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.
It is well known that smoking is dangerous in many different ways. Smoking over a period of time leads to many different health problems. Smoking is particularly damaging to the heart and lungs. Smoking can lead to a number of lung diseases or disorders including COPD (Chronic Obstructive Pulmonary Disorder), lung cancer, Emphysema, and shortness of breath. But exactly how can smoking destroy your lungs.
@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.
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.
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.
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.
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.
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.
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.
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.
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.
It is well known that smoking is dangerous in many different ways. Smoking over a period of time leads to many different health problems. Smoking is particularly damaging to the heart and lungs. Smoking can lead to a number of lung diseases or disorders including COPD (Chronic Obstructive Pulmonary Disorder), lung cancer, Emphysema, and shortness of breath. But exactly how can smoking destroy your lungs.
Article source : http://1betteroff.blogspot....
@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."
http://jama.ama-assn.org/co...
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.
How do you know who's an expert? You ask the experts. Hmmm. Problem.
If you think Robin's an expert on this, you're quite wrong.
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.
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.
Nice.
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.
http://books.google.com/boo...
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.
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.
Robin here is a study that shows reduction in all-cause mortality from smoking intervention
http://www.annals.org/conte...
I'd like to know how far you can take this.
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.
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.
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.
> 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.