’t hurt more by smoking than other smokers, we aren’t quite at the point of seeing a clear contradiction.  Apparently we need bigger trials if we are going to see clearly if smoking kills on net.   Alas the era of the large risk trial seems to be over, at least for now; it seems it will be a long time before we really know.

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  • drewster

    Smoking does not kill. It damages your lungs, and increases the rate of cellular mutation.

    • anon

      Smoking does not kill people, lung cancer kills people.

      • Cecil

        Lung cancer does not kill people, cessation of neural activity kills people.

        How far did you want to take this?

      • josh

        I’d like to know how far you can take this.

  • retired phlebotomist

    Is it possible this means that the damage is done early, and quitting does not reduce it?
    I’ve read COPD can emerge during someone’s 50’s or 60’s, even if they quit decades before.

    • retired phlebotomist

      Also, the conventional story is that lung cancer did not emerge as a common cause of death prior to WWI, when cigs were rationed out to soldiers.

    • This is the first thing I thought of.

    • Curt Adams

      That’s how it works with skin cancer. Childhood and young adult exposure is considerably more important than late-life exposure.

      Also, insofar as the damage is cumulative, quitting would take a long time for the benefit to show up. After 20 years of smoking, a 5 year cessation would crudely be expected to generate an improvement of only 20% of the hazard of smoking, and these studies are underpowered for that.

      The general problem of these studies is that they are underpowered, and people naive to the meaning of statistical tests are interpreting them as indicating smoking cessation doesn’t work. The proper Bayesian interpretation is that these studies should raise your confidence that smoking cessation works, but only a few fold per study.

      • Are you making a worst case assumption about how long cessation continues? Your view would suggest shorter time data would show a clearer effect, yet in the MFIRT ten year data the SI group had higher total mortality than UC.

      • Curt Adams

        No, my view would indicate improvements from cessation should increase over time assumed cessation continues. I’m hypothesizing the increased risk is proportional to years of smoking. As time wears on, the difference in years of smoking between quitters and continuers increases. Indeed, the 20-year data shows a 13% drop in CHD, and that’s pretty good although the size of the study leaves the result inconclusive.

        Also, since this is looking at deaths, a study of n years is looking at the difference resulting from less than n years, because all the deaths occurred before n years. The “effective time” of the study would be the average years to death, which would be about n/2 for the shorter study.

    • If so, why are smokers urged so strongly to quit?

      • I can think of multiple possible reasons. The one I think the most likely is last.

        Because it’s something you have control of that has at least some effect on your health.

        Because the smaller the number of current smokers the smaller the number of people who start smoking.

        Because it’s ingrained in our culture.

      • retired phlebotomist

        What does what smokers are urged to do have to do with the health effects of smoking?

        “Apparently we need bigger trials if we are going to see clearly if smoking kills”

        If the data clearly show a rise in lung cancer and other diseases that strongly correlates with the advent and increase of smoking, I’d like to see some stronger evidence for “self selection” that the fact that the 10% highest risk smokers did not get a benefit by quitting.

        As for: “They obviously wouldn’t have done these studies if they hadn’t thought they had a chance of seeing something”

        I’d love to know where they got their funding for this study.

      • anon

        Smokers are not strongly urged to quit. People in general however are strongly urged not to smoke, which makes sense if the damage from smoking is cumulative.

  • jonathan

    One issue is that smoking cessation rates changed in both groups and that may have a substantial effect. Consider only the regular care group in one of the studies you excerpt and note that cessation rates over doubled versus a relatively small increase in cessation rates in the intervention group.

  • Daniel Lakeland

    There are some studies purporting to show a significant reduction in heart attack risk in the general population during periods of reduced secondhand smoking due to bans. The famous first one was the “Helena Montana” study, and there have been some others in other areas as well since then.

    If *secondhand* smoking seriously increases heart attack risk, do we really expect any kind of linear response from reduction of say 1 pack per day to 3 cigarettes per day?

    This stuff you’re citing, together with the causal data on biochemical processes involved in smoking response all just strongly suggests to me that cigarette smoke is highly toxic and that the bulk of its dose-response function transition region occurs at doses around or lower than 1 cigarette per day.

  • Psychohistorian

    “People who quit smoking in their forties and fifties did not see a strong drop in mortality,” is an ENORMOUS leap from, “smoking does not have a direct effect on health,” given the rather significant evidence that smoking does affect health. “Smoking later in life does not have a significant marginal effect on health if one has already been smoking a long time” seems like a much more likely hypothesis.

  • Bill

    Sometimes it is cute to be countercultural. It might give you a feeling of superiority, separteness, uniqueness.

    But, not when it endangers others health.

    Do your research.

    • drewster

      The simple fact of the matter is that if you’re going to make a habit of taking the contrary position to stimulate discussion, you’ll have to get used to habitually being on wrong side of the discussion. Robin seems to have forgotten that aspect of contrarianism.

  • retired phlebotomist


    plenty of interesting charts of smoking rates and lung cancer deaths thru the 20th century in this. (pg 27 of the pdf for example)

  • How is it that you selectively forget basics of Bayesian statistics the moment the study has anything to do with medicine?

    If we expect effect size to be 5%-10% difference, and 5%-10% difference would not be “statistically significant” when actually observed, it means “statistical significance” analysis is worthless due to small sample size. It’s as simple as that.

    That’s pretty much why you can cherry pick trials showing “no statistical significance” of this or that in medicine.

    • They obviously wouldn’t have done these studies if they hadn’t thought they had a chance of seeing something. Since they didn’t, that is weak evidence against the basis of their expectations.

      • Curt Adams

        C’mon Robin, you know better than that! First of all, people almost never did power studies (it’s getting better, but still pretty bad) so they really had no idea whether they’d see something. Second, insofar as they did have power estimates, that means the effect is less *than they were expecting*, which is not the same as absent. The data is still more likely if quitting benefits that if it doesn’t and so supports (albeit not strongly) a benefit from quitting.

      • Eric Johnson

        I agree. I’ve heard more than one stats jock bellyache about the statistical power of medical studies in general

      • Eric Johnson

        I agree w/ Curt I mean

      • If you find this obvious, your and my expectations about amount of statistical cluefulness of an average scientists are wildly different.

      • Tomasz, I didn’t say they had accurately or correctly calculated their expectations.

  • Phil

    “strongly suggests to me that cigarette smoke is highly toxic and that the bulk of its dose-response function transition region occurs at doses around or lower than 1 cigarette per day.”

    So you’re saying that if I smoke three cigarettes a day, and I increase to two packs a day, there won’t be much change in my health risk?

    Possible, I guess, but it doesn’t sound intuitively likely.

    • Eric Johnson

      > bulk of its dose-response function transition region occurs

      Maybe not at one cig a day, but I’m 95% I’ve heard (in the media) of a study finding that a few a day is nearly as bad as a lot.

      • Eric Johnson

        Hmm, could be that I’m wrong, or that the study I remember is false. This calls it into question without answering the question:

        But studies have shown that lung cancer risk is greatest among those who smoke the most cigarettes over the longest period of time.

        The length of time spent smoking seems to be the more important of these two factors. The British Doctors’ Study found that people who had smoked for 45 years had 100 times the lung cancer risk of people who had smoked for 15 years, regardless of whether they smoked heavily or moderately. And smoking one packet a day for 40 years is about 8 times more dangerous than smoking two packets a day for 20 years.

  • There is a *lot* more pertinent evidence than this – e.g. see:


    • What is the single strongest piece of evidence you would point me to look at first?

      • George

        There isn’t one single piece of evidence. You should talk to an epidemiologist and ask for their teaching material on inferring causality – smoking is usually the case study used. You’ll also learn how evidence for causality is gathered in the health sciences, which I’m sure will give you more confidence in their findings.

        Briefly, a strong association was observed, then decades of studies were performed to eliminate every other causal explanation anyone could think of. Also, the “smoking causes cancer” theory explain a huge amount of observed data. There’s no RCT, but even just one RCT is not enough evidence anyway (see http://www.cochrane.org).

      • George, so I shouldn’t look at anything first?

      • retired phlebotomist

        just from wikipedia:

        17.2% of smokers develop lung cancer
        1.4% of nonsmokers do

        Given that, I dunno how you get to “Apparently we need bigger trials if we are going to see clearly if smoking kills”

        over Psychohistorian’s:
        “Smoking later in life does not have a significant marginal effect on health if one has already been smoking a long time”

        especially with the historical tie in between smoking and lung cancer rates from the pdf link I already posted.

      • Retired, that is exactly the sort of huge difference that led folks to think they would see a lung cancer rate difference in a randomized trial of this size.

    • That link seems informative to whether smoking relates to cancer, but not at all to whether it on net shortens lifespan after taking all other factors into account. There are lots of ways it might not. For instance, smoking promotes weight loss, which reduces risk for various problems. Or there’s the hormesis factor – irritants at low levels can stimulate the immune system and make organisms healthier as a result. There is a definite problem in the medicine of looking at one problem at a time while ignoring the larger picture; this link does seem to follow that pattern.

  • Robert Koslover

    Surely, this is a prediction markets question! 🙂 After all, life Insurance companies charge higher rates for smokers. For example, see http://www.profam.com/insurance/smoker-vs-non-smoker.asp In that example, smokers are charged more than double! Thus, we can have high confidence that smoking is deadly. QED!

    • Robert Koslover

      And before anyone leaps in, let me say that I am very well aware that correlation and cause are not the same thing. But the correlation is undeniable.

    • Robert Rush

      This is exactly what you would predict if smoking didn’t make you worse off but people who choose to smoke tend to be more likely to die young(because they are poorer on average etc.) . Its also what you would predict if smoking made you less healthy so it is not solid proof either way. The question isn’t do smokers die more, they undoubtedly do, the question is instead whether or not they die more because of smoking.

      • Robert Koslover

        And that’s why I added the note about correlation vs cause.

  • Eric Johnson

    I think the study where people just smoked less can be dismissed, since (for relevant values) smoking for X-fold more years tends to be worse than smoking X more per day (all based on observational data of course).

    That leaves MRFIT. Someone should just actually calculate the statistical power of that study. I may be able to later, if I successfully look a bunch of stuff up, which I may or may not attempt (probably not).

  • Maybe because smoking is correlated with lower socio-economic class; and lower life expectancy is strongly correlated with lower SEC. Part of the effect could be that investigators expected smoking to shorten life, so they misinterpreted part of the life shortening effects of SEC to be from smoking instead.

    I dislike smoking and being around smokers, which was tough on me as a kid because both parents and starting in their teens all three of my brothers smoked. So I have always been wary about the anti-smoking literature, since I would have liked it to be true. But there have always been things that didn’t look right about it, and they haven’t gotten anything but more irritating since the gov’t has started using the second-hand smoking pseudoscience to justify increasingly wider bans.

    One thing that has bothered me since I was a teen, is that I have known a lot of smokers and never-smoked and I have never noticed any difference in health problems between the groups. The numbers are too small for any sort of significance, but it was another reason I have been suspicious of the gov’t’s claims.

    • Eric Johnson


      How strongly?

      And how strong is the SES to smoking correlation? 0.50? 0.60?

      • Typical mortality risk ratios for high vs low status are roughly a factor of two or three.

  • diogenese

    Robin — you have killed any credibility you have on healthcare with this post. I have not seen any observational data link any exposure TO cancer as strong as smoking. The relative risk is on the order of 10-20. I can’t even think of any observational data that is THAT strong for ANY EFFECT. Seriously, I would love to see somoene post observational data with a STRONGER effect size with as large an N.

    You aren’t as smart as you think you are — or original RA FISHER made the exact same arguments when the initial observational data came out. . Daphne Koller (I think Pearl too) have graphical models in their text providing causal explanations. Unfortunately its been a years since I looked at them, but you can look it up yourself.

    You have had some outrageous posts on healthcare before — but this is sheer QUACKERY. This post is equivalent to a creationist post — mostly because through sheer laziness you refuse to read about the history whatsoever.

    This history isn’t event CONFINED to the medical literature — its reviewed in innumerable statistics textbooks as well.

    BTW — interventions to quit smoking are horribly unsuccessful — it appears you forgot to consider that in your “analysis”.

  • Hey everyone, take a deep breath and chill for a minute. I didn’t deny that smoking hurts; I in fact said:

    Experts say there is a substantial causal component, and for now I’m accepting that claim, but this lack of clear evidence is suspicious, and disturbing.

    It is hard to imagine that smoking doesn’t effect our bodies, and I’d be surprised if some of these effect weren’t negative. But the important issue is the overall health effect. Even if I were absolutely convinced that smoking caused some lung cancer, that still wouldn’t settle the overall health effect issue.

    • Robert Koslover

      Well said. Of course, it is only because I am a nonsmoker that I am even capable of taking a deep breath. 🙂

    • retired phlebotomist

      It is interesting that someone who champions the idea of the irrationality of disagreement (& weighing others’ reasoned opinions as evidence) is so consistently smitten by contrarian notions presented by a lone source. This, the “Loose Change” 9/11 documentary, etc.

      And sure, you might couch them with half-hearted disclaimers, but I think diogenese may be right on this one. Your posts and comments here should be taken into consideration by anyone weighing your more unconventional views.

      I think Cowen really had you pegged in your bloggingheads.

  • I’ve added Robin’s opinion to a summary of experts who agree and disagree with the belief that smoking causes cancer:


    I had trouble finding an expert who was skeptical of the actual mechanism through which smoking causes cancer (the skeptics’ doubt seems to be focused on the statistics). If anyone can find such a source, let me know.

    • drewster

      If you think Robin’s an expert on this, you’re quite wrong.

      • Constant

        How do you know who’s an expert? You ask the experts. Hmmm. Problem.

  • It looks like being strongly advised to do something is correlated by increased mortality.

  • Eric Johnson

    > Even if I were absolutely convinced that smoking caused some lung cancer

    With a 23x risk ratio, its implausible that it doesnt cause a large majority of it.

    > that still wouldn’t settle the overall health effect issue

    I guess that is somewhat defendable, especially without knowing the power of MRFIT.

    What may be more questionable is the second-hand smoke crusade. I vaguely recall hearing some reasonable person sort of take it down.

  • Dan

    Robin, there may be a good indicator for the lung cancer. Small cell lung cancer is almost always observed in smokers only… what kind of cancer is observed? If the intervention group is mostly small cell then the statistic is ominous, the damaged cannot be reversed by quitting.

  • Empirics isn’t the whole picture. There is a very plausible mechanism by which cigarette smoke causes lung cancer, and even absent any experimental evidence, correlation + deduction is enough for me. That’s why it’s painfully obvious to everyone that the causal effect is there, even though the “scientific” case is, as Robin points out, quite weak.

  • Robin here is a study that shows reduction in all-cause mortality from smoking intervention


    • Eric Johnson


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  • You report that in the intervention groups, from 22.7% to 51.3% quit smoking.

    Suppose that, in the intervention groups, one-quarter of the subjects were already so unhealthy that their doctors told them they would die if they didn’t stop smoking. Suppose these people are much more likely to stop smoking.

    Then the protective effect of not smoking is concentrated among people who were already likely to die.

  • jonathan

    I’ve thought about this post and though I understand the point of this blog, you’re cherry picking an issue. I can easily cite a large number of statistical studies that show mortality for smoking, but you note a knowledge of only one specific type of study, which means you’ve decided to bias the case by focusing your argument on a point that may or may not be meaningful at all. (And I noted above that even your description contains certain issue that make me question the results are quite as simple as they appear.)

    My guess is that you accept statistical studies in a vast number of areas, that in fact you rely on them often. So here you want to debate to make a contrarian or skeptical point and you do that by narrowing the focus of the facts at hand while not narrowing the focus of the debate. One might say that given the study you note it would make sense to at least look for other primary data that either supports or does not support increased mortality. But that’s about all you can say without being intellectually dishonest.

    Secondly, you focus on mortality and that is of course an issue but you leave out incidences of cancer and the like. That again is a game of hiding the pea because the issue isn’t solely about mortality and everyone knows that. To make an unjustified statement, let’s say mortality was the same but smokers suffered in dreadful pain for 5 years before dying. Is that meaningful? Not if you twist the argument to only be about mortality.

    If you want to look at a health issue, a better candidate for skepticism is the relation between dietary cholesterol and your personal cholesterol levels (and then to heart disease). Unlike blood pressure, high cholesterol is not much of a risk factor if you don’t have a family history – and by history I don’t mean a 78 year old with some angina or mild coronary artery disease because the analysis of aging-related disease is different. As to dietary cholesterol, it not only affects some people more than others but the relation may be weaker than that of salt to hypertension. This has been relatively hard to analyze because people have become so much fatter.

    • Eric Johnson

      Agreed that death is not good as a sole metric, and that Robin’s thoughts are probably pushing untenable. But you seem to be missing or eliding his focus on observational vs interventional data.

      This book by a Mason physics prof, like his other book, addresses the insurgent position on cholesterol, and several other similar positions. Its not really a heavyweight review of any of the controversies in question, but the guy has an outsider’s freshness on these disputes, and of course the fine epistemology any physicist would have. And he’s very readable.


  • GoOpenOrPoly

    On the broader issue of smoking regulation and the drug war:

    I think we should make smoking anything illegal and legalize everything else – whether inhaled, injected, swallowed or absorbed – all drugs. The only places you should be allowed to smoke are designated private smoking facilities with air filtration systems. I cannot refuse or consent to inhaling smoke (and where I live, it’s a constant assault on your respiratory system). Otherwise, just legalize and regulate; you should have to go through a lengthy process to determine whether you’re fit to use drugs (including alcohol) and you’d have to sign consent forms, and agree that any costs incurred due to potential addiction are your own and will not be borne by the state (except addiction programs themselves, of course). If you agree, you’re sold drugs by state-chartered companies that are tightly regulated, including pricing, to eliminate the black market.

    Regulation should focus on direct, material harm to others (not things like attendant loss of income or someone being mean) and should be about methods, not substances.

  • I hope Robin will return to this thread to respond to the study Karl Smith identified. Does it take more than one controlled experimental study to convince Robin that smoking is linked to mortality (to supplement, of course, the many econometric studies that attempt to control for self-selection and other correlated variables)? Robin might also speak to whether he is a Bayesian, and if so, how are his prior beliefs influenced by the obvious physiological damage caused by smoking. Similarly, how are his priors affected by his strong belief that low-status people smoke, and status is (in Robin’s view) very important.

    I sure hope the answer isn’t of the form ‘it takes one more controlled experimental study than has been conducted’,a typical ruse of people unwilling to be convinced by any degree of evidence, either because they have financial interests involved (the tobacco companies) or because they are emotionally invested in being contrarian.

    Btw, technically these controlled studies actually test the hypothesis “does an intervention intended to reduce smoking delay death,” not “does quitting smoking delay death.” Robin wants to use the (non)results to argue that there is no evidence of the latter, because those who quit are self-selecting. However, the results of the non-results studies are not particularly damning evidence against the quitting-living association, because there are other ways to address self-selection biases.

    The results of Karl’s study show that the intervention helps *because* those who quit live longer–a very strong result, because it shows the path of the effect.

    • @Robert Bloomfield: I’m not sure this study (mentioned by Karl Smith) can be called a randomised controlled trial. It was not set up to test the hypothesis “does an intervention intended to reduce smoking delay death?” Instead it was set up to:

      “… determine whether a program incorporating smoking intervention and use of an inhaled bronchodilator can slow the rate of decline in forced expiratory volume in 1 second (FEV1) in smokers aged 35 to 60 years who have mild obstructive pulmonary disease.”


      The original paper shows the 5-year results, which were positive: The program slowed the rates. But no difference in mortality between the two intervention groups and the usual care-group were recorded. However it is noted in the paper that “nearly half (of the participants) gave a history of exposure to dust and/or fumes”.

      It is well known that exposure to dust and fumes are important risk factors for lung cancer disease and death for both smokers, ex-smokers and nonsmokers. The inclusion of these people in a study of smoking/quitting risks with a death endpoint multiply the risk of bias.

      The authors write in the 14,5 year follow up article: “Since death rates between special intervention and usual care participants with similar smoking habits did not differ, the differences observed in the groups as a whole were almost certainly due to differential cessation rates.”

      “Almost certainly,” is hardly a “strong result”. And it does not make the case better that the authors refused to publish the actual figures when asked in the letters to the editor.

      So I do not think this paper adds anything new to the Johnstone & Finch article.

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