CATCH-13

Rich White returns.

Chris has presented a number of points to be addressed, so this post is somewhat lengthy but I have tried to refrain from over embellishing anything or making unnecessary statements. Also for the sake of brevity I have not tended to every single sentence from Chris; some were unnecessary to respond to, others don’t need to be dealt with to add anything to this debate and others have had responses in the comments.

“So, first up is the idea that because “only” around 10% of smokers develop lung cancer, smoking does not really ‘cause’ lung cancer at all.”

This is a tricky argument for both sides. I do agree with Chris that just because something is caused in a minority, it can still be causal. However the Cholera argument also serves both points. Chris is right Cholera was from the water (not the pump, which was very aptly pointed out in the comments); however, we know not everyone was affected by the water because of their immunity. On his death bed, Louis Pasteur said that ‘the terrain is everything’, meaning it is much more than just any given substance that can do harm, but how healthy our body is in general that determines whether a negative effect will ensue. Robert Koch developed the germ theory went on to say that it isn’t the bacteria itself, but the terrain i.e. your own immune system, and proved this by drinking a glass of vicrio cholera and remained symptom free 

The 10% itself, I think everyone here besides Chris agrees that that is more indicative of a ‘factor’ than a ‘cause’. Timbone made the point earlier in the CATCH discussion that a ‘cause’ has a direct effect and used the example of slitting your wrists leading to blood loss. A factor is something that may increase your chances of something happening. I think that’s far more accurate with smoking and LC.

“We can say, quite literally, that drink-driving kills.”

This is a good way to prove the above. It is not drink driving that kills, it is being hit by a car that can damage your body beyond repair and causing death. Drinking simply makes you more likely to be in an accident because of the neurological effects alcohol has on the body. From the victim’s point of view though, it won’t matter how sober or drunk the driver is – it’s the collision that does the damage.

“unlike Rich they don’t reject what we do know in the mean time, just because our knowledge is not perfect in the here and now.”

I’ve never said that. I have stated in the CATCH debate that I have never stated smoking doesn’t cause lung cancer, just that the evidence for the claim is underwhelming. I also put in my last entry about primary and secondary lung cancer i.e. whether smoking doesn’t cause lung cancer but sets up ideal conditions in the lungs for cancer to migrate to that site once it is established in the body. I’m actually a little disappointed Chris didn’t respond to this point, because I think it should be explored.

“Then we would expect smokers and nonsmokers alike to be dropping dead of lung cancer at the same rate. We would also expect some canny scientist to have spotted this massive global outdoor carcinogen.”

We wouldn’t expect them to drop dead at the same rate because, as Chris did rightly point out, we won’t expect everyone to suffer from any individual factor. Nor, as he also said, do we need a large percentage of victims to cry causation. And the massive outdoor carcinogen, well, it has. Rose has gone to great lengths to share information on air pollution, radioactive particles, mustard gas and so on.

“They used between 25mg and 75mg of tar. It was painted on their backs, as I would have thought Rich would know, really.”

I did know that, as I stated in CATCH-9: “And the animal studies, the carcinogenity was only really demonstrated by taking extracts, like tobacco condensate on bald mice (any irritant will cause skin cancer on bald mice).” While I’m not denying carcinogens exist in tobacco smoke, I will point out skin cancer developing on bald mice isn’t indicative of carcinogens, because skin cancer can be caused simply by irritation. Moreover, it wasn’t smoke that was used but condensate, which is different. (In fact, in looking through the McTear case to answer points further down, I found this:

‘The authors of the reports stated that the results of animal skin-painting experiments supported the proposition that the statistical association between cigarette smoking and lung cancer was causal. But Sir Richard Doll and Professor Friend said that the results of these experiments were of no value in determining whether smoking could cause lung cancer.’)

Finally, as I have said multiple times, it’s all about the dosage.

“On the criticism that there weren’t enough control dogs, same answer again, really. Since every one of the controls were absolutely fine and all the cases were dead, dying or in a bad way, we don’t need hundreds of controls to tell us what we already know – that healthy beagles don’t just suddenly get a range of smoking-related diseases for no reason.”

I wholly disagree here. Firstly, not every smoking dog was dead, dying or in a bad way. Plus, it is simply not scientific to compare a lot of smoking dogs (you’re right my number was wrong, i was working from memory, (I said 76, the 1971 report says 86, the 1982 report says 78, presumably the 78 were the remaining dogs after others were ‘sacrificed’ early on) but boosting the amount of smoking dogs and keeping the same amount non-smoking dogs isn’t helping your argument here) to only eight non-smoking dogs. I have just been looking through the 1971 Report and found the study details. The facts are there were 86 smoking dogs and 8 non-smoking dogs, which means the non-smoking group was roughly only 10% that of the smoking group. There were only 28 deaths in total, between days 57-875, while 58 of the smoking group survived to the final day. Of the non-smoking dogs, none died but there were two tumours, meaning 25% of the non-smoking dogs developed tumours. So, what does this tell us? The control group didn’t have any deaths, but did develop tumours. The smoking group developed more tumours but then there were far more of them – which reinforces my earlier point that the results may well have been very different had there been an equal number of smoking and non-smoking dogs. This is further backed up by the fact that in the smoking group, more than 8 dogs didn’t get tumours or die. It would therefore be possible to have 8 smoking dogs that had no ill effects and 8 non-smoking dogs, two of whom got tumours. This would indicate smoking as protective or harmless. Or, we could have 8 dogs of each camp neither of whom had any ill effect. The point here is that by changing the numbers the results vary massively, and the mere presence of tumours in the non-smoking group surely indicates that at least some of the tumours in the smoking group were caused by something other than tobacco. (pg 269-275 1971 report). Also, the 1982 Report says, on page 185, that “However, this observation has not been repeated so far (137).”

I think it’s suspicious too, because no doubt the researchers were aware that it should be more equal and could have had 60% smoking dogs, 40% non-smoking dogs. But with over 80 smoking dogs and less than 10 non-smoking, it’s hard to really call it worthy of praise. But, nonetheless, why give this one precedence over the myriad of other animal studies that failed? How can it be if this was such a gold standard, case-closed undeniable study that it has not been held up in court to prove that smoking has caused lung cancer in animals? From the McTear court case:

‘Mr McEachran said that Professor Idle was a witness who had had tobacco funding for research. His report concentrated on the biological and carcinogenesis studies which had so far failed to show how lung cancer developed. Researchers had failed to produce squamous cell carcinoma in laboratory animals exposed to cigarette smoke. No constituent or group of constituents as they existed in cigarette smoke had been shown to be a cause of lung cancer.’

‘Mr McEachran said that Dr Cohen was another witness who did not know whether smoking killed. He concluded that laboratory studies using whole cigarette smoke had not produced squamous cell carcinoma of the lung in experimental animals.’

‘He [Dr Cohen] also concluded that laboratory studies using whole cigarette smoke had not produced squamous cell carcinoma of the lung in experimental animals.’

‘Professor Idle was well qualified to express a view on whether smoking had been established as a cause of lung cancer. He noted repeatedly the limited understanding that science had of the mechanisms of cancer and the causation of the disease. He described the various theories of cancer causation and noted how theories that were once considered highly credible had been discarded at times, then revived. He described the inability of laboratory experiments to produce lung cancer in animals exposed to cigarette smoke, and the similar failure, despite long-standing efforts, to identify what ingredient or ingredients in cigarette smoke might be responsible for the development of lung cancer.’

‘Both Professor Idle and Dr Cohen gave evidence that laboratory studies had not produced lung cancer in animals exposed to cigarette smoke. What was interesting, counsel submitted, was not just that squamous cell carcinoma had not been induced in the lungs of laboratory animals, but that great care had been taken to create experiments which would produce positive results.’

(As an interesting bit of information in keeping with the debate, from the same case: ‘Professor Idle looked at the question of complex mixtures, and whether any ingredient had been identified as a cause of lung cancer, and concluded that it had not. He finally concluded that, in his judgment, cigarette smoking had not been established as a cause of human lung cancer and indeed the cause of cancer was unknown. Dr Cohen gave evidence that the majority of chemicals that had been shown to develop tumours in animals had been reported to show an increased risk in humans, and he could think of no examples where the human data were in conflict with the animal data. This rather underlined an expectation that when animal experiments were being carried out, they might produce a result to confirm that cigarette smoking could cause lung cancer. Dr Cohen gave evidence that studies had been carried out on animals in whom it had been demonstrated that cancer could be induced within their lifespan. Professor Platz gave evidence that it was not possible to distinguish between a smoker and a non-smoker, or indeed an individual with any other exposure that might be associated with lung cancer, on examination of pathological material.’)

So yes, we can discuss Auerbach all day long and Chris, feel free to tout it as the unshakable proof all you want. But everyone else is able to see the massive shortcomings and the absence of lung cancer. And, if it were as wonderful and conclusive as you are convinced then none of the above excerpts would exist.

“Stress is the perfect excuse for the critics because it can’t be measured very reliably, it’s vague in meaning and whatever effect it has on health is impossible to quantify”

I will simply paste a reply from the comments for this: ‘Does this therefore mean that it should be discounted? Research into the effects of stress are in their infancy and, as Chris says, it is hard to measure accurately. But studies do seem to be increasingly showing that again, whilst not in and of itself a hard-and-fast cause of many illnesses, it would seem to be a contributory factor. Probably not dissimilar to smoking itself ……’

“Rich tries to have his cake and eat it by suggesting that stress causes lung cancer (“Who’s to say that the cancer was not caused by post-operative complications? Or indeed the stress.”) while insisting that he’s not putting forward an alternative explanation (“I didn’t assert the real cause was stress”) because it would be ripped to shreds”

Chris, stop pretending to be a psychic or a psychologist. You’re an intelligent man so stop acting dumb. Let me clarify though: “Who’s to say that the cancer was not caused by post-operative complications? Or indeed the stress” those were postulates, food for thought, potential possibilities. Not alternative explanations – I am providing no alternative explanations because I have no evidence. But remember something, evidence only comes after something is already a fact. I don’t think a hypothesis on stress would at all be ripped to shreds, and such a silly claim suggests you know very little about the effects long term and chronic stress can have on the body.

“And we know that the percentage of nonsmokers who get lung cancer is much, much lower.”

Ah but we don’t. We know the figures show that, but we also know that misclassification and detection bias very much exist and, as Frank so wonderfully demonstrated, have a massive effect on the actual figures. And, anyway, if we run with your comment there, it still isn’t proof. It’s suggestive, yes. But look, smokers around the world know the purported health effects of smoking, and it’s known most smokers don’t have the greatest health – for most people, if you’re willing to engage in something you are pretty sure will kill you, the rest of your health isn’t top priority either. About 77% of cancer occurs in non-smokers, so they get quite a lot of it. Beyond misclassification and detection bias we have other things to consider – my nan, for example, had secondary bone cancer but they never located the primary site, I doubt that was a one-off occurrence. As I have stated previously, it would be very interesting to be provided data on primary/secondary cancer in smokers.

““No biological evidence exists, whatsoever, and animals studied have failed.”

Both these statements are, quite simply, lies, and transparent ones at that, considering Rich has just admitted that at least one animal study succeeded.”

I think you’ll find the above court case quotes quite adequate that neither are lies or transparent. I don’t remember admitting any animal study succeeded either.

“Rich complains that graphs showing cigarette consumption against lung cancer don’t “take into account such facts as, for instance, US tobacco being more radiaoctive than foreign tobacco, which should be explored.” He has since admitted that there is no evidence for this claim and the source he gave me is comically inept.”

Did I admit there’s no evidence for it? And, again, let me paste an earlier comment of mine just to dispel your lies that I’m backtracking: ‘I don’t actually think the Polonium does cause cancer (which i probably should have specified), for reasons I deal with in my book. It was just something else i’m throwing out there as stuff that simply hasn’t been looked at in smoking studies, when really, something as huge as that premise should look at as many avenues as possible.’

Frank also mentioned he had heard about high-phosphate fertilisers being used at one point, and it is precisely in this high-phosphate fertilisers that extra polonium would come from.

“So let me be more explicit: Very few women smoked until the 1920s and very few women got lung cancer. By the 1970s, very many women were smoking and very many women were getting lung cancer.”

From Frank’s ‘misclassification error’ entry is this comment from HarleyRider: “For some unknown reason, never smokers who get lung cancer are more likely to be female.” 

So if never smokers with lung cancer are more likely to be female, and more female smokers are getting lung cancer, doesn’t that demonstrate other factors coming to play? Your premise only really works Chris if the smokers get the disease and non-smokers don’t.

“On the wacky idea that the chemicals and toxins in cigarettes “are tiny, less than we inhale in normal air”, I pointed out that all of Rich’s examples involved secondhand smoke, not directly inhaled smoke.

My figures were how much a cigarette contains, yes. Higher, yes, but how much?

It varies greatly depending on the chemical, but 1,000 times higher is the frequently given estimate. Whatever the dilution, it is completely fatuous to equate secondhand smoke with directly inhaled smoke.”

I wasn’t comparing SHS to active smoking. My figures were how much a cigarette contained or produces. And you’ll forgive me for not immediately swallowing the ‘estimate’ i’m sure, given everyone here knows what ‘estimate’ means in tobacco control.

“You’re confusing acute health problems with chronic health problems. CO converts haemoglobin to carboxyhaemoglobin. This is not great in the short-term but can be very bad in the long-term as it starves your organs of oxygen and leads to chronic disease.”

Right, but you keep repeatedly missing the point of dosage. For instance, how many cigarettes does it take over what timeframe to develop chronic disease from the carbon monoxide? How long would it take for the oxygen levels and haemoglobin to return to normal? Such questions are important here. It’s like saying ‘smoking causes cancer’ and the latest SG statement that even one puff can kill. Context, dosage, timeframe.

“A massive straw man, there. My point was—and I think this is crystal clear as it was the point of the whole post—that all studies have flaws and we must decide whether the flaws are big enough to invalidate the study’s finding. Since the flaws raised by the defence are petty issues like ‘they didn’t have enough control dogs’ and ‘my mate smoked 105 cigarettes but he calls himself a nonsmoker’, the answer in this case is no.”

If those are the only flaws you think we’ve found I guess you haven’t been doing much reading here. I think most of us here are able to acknowledge that Frank’s recent graphs and other findings in the comments destroy the hospital study, just for starters.

“Show me one person who says ‘eating causes heart disease’.”

Really? The findings of a high-fat or generally poor diet contributing to heart disease hasn’t reached you yet? My actual point there was that we know some foods can lead to heart problems, but other foods can help prevent, so how can we be confident that all tobacco causes lung cancer and not, perhaps, certain brands? Or tobacco cured in certain ways?

“Which would surely suggest the cigarettes are responsible in your argument, correct? In which case, the aforementioned resistance isn’t quite so prominent as is being made out.

See what he did there? I said that Asian people had a resistance to lung cancer and he responded as if I said Asian people were immune from lung cancer. Even though I’d already corrected him on this in a previous post. Would you like a light for your straw man, Rich?”

Even though I dealt with this in the comments, it’s just an outright display of dishonesty I want to mention it again. Anyone, besides you apparently Chris, can see I have not said that in that excerpt at all. ‘The very quote of mine you used says ‘resistance’ and no mention of ‘immune’. It says, and you copied it, ‘resistance isn’t quite so prominent as is being made out’.’

“Because if it was less than 98% then there were a disproportionately large number of smokers in hospital, which ‘anti-smoking fanatics’ like me would suggest is evidence that smoking isn’t too good for you. And since 99.7% of lung cancer patients were smokers, we’d need 99.7% of Londoners to be smokers for there not to be a positive association when measured against the general population.”

Not necessarily. The percentage of a population of a whole city needs to be mirrored in a hospital sample to show it one way or the other? Nonsense. I think you’ll find the original point made on this was simply that with such a vast majority of Londoners being smokers, it is not surprising to find a huge percentage of smokers in hospital.

“Rich, that’s because you’re a young lad who started smoking a few years ago. The people dying of lung cancer in the hospital were not. And, yes, smoking habits do change and that’s why Doll and Hill asked for the average amount smoked over 20 years. As I said in the post, a bit of inaccuracy here or there on this sort of question really is a trivial issue.”

I’ll agree with this, most older people do tend to keep the same smoking habits (within a range, say ’20-25’ a day rather than a flat 23).

“No, God, don’t repeat things. I read it. Just give me a source for your claim that the study didn’t take note of smoking status and explain what you mean about comparing people in their 30s to people in their 80s.”

If you read it, then this excerpt would be perfectly clear: ‘What we do know is that during the time period of twenty-two months there was a total of 11,612, which is a figure much lower than the overall death rate for white males. The Surgeon General acknowledged this and claimed that the participants in the survey were considerably healthier than the average person.’

I didn’t say the study didn’t take note of smoking status, I said the Report doesn’t inform us how many of the participants were smokers and non-smokers. The age range was 35-89 and the results appear to talk only of total deaths, total incidence etc, with age only being mentioned with this: ‘For cigarette smokers, the studies show that the mortality ratio declines with increasing age, being higher for men aged 40-50 than for men over 70. This effect is illustrated in Table 6 from the study of men in 25 states,’

There are some other interesting things mentioned in the ’64 Report:

‘The studies of men in nine states and men in 25 States, for instance, suffer from the difficulties that the populations studied are hard to define, that the smokers and non-smokers were recruited by a large number of volunteer workers, and that completeness in the reporting of deaths was hard to achieve, since this depends on reports from the volunteers.’

‘In all studies the death rates for non-smokers are markedly below those of U.S. white males in 1960. Even the smokers of one pack of cigarettes or more daily have death rates that average slightly below the U.S. white male figure. To some extent this is to be expected, since hospitalized and other seriously ill persons are not recruited in such studies. The sizes of the differences appear, however, surprising for the studies with United States populations. Hammond and Horn (lo), in a special investigation on this question, concluded that the discrepancy in their study was due to the screening out of sick persons in recruiting plus probably a selection towards men of higher economic levels.’

‘So far as interpretation of results is concerned, the discrepancy raises two points. It is clear that the seven prospective studies involve populations which are healthier than U.S. males as a whole. Secondly, the low death rates for non-smokers suggest the possibility that the studies recruited unusually healthy groups of non-smokers.’

Ultimately, I think we’re lost as to where this debate is. It started with Chris telling Frank he was wrong smoking doesn’t cause lung cancer and a debate should ensue. It has, and it’s been interesting. But where do we go from here? For a lot of people, the debate could end with ‘1 in 10 heavy smokers get lung cancer, i call that a factor not a cause’. Has the ‘cause’ debate concluded and we just looking at incidence of smoking and lung cancer rates, or are we just analysing the smoking studies? Either suits me, I’m just curious about the direction.