CATCH-14

Frank Davis writes.

In CATCH-4, a week or so back, Chris Snowdon wrote:

Since the obvious explanation for this strong, dose-sensitive association is that chronic smoking raises the risk of lung cancer significantly, any defence of smoking as the causative factor must provide an alternative. That alternative must be closely correlated with smoking itself and must have a correlation with lung cancer that is at least as strong as the correlations found for smoking and lung cancer.

A couple of days ago I called this ‘dose-sensitive relationship’ into question, pointing out that the number of cigarettes somebody smoked per day was not a measure of the dose they received in terms of the amount of tobacco smoke inhaled (assuming it was inhaled at all). I was able to show that the dose was dependent not just on the number of cigarettes smoked, but the fraction of those cigarettes’ smoke which was inhaled, and that this was dependent on the rate at which they were smoked. If the rate at which cigarettes were smoked was unknown, then the dose was unknown, and it wasn’t possible to say that there was a ‘strong, dose-sensitive relationship’.

There’s been no response from Chris to this argument of mine. And that’s probably because it’s a new argument, or at least one which has not much been advanced in debates of this sort. Nevertheless, new or not, it was an argument which, I would dare to say, largely undermines Chris’ confident claim.

A few days earlier, I called into question his claim that the London Hospitals study had shown a Relative Risk of 7 for smokers contracting lung cancer, by showing that this RR fell rapidly when fairly small smoker or cancer misclassification errors were assumed. And there would have been misclassification errors. There are always errors in measurements. I dare say exactly the same analysis could be applied to a great many studies of smoking, with much the same effect.

There’s been no response from Chris to this argument either. And this one isn’t a new argument.

The truth of the matter, I fear, is that the association between smoking and lung cancer doesn”t bear much in the way of close scrutiny. It only holds up if the numbers are taken at face value – that there were exactly so many smokers, and they got exactly this much lung cancer -. Question the numbers at all, and the claims rapidly falls apart. It’s a house of cards, which will only remain standing if nobody touches it, or even breathes upon it.

In fact, I would say that there really shouldn’t be any need to go to the lengths of performing mathematical operations on the given numbers as I have been doing. All that needs to be done is to point out that all the published numbers do not consist of accurate measurements of any sort, but almost entirely of guesses. For it’s a pure guess what number anyone gives for the number of cigarettes they smoke in a day or a lifetime. And it’s a pure guess what anyone may be said to have died from, whether it be lung cancer or emphysema or bronchitis or heart disease.

What other science relies upon guesses to provide it with its raw data? Does this epidemiology actually deserve the name of ‘science’ at all? The best that it offers is a vague intimation of what might be cause and what might be effect. It is as accurate as wetting a finger to gauge the direction of the wind.

Nevertheless, it’s upon the basis of this risible ‘science’ that the doctrine that smoking causes lung cancer has been almost entirely erected.

For neither have animal studies helped very much either. It appears that, except perhaps for one case, studies of smoking animals have never been shown to produce lung cancers – something Chris puts down to animals breathing through their noses, and filtering  the smoke (as if somehow nature had equipped them with better nasal filters than any cigarette manufacturer have managed to mount on the end of a cigarette). The one exception was when beagles were given tracheotomies, in an experiment that was never repeated, but which Chris seemed to think was a more ‘natural’ way of smoking, although if it was done to me would entirely negate my own presumably ‘unnatural’ way of smoking (I first draw a little smoke into my mouth, and then open my mouth and inhale both smoke and air into my lungs)..

I’d also like to call into question Chris’ assertion, in the fragment quoted above, that  "any defence of smoking as the causative factor must provide an alternative". I think that what he means here is that if people don’t believe that smoking causes lung cancer, then they must tell us what does.

But do they? Isn’t it enough to simply create sufficient doubt about the old hypothesis, by pointing out its innumerable deficiencies? Isn’t it that the old hypothesis first has to be seen to fail before some new hypothesis can be entertained? As the measurement of planetary motions became more and more accurate, ever more epicycles had to be added to the old earth-centred Ptolemaic model of the solar system in order to keep it working. There was already a need for a new model by the time Copernicus showed up with his new heliocentric scheme of things. In the same way, I don’t think that I (or anybody else) needs to advance a plausible hypothesis to replace the cigarette/smoking hypothesis in order to show its inadequacy.. Nor is it that there is any lack of alternative hypotheses. There’s the diesel exhaust hypothesis (diesel driven vehicles started appearing on the roads just when lung cancer started becoming more frequent). The fallout/radioactivity hypothesis (highly carcinogenic radioactive elements, beginning with radium, began to become abundant at the same time, and eventually got showered all over the world thanks to nuclear weapons testing). The HPV hypothesis (Human papilloma virus is now believed to be the cause of cervical cancer, and HPV has been found present in a number of other cancers, including lung cancer).. And more.

But in considering possible causes of lung cancer, we’ve mostly been considering a few post-war studies – Doll and Hill (1950) and (1954 – 2004), the Kaiser Permanente experiment (1979 – 1987) -. Since then the same questionnaire-driven methodology  has been used to build the even giddier card house of secondhand smoking studies. Even though Chris respects the active smoking studies that preceded these, he doesn’t have much respect for these studies, or for the weight that has been placed upon them (as his own book testifies).

Nor, it seemed, does Chris place much weight on the Nazi studies by Lickint, Muller, et al, from about 1930 to 1945.

It would seem then that he rejects the Nazi studies, but accepts the post-war active smoking studies (which were arguably just a continuation of the Nazi studies), and then rejects the subsequent passive smoking studies.

Why pick and choose? Wouldn’t it be simpler to just reject the whole lot, from start to finish?

Furthermore, I would suggest that there are a number of very good reasons for rejecting the whole lot. In the first place, it creates a much more easily defensible position – it straightens the trenches, and gets rid of a Ypres salient, so to speak.  Secondly, as I have said before, the passive smoking hypothesis is built upon and depends upon the active smoking hypothesis. Once someone has accepted that active or primary smoking can cause a lot of lung cancer (never mind what is meant by ‘a lot’) then it is perfectly plausible that passive or secondhand smoking can cause a little bit of lung cancer (and by extension so also all the other mystical degrees of smoke – thirdhand, fourthhand, etc, etc -) While the tree of primary smoking remains standing, it will continue to keep sprouting new secondary and tertiary branches. The only way to stop it is to cut the tree down at its base, or better still entirely uproot it.

Furthermore, this is no longer some sort of academic debate (as it was perhaps in the 1950s when Sir Ronald Fisher was a friend of Bradford Hill). Sixty years on from those civilised times, smoking research is being used to persecute and demonise smokers, expel them from pubs, refuse them medical treatment (Dick Puddlecote has a new example of this just yesterday), fire them from their jobs, and evict them from their homes (see a comment by Michael McFadden I received today). It has become an accelerating modern pogrom.

On a cold October night in upstate New York, an elderly woman named Pearl huddled in her overcoat on the unlit porch of her adult group home, smoking a cigarette.

"A lot of us smoke, and we had a meeting about it, but [the manager] told us if anyone was caught smoking inside, he’d throw us out," Pearl said.

I asked Pearl if she couldn’t move somewhere else, but immediately regretted the question. Even in the dark, I could see her eyes fill with tears as she looked away and shook her head.

In this circumstance, it has become as absurd for any smoker to give credit to any of the ‘research’ that is being used to persecute them as it would have been for a Jew to give credit to any Nazi racial ‘research’.

And this is why I believe that smokers will increasingly be driven to reject the entire set of epidemiological studies that have been conducted over the past 80 years, and also the entire system of  eugenic ‘lifestyle’ medicine in which it is embedded. All of it must go. The whole filthy thing must be uprooted and burned. None of it can be allowed to remain.

Because we are not really engaged in any sort of nice, civilised debate any more. We are engaged in a war. And in this war there can be no compromises and no concessions. We can’t afford such luxuries. It is a war of annihilation. And the sooner smokers and their friends see this, the better.

About Frank Davis

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289 Responses to CATCH-14

  1. richwhite09 says:

    To play devil’s advocate, i believe a continuity fault exists in your post Frank. Let me state from the offset that I do agree with the claims, but I also see a flawed continuation that I suspect Chris has also seen. Quite simply, the flaw is that we cannot do away with any harm of active smoking just because we know passive smoking to be a fraud. In such instances where the active is true and the passive false, the correct method would be to expose the political ties and agenda in the latter. For instance, you say “Why pick and choose? Wouldn’t it be simpler to just reject the whole lot, from start to finish?”
    Yes it would be simpler, but i must say that wouldn’t be at all scientific. I also think it’s becoming increasingly apparent from this debate that we don’t need to reject it for matters of simplicity – it’s just crying out to be rejected.
    Now that’s out the way, i want to say it’s an excellent post. You touched upon a couple tihngs I have briefly mentioned too, namely that Chris rejected the SHS studies because they were questionnaires and were not solid science; in an earlier CATCH instalment I provided a questionnaire from Wynder to demonstrate how it wasn’t far removed from SHS questionnaires at all.
    Also the point on animal studies and breathing it in nasally. Chris seems to be quite confused with the animal studies, and while he’s quick to call me a liar or making transparent claims if i make a slight recollection error, I won’t do that here. However, in response to Chris’ claims about the animals only breathing in their nose, I provided excerpts from surgeon general reports that, actually, ‘advanced inhalation’ equipment has been in existence and used for decades. Chris didn’t reply to this. And as I showed in my last post, Chris is also very confused about Auerbach’s findings, asserting that every smoking dog was dead, dying or in a bad way, while the controls were all fine. As i showed from the SG report findings, actually 2 non-smoking dogs developed tumours and not nearly every smoking dog was dead, dying or ill. Ultimately, this has been laid to rest in the multiple court cases that show that no animal has contracted lung cancer through exposure to tobacco smoke.
    I would like to respond to the quote from Chris you provided:
    “Since the obvious explanation for this strong, dose-sensitive association is that chronic smoking raises the risk of lung cancer significantly, any defence of smoking as the causative factor must provide an alternative. That alternative must be closely correlated with smoking itself and must have a correlation with lung cancer that is at least as strong as the correlations found for smoking and lung cancer.”
    Firstly, Frank I agree we don’t need to provide an alternative at all. If an alternative exists and we just don’t know about it yet (and with all the focus on tobacco over the decades who knows what has been missed), we can’t pin the blame on something else just to keep things neat and tidy.
    But secondly, I was reading a post from Nightlight earlier today and it’s a very good point indeed:
    “Of course, as any other therapy or medicine, smoking will statistically correlate with diseases it is therapeutic or protective against, just as taking aspirin will statistically correlate with headaches, or using breathing ventilators with breathing problems, or using vitamins and health supplements with poorer general health”
    Now, before Chris takes this and puts his ‘see what he did there?’ spin on it, I’m not saying smoking wards off lung cancer (we’ll save that topic for another discussion i think), but the point itself is irrefutable: statistically, positive things appear negative. All i’m offering this for here is just for further reflection on the inadequacy of statistics. Statistics have their place, and in conjunction with other evidence they can help solidify a fact, but taken alone they cannot.

  2. richwhite09 says:

    To play devil’s advocate, i believe a continuity fault exists in your post Frank. Let me state from the offset that I do agree with the claims, but I also see a flawed continuation that I suspect Chris has also seen. Quite simply, the flaw is that we cannot do away with any harm of active smoking just because we know passive smoking to be a fraud. In such instances where the active is true and the passive false, the correct method would be to expose the political ties and agenda in the latter. For instance, you say “Why pick and choose? Wouldn’t it be simpler to just reject the whole lot, from start to finish?”
    Yes it would be simpler, but i must say that wouldn’t be at all scientific. I also think it’s becoming increasingly apparent from this debate that we don’t need to reject it for matters of simplicity – it’s just crying out to be rejected.
    Now that’s out the way, i want to say it’s an excellent post. You touched upon a couple tihngs I have briefly mentioned too, namely that Chris rejected the SHS studies because they were questionnaires and were not solid science; in an earlier CATCH instalment I provided a questionnaire from Wynder to demonstrate how it wasn’t far removed from SHS questionnaires at all.
    Also the point on animal studies and breathing it in nasally. Chris seems to be quite confused with the animal studies, and while he’s quick to call me a liar or making transparent claims if i make a slight recollection error, I won’t do that here. However, in response to Chris’ claims about the animals only breathing in their nose, I provided excerpts from surgeon general reports that, actually, ‘advanced inhalation’ equipment has been in existence and used for decades. Chris didn’t reply to this. And as I showed in my last post, Chris is also very confused about Auerbach’s findings, asserting that every smoking dog was dead, dying or in a bad way, while the controls were all fine. As i showed from the SG report findings, actually 2 non-smoking dogs developed tumours and not nearly every smoking dog was dead, dying or ill. Ultimately, this has been laid to rest in the multiple court cases that show that no animal has contracted lung cancer through exposure to tobacco smoke.
    I would like to respond to the quote from Chris you provided:
    “Since the obvious explanation for this strong, dose-sensitive association is that chronic smoking raises the risk of lung cancer significantly, any defence of smoking as the causative factor must provide an alternative. That alternative must be closely correlated with smoking itself and must have a correlation with lung cancer that is at least as strong as the correlations found for smoking and lung cancer.”
    Firstly, Frank I agree we don’t need to provide an alternative at all. If an alternative exists and we just don’t know about it yet (and with all the focus on tobacco over the decades who knows what has been missed), we can’t pin the blame on something else just to keep things neat and tidy.
    But secondly, I was reading a post from Nightlight earlier today and it’s a very good point indeed:
    “Of course, as any other therapy or medicine, smoking will statistically correlate with diseases it is therapeutic or protective against, just as taking aspirin will statistically correlate with headaches, or using breathing ventilators with breathing problems, or using vitamins and health supplements with poorer general health”
    Now, before Chris takes this and puts his ‘see what he did there?’ spin on it, I’m not saying smoking wards off lung cancer (we’ll save that topic for another discussion i think), but the point itself is irrefutable: statistically, positive things appear negative. All i’m offering this for here is just for further reflection on the inadequacy of statistics. Statistics have their place, and in conjunction with other evidence they can help solidify a fact, but taken alone they cannot.

    • richwhite09 says:

      Oh, to add, as i missed this before, “Nor, it seemed, does Chris place much weight on the Nazi studies by Lickint, Muller, et al, from about 1930 to 1945.”
      Well, they most definitely formed the basis for Doll etc, Doll even referenced Muller, and it was pointed out earlier in the CATCH discussion that the Nazi scientists gave lectures to the subsequent British and American epidemiologists. So there’s no denying their influence. But why does Chris reject these and not Doll etc? What made Doll and Hill better than Muller?
      Also, one other thing, when I said no biological evidence exists of how smoking causes cancer, in humans or animals, he called it transparent and a lie, but offered no proof to the contrary. As Gary K pointed out, that’s ‘not very gentlemanly’. Chris, this debate cannot be solved with rhetoric and a sweeping hand of rejection. If you do know of the mechanisms of how tobacco smoke causes cancer, I, the other commenters and indeed the prosecution and defence of the courts would love to see it.

      • cjsnowdon says:

        Animal experiments are biological evidence, FFS.

        • richwhite09 says:

          Yes, and they failed! So how, exactly, is it that my statement ‘no biological evidence exists and animal studies have failed’ is a transparent lie, when i have shown the transcripts from court from multiple scientists that actually it is true? You say ‘animal experiments are biological evidence’, and indeed this is true – but the studies have failed, so what biological evidence are you taking from this?
          You’re dragging this round and round in circles, all on the hope that apparently the facts will change

        • richwhite09 says:

          Chris, i’m going out in a few minutes and won’t be back until about lunchtime tomorrow. If i can’t reply to anything until then don’t take it that i’m ignoring you. If you leave me any comments/replies, i’ll look at them when i get back.

    • richwhite09 says:

      Oh, to add, as i missed this before, “Nor, it seemed, does Chris place much weight on the Nazi studies by Lickint, Muller, et al, from about 1930 to 1945.”
      Well, they most definitely formed the basis for Doll etc, Doll even referenced Muller, and it was pointed out earlier in the CATCH discussion that the Nazi scientists gave lectures to the subsequent British and American epidemiologists. So there’s no denying their influence. But why does Chris reject these and not Doll etc? What made Doll and Hill better than Muller?
      Also, one other thing, when I said no biological evidence exists of how smoking causes cancer, in humans or animals, he called it transparent and a lie, but offered no proof to the contrary. As Gary K pointed out, that’s ‘not very gentlemanly’. Chris, this debate cannot be solved with rhetoric and a sweeping hand of rejection. If you do know of the mechanisms of how tobacco smoke causes cancer, I, the other commenters and indeed the prosecution and defence of the courts would love to see it.

    • Frank Davis says:

      “Why pick and choose? Wouldn’t it be simpler to just reject the whole lot, from start to finish?”
      Yes it would be simpler, but i must say that wouldn’t be at all scientific.

      The ‘continuity fault’ you point out is where I switch from a scientific or ‘academic’ argument to a political argument. I’m not arguing as a scientific point that just because the passive smoking science is lousy, the active smoking science must be lousy too. I’m saying that, in a political confrontation, we absolutely have to throw the whole lot away, regardless of the science.
      Frank

    • Frank Davis says:

      “Why pick and choose? Wouldn’t it be simpler to just reject the whole lot, from start to finish?”
      Yes it would be simpler, but i must say that wouldn’t be at all scientific.

      The ‘continuity fault’ you point out is where I switch from a scientific or ‘academic’ argument to a political argument. I’m not arguing as a scientific point that just because the passive smoking science is lousy, the active smoking science must be lousy too. I’m saying that, in a political confrontation, we absolutely have to throw the whole lot away, regardless of the science.
      Frank

  3. richwhite09 says:

    To play devil’s advocate, i believe a continuity fault exists in your post Frank. Let me state from the offset that I do agree with the claims, but I also see a flawed continuation that I suspect Chris has also seen. Quite simply, the flaw is that we cannot do away with any harm of active smoking just because we know passive smoking to be a fraud. In such instances where the active is true and the passive false, the correct method would be to expose the political ties and agenda in the latter. For instance, you say “Why pick and choose? Wouldn’t it be simpler to just reject the whole lot, from start to finish?”
    Yes it would be simpler, but i must say that wouldn’t be at all scientific. I also think it’s becoming increasingly apparent from this debate that we don’t need to reject it for matters of simplicity – it’s just crying out to be rejected.
    Now that’s out the way, i want to say it’s an excellent post. You touched upon a couple tihngs I have briefly mentioned too, namely that Chris rejected the SHS studies because they were questionnaires and were not solid science; in an earlier CATCH instalment I provided a questionnaire from Wynder to demonstrate how it wasn’t far removed from SHS questionnaires at all.
    Also the point on animal studies and breathing it in nasally. Chris seems to be quite confused with the animal studies, and while he’s quick to call me a liar or making transparent claims if i make a slight recollection error, I won’t do that here. However, in response to Chris’ claims about the animals only breathing in their nose, I provided excerpts from surgeon general reports that, actually, ‘advanced inhalation’ equipment has been in existence and used for decades. Chris didn’t reply to this. And as I showed in my last post, Chris is also very confused about Auerbach’s findings, asserting that every smoking dog was dead, dying or in a bad way, while the controls were all fine. As i showed from the SG report findings, actually 2 non-smoking dogs developed tumours and not nearly every smoking dog was dead, dying or ill. Ultimately, this has been laid to rest in the multiple court cases that show that no animal has contracted lung cancer through exposure to tobacco smoke.
    I would like to respond to the quote from Chris you provided:
    “Since the obvious explanation for this strong, dose-sensitive association is that chronic smoking raises the risk of lung cancer significantly, any defence of smoking as the causative factor must provide an alternative. That alternative must be closely correlated with smoking itself and must have a correlation with lung cancer that is at least as strong as the correlations found for smoking and lung cancer.”
    Firstly, Frank I agree we don’t need to provide an alternative at all. If an alternative exists and we just don’t know about it yet (and with all the focus on tobacco over the decades who knows what has been missed), we can’t pin the blame on something else just to keep things neat and tidy.
    But secondly, I was reading a post from Nightlight earlier today and it’s a very good point indeed:
    “Of course, as any other therapy or medicine, smoking will statistically correlate with diseases it is therapeutic or protective against, just as taking aspirin will statistically correlate with headaches, or using breathing ventilators with breathing problems, or using vitamins and health supplements with poorer general health”
    Now, before Chris takes this and puts his ‘see what he did there?’ spin on it, I’m not saying smoking wards off lung cancer (we’ll save that topic for another discussion i think), but the point itself is irrefutable: statistically, positive things appear negative. All i’m offering this for here is just for further reflection on the inadequacy of statistics. Statistics have their place, and in conjunction with other evidence they can help solidify a fact, but taken alone they cannot.

  4. richwhite09 says:

    Oh, to add, as i missed this before, “Nor, it seemed, does Chris place much weight on the Nazi studies by Lickint, Muller, et al, from about 1930 to 1945.”
    Well, they most definitely formed the basis for Doll etc, Doll even referenced Muller, and it was pointed out earlier in the CATCH discussion that the Nazi scientists gave lectures to the subsequent British and American epidemiologists. So there’s no denying their influence. But why does Chris reject these and not Doll etc? What made Doll and Hill better than Muller?
    Also, one other thing, when I said no biological evidence exists of how smoking causes cancer, in humans or animals, he called it transparent and a lie, but offered no proof to the contrary. As Gary K pointed out, that’s ‘not very gentlemanly’. Chris, this debate cannot be solved with rhetoric and a sweeping hand of rejection. If you do know of the mechanisms of how tobacco smoke causes cancer, I, the other commenters and indeed the prosecution and defence of the courts would love to see it.

  5. Anonymous says:

    And we fight as I have done since day 1…………..Feck anti-smoking nazis,we need to persecute them for a change!

  6. Anonymous says:

    And we fight as I have done since day 1…………..Feck anti-smoking nazis,we need to persecute them for a change!

  7. Anonymous says:

    And we fight as I have done since day 1…………..Feck anti-smoking nazis,we need to persecute them for a change!

  8. Frank Davis says:

    “Why pick and choose? Wouldn’t it be simpler to just reject the whole lot, from start to finish?”
    Yes it would be simpler, but i must say that wouldn’t be at all scientific.

    The ‘continuity fault’ you point out is where I switch from a scientific or ‘academic’ argument to a political argument. I’m not arguing as a scientific point that just because the passive smoking science is lousy, the active smoking science must be lousy too. I’m saying that, in a political confrontation, we absolutely have to throw the whole lot away, regardless of the science.
    Frank

  9. Anonymous says:

    At least big tobacco never pushed for laws to outlaw people!

  10. Anonymous says:

    At least big tobacco never pushed for laws to outlaw people!

  11. Anonymous says:

    At least big tobacco never pushed for laws to outlaw people!

  12. richwhite09 says:

    I agree; as i say, just picking it up before the prosecution

  13. Anonymous says:

    Sorry – More on Beagles
    In Catch11, I had a discussion with Chris about his evidence on Auerbach having produced evidence of smoke inhalation causing cancer in beagles:
    http://frank-davis.livejournal.com/128390.html?thread=1253766#t1253766
    His evidence essentially boiled down to one document and in particular the quote given on page 40 which was attributed to the General Manager of Research at Gallaher on 3rd April 1970:
    http://tobaccodocuments.org/batco/321481589-1857.html?zoom=750&ocr_position=above_foramatted&start_page=31
    Looking at this further, I still can’t find the full memo from which the quote was taken. Which means it remains unclear whether caveats were added or for that matter whether the original author was actually quoting someone else in his memo.
    I also noted that the document (link above) is actually the case for the prosecution brought by Tobacco Control Australia in 1976. I have no idea what the outcome was and whether the evidence held up in court.
    I did however, come across an R..J. Reynolds statement to stockholders from May 1970:
    http://tobaccodocuments.org/atc/60268526.html?zoom=750&ocr_position=above_foramatted&start_page=11
    This contains the following statement:
    Early this year an experiment on 56 beagles was press-released in terms calculated to drown out these voices of scientific reason. I will not go into the details of that dog act. but with your permission I will cite this comment by one disinterested biologist. After analyzing the beagle experiment, he concluded: “What does bother me is the misuse of so-called scientific results by one group with vested interests to attack another. All this experiment proves is: Whether or not smoking causes lung cancer in beagles is as inconclusive now as it was before the experiment was carried out.”
    Of course this also matches the conclusions of the independent scientists, the defence team AND the pursuers in the ITL vs McTear case.
    Just thought it might be of interest.
    P.S. To be fair, Chris actually stated (Catch-11):
    No, as I said in the last post they delivered invasive tumours which is the step before lung cancer, and they developed lots of them. The nonsmoking dogs didn’t develop any.
    Tony

  14. Anonymous says:

    Sorry – More on Beagles
    In Catch11, I had a discussion with Chris about his evidence on Auerbach having produced evidence of smoke inhalation causing cancer in beagles:
    http://frank-davis.livejournal.com/128390.html?thread=1253766#t1253766
    His evidence essentially boiled down to one document and in particular the quote given on page 40 which was attributed to the General Manager of Research at Gallaher on 3rd April 1970:
    http://tobaccodocuments.org/batco/321481589-1857.html?zoom=750&ocr_position=above_foramatted&start_page=31
    Looking at this further, I still can’t find the full memo from which the quote was taken. Which means it remains unclear whether caveats were added or for that matter whether the original author was actually quoting someone else in his memo.
    I also noted that the document (link above) is actually the case for the prosecution brought by Tobacco Control Australia in 1976. I have no idea what the outcome was and whether the evidence held up in court.
    I did however, come across an R..J. Reynolds statement to stockholders from May 1970:
    http://tobaccodocuments.org/atc/60268526.html?zoom=750&ocr_position=above_foramatted&start_page=11
    This contains the following statement:
    Early this year an experiment on 56 beagles was press-released in terms calculated to drown out these voices of scientific reason. I will not go into the details of that dog act. but with your permission I will cite this comment by one disinterested biologist. After analyzing the beagle experiment, he concluded: “What does bother me is the misuse of so-called scientific results by one group with vested interests to attack another. All this experiment proves is: Whether or not smoking causes lung cancer in beagles is as inconclusive now as it was before the experiment was carried out.”
    Of course this also matches the conclusions of the independent scientists, the defence team AND the pursuers in the ITL vs McTear case.
    Just thought it might be of interest.
    P.S. To be fair, Chris actually stated (Catch-11):
    No, as I said in the last post they delivered invasive tumours which is the step before lung cancer, and they developed lots of them. The nonsmoking dogs didn’t develop any.
    Tony

    • richwhite09 says:

      Re: Sorry – More on Beagles
      Not just McTear, it was also concluded in the Minnesota case in, i think, 1997 that no animal had contracted lung cancer from tobacco smoke.
      I also showed in catch13 that chris is wrong and being misleading (deliberately or not i don’t know) with his claims about the beagles. 2 of 8 (25%) non-smoking dogs got tumours.

      • cjsnowdon says:

        Re: Sorry – More on Beagles
        And what Rich is not saying (deliberately or not i don’t know) is that the tumours were non-invasive and that’s not unusual in humans or dogs. However, ALL the invasive tumours were found in the smoking dogs and NONE of the nonsmoking dogs had an invasive tumour. There was also a dose-response relationship for the non-invasive tumours, which went 25% (nonsmoking), 40% (filter-tip), 50% (non-filter tip), 100% (non-filter tip, heavy smoking). In that last category, 10 out of 24 dogs had invasive tumours, and it no doubt would have been higher still if half of them hadn’t died before the experiment ended.
        Still, probably just the stress, eh?

        • Frank Davis says:

          Re: Sorry – More on Beagles
          What does it matter? There was only one experiment, as far as I understand, which was never repeated. Nobody pays any attention to a single experiment until somebody else replicates it.
          Frank

        • cjsnowdon says:

          Re: Sorry – More on Beagles
          It doesn’t matter. Not to me. I’m interested in whether smoking causes lung cancer in humans. I only mentioned Auerbach in the first place because you said (in CATCH-3):
          “No laboratory studies of smoking animals have shown them developing lung cancer”
          And Rich said (in CATCH-2):
          “To this day, scientists have not managed to induce lung cancer in any animal through tobacco smoke”

        • richwhite09 says:

          Re: Sorry – More on Beagles
          And that statement is true. Shall I keep repeating quotes from the scientists of the court cases until it sinks in? Both sides, including the one who would benefit enormously from showing tobacco smoke caused lung cancer, conceded the animal studies have failed.
          The assertion has never been that no animal has suffered lung cancer in a study, because they have. The assertion is the tobacco smoke hasn’t caused it.
          Fact of the matter is, Chris, you were plainly wrong about the experiment. You said all the controls were fine and all the smoking dogs were dead, dying or in a bad way. You then accused me of not reading the study – when clearly, you hadn’t read it very well because what you said was wrong! It’s time to stop relying on personal digs, it’s not going to help your cause of showing us all wrong at all; neither will reliance on studies that do not show what you say they do.

        • richwhite09 says:

          Re: Sorry – More on Beagles
          Also, “It doesn’t matter. Not to me.”
          So now you’re wrong it doesn’t matter? Before you were all over Auerbach’s study, stating:
          “12 of the 86 dogs did get lung cancer” in CATCH 4. When it was pointed out they didn’t, you said the what they had was the stage before lung cancer. When you found out the non-smoking dogs had tumours, you wriggled by saying they were non-invasive, as if somehow that made it more damning to tobacco. Non-invasive tumours have the potential to become invasive if left untreated, so that doesn’t do anything to the argument except show how you’re willing to use one single point as both a defence and an attach. And, as I have said repeatedly, with only 10% of the amount of controls as smoking dogs, it’s not valid to use the numbers as conclusive because had the numbers been more equal the rates of cancer may also have been more equal. The only dog to die from aspiration of food was in the smoking group, so are we to suggest smoking was the cause of that too? Or perhaps stress really was an underlying factor, which explains why that group had more ‘other’ deaths, and if it was the tobacco that stressed them that would explain the dose dependency. This is a hypothesis, before you run around with ‘oh so now you’re saying stress caused it again?’ I know you’ll reject this too, but i also know you’ll do so without actually providing any basis

        • cjsnowdon says:

          Re: Sorry – More on Beagles
          The nonsmoking dogs were fine. They didn’t have non-invasive tumours or any other disease. All the smoking dogs were dead, dying or in a bad way. Even the one that didn’t have invasive tumours all had emphysema.

        • richwhite09 says:

          Re: Sorry – More on Beagles
          “The nonsmoking dogs were fine. They didn’t have non-invasive tumours or any other disease”
          So now you’re bold enough to say the results in the SG reports are wrong? The dogs didn’t have non-invasive tumours despite, well, the results showing they did?

        • cjsnowdon says:

          Re: Sorry – More on Beagles
          Sorry, should have been “invasive tumours”.

        • richwhite09 says:

          Re: Sorry – More on Beagles
          Sure, true enough. But non-invasive tumours can progress to invasive tumours, and as i keep repeating, how can you be so sure that different results wouldn’t have occured had there been even 15 or 20 non-smoking dogs? Surely even you must concede it’s a bit odd for the researchers not to make the numbers a bit more balanced.

        • cjsnowdon says:

          Re: Sorry – More on Beagles
          No I don’t. The evidence from it is clear and since none of the nonsmoking dogs had smoking-related diseases or symptoms, there’s no reason to think that this would have changed if there had been 80 controls. We know that beagles don’t just develop these diseases for no reason. The control group was large enough to confirm that tracheotomies don’t cause these diseases either (not that anyone thought they would). Mutilating more dogs for no good reason would have gone down very badly with the public. Auerbach was getting death threats from animal rights campaigners and had to do is work in secret.

        • richwhite09 says:

          Re: Sorry – More on Beagles
          “there’s no reason to think that this would have changed if there had been 80 controls”
          Rubbish. Let’s take the 8 healthiest dogs from the smoking section and say that nothing would change if there were 80. Or take 8 healthy 90 year old humans and say having 80 would’t change their health status.
          “Mutilating more dogs for no good reason would have gone down very badly with the public. Auerbach was getting death threats from animal rights campaigners and had to do is work in secret.”
          So? What’s that got to do with the results?
          Once again Chris, if this study really proved what you claim, the McTear case and the Minnesota case would be all over it. Instead, it was found from both sides that the animal studies have failed.

        • richwhite09 says:

          Re: Sorry – More on Beagles
          And that statement is true. Shall I keep repeating quotes from the scientists of the court cases until it sinks in? Both sides, including the one who would benefit enormously from showing tobacco smoke caused lung cancer, conceded the animal studies have failed.
          The assertion has never been that no animal has suffered lung cancer in a study, because they have. The assertion is the tobacco smoke hasn’t caused it.
          Fact of the matter is, Chris, you were plainly wrong about the experiment. You said all the controls were fine and all the smoking dogs were dead, dying or in a bad way. You then accused me of not reading the study – when clearly, you hadn’t read it very well because what you said was wrong! It’s time to stop relying on personal digs, it’s not going to help your cause of showing us all wrong at all; neither will reliance on studies that do not show what you say they do.

        • cjsnowdon says:

          Re: Sorry – More on Beagles
          It doesn’t matter. Not to me. I’m interested in whether smoking causes lung cancer in humans. I only mentioned Auerbach in the first place because you said (in CATCH-3):
          “No laboratory studies of smoking animals have shown them developing lung cancer”
          And Rich said (in CATCH-2):
          “To this day, scientists have not managed to induce lung cancer in any animal through tobacco smoke”

        • richwhite09 says:

          Re: Sorry – More on Beagles
          The experiment may have been repeated. All the SG actually says is the “observation has not been repeated”, which could quite easily be interpreted as ‘the study has been repeated, but the results were different’.

        • Frank Davis says:

          Re: Sorry – More on Beagles
          What does it matter? There was only one experiment, as far as I understand, which was never repeated. Nobody pays any attention to a single experiment until somebody else replicates it.
          Frank

      • cjsnowdon says:

        Re: Sorry – More on Beagles
        And what Rich is not saying (deliberately or not i don’t know) is that the tumours were non-invasive and that’s not unusual in humans or dogs. However, ALL the invasive tumours were found in the smoking dogs and NONE of the nonsmoking dogs had an invasive tumour. There was also a dose-response relationship for the non-invasive tumours, which went 25% (nonsmoking), 40% (filter-tip), 50% (non-filter tip), 100% (non-filter tip, heavy smoking). In that last category, 10 out of 24 dogs had invasive tumours, and it no doubt would have been higher still if half of them hadn’t died before the experiment ended.
        Still, probably just the stress, eh?

    • richwhite09 says:

      Re: Sorry – More on Beagles
      Not just McTear, it was also concluded in the Minnesota case in, i think, 1997 that no animal had contracted lung cancer from tobacco smoke.
      I also showed in catch13 that chris is wrong and being misleading (deliberately or not i don’t know) with his claims about the beagles. 2 of 8 (25%) non-smoking dogs got tumours.

  15. Anonymous says:

    Sorry – More on Beagles
    In Catch11, I had a discussion with Chris about his evidence on Auerbach having produced evidence of smoke inhalation causing cancer in beagles:
    http://frank-davis.livejournal.com/128390.html?thread=1253766#t1253766
    His evidence essentially boiled down to one document and in particular the quote given on page 40 which was attributed to the General Manager of Research at Gallaher on 3rd April 1970:
    http://tobaccodocuments.org/batco/321481589-1857.html?zoom=750&ocr_position=above_foramatted&start_page=31
    Looking at this further, I still can’t find the full memo from which the quote was taken. Which means it remains unclear whether caveats were added or for that matter whether the original author was actually quoting someone else in his memo.
    I also noted that the document (link above) is actually the case for the prosecution brought by Tobacco Control Australia in 1976. I have no idea what the outcome was and whether the evidence held up in court.
    I did however, come across an R..J. Reynolds statement to stockholders from May 1970:
    http://tobaccodocuments.org/atc/60268526.html?zoom=750&ocr_position=above_foramatted&start_page=11
    This contains the following statement:
    Early this year an experiment on 56 beagles was press-released in terms calculated to drown out these voices of scientific reason. I will not go into the details of that dog act. but with your permission I will cite this comment by one disinterested biologist. After analyzing the beagle experiment, he concluded: “What does bother me is the misuse of so-called scientific results by one group with vested interests to attack another. All this experiment proves is: Whether or not smoking causes lung cancer in beagles is as inconclusive now as it was before the experiment was carried out.”
    Of course this also matches the conclusions of the independent scientists, the defence team AND the pursuers in the ITL vs McTear case.
    Just thought it might be of interest.
    P.S. To be fair, Chris actually stated (Catch-11):
    No, as I said in the last post they delivered invasive tumours which is the step before lung cancer, and they developed lots of them. The nonsmoking dogs didn’t develop any.
    Tony

  16. Anonymous says:

    Psychological props
    A little speculation on Frank’s idea that people who consume more cigarettes might actually smoke/inhale the same amount. Rich noted previously that his friend used a cigarette as a psychological prop and that certainly matches my own observations. So maybe cigarette consumption is dominated by the need for a psychological prop and the dose response relationship seen in the RRs is more to do with the type of person than the actual exposure.
    Which is pretty close to what Fisher and Eysenck argued.
    Tony

  17. Anonymous says:

    Psychological props
    A little speculation on Frank’s idea that people who consume more cigarettes might actually smoke/inhale the same amount. Rich noted previously that his friend used a cigarette as a psychological prop and that certainly matches my own observations. So maybe cigarette consumption is dominated by the need for a psychological prop and the dose response relationship seen in the RRs is more to do with the type of person than the actual exposure.
    Which is pretty close to what Fisher and Eysenck argued.
    Tony

    • richwhite09 says:

      Re: Psychological props
      which also perfectly ties in perfectly with smoking being a sympton rather than a cause i.e. why do people smoke? if it is to relieve stress, tension or a mental imbalance then that could be another huge arrow through tobacco control.

    • richwhite09 says:

      Re: Psychological props
      which also perfectly ties in perfectly with smoking being a sympton rather than a cause i.e. why do people smoke? if it is to relieve stress, tension or a mental imbalance then that could be another huge arrow through tobacco control.

    • Frank Davis says:

      Re: Psychological props
      I think that it might be possible to get to the bottom of this matter by simply videoing smokers in various environments – e.g. sitting and talking with friends, at home doing other things, etc, etc. It should be possible from the videos to find out how much they’re smoking in those different circumstances, by noting when they light a cigarette, and when they take drags on them, and use that to figure out how much of the cigarette they’re actually smoking.
      The trouble with smokers trying to watch their own behaviour is that it all gets self-conscious, and most likely distorted by that self-consciousness. I can’t watch what I myself do without the watching intruding on what I do.
      Back in the days when I spent a lot of time intensively programming computers, I quite often found that I seemed to smoke a lot more when I was doing that. But I now wonder whether I was actually smoking more, because using a keyboard is very much a two-handed task for me, and that effectively precludes smoking. So I think that what I must have been doing was leaving the cigarette on an ashtray most of the time to slowly burn out, and having to keep rolling new ones. It may have looked to me like I was smoking more than usual (and perhaps I was in terms of number of cigarettes), but I was quite likely actually getting a lot less from each one than I usually do, because my hands were too busy. And because I was getting less, I compensated by smoking more cigarettes.
      If that makes sense…
      Frank

      • cjsnowdon says:

        Re: Psychological props
        “I think that it might be possible to get to the bottom of this matter by simply videoing smokers in various environments – e.g. sitting and talking with friends, at home doing other things, etc, etc.”
        Takes me back to what I said in CATCH-8:
        “This criticism, like so many in this debate, expects an impossible level of accuracy that could only be achieved by having a video camera pointed at every single subject every day of their lives for 20 years. Anything short of that is considered to be ‘flawed’, irrespective of the fact that the supposed flaws are so incidental to the larger body of evidence that they are little more than distractions.”

        • Frank Davis says:

          Re: Psychological props
          Anything short of that is considered to be ‘flawed’,
          Perhaps because it actually is flawed.
          Unless I am mistaken, you seem to be quite happy to work with the most flawed and imperfect raw data. Anything is better than nothing.
          To go back to Copernicus (or, more exactly, Kepler) it was only because Tycho Brahe had produced much more accurate data on the motion of the planets that he (Kepler) was able to construct his elliptical theory of orbital motion. Accuracy matters! Science depends upon it, and depends utterly. Where there is no accuracy of measurement, there is no science. And that is the deepest and most damning charge that I bring against the farago of smoking ‘science’: all the numbers are guesses.
          Frank

        • Anonymous says:

          Re: Psychological props
          Hope you don’t mind if I expand a little on the reproducibility of any measurements. It is precision and accuracy which matter.
          http://en.wikipedia.org/wiki/Accuracy_and_precision

        • Anonymous says:

          Re: Psychological props
          Hope you don’t mind if I expand a little on the reproducibility of any measurements. It is precision and accuracy which matter.
          http://en.wikipedia.org/wiki/Accuracy_and_precision

        • Frank Davis says:

          Re: Psychological props
          Anything short of that is considered to be ‘flawed’,
          Perhaps because it actually is flawed.
          Unless I am mistaken, you seem to be quite happy to work with the most flawed and imperfect raw data. Anything is better than nothing.
          To go back to Copernicus (or, more exactly, Kepler) it was only because Tycho Brahe had produced much more accurate data on the motion of the planets that he (Kepler) was able to construct his elliptical theory of orbital motion. Accuracy matters! Science depends upon it, and depends utterly. Where there is no accuracy of measurement, there is no science. And that is the deepest and most damning charge that I bring against the farago of smoking ‘science’: all the numbers are guesses.
          Frank

      • cjsnowdon says:

        Re: Psychological props
        “I think that it might be possible to get to the bottom of this matter by simply videoing smokers in various environments – e.g. sitting and talking with friends, at home doing other things, etc, etc.”
        Takes me back to what I said in CATCH-8:
        “This criticism, like so many in this debate, expects an impossible level of accuracy that could only be achieved by having a video camera pointed at every single subject every day of their lives for 20 years. Anything short of that is considered to be ‘flawed’, irrespective of the fact that the supposed flaws are so incidental to the larger body of evidence that they are little more than distractions.”

    • Frank Davis says:

      Re: Psychological props
      I think that it might be possible to get to the bottom of this matter by simply videoing smokers in various environments – e.g. sitting and talking with friends, at home doing other things, etc, etc. It should be possible from the videos to find out how much they’re smoking in those different circumstances, by noting when they light a cigarette, and when they take drags on them, and use that to figure out how much of the cigarette they’re actually smoking.
      The trouble with smokers trying to watch their own behaviour is that it all gets self-conscious, and most likely distorted by that self-consciousness. I can’t watch what I myself do without the watching intruding on what I do.
      Back in the days when I spent a lot of time intensively programming computers, I quite often found that I seemed to smoke a lot more when I was doing that. But I now wonder whether I was actually smoking more, because using a keyboard is very much a two-handed task for me, and that effectively precludes smoking. So I think that what I must have been doing was leaving the cigarette on an ashtray most of the time to slowly burn out, and having to keep rolling new ones. It may have looked to me like I was smoking more than usual (and perhaps I was in terms of number of cigarettes), but I was quite likely actually getting a lot less from each one than I usually do, because my hands were too busy. And because I was getting less, I compensated by smoking more cigarettes.
      If that makes sense…
      Frank

  18. Anonymous says:

    Psychological props
    A little speculation on Frank’s idea that people who consume more cigarettes might actually smoke/inhale the same amount. Rich noted previously that his friend used a cigarette as a psychological prop and that certainly matches my own observations. So maybe cigarette consumption is dominated by the need for a psychological prop and the dose response relationship seen in the RRs is more to do with the type of person than the actual exposure.
    Which is pretty close to what Fisher and Eysenck argued.
    Tony

  19. richwhite09 says:

    Re: Psychological props
    which also perfectly ties in perfectly with smoking being a sympton rather than a cause i.e. why do people smoke? if it is to relieve stress, tension or a mental imbalance then that could be another huge arrow through tobacco control.

  20. richwhite09 says:

    Re: Sorry – More on Beagles
    Not just McTear, it was also concluded in the Minnesota case in, i think, 1997 that no animal had contracted lung cancer from tobacco smoke.
    I also showed in catch13 that chris is wrong and being misleading (deliberately or not i don’t know) with his claims about the beagles. 2 of 8 (25%) non-smoking dogs got tumours.

  21. cjsnowdon says:

    Frank,
    The reason I haven’t replied to your theory about the dose-response relationship is – as I would must have noticed – because I haven’t actually posted anything since you wrote about it. Having said that, what can be said about a theory that says that people who smoke 40 a day inhale less smoke than someone who smokes 20 a day? When we get to that degree of self-delusion, it does tend to leave me speechless.
    I’ve read and reread your post about misclassification and haven’t commented because I really can’t see where you’re getting your calculations from. However, I’d be interested to see you do the same reassessment of some of the other studies.
    I hope you appreciate that it is physically impossible for me to keep with, and reply to, the barrage of comments being made. Please do not – for a second -think that’s because I think you might have a point. Partly it is because of time, partly because I’ve answered them before and partly because some of them are so obviously bonkers that I expect anyone reading to see that for themselves. And I’m definitely not going to respond to the comments which use the approach of “I think it might be this but I know nothing about it, so you look into it and prove me wrong’. However, I will try and respond to some of the main points this week.
    In the mean time, I’ve noticed that no one has made any attempt to debunk the one piece of evidence I presented in my last post. I made an effort to get this debate back on track by sticking to a few points at a time but all I’m getting is questions and no answers to the straightforward evidence I’m presenting. Continually bitching about Doll and Hill 1950 is not getting us anywhere.
    This shouldn’t be one-way traffic and the defence DOES need to put some ideas of their own forward and defend them without squealing ‘I was only throwing it out there’ and moving on at the first sign of trouble. It is not enough to say that smoking is innocent until proven guilty as if it was still the ’50s because as far as the vast majority of the world is concerned, smoking has been proven guilty and people who think it hasn’t are perceived as a pocket of denialists at the outer reaches of crankdom. That isn’t going to change unless you can give a halfway plausible explanation for why lung cancer kills smokers many times more often than it kills nonsmokers.
    CJS
    PS. What makes you think I reject the studies but Muller et al.?

  22. cjsnowdon says:

    Frank,
    The reason I haven’t replied to your theory about the dose-response relationship is – as I would must have noticed – because I haven’t actually posted anything since you wrote about it. Having said that, what can be said about a theory that says that people who smoke 40 a day inhale less smoke than someone who smokes 20 a day? When we get to that degree of self-delusion, it does tend to leave me speechless.
    I’ve read and reread your post about misclassification and haven’t commented because I really can’t see where you’re getting your calculations from. However, I’d be interested to see you do the same reassessment of some of the other studies.
    I hope you appreciate that it is physically impossible for me to keep with, and reply to, the barrage of comments being made. Please do not – for a second -think that’s because I think you might have a point. Partly it is because of time, partly because I’ve answered them before and partly because some of them are so obviously bonkers that I expect anyone reading to see that for themselves. And I’m definitely not going to respond to the comments which use the approach of “I think it might be this but I know nothing about it, so you look into it and prove me wrong’. However, I will try and respond to some of the main points this week.
    In the mean time, I’ve noticed that no one has made any attempt to debunk the one piece of evidence I presented in my last post. I made an effort to get this debate back on track by sticking to a few points at a time but all I’m getting is questions and no answers to the straightforward evidence I’m presenting. Continually bitching about Doll and Hill 1950 is not getting us anywhere.
    This shouldn’t be one-way traffic and the defence DOES need to put some ideas of their own forward and defend them without squealing ‘I was only throwing it out there’ and moving on at the first sign of trouble. It is not enough to say that smoking is innocent until proven guilty as if it was still the ’50s because as far as the vast majority of the world is concerned, smoking has been proven guilty and people who think it hasn’t are perceived as a pocket of denialists at the outer reaches of crankdom. That isn’t going to change unless you can give a halfway plausible explanation for why lung cancer kills smokers many times more often than it kills nonsmokers.
    CJS
    PS. What makes you think I reject the studies but Muller et al.?

    • Frank Davis says:

      The reason I haven’t replied to your theory about the dose-response relationship is – as I would must have noticed – because I haven’t actually posted anything since you wrote about it.
      Yes, I had noticed. But I couldn’t help but use it to my own advantage.
      Having said that, what can be said about a theory that says that people who smoke 40 a day inhale less smoke than someone who smokes 20 a day? When we get to that degree of self-delusion, it does tend to leave me speechless.
      Seriously, unless you can fault my mathematics, there’s absolutely no self-delusion about it. It’s perfectly possible. I explained it in simple mathematical terms. And if my explanation wasn’t clear to you, I’ll be more than happy to explain it again, perhaps without any mathematics. Anyway, Tony (writing above) certainly seems to have understood what I was saying.
      The number of cigarettes that somebody smokes a day simply is not a measure of the dose of tobacco smoke they inhale. It’s just part of the measure.
      I agree that this seems highly paradoxical. That was what delighted me about the argument. And I doubt that you have encountered this particular argument before, so I didn’t really expect you to be able to come up with a ready answer.
      If I put myself in your shoes, I think I’d reply with something along these lines: “Yes, you’re quite right that it’s possible that somebody who is smoking 40 a day could well be inhaling less than someone who smokes 20 a day. That said, is it probable that this is happening?” Something along those lines.
      In the mean time, I’ve noticed that no one has made any attempt to debunk the one piece of evidence I presented in my last post.
      I could make the same complaint. But unless I’m mistaken, much of that post was directed towards Rich. And for the most part I leave it to Rich to respond to replies made to him.
      As CATCH has developed, it’s very much turned into Chris vs. Rich, and has become rather acrimonious in the process. But perhaps it will yet widen a bit.
      Tomorrow I’ll publish something from Dave Atherton.
      Frank

      • cjsnowdon says:

        Don’t get me wrong. I understood what you were saying: some people might smoke lots of cigarettes but smoke lightly and other people might smoke few cigarettes but inhale a lot. I get it. I just think it’s clutching at straws when you look at the studies which are remarkably consistent in showing – again and again – the heavier smokers (as in number of cigs smoked) to have the biggest increase in risk. The chances of this dose-response relationship happening if cigarettes don’t cause lung cancer are billions to one.
        And, of course, some people who smoke heavily will smoke harder and those who don’t smoke as much will inhale less (per cig). This is at least as likely as your proposition, and so, as with most classification issues, it evens out once you study large populations.

        • Frank Davis says:

          The chances of this dose-response relationship happening if cigarettes don’t cause lung cancer are billions to one.
          Not if my secondary hypothesis – that smokers are generally simply trying to maintain some inner equilibrium (of nicotine, say) – has any validity.
          Heavy smokers may simply be people who seldom get the opportunity to smoke, and who light up at every opportunity they get.
          This would apply particularly to all kinds of manual labour, because you need at least one hand free to smoke a cigarette. For the most part, the middle classes sitting at their desks very often have both hands free.
          And, of course, some people who smoke heavily will smoke harder and those who don’t smoke as much will inhale less (per cig). This is at least as likely as your proposition, and so, as with most classification issues, it evens out once you study large populations.
          There’s no “of course” about it. Unless there is some data available about this, we really can’t say one way or the other.
          Frank

        • cjsnowdon says:

          Yes, even if your secondary hypothesis is correct. It makes no difference at all to the outlandish odds.
          I’ll explain again. Every study that I’ve seen shows a remarkable consistency in that the people with the highest cigarette consumption have the highest risk and the people who smoke for the most years have the highest risk. There is a crystal clear dose-response relationship that affects all ages, sexes and races. If smoking doesn’t cause lung cancer, this must be the result of chance and the chances of it happening are infinitesimally small. It simply wouldn’t happen. Whether the smokers all actually inhale the same amount (a theory that runs contrary to observation and common sense) makes no difference to those odds.

        • Frank Davis says:

          The chances of this dose-response relationship happening if cigarettes don’t cause lung cancer are billions to one.
          Not if my secondary hypothesis – that smokers are generally simply trying to maintain some inner equilibrium (of nicotine, say) – has any validity.
          Heavy smokers may simply be people who seldom get the opportunity to smoke, and who light up at every opportunity they get.
          This would apply particularly to all kinds of manual labour, because you need at least one hand free to smoke a cigarette. For the most part, the middle classes sitting at their desks very often have both hands free.
          And, of course, some people who smoke heavily will smoke harder and those who don’t smoke as much will inhale less (per cig). This is at least as likely as your proposition, and so, as with most classification issues, it evens out once you study large populations.
          There’s no “of course” about it. Unless there is some data available about this, we really can’t say one way or the other.
          Frank

      • cjsnowdon says:

        Don’t get me wrong. I understood what you were saying: some people might smoke lots of cigarettes but smoke lightly and other people might smoke few cigarettes but inhale a lot. I get it. I just think it’s clutching at straws when you look at the studies which are remarkably consistent in showing – again and again – the heavier smokers (as in number of cigs smoked) to have the biggest increase in risk. The chances of this dose-response relationship happening if cigarettes don’t cause lung cancer are billions to one.
        And, of course, some people who smoke heavily will smoke harder and those who don’t smoke as much will inhale less (per cig). This is at least as likely as your proposition, and so, as with most classification issues, it evens out once you study large populations.

    • Frank Davis says:

      The reason I haven’t replied to your theory about the dose-response relationship is – as I would must have noticed – because I haven’t actually posted anything since you wrote about it.
      Yes, I had noticed. But I couldn’t help but use it to my own advantage.
      Having said that, what can be said about a theory that says that people who smoke 40 a day inhale less smoke than someone who smokes 20 a day? When we get to that degree of self-delusion, it does tend to leave me speechless.
      Seriously, unless you can fault my mathematics, there’s absolutely no self-delusion about it. It’s perfectly possible. I explained it in simple mathematical terms. And if my explanation wasn’t clear to you, I’ll be more than happy to explain it again, perhaps without any mathematics. Anyway, Tony (writing above) certainly seems to have understood what I was saying.
      The number of cigarettes that somebody smokes a day simply is not a measure of the dose of tobacco smoke they inhale. It’s just part of the measure.
      I agree that this seems highly paradoxical. That was what delighted me about the argument. And I doubt that you have encountered this particular argument before, so I didn’t really expect you to be able to come up with a ready answer.
      If I put myself in your shoes, I think I’d reply with something along these lines: “Yes, you’re quite right that it’s possible that somebody who is smoking 40 a day could well be inhaling less than someone who smokes 20 a day. That said, is it probable that this is happening?” Something along those lines.
      In the mean time, I’ve noticed that no one has made any attempt to debunk the one piece of evidence I presented in my last post.
      I could make the same complaint. But unless I’m mistaken, much of that post was directed towards Rich. And for the most part I leave it to Rich to respond to replies made to him.
      As CATCH has developed, it’s very much turned into Chris vs. Rich, and has become rather acrimonious in the process. But perhaps it will yet widen a bit.
      Tomorrow I’ll publish something from Dave Atherton.
      Frank

    • Frank Davis says:

      PS. What makes you think I reject the studies but Muller et al.?
      Because you’ve said nothing supportive of them. You’ve said nothing at all.
      Would you care to elaborate on what you mean?
      Frank

    • Frank Davis says:

      PS. What makes you think I reject the studies but Muller et al.?
      Because you’ve said nothing supportive of them. You’ve said nothing at all.
      Would you care to elaborate on what you mean?
      Frank

    • Frank Davis says:

      as far as the vast majority of the world is concerned, smoking has been proven guilty and people who think it hasn’t are perceived as a pocket of denialists at the outer reaches of crankdom. That isn’t going to change unless you can give a halfway plausible explanation for why lung cancer kills smokers many times more often than it kills nonsmokers.
      Perceived.
      That’s the key word.
      And since the term “denialist” is usually reserved for AGW sceptics, it’s interesting to observe how perception of AGW has changed over the past year in the aftermath of Climategate, which changed the perception of climate science for a great many people.
      This year’s crank is next year’s visionary. And this year’s visionary is next year’s crank.
      I still think that before there is any change in belief about what causes lung cancer, there’ll have to be growing dissatisfaction with the current orthodoxy on the matter. A new explanation is only likely to attract interest if the old explanation increasingly seems implausible. e.g. because more and more never-smokers seem to be getting lung cancer.
      Frank

      • cjsnowdon says:

        Even if Climategate disproved AGW, which it didn’t it, it’s a logical fallacy to say that because people thought x was crazy and turned out to be right that y is right because people think he’s crazy. This year’s crank is usually just a crank.
        I used ‘perceived’ to be polite. ‘Recognised’ might have been better.

        • Frank Davis says:

          I agree (from what I know of it) that Climategate didn’t disprove AGW. But it changed the perception of the climate scientists. And I think ‘perception’ was actually the right word.
          As for cranks who become visionaries, how about that chap you mentioned in your book – Johnstone, I think his name was – who used to inject himself with nicotine? I rather suspect that he’s regarded as something of a patron saint by the current bunch of antismoking zealots.
          Frank

        • cjsnowdon says:

          Lennox Johnston? He’s still a forgotten man. I’m one of the very few people who’ve ever mentioned him, even in books about smoking. The fact that odd crank is later recognised as being right gives cranks something to hold onto (usually they like to compare themselves to Gallileo). It doesn’t alter the fact that the vast majority of cranks are just cranks.

        • Anonymous says:

          “The first opportunity for change offered itself most forcefully when in 1942 Lennox Johnston’s landmark report in the British medical journal The Lancet identified nicotine as the active agent in tobacco responsible for the pleasant sensations experienced by the smoker. Johnston proposed that smoking tobacco was essentially a means of administering nicotine, just as smoking opium was a means of administering morphine. In 35 volunteers he found that nicotine injections not only simulated cigarette smoke inhalation but were also actually preferred to a cigarette”
          http://www.acsh.org/healthissues/newsID.574/healthissue_detail.asp
          The first modern scientific evidence for this conclusion appeared in the English medical journal Lancet in 1942. Dr. Lennox Johnston there reported that he had given small injections of nicotine solution to 35 volunteers, including himself. “Smokers almost invariably thought the sensation pleasant,” Dr. Johnston declared, “and, given an adequate dose, were disinclined to smoke for a time thereafter…. After a course of 80 injections of nicotine, an injection was preferred to a cigarette.” If the nicotine injections were abruptly discontinued, craving arose. Dr. Johnston found that in satisfying this craving, one milligram of injected nicotine was roughly the equivalent of smoking one cigarette. He concluded that “smoking tobacco is essentially a means of administering nicotine, just as smoking opium is a means of administering morphine.”
          http://www.drugtext.org/library/reports/cu/CU25.html
          Dr. Doll had little to say about Dr. Lennox Johnston, who has been most vigorously campaigning against tobacco in England. Dr. Doll felt that most physicians did not take Dr. Johnston too seriously, either in this or most other professional matters.
          http://tobaccodocuments.org/pm/2024998686-8708.html
          Rose

    • Frank Davis says:

      as far as the vast majority of the world is concerned, smoking has been proven guilty and people who think it hasn’t are perceived as a pocket of denialists at the outer reaches of crankdom. That isn’t going to change unless you can give a halfway plausible explanation for why lung cancer kills smokers many times more often than it kills nonsmokers.
      Perceived.
      That’s the key word.
      And since the term “denialist” is usually reserved for AGW sceptics, it’s interesting to observe how perception of AGW has changed over the past year in the aftermath of Climategate, which changed the perception of climate science for a great many people.
      This year’s crank is next year’s visionary. And this year’s visionary is next year’s crank.
      I still think that before there is any change in belief about what causes lung cancer, there’ll have to be growing dissatisfaction with the current orthodoxy on the matter. A new explanation is only likely to attract interest if the old explanation increasingly seems implausible. e.g. because more and more never-smokers seem to be getting lung cancer.
      Frank

    • richwhite09 says:

      “all I’m getting is questions and no answers to the straightforward evidence I’m presenting”
      The comments are full of people who have responded to your various claims.
      “Continually bitching about Doll and Hill 1950 is not getting us anywhere.”
      You must appreciate though that with Doll and Hill’s being the first ‘landmark’ study on it, it requires much attention. It’s the root of this whole thing.
      “This shouldn’t be one-way traffic and the defence DOES need to put some ideas of their own forward and defend them without squealing ‘I was only throwing it out there’ and moving on at the first sign of trouble.”
      A backhanded remark about me, again.
      Firstly, i haven’t moved on at the first sign of trouble; actually, there hasn’t been any trouble. The only whiff of trouble has been your rapid ‘nonsense!’ to everything, rather than any demonstrable scientific rejections. In fact, Frank went ahead and posted a series of links on radiation in tobacco, the article of mine you posted only served to show that it did indeed exist, and it was mentioned by a commenter that stress is continuing to be realised as a factor.
      “It is not enough to say that smoking is innocent until proven guilty as if it was still the ’50s because as far as the vast majority of the world is concerned, smoking has been proven guilty and people who think it hasn’t are perceived as a pocket of denialists at the outer reaches of crankdom”
      I disagree. I said earlier that a fact is a fact before evidence supports it, and honestly, because people believe something we must go with it? Ok, then remove VGIF from the market because people who don’t actively research this stuff like we here have believe SHS has been proven guilty. Just because we don’t know what the real culprit is doesn’t mean anything, and to repeat myself once more, we may well not know what it is because the focus on tobacco has stalled research elsewhere.

      • cjsnowdon says:

        I said earlier that a fact is a fact before evidence supports it, and honestly, because people believe something we must go with it?
        Straw man. I’m saying that if you want to convince more than a handful of Frank’s readers, you’ll need to come up with something more concrete that ‘someone should look into this..’
        I’ll come to the differences between SHS and smoking in my post after the next one.

        • richwhite09 says:

          First off, i’m not trying to convince anyone of anything, this debate was your idea because it was you who wanted to convince of something. Secondly, reading the posts, it would appear Frank’s readers are in agreement with Frank and myself.
          Finally, as was my initial point, it has nothing to do with convincing anyone of anything. Facts are facts. If the point of this debate was to find the cause of lung cancer then it appears Frank and I were left out of the loop. If, though, it’s to look at the smoking studies to see if they’re convincing (which it is) then we need not provide any alternate explanation, which has been stated already. In fact, given the vast gaps in knowledge of cancer it’s a massive leap to suggest we must! Considering the finer points of cancer still elude scientists, and we have patchy knowledge at best, it’s an outrageous claim. And considering even further that everyone, yourself included, knows full well that various things are factors or causes of lung cancer, yet we know precious little about what, how, or what dosage actually leads to the disease, your claim sinks even further.
          More concrete than ‘someone should look into this…’, sure, if i were attempting to show demonstrative proof of another cause, but i’m not. As I said earlier today but will repeat in case you haven’t seen it, those individual things i mentioned were just to demonstrate that not every avenue has been investigated as you so confidently (and wrongly) asserted.
          Now, Chris, you are very fond of saying that we, the defence, must proof this, must demonstrate that and so forth. In actuality, our job as the defence is to show our dissatisfaction with the smoking studies. It is your job as the prosecution to squash our grievances and show us why, actually, they do hold up. That doesn’t mean divert all attention to ‘well unless you can show another cause then this must be the real one’.
          And if you want to convince anyone of anything, you’re going to have to do much better than a) the above, b) dismissing everything as ‘straw man’ or ‘clutching at straws’ despite Frank giving very rational thought and demonstratable figures on his numbers, c) employing rhetoric to avoid the crux of the issues and cast a shadow over individuals, and d) talking about studies such as Auerbach before you know what they say.

        • cjsnowdon says:

          Considering you only read the Auerbach study the other day (and, until then, based your spurious argument on the belief that the control dogs didn’t have tracheotomies), it’s a bit rich for you to accuse me of not knowing what it says.
          And if you think your job is just to debunk the studies, why don’t you stop muddying the waters with rubbish about lung cancer being caused by people taking showers and say something about the study that I prominently featured in my last post? It’s notable that whenever the topic veers off from animal studies and Richard Doll, you don’t have much to say.

        • richwhite09 says:

          No, I read the study 3 years ago and briefly last year, while I was writing Smoke Screens. Forgive me for getting a few points wrong; the basic point remains though.
          “It’s notable that whenever the topic veers off from animal studies and Richard Doll, you don’t have much to say.”
          Really? Is that why i’ve responded to just about every comment asked of me then? What’s more notable, and mentioned by more than just me, is your lack of responses to numerous comments that disagree with you.
          I haven’t commented on the study you mentioned in your last post simply because Frank already did so.

        • cjsnowdon says:

          Rich, I have done nothing else in this debate other than repeatedly respond to comments from you, Frank and other readers. Not only that, I have also explicitly laid out what I will be discussing in future posts. On the other hand, the one piece of evidence I put out in my last post has been completely ignored. Frank did not respond to it at all, as he said earlier in this thread: “unless I’m mistaken, much of that post was directed towards Rich. And for the most part I leave it to Rich to respond to replies made to him.”
          I’ve linked to the study, so all you have to do is read it and tell us what’s wrong with it.

        • richwhite09 says:

          “Rich, I have done nothing else in this debate other than repeatedly respond to comments from you, Frank and other readers.”
          I’m not saying you haven’t responded at all, but there are plenty of comments that you have totally ignored despite appearing to be quite important.
          “Frank did not respond to it at all, as he said earlier in this thread: “unless I’m mistaken, much of that post was directed towards Rich. And for the most part I leave it to Rich to respond to replies made to him.””
          Do you mean Kaiser’s study? I thought Frank had responded saying about it being more face-value numbers, maybe I was wrong. If so i apologise.
          At 24 pages, i’ve only thoroughly skimmed it. But from the first couple of pages it appears we hit the same problem we get with Doll: classification. Current smokers are those who admit to smoking regularly for a year, which is much better than Doll’s but what does it mean? Smoking 5 every friday is regular.
          “If they did not affirm never using any tobacco product, never-smokers had to deny ever smoking cigarettes regularly for at least 1 year”
          Immediately that is the same i have put above. It comes down to the participant’s understanding of ‘regular’. It also all comes down to honesty, did the number of never smokers registered really all never try a tobacco product? Perhaps, but perhaps not.
          Then there’s the smoking categories – why less than 20, not less than 10? The 1964 SG report showed those who smoked 10 or less a day had less mortality than non-smokers (or less LC, i can’t remember off the top of my head), and Kaiser’s grouping would completely eradicate that, even if it were to show again.
          Then they say “under the assumption that smoking habits remained as initially reported”
          Assumption doesn’t belong in science, it only takes a small percentage to change their smoking habits relatively slightly to alter the results drastically.
          The mean age of study was 50.9, or 51 for argument’s sake, and the age range was 50-64. This is a difficult age bracket because it’s in the 60s that such diseases as cancer and emphysema become much more prominent. The study finds the rates increase with age – yeah, no shit.
          And where are the confounders? I see no mention of diet, background, social class, exercise, purported stress levels from work, environment, exposure to chemicals in work or home etc etc. This is pretty terrible – you’re providing this study as proof of the dose dependent relationship and yet it has no confounders? They’ve simply looked at smoking rates, looked at disease rates, and put two and two together. Maybe those confounders are in there and i didn’t spot them because i skim-read it, if they are maybe you’ll point them out to be.
          But at first glance, if that’s your offering of proof of smoking and cancer…. damn.

        • richwhite09 says:

          Chris, i can’t find the comment thread from earlier today about alternative explanations. Now, this isn’t one, but questions to you along the same lines. Has there been any investigations into roll ups versus premades? Organic tobacco vs high-phosphate fertiliser (or even non-organic fertiliser)? Do you accept/agree that 10 roll-ups with slim filters are different in quantity to 10 premades because they contain less tobacco?
          Removing all sarcasm and snide tones, this is really what i was getting at at the start of this topic about things that haven’t been investigated. As Frank has pointed out (and Leg Iron), one big problem with smoking studies is that a cigarette is just a cigarette, but in reality there are many types of cigarette, varying in tobacco (Virginia, Burley, blond, dark etc), curing methods (air cured, flue cured, the fuel used to power the machines), size (length, width and quantity of tobacco), length of filter and so on and so forth. Do you think, in your opinion or from studies you know of, that a cigarette is just a cigarette? Or that any of these factors could play a role in how harmful smoking could be?
          I’d like to draw a line in the sand at this point, i think we’re both frustrated with certain statements and this debate isn’t as civil as it could or should be. I don’t think it needs to descend to any level of immaturity, and the questions in this comment can be answered sensibly, just as they were posed.
          So, do you have any thoughts on this?

        • cjsnowdon says:

          Are you offering this as a serious explanation which you’re willing to defend or will you say you were just throwing it out there when I shoot it down? I ask in all seriousness because I really don’t have time for any more wild geese chases. In fact, it would be more appropriate if you provided the reasons why you think it’s a useful area of research and the I could respond. That would be more normal in a debate.

        • richwhite09 says:

          I said explicitly i’m not offering anything, just asking a few questions.

        • cjsnowdon says:

          In that case I’ll state explicitly that I’m not here to do your research for you. If you think you’ve found something of interest then find some evidence, organise your thoughts and put them down in a post.

        • richwhite09 says:

          i’m not asking for research, i’m asing for your opinion

        • cjsnowdon says:

          But from the first couple of pages it appears we hit the same problem we get with Doll: classification. Current smokers are those who admit to smoking regularly for a year, which is much better than Doll’s but what does it mean? Smoking 5 every friday is regular.
          Then you’re obviously not a nonsmoker and you get classified as a light smoker. Is there some problem with that?
          Then there’s the smoking categories – why less than 20, not less than 10?
          Why not? If it had been the other way round you would have said ‘why not less 10, not less than 5’. The point is to divide up lighter and heavier smokers. Smoking more than 20 a day is perfectly reasonable definition of a heavier smoker.
          Assumption doesn’t belong in science, it only takes a small percentage to change their smoking habits relatively slightly to alter the results drastically.
          Absolute rubbish. It would take a huge change. And, as you and Frank always ignore, misclassification is minimal in these studies and, in any case, it works both ways.
          The mean age of study was 50.9, or 51 for argument’s sake, and the age range was 50-64. This is a difficult age bracket because it’s in the 60s that such diseases as cancer and emphysema become much more prominent.
          Well, dur. This is a bad thing? Perhaps they should just have studies healthy teenagers? . The study compares like with like and the results are stratified by age and age-adjusted, always with the same result.
          And where are the confounders? I see no mention of diet, background, social class, exercise, purported stress levels from work, environment, exposure to chemicals in work or home etc etc.
          None of these factors are anywhere near strong enough to explain the RRs in the study and some of them are not causal factors for lung cancer at all.

        • richwhite09 says:

          point 1: yes it’s a problem, because your statement wouldn’t classify them as a non-smoker.
          2: more than 20 yes, i’m talking under under it because 20 and 4 are different in terms of light moderate and heavy, at the lower levels smaller categories make more sense. and as i said before, smokers of less than 10 in the 64 report had less disease incidence, while 10-20 didn’t.
          3: perhaps.
          4: you miss my point, i was saying 60+ should be separate to 50s
          5: so basically there are no confounders. what a stellar piece of research

        • cjsnowdon says:

          1. Well guess what? Someone who smokes in a smoker.
          2. How would this turn a null study into a very strong correlation between smoking and lung cancer? (It wouldn’t. It’s utterly irrelevant.)
          4. For what earthly reason? How does the age stratification lead to a bias towards the smoking theory? (It doesn’t. You just don’t understand epidemiology.)
          5. Yep, there are no confounders that come anywhere near the risk of smoking. Especially things like ‘background’ and ‘social class’ which clearly aren’t causal, and are themselves confounded by real causal factors of which the largest, by a very long way, is smoking.

        • richwhite09 says:

          christ, can you read?
          until you get over yourself and learn how to hold a discussion, this will go nowhere. when someone disagrees, that isn’t a green light for insults, just so you know.

        • cjsnowdon says:

          Yes, I’ve read your comments. That’s how I know you don’t understand epidemiology. That’s not an insult, by the way, just a statement of fact. No one who understands the basics of epidemiology would claim that showing the results in a certain age range was a flaw in a study, especially when all the age ranges show similar, strong, positive results. Nor would they claim that starting the age range at 60 would be a superior or any less arbitrary way of doing it.
          This is not even trivial. It’s just nothing. Nothing at all. It’s as if you went through the study and looked at what they could have done differently and then called their choices flawed, even though they had precisely zero effect on the results. Either that’s the behaviour of a man who doesn’t understand the discipline or who is deliberately muddying the water in the hope that some people will be daft enough to believe that you’ve identified some genuine problems.

        • richwhite09 says:

          this just basically goes back to a point Frank made earlier – you’re exceptionally willing to accept any smoking study regardless of the flaws. Highlighting the flaws means i either am being ignorant or don’t understand epidemiology. another spurious claim from you chris that simply shows your pig headedness on the issue.
          they had precisely zero effects on the results? how can you possibly determine that? in the studies where a few confounders are mentioned you say that’s good. in studies showing social class is a confounder because those people are more likely to suffer from various illnesses, that’s fine. and in studies where there are no confounders, well it doesn’t matter because they make no difference?! it really is like arguing with a child. you proposed this debate and presumably thought it would be easy to prove your point. yet you haven’t tried very hard (from catch3 someone mentioned your reliance on rhetoric) and quickly resorted to behaviour that, as correctly noted by brfian bond, resembles that of a hormonal teenager. almos everyone here is making good posts, positions, relaying of facts, and you retaliate with snide marks, personal attacks, dismissal of everything when you know nothing about the topic, ignoring people, and generally bullish attitudes. it’s not nice or pleasant and quite frankly it’s pathetic.
          if your claim was so stronly proved as you assert it would have been a piece of cake to show it. instead it turns out that everyone else can find huge problems with the studies and that seems to dent your ego. and remember: i’m not the first or only one to mention your attitude and arrogance in the posts, and secondly, you are quite simply the only one of everyone to be called out for it by commenters.

        • cjsnowdon says:

          OK then. Explain how the age stratification is a flaw in the study.

        • richwhite09 says:

          it’s not a ‘flaw’ so much, just an observation that it would be better to separate the age group who is far more likely to have cancer anyway from the group that isn’t.
          i’m much more concerned about the complete lack of any confounders whatsoever. you want us to take this seriously as proof of smoking causing cancer, when there were no other factors even considered? i know, i know , you’re going to say that it makes no difference. well even wynder concluded from one of his studies that other factors were clearly involved in the onset of lung cancer, also shown by lung cancer rising in non smokers and the simple fact we know other factors contribute to the disease. for you to say confounders would make no difference is just unbelievable

        • cjsnowdon says:

          it would be better to separate the age group who is far more likely to have cancer anyway from the group that isn’t.
          Why?

        • richwhite09 says:

          er, for the same reason 70 year olds aren’t compared to 50 year olds?because if you’re studying an isolated factor to work out it’s imppact on health, lumping in people who are already at hugely increased odds of getting it with an age group of less risk isn’t very good methodology. but let’s face it, you already knew that.

        • cjsnowdon says:

          But whatever age group of smokers is selected is being compared to the SAME AGE GROUP of nonsmokers! They’re not comparing 70 year olds to 50 year olds. It’s a completely apples and apples comparison with the only key variable being the smoking.
          You really don’t get this at all, do you?

        • richwhite09 says:

          Yes, i do, hence me saying that i don’t think it’s much of a flaw, just an observation. But, as ever, you singled out the lesser part of my post and ignored the rest.

        • cjsnowdon says:

          No, I’m testing your criticisms to see if they’re valid. Now let’s take another ‘flaw’ you mentioned. You think that someone who smokes 5 cigarettes a week should be classed as a nonsmoker. That, I think, is very questionable, but let’s go with it. If we have a few people who smoke 5 cigarettes a week classed as smokers, what will be the effect on the results if (a) some of them get lung cancer, or (b) none of them don’t get lung cancer?

        • richwhite09 says:

          No, sorry, it appears i wasn’t clear. I didn’t say someone who smokes 5 a week is a non-smoker. The study paper says a smoker was someone who admits to smoking regularly, and my point was ‘regular’ is very much open to debate on a person’s interpretation. I just used 5 a week as an example. Someone could equally think going out to the local once a month and smoking 3, 4, or 100 is ‘regular’. My follow on from that was “”If they did not affirm never using any tobacco product, never-smokers had to deny ever smoking cigarettes regularly for at least 1 year””, from the paper itself. So a never-smoker in the study is someone who has smoked, but abstained for a year – except not total abstain, just irregular. To some people, that could mean 5 one week, none for a couple months, smoke every day for a week, quit again. That’s irregular.
          The bulk of CATCH so far has revolved around such problems with definition – Doll apparently omitted the inhalation question in case some people didn’t know what it meant; I think it’s a safe bet that more people understand ‘inhale’ than ‘regular’, because ‘regular’ is a very flexible word that depends on context.

        • cjsnowdon says:

          Understood. But the question remains, what would be the effect on the results of having a number of very light smokers classified as smokers?

        • richwhite09 says:

          That depends on how many were misclassified i suppose. But then this is part of the other problem of smoking rates starting with 0-20, rather than smaller increments. It’s just not thorough research to say someone who smokes even a pack a month belongs in the same category as someone who smokes 20 a day. mind you it’s not thorough research to conduct a study with no confounders whatsoever; it’s been posted in CATCH 15 from a study that found vitamin B6 has an inverse effect on lung cancer, with those deficient in it more likely to have the disease while those who had adequate levels were much less likely to. In a study that made no attempt to see if smokers ate worse, ate better, exercised more or less or anything outside of smoking whatsoever, it’s not particularly logical to take the results as gospel anymore than it makes sense to look at statistics of those who take paracetamol – the more headaches they get, the more pills they take, so we could say from the figure paracetamol is conclusively linked to headaches with a dose-dependent relationship.

        • cjsnowdon says:

          The effects of diet are very weak compared to the risks found with smoking, but that’s a different point (and I’ll come to that in tonight’s post). The rate of misclassification are low, and this has been shown through chemical testing on many occasions (see my posts yesterday).
          The answer to the question is that if a few light smokers are classified as smokers and they don’t get lung cancer (which is most likely), it will actually weaken to relationship between smoking and lung cancer. If smoking doesn’t cause lung cancer then the rates of lung cancer will be evenly spread over the cohort and there wouldn’t be an association at all. So the effect of the misclassification you’re talking about will tend to lead to the risks of smoking being underestimated, not overestimated.

        • richwhite09 says:

          “The effects of diet are very weak compared to the risks found with smoking”
          The risks found with smoking are still correlation though, which Fisher spoke out against in 1958 and we still haven’t progressed from, and which as i said in my last post is like looking at people with headaches and take paracetamol and say the tablet causes the headache. The effects of diet could play a massive part, B6 alone has been shown to cut the risk of LC, as has vitamin E. Considering what we eat affects all of our cells, pH levels and general internal wellbeing, it could easily impact on cancer.
          “So the effect of the misclassification you’re talking about will tend to lead to the risks of smoking being underestimated, not overestimated.”
          In theory. But what if, for some other reason, the smokers of 15-20 a day had huge incidence of LC, which was offset in the results by the lack of cancer in the lighter smokers? It could have been that the 15-20 a day had the highest peak of all, but remained undiscovered in the results table. And none of this considers detection bias either, which has been well and truly documented and shown to be real, before this study was conducted. And as the researchers only looked at smoking, and nothing else, they were clearly aware of the association and expecting the results they found to turn up, so detection bias here is an almost certainty (if for no other reason than the fact that even nowadays diagnosis is not 100%, or anywhere near it, so going back 30, 40 years, we must acknowledge that much of the cancers didn’t even really exist).
          And also still nothing has been said about my earlier posts about primary and secondary cancers.

        • cjsnowdon says:

          But what if, for some other reason, the smokers of 15-20 a day had huge incidence of LC, which was offset in the results by the lack of cancer in the lighter smokers? It could have been that the 15-20 a day had the highest peak of all, but remained undiscovered in the results table.
          Sorry. Read it 4 times. Still don’t see what you’re getting at in theory or in practice.

        • richwhite09 says:

          ok, what if (and this is hypothetical) people who smoked 15-20 a day had the most incidence of lung cancer across the entire study population. If the people who smoked 0-10 had the lowest incidence then the entire category of 0-20 would sort of meet in the middle and bring the LC number for that category lower than the other categories (say, 20-30, 40-50 a day etc). So the end result graph wouldn’t be an accurate representation of the actual LC incidence.

        • cjsnowdon says:

          If that (admittedly inexplicable) event happened, the two would cancel each other out and you would have an RR for the 1-10 cigarette group that was the same as the nonsmoking group, and therefore a null study. It would suggest that smoking doesn’t cause cancer. Alas, that’s not what happens.
          Note also that chopping the sample group into smaller and smaller subdivisions is a trick usually performed by junk scientists to claim individual associations where there is no overall association (eg. the recent Isle of Man study that looked at the over 55s).

        • richwhite09 says:

          “the two would cancel each other out and you would have an RR for the 1-10 cigarette group that was the same as the nonsmoking group, and therefore a null study. It would suggest that smoking doesn’t cause cancer.”
          Not necessarily, if the excess of the 15-20 exceeded the lack of Lc in 0-15 then there would still be an increase over the non-smokers. It would be higher than non-smokers and lower than 20-30, thus creating the linear graph.
          “Note also that chopping the sample group into smaller and smaller subdivisions is a trick usually performed by junk scientists to claim individual associations where there is no overall association (eg. the recent Isle of Man study that looked at the over 55s).”
          I’m not suggesting to have only small subdivisions, i don’t see the benefit of that. I’m talking about 0-20 specifically, because that range accounts for very light, light and moderate smokers (perhaps even by some standards ‘heavy’). In light of the fact that the 1964 SG Report had a table showing smokers of up to 10 a day had lower incidence of LC, i don’t think it’s an outrageous thing to say in subsequent studies that group should have its own category, which is all i’m saying. And, going back to the previous point, let’s assume that smoking can cause cancer in the right dosage, and the right dosage is 15+. In which case, my hypothetical situation would begin to look much more plausbile

        • cjsnowdon says:

          If you were to say that smoking causes cancer beyond a certain dosage that would, I do believe, be a victory for the ‘smoking causes lung cancer’ hypothesis.
          Other studies have broken down the results by more specific measures of cigarette consumption and have found the same dose-response relationship.
          eg:
          http://tobaccocontrol.bmj.com/content/14/5/315/T3.expansion.html

        • richwhite09 says:

          “If you were to say that smoking causes cancer beyond a certain dosage that would, I do believe, be a victory for the ‘smoking causes lung cancer’ hypothesis.”
          It would indeed. Note, though, I didn’t say it does, I said ‘let’s assume that smoking can cause cancer in the right dosage.’
          This is unrelated to this thread (but in keeping with the CATCH debate), have you read Nighlight’s forum posts? I’m currently about 1/3 way through one partocular discussion, so too soon to draw any conclusions, but i wondered if you’d give your thoughts on it if and when you have the time to read it? Obviously i don’t expect a reply today or even this week; i’d just be interested in your thoughts to his thoughts on the correlation and human studies etc
          http://www.imminst.org/forum/topic/38868-smoking-is-good-for-you/

        • richwhite09 says:

          As an addendum to this, remember the primary/secondary cancer I mentioned and how it would be interesting to find out how much lung cancer in smokers is primary and secondary? From that link above Nighlight posted this:
          Chronic Inhalation of Cigarette Smoke by F344 rats
          W.E. Dalbey at al., Oak Ridge Nat. Lab., Inst. Environ. Health…
          J. National Cancer Inst., 64 (2): 383-390 (Feb 1980)
          “”Smoke exposure did not change the total number of tumor-bearing animals relative to controls; however [smoke] exposed rats had significantly fewer tumors in the hypophyses, hematopletic-lymphoid system, uteri and ovaries, but an increased number of tumors in the respiratory tracts and dermes.”
          These animal data fit in with the concepts of Prof. Oeser in Berlin and Dr. Lock in Hamburg, that, if properly assessed, the epidemiological data on cancers in general and for specific organs, indicate that total cancer rates have not changed, and that the only thing which has changed is that the increase in one type of cancer is compensated for by a decrease in other organ cancers.””
          This links in with my primary/secondary suggestion. We have on the one hand a scientific fact that cancer can migrate and will migrate to the area it is most likely to survive. So do we have data on total incidence of cancer since 1930s or 1950s? This will help inform us if cancer itself has increased exponentially, or if the total rate is the same with variations in individual sites.

        • cjsnowdon says:

          Where can I see the full study?

        • cjsnowdon says:

          I think I’ve got enough to reply to on this blog without discussing the thoughts of someone who thinks that showing photos of elderly smokers is a compelling way to put forward the argument that ‘smoking is healthy’. His first claim is that ‘smoking animals live longer’ and his source is another message-board. I think I’ll give it a miss, thanks.

        • richwhite09 says:

          That’s not nearly the extent of his argument, and he goes into much, much more details further in (i’m on page 11 of 25), and he does indeed show studies where smoking animals live longer

        • cjsnowdon says:

          Good for him. I’m sure he won’t mind if you introduce some of his killer arguments into your next post.

        • richwhite09 says:

          I’m sure he won’t either. But we’ll see how the debate continues as to whether they’re relevant; plus the fact it’s looking likely i won’t be contributing much here after Saturday.

    • richwhite09 says:

      “all I’m getting is questions and no answers to the straightforward evidence I’m presenting”
      The comments are full of people who have responded to your various claims.
      “Continually bitching about Doll and Hill 1950 is not getting us anywhere.”
      You must appreciate though that with Doll and Hill’s being the first ‘landmark’ study on it, it requires much attention. It’s the root of this whole thing.
      “This shouldn’t be one-way traffic and the defence DOES need to put some ideas of their own forward and defend them without squealing ‘I was only throwing it out there’ and moving on at the first sign of trouble.”
      A backhanded remark about me, again.
      Firstly, i haven’t moved on at the first sign of trouble; actually, there hasn’t been any trouble. The only whiff of trouble has been your rapid ‘nonsense!’ to everything, rather than any demonstrable scientific rejections. In fact, Frank went ahead and posted a series of links on radiation in tobacco, the article of mine you posted only served to show that it did indeed exist, and it was mentioned by a commenter that stress is continuing to be realised as a factor.
      “It is not enough to say that smoking is innocent until proven guilty as if it was still the ’50s because as far as the vast majority of the world is concerned, smoking has been proven guilty and people who think it hasn’t are perceived as a pocket of denialists at the outer reaches of crankdom”
      I disagree. I said earlier that a fact is a fact before evidence supports it, and honestly, because people believe something we must go with it? Ok, then remove VGIF from the market because people who don’t actively research this stuff like we here have believe SHS has been proven guilty. Just because we don’t know what the real culprit is doesn’t mean anything, and to repeat myself once more, we may well not know what it is because the focus on tobacco has stalled research elsewhere.

    • Anonymous says:

      Ad hominem
      “as far as the vast majority of the world is concerned, smoking has been proven guilty and people who think it hasn’t are perceived as a pocket of denialists at the outer reaches of crankdom”
      I find it hard to believe that this was said by someone from ‘our’ side, and not a die-hard ASHite!
      Chris, please learn to conduct a debate without resorting to this kind of offensive language. You are talking to many intelligent and experienced people here (including some who are far more skilled than yourself in interpreting statistics), yet who are sceptical about the true role that smoking plays in lung carcinogenesis. Scepticism is not denial, my friend!
      I expect a better standard of argument than I get from my teenage daughter when she is in a bratty, hormonal mood, Sadly, I’m not seeing enough of it in this debate.
      You are capable of making a strong case, Chris, and you certainly have the “vast majority of the world” opinion on your side (for what that is worth) so why spoil it?
      Thank you
      Brian Bond

      • cjsnowdon says:

        Re: Ad hominem
        Brian, you’ve completely missed the point of what I’m saying. I would never argue that something is true just because a majority believes it. I was simply pointing out that if Frank and Rich want to convince people outside of this forum that smoking doesn’t cause lung cancer, they are going to have to come up with a vaguely plausible explanation for the fact that smokers get lung cancer at a far higher rate than nonsmokers. It’s not sufficient to say that ‘we don’t have to prove anything, you do’ when, in fact, it is Rich and Frank who are in a tiny minority of people who take a view that is seen as not just unconventional but laughable. The onus is very much on Rich and Frank to make an alternative case because they are the ones challenging the conventional wisdom. Unless the aim is solely to convince the self-selecting sample of smokers’ rights visitors who comment on this blog.

        • richwhite09 says:

          Re: Ad hominem
          No Chris, our duty here is not to provide another explanation, but to deconstruct the smoking studies as they stand. As I’ve stated, it may well be that actually the true cause isn’t yet known, so how can we find it?
          And Frank has provided multiple very plausible, and demonstrated, reasons why smokers appear to get more lung cancer than non-smokers, from misclassification of a smoker and lung cancer, to perceived dosage and so on. And i provided quotes form Fisher one of which explained how once something is in the mind, it is more eagerly looked for, meaning it’s self fulfilled without being strictly true. And, myself and others have provided study quotes showing that lung cancer is now rising quite fast in non-smokers and one quote even showed that in never smokers it’s rising mostly in women rather than men. All of which can demonstrate perhaps that smoking has just masked this because so many people smoked – as smoking rates decline, lung cancer appears more in non-smokers and never-smokers.
          But regardless, no matter how many times you say it, we aren’t here to provide a different hypothesis – just to question this one.
          (later leaving than i thought, so this is my last post today most probably)

        • cjsnowdon says:

          Re: Ad hominem
          I don’t know how many more ways I can explain that the point is that if, as Frank says “in a political confrontation, we absolutely have to throw the whole lot away, regardless of the science”, that will not be achieved with the arguments being presented here. I can’t force anyone on this blog to discuss things they don’t want to discuss, but while the ‘it’s only statistics, nothing’s been proven’ approach might play well on this blog, outside of this corner of the net it’ll be ripped apart like a bread roll, as Rich found out earlier this year (http://www.badscience.net/forum/viewtopic.php?f=3&t=14107&start=0).
          I’m quite prepared to carry on presenting my side of the debate even with the proviso that the defence only has to ask questions and never has to provide answers, but that won’t get you far in the real world.
          That’s all I’m saying.

        • cjsnowdon says:

          Re: Ad hominem
          By the way, I’ve already responded to Frank’s point about misclassification and amount on tobacco inhaled. As usual in this debate it boiled down to: “Why don’t scientists investigate this!? … Oh, they have.”
          http://frank-davis.livejournal.com/129267.html?thread=1290483#t1290483

        • richwhite09 says:

          Re: Ad hominem
          great, we can have an earnest debate then, from the figures instead of bullish remarks about it all being rubbish. Of course,if you were right initially that no scientist would go down this blind alley then you wouldn’t have such evidence to post, so maybe now the catty comments can cease

        • richwhite09 says:

          Re: Ad hominem
          fair enough, but Frank mentioned he never intended that statement as a scientific one but political.
          The bad science blog was a joke, i actually had some sensible discussions with a few of them privately though. It isn’t the real world, i’ve spoken to various people in the real world including medical practitioners, it’s always been amicable and some even changed their minds a bit.
          And anyway, the defence has answered a lot and posed a lot, but questions are the nature of debate. We have shied away from nothing, but a few of us have said you have.
          lastly, what’s this talk of the real world? we’re on a blog and not taking it to the press. We are just discussing purported facts, that’s all.

        • Frank Davis says:

          Re: Ad hominem
          if Frank and Rich want to convince people outside of this forum that smoking doesn’t cause lung cancer
          Why should we want to do that? All I’m doing is airing a few of my reservations about the theory, which have arisen in response to a number of concerns.
          I’m not even sure that anyone’s mind can be changed on this matter anyway.
          in fact, it is Rich and Frank who are in a tiny minority of people who take a view that is seen as not just unconventional but laughable.
          I can’t see that it matters a damn if I belong to a ‘tiny minority’, or if anybody laughs at me. I perfectly well understand that for most people, “the debate is over” on this subject. But it isn’t for me. In fact, my debate only got started about 4 or 5 years ago. Before that my views were indistinguishable from anybody else’s.
          Frank

        • cjsnowdon says:

          Re: Ad hominem
          if Frank and Rich want to convince people outside of this forum that smoking doesn’t cause lung cancer
          Why should we want to do that?

          Because you want to “kill the many-headed hydra” and because “in a political confrontation, we absolutely have to throw the whole lot away, regardless of the science”?

        • richwhite09 says:

          Re: Ad hominem
          Chris, to revert to your claim we must provide alternate reasons, why is that for us to do any more than it is for you to state other reasons, to antis, for non smokers getting LC other than SHS?

        • cjsnowdon says:

          Re: Ad hominem
          What?

        • richwhite09 says:

          Re: Ad hominem
          it’s very simple. you say we who doubt the active smoking/cancer link must provide an alternative. you doubt the SHS/cancer link, have you provided alternatives to those who think it does cause lung cancer?
          btw, you say most of the world agrees smoking causes cancer. but so too do most believe SHS can cause lung cancer, yet that doesn’t deter your thoughts on it. your ‘logic’ is so riddled with holes it’s quite stunning

        • cjsnowdon says:

          Re: Ad hominem
          Gee, you must have missed my comment early today when I said: “I would never argue that something is true just because a majority believes it.”
          http://frank-davis.livejournal.com/129267.html?thread=1289971#t1289971
          Oh, but hang on, you were the first person to reply so I guess you’ve just got a very short memory.
          Re: SHS, the reason I am doubtful is not because I think there is an alternative explanation for the association, it’s because I don’t see that there is an association there to begin with. So it’s more of a data collection issue rather than a cause/correlation issue. The magnitude of the association with SHS is ultra-low, in complete contrast to the risk of active smoking. I’m going to write about this in my post after next.

        • richwhite09 says:

          Re: Ad hominem
          riiight, let me explain again and maybe you’ll get it. We all here know about the SHS fraud, you don’t need to point out the lack of association. My point was, you have plucked from the air the ridiculous demand that we must provide an alternative reason for smokers getting lung cancer if not smoking. Many people believe SHS is a cause of thousands of deaths of lung cancer each year – so to those people, should you not provide an alternative reason for the deaths?
          no, of course not. and seemingly this whole debate has gone over your head, because by challenging the data and figures we’re calling the strength of association into question. in turn, you are meant to be showing why it is as strong as we’re told.

        • cjsnowdon says:

          Re: Ad hominem
          Has it been a long night on the beer or are you just a bit slow? Read what I said and think it through.

        • richwhite09 says:

          Re: Ad hominem
          neither chris, neither. it’s evidently just another post in this debate that you have not managed to get your head around and instead you sidestep and throw an insult. anyone can see what my post meant and how your reply didn’t answer it.

        • cjsnowdon says:

          Re: Ad hominem
          *sigh*
          Let’s try one more time then…
          My doubts about the SHS studies is that the statistical correlations are usually nonsignificant and are so close to 1.0 that it’s questionable whether they exist at all. If they don’t exist at all, I don’t need to provide an alternative explanation for the hypothetical deaths.
          With active smoking, the relative risks are solid, strong and statistically significant, so anyone who denies causation really needs to come up with an alternative explanation for the strong correlation. Otherwise people are going to assume – very understandably indeed – that the reason smokers’ risk of lung cancer is greatly higher than nonsmokers is because they smoke.
          Got it?

        • richwhite09 says:

          Re: Ad hominem
          oh i get your point, i just don’t agree with it. let’s take frank’s example of misclassification from doll as an example, ok? with a pretty low misclassification rate, he took the RR down very low indeed. so by your own logic, we only need to show the correlation isn’t as strong as suggested or seemingly shown.

        • cjsnowdon says:

          Re: Ad hominem
          Now we’re getting somewhere! If you show me that the statistical correlations are actually very weak then I’ll change my mind. The problem you face is that they aren’t weak at all. They’re very strong and consistent. But I will continue to present evidence post-Doll and you can pick holes in it. That’s why I’m prepared to continue this debate – so that the rest of the evidence (a lot of which is fairly new to me) can be examined and assessed. Unfortunately, it took a lot of coaxing for me to get anyone to discuss the (randomly selected) study I presented last time and I haven’t heard anything since to make me think it, or any of the rest, have a major problem.

        • richwhite09 says:

          Re: Ad hominem
          With all due respect Chris, you haven’t posted much in the way of studies on active smoking. I didn’t respond about Kaiser because I genuinely thought Frank had, but it must have been a comment referring to something else, so i then replied straight away.

  23. cjsnowdon says:

    Frank,
    The reason I haven’t replied to your theory about the dose-response relationship is – as I would must have noticed – because I haven’t actually posted anything since you wrote about it. Having said that, what can be said about a theory that says that people who smoke 40 a day inhale less smoke than someone who smokes 20 a day? When we get to that degree of self-delusion, it does tend to leave me speechless.
    I’ve read and reread your post about misclassification and haven’t commented because I really can’t see where you’re getting your calculations from. However, I’d be interested to see you do the same reassessment of some of the other studies.
    I hope you appreciate that it is physically impossible for me to keep with, and reply to, the barrage of comments being made. Please do not – for a second -think that’s because I think you might have a point. Partly it is because of time, partly because I’ve answered them before and partly because some of them are so obviously bonkers that I expect anyone reading to see that for themselves. And I’m definitely not going to respond to the comments which use the approach of “I think it might be this but I know nothing about it, so you look into it and prove me wrong’. However, I will try and respond to some of the main points this week.
    In the mean time, I’ve noticed that no one has made any attempt to debunk the one piece of evidence I presented in my last post. I made an effort to get this debate back on track by sticking to a few points at a time but all I’m getting is questions and no answers to the straightforward evidence I’m presenting. Continually bitching about Doll and Hill 1950 is not getting us anywhere.
    This shouldn’t be one-way traffic and the defence DOES need to put some ideas of their own forward and defend them without squealing ‘I was only throwing it out there’ and moving on at the first sign of trouble. It is not enough to say that smoking is innocent until proven guilty as if it was still the ’50s because as far as the vast majority of the world is concerned, smoking has been proven guilty and people who think it hasn’t are perceived as a pocket of denialists at the outer reaches of crankdom. That isn’t going to change unless you can give a halfway plausible explanation for why lung cancer kills smokers many times more often than it kills nonsmokers.
    CJS
    PS. What makes you think I reject the studies but Muller et al.?

  24. Frank Davis says:

    Re: Psychological props
    I think that it might be possible to get to the bottom of this matter by simply videoing smokers in various environments – e.g. sitting and talking with friends, at home doing other things, etc, etc. It should be possible from the videos to find out how much they’re smoking in those different circumstances, by noting when they light a cigarette, and when they take drags on them, and use that to figure out how much of the cigarette they’re actually smoking.
    The trouble with smokers trying to watch their own behaviour is that it all gets self-conscious, and most likely distorted by that self-consciousness. I can’t watch what I myself do without the watching intruding on what I do.
    Back in the days when I spent a lot of time intensively programming computers, I quite often found that I seemed to smoke a lot more when I was doing that. But I now wonder whether I was actually smoking more, because using a keyboard is very much a two-handed task for me, and that effectively precludes smoking. So I think that what I must have been doing was leaving the cigarette on an ashtray most of the time to slowly burn out, and having to keep rolling new ones. It may have looked to me like I was smoking more than usual (and perhaps I was in terms of number of cigarettes), but I was quite likely actually getting a lot less from each one than I usually do, because my hands were too busy. And because I was getting less, I compensated by smoking more cigarettes.
    If that makes sense…
    Frank

  25. cjsnowdon says:

    Re: Sorry – More on Beagles
    And what Rich is not saying (deliberately or not i don’t know) is that the tumours were non-invasive and that’s not unusual in humans or dogs. However, ALL the invasive tumours were found in the smoking dogs and NONE of the nonsmoking dogs had an invasive tumour. There was also a dose-response relationship for the non-invasive tumours, which went 25% (nonsmoking), 40% (filter-tip), 50% (non-filter tip), 100% (non-filter tip, heavy smoking). In that last category, 10 out of 24 dogs had invasive tumours, and it no doubt would have been higher still if half of them hadn’t died before the experiment ended.
    Still, probably just the stress, eh?

  26. cjsnowdon says:

    Re: Psychological props
    “I think that it might be possible to get to the bottom of this matter by simply videoing smokers in various environments – e.g. sitting and talking with friends, at home doing other things, etc, etc.”
    Takes me back to what I said in CATCH-8:
    “This criticism, like so many in this debate, expects an impossible level of accuracy that could only be achieved by having a video camera pointed at every single subject every day of their lives for 20 years. Anything short of that is considered to be ‘flawed’, irrespective of the fact that the supposed flaws are so incidental to the larger body of evidence that they are little more than distractions.”

  27. Frank Davis says:

    The reason I haven’t replied to your theory about the dose-response relationship is – as I would must have noticed – because I haven’t actually posted anything since you wrote about it.
    Yes, I had noticed. But I couldn’t help but use it to my own advantage.
    Having said that, what can be said about a theory that says that people who smoke 40 a day inhale less smoke than someone who smokes 20 a day? When we get to that degree of self-delusion, it does tend to leave me speechless.
    Seriously, unless you can fault my mathematics, there’s absolutely no self-delusion about it. It’s perfectly possible. I explained it in simple mathematical terms. And if my explanation wasn’t clear to you, I’ll be more than happy to explain it again, perhaps without any mathematics. Anyway, Tony (writing above) certainly seems to have understood what I was saying.
    The number of cigarettes that somebody smokes a day simply is not a measure of the dose of tobacco smoke they inhale. It’s just part of the measure.
    I agree that this seems highly paradoxical. That was what delighted me about the argument. And I doubt that you have encountered this particular argument before, so I didn’t really expect you to be able to come up with a ready answer.
    If I put myself in your shoes, I think I’d reply with something along these lines: “Yes, you’re quite right that it’s possible that somebody who is smoking 40 a day could well be inhaling less than someone who smokes 20 a day. That said, is it probable that this is happening?” Something along those lines.
    In the mean time, I’ve noticed that no one has made any attempt to debunk the one piece of evidence I presented in my last post.
    I could make the same complaint. But unless I’m mistaken, much of that post was directed towards Rich. And for the most part I leave it to Rich to respond to replies made to him.
    As CATCH has developed, it’s very much turned into Chris vs. Rich, and has become rather acrimonious in the process. But perhaps it will yet widen a bit.
    Tomorrow I’ll publish something from Dave Atherton.
    Frank

  28. Frank Davis says:

    Re: Psychological props
    Anything short of that is considered to be ‘flawed’,
    Perhaps because it actually is flawed.
    Unless I am mistaken, you seem to be quite happy to work with the most flawed and imperfect raw data. Anything is better than nothing.
    To go back to Copernicus (or, more exactly, Kepler) it was only because Tycho Brahe had produced much more accurate data on the motion of the planets that he (Kepler) was able to construct his elliptical theory of orbital motion. Accuracy matters! Science depends upon it, and depends utterly. Where there is no accuracy of measurement, there is no science. And that is the deepest and most damning charge that I bring against the farago of smoking ‘science’: all the numbers are guesses.
    Frank

  29. Frank Davis says:

    PS. What makes you think I reject the studies but Muller et al.?
    Because you’ve said nothing supportive of them. You’ve said nothing at all.
    Would you care to elaborate on what you mean?
    Frank

  30. Frank Davis says:

    Re: Sorry – More on Beagles
    What does it matter? There was only one experiment, as far as I understand, which was never repeated. Nobody pays any attention to a single experiment until somebody else replicates it.
    Frank

  31. cjsnowdon says:

    Don’t get me wrong. I understood what you were saying: some people might smoke lots of cigarettes but smoke lightly and other people might smoke few cigarettes but inhale a lot. I get it. I just think it’s clutching at straws when you look at the studies which are remarkably consistent in showing – again and again – the heavier smokers (as in number of cigs smoked) to have the biggest increase in risk. The chances of this dose-response relationship happening if cigarettes don’t cause lung cancer are billions to one.
    And, of course, some people who smoke heavily will smoke harder and those who don’t smoke as much will inhale less (per cig). This is at least as likely as your proposition, and so, as with most classification issues, it evens out once you study large populations.

  32. cjsnowdon says:

    There’s a very simple explanation answer for that: I haven’t read them. It’s a bit much to assume I reject something just because I haven’t mentioned it.

  33. cjsnowdon says:

    Re: Sorry – More on Beagles
    It doesn’t matter. Not to me. I’m interested in whether smoking causes lung cancer in humans. I only mentioned Auerbach in the first place because you said (in CATCH-3):
    “No laboratory studies of smoking animals have shown them developing lung cancer”
    And Rich said (in CATCH-2):
    “To this day, scientists have not managed to induce lung cancer in any animal through tobacco smoke”

  34. Frank Davis says:

    as far as the vast majority of the world is concerned, smoking has been proven guilty and people who think it hasn’t are perceived as a pocket of denialists at the outer reaches of crankdom. That isn’t going to change unless you can give a halfway plausible explanation for why lung cancer kills smokers many times more often than it kills nonsmokers.
    Perceived.
    That’s the key word.
    And since the term “denialist” is usually reserved for AGW sceptics, it’s interesting to observe how perception of AGW has changed over the past year in the aftermath of Climategate, which changed the perception of climate science for a great many people.
    This year’s crank is next year’s visionary. And this year’s visionary is next year’s crank.
    I still think that before there is any change in belief about what causes lung cancer, there’ll have to be growing dissatisfaction with the current orthodoxy on the matter. A new explanation is only likely to attract interest if the old explanation increasingly seems implausible. e.g. because more and more never-smokers seem to be getting lung cancer.
    Frank

  35. junican says:

    Catch 14
    I have just downloaded the US Surgeon General’s report on smoking. I have read the SG’s foreword. The picture she paints is HORRIFIC! Smoking, and only smoking, causes every disease you can think of.
    The picture that she paints has the following undeniable conclusions:
    All cultivation of the the tobacco plant must cease at once and all plantations burnt to the ground.
    The manufacture of tobacco products must be forbidden with the legal penalty of death for infringement.
    With effect from tomorrow, anyone caught with a cigarette or any other form of tobacco product will face a similar penalty (between now and midnight tonight, an amnesty is declared so that such products may be delivered to a collecting point where they will be incinerated (no,…disposed of).
    Everyone who has ever smoked is to be interned until he/she dies.
    All buildings where anyone has ever smoked are to be raised to the ground and the land thereabouts declared unfit for human habitation.
    The President of the US must stand down forthwith as a mass murderer.
    The bodies of soldiers who have died in the service of their country are to be disinterred, crushed into dust and sold to China as fertiliser.
    Only professors and scientists contributing to this study are to be regarded as fit to procreate. All nubile young, non-smoking women are to make themselves available forthwith.
    Anyone thought to be in possession of tobacco may be shot on sight. A bounty of one million dollars per person those exterminated is offered. NB NO PROOF IS REQUIRED.
    This list is not complete.
    Seriously though, regardless of how accurate the scientists’ work on this report is, the Surgeon General has completely rendered the report a joke. Why? Because the actual event of a person, apparently in good health actually collapsing and dying during the course of smoking a cigarette must be minuscule beyond imagining.
    More seriously, the SG’s statement MUST throw doubt on every study ever conducted.The reason is the reliance upon chemicals in tobacco smoke. But note how they have got around the fact that many of these chemical occur naturally in food anyway – they claim that tobacco smoke EXAGGERATES the natural effects! So there are no confounding factors since tobacco smoke exaggerates EVERY disease known to man. It isn’t just the papilpoma virus which is instrumental in cancer of the cervix, it is papiloma PLUS tobacco smoke.
    My final comment. This report appeared in the Mail on Line on Sunday. It did not appear in the print edition of Sunday in the Telegraph or the News of the World. Not a mention. Not a word. I wonder why?

  36. junican says:

    Catch 14
    I have just downloaded the US Surgeon General’s report on smoking. I have read the SG’s foreword. The picture she paints is HORRIFIC! Smoking, and only smoking, causes every disease you can think of.
    The picture that she paints has the following undeniable conclusions:
    All cultivation of the the tobacco plant must cease at once and all plantations burnt to the ground.
    The manufacture of tobacco products must be forbidden with the legal penalty of death for infringement.
    With effect from tomorrow, anyone caught with a cigarette or any other form of tobacco product will face a similar penalty (between now and midnight tonight, an amnesty is declared so that such products may be delivered to a collecting point where they will be incinerated (no,…disposed of).
    Everyone who has ever smoked is to be interned until he/she dies.
    All buildings where anyone has ever smoked are to be raised to the ground and the land thereabouts declared unfit for human habitation.
    The President of the US must stand down forthwith as a mass murderer.
    The bodies of soldiers who have died in the service of their country are to be disinterred, crushed into dust and sold to China as fertiliser.
    Only professors and scientists contributing to this study are to be regarded as fit to procreate. All nubile young, non-smoking women are to make themselves available forthwith.
    Anyone thought to be in possession of tobacco may be shot on sight. A bounty of one million dollars per person those exterminated is offered. NB NO PROOF IS REQUIRED.
    This list is not complete.
    Seriously though, regardless of how accurate the scientists’ work on this report is, the Surgeon General has completely rendered the report a joke. Why? Because the actual event of a person, apparently in good health actually collapsing and dying during the course of smoking a cigarette must be minuscule beyond imagining.
    More seriously, the SG’s statement MUST throw doubt on every study ever conducted.The reason is the reliance upon chemicals in tobacco smoke. But note how they have got around the fact that many of these chemical occur naturally in food anyway – they claim that tobacco smoke EXAGGERATES the natural effects! So there are no confounding factors since tobacco smoke exaggerates EVERY disease known to man. It isn’t just the papilpoma virus which is instrumental in cancer of the cervix, it is papiloma PLUS tobacco smoke.
    My final comment. This report appeared in the Mail on Line on Sunday. It did not appear in the print edition of Sunday in the Telegraph or the News of the World. Not a mention. Not a word. I wonder why?

  37. junican says:

    Catch 14
    I have just downloaded the US Surgeon General’s report on smoking. I have read the SG’s foreword. The picture she paints is HORRIFIC! Smoking, and only smoking, causes every disease you can think of.
    The picture that she paints has the following undeniable conclusions:
    All cultivation of the the tobacco plant must cease at once and all plantations burnt to the ground.
    The manufacture of tobacco products must be forbidden with the legal penalty of death for infringement.
    With effect from tomorrow, anyone caught with a cigarette or any other form of tobacco product will face a similar penalty (between now and midnight tonight, an amnesty is declared so that such products may be delivered to a collecting point where they will be incinerated (no,…disposed of).
    Everyone who has ever smoked is to be interned until he/she dies.
    All buildings where anyone has ever smoked are to be raised to the ground and the land thereabouts declared unfit for human habitation.
    The President of the US must stand down forthwith as a mass murderer.
    The bodies of soldiers who have died in the service of their country are to be disinterred, crushed into dust and sold to China as fertiliser.
    Only professors and scientists contributing to this study are to be regarded as fit to procreate. All nubile young, non-smoking women are to make themselves available forthwith.
    Anyone thought to be in possession of tobacco may be shot on sight. A bounty of one million dollars per person those exterminated is offered. NB NO PROOF IS REQUIRED.
    This list is not complete.
    Seriously though, regardless of how accurate the scientists’ work on this report is, the Surgeon General has completely rendered the report a joke. Why? Because the actual event of a person, apparently in good health actually collapsing and dying during the course of smoking a cigarette must be minuscule beyond imagining.
    More seriously, the SG’s statement MUST throw doubt on every study ever conducted.The reason is the reliance upon chemicals in tobacco smoke. But note how they have got around the fact that many of these chemical occur naturally in food anyway – they claim that tobacco smoke EXAGGERATES the natural effects! So there are no confounding factors since tobacco smoke exaggerates EVERY disease known to man. It isn’t just the papilpoma virus which is instrumental in cancer of the cervix, it is papiloma PLUS tobacco smoke.
    My final comment. This report appeared in the Mail on Line on Sunday. It did not appear in the print edition of Sunday in the Telegraph or the News of the World. Not a mention. Not a word. I wonder why?

  38. Frank Davis says:

    The chances of this dose-response relationship happening if cigarettes don’t cause lung cancer are billions to one.
    Not if my secondary hypothesis – that smokers are generally simply trying to maintain some inner equilibrium (of nicotine, say) – has any validity.
    Heavy smokers may simply be people who seldom get the opportunity to smoke, and who light up at every opportunity they get.
    This would apply particularly to all kinds of manual labour, because you need at least one hand free to smoke a cigarette. For the most part, the middle classes sitting at their desks very often have both hands free.
    And, of course, some people who smoke heavily will smoke harder and those who don’t smoke as much will inhale less (per cig). This is at least as likely as your proposition, and so, as with most classification issues, it evens out once you study large populations.
    There’s no “of course” about it. Unless there is some data available about this, we really can’t say one way or the other.
    Frank

  39. Frank Davis says:

    Fair enough.
    Perhaps you’d like to cast an eye over Schairer and Schoeniger, 1944. These lads were personally funded by Hitler, I believe.
    Or First Reports, Why Ignored? by George Davey Smith.
    Or Robert Proctor on Schairer and Schöniger’s forgotten tobacco epidemiology.
    Or my own response to Proctor’s claim that Nazi smoking science was an example of ‘good’ Nazi science.
    Always bearing in mind that this is all about perception.
    Frank

  40. Frank Davis says:

    Re: Catch 14
    I have just downloaded the US Surgeon General’s report on smoking.
    Which one? What year?
    Frank

  41. Anonymous says:

    Re: Catch 14
    Surgeon-General Report (2010) on Tobacco Smoke
    It was released just a few days ago.

    Click to access full_report.pdf


    See also Siegel’s blog

  42. Anonymous says:

    Re: Catch 14
    Surgeon-General Report (2010) on Tobacco Smoke
    It was released just a few days ago.

    Click to access full_report.pdf


    See also Siegel’s blog

  43. Anonymous says:

    Re: Catch 14
    Surgeon-General Report (2010) on Tobacco Smoke
    It was released just a few days ago.

    Click to access full_report.pdf


    See also Siegel’s blog

  44. Anonymous says:

    Re: Psychological props
    Hope you don’t mind if I expand a little on the reproducibility of any measurements. It is precision and accuracy which matter.
    http://en.wikipedia.org/wiki/Accuracy_and_precision

  45. richwhite09 says:

    Re: Sorry – More on Beagles
    And that statement is true. Shall I keep repeating quotes from the scientists of the court cases until it sinks in? Both sides, including the one who would benefit enormously from showing tobacco smoke caused lung cancer, conceded the animal studies have failed.
    The assertion has never been that no animal has suffered lung cancer in a study, because they have. The assertion is the tobacco smoke hasn’t caused it.
    Fact of the matter is, Chris, you were plainly wrong about the experiment. You said all the controls were fine and all the smoking dogs were dead, dying or in a bad way. You then accused me of not reading the study – when clearly, you hadn’t read it very well because what you said was wrong! It’s time to stop relying on personal digs, it’s not going to help your cause of showing us all wrong at all; neither will reliance on studies that do not show what you say they do.

  46. Anonymous says:

    Chuckles
    Frank, Like you I have conducted the software development/smoking experiment over a number of years, and you are absolutely correct. The ashtray smokes 90+% of the cigarettes.
    Light cigarette, take a couple of puffs, place on ashtray, concentrate of bug detection. Stub out and cigarette.
    And the claim –
    “any defence of smoking as the causative factor must provide an alternative”.
    is lifted straight from the AGW play-book. Complete nonsense.
    There is nothing in science that says that one must propose an alternate to inherently defective data, and what is being questioned is the supposed evidence that smoking causes cancer. Without that evidence there is nothing to which an alternative must be proposed, no hypothesis exists.

  47. Anonymous says:

    Chuckles
    Frank, Like you I have conducted the software development/smoking experiment over a number of years, and you are absolutely correct. The ashtray smokes 90+% of the cigarettes.
    Light cigarette, take a couple of puffs, place on ashtray, concentrate of bug detection. Stub out and cigarette.
    And the claim –
    “any defence of smoking as the causative factor must provide an alternative”.
    is lifted straight from the AGW play-book. Complete nonsense.
    There is nothing in science that says that one must propose an alternate to inherently defective data, and what is being questioned is the supposed evidence that smoking causes cancer. Without that evidence there is nothing to which an alternative must be proposed, no hypothesis exists.

    • Anonymous says:

      Re: Chuckles
      “any defence of smoking as the causative factor must provide an alternative”.
      “There is nothing in science that says that one must propose an alternate to inherently defective data, and what is being questioned is the supposed evidence that smoking causes cancer. Without that evidence there is nothing to which an alternative must be proposed, no hypothesis exists”
      No, an alternative as a (?one) causative factor is not compulsory and never has been. It is sufficient to dissect and question the “evidence” provided. However, in order to do so, it is always a good idea to add, e.g. other factors/conditions influencing.

  48. Anonymous says:

    Chuckles
    Frank, Like you I have conducted the software development/smoking experiment over a number of years, and you are absolutely correct. The ashtray smokes 90+% of the cigarettes.
    Light cigarette, take a couple of puffs, place on ashtray, concentrate of bug detection. Stub out and cigarette.
    And the claim –
    “any defence of smoking as the causative factor must provide an alternative”.
    is lifted straight from the AGW play-book. Complete nonsense.
    There is nothing in science that says that one must propose an alternate to inherently defective data, and what is being questioned is the supposed evidence that smoking causes cancer. Without that evidence there is nothing to which an alternative must be proposed, no hypothesis exists.

  49. richwhite09 says:

    “all I’m getting is questions and no answers to the straightforward evidence I’m presenting”
    The comments are full of people who have responded to your various claims.
    “Continually bitching about Doll and Hill 1950 is not getting us anywhere.”
    You must appreciate though that with Doll and Hill’s being the first ‘landmark’ study on it, it requires much attention. It’s the root of this whole thing.
    “This shouldn’t be one-way traffic and the defence DOES need to put some ideas of their own forward and defend them without squealing ‘I was only throwing it out there’ and moving on at the first sign of trouble.”
    A backhanded remark about me, again.
    Firstly, i haven’t moved on at the first sign of trouble; actually, there hasn’t been any trouble. The only whiff of trouble has been your rapid ‘nonsense!’ to everything, rather than any demonstrable scientific rejections. In fact, Frank went ahead and posted a series of links on radiation in tobacco, the article of mine you posted only served to show that it did indeed exist, and it was mentioned by a commenter that stress is continuing to be realised as a factor.
    “It is not enough to say that smoking is innocent until proven guilty as if it was still the ’50s because as far as the vast majority of the world is concerned, smoking has been proven guilty and people who think it hasn’t are perceived as a pocket of denialists at the outer reaches of crankdom”
    I disagree. I said earlier that a fact is a fact before evidence supports it, and honestly, because people believe something we must go with it? Ok, then remove VGIF from the market because people who don’t actively research this stuff like we here have believe SHS has been proven guilty. Just because we don’t know what the real culprit is doesn’t mean anything, and to repeat myself once more, we may well not know what it is because the focus on tobacco has stalled research elsewhere.

  50. richwhite09 says:

    Re: Sorry – More on Beagles
    The experiment may have been repeated. All the SG actually says is the “observation has not been repeated”, which could quite easily be interpreted as ‘the study has been repeated, but the results were different’.

  51. richwhite09 says:

    Re: Sorry – More on Beagles
    Also, “It doesn’t matter. Not to me.”
    So now you’re wrong it doesn’t matter? Before you were all over Auerbach’s study, stating:
    “12 of the 86 dogs did get lung cancer” in CATCH 4. When it was pointed out they didn’t, you said the what they had was the stage before lung cancer. When you found out the non-smoking dogs had tumours, you wriggled by saying they were non-invasive, as if somehow that made it more damning to tobacco. Non-invasive tumours have the potential to become invasive if left untreated, so that doesn’t do anything to the argument except show how you’re willing to use one single point as both a defence and an attach. And, as I have said repeatedly, with only 10% of the amount of controls as smoking dogs, it’s not valid to use the numbers as conclusive because had the numbers been more equal the rates of cancer may also have been more equal. The only dog to die from aspiration of food was in the smoking group, so are we to suggest smoking was the cause of that too? Or perhaps stress really was an underlying factor, which explains why that group had more ‘other’ deaths, and if it was the tobacco that stressed them that would explain the dose dependency. This is a hypothesis, before you run around with ‘oh so now you’re saying stress caused it again?’ I know you’ll reject this too, but i also know you’ll do so without actually providing any basis

  52. Frank Davis says:

    To further pin down this matter of what daily inhaled ‘dose’ a smoker gets from smoking, I think it’s possible to identify 3 factors.

    N, the number of cigarettes smoked per day.
    F, the fraction of each cigarette that is drawn into the mouth, and is in the range 0 to 1.
    I, the amount of each puff or toke on a cigarette that is inhaled into the lungs, and is in the range 0 to 1.

    So that daily dose = F . I . N
    For non-inhalers, I will be somewhere near zero. If a smoker draws the smoke straight out of the cigarette and down into the lungs, I will approach 1.
    Determining the size of F was the subject of my last post (CATCH-12?), and my conclusion was that the fraction of the cigarette smoke which was drawn into the mouth depended on the speed at which it was smoked.
    F = ( tl . tr ) / ( nbr + tl . tr )
    where tl is toke length (mm of cigarette burned with each toke or pull), tr is toke rate (tokes per minute), and nbr is the cigarette natural burn rate (mm/minute). F increases with increased toke rate.
    There may be other factors to take into account.
    I believe that Ernst Wynder entirely dismissed the phenomenon of non-inhalation, and simply didn’t believe it happened. Doll and Hill asked about it once.
    One thing that daily dose definitely is NOT is N. If this is actually what researchers suppose it is then they’re just plain wrong

  53. Frank Davis says:

    To further pin down this matter of what daily inhaled ‘dose’ a smoker gets from smoking, I think it’s possible to identify 3 factors.

    N, the number of cigarettes smoked per day.
    F, the fraction of each cigarette that is drawn into the mouth, and is in the range 0 to 1.
    I, the amount of each puff or toke on a cigarette that is inhaled into the lungs, and is in the range 0 to 1.

    So that daily dose = F . I . N
    For non-inhalers, I will be somewhere near zero. If a smoker draws the smoke straight out of the cigarette and down into the lungs, I will approach 1.
    Determining the size of F was the subject of my last post (CATCH-12?), and my conclusion was that the fraction of the cigarette smoke which was drawn into the mouth depended on the speed at which it was smoked.
    F = ( tl . tr ) / ( nbr + tl . tr )
    where tl is toke length (mm of cigarette burned with each toke or pull), tr is toke rate (tokes per minute), and nbr is the cigarette natural burn rate (mm/minute). F increases with increased toke rate.
    There may be other factors to take into account.
    I believe that Ernst Wynder entirely dismissed the phenomenon of non-inhalation, and simply didn’t believe it happened. Doll and Hill asked about it once.
    One thing that daily dose definitely is NOT is N. If this is actually what researchers suppose it is then they’re just plain wrong

  54. cjsnowdon says:

    Even if Climategate disproved AGW, which it didn’t it, it’s a logical fallacy to say that because people thought x was crazy and turned out to be right that y is right because people think he’s crazy. This year’s crank is usually just a crank.
    I used ‘perceived’ to be polite. ‘Recognised’ might have been better.

  55. cjsnowdon says:

    I said earlier that a fact is a fact before evidence supports it, and honestly, because people believe something we must go with it?
    Straw man. I’m saying that if you want to convince more than a handful of Frank’s readers, you’ll need to come up with something more concrete that ‘someone should look into this..’
    I’ll come to the differences between SHS and smoking in my post after the next one.

  56. cjsnowdon says:

    Thanks for the links. I know what I’m writing for my next 2 posts but if I’m still here after that I might discuss them. I think it’s fair to guess that the ‘debunking’ of them will consist of some variation of ‘what do you expect, they were Nazis!’ though.

  57. cjsnowdon says:

    Yes, even if your secondary hypothesis is correct. It makes no difference at all to the outlandish odds.
    I’ll explain again. Every study that I’ve seen shows a remarkable consistency in that the people with the highest cigarette consumption have the highest risk and the people who smoke for the most years have the highest risk. There is a crystal clear dose-response relationship that affects all ages, sexes and races. If smoking doesn’t cause lung cancer, this must be the result of chance and the chances of it happening are infinitesimally small. It simply wouldn’t happen. Whether the smokers all actually inhale the same amount (a theory that runs contrary to observation and common sense) makes no difference to those odds.

  58. Frank Davis says:

    I agree (from what I know of it) that Climategate didn’t disprove AGW. But it changed the perception of the climate scientists. And I think ‘perception’ was actually the right word.
    As for cranks who become visionaries, how about that chap you mentioned in your book – Johnstone, I think his name was – who used to inject himself with nicotine? I rather suspect that he’s regarded as something of a patron saint by the current bunch of antismoking zealots.
    Frank

  59. Frank Davis says:

    Re: hpv
    Should I delete this?

  60. Frank Davis says:

    I just think it’s clutching at straws when you look at the studies which are remarkably consistent in showing – again and again – the heavier smokers (as in number of cigs smoked) to have the biggest increase in risk. The chances of this dose-response relationship happening if cigarettes don’t cause lung cancer are billions to one.
    For the Nth time, the inhaled dose that a smoker gets is not necessarily proportional to the number of cigarettes, N, being smoked! Unless it is assumed that all smokers smoke cigarettes at more or less the same rate, and inhale roughly the same amount. They may do, or they may not. I suspect that there are probably as many ways of smoking cigarettes as there are smokers.
    A ‘heavy’ smoker may often be someone who only takes occasional drags on a cigarette, or inhales comparatively little of the smoke, and who is smoking more cigarettes because he’s getting less out of each one.
    For serious research purposes, smokers ought to be asked how quickly they smoke cigarettes, and whether they inhale the smoke. In the absence of this information, no proper estimate of dose can be made.
    It would be like taking the gas law P.V = k. T and measuring pressure, but neglecting to read volume. And there’s no use waving it away by saying we can’t have perfect information.
    If, for example, it actually is true that ‘heavy’ smokers get more lung cancer, but also the heavy smokers don’t actually inhale any more smoke than lighter smokers, then some other agent than tobacco smoke would have to be considered. For example the suggestion that’s been floating round these threads that the means of lighting cigarettes may be the culprit, because 40-a-day smokers will very likely be getting 8 times as much gases from matches, lighters, or whatever else they use, than a 5-a-day smoker.
    It’s only by asking these sorts of questions that the matter will be unveiled. There’s no excuse for not asking.
    Frank

  61. Frank Davis says:

    I just think it’s clutching at straws when you look at the studies which are remarkably consistent in showing – again and again – the heavier smokers (as in number of cigs smoked) to have the biggest increase in risk. The chances of this dose-response relationship happening if cigarettes don’t cause lung cancer are billions to one.
    For the Nth time, the inhaled dose that a smoker gets is not necessarily proportional to the number of cigarettes, N, being smoked! Unless it is assumed that all smokers smoke cigarettes at more or less the same rate, and inhale roughly the same amount. They may do, or they may not. I suspect that there are probably as many ways of smoking cigarettes as there are smokers.
    A ‘heavy’ smoker may often be someone who only takes occasional drags on a cigarette, or inhales comparatively little of the smoke, and who is smoking more cigarettes because he’s getting less out of each one.
    For serious research purposes, smokers ought to be asked how quickly they smoke cigarettes, and whether they inhale the smoke. In the absence of this information, no proper estimate of dose can be made.
    It would be like taking the gas law P.V = k. T and measuring pressure, but neglecting to read volume. And there’s no use waving it away by saying we can’t have perfect information.
    If, for example, it actually is true that ‘heavy’ smokers get more lung cancer, but also the heavy smokers don’t actually inhale any more smoke than lighter smokers, then some other agent than tobacco smoke would have to be considered. For example the suggestion that’s been floating round these threads that the means of lighting cigarettes may be the culprit, because 40-a-day smokers will very likely be getting 8 times as much gases from matches, lighters, or whatever else they use, than a 5-a-day smoker.
    It’s only by asking these sorts of questions that the matter will be unveiled. There’s no excuse for not asking.
    Frank

  62. cjsnowdon says:

    Re: Sorry – More on Beagles
    The nonsmoking dogs were fine. They didn’t have non-invasive tumours or any other disease. All the smoking dogs were dead, dying or in a bad way. Even the one that didn’t have invasive tumours all had emphysema.

  63. cjsnowdon says:

    Lennox Johnston? He’s still a forgotten man. I’m one of the very few people who’ve ever mentioned him, even in books about smoking. The fact that odd crank is later recognised as being right gives cranks something to hold onto (usually they like to compare themselves to Gallileo). It doesn’t alter the fact that the vast majority of cranks are just cranks.

  64. cjsnowdon says:

    Animal experiments are biological evidence, FFS.

  65. cjsnowdon says:

    Re: hpv
    Most definitely.

  66. richwhite09 says:

    First off, i’m not trying to convince anyone of anything, this debate was your idea because it was you who wanted to convince of something. Secondly, reading the posts, it would appear Frank’s readers are in agreement with Frank and myself.
    Finally, as was my initial point, it has nothing to do with convincing anyone of anything. Facts are facts. If the point of this debate was to find the cause of lung cancer then it appears Frank and I were left out of the loop. If, though, it’s to look at the smoking studies to see if they’re convincing (which it is) then we need not provide any alternate explanation, which has been stated already. In fact, given the vast gaps in knowledge of cancer it’s a massive leap to suggest we must! Considering the finer points of cancer still elude scientists, and we have patchy knowledge at best, it’s an outrageous claim. And considering even further that everyone, yourself included, knows full well that various things are factors or causes of lung cancer, yet we know precious little about what, how, or what dosage actually leads to the disease, your claim sinks even further.
    More concrete than ‘someone should look into this…’, sure, if i were attempting to show demonstrative proof of another cause, but i’m not. As I said earlier today but will repeat in case you haven’t seen it, those individual things i mentioned were just to demonstrate that not every avenue has been investigated as you so confidently (and wrongly) asserted.
    Now, Chris, you are very fond of saying that we, the defence, must proof this, must demonstrate that and so forth. In actuality, our job as the defence is to show our dissatisfaction with the smoking studies. It is your job as the prosecution to squash our grievances and show us why, actually, they do hold up. That doesn’t mean divert all attention to ‘well unless you can show another cause then this must be the real one’.
    And if you want to convince anyone of anything, you’re going to have to do much better than a) the above, b) dismissing everything as ‘straw man’ or ‘clutching at straws’ despite Frank giving very rational thought and demonstratable figures on his numbers, c) employing rhetoric to avoid the crux of the issues and cast a shadow over individuals, and d) talking about studies such as Auerbach before you know what they say.

  67. Anonymous says:

    “The first opportunity for change offered itself most forcefully when in 1942 Lennox Johnston’s landmark report in the British medical journal The Lancet identified nicotine as the active agent in tobacco responsible for the pleasant sensations experienced by the smoker. Johnston proposed that smoking tobacco was essentially a means of administering nicotine, just as smoking opium was a means of administering morphine. In 35 volunteers he found that nicotine injections not only simulated cigarette smoke inhalation but were also actually preferred to a cigarette”
    http://www.acsh.org/healthissues/newsID.574/healthissue_detail.asp
    The first modern scientific evidence for this conclusion appeared in the English medical journal Lancet in 1942. Dr. Lennox Johnston there reported that he had given small injections of nicotine solution to 35 volunteers, including himself. “Smokers almost invariably thought the sensation pleasant,” Dr. Johnston declared, “and, given an adequate dose, were disinclined to smoke for a time thereafter…. After a course of 80 injections of nicotine, an injection was preferred to a cigarette.” If the nicotine injections were abruptly discontinued, craving arose. Dr. Johnston found that in satisfying this craving, one milligram of injected nicotine was roughly the equivalent of smoking one cigarette. He concluded that “smoking tobacco is essentially a means of administering nicotine, just as smoking opium is a means of administering morphine.”
    http://www.drugtext.org/library/reports/cu/CU25.html
    Dr. Doll had little to say about Dr. Lennox Johnston, who has been most vigorously campaigning against tobacco in England. Dr. Doll felt that most physicians did not take Dr. Johnston too seriously, either in this or most other professional matters.
    http://tobaccodocuments.org/pm/2024998686-8708.html
    Rose

  68. richwhite09 says:

    Re: Sorry – More on Beagles
    “The nonsmoking dogs were fine. They didn’t have non-invasive tumours or any other disease”
    So now you’re bold enough to say the results in the SG reports are wrong? The dogs didn’t have non-invasive tumours despite, well, the results showing they did?

  69. richwhite09 says:

    Yes, and they failed! So how, exactly, is it that my statement ‘no biological evidence exists and animal studies have failed’ is a transparent lie, when i have shown the transcripts from court from multiple scientists that actually it is true? You say ‘animal experiments are biological evidence’, and indeed this is true – but the studies have failed, so what biological evidence are you taking from this?
    You’re dragging this round and round in circles, all on the hope that apparently the facts will change

  70. cjsnowdon says:

    Considering you only read the Auerbach study the other day (and, until then, based your spurious argument on the belief that the control dogs didn’t have tracheotomies), it’s a bit rich for you to accuse me of not knowing what it says.
    And if you think your job is just to debunk the studies, why don’t you stop muddying the waters with rubbish about lung cancer being caused by people taking showers and say something about the study that I prominently featured in my last post? It’s notable that whenever the topic veers off from animal studies and Richard Doll, you don’t have much to say.

  71. cjsnowdon says:

    Re: Sorry – More on Beagles
    Sorry, should have been “invasive tumours”.

  72. richwhite09 says:

    No, I read the study 3 years ago and briefly last year, while I was writing Smoke Screens. Forgive me for getting a few points wrong; the basic point remains though.
    “It’s notable that whenever the topic veers off from animal studies and Richard Doll, you don’t have much to say.”
    Really? Is that why i’ve responded to just about every comment asked of me then? What’s more notable, and mentioned by more than just me, is your lack of responses to numerous comments that disagree with you.
    I haven’t commented on the study you mentioned in your last post simply because Frank already did so.

  73. richwhite09 says:

    Re: Sorry – More on Beagles
    Sure, true enough. But non-invasive tumours can progress to invasive tumours, and as i keep repeating, how can you be so sure that different results wouldn’t have occured had there been even 15 or 20 non-smoking dogs? Surely even you must concede it’s a bit odd for the researchers not to make the numbers a bit more balanced.

  74. cjsnowdon says:

    Rich, I have done nothing else in this debate other than repeatedly respond to comments from you, Frank and other readers. Not only that, I have also explicitly laid out what I will be discussing in future posts. On the other hand, the one piece of evidence I put out in my last post has been completely ignored. Frank did not respond to it at all, as he said earlier in this thread: “unless I’m mistaken, much of that post was directed towards Rich. And for the most part I leave it to Rich to respond to replies made to him.”
    I’ve linked to the study, so all you have to do is read it and tell us what’s wrong with it.

  75. cjsnowdon says:

    Re: Sorry – More on Beagles
    No I don’t. The evidence from it is clear and since none of the nonsmoking dogs had smoking-related diseases or symptoms, there’s no reason to think that this would have changed if there had been 80 controls. We know that beagles don’t just develop these diseases for no reason. The control group was large enough to confirm that tracheotomies don’t cause these diseases either (not that anyone thought they would). Mutilating more dogs for no good reason would have gone down very badly with the public. Auerbach was getting death threats from animal rights campaigners and had to do is work in secret.

  76. richwhite09 says:

    “Rich, I have done nothing else in this debate other than repeatedly respond to comments from you, Frank and other readers.”
    I’m not saying you haven’t responded at all, but there are plenty of comments that you have totally ignored despite appearing to be quite important.
    “Frank did not respond to it at all, as he said earlier in this thread: “unless I’m mistaken, much of that post was directed towards Rich. And for the most part I leave it to Rich to respond to replies made to him.””
    Do you mean Kaiser’s study? I thought Frank had responded saying about it being more face-value numbers, maybe I was wrong. If so i apologise.
    At 24 pages, i’ve only thoroughly skimmed it. But from the first couple of pages it appears we hit the same problem we get with Doll: classification. Current smokers are those who admit to smoking regularly for a year, which is much better than Doll’s but what does it mean? Smoking 5 every friday is regular.
    “If they did not affirm never using any tobacco product, never-smokers had to deny ever smoking cigarettes regularly for at least 1 year”
    Immediately that is the same i have put above. It comes down to the participant’s understanding of ‘regular’. It also all comes down to honesty, did the number of never smokers registered really all never try a tobacco product? Perhaps, but perhaps not.
    Then there’s the smoking categories – why less than 20, not less than 10? The 1964 SG report showed those who smoked 10 or less a day had less mortality than non-smokers (or less LC, i can’t remember off the top of my head), and Kaiser’s grouping would completely eradicate that, even if it were to show again.
    Then they say “under the assumption that smoking habits remained as initially reported”
    Assumption doesn’t belong in science, it only takes a small percentage to change their smoking habits relatively slightly to alter the results drastically.
    The mean age of study was 50.9, or 51 for argument’s sake, and the age range was 50-64. This is a difficult age bracket because it’s in the 60s that such diseases as cancer and emphysema become much more prominent. The study finds the rates increase with age – yeah, no shit.
    And where are the confounders? I see no mention of diet, background, social class, exercise, purported stress levels from work, environment, exposure to chemicals in work or home etc etc. This is pretty terrible – you’re providing this study as proof of the dose dependent relationship and yet it has no confounders? They’ve simply looked at smoking rates, looked at disease rates, and put two and two together. Maybe those confounders are in there and i didn’t spot them because i skim-read it, if they are maybe you’ll point them out to be.
    But at first glance, if that’s your offering of proof of smoking and cancer…. damn.

  77. richwhite09 says:

    Re: Sorry – More on Beagles
    “there’s no reason to think that this would have changed if there had been 80 controls”
    Rubbish. Let’s take the 8 healthiest dogs from the smoking section and say that nothing would change if there were 80. Or take 8 healthy 90 year old humans and say having 80 would’t change their health status.
    “Mutilating more dogs for no good reason would have gone down very badly with the public. Auerbach was getting death threats from animal rights campaigners and had to do is work in secret.”
    So? What’s that got to do with the results?
    Once again Chris, if this study really proved what you claim, the McTear case and the Minnesota case would be all over it. Instead, it was found from both sides that the animal studies have failed.

  78. richwhite09 says:

    Chris, i’m going out in a few minutes and won’t be back until about lunchtime tomorrow. If i can’t reply to anything until then don’t take it that i’m ignoring you. If you leave me any comments/replies, i’ll look at them when i get back.

  79. junican says:

    Surgeon General report 2010
    The Surgeon General report 2010 On Tobacco and Health
    URL
    http://www.surgeongeneral.gov/library/tobaccosmoke/index.html

  80. junican says:

    Surgeon General report 2010
    The Surgeon General report 2010 On Tobacco and Health
    URL
    http://www.surgeongeneral.gov/library/tobaccosmoke/index.html

  81. Anonymous says:

    Ad hominem
    “as far as the vast majority of the world is concerned, smoking has been proven guilty and people who think it hasn’t are perceived as a pocket of denialists at the outer reaches of crankdom”
    I find it hard to believe that this was said by someone from ‘our’ side, and not a die-hard ASHite!
    Chris, please learn to conduct a debate without resorting to this kind of offensive language. You are talking to many intelligent and experienced people here (including some who are far more skilled than yourself in interpreting statistics), yet who are sceptical about the true role that smoking plays in lung carcinogenesis. Scepticism is not denial, my friend!
    I expect a better standard of argument than I get from my teenage daughter when she is in a bratty, hormonal mood, Sadly, I’m not seeing enough of it in this debate.
    You are capable of making a strong case, Chris, and you certainly have the “vast majority of the world” opinion on your side (for what that is worth) so why spoil it?
    Thank you
    Brian Bond

  82. richwhite09 says:

    Chris, i can’t find the comment thread from earlier today about alternative explanations. Now, this isn’t one, but questions to you along the same lines. Has there been any investigations into roll ups versus premades? Organic tobacco vs high-phosphate fertiliser (or even non-organic fertiliser)? Do you accept/agree that 10 roll-ups with slim filters are different in quantity to 10 premades because they contain less tobacco?
    Removing all sarcasm and snide tones, this is really what i was getting at at the start of this topic about things that haven’t been investigated. As Frank has pointed out (and Leg Iron), one big problem with smoking studies is that a cigarette is just a cigarette, but in reality there are many types of cigarette, varying in tobacco (Virginia, Burley, blond, dark etc), curing methods (air cured, flue cured, the fuel used to power the machines), size (length, width and quantity of tobacco), length of filter and so on and so forth. Do you think, in your opinion or from studies you know of, that a cigarette is just a cigarette? Or that any of these factors could play a role in how harmful smoking could be?
    I’d like to draw a line in the sand at this point, i think we’re both frustrated with certain statements and this debate isn’t as civil as it could or should be. I don’t think it needs to descend to any level of immaturity, and the questions in this comment can be answered sensibly, just as they were posed.
    So, do you have any thoughts on this?

  83. cjsnowdon says:

    Re: Ad hominem
    Brian, you’ve completely missed the point of what I’m saying. I would never argue that something is true just because a majority believes it. I was simply pointing out that if Frank and Rich want to convince people outside of this forum that smoking doesn’t cause lung cancer, they are going to have to come up with a vaguely plausible explanation for the fact that smokers get lung cancer at a far higher rate than nonsmokers. It’s not sufficient to say that ‘we don’t have to prove anything, you do’ when, in fact, it is Rich and Frank who are in a tiny minority of people who take a view that is seen as not just unconventional but laughable. The onus is very much on Rich and Frank to make an alternative case because they are the ones challenging the conventional wisdom. Unless the aim is solely to convince the self-selecting sample of smokers’ rights visitors who comment on this blog.

  84. richwhite09 says:

    Re: Ad hominem
    No Chris, our duty here is not to provide another explanation, but to deconstruct the smoking studies as they stand. As I’ve stated, it may well be that actually the true cause isn’t yet known, so how can we find it?
    And Frank has provided multiple very plausible, and demonstrated, reasons why smokers appear to get more lung cancer than non-smokers, from misclassification of a smoker and lung cancer, to perceived dosage and so on. And i provided quotes form Fisher one of which explained how once something is in the mind, it is more eagerly looked for, meaning it’s self fulfilled without being strictly true. And, myself and others have provided study quotes showing that lung cancer is now rising quite fast in non-smokers and one quote even showed that in never smokers it’s rising mostly in women rather than men. All of which can demonstrate perhaps that smoking has just masked this because so many people smoked – as smoking rates decline, lung cancer appears more in non-smokers and never-smokers.
    But regardless, no matter how many times you say it, we aren’t here to provide a different hypothesis – just to question this one.
    (later leaving than i thought, so this is my last post today most probably)

  85. cjsnowdon says:

    Contrary to what Frank says, there have been many, many studies undertaken to test the reliability of self-reported smoking status and the amount of tobacco smoke inhaled. It’s not a new argument in the slightest. Scientists have measured levels of nicotine, cotinine and carbon monoxide in smokers blood, urine and saliva and have found that those with a high cigarette consumption really do inhale more smoke. They’ve also found (equally unsurprisingly) a strong correlation between people saying they smoke and high levels of nicotine, cotinine and CO. See, for example:
    “In a sample of the general population in Finland the validity of self reported smoking is high, and most of the few self reported non-smokers who had cotinine in their serum had only low or moderate levels.”
    http://jech.bmj.com/content/56/3/167.full
    “There were significant positive correlation between CO levels and daily cigarette consumption, and CO levels and duration of smoking in healthy smokers (r=+0.550, P<0.001, r=+0.265, P<0.001, respectively. Spearman's test). When smokers and non-smokers were looked at as a whole, a cutoff of 6.5 ppm had a sensitivity of 90% and specificity of 83%. In conclusion, exhaled CO level provides an easy, an immediate way of assessing a subject's smoking status."
    http://www.ncbi.nlm.nih.gov/pubmed/15191041?dopt=Abstract
    “Exhaled carbon monoxide levels were higher in self-reported smokers than in nonsmokers and were also higher than those seen among former smokers. There were also significant correlations between the number of cigarettes smoked per day and the exhaled carbon monoxide measurements, confirming previous findings”
    http://chestjournal.chestpubs.org/content/128/3/1233.full
    “A significant correlation was observed between the number of cigarettes smoked and hair measurements of nicotine (r = 0.48, p = 0.004) and cotinine (r = 0.57, p = 0.0008). In addition, a good correlation was found between the reported number of cigarettes smoked and plasma nicotine, plasma cotinine, and carboxyhemoglobin levels.”
    http://ukpmc.ac.uk/abstract/MED/8885115
    “The sensitivity of self-reported smoking status was 97.6%, and the specificity was 100%. Comparing the reported number of cigarettes smoked and the serum cotinine level, the Spearman correlation coefficient was 0.92 (p=0.015) overall and 0.67 (p=0.088) for the subgroup of smokers. This study demonstrates that self-reported smoking exposure during pregnancy is highly accurate. The high correlation coefficient suggests that this is a robust surrogate for cotinine levels.”
    http://bit.ly/dU1BcQ
    “The association between the number of cigarettes smoked per day and the saliva cotinine levels was almost linear. Each additional cigarette smoked per day was associated with an increase of 14 ng/ml in saliva cotinine.”

    Click to access 251.full.pdf


    “This study shows that salivary cotinine concentration is significantly associated with the number of cigarettes smoked and sex, but not with other smoking-related variables.”
    http://www.biomedcentral.com/1471-2458/9/320
    The argument about misclassification has long been resolved by using these methods. In no way is it something that’s been overlooked. Smoker misclassification is minimal and the number of cigarettes consumed is directly correlated with the amount of smoke inhaled.

  86. cjsnowdon says:

    Contrary to what Frank says, there have been many, many studies undertaken to test the reliability of self-reported smoking status and the amount of tobacco smoke inhaled. It’s not a new argument in the slightest. Scientists have measured levels of nicotine, cotinine and carbon monoxide in smokers blood, urine and saliva and have found that those with a high cigarette consumption really do inhale more smoke. They’ve also found (equally unsurprisingly) a strong correlation between people saying they smoke and high levels of nicotine, cotinine and CO. See, for example:
    “In a sample of the general population in Finland the validity of self reported smoking is high, and most of the few self reported non-smokers who had cotinine in their serum had only low or moderate levels.”
    http://jech.bmj.com/content/56/3/167.full
    “There were significant positive correlation between CO levels and daily cigarette consumption, and CO levels and duration of smoking in healthy smokers (r=+0.550, P<0.001, r=+0.265, P<0.001, respectively. Spearman's test). When smokers and non-smokers were looked at as a whole, a cutoff of 6.5 ppm had a sensitivity of 90% and specificity of 83%. In conclusion, exhaled CO level provides an easy, an immediate way of assessing a subject's smoking status."
    http://www.ncbi.nlm.nih.gov/pubmed/15191041?dopt=Abstract
    “Exhaled carbon monoxide levels were higher in self-reported smokers than in nonsmokers and were also higher than those seen among former smokers. There were also significant correlations between the number of cigarettes smoked per day and the exhaled carbon monoxide measurements, confirming previous findings”
    http://chestjournal.chestpubs.org/content/128/3/1233.full
    “A significant correlation was observed between the number of cigarettes smoked and hair measurements of nicotine (r = 0.48, p = 0.004) and cotinine (r = 0.57, p = 0.0008). In addition, a good correlation was found between the reported number of cigarettes smoked and plasma nicotine, plasma cotinine, and carboxyhemoglobin levels.”
    http://ukpmc.ac.uk/abstract/MED/8885115
    “The sensitivity of self-reported smoking status was 97.6%, and the specificity was 100%. Comparing the reported number of cigarettes smoked and the serum cotinine level, the Spearman correlation coefficient was 0.92 (p=0.015) overall and 0.67 (p=0.088) for the subgroup of smokers. This study demonstrates that self-reported smoking exposure during pregnancy is highly accurate. The high correlation coefficient suggests that this is a robust surrogate for cotinine levels.”
    http://bit.ly/dU1BcQ
    “The association between the number of cigarettes smoked per day and the saliva cotinine levels was almost linear. Each additional cigarette smoked per day was associated with an increase of 14 ng/ml in saliva cotinine.”

    Click to access 251.full.pdf


    “This study shows that salivary cotinine concentration is significantly associated with the number of cigarettes smoked and sex, but not with other smoking-related variables.”
    http://www.biomedcentral.com/1471-2458/9/320
    The argument about misclassification has long been resolved by using these methods. In no way is it something that’s been overlooked. Smoker misclassification is minimal and the number of cigarettes consumed is directly correlated with the amount of smoke inhaled.

    • Frank Davis says:

      I can well imagine that cotinine levels correspond well with current reported smoking. But they will be of no use whatsoever in determining past smoking. e.g. whether people have smoked more or less than 100 or 365 cigarettes in their lifetime, and are therefore deemed to be ‘smokers’ or ‘non-smokers’.
      Furthermore, if researchers are able to assess smoking status in this manner, why do they bother asking people whether they’re smokers or not, when all they need do is run the test? As a matter of interest, I don’t believe I’ve ever been tested in this manner.
      Incidentally, in respect of the Kaiser study, I did glance at it. But there’s no way I’m going to be able to comment on it, and ‘say what’s wrong with it’ in a day or even a week. My criticisms of the Doll and Hill studies have anyway been ones which have developed over some years.
      Frank

      • cjsnowdon says:

        Would you accept that it rather ruins your theory about there being no proof that people who smoke more cigarettes inhale more smoke? That idea seems to have excited a few people on this blog in the last couple of days, but the evidence is clear that it’s groundless.
        Sometimes they do test people by taking blood, urine, salvia or hair samples. But the main purpose of the studies above (and there are many more) was to see if self-reporting was accurate in general. And, indeed, it seems to be pretty good. The misclassification rate is always a few percent and is nowhere near strong enough to confound the results of smoking studies, hence the consistency of the results.

        • Frank Davis says:

          Would you accept that it rather ruins your theory about there being no proof that people who smoke more cigarettes inhale more smoke?
          Not as yet.
          Apart from the one study (which found an almost linear relationship between number of cigarettes smoked and CO levels) it didn’t seem that these tests could do very much more than indicate whether someone had been smoking or not. i.e. they couldn’t measure how much people had been smoking.
          Furthermore, CO is present in engine exhausts, so I’d imagine that someone who lives in an area where there is a lot of traffic would have a higher reading.
          I also don’t know how long it takes for CO levels to build up in the bloodstream, and how long to decay after stopping smoking. This would also have an effect.
          Also, these studies appear to be checking the accuracy of the tests, in that it seems to be taken that they know how much people are smoking, and finding how accurately the test does. They appear to be calibrating the test. And to do so they’d have to ask people to smoke a lot or a little or nothing at all for some period prior to the test. It’s not clear to me that they tried it out the other way round, using the test to determine how much anyone was smoking.
          But regardless of whether these tests can accurately assess how much anyone has been smoking, it remains the case that someone who smokes a cigarette very rapidly is going to get a higher dose of nicotine/CO than someone who just lets the cigarette burn down in an ashtray. Same for someone who doesn’t inhale. And we all know perfectly well that cigarettes are smoked in these various different ways. Are you seriously suggesting that the way cigarettes are smoked, fast or slow, inhaled or not inhaled, would have no effect on the resulting reading?
          In short, I’d like to see a test that was specifically designed to look at different ways of smoking.
          Frank

        • cjsnowdon says:

          Frank,
          Apart from the first study in the list, they all clearly state that there is a dose-response relationship between the number of cigarettes smoked and the biomarker examined. The graph on p 253 of the sixth study down shows this quite explicitly.
          CO is present on busy streets but the levels found in smokers is much higher than people who live there so that isn’t a confounder.
          I don’t know exactly how long CO remains in the bloodstream and I don’t see how it’s going to affect things. It’s a relatively brief period I think (less than a day), but for once I’ll let someone else do the googling and find out.
          Your description of the experiments isn’t right. They ask people what they smoke in the usual questionnaire way but then, or at a later date, take a reading to confirm or refute it. They’re not asking anyone to smoke anything, and they’re not conducting a sit-down trial in a lab. It’s all to test self-reported smoking. The studies I’ve listed, and the many others available, all show that misclassification of smoking status from questionnaires is minimal and that the dose is closely correlated with the quantity smoked (which really shouldn’t be a big shock).
          Someone who smokes intensely will also get more nicotine and other biomarkers. That, too, has been shown (although the evidence is mixed), but there is no evidence whatsoever that people who smoke 40 cigarettes take in less smoke than someone who smokes 20 cigarettes (am I really having this discussion!?)
          The point of all this is that the arguments about smoker misclassification are a relic from the 1950s when people used the argument about Doll and Hill. This is quite understandable, particularly since the smoking prevalence in Doll/Hill 1950 was so high in both groups that people found it intuitively difficult to see how anyone could make firm conclusions, despite the relative risk.
          I have some sympathy with that position. What I have no sympathy with is the pretense that the whole smoking theory revolves around Doll and Hill and that nobody bothered to take the criticisms of Doll/Hill into account in future studies. The fact that there is a vast literature on the niche issue of smoker misclassification is indicative of how much work has gone into every area of this subject. There really isn’t anything that Rich and yourself are going to come up with now that scientists, sceptics and the tobacco industry haven’t thrown up, and had thrown out, in the past.

    • richwhite09 says:

      “The argument about misclassification has long been resolved by using these methods. In no way is it something that’s been overlooked.”
      only when the methods are employed in the epidemiological studies. Without it, it just proves such measures and tests are demonstrative in a lab and remain unemployed in real life studies.
      Also (i’m writing from the car so haven’t read the links yet) were those results from a lab where they told participants to smoke? it seems so, and if that’s what happens it has zero effect on inhalation in the real world or misclassification in real life epidemiology.

  87. cjsnowdon says:

    Re: Ad hominem
    I don’t know how many more ways I can explain that the point is that if, as Frank says “in a political confrontation, we absolutely have to throw the whole lot away, regardless of the science”, that will not be achieved with the arguments being presented here. I can’t force anyone on this blog to discuss things they don’t want to discuss, but while the ‘it’s only statistics, nothing’s been proven’ approach might play well on this blog, outside of this corner of the net it’ll be ripped apart like a bread roll, as Rich found out earlier this year (http://www.badscience.net/forum/viewtopic.php?f=3&t=14107&start=0).
    I’m quite prepared to carry on presenting my side of the debate even with the proviso that the defence only has to ask questions and never has to provide answers, but that won’t get you far in the real world.
    That’s all I’m saying.

  88. Anonymous says:

    Chris, I doubt people lied about smoking status until recently but here was a New Zealand paper a couple of years ago claiming that in the current climate, a substantial proportion of smokers in NZ do lie.
    JB

  89. Anonymous says:

    Chris, I doubt people lied about smoking status until recently but here was a New Zealand paper a couple of years ago claiming that in the current climate, a substantial proportion of smokers in NZ do lie.
    JB

  90. cjsnowdon says:

    Re: Ad hominem
    By the way, I’ve already responded to Frank’s point about misclassification and amount on tobacco inhaled. As usual in this debate it boiled down to: “Why don’t scientists investigate this!? … Oh, they have.”
    http://frank-davis.livejournal.com/129267.html?thread=1290483#t1290483

  91. richwhite09 says:

    Re: Ad hominem
    fair enough, but Frank mentioned he never intended that statement as a scientific one but political.
    The bad science blog was a joke, i actually had some sensible discussions with a few of them privately though. It isn’t the real world, i’ve spoken to various people in the real world including medical practitioners, it’s always been amicable and some even changed their minds a bit.
    And anyway, the defence has answered a lot and posed a lot, but questions are the nature of debate. We have shied away from nothing, but a few of us have said you have.
    lastly, what’s this talk of the real world? we’re on a blog and not taking it to the press. We are just discussing purported facts, that’s all.

  92. Frank Davis says:

    I can well imagine that cotinine levels correspond well with current reported smoking. But they will be of no use whatsoever in determining past smoking. e.g. whether people have smoked more or less than 100 or 365 cigarettes in their lifetime, and are therefore deemed to be ‘smokers’ or ‘non-smokers’.
    Furthermore, if researchers are able to assess smoking status in this manner, why do they bother asking people whether they’re smokers or not, when all they need do is run the test? As a matter of interest, I don’t believe I’ve ever been tested in this manner.
    Incidentally, in respect of the Kaiser study, I did glance at it. But there’s no way I’m going to be able to comment on it, and ‘say what’s wrong with it’ in a day or even a week. My criticisms of the Doll and Hill studies have anyway been ones which have developed over some years.
    Frank

  93. richwhite09 says:

    Re: Ad hominem
    great, we can have an earnest debate then, from the figures instead of bullish remarks about it all being rubbish. Of course,if you were right initially that no scientist would go down this blind alley then you wouldn’t have such evidence to post, so maybe now the catty comments can cease

  94. richwhite09 says:

    “The argument about misclassification has long been resolved by using these methods. In no way is it something that’s been overlooked.”
    only when the methods are employed in the epidemiological studies. Without it, it just proves such measures and tests are demonstrative in a lab and remain unemployed in real life studies.
    Also (i’m writing from the car so haven’t read the links yet) were those results from a lab where they told participants to smoke? it seems so, and if that’s what happens it has zero effect on inhalation in the real world or misclassification in real life epidemiology.

  95. cjsnowdon says:

    Would you accept that it rather ruins your theory about there being no proof that people who smoke more cigarettes inhale more smoke? That idea seems to have excited a few people on this blog in the last couple of days, but the evidence is clear that it’s groundless.
    Sometimes they do test people by taking blood, urine, salvia or hair samples. But the main purpose of the studies above (and there are many more) was to see if self-reporting was accurate in general. And, indeed, it seems to be pretty good. The misclassification rate is always a few percent and is nowhere near strong enough to confound the results of smoking studies, hence the consistency of the results.

  96. cjsnowdon says:

    No. Hence ‘self-reported’ smoking status.

  97. Frank Davis says:

    Re: Ad hominem
    if Frank and Rich want to convince people outside of this forum that smoking doesn’t cause lung cancer
    Why should we want to do that? All I’m doing is airing a few of my reservations about the theory, which have arisen in response to a number of concerns.
    I’m not even sure that anyone’s mind can be changed on this matter anyway.
    in fact, it is Rich and Frank who are in a tiny minority of people who take a view that is seen as not just unconventional but laughable.
    I can’t see that it matters a damn if I belong to a ‘tiny minority’, or if anybody laughs at me. I perfectly well understand that for most people, “the debate is over” on this subject. But it isn’t for me. In fact, my debate only got started about 4 or 5 years ago. Before that my views were indistinguishable from anybody else’s.
    Frank

  98. Anonymous says:

    It appears a war broke out while I was gone!

  99. Anonymous says:

    It appears a war broke out while I was gone!

  100. cjsnowdon says:

    Re: Ad hominem
    if Frank and Rich want to convince people outside of this forum that smoking doesn’t cause lung cancer
    Why should we want to do that?

    Because you want to “kill the many-headed hydra” and because “in a political confrontation, we absolutely have to throw the whole lot away, regardless of the science”?

  101. cjsnowdon says:

    Are you offering this as a serious explanation which you’re willing to defend or will you say you were just throwing it out there when I shoot it down? I ask in all seriousness because I really don’t have time for any more wild geese chases. In fact, it would be more appropriate if you provided the reasons why you think it’s a useful area of research and the I could respond. That would be more normal in a debate.

  102. richwhite09 says:

    right, sorry, but did they know they were going to be in a study or tested?

  103. richwhite09 says:

    I said explicitly i’m not offering anything, just asking a few questions.

  104. Anonymous says:

    Re: Chuckles
    “any defence of smoking as the causative factor must provide an alternative”.
    “There is nothing in science that says that one must propose an alternate to inherently defective data, and what is being questioned is the supposed evidence that smoking causes cancer. Without that evidence there is nothing to which an alternative must be proposed, no hypothesis exists”
    No, an alternative as a (?one) causative factor is not compulsory and never has been. It is sufficient to dissect and question the “evidence” provided. However, in order to do so, it is always a good idea to add, e.g. other factors/conditions influencing.

  105. cjsnowdon says:

    But from the first couple of pages it appears we hit the same problem we get with Doll: classification. Current smokers are those who admit to smoking regularly for a year, which is much better than Doll’s but what does it mean? Smoking 5 every friday is regular.
    Then you’re obviously not a nonsmoker and you get classified as a light smoker. Is there some problem with that?
    Then there’s the smoking categories – why less than 20, not less than 10?
    Why not? If it had been the other way round you would have said ‘why not less 10, not less than 5’. The point is to divide up lighter and heavier smokers. Smoking more than 20 a day is perfectly reasonable definition of a heavier smoker.
    Assumption doesn’t belong in science, it only takes a small percentage to change their smoking habits relatively slightly to alter the results drastically.
    Absolute rubbish. It would take a huge change. And, as you and Frank always ignore, misclassification is minimal in these studies and, in any case, it works both ways.
    The mean age of study was 50.9, or 51 for argument’s sake, and the age range was 50-64. This is a difficult age bracket because it’s in the 60s that such diseases as cancer and emphysema become much more prominent.
    Well, dur. This is a bad thing? Perhaps they should just have studies healthy teenagers? . The study compares like with like and the results are stratified by age and age-adjusted, always with the same result.
    And where are the confounders? I see no mention of diet, background, social class, exercise, purported stress levels from work, environment, exposure to chemicals in work or home etc etc.
    None of these factors are anywhere near strong enough to explain the RRs in the study and some of them are not causal factors for lung cancer at all.

  106. richwhite09 says:

    Re: Ad hominem
    Chris, to revert to your claim we must provide alternate reasons, why is that for us to do any more than it is for you to state other reasons, to antis, for non smokers getting LC other than SHS?

  107. cjsnowdon says:

    Rich,
    I have a life to lead and it doesn’t involve spoon-feeding you information. Why don’t you wait till you get back home and read the studies then?
    CJS

  108. richwhite09 says:

    point 1: yes it’s a problem, because your statement wouldn’t classify them as a non-smoker.
    2: more than 20 yes, i’m talking under under it because 20 and 4 are different in terms of light moderate and heavy, at the lower levels smaller categories make more sense. and as i said before, smokers of less than 10 in the 64 report had less disease incidence, while 10-20 didn’t.
    3: perhaps.
    4: you miss my point, i was saying 60+ should be separate to 50s
    5: so basically there are no confounders. what a stellar piece of research

  109. cjsnowdon says:

    In that case I’ll state explicitly that I’m not here to do your research for you. If you think you’ve found something of interest then find some evidence, organise your thoughts and put them down in a post.

  110. cjsnowdon says:

    Re: Ad hominem
    What?

  111. cjsnowdon says:

    1. Well guess what? Someone who smokes in a smoker.
    2. How would this turn a null study into a very strong correlation between smoking and lung cancer? (It wouldn’t. It’s utterly irrelevant.)
    4. For what earthly reason? How does the age stratification lead to a bias towards the smoking theory? (It doesn’t. You just don’t understand epidemiology.)
    5. Yep, there are no confounders that come anywhere near the risk of smoking. Especially things like ‘background’ and ‘social class’ which clearly aren’t causal, and are themselves confounded by real causal factors of which the largest, by a very long way, is smoking.

  112. richwhite09 says:

    i’m not asking for research, i’m asing for your opinion

  113. richwhite09 says:

    christ, can you read?
    until you get over yourself and learn how to hold a discussion, this will go nowhere. when someone disagrees, that isn’t a green light for insults, just so you know.

  114. richwhite09 says:

    Re: Ad hominem
    it’s very simple. you say we who doubt the active smoking/cancer link must provide an alternative. you doubt the SHS/cancer link, have you provided alternatives to those who think it does cause lung cancer?
    btw, you say most of the world agrees smoking causes cancer. but so too do most believe SHS can cause lung cancer, yet that doesn’t deter your thoughts on it. your ‘logic’ is so riddled with holes it’s quite stunning

  115. cjsnowdon says:

    Yes, I’ve read your comments. That’s how I know you don’t understand epidemiology. That’s not an insult, by the way, just a statement of fact. No one who understands the basics of epidemiology would claim that showing the results in a certain age range was a flaw in a study, especially when all the age ranges show similar, strong, positive results. Nor would they claim that starting the age range at 60 would be a superior or any less arbitrary way of doing it.
    This is not even trivial. It’s just nothing. Nothing at all. It’s as if you went through the study and looked at what they could have done differently and then called their choices flawed, even though they had precisely zero effect on the results. Either that’s the behaviour of a man who doesn’t understand the discipline or who is deliberately muddying the water in the hope that some people will be daft enough to believe that you’ve identified some genuine problems.

  116. cjsnowdon says:

    Re: Ad hominem
    Gee, you must have missed my comment early today when I said: “I would never argue that something is true just because a majority believes it.”
    http://frank-davis.livejournal.com/129267.html?thread=1289971#t1289971
    Oh, but hang on, you were the first person to reply so I guess you’ve just got a very short memory.
    Re: SHS, the reason I am doubtful is not because I think there is an alternative explanation for the association, it’s because I don’t see that there is an association there to begin with. So it’s more of a data collection issue rather than a cause/correlation issue. The magnitude of the association with SHS is ultra-low, in complete contrast to the risk of active smoking. I’m going to write about this in my post after next.

  117. Anonymous says:

    Re: Surgeon General report 2010
    Surgeon General’s Office Again Misrepresents and Distorts the Science in Report Press Release; Why the Need to Lie to the American Public?
    http://tobaccoanalysis.blogspot.com/2010_12_01_archive.html

  118. Anonymous says:

    “The onus is very much on Rich and Frank to make an alternative case because they are the ones challenging the conventional wisdom.
    Unless the aim is solely to convince the self-selecting sample of smokers’ rights visitors who comment on this blog.”
    http://frank-davis.livejournal.com/129267.html?thread=1289971#t1289971
    Better than calling us right-to-smoke-zealots I suppose.
    Why all this matters to everyone, whether they know it or not.
    FINAL ASSESSMENT REPORT
    “Many commonly and widely consumed vegetables of the nightshade family (Solanaceae)
    such as potatoes, tomatoes, eggplants and capsicums naturally contain low levels of nicotine.
    Nicotine has also been detected in cauliflower and tea – two non-solanaceous plants.”
    “A concern expressed by health authorities is that the addition of tobacco or nicotine in food may promote or legitimise the smoking of tobacco or the use of smokeless tobacco products.
    VicHealth proposed a modified Option 2 – Allow the use of Nicotiana species in all foods but restrict the level of nicotine to the level demonstrated to be safe and not to be therapeutic or psychoactive.” ?
    “The option was raised to prevent foods such as the nightshades, known to naturally contain low levels of nicotine, from being banned.”

    Click to access P278_Nicotine_FAR_Final.pdf


    “Consider, for example, the most famous of the one-ring type alkaloids (monocyclic alkaloids) found in the highest concentrations in tobacco (Nicotiana tabacum): nicotine. This alkaloid is found not only in non-food nightshades like tobacco, but also in the food nightshades including eggplant and tomato.”
    But there is one important difference here: while alkaloids like nicotine are definitely found in nightshade foods, the amount involved is dramatically less. Even in the case of eggplant, which is the food nightshade that appears to have the highest nicotine content after tobacco, the amount of nicotine is far lower than the amount found in tobacco.
    The levels of nicotine in all nightshade foods are so low that most healthcare practitioners have simply ignored the presence of nicotine in these foods as a potential compromising factor in our health”
    http://www.whfoods.com/genpage.php?tname=george&dbid=62
    ENVIRONMENTAL TOBACCO SMOKE –
    ESTIMATION OF ITS CONTRIBUTION TO RESPIRABLE SUSPENDED PARTICLES –
    METHOD BASED ON SOLANESOL DETERMINATION
    “Many plants of the Solanaceae family, which includes the genus Nicotiana, of which the tobacco
    plant is a member, contain solanesol; particularly those that contain trace amounts of nicotine.
    These include the tomato, eggplant, potato, and pepper.
    The potential interference due to these sources is negligible, cooking being the only likely potential source of interference. An interference of this type would bias results high, overestimating the contribution of ETS to RSP.

    Click to access CRM_52.pdf


    Study raises concerns about outdoor second-hand smoke
    “To put that number into context, a widely cited study has determined that an average cotinine level of 0.4 ng/ml increases lung cancer deaths by 1 for every 1,000 people and increases heart disease deaths by 1 for every 100 people.”
    http://www.eurekalert.org/pub_releases/2009-11/uog-src111809.php
    EVALUATION
    “The Committee considered that, despite the long history of human consumption of plants containing glycoalkaloids, the available epidemiological and experimental data from human and laboratory animal studies did not permit the determination of a safe level of intake.
    The Committee recognized that the development of empirical data to support such a level would require considerable effort”
    http://www.inchem.org/documents/jecfa/jecmono/v30je19.htm
    But for how long?
    Think that they would never do it?
    Well that’s what I thought and for exactly the same reasons.
    Rose

  119. Anonymous says:

    “The onus is very much on Rich and Frank to make an alternative case because they are the ones challenging the conventional wisdom.
    Unless the aim is solely to convince the self-selecting sample of smokers’ rights visitors who comment on this blog.”
    http://frank-davis.livejournal.com/129267.html?thread=1289971#t1289971
    Better than calling us right-to-smoke-zealots I suppose.
    Why all this matters to everyone, whether they know it or not.
    FINAL ASSESSMENT REPORT
    “Many commonly and widely consumed vegetables of the nightshade family (Solanaceae)
    such as potatoes, tomatoes, eggplants and capsicums naturally contain low levels of nicotine.
    Nicotine has also been detected in cauliflower and tea – two non-solanaceous plants.”
    “A concern expressed by health authorities is that the addition of tobacco or nicotine in food may promote or legitimise the smoking of tobacco or the use of smokeless tobacco products.
    VicHealth proposed a modified Option 2 – Allow the use of Nicotiana species in all foods but restrict the level of nicotine to the level demonstrated to be safe and not to be therapeutic or psychoactive.” ?
    “The option was raised to prevent foods such as the nightshades, known to naturally contain low levels of nicotine, from being banned.”

    Click to access P278_Nicotine_FAR_Final.pdf


    “Consider, for example, the most famous of the one-ring type alkaloids (monocyclic alkaloids) found in the highest concentrations in tobacco (Nicotiana tabacum): nicotine. This alkaloid is found not only in non-food nightshades like tobacco, but also in the food nightshades including eggplant and tomato.”
    But there is one important difference here: while alkaloids like nicotine are definitely found in nightshade foods, the amount involved is dramatically less. Even in the case of eggplant, which is the food nightshade that appears to have the highest nicotine content after tobacco, the amount of nicotine is far lower than the amount found in tobacco.
    The levels of nicotine in all nightshade foods are so low that most healthcare practitioners have simply ignored the presence of nicotine in these foods as a potential compromising factor in our health”
    http://www.whfoods.com/genpage.php?tname=george&dbid=62
    ENVIRONMENTAL TOBACCO SMOKE –
    ESTIMATION OF ITS CONTRIBUTION TO RESPIRABLE SUSPENDED PARTICLES –
    METHOD BASED ON SOLANESOL DETERMINATION
    “Many plants of the Solanaceae family, which includes the genus Nicotiana, of which the tobacco
    plant is a member, contain solanesol; particularly those that contain trace amounts of nicotine.
    These include the tomato, eggplant, potato, and pepper.
    The potential interference due to these sources is negligible, cooking being the only likely potential source of interference. An interference of this type would bias results high, overestimating the contribution of ETS to RSP.

    Click to access CRM_52.pdf


    Study raises concerns about outdoor second-hand smoke
    “To put that number into context, a widely cited study has determined that an average cotinine level of 0.4 ng/ml increases lung cancer deaths by 1 for every 1,000 people and increases heart disease deaths by 1 for every 100 people.”
    http://www.eurekalert.org/pub_releases/2009-11/uog-src111809.php
    EVALUATION
    “The Committee considered that, despite the long history of human consumption of plants containing glycoalkaloids, the available epidemiological and experimental data from human and laboratory animal studies did not permit the determination of a safe level of intake.
    The Committee recognized that the development of empirical data to support such a level would require considerable effort”
    http://www.inchem.org/documents/jecfa/jecmono/v30je19.htm
    But for how long?
    Think that they would never do it?
    Well that’s what I thought and for exactly the same reasons.
    Rose

  120. Frank Davis says:

    Would you accept that it rather ruins your theory about there being no proof that people who smoke more cigarettes inhale more smoke?
    Not as yet.
    Apart from the one study (which found an almost linear relationship between number of cigarettes smoked and CO levels) it didn’t seem that these tests could do very much more than indicate whether someone had been smoking or not. i.e. they couldn’t measure how much people had been smoking.
    Furthermore, CO is present in engine exhausts, so I’d imagine that someone who lives in an area where there is a lot of traffic would have a higher reading.
    I also don’t know how long it takes for CO levels to build up in the bloodstream, and how long to decay after stopping smoking. This would also have an effect.
    Also, these studies appear to be checking the accuracy of the tests, in that it seems to be taken that they know how much people are smoking, and finding how accurately the test does. They appear to be calibrating the test. And to do so they’d have to ask people to smoke a lot or a little or nothing at all for some period prior to the test. It’s not clear to me that they tried it out the other way round, using the test to determine how much anyone was smoking.
    But regardless of whether these tests can accurately assess how much anyone has been smoking, it remains the case that someone who smokes a cigarette very rapidly is going to get a higher dose of nicotine/CO than someone who just lets the cigarette burn down in an ashtray. Same for someone who doesn’t inhale. And we all know perfectly well that cigarettes are smoked in these various different ways. Are you seriously suggesting that the way cigarettes are smoked, fast or slow, inhaled or not inhaled, would have no effect on the resulting reading?
    In short, I’d like to see a test that was specifically designed to look at different ways of smoking.
    Frank

  121. cjsnowdon says:

    Frank,
    Apart from the first study in the list, they all clearly state that there is a dose-response relationship between the number of cigarettes smoked and the biomarker examined. The graph on p 253 of the sixth study down shows this quite explicitly.
    CO is present on busy streets but the levels found in smokers is much higher than people who live there so that isn’t a confounder.
    I don’t know exactly how long CO remains in the bloodstream and I don’t see how it’s going to affect things. It’s a relatively brief period I think (less than a day), but for once I’ll let someone else do the googling and find out.
    Your description of the experiments isn’t right. They ask people what they smoke in the usual questionnaire way but then, or at a later date, take a reading to confirm or refute it. They’re not asking anyone to smoke anything, and they’re not conducting a sit-down trial in a lab. It’s all to test self-reported smoking. The studies I’ve listed, and the many others available, all show that misclassification of smoking status from questionnaires is minimal and that the dose is closely correlated with the quantity smoked (which really shouldn’t be a big shock).
    Someone who smokes intensely will also get more nicotine and other biomarkers. That, too, has been shown (although the evidence is mixed), but there is no evidence whatsoever that people who smoke 40 cigarettes take in less smoke than someone who smokes 20 cigarettes (am I really having this discussion!?)
    The point of all this is that the arguments about smoker misclassification are a relic from the 1950s when people used the argument about Doll and Hill. This is quite understandable, particularly since the smoking prevalence in Doll/Hill 1950 was so high in both groups that people found it intuitively difficult to see how anyone could make firm conclusions, despite the relative risk.
    I have some sympathy with that position. What I have no sympathy with is the pretense that the whole smoking theory revolves around Doll and Hill and that nobody bothered to take the criticisms of Doll/Hill into account in future studies. The fact that there is a vast literature on the niche issue of smoker misclassification is indicative of how much work has gone into every area of this subject. There really isn’t anything that Rich and yourself are going to come up with now that scientists, sceptics and the tobacco industry haven’t thrown up, and had thrown out, in the past.

  122. richwhite09 says:

    this just basically goes back to a point Frank made earlier – you’re exceptionally willing to accept any smoking study regardless of the flaws. Highlighting the flaws means i either am being ignorant or don’t understand epidemiology. another spurious claim from you chris that simply shows your pig headedness on the issue.
    they had precisely zero effects on the results? how can you possibly determine that? in the studies where a few confounders are mentioned you say that’s good. in studies showing social class is a confounder because those people are more likely to suffer from various illnesses, that’s fine. and in studies where there are no confounders, well it doesn’t matter because they make no difference?! it really is like arguing with a child. you proposed this debate and presumably thought it would be easy to prove your point. yet you haven’t tried very hard (from catch3 someone mentioned your reliance on rhetoric) and quickly resorted to behaviour that, as correctly noted by brfian bond, resembles that of a hormonal teenager. almos everyone here is making good posts, positions, relaying of facts, and you retaliate with snide marks, personal attacks, dismissal of everything when you know nothing about the topic, ignoring people, and generally bullish attitudes. it’s not nice or pleasant and quite frankly it’s pathetic.
    if your claim was so stronly proved as you assert it would have been a piece of cake to show it. instead it turns out that everyone else can find huge problems with the studies and that seems to dent your ego. and remember: i’m not the first or only one to mention your attitude and arrogance in the posts, and secondly, you are quite simply the only one of everyone to be called out for it by commenters.

  123. richwhite09 says:

    Re: Ad hominem
    riiight, let me explain again and maybe you’ll get it. We all here know about the SHS fraud, you don’t need to point out the lack of association. My point was, you have plucked from the air the ridiculous demand that we must provide an alternative reason for smokers getting lung cancer if not smoking. Many people believe SHS is a cause of thousands of deaths of lung cancer each year – so to those people, should you not provide an alternative reason for the deaths?
    no, of course not. and seemingly this whole debate has gone over your head, because by challenging the data and figures we’re calling the strength of association into question. in turn, you are meant to be showing why it is as strong as we’re told.

  124. cjsnowdon says:

    OK then. Explain how the age stratification is a flaw in the study.

  125. cjsnowdon says:

    Re: Ad hominem
    Has it been a long night on the beer or are you just a bit slow? Read what I said and think it through.

  126. richwhite09 says:

    it’s not a ‘flaw’ so much, just an observation that it would be better to separate the age group who is far more likely to have cancer anyway from the group that isn’t.
    i’m much more concerned about the complete lack of any confounders whatsoever. you want us to take this seriously as proof of smoking causing cancer, when there were no other factors even considered? i know, i know , you’re going to say that it makes no difference. well even wynder concluded from one of his studies that other factors were clearly involved in the onset of lung cancer, also shown by lung cancer rising in non smokers and the simple fact we know other factors contribute to the disease. for you to say confounders would make no difference is just unbelievable

  127. richwhite09 says:

    Re: Ad hominem
    neither chris, neither. it’s evidently just another post in this debate that you have not managed to get your head around and instead you sidestep and throw an insult. anyone can see what my post meant and how your reply didn’t answer it.

  128. cjsnowdon says:

    it would be better to separate the age group who is far more likely to have cancer anyway from the group that isn’t.
    Why?

  129. richwhite09 says:

    er, for the same reason 70 year olds aren’t compared to 50 year olds?because if you’re studying an isolated factor to work out it’s imppact on health, lumping in people who are already at hugely increased odds of getting it with an age group of less risk isn’t very good methodology. but let’s face it, you already knew that.

  130. cjsnowdon says:

    Re: Ad hominem
    *sigh*
    Let’s try one more time then…
    My doubts about the SHS studies is that the statistical correlations are usually nonsignificant and are so close to 1.0 that it’s questionable whether they exist at all. If they don’t exist at all, I don’t need to provide an alternative explanation for the hypothetical deaths.
    With active smoking, the relative risks are solid, strong and statistically significant, so anyone who denies causation really needs to come up with an alternative explanation for the strong correlation. Otherwise people are going to assume – very understandably indeed – that the reason smokers’ risk of lung cancer is greatly higher than nonsmokers is because they smoke.
    Got it?

  131. cjsnowdon says:

    But whatever age group of smokers is selected is being compared to the SAME AGE GROUP of nonsmokers! They’re not comparing 70 year olds to 50 year olds. It’s a completely apples and apples comparison with the only key variable being the smoking.
    You really don’t get this at all, do you?

  132. richwhite09 says:

    Re: Ad hominem
    oh i get your point, i just don’t agree with it. let’s take frank’s example of misclassification from doll as an example, ok? with a pretty low misclassification rate, he took the RR down very low indeed. so by your own logic, we only need to show the correlation isn’t as strong as suggested or seemingly shown.

  133. cjsnowdon says:

    Re: Ad hominem
    Now we’re getting somewhere! If you show me that the statistical correlations are actually very weak then I’ll change my mind. The problem you face is that they aren’t weak at all. They’re very strong and consistent. But I will continue to present evidence post-Doll and you can pick holes in it. That’s why I’m prepared to continue this debate – so that the rest of the evidence (a lot of which is fairly new to me) can be examined and assessed. Unfortunately, it took a lot of coaxing for me to get anyone to discuss the (randomly selected) study I presented last time and I haven’t heard anything since to make me think it, or any of the rest, have a major problem.

  134. richwhite09 says:

    Yes, i do, hence me saying that i don’t think it’s much of a flaw, just an observation. But, as ever, you singled out the lesser part of my post and ignored the rest.

  135. richwhite09 says:

    Re: Ad hominem
    With all due respect Chris, you haven’t posted much in the way of studies on active smoking. I didn’t respond about Kaiser because I genuinely thought Frank had, but it must have been a comment referring to something else, so i then replied straight away.

  136. cjsnowdon says:

    No, I’m testing your criticisms to see if they’re valid. Now let’s take another ‘flaw’ you mentioned. You think that someone who smokes 5 cigarettes a week should be classed as a nonsmoker. That, I think, is very questionable, but let’s go with it. If we have a few people who smoke 5 cigarettes a week classed as smokers, what will be the effect on the results if (a) some of them get lung cancer, or (b) none of them don’t get lung cancer?

  137. richwhite09 says:

    No, sorry, it appears i wasn’t clear. I didn’t say someone who smokes 5 a week is a non-smoker. The study paper says a smoker was someone who admits to smoking regularly, and my point was ‘regular’ is very much open to debate on a person’s interpretation. I just used 5 a week as an example. Someone could equally think going out to the local once a month and smoking 3, 4, or 100 is ‘regular’. My follow on from that was “”If they did not affirm never using any tobacco product, never-smokers had to deny ever smoking cigarettes regularly for at least 1 year””, from the paper itself. So a never-smoker in the study is someone who has smoked, but abstained for a year – except not total abstain, just irregular. To some people, that could mean 5 one week, none for a couple months, smoke every day for a week, quit again. That’s irregular.
    The bulk of CATCH so far has revolved around such problems with definition – Doll apparently omitted the inhalation question in case some people didn’t know what it meant; I think it’s a safe bet that more people understand ‘inhale’ than ‘regular’, because ‘regular’ is a very flexible word that depends on context.

  138. cjsnowdon says:

    Understood. But the question remains, what would be the effect on the results of having a number of very light smokers classified as smokers?

  139. richwhite09 says:

    That depends on how many were misclassified i suppose. But then this is part of the other problem of smoking rates starting with 0-20, rather than smaller increments. It’s just not thorough research to say someone who smokes even a pack a month belongs in the same category as someone who smokes 20 a day. mind you it’s not thorough research to conduct a study with no confounders whatsoever; it’s been posted in CATCH 15 from a study that found vitamin B6 has an inverse effect on lung cancer, with those deficient in it more likely to have the disease while those who had adequate levels were much less likely to. In a study that made no attempt to see if smokers ate worse, ate better, exercised more or less or anything outside of smoking whatsoever, it’s not particularly logical to take the results as gospel anymore than it makes sense to look at statistics of those who take paracetamol – the more headaches they get, the more pills they take, so we could say from the figure paracetamol is conclusively linked to headaches with a dose-dependent relationship.

  140. cjsnowdon says:

    The effects of diet are very weak compared to the risks found with smoking, but that’s a different point (and I’ll come to that in tonight’s post). The rate of misclassification are low, and this has been shown through chemical testing on many occasions (see my posts yesterday).
    The answer to the question is that if a few light smokers are classified as smokers and they don’t get lung cancer (which is most likely), it will actually weaken to relationship between smoking and lung cancer. If smoking doesn’t cause lung cancer then the rates of lung cancer will be evenly spread over the cohort and there wouldn’t be an association at all. So the effect of the misclassification you’re talking about will tend to lead to the risks of smoking being underestimated, not overestimated.

  141. richwhite09 says:

    “The effects of diet are very weak compared to the risks found with smoking”
    The risks found with smoking are still correlation though, which Fisher spoke out against in 1958 and we still haven’t progressed from, and which as i said in my last post is like looking at people with headaches and take paracetamol and say the tablet causes the headache. The effects of diet could play a massive part, B6 alone has been shown to cut the risk of LC, as has vitamin E. Considering what we eat affects all of our cells, pH levels and general internal wellbeing, it could easily impact on cancer.
    “So the effect of the misclassification you’re talking about will tend to lead to the risks of smoking being underestimated, not overestimated.”
    In theory. But what if, for some other reason, the smokers of 15-20 a day had huge incidence of LC, which was offset in the results by the lack of cancer in the lighter smokers? It could have been that the 15-20 a day had the highest peak of all, but remained undiscovered in the results table. And none of this considers detection bias either, which has been well and truly documented and shown to be real, before this study was conducted. And as the researchers only looked at smoking, and nothing else, they were clearly aware of the association and expecting the results they found to turn up, so detection bias here is an almost certainty (if for no other reason than the fact that even nowadays diagnosis is not 100%, or anywhere near it, so going back 30, 40 years, we must acknowledge that much of the cancers didn’t even really exist).
    And also still nothing has been said about my earlier posts about primary and secondary cancers.

  142. cjsnowdon says:

    But what if, for some other reason, the smokers of 15-20 a day had huge incidence of LC, which was offset in the results by the lack of cancer in the lighter smokers? It could have been that the 15-20 a day had the highest peak of all, but remained undiscovered in the results table.
    Sorry. Read it 4 times. Still don’t see what you’re getting at in theory or in practice.

  143. richwhite09 says:

    ok, what if (and this is hypothetical) people who smoked 15-20 a day had the most incidence of lung cancer across the entire study population. If the people who smoked 0-10 had the lowest incidence then the entire category of 0-20 would sort of meet in the middle and bring the LC number for that category lower than the other categories (say, 20-30, 40-50 a day etc). So the end result graph wouldn’t be an accurate representation of the actual LC incidence.

  144. cjsnowdon says:

    If that (admittedly inexplicable) event happened, the two would cancel each other out and you would have an RR for the 1-10 cigarette group that was the same as the nonsmoking group, and therefore a null study. It would suggest that smoking doesn’t cause cancer. Alas, that’s not what happens.
    Note also that chopping the sample group into smaller and smaller subdivisions is a trick usually performed by junk scientists to claim individual associations where there is no overall association (eg. the recent Isle of Man study that looked at the over 55s).

  145. richwhite09 says:

    “the two would cancel each other out and you would have an RR for the 1-10 cigarette group that was the same as the nonsmoking group, and therefore a null study. It would suggest that smoking doesn’t cause cancer.”
    Not necessarily, if the excess of the 15-20 exceeded the lack of Lc in 0-15 then there would still be an increase over the non-smokers. It would be higher than non-smokers and lower than 20-30, thus creating the linear graph.
    “Note also that chopping the sample group into smaller and smaller subdivisions is a trick usually performed by junk scientists to claim individual associations where there is no overall association (eg. the recent Isle of Man study that looked at the over 55s).”
    I’m not suggesting to have only small subdivisions, i don’t see the benefit of that. I’m talking about 0-20 specifically, because that range accounts for very light, light and moderate smokers (perhaps even by some standards ‘heavy’). In light of the fact that the 1964 SG Report had a table showing smokers of up to 10 a day had lower incidence of LC, i don’t think it’s an outrageous thing to say in subsequent studies that group should have its own category, which is all i’m saying. And, going back to the previous point, let’s assume that smoking can cause cancer in the right dosage, and the right dosage is 15+. In which case, my hypothetical situation would begin to look much more plausbile

  146. cjsnowdon says:

    If you were to say that smoking causes cancer beyond a certain dosage that would, I do believe, be a victory for the ‘smoking causes lung cancer’ hypothesis.
    Other studies have broken down the results by more specific measures of cigarette consumption and have found the same dose-response relationship.
    eg:
    http://tobaccocontrol.bmj.com/content/14/5/315/T3.expansion.html

  147. richwhite09 says:

    “If you were to say that smoking causes cancer beyond a certain dosage that would, I do believe, be a victory for the ‘smoking causes lung cancer’ hypothesis.”
    It would indeed. Note, though, I didn’t say it does, I said ‘let’s assume that smoking can cause cancer in the right dosage.’
    This is unrelated to this thread (but in keeping with the CATCH debate), have you read Nighlight’s forum posts? I’m currently about 1/3 way through one partocular discussion, so too soon to draw any conclusions, but i wondered if you’d give your thoughts on it if and when you have the time to read it? Obviously i don’t expect a reply today or even this week; i’d just be interested in your thoughts to his thoughts on the correlation and human studies etc
    http://www.imminst.org/forum/topic/38868-smoking-is-good-for-you/

  148. richwhite09 says:

    As an addendum to this, remember the primary/secondary cancer I mentioned and how it would be interesting to find out how much lung cancer in smokers is primary and secondary? From that link above Nighlight posted this:
    Chronic Inhalation of Cigarette Smoke by F344 rats
    W.E. Dalbey at al., Oak Ridge Nat. Lab., Inst. Environ. Health…
    J. National Cancer Inst., 64 (2): 383-390 (Feb 1980)
    “”Smoke exposure did not change the total number of tumor-bearing animals relative to controls; however [smoke] exposed rats had significantly fewer tumors in the hypophyses, hematopletic-lymphoid system, uteri and ovaries, but an increased number of tumors in the respiratory tracts and dermes.”
    These animal data fit in with the concepts of Prof. Oeser in Berlin and Dr. Lock in Hamburg, that, if properly assessed, the epidemiological data on cancers in general and for specific organs, indicate that total cancer rates have not changed, and that the only thing which has changed is that the increase in one type of cancer is compensated for by a decrease in other organ cancers.””
    This links in with my primary/secondary suggestion. We have on the one hand a scientific fact that cancer can migrate and will migrate to the area it is most likely to survive. So do we have data on total incidence of cancer since 1930s or 1950s? This will help inform us if cancer itself has increased exponentially, or if the total rate is the same with variations in individual sites.

  149. cjsnowdon says:

    I think I’ve got enough to reply to on this blog without discussing the thoughts of someone who thinks that showing photos of elderly smokers is a compelling way to put forward the argument that ‘smoking is healthy’. His first claim is that ‘smoking animals live longer’ and his source is another message-board. I think I’ll give it a miss, thanks.

  150. richwhite09 says:

    That’s not nearly the extent of his argument, and he goes into much, much more details further in (i’m on page 11 of 25), and he does indeed show studies where smoking animals live longer

  151. cjsnowdon says:

    Good for him. I’m sure he won’t mind if you introduce some of his killer arguments into your next post.

  152. richwhite09 says:

    I’m sure he won’t either. But we’ll see how the debate continues as to whether they’re relevant; plus the fact it’s looking likely i won’t be contributing much here after Saturday.

  153. cjsnowdon says:

    Where can I see the full study?

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