CATCH-17

Rich White again

This is likely to be my last post, for the time being at least. The next few weeks are going to be extremely hectic for me and I won’t have time to submit any more posts, except possibly the occasional comment. Although if Frank is putting this on hiatus over Christmas then it won’t matter anyway.

This debate has become somewhat circular, with continued discussion on the merits of epidemiology and the relevance of animal studies. From the looks of it, we’re never going to get anywhere if we continue with this. Some of the most interesting discussions and points have been raised by Frank’s deterring from the main body of points and putting forth different theories, like actual dosage from cigarettes smoked etc. With that in mind, I am taking a slightly different path with this post and will be looking beyond the correlations and statistics and into areas that are new for CATCH and hopefully readers will find it interesting.

Smoking is a funny topic. Even the most rational, level-headed and sceptical person can suddenly turn into something of a wreck with emotions running high. While we can question the evidence of such about anything – even if it just serves to reinforce the belief it perpetuates – with smoking, challenging the evidence makes us crazy, denialists, cranks; we’re ignored, ridiculed, met with derision – by apparently people on our own side.

But what is the basis for all this? It’s flimsy indeed. Chris bases his entire faith on the smoking/cancer premise on the statistics. It’s interesting to note than despite tobacco being so intensively studied for over 60 years, all we still have is statistics. To some, that isn’t a problem. To others, it’s a big red flag. Statistically, we could show a dose-dependent relationship between almost anything. People with headaches will take paracetamol, and the worse/more frequent the headaches, the more paracetamol they take. Statistically then, paracetamol causes headaches. Or respiration equipment is linked with difficulty breathing, in a dose-dependent way (the worse the breathing, the more respiration equipment), and so statistically respiration equipment causes difficulty breathing.

Of course, causation is always linked with correlation, but the opposite isn’t true at all, and as shown above, correlation alone can be hugely misleading. The soft science of epidemiology and statistics provide clues for hard science to investigate. The hard science would be animal studies and randomized clinical trials. The latter cannot really be done in smoking studies because it would be deemed unethical to make people start smoking (although intervention trials have been conducted, with underwhelming results for the investigators – look for Whitehall and MRFIT), but the former has been done.

So what do we find from animal studies? In addition to the fact that tobacco smoke has not induced lung cancer in any animal (Chris still refutes this, but we’ll stick to the legal and medical professionals who quite readily admit they failed. And of course, if the animals were dying from smoke, they would never have needed to use the F344 rats and A/J mice, genetically bred to develop vast amounts of tumours), there are a great many study where smoke-exposed animals outlived the non-smoking ones, whose maximum lifespans were actually increased, and in other studies where animals exposed to radon or radioactive particules all died, those exposed to tobacco smoke had a massively decreased mortality rate. In a critique of the 1982 SG Report we are told various things about animal studies.

“Chronic Inhalation of Cigarette Smoke by F344 Rats”: ‘smoke exposure did not change the total number of tumor-bearing animals relative to controls; however exposed rats had significantly fewer tumors in the hyphphyses, hematopietic-lymphoid systems, 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 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 cancer’ [For those who missed it, I explained in a comment in CATCH-14 how one plausible explanation for this is that nicotine stimulates vascular growth, i.e. rich blood supply in the lungs and aerodigestive tract. Cancer can, and will, migrate to the site that will benefit it most. This would mean smokers do get more lung cancer, but no more actual cancer than had they not smoked – the cancer just moves to the lungs. I then said it would be interesting to see the percentage of primary and secondary lung cancers in smokers.)

“A.P. Wenner et al”

‘The results show that the highest number of tumors occurred in the untreated control rats. The next highest number of tumors occurred in rats subjected to sham smoking, i.e. rats which were placed in the smoking machine without smoke exposure, and the lowest number of tumors occurred in the smoke-exposed rats…The bottom line of this research is that again, in spite of tremendous efforts and millions of dollars of expenditures, all efforts have failed to induce tumors having any resemblance to human tumors, by exposing animals to cigarette smoke.’

The notorious Nightlight posted in a forum:

“The most interesting tidbit though, buried deep in the dogs experiments section (experiments by Cross et al, 1982), at the end of a sentence (p. 555), are the results of combined effects of radon (via uranium dusts) inhalation and tobacco smoke. While the radon alone had no problems in inducing lung cancers in dogs (or any other animals), the combined effect of tobacco smoke and radon resulted in significant protection against lung cancers in smoking dogs — while the nonsmoking dogs exposed to radon had 37% incidence of lung tumors, the smoking dogs exposed to radon had only 5% lung tumor incidence (from the original Cross et al. 1982 paper, p. 48):

“Results of this experiment indicate that cigarette-smoke exposure, under the conditions of the experiment, had a mitigating effect of radon-daughter induced respiratory tract cancer in dogs… This difference is significant (p=0.03 Fischer’s Exact test).”

(source)

Further still:

“Inhalation Studies with Syrian Golden Hamsters”

‘The authors confirmed their previous data of experiments financed by the National Cancer Institute, of a “significantly longer lifespan of the smoke exposed hamsters”, as compared to non-smoking hamsters.


(The increased lifespan of animals became so common, and clearly problematic to the researchers, that animals were ‘terminated’ before they died naturally. This solved the little indiscrepancy.)

Bear in mind that in all these studies, the researchers tried very hard to cause cancer, exposing them to so much smoke that they were borderline asphyxiated (the researchers called it Maximum Dosage Tolerance, MDT), and yet they still couldn’t get the desired result. These animals sometimes smoked more than is humanly possible for us to smoke without vomiting, and they still outlived the non-smoking animals.

So if animals aren’t dying from smoke, and are outliving the non-smoking animals, why are we dying from smoke? We’re either the only single living animal to die from smoking (albeit after 50 or 60 years of doing it, which to many is rather peculiar, myself included), or we’ve made an error somewhere along the way. After 60 years, we have no biological evidence of how smoking causes cancer (Chris stated the animal studies are biological evidence, momentarily forgetting the animal studies have failed in inducing lung cancer in animals.) Given that the world’s oldest people were all smokers, and Dr Denson found that smokers who eat well and exercise outlive non-smokers, it does warrant investigation.

We’ve already discussed the initial epidemiology (which Doll conducted while under the pay of an asbestos company, and subsequent studies didn’t advance much on, as Fisher noted they were just repetition. Chris produced the Kaiser report in CATCH 14, a study which took account of absolutely no confounders. Chris said it didn’t matter as they wouldn’t have any effect on the results!), so what else do we know? In his study Comparative Epidemiology of Cancer Between the United States and Japan, Wynder stated the Japanese smoked less than the Americans. Chris has said the researchers of the 1950s were honest. But really? Wynder said: “The age adjusted mortality rates for laryngeal cancer during 1955 are higher in US White[s] than in the Japanese. These differences can be partially explained by the higher levels of cigarette and alcohol consumption in the US” even though his own tables demonstrated the Japanese smoked more. And if the research in the ‘50s was really objective and not affected by bias, why was smoking singled out and not looked at collectively with other factors? The very fact that Doll and Hill decided to straight away look at tobacco usage shows an element of bias. It’s odd that Chris thinks researchers were more honest then, because his own book is a demonstration of how far back negative attitudes towards tobacco go.

So what’s causing the deaths in smokers? It’s easy to say smoking is killing them, but this is too simplified. If tobacco is really ‘unique’ and such a huge killer, we would expect more deaths. Chris asserts 10% is a big risk, and perhaps in risk terms it is; but in real terms, a 90% chance of not getting ill is pretty good. If I had a 90% chance of winning the lottery, i’d play it. One of Chris’s champion reasons for accepting smoking=cancer is the statistics of females. Yet Chris also argues that different races are less likely to get lung cancer, so who’s to say women simply don’t have more resistance than men? Or, going back to the quote above about total cancer being constant but cancers of varying organs changing in regularity, perhaps women have the same total cancer as they did previously but more in the lungs. In which case, it could be explained by my aforementioned theory on cancer migrating i.e. secondary cancer. Let’s not forget, breast cancer affects men as well as women, but the rates are very low in men while seemingly increasing in women. There’s a strong statistical correlation between wearing a bra and developing breast cancer. But then again, maybe women have less lung cancer because they have more breast cancer – and their lung cancer rates are caused by secondary cancer, migrating to the lungs.

The negative placebo, or ‘nocebo’ effect, is very real with much research conducted into it. Nightlight posted on a forum the following:

There was a study in Heidelberg, described by Professor Eysenck in Psychological Reports (1989) in which 528 men were asked whether they, as smokers, were convinced that they would be very likely to develop lung cancer, heart disease, or other ‘smoking related diseases’. The 72 who answered ‘yes’, while admitting that their views were taken from information in the media, had an almost three times higher death rate at the end of 13 years than those who were not so influenced.

Fear can kill. This has been known since disease was first studied. We are entitled to wonder how many people have been killed more by the fear of ‘smoking related diseases’ than by any actual disease itself.

This is relevant nowadays, but what of disease in the 1950s when people weren’t worried about smoking? The self medication hypothesis could go some way to explaining it. We know smokers smoke for various reasons, and people note that it wakes them up in the morning, perks them up when they’re tired, suppresses hunger, and various other things. And yet fatigue is just one sign of various diseases, so how can we know that people don’t have an underlying or developing disease and smoke more to mask the symptoms? Indeed, this would perfectly correlate with the dose-dependency shown in the statistics of ‘the more you smoke the more you die’. Certainly none of Chris’s beloved epidemiology looks into it. The fact is, the epidemiology simply makes no attempt to learn why people smoke. There is a lot of research into the possibility that people are genetically predisposed to want to smoke, and independently develop lung cancer also. Does the epidemiology consider this? No, it doesn’t. If true, we realise that the smoking is just a correlation – the people have alleles in certain genes that predispose them to lung cancer regardless, but the fact they smoke confuses the results. I have repeatedly made the point that as more non-smokers and never smokers are now seemingly getting cancer than before, in lieu of the fact there are simply more non/never smokers now than ever before, it is entirely possible that the same overall rates exist but before they were in smokers and so hidden under ‘smoking related deaths’. This theory perfectly correlates with the above studies.

Back to self-medication, there is some validation of this in schizophrenia sufferers, as over 90% of them smoke and smoking helps alleviate the symptoms. Statistically, smoking could be shown to cause schizophrenia, but in reality the victims use smoking to help them – just like paracetamol and headaches. There is a lot of research into self-medication and it isn’t a crackpot theory designed to make us feel better about our filthy habit.

Nicotine is just one of many compounds of tobacco smoke; we are aware of the MAO B inhibitors in the smoke, which we can use to ‘self medicate’ to feel happier for instance. But what of physical ailments? Smoking has anti-inflammatory effects too, so we can ‘self medicate’ for various other problems. There’s more too, and I will quote again from Nightlight:

Specifically, some still unknown components of tobacco smoke upregulate substantially the key internal antioxidants and detox enzymes (glutathione [or more recent ref cf. Fig 4, p. L1076], catalase and SOD, all nearly doubled). These (families of) enzymes are responsible for neutralizing and excreting virtually every environmental or industraial toxin and carcinogen we are exposed to (WIKI: glutathione, SOD, catalase).

I stated some time ago about people smoking for different reasons and used the single example of stress. Dr Ian Dunbar spent much of his career looking at psychopharmacology and noticed the effects stress or insecurity can have on physical wellbeing. He explained it quite succinctly for this debate, but this brief quote is by no means exhaustive of the whole issue:

I am afraid that all the statistics about tobacco are worthless because they omit a common variable from their compilation.

I have gone on before about the importance of the mind. It is still generally dismissed by those who profess to be scientists as a figment of the imagination and ignored. However, it must be regarded as a physical entity with its own physiology and biochemistry like the kidneys or lungs.

Had scientists been more scientific they would be able to confirm that the mind is linked to the body by three hormone/neurotransmitter systems. The chemistry of those systems varies according to whether the individual sees itself as being secure in the environment or insecure in the environment.

That perception can be physical, intellectual or emotional and the security or insecurity acute or chronic.

If the individual is chronically insecure, physically, intellectually or emotionally then the body can become poisoned by the associated biochemistry just as cirrhosis of the liver is caused by chronic consumption of alcohol. I would submit that it is that poisoning that lies at the root not only of cancer but of ageing and of illness generally. People who are chronically insecure seek respite with sedative activities such as food, drink, drugs and sex all of which can be hazardous to health.

They also tend to smoke tobacco and inhale it deeply but that is a trivial side issue distracting people from facing up to the real problem.

So where does that take us? I’m not sure Chris realises the existence of psychopharmacology, but it is very real and recognised (stress produces cortisol for instance, while other ‘psychological’ distress causes a surge in adrenaline, and so on. Before Chris turns this into accusing me of making the claim that adrenaline is causing cancer, I’m really just making a couple of brief examples of the very real existence of ‘psychopharmacology’). Chris asked for some other reasons why smokers get more disease than non-smokers, and these are just a few very real, plausible, possible and recognised suggestions. Beyond that, what could it be? Why was there a surge in lung cancer in the 1930s? I already explained about advanced diagnostic tools that became used in the 1930s which caused an immediate surge in LC – the surge itself wasn’t real in terms of cases, but those now correctly diagnosed showed an increase. But around the 1880s, a case of lung cancer was found and it caused a stir in the medical community because it was believed they would never see it again. What does this mean? People were smoking long before this, the first cigarette maker was patented in 1881, and the first cigarette shop opened in, I believe, 1860 (correct date mentioned in an earlier CATCH, but it was around this time). So we know people were smoking, we know lung cancer existed but apparently not particularly common, even making allowances for misdiagnosis to consumption and TB, and we know this changed in the 20th century. Is it very likely that tobacco suddenly became dangerous? Not really. To go back to Nightlight once again, he briefly explains the inherent problems with secular graphs, but the second paragraph he gives some possible explanations for the rise in LC:

The secular trends are by far the weakest and the lowest resolution tool, among already low-res statistical methods on self-selected subjects, for reconstructing the complex graphs of causes and effects leading to diseases. They lump up far too many factors, quantified in extremely coarse grained, fuzzy paramatrizations or largely ignored altogether, to get close to even pretending to resolve between the models (a), (b) or ©. There are so many other secular trends going up or down at every scale, intertwined in myriad ways, that to pin anything on anything is a pure act of faith. It’s fine if one looks at it as a heuristic, providing coarse grained hints for subsequent use of more precise epidemiological tools, which in turn will provide hints for hard science to actually resolve the complex cause-effect graphs.

Regarding smoking & LC, how do you account for and adjust for the effect of nuclear fallouts, which also rose rapidly with atmospheric nuclear tests in early 1950s, coinciding in time and often in space, with rapid rise in lung cancers and melanomas (lungs & skin are the frontline interface of our bodies to the external air). Or simultaneous rise in EMF pollution, especially in high frequency ranges (whose quanta energies increasingly overlap in spectrum with the sectra of cellular biochemical processes)? Or trends in traffic pollution, fuel & engines trends,…? Or about myriad of other environmental, nutritional, medical, social,… trends, be it known, unknown, unquantified or unquantifiable, unfolding all in parallel on the same populations? It just can’t be done through such coarse grained methods. At most you can honestly get out of it is a hunch about a rough domain where to look for a better hint (e.g. using case control epidemiological studies), before focusing the finer tools of hard science to actually resolve between the alternative models (a), (b) or ©.

Interjecting this trail, Chris says that Asians have a resistance to lung cancer than westerners don’t have and thus have lower lung cancer rates. Perhaps that’s true, let’s run with it. Japan has the top life expectancy in the world right now, which depends on more than lung cancer. Chris asserted that lung cancer isn’t higher in smokers because of emphysema and heart disease carrying them off beforehand. So are we now to accept than Asians have resistance to all smoking related diseases, allowing them to puff away and still have the top life expectancy? The USA ranks a lowly 36 in the list despite having low smoking rates in terms of its own population, and the UK sits at number 20, while France and Spain, heavy smokers without the lung cancer resistance, are above us. In fact the Spanish smoke far, far more than nearby Portugal, share similar diets and culture, and outlive the Portuguese by some margin. You’d think really that if smoking was wiping them out in their droves, that would seriously hamper the life expectancy of these countries.

So basically, we have: the fact that statistics are misleading; the fact that epidemiology cannot prove anything and has missed (intentionally or accidentally) confounding factors and made no attempt to look at why people smoke; psychopharmacology providing some insight into reasons why people smoke and the effect these underlying reasons can have on physical health; scientific studies showing that some people have a genetic code that prompts them to smoke, and independently causes them to have lung cancer later in life; and a self-medication hypothesis that fits perfectly with the statistics, fits perfectly with other ‘medication/illness’ statistics, has a multitude of studies and is backed up by the rest of this paragraph.

At the end of the day, only epidemiology and statistics exist to link smoking to cancer. And when you only have epidemiology and statistics, you’re asking for trouble. If, after 60 years of intensive research, nothing of more substance exists, you’re asking for trouble. Especially when there are theories and evidence that explain away those statistics.

About Frank Davis

smoker
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183 Responses to CATCH-17

  1. richwhite09 says:

    To clarify before Chris pounces, when I mentioned Doll and asbestos I meant the general period, not the Hospital’s study, which I didn’t explain clearly by saying ‘the initial epidemiology’.

  2. richwhite09 says:

    To clarify before Chris pounces, when I mentioned Doll and asbestos I meant the general period, not the Hospital’s study, which I didn’t explain clearly by saying ‘the initial epidemiology’.

  3. richwhite09 says:

    Links missing
    The quote from Nightlight should had links:
    Specifically, some still unknown components of tobacco smoke upregulate substantially the key internal antioxidants and detox enzymes(glutathione [1] [or more recent ref [2] cf. Fig 4, p. L1076], catalase and SOD [3], all nearly doubled). These (families of) enzymes are responsible for neutralizing and excreting virtually every environmental or industraial toxin and carcinogen we are exposed to (WIKI: glutathione[4], SOD[5]. catalase[6]).
    [1] http://jap.physiology.org/content/63/1/152.citation?ijkey=3ea8cff64c6d72a42e1d4ef7cf9f6fd2485e5921&keytype2=tf_ipsecsha
    [2] http://ajplung.physiology.org/content/277/6/L1067.abstract
    [3] http://www.ncbi.nlm.nih.gov/pubmed/2310098?dopt=Citation
    [4] http://en.wikipedia.org/wiki/Gluthathione
    [5] http://en.wikipedia.org/wiki/Superoxide_dismutase
    [6] http://en.wikipedia.org/wiki/Catalase

  4. richwhite09 says:

    Links missing
    The quote from Nightlight should had links:
    Specifically, some still unknown components of tobacco smoke upregulate substantially the key internal antioxidants and detox enzymes(glutathione [1] [or more recent ref [2] cf. Fig 4, p. L1076], catalase and SOD [3], all nearly doubled). These (families of) enzymes are responsible for neutralizing and excreting virtually every environmental or industraial toxin and carcinogen we are exposed to (WIKI: glutathione[4], SOD[5]. catalase[6]).
    [1] http://jap.physiology.org/content/63/1/152.citation?ijkey=3ea8cff64c6d72a42e1d4ef7cf9f6fd2485e5921&keytype2=tf_ipsecsha
    [2] http://ajplung.physiology.org/content/277/6/L1067.abstract
    [3] http://www.ncbi.nlm.nih.gov/pubmed/2310098?dopt=Citation
    [4] http://en.wikipedia.org/wiki/Gluthathione
    [5] http://en.wikipedia.org/wiki/Superoxide_dismutase
    [6] http://en.wikipedia.org/wiki/Catalase

  5. cjsnowdon says:

    Chris has said the researchers of the 1950s were honest. But really? Wynder said: “The age adjusted mortality rates for laryngeal cancer during 1955 are higher in US White[s] than in the Japanese. These differences can be partially explained by the higher levels of cigarette and alcohol consumption in the US” even though his own tables demonstrated the Japanese smoked more.
    Er, no. Figure 1 of that study shows that Americans consumed more than 3 times as many cigarettes than the Japanese in 1950 and consistently smoked more cigarettes throughout the whole period of the study (1920-1985). And Figure 4 shows that Americans drunk more alcohol, which is also a major risk factor for laryngeal. So who’s being ‘dishonest’ here?

  6. cjsnowdon says:

    Chris has said the researchers of the 1950s were honest. But really? Wynder said: “The age adjusted mortality rates for laryngeal cancer during 1955 are higher in US White[s] than in the Japanese. These differences can be partially explained by the higher levels of cigarette and alcohol consumption in the US” even though his own tables demonstrated the Japanese smoked more.
    Er, no. Figure 1 of that study shows that Americans consumed more than 3 times as many cigarettes than the Japanese in 1950 and consistently smoked more cigarettes throughout the whole period of the study (1920-1985). And Figure 4 shows that Americans drunk more alcohol, which is also a major risk factor for laryngeal. So who’s being ‘dishonest’ here?

    • richwhite09 says:

      Can we keep this one amicable Chris? No need for snide remarks or accusations.
      Figure 1 is cigarettes consumed in a graph. Table 1 gives the data on smokers per country and shows far more smokers in Japan than the USA.
      The graph also has no adjustment for the sexes of either country, which has an effect because the lower rates of female smokers in Japan brings the overall rate down thus purporting Japan as having a lower smoking rate, whereas an adjustment would have corrected this.

      • cjsnowdon says:

        So what’s dishonest about Wynder saying that cigarette consumption was higher in America?

        • richwhite09 says:

          Besides what i said above, he didn’t consider something. He told us that cigarette consumption dropped to a third of the rate during the war as it was before the war. Yet if we look in International Smoking Statistics, which provdies Japan’s annual cigarette consumption for each year from 1920-1990, we are told that the Japanese switched from premade cigarette to roll-ups. In 1941 the Japanese smoked 71,158 million cigarettes (premade and roll ups combined), and the rate remained constant until 1944. It dropped until 1950 to 64,280m and in 1950 rose to 75,138m. So the dip was much smaller than the touted one third, and only for a 5 year period.

        • richwhite09 says:

          “It dropped until 1950 to 64,280m and in 1950 rose to 75,138m”
          To clarify, that should read “it dropped and remained constant until 1950”, in case it’s misinterpreted as dropping constantly until 1950.

      • richwhite09 says:

        (while we’re talking about researcher honesty in the ’50s, you can also see that while we are told smoking rates are looked at in the USA with no mention of ethnic demographic, the lung cancer death rates (LCDRs) only looked at caucasians, omitting African-Americans and American-Indians. This cut out quite a section of the population, and they give no reason. Although it isn’t hard to assume that it’s because it would’ve ‘bodged’ the results up a bit. So they looked at smoking rates of the populations of both countries, and the LCDRs of Japan as a nation, but selected which ethnic group to look at the LCDRs for in the USA.

        • cjsnowdon says:

          Answer the question.

        • richwhite09 says:

          “Answer the question”
          LOL! “hello, pot? Yeah, it’s kettle. you’re black”
          And i answered the question after posting the one you just replied to.

        • cjsnowdon says:

          I’ll try again. Assuming you understand the difference between smoking prevalence and cigarette consumption, what’s dishonest about Wynder saying that cigarette consumption was higher in America?

        • richwhite09 says:

          Graph 1 that you referenced shows higher consumption in America, because of what it’s told to show. The discrepancy is between the sexes, as shown in Figure 2 where we can see the Japanese males outsmoke the American males, but the Japanese women smoke less than the American women. The graph doesn’t take this into account, if it did, it would look different.
          And if you read the post above, you’d see i said about Wynder saying that Japanese smoking rates dropped to one third of the rate they were before the war. In actual fact, the Japanese just switched the types of cigarettes they smoked and Wynder didn’t consider this. There was a dip of a few years, but only by 7million, before rising to 4million higher to what it was previously (71-64-75). So the consumption of the Japanese in Wynder’s study is wrong, which in turn affects the graph.
          I don’t have time to post anymore tonight, I may have time to post a bit tomorrow depending how the day pans out, i’ve already said a few days ago that my time is getting short now. But regardless, i’m not prepared to discuss the epidemiology endlessly, I stated at the start of this CATCH entry that it isn’t getting us anywhere. Even if we continue this discussion on Wynder and neither of us budge (or even if, for argument’s sake, i do), it makes no difference to the overall debate because all we’re left with is another epidemiological statistical link. The whole purpose of this entry was to move beyond that.

        • richwhite09 says:

          To save you scrolling up, i said in paragraph 2:
          “This debate has become somewhat circular, with continued discussion on the merits of epidemiology and the relevance of animal studies. From the looks of it, we’re never going to get anywhere if we continue with this… With that in mind, I am taking a slightly different path with this post and will be looking beyond the correlations and statistics and into areas that are new for CATCH”
          Hence my statement above that i’m not prepared to discuss the epidemiology endlessly.

      • richwhite09 says:

        To add to this point about the graph not accounting for the sexes, Figure 2 shows the Japanese males smoking more cigarettes than US males, and Japanese women smoking less than American women. The discrepancy is not accounted for in the graph.

  7. Frank Davis says:

    Re: Links missing
    Whoops! Corrected now.
    The links were embedded, and dropped out when I copied the text from your email to the Livejournal edit window.
    Frank

  8. richwhite09 says:

    Re: Links missing
    I thought so, not to worry.

  9. richwhite09 says:

    Can we keep this one amicable Chris? No need for snide remarks or accusations.
    Figure 1 is cigarettes consumed in a graph. Table 1 gives the data on smokers per country and shows far more smokers in Japan than the USA.
    The graph also has no adjustment for the sexes of either country, which has an effect because the lower rates of female smokers in Japan brings the overall rate down thus purporting Japan as having a lower smoking rate, whereas an adjustment would have corrected this.

  10. cjsnowdon says:

    So what’s dishonest about Wynder saying that cigarette consumption was higher in America?

  11. richwhite09 says:

    (while we’re talking about researcher honesty in the ’50s, you can also see that while we are told smoking rates are looked at in the USA with no mention of ethnic demographic, the lung cancer death rates (LCDRs) only looked at caucasians, omitting African-Americans and American-Indians. This cut out quite a section of the population, and they give no reason. Although it isn’t hard to assume that it’s because it would’ve ‘bodged’ the results up a bit. So they looked at smoking rates of the populations of both countries, and the LCDRs of Japan as a nation, but selected which ethnic group to look at the LCDRs for in the USA.

  12. richwhite09 says:

    Besides what i said above, he didn’t consider something. He told us that cigarette consumption dropped to a third of the rate during the war as it was before the war. Yet if we look in International Smoking Statistics, which provdies Japan’s annual cigarette consumption for each year from 1920-1990, we are told that the Japanese switched from premade cigarette to roll-ups. In 1941 the Japanese smoked 71,158 million cigarettes (premade and roll ups combined), and the rate remained constant until 1944. It dropped until 1950 to 64,280m and in 1950 rose to 75,138m. So the dip was much smaller than the touted one third, and only for a 5 year period.

  13. cjsnowdon says:

    Answer the question.

  14. richwhite09 says:

    “Answer the question”
    LOL! “hello, pot? Yeah, it’s kettle. you’re black”
    And i answered the question after posting the one you just replied to.

  15. richwhite09 says:

    To add to this point about the graph not accounting for the sexes, Figure 2 shows the Japanese males smoking more cigarettes than US males, and Japanese women smoking less than American women. The discrepancy is not accounted for in the graph.

  16. cjsnowdon says:

    I’ll try again. Assuming you understand the difference between smoking prevalence and cigarette consumption, what’s dishonest about Wynder saying that cigarette consumption was higher in America?

  17. richwhite09 says:

    Graph 1 that you referenced shows higher consumption in America, because of what it’s told to show. The discrepancy is between the sexes, as shown in Figure 2 where we can see the Japanese males outsmoke the American males, but the Japanese women smoke less than the American women. The graph doesn’t take this into account, if it did, it would look different.
    And if you read the post above, you’d see i said about Wynder saying that Japanese smoking rates dropped to one third of the rate they were before the war. In actual fact, the Japanese just switched the types of cigarettes they smoked and Wynder didn’t consider this. There was a dip of a few years, but only by 7million, before rising to 4million higher to what it was previously (71-64-75). So the consumption of the Japanese in Wynder’s study is wrong, which in turn affects the graph.
    I don’t have time to post anymore tonight, I may have time to post a bit tomorrow depending how the day pans out, i’ve already said a few days ago that my time is getting short now. But regardless, i’m not prepared to discuss the epidemiology endlessly, I stated at the start of this CATCH entry that it isn’t getting us anywhere. Even if we continue this discussion on Wynder and neither of us budge (or even if, for argument’s sake, i do), it makes no difference to the overall debate because all we’re left with is another epidemiological statistical link. The whole purpose of this entry was to move beyond that.

  18. richwhite09 says:

    “It dropped until 1950 to 64,280m and in 1950 rose to 75,138m”
    To clarify, that should read “it dropped and remained constant until 1950”, in case it’s misinterpreted as dropping constantly until 1950.

  19. richwhite09 says:

    To save you scrolling up, i said in paragraph 2:
    “This debate has become somewhat circular, with continued discussion on the merits of epidemiology and the relevance of animal studies. From the looks of it, we’re never going to get anywhere if we continue with this… With that in mind, I am taking a slightly different path with this post and will be looking beyond the correlations and statistics and into areas that are new for CATCH”
    Hence my statement above that i’m not prepared to discuss the epidemiology endlessly.

  20. cjsnowdon says:

    We’re not talking about the epidemiology. We’re talking about the integrity of individuals. You’re claiming the people who discovered the smoking-lung cancer link were dishonest or compromised. That’s a serious claim and if you’re going to denigrate well-respected scientists like Wynder you need to be able to defend that claim.
    So far you’ve said that Richard Doll was in the pay of the asbestos industry when he made the smoking-lung cancer discovery. That’s not true. Now you use this study by Wynder to suggest that he is lying when he says that cigarette consumption was lower in Japan than America in 1950. But it was lower – much lower – in America, and that fits perfectly with what he says about laryngeal cancer.
    Whether cigarette consumption in Japan was 64,280m or 75,138m (and you’re right that it was even lower in 1945), it was much less than in the US. Wynder’s graph is not wrong. You’re wrong, because you’re assuming all the Japanese smokers smoked cigarettes. But Wynder makes it quite clear what was going on: “Cigarette smoking did not become popular in Japan until approximately 10 years after World War II, whereas mass production and consumption of cigarettes occurred in the US several decades earlier.”
    (He also says: “As predicted, rapid acceleration in mortality rates due to cancers of the lung and oropharynx have recently been observed in the heavy smoking male population in Japan”, which is entirely compatible with cigarette smoking causing lung cancer.)
    So, I’ll ask again, why was it dishonest of Wynder to say that cigarette consumption was higher in America than in Japan?

  21. cjsnowdon says:

    We’re not talking about the epidemiology. We’re talking about the integrity of individuals. You’re claiming the people who discovered the smoking-lung cancer link were dishonest or compromised. That’s a serious claim and if you’re going to denigrate well-respected scientists like Wynder you need to be able to defend that claim.
    So far you’ve said that Richard Doll was in the pay of the asbestos industry when he made the smoking-lung cancer discovery. That’s not true. Now you use this study by Wynder to suggest that he is lying when he says that cigarette consumption was lower in Japan than America in 1950. But it was lower – much lower – in America, and that fits perfectly with what he says about laryngeal cancer.
    Whether cigarette consumption in Japan was 64,280m or 75,138m (and you’re right that it was even lower in 1945), it was much less than in the US. Wynder’s graph is not wrong. You’re wrong, because you’re assuming all the Japanese smokers smoked cigarettes. But Wynder makes it quite clear what was going on: “Cigarette smoking did not become popular in Japan until approximately 10 years after World War II, whereas mass production and consumption of cigarettes occurred in the US several decades earlier.”
    (He also says: “As predicted, rapid acceleration in mortality rates due to cancers of the lung and oropharynx have recently been observed in the heavy smoking male population in Japan”, which is entirely compatible with cigarette smoking causing lung cancer.)
    So, I’ll ask again, why was it dishonest of Wynder to say that cigarette consumption was higher in America than in Japan?

    • richwhite09 says:

      This is my last post on this, whether you reply or not.
      “he says that cigarette consumption was lower in Japan than America in 1950. But it was lower – much lower – in America”
      I’ll assume you made a mistake here?
      “You’re wrong, because you’re assuming all the Japanese smokers smoked cigarettes.”
      No, i’m not. I’m looking at the consumption of cigarettes, not the consumption of tobacco (what on earth made you think i was doing that?)
      Let’s drop the honesty thing, you’re getting hung up on it. Let’s just say maybe the researchers were wrong in the 50s. I did say much earlier that just because something is honest doesn’t mean it’s right or valid. So let’s forget the terminology.
      “why was it dishonest of Wynder to say that cigarette consumption was higher in America than in Japan?”
      I’ve answered this more than once. Figure 2 shows the Japanese males smoke more cigarettes than the American males. The American women smoke more cigarettes than the Japanese women. Table 1 one shows Japanese have a higher amount of smokers, and Figure 2 shows they have a higher consumption also.
      And just to really nail it home for you, Wynder said:
      “[lung cancer rates are] higher in US White men than in Japanese men which is discrepant with the higher prevalence of cigarette smoking among Japanese males for the same period of time.”
      Now let’s drop this and move on.

  22. Anonymous says:

    Thanks Rich — nice post.
    FYI — I am a PhD health statistician, 25 years experience analyzing stats such as these, (not related to tobacco) and I basically agree with you.
    Chris – I’m not even going to go look at Table 2 (the subject of the last group of comments) for myself — because IT DOESN”T MATTER. The point is, (for me) — Well, for the sake of argument, let’s concede the epidemiology. Let’s just say that some (many, most, all…) studies have found that people who smoke are more likely to be the people who get LC (which is THE LIMIT to what even the very best health stats could possibly tell you). Okay fine — let’s move on to animal studies (which might tell us something more). (You can forget the randomized trials of smoking cessation, because as Rich pointed out — they (MRFIT, Whitehall) do tend to backfire on the anti-smoking position.)
    I know Chris refused to read Nightlight’s argument (apprently because Nightlight began his discussion with pics of older smokers — for shame!) — Too bad Chris – because Nightlight has a very good way of presenting evidence in an easy to follow manner. I’ve asked him before if I could quote some of his arguments – and he hs given permission — so here goes. If Chris won’t go to the mountain — we’ll have to bring the mountain to Chris.
    From Nightlight:
    “As I reread the experimental papers I realized this phenomenon was always there right in front of me, it was noticed and studied by researchers, including the potential treatments (with none other than those same ‘scary’ tobacco smoke components, which we are told in the other story, before quitting, cause lung cancers), but the very carefully worded, circumspect descriptions had made it invisible to a reader unaware of its existence from some other source. The exemplary in this regard is masterfully weasel-worded recent review of animal experiments by the leading authority in the field, Dr. S.S. Hecht:
    “Carcinogenicity studies of inhaled cigarette smoke in laboratory animals: old and new”
    S.S. Hecht, Carcinogenesis 2005 26(9):1488
    [p.1489]…The animals were exposed for 5 months, then allowed a 4 month recovery period…. The increases in tumor multiplicity were generally small, from ~1 tumor per mouse to ~2.8, following exposure to 50-170 mg/m3 of total suspended particulates. The increase in tumor multiplicity observed in this model was due to a component of the gas phase of tobacco smoke….The 4-month recovery period is absolutely necessary for observation of increased lung tumor multiplicity, but the reason for this is not clear.
    [p.1492] Note added in proof: A recent study (W. Stinn et al. 2005) indicated that the recovery period in the A/J mouse smoke inhalation model is necessary to overcome stress induced inhibition of lung tumorigenesis, and that the lack of weight gain during the smoke inhalation period was unrelated to the final tumor multiplicity.
    Well, there it is — increased lung tumors were observed (in A/J mice, a specially bred cancer-mice which gets lung tumors spontaneously), attributed of course to inhalation of tobacco smoke, but somehow, for the smoking to “cause” these lung tumors, the mice has to quit smoking, then it has go through the perversely named “recovery period” (non-smoking) of similar duration as previous smoking, and only then “smoking” will somehow cause increase in tumors. But had they continued smoking instead of ostensibly “recovering” from the ravages of smoking, smoking would not have caused increase in tumors (and it would have even extended their lifespan well beyond that of the non-smoking mice). Orwell was an amateur for these newspeak magicians.
    (continued)

  23. Anonymous says:

    Thanks Rich — nice post.
    FYI — I am a PhD health statistician, 25 years experience analyzing stats such as these, (not related to tobacco) and I basically agree with you.
    Chris – I’m not even going to go look at Table 2 (the subject of the last group of comments) for myself — because IT DOESN”T MATTER. The point is, (for me) — Well, for the sake of argument, let’s concede the epidemiology. Let’s just say that some (many, most, all…) studies have found that people who smoke are more likely to be the people who get LC (which is THE LIMIT to what even the very best health stats could possibly tell you). Okay fine — let’s move on to animal studies (which might tell us something more). (You can forget the randomized trials of smoking cessation, because as Rich pointed out — they (MRFIT, Whitehall) do tend to backfire on the anti-smoking position.)
    I know Chris refused to read Nightlight’s argument (apprently because Nightlight began his discussion with pics of older smokers — for shame!) — Too bad Chris – because Nightlight has a very good way of presenting evidence in an easy to follow manner. I’ve asked him before if I could quote some of his arguments – and he hs given permission — so here goes. If Chris won’t go to the mountain — we’ll have to bring the mountain to Chris.
    From Nightlight:
    “As I reread the experimental papers I realized this phenomenon was always there right in front of me, it was noticed and studied by researchers, including the potential treatments (with none other than those same ‘scary’ tobacco smoke components, which we are told in the other story, before quitting, cause lung cancers), but the very carefully worded, circumspect descriptions had made it invisible to a reader unaware of its existence from some other source. The exemplary in this regard is masterfully weasel-worded recent review of animal experiments by the leading authority in the field, Dr. S.S. Hecht:
    “Carcinogenicity studies of inhaled cigarette smoke in laboratory animals: old and new”
    S.S. Hecht, Carcinogenesis 2005 26(9):1488
    [p.1489]…The animals were exposed for 5 months, then allowed a 4 month recovery period…. The increases in tumor multiplicity were generally small, from ~1 tumor per mouse to ~2.8, following exposure to 50-170 mg/m3 of total suspended particulates. The increase in tumor multiplicity observed in this model was due to a component of the gas phase of tobacco smoke….The 4-month recovery period is absolutely necessary for observation of increased lung tumor multiplicity, but the reason for this is not clear.
    [p.1492] Note added in proof: A recent study (W. Stinn et al. 2005) indicated that the recovery period in the A/J mouse smoke inhalation model is necessary to overcome stress induced inhibition of lung tumorigenesis, and that the lack of weight gain during the smoke inhalation period was unrelated to the final tumor multiplicity.
    Well, there it is — increased lung tumors were observed (in A/J mice, a specially bred cancer-mice which gets lung tumors spontaneously), attributed of course to inhalation of tobacco smoke, but somehow, for the smoking to “cause” these lung tumors, the mice has to quit smoking, then it has go through the perversely named “recovery period” (non-smoking) of similar duration as previous smoking, and only then “smoking” will somehow cause increase in tumors. But had they continued smoking instead of ostensibly “recovering” from the ravages of smoking, smoking would not have caused increase in tumors (and it would have even extended their lifespan well beyond that of the non-smoking mice). Orwell was an amateur for these newspeak magicians.
    (continued)

  24. Anonymous says:

    (Mightlight continues)
    “What an excruciatingly round about way of saying plainly — quitting smoking will trigger any latent tumors (that smoking had kept suppressed). But since this is antismoking “science” which provides the “scientific” pretext for hounding and extorting countless millions of human smokers, to force them to quit, Dr. S.S. Hecht simply cannot say it that way. And of curse, as a matter of routine, researchers terminate these experiments (kill mice) safely before the expiration of their natural life-expectancy (otherwise they would have to watch out for the wrath from the vengeful ancient gods of prairies that endowed us this medicinal miracle plant — the life-extending effects of tobacco smoking).
    Another experimental paper (G.M. Curtin et al, 2004) explains the “recovery period” somewhat more bluntly:
    [p. 26] Demonstration of increased tumor formation required that the standardized 20-week exposure period be followed by a 16-week recovery period, during which mice were provided filtered air. Bogen and Witschi (2002) provided justification for the recovery period; more specifically, it was suggested that tobacco smoke exposure suppresses the growth of premalignant foci, and that smoke induced lung tumor risk occurs predominantly via a genotoxic mechanism. Consequently, the recovery period allows tobacco smoke-induced genetic damage to progress to tumors.
    We should also recall that this scheme also relies on vascular effects of nicotine to demonstrate “carcinogenicity” of tobacco smoke in mice susceptible to lung tumors or in mice seeded with tumors in the beginning of the experiment (they observe rates of growth and misattribute vascular effect to ‘genetic damage’, which obviously contradicts the fact that extending smoking somehow cancels the effects of the alleged genotoxic damage from smoking during the first half of the experiment). What they are in fact fighting with “recovery period” is the tumor suppressive effects of tobacco smoke (explicitly demonstrated in that [Stinn 2005] experiment), that are overriding the vascular effect on the growth in A/J mice. The recovery period simply removes the carcinogenic protection by tobacco smoke leaving the vascular effect to help the existent tumors (caused by injected seed or from genetically bred traits) in the respiratory system grow faster.
    (continued)

  25. Anonymous says:

    (Mightlight continues)
    “What an excruciatingly round about way of saying plainly — quitting smoking will trigger any latent tumors (that smoking had kept suppressed). But since this is antismoking “science” which provides the “scientific” pretext for hounding and extorting countless millions of human smokers, to force them to quit, Dr. S.S. Hecht simply cannot say it that way. And of curse, as a matter of routine, researchers terminate these experiments (kill mice) safely before the expiration of their natural life-expectancy (otherwise they would have to watch out for the wrath from the vengeful ancient gods of prairies that endowed us this medicinal miracle plant — the life-extending effects of tobacco smoking).
    Another experimental paper (G.M. Curtin et al, 2004) explains the “recovery period” somewhat more bluntly:
    [p. 26] Demonstration of increased tumor formation required that the standardized 20-week exposure period be followed by a 16-week recovery period, during which mice were provided filtered air. Bogen and Witschi (2002) provided justification for the recovery period; more specifically, it was suggested that tobacco smoke exposure suppresses the growth of premalignant foci, and that smoke induced lung tumor risk occurs predominantly via a genotoxic mechanism. Consequently, the recovery period allows tobacco smoke-induced genetic damage to progress to tumors.
    We should also recall that this scheme also relies on vascular effects of nicotine to demonstrate “carcinogenicity” of tobacco smoke in mice susceptible to lung tumors or in mice seeded with tumors in the beginning of the experiment (they observe rates of growth and misattribute vascular effect to ‘genetic damage’, which obviously contradicts the fact that extending smoking somehow cancels the effects of the alleged genotoxic damage from smoking during the first half of the experiment). What they are in fact fighting with “recovery period” is the tumor suppressive effects of tobacco smoke (explicitly demonstrated in that [Stinn 2005] experiment), that are overriding the vascular effect on the growth in A/J mice. The recovery period simply removes the carcinogenic protection by tobacco smoke leaving the vascular effect to help the existent tumors (caused by injected seed or from genetically bred traits) in the respiratory system grow faster.
    (continued)

  26. Anonymous says:

    Nightlight continues)
    “So, what is the lesson for humans(smokers and non-smokers) from all this? The basic fact established in animal experiments is that lifelong tobacco smoking will extend lifespan, regardless of genetic predisposition to cancers or carcinogenic exposures. If someone is genetically predisposed to cancers or is exposed to real carcinogens, tobacco smoke will still be protective throughout (e.g. via nearly doubled detox rates as well via the mechanisms mentioned in Indian paper at the top), as the experiment with dogs inhaling radon clearly demonstrated (similarly in other hamster, mice, rat experiments with co-exposures). The vascular effect (better angiogenesis in the lungs, which is normally quite beneficial, such as for physical laborers, athletes, soldiers or the 101 year marathon runners) implies that if a cancer eventually gets started despite the protective effects of tobacco smoke, depending on its location it may grow ‘potentially faster’ (in respiratory system) or always slower (elsewhere, since the protection still exists, it’s just not strong enough, while vascular effect is absent or much smaller). Regarding the case of ‘potentially faster’ growth for respiratory cancers, the net effect again depends on the precise balance between the ongoing protective effects and the vascular effect, which now amplifies the cancer growth rate (but it helps amplify protective tobacco effects, too). Hence, it is the same kind of battle as elsewhere in the body (where protective effects of TS battle the growth of cancer), except that in the respiratory system, both sides are amplified by the vascular effect. So the net result in the respiratory system is down to the same kind of balance as elsewhere.
    The case of someone quitting smoking removes the protective effects of tobacco smoke, while leaving the vascular effect (the extra blood vessels and higher circulation remain) to help the cancer, whenever its natural onset begins (from genetic or environmental causes). That is the worst possible combination, worse than had he never-smoked, in which case the vascular effect in the lungs would have been absent. On the other hand, a lifelong smoker is always better off than had he never started smoking. He will live longer and age better than had he not started, regardless of when the cancers are set to start in his case. As the cancer-mice/rat experiments show, even in the cases of the extremely strong propensity to cancers (including in lungs), the net protective effect is beneficial — smoking mice/rats still outlive the nonsmoking ones (despite the experiments & exposures being optimized to go the other way; human smoker optimizes the exposure in opposite direction than antismoking scientists did for the test animals).”
    *******
    Okay — done with Nightlight and back to me —
    Something else I wanted to mention. Doll pointed out early on that smokers tend to consume more sugar, which he attributed to greater consumption of hot drinks, and then dismissed as unimportant (I don’t have the ref handy but can provide on request). Also — WRT to the DOLL study, I’ve always wondered whether, if the purpose of the study was known, if the smoking doctors tended to get chest X-rays more than the non-smoking (not so important, just something I’ve wondered).
    A final thought. The connection between nicotine and niacin, as well as the apparent chemo-protective effects of substances related to the B vitamin family (niacin, myo-inositol for example) — make me suspicious that LC may be related to various B vitamin deficiencies. Might be intersting to compare LC rates to patterns of grain refining and fortification. — (But all in all, I’m sure the issue is very complex and not likely to be solved with the simple statistical tools we apply these days.)
    GDF

  27. Anonymous says:

    Nightlight continues)
    “So, what is the lesson for humans(smokers and non-smokers) from all this? The basic fact established in animal experiments is that lifelong tobacco smoking will extend lifespan, regardless of genetic predisposition to cancers or carcinogenic exposures. If someone is genetically predisposed to cancers or is exposed to real carcinogens, tobacco smoke will still be protective throughout (e.g. via nearly doubled detox rates as well via the mechanisms mentioned in Indian paper at the top), as the experiment with dogs inhaling radon clearly demonstrated (similarly in other hamster, mice, rat experiments with co-exposures). The vascular effect (better angiogenesis in the lungs, which is normally quite beneficial, such as for physical laborers, athletes, soldiers or the 101 year marathon runners) implies that if a cancer eventually gets started despite the protective effects of tobacco smoke, depending on its location it may grow ‘potentially faster’ (in respiratory system) or always slower (elsewhere, since the protection still exists, it’s just not strong enough, while vascular effect is absent or much smaller). Regarding the case of ‘potentially faster’ growth for respiratory cancers, the net effect again depends on the precise balance between the ongoing protective effects and the vascular effect, which now amplifies the cancer growth rate (but it helps amplify protective tobacco effects, too). Hence, it is the same kind of battle as elsewhere in the body (where protective effects of TS battle the growth of cancer), except that in the respiratory system, both sides are amplified by the vascular effect. So the net result in the respiratory system is down to the same kind of balance as elsewhere.
    The case of someone quitting smoking removes the protective effects of tobacco smoke, while leaving the vascular effect (the extra blood vessels and higher circulation remain) to help the cancer, whenever its natural onset begins (from genetic or environmental causes). That is the worst possible combination, worse than had he never-smoked, in which case the vascular effect in the lungs would have been absent. On the other hand, a lifelong smoker is always better off than had he never started smoking. He will live longer and age better than had he not started, regardless of when the cancers are set to start in his case. As the cancer-mice/rat experiments show, even in the cases of the extremely strong propensity to cancers (including in lungs), the net protective effect is beneficial — smoking mice/rats still outlive the nonsmoking ones (despite the experiments & exposures being optimized to go the other way; human smoker optimizes the exposure in opposite direction than antismoking scientists did for the test animals).”
    *******
    Okay — done with Nightlight and back to me —
    Something else I wanted to mention. Doll pointed out early on that smokers tend to consume more sugar, which he attributed to greater consumption of hot drinks, and then dismissed as unimportant (I don’t have the ref handy but can provide on request). Also — WRT to the DOLL study, I’ve always wondered whether, if the purpose of the study was known, if the smoking doctors tended to get chest X-rays more than the non-smoking (not so important, just something I’ve wondered).
    A final thought. The connection between nicotine and niacin, as well as the apparent chemo-protective effects of substances related to the B vitamin family (niacin, myo-inositol for example) — make me suspicious that LC may be related to various B vitamin deficiencies. Might be intersting to compare LC rates to patterns of grain refining and fortification. — (But all in all, I’m sure the issue is very complex and not likely to be solved with the simple statistical tools we apply these days.)
    GDF

  28. Anonymous says:

    Okay — one more thing.
    I mentioned the sugar and hot drinks connection (as well as the B vitamins) because my own suspicion is that people who smoke may be craving something(s) due to a genetic(?) lack. We’ve all lost the ability to synthesize vitamin C (humans- along with some primates, fruit bats and guinea pigs) — perhaps some of us have the ability to synthesize other vitamins or substances to varying degrees and some of us do not. This seems to me to be consistent with a self-medication theory of smoking, also consistent with some recent research on “smoker’s genes” and if the “medication” was less than %100 effective, would be consistent with your epidemiology as well Chris(i.e., differences in internal bio-chemistry being the missing strong confounder(s) that hasn’t even been looked for) .
    Hope that clarifies why I presented all of that.

  29. Anonymous says:

    Okay — one more thing.
    I mentioned the sugar and hot drinks connection (as well as the B vitamins) because my own suspicion is that people who smoke may be craving something(s) due to a genetic(?) lack. We’ve all lost the ability to synthesize vitamin C (humans- along with some primates, fruit bats and guinea pigs) — perhaps some of us have the ability to synthesize other vitamins or substances to varying degrees and some of us do not. This seems to me to be consistent with a self-medication theory of smoking, also consistent with some recent research on “smoker’s genes” and if the “medication” was less than %100 effective, would be consistent with your epidemiology as well Chris(i.e., differences in internal bio-chemistry being the missing strong confounder(s) that hasn’t even been looked for) .
    Hope that clarifies why I presented all of that.

    • richwhite09 says:

      Thanks for the comments GDF, much appreciated.
      What Nightlight points out about the animal’s ‘recovery period’ is also in keeping with the observed effect in humans, as pointed out by Rose numerous times in this debate, that the odds of lung cancer appear to increase in ex-smokers with a seeming surge in the immediate 18-month follow-up period of smoking cessation.
      Thanks for the input and detailed points. This post was intended to move the debate beyond epidemiology and look into other possibilities that could call into doubt the reliability of the statistics while still maintaining the statistical link. I maintained that no matter how strong the epidemiology is, it’s still only suggestive, and my paracetamol/headaches example should have served to highlight this. Whereas many will be content with the correlation, I think in order to truly know what’s going on and make a balanced decision on how convincing it is, we must extend the scope and look elsewhere – sort of a large scale cross reference – to see if the link remains strong from each angle.

    • richwhite09 says:

      “if the “medication” was less than %100 effective, would be consistent with your epidemiology as well Chris(i.e., differences in internal bio-chemistry being the missing strong confounder(s) that hasn’t even been looked for) . ”
      I was pondering over something along these lines yesterday. Basically my thought processes were that while smoking is linked to increased LC, it’s still a small minority of 10% who develop the disease (so ‘statistically’, smoking is linked more with not dying than it is with dying :o ) but more than that, if we accept smoking causes lung cancer, why in so few people? I’m not saying it can’t be the cause just because relatively few people suffer from it, but in real terms, if it’s so carcinogenic, why is it so low? The self medication theory fills in the gaps here, as does the suggestion of a genetic need to smoke. To bring it round to your own comment, if certain individuals are lacking certain things from their biochemistry, that could be the real indicator of their later developing LC. That they also happen to smoke (coincidentally or to try to rectify their deficiency) would simply mask the real cause, while simultaenously providing all this ‘solid’ statistically correlations that Chris is providing.
      Of course, you already know this as you’ve said it. I’m just putting my own thoughts on the matter.

    • Anonymous says:

      “The connection between nicotine and niacin, as well as the apparent chemo-protective effects of substances related to the B vitamin family (niacin, myo-inositol for example) — make me suspicious that LC may be related to various B vitamin deficiencies. Might be interesting to compare LC rates to patterns of grain refining and fortification.”
      GDF
      My thoughts have been running along the same lines.
      Pellagra
      “Early neurological symptoms associated with pellagra include anxiety, depression, and fatigue; later symptoms include apathy, headache, dizziness, irritability and tremors.”

      Click to access pellagra_prevention_control.pdf


      “The only certain method used by early pellagrologists was to give their patients in the mental hospitals small amounts of nicotinic acid. If they recovered they diagnosed them pellagra, if they did not they diagnosed them schizophrenia”
      http://www.doctoryourself.com/hoffer_niacin.html
      Even though Doctor Goldberger proved that pellagra was a vitamin deficiency, many of the doctors still clung on to the germ theory.
      “Although many scientific colleagues sang Goldberger’s praises, even mentioning a Nobel nomination, others still doubted. In the pages of the Journal of the American Medical Association, critic W.J. MacNeal challenged the results. One Birmingham physician referred to the experiment as “half-baked.” Still others thought the whole experiment a fraud.”
      http://history.nih.gov/exhibits/goldberger/docs/pellegra_5.htm
      Medicine: The Nation’s Food
      Monday, Jun. 09, 1941
      “A necessary vitamin is B—a group of at least half a dozen different chemicals. Most radio listeners, said Vice President Wallace last week, know B as the “oomph vitamin, that puts the sparkle in your eye, the spring in your step, the zip in your soul!” Vitamin B is found abundantly in whole wheat and coarse grains, is appreciably reduced in the milling process, when the rough coat is “scalped”‘ from wheat kernel.
      Most of the big flour mills and bakers have recently agreed to put vitamin B1; nicotinic acid and iron back into their flour and bread. But experts last week pointed out that such “enriched bread,” although a step forward, was not the ideal solution of the problem.”
      http://www.time.com/time/magazine/article/0,9171,795342,00.html
      Hot drinks
      Basic Chemical Reactions Occurring in the Roasting Process
      “The best cup characteristic are produced when the ratio of the degradation of trigonelline to the derivation of Nicotinic Acid remains linear. The control model of this reaction ratio is a time/temperature/energy relationship. The environment temperature (ET) establishes the pyrolysis region for the desired chemical reactions while the energy value (BTU) and system transfer efficiency (STE) determines the rate of reaction propagation and linearity of Nicotinic Acid derivation to degradation of trigonelline”
      http://www.sweetmarias.com/roast.carlstaub.html
      ” Niacin is formed during the roasting process, and coffee can contain 10-40mg of niacin per 100 g, depending on the extent of roasting, thus making a significant contribution to average intakes of niacin”
      http://www.answers.com/topic/coffee
      Incidentally
      “A laboratory study by the Institute of Food Research found modified pectin releases a molecular fragment that curbs all stages of cancer progression”
      “Pectin supplements that claim to detoxify the body and protect against cancer are already sold on the internet, and a laboratory study published in the journal Glycobiology last year showed pectin can slow the growth of prostate cancer.”
      Scientists at the University of Georgia in the US found when prostate cancer cells were exposed to pectin powder or heat-treated citrus pectin, up to 40 per cent died.
      The cells were made to “commit suicide” through a natural process called apoptosis that halts the creation of tumours.
      Other studies on rats and cell cultures suggest pectin also fights lung and colon cancers”
      http://www.telegraph.co.uk/health/3183821/Jam-can-curb-cancer-say-food-scientists.html
      Characteristics of tobacco pectin
      http://legacy.library.ucsf.edu/action/document/page?tid=ngp65d00
      The more I look, the more amazing things I find, and the more it all begins to make sense.
      Rose

      • richwhite09 says:

        The part about B vitamins in the milling process is interesting and reinforces the social classes point, because the poorer classes pay less attention to their diet and consume more refined flour products (bread and pasta).
        “But experts last week pointed out that such “enriched bread,” although a step forward, was not the ideal solution of the problem.”
        This is true too. Adding something in manually makes the body less able to assimilate it properly, which is why ‘omega-3 enriched’ food products are a waste of time. When we add something, it’s standalone. When it’s found there naturally, it’s a harmonious effect and the compounds and nutrients of one part react with another, making it more potent or easily assimilated by the body. I bring this up because it ties in with a point i made before about using tobacco condensate to induce skin cancer – it’s a standalone product, and doesn’t take into account the effect the rest of the compounds in smoke on the isolated one.
        “The more I look, the more amazing things I find, and the more it all begins to make sense.”
        Yep

    • Anonymous says:

      Most vitamins are not synthesised by the human body, we depend on dietary uptake, so a lot points to diet.
      The biochemistry of the human body and it’s variation in individuals is something which needs to be looked at. Some hormones e.g. cortisol, varies greatly in a space of 24 hrs; others (e.g. Thyroid hormones) depend on positive/negative feedbacks; and so on.
      Then we have individuals affected by chronic conditions e.g. diabetics, which have altered biochemical processes. And so on.
      Molecular biology provides great tools to investigate and manipulate DNA but it is only a small part of the full picture.

  30. richwhite09 says:

    Thanks for the comments GDF, much appreciated.
    What Nightlight points out about the animal’s ‘recovery period’ is also in keeping with the observed effect in humans, as pointed out by Rose numerous times in this debate, that the odds of lung cancer appear to increase in ex-smokers with a seeming surge in the immediate 18-month follow-up period of smoking cessation.
    Thanks for the input and detailed points. This post was intended to move the debate beyond epidemiology and look into other possibilities that could call into doubt the reliability of the statistics while still maintaining the statistical link. I maintained that no matter how strong the epidemiology is, it’s still only suggestive, and my paracetamol/headaches example should have served to highlight this. Whereas many will be content with the correlation, I think in order to truly know what’s going on and make a balanced decision on how convincing it is, we must extend the scope and look elsewhere – sort of a large scale cross reference – to see if the link remains strong from each angle.

  31. richwhite09 says:

    “if the “medication” was less than %100 effective, would be consistent with your epidemiology as well Chris(i.e., differences in internal bio-chemistry being the missing strong confounder(s) that hasn’t even been looked for) . ”
    I was pondering over something along these lines yesterday. Basically my thought processes were that while smoking is linked to increased LC, it’s still a small minority of 10% who develop the disease (so ‘statistically’, smoking is linked more with not dying than it is with dying :o ) but more than that, if we accept smoking causes lung cancer, why in so few people? I’m not saying it can’t be the cause just because relatively few people suffer from it, but in real terms, if it’s so carcinogenic, why is it so low? The self medication theory fills in the gaps here, as does the suggestion of a genetic need to smoke. To bring it round to your own comment, if certain individuals are lacking certain things from their biochemistry, that could be the real indicator of their later developing LC. That they also happen to smoke (coincidentally or to try to rectify their deficiency) would simply mask the real cause, while simultaenously providing all this ‘solid’ statistically correlations that Chris is providing.
    Of course, you already know this as you’ve said it. I’m just putting my own thoughts on the matter.

  32. Anonymous says:

    “The connection between nicotine and niacin, as well as the apparent chemo-protective effects of substances related to the B vitamin family (niacin, myo-inositol for example) — make me suspicious that LC may be related to various B vitamin deficiencies. Might be interesting to compare LC rates to patterns of grain refining and fortification.”
    GDF
    My thoughts have been running along the same lines.
    Pellagra
    “Early neurological symptoms associated with pellagra include anxiety, depression, and fatigue; later symptoms include apathy, headache, dizziness, irritability and tremors.”

    Click to access pellagra_prevention_control.pdf


    “The only certain method used by early pellagrologists was to give their patients in the mental hospitals small amounts of nicotinic acid. If they recovered they diagnosed them pellagra, if they did not they diagnosed them schizophrenia”
    http://www.doctoryourself.com/hoffer_niacin.html
    Even though Doctor Goldberger proved that pellagra was a vitamin deficiency, many of the doctors still clung on to the germ theory.
    “Although many scientific colleagues sang Goldberger’s praises, even mentioning a Nobel nomination, others still doubted. In the pages of the Journal of the American Medical Association, critic W.J. MacNeal challenged the results. One Birmingham physician referred to the experiment as “half-baked.” Still others thought the whole experiment a fraud.”
    http://history.nih.gov/exhibits/goldberger/docs/pellegra_5.htm
    Medicine: The Nation’s Food
    Monday, Jun. 09, 1941
    “A necessary vitamin is B—a group of at least half a dozen different chemicals. Most radio listeners, said Vice President Wallace last week, know B as the “oomph vitamin, that puts the sparkle in your eye, the spring in your step, the zip in your soul!” Vitamin B is found abundantly in whole wheat and coarse grains, is appreciably reduced in the milling process, when the rough coat is “scalped”‘ from wheat kernel.
    Most of the big flour mills and bakers have recently agreed to put vitamin B1; nicotinic acid and iron back into their flour and bread. But experts last week pointed out that such “enriched bread,” although a step forward, was not the ideal solution of the problem.”
    http://www.time.com/time/magazine/article/0,9171,795342,00.html
    Hot drinks
    Basic Chemical Reactions Occurring in the Roasting Process
    “The best cup characteristic are produced when the ratio of the degradation of trigonelline to the derivation of Nicotinic Acid remains linear. The control model of this reaction ratio is a time/temperature/energy relationship. The environment temperature (ET) establishes the pyrolysis region for the desired chemical reactions while the energy value (BTU) and system transfer efficiency (STE) determines the rate of reaction propagation and linearity of Nicotinic Acid derivation to degradation of trigonelline”
    http://www.sweetmarias.com/roast.carlstaub.html
    ” Niacin is formed during the roasting process, and coffee can contain 10-40mg of niacin per 100 g, depending on the extent of roasting, thus making a significant contribution to average intakes of niacin”
    http://www.answers.com/topic/coffee
    Incidentally
    “A laboratory study by the Institute of Food Research found modified pectin releases a molecular fragment that curbs all stages of cancer progression”
    “Pectin supplements that claim to detoxify the body and protect against cancer are already sold on the internet, and a laboratory study published in the journal Glycobiology last year showed pectin can slow the growth of prostate cancer.”
    Scientists at the University of Georgia in the US found when prostate cancer cells were exposed to pectin powder or heat-treated citrus pectin, up to 40 per cent died.
    The cells were made to “commit suicide” through a natural process called apoptosis that halts the creation of tumours.
    Other studies on rats and cell cultures suggest pectin also fights lung and colon cancers”
    http://www.telegraph.co.uk/health/3183821/Jam-can-curb-cancer-say-food-scientists.html
    Characteristics of tobacco pectin
    http://legacy.library.ucsf.edu/action/document/page?tid=ngp65d00
    The more I look, the more amazing things I find, and the more it all begins to make sense.
    Rose

  33. richwhite09 says:

    The part about B vitamins in the milling process is interesting and reinforces the social classes point, because the poorer classes pay less attention to their diet and consume more refined flour products (bread and pasta).
    “But experts last week pointed out that such “enriched bread,” although a step forward, was not the ideal solution of the problem.”
    This is true too. Adding something in manually makes the body less able to assimilate it properly, which is why ‘omega-3 enriched’ food products are a waste of time. When we add something, it’s standalone. When it’s found there naturally, it’s a harmonious effect and the compounds and nutrients of one part react with another, making it more potent or easily assimilated by the body. I bring this up because it ties in with a point i made before about using tobacco condensate to induce skin cancer – it’s a standalone product, and doesn’t take into account the effect the rest of the compounds in smoke on the isolated one.
    “The more I look, the more amazing things I find, and the more it all begins to make sense.”
    Yep

  34. richwhite09 says:

    This is my last post on this, whether you reply or not.
    “he says that cigarette consumption was lower in Japan than America in 1950. But it was lower – much lower – in America”
    I’ll assume you made a mistake here?
    “You’re wrong, because you’re assuming all the Japanese smokers smoked cigarettes.”
    No, i’m not. I’m looking at the consumption of cigarettes, not the consumption of tobacco (what on earth made you think i was doing that?)
    Let’s drop the honesty thing, you’re getting hung up on it. Let’s just say maybe the researchers were wrong in the 50s. I did say much earlier that just because something is honest doesn’t mean it’s right or valid. So let’s forget the terminology.
    “why was it dishonest of Wynder to say that cigarette consumption was higher in America than in Japan?”
    I’ve answered this more than once. Figure 2 shows the Japanese males smoke more cigarettes than the American males. The American women smoke more cigarettes than the Japanese women. Table 1 one shows Japanese have a higher amount of smokers, and Figure 2 shows they have a higher consumption also.
    And just to really nail it home for you, Wynder said:
    “[lung cancer rates are] higher in US White men than in Japanese men which is discrepant with the higher prevalence of cigarette smoking among Japanese males for the same period of time.”
    Now let’s drop this and move on.

  35. Anonymous says:

    Because some people are being forced to give up smoking, I’ve been trying to find the exact part of the smoke that works the magic, so they can substitute where possible.
    Some are rather tricky because no alternative yet exists.
    Ulcerative Colitis
    “Compared with those who had never smoked, current smokers were much less likely to have ulcerative colitis (odds ratio 0.13, 95% CI 0.05 to 0.3 – that is they were about eight times less likely to have ulcerative colitis. Former smokers’ risk was no different from non-smokers.”
    http://www.medicine.ox.ac.uk/bandolier/band39/b39-5.html
    “It’s currently estimated that there are about 700,000 people with ulcerative colitis,” said Dr. David Rubin, of the University of Chicago.
    “The numbers of people are rising every year and we don’t know why.”
    Ulcerative colitis is an auto-immune disease which causes inflammation of the colon. Its symptoms include abdominal pain, cramping, and diarrhea. A treatment exists, but not a cure”
    http://abcnews.go.com/GMA/OnCall/story?id=3274894&page=1
    “About 5 percent of people with ulcerative colitis develop colon cancer. The risk of cancer increases with the duration and the extent of involvement of the colon. For example, if only the lower colon and rectum are involved, the risk of cancer is not higher than normal.
    However, if the entire colon is involved, the risk of cancer may be as great as 32 times the normal rate”
    http://www.medhelp.org/NIHlib/GF-381.html
    Because the chemistry of tobacco smoking has been so thoroughly obscured, mistakes are understandable.
    Nicotine: does it have a role in the treatment of ulcerative colitis?
    “Ulcerative colitis is a chronic inflammatory disease state of unknown etiology. Its progression is erratic, with patients experiencing periods of exacerbations and remissions. Current therapeutic options have yielded less than satisfactory results.
    With the discovery of the potential relationship between nonsmoking status and the onset of ulcerative colitis and the development of various nicotine dosage forms came the hypothesis that nicotine may play a protective role against the development of ulcerative colitis and maintenance of remission.
    Hence, investigators began conducting clinical trials on the use of available nicotine dosage forms in the management of ulcerative colitis.”
    “Overall, investigation of nicotine in the treatment of ulcerative colitis has yielded disappointing results.
    CONCLUSION: Nicotine cannot be recommended as adjunctive or single therapy for the treatment of ulcerative colitis and will not alter current treatment options.”
    http://www.ncbi.nlm.nih.gov/pubmed/10423604
    Rose

  36. Anonymous says:

    Because some people are being forced to give up smoking, I’ve been trying to find the exact part of the smoke that works the magic, so they can substitute where possible.
    Some are rather tricky because no alternative yet exists.
    Ulcerative Colitis
    “Compared with those who had never smoked, current smokers were much less likely to have ulcerative colitis (odds ratio 0.13, 95% CI 0.05 to 0.3 – that is they were about eight times less likely to have ulcerative colitis. Former smokers’ risk was no different from non-smokers.”
    http://www.medicine.ox.ac.uk/bandolier/band39/b39-5.html
    “It’s currently estimated that there are about 700,000 people with ulcerative colitis,” said Dr. David Rubin, of the University of Chicago.
    “The numbers of people are rising every year and we don’t know why.”
    Ulcerative colitis is an auto-immune disease which causes inflammation of the colon. Its symptoms include abdominal pain, cramping, and diarrhea. A treatment exists, but not a cure”
    http://abcnews.go.com/GMA/OnCall/story?id=3274894&page=1
    “About 5 percent of people with ulcerative colitis develop colon cancer. The risk of cancer increases with the duration and the extent of involvement of the colon. For example, if only the lower colon and rectum are involved, the risk of cancer is not higher than normal.
    However, if the entire colon is involved, the risk of cancer may be as great as 32 times the normal rate”
    http://www.medhelp.org/NIHlib/GF-381.html
    Because the chemistry of tobacco smoking has been so thoroughly obscured, mistakes are understandable.
    Nicotine: does it have a role in the treatment of ulcerative colitis?
    “Ulcerative colitis is a chronic inflammatory disease state of unknown etiology. Its progression is erratic, with patients experiencing periods of exacerbations and remissions. Current therapeutic options have yielded less than satisfactory results.
    With the discovery of the potential relationship between nonsmoking status and the onset of ulcerative colitis and the development of various nicotine dosage forms came the hypothesis that nicotine may play a protective role against the development of ulcerative colitis and maintenance of remission.
    Hence, investigators began conducting clinical trials on the use of available nicotine dosage forms in the management of ulcerative colitis.”
    “Overall, investigation of nicotine in the treatment of ulcerative colitis has yielded disappointing results.
    CONCLUSION: Nicotine cannot be recommended as adjunctive or single therapy for the treatment of ulcerative colitis and will not alter current treatment options.”
    http://www.ncbi.nlm.nih.gov/pubmed/10423604
    Rose

    • Anonymous says:

      cont.
      This sounds more likely though.
      Carbon Monoxide Soothes Inflammatory Bowel Disease
      “Doctors have long known that smokers rarely suffer from a common form of inflammatory bowel disease (IBD) called ulcerative colitis, but they didn’t know why.
      A new study in the December 19 issue of The Journal of Experimental Medicine might help explain this apparent resistance. Scott Plevy and his colleagues at the University of Pittsburgh now show that carbon monoxide (CO), a component of cigarette smoke, helps shut down the intestinal inflammation that causes ulcerative colitis.”
      “But recent scientific studies have shown that CO — at least at low concentrations — has a redeeming quality: it acts as an anti-inflammatory agent”
      “The group traced the action of inhaled CO to a protein that is produced by immune cells called interleukin (IL)-12. IL-12 is normally produced during infection and helps activate the immune cells that fight off the invading pathogens.
      But chronic production of IL-12 in the gut also drives the inflammation that causes ulcerative colitis.
      Inhaled CO inhibited the production of IL-12, short-circuiting the disease-causing inflammation.”
      http://www.sciencedaily.com/releases/2006/01/060103084934.htm
      Carbon monoxide plays role in orchestrating digestive tract function
      “Farrugia and an associate, Dr. Joseph Szurszewski, headed the study, which focused on carbon monoxide’s role in orchestrating movements of muscles in the digestive system.”
      “They showed that cells in the digestive system manufacture tiny amounts of carbon monoxide, which then regulates muscle contractions. The contractions occur with great precision to properly move food ahead through the stomach and intestines”
      “Farrugia pointed out that carbon monoxide probably orchestrates other body processes, since the biochemical apparatus for making it also exists in brain, heart, liver, kidney and other cells.
      Carbon monoxide works as a so-called neurotransmitter, a chemical that carries signals from one nerve cell to another. It joins nitric oxide as an oddball in that genre.”
      http://www.post-gazette.com/healthscience/20030617carbon0617p3.asp
      Rose

  37. Anonymous says:

    cont.
    This sounds more likely though.
    Carbon Monoxide Soothes Inflammatory Bowel Disease
    “Doctors have long known that smokers rarely suffer from a common form of inflammatory bowel disease (IBD) called ulcerative colitis, but they didn’t know why.
    A new study in the December 19 issue of The Journal of Experimental Medicine might help explain this apparent resistance. Scott Plevy and his colleagues at the University of Pittsburgh now show that carbon monoxide (CO), a component of cigarette smoke, helps shut down the intestinal inflammation that causes ulcerative colitis.”
    “But recent scientific studies have shown that CO — at least at low concentrations — has a redeeming quality: it acts as an anti-inflammatory agent”
    “The group traced the action of inhaled CO to a protein that is produced by immune cells called interleukin (IL)-12. IL-12 is normally produced during infection and helps activate the immune cells that fight off the invading pathogens.
    But chronic production of IL-12 in the gut also drives the inflammation that causes ulcerative colitis.
    Inhaled CO inhibited the production of IL-12, short-circuiting the disease-causing inflammation.”
    http://www.sciencedaily.com/releases/2006/01/060103084934.htm
    Carbon monoxide plays role in orchestrating digestive tract function
    “Farrugia and an associate, Dr. Joseph Szurszewski, headed the study, which focused on carbon monoxide’s role in orchestrating movements of muscles in the digestive system.”
    “They showed that cells in the digestive system manufacture tiny amounts of carbon monoxide, which then regulates muscle contractions. The contractions occur with great precision to properly move food ahead through the stomach and intestines”
    “Farrugia pointed out that carbon monoxide probably orchestrates other body processes, since the biochemical apparatus for making it also exists in brain, heart, liver, kidney and other cells.
    Carbon monoxide works as a so-called neurotransmitter, a chemical that carries signals from one nerve cell to another. It joins nitric oxide as an oddball in that genre.”
    http://www.post-gazette.com/healthscience/20030617carbon0617p3.asp
    Rose

  38. Anonymous says:

    “Because some people are being forced to give up smoking, I’ve been trying to find the exact part of the smoke that works the magic, so they can substitute where possible.”
    Rose, so have I. One area has been the electro-fag. For some this works yet for others it does not. I had thought about B vitamins (B3 esp) and MAOIs in inhaled smoke as well as the Psychological aspect of smoking.
    In order to compensate some use Snus and again this seems to work, indicating that there is something in tobacco that is missing in the e-cig. Still for some this is not enough and only smoked tobacco is sufficient. The common theory of ‘Nicotine addiction’ is clearly not the explanation.
    So returning to the current debate, is there something in tobacco smoke that some are using to offset the risk of cancer? This seems a strange thing to say as ‘everyone’ knows cigarettes cause cancer. Having read Rich’s comment about LC possibly being a secondary or migratory cancer, is it possible that overall cancer rates will increase as smoking rates decrease due to this affect? Is it possible that the rise in Female LC is a result of an increase in the number of women now in work and exposed to primary cancer agents that migrate to the Lung if they smoke?
    It is interesting to note that countries that have high asthma rates (US) have relatively low smoking rates and those with low rates of asthma (Russia, China) have high rates of smoking. In any ordinary analysis this would suggest that there is some protective effect. Is it possible that we are looking at people who are 1) really affected (small group) and 2) affected by some other source (larger group) and blown out of all proportion the effect smoking and SHS has? Is this same thing happening with LC?
    west2

  39. Anonymous says:

    “Because some people are being forced to give up smoking, I’ve been trying to find the exact part of the smoke that works the magic, so they can substitute where possible.”
    Rose, so have I. One area has been the electro-fag. For some this works yet for others it does not. I had thought about B vitamins (B3 esp) and MAOIs in inhaled smoke as well as the Psychological aspect of smoking.
    In order to compensate some use Snus and again this seems to work, indicating that there is something in tobacco that is missing in the e-cig. Still for some this is not enough and only smoked tobacco is sufficient. The common theory of ‘Nicotine addiction’ is clearly not the explanation.
    So returning to the current debate, is there something in tobacco smoke that some are using to offset the risk of cancer? This seems a strange thing to say as ‘everyone’ knows cigarettes cause cancer. Having read Rich’s comment about LC possibly being a secondary or migratory cancer, is it possible that overall cancer rates will increase as smoking rates decrease due to this affect? Is it possible that the rise in Female LC is a result of an increase in the number of women now in work and exposed to primary cancer agents that migrate to the Lung if they smoke?
    It is interesting to note that countries that have high asthma rates (US) have relatively low smoking rates and those with low rates of asthma (Russia, China) have high rates of smoking. In any ordinary analysis this would suggest that there is some protective effect. Is it possible that we are looking at people who are 1) really affected (small group) and 2) affected by some other source (larger group) and blown out of all proportion the effect smoking and SHS has? Is this same thing happening with LC?
    west2

    • richwhite09 says:

      “would suggest that there is some protective effect.”
      There is much evidence that smoking protects against many things. The investigation into a protective effect on cancer has been overlooked because the epidemiology shows a correlation between cancer and smoking – yet, once again, any protective medicine will have a correlation to the disease it prevents or treats (paracetamol/headaches, breathing problems/respirators etc etc)
      “is it possible that overall cancer rates will increase as smoking rates decrease due to this affect?”
      One of my excerpts in the main post from the animal studies was of a medical professional saying that there is evidence overall cancer rates have remained constant, while the rates vary for individual organs. In other words, that could mean (using hypothetical figures), that for the past 100 years there have been 100million cases of cancer of every part of the body (combined figure), while LC was perhaps 500,000 in one year, 1.5million another year, and the rise in one year correlated with a drop in another organ, and vice versa.
      As for your actual question though, there’s no reason to see why not, if the self-medication theory holds true. The 10% of smokers who succumb to the disease may be at the lwoer end of the gene pool, while for perhaps 40% of the remaining 90% it is being a huge benefit (the remaining 50% may not need any protection but smoke anyway). If this were to be the case, we could see a growth in cancer of anywhere up to 40% if smoking were to be eradicated.

    • Anonymous says:

      “So returning to the current debate, is there something in tobacco smoke that some are using to offset the risk of cancer?”
      West2
      According to modern science there is, see Catch2
      http://frank-davis.livejournal.com/125361.html?thread=1153713#t1153713
      There are loads more studies in the Garden saying the same.
      Also the Ubiquinone in a tobacco leaf is said to be anti-carcinogenic, but I can’t find anything definate about what happens when its oxidized.
      TC has ruled the roost for so long that any research on tobacco is dubious at best.
      I’ve had to get the information from scientific studies where the writers probably have no clue that the plant chemical is also in tobacco.
      Luckily I can use pre-sixties tobacco company R&D as confirmation.
      After the RCP report the tobacco company scientists might have got spooked.
      TC were screeching so loudly about cancer without doing any research on the plant that I can find, it was pretty obvious where to look.
      “It is interesting to note that countries that have high asthma rates (US) have relatively low smoking rates and those with low rates of asthma (Russia, China) have high rates of smoking.
      In any ordinary analysis this would suggest that there is some protective effect.”
      As anti-tobacco science seems to work in reverse, there probably is.
      Treatment of Asthma by Nicotinic Acid
      http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2282923/
      But I’m sure that it’s far more complex than that.
      Rose

  40. Anonymous says:

    2009
    Estimated costs for treating Ulcerative Colitis in the UK are-
    adalimumab 40mg injection pen every other week for a year £9,295
    Infliximab at 2, 6 and every 8 weeks for a year £13,428
    http://www.haps.bham.ac.uk/publichealth/horizon/outputs/documents/2009/may-aug/Adalimumab.pd
    Rose

  41. richwhite09 says:

    “would suggest that there is some protective effect.”
    There is much evidence that smoking protects against many things. The investigation into a protective effect on cancer has been overlooked because the epidemiology shows a correlation between cancer and smoking – yet, once again, any protective medicine will have a correlation to the disease it prevents or treats (paracetamol/headaches, breathing problems/respirators etc etc)
    “is it possible that overall cancer rates will increase as smoking rates decrease due to this affect?”
    One of my excerpts in the main post from the animal studies was of a medical professional saying that there is evidence overall cancer rates have remained constant, while the rates vary for individual organs. In other words, that could mean (using hypothetical figures), that for the past 100 years there have been 100million cases of cancer of every part of the body (combined figure), while LC was perhaps 500,000 in one year, 1.5million another year, and the rise in one year correlated with a drop in another organ, and vice versa.
    As for your actual question though, there’s no reason to see why not, if the self-medication theory holds true. The 10% of smokers who succumb to the disease may be at the lwoer end of the gene pool, while for perhaps 40% of the remaining 90% it is being a huge benefit (the remaining 50% may not need any protection but smoke anyway). If this were to be the case, we could see a growth in cancer of anywhere up to 40% if smoking were to be eradicated.

  42. Anonymous says:

    “So returning to the current debate, is there something in tobacco smoke that some are using to offset the risk of cancer?”
    West2
    According to modern science there is, see Catch2
    http://frank-davis.livejournal.com/125361.html?thread=1153713#t1153713
    There are loads more studies in the Garden saying the same.
    Also the Ubiquinone in a tobacco leaf is said to be anti-carcinogenic, but I can’t find anything definate about what happens when its oxidized.
    TC has ruled the roost for so long that any research on tobacco is dubious at best.
    I’ve had to get the information from scientific studies where the writers probably have no clue that the plant chemical is also in tobacco.
    Luckily I can use pre-sixties tobacco company R&D as confirmation.
    After the RCP report the tobacco company scientists might have got spooked.
    TC were screeching so loudly about cancer without doing any research on the plant that I can find, it was pretty obvious where to look.
    “It is interesting to note that countries that have high asthma rates (US) have relatively low smoking rates and those with low rates of asthma (Russia, China) have high rates of smoking.
    In any ordinary analysis this would suggest that there is some protective effect.”
    As anti-tobacco science seems to work in reverse, there probably is.
    Treatment of Asthma by Nicotinic Acid
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2282923/
    But I’m sure that it’s far more complex than that.
    Rose

  43. Anonymous says:

    “Let’s just say that some (many, most, all…) studies have found that people who smoke are more likely to be the people who get LC (which is THE LIMIT to what even the very best health stats could possibly tell you).”
    Here is a very interesting article on causal inference in statistics:

    Click to access r350.pdf

  44. Anonymous says:

    “Let’s just say that some (many, most, all…) studies have found that people who smoke are more likely to be the people who get LC (which is THE LIMIT to what even the very best health stats could possibly tell you).”
    Here is a very interesting article on causal inference in statistics:

    Click to access r350.pdf

  45. cjsnowdon says:

    My earlier comment should have read “he says that cigarette consumption was lower in Japan than America in 1950. But it was lower – much lower – in JAPAN” – what can I say, it was 3 am.
    As Rich is not replying, I’ll post this for any passing visitors, because it’s important for several reasons. (1) It’s being used it as an example of scientists being dishonest, (2) it’s being used as evidence that cigarette consumption is not being linked cancer, and (3) it tells us a lot about Rich’s own integrity and competence.
    This is the study he cites:
    http://bit.ly/ihhizi
    He says that Wynder is lying when he says that cigarette consumption in 1950 was higher in America and Japan. As you can see from table 2 on the third page, Wynder was quite correct. What Rich has done is look at table 1 which shows higher smoking prevalence in Japan and confused that with cigarette consumption.
    Japan had a higher smoking prevalence but much lower cigarette consumption because cigarettes didn’t taken off there until the mid-1950s. Before that the Japanese smoked pipes and other forms of tobacco. Wynder, and everyone else, knew perfectly well that it was the cigarette specifically that was linked to lung and laryngeal cancer, and America’s much higher rate of cigarette and alcohol consumption is a entirely reasonable explanation for its higher rate of laryngeal cancer.
    It’s a very basic mistake and Rich is now trying to squirm out of it by pointing to figure 2 which shows Japanese MEN smoking more cigarettes per day than American MEN in the 1970s and 1980s. This is cherry-picking of gender (overall consumption was still lower) and he’s picking an entirely different time period.
    Rich then takes a sentence from the study out of context, without including the following passage which explains why higher prevalence of cigarette smoking and lung cancer were discrepant “for the same period of time” ie. there is a time-lag between smoking initiation and lung cancer.
    So Wynder was quite right and what he said was grounded in facts. What Rich said was a slur based on his own misreading of the study.

  46. cjsnowdon says:

    My earlier comment should have read “he says that cigarette consumption was lower in Japan than America in 1950. But it was lower – much lower – in JAPAN” – what can I say, it was 3 am.
    As Rich is not replying, I’ll post this for any passing visitors, because it’s important for several reasons. (1) It’s being used it as an example of scientists being dishonest, (2) it’s being used as evidence that cigarette consumption is not being linked cancer, and (3) it tells us a lot about Rich’s own integrity and competence.
    This is the study he cites:
    http://bit.ly/ihhizi
    He says that Wynder is lying when he says that cigarette consumption in 1950 was higher in America and Japan. As you can see from table 2 on the third page, Wynder was quite correct. What Rich has done is look at table 1 which shows higher smoking prevalence in Japan and confused that with cigarette consumption.
    Japan had a higher smoking prevalence but much lower cigarette consumption because cigarettes didn’t taken off there until the mid-1950s. Before that the Japanese smoked pipes and other forms of tobacco. Wynder, and everyone else, knew perfectly well that it was the cigarette specifically that was linked to lung and laryngeal cancer, and America’s much higher rate of cigarette and alcohol consumption is a entirely reasonable explanation for its higher rate of laryngeal cancer.
    It’s a very basic mistake and Rich is now trying to squirm out of it by pointing to figure 2 which shows Japanese MEN smoking more cigarettes per day than American MEN in the 1970s and 1980s. This is cherry-picking of gender (overall consumption was still lower) and he’s picking an entirely different time period.
    Rich then takes a sentence from the study out of context, without including the following passage which explains why higher prevalence of cigarette smoking and lung cancer were discrepant “for the same period of time” ie. there is a time-lag between smoking initiation and lung cancer.
    So Wynder was quite right and what he said was grounded in facts. What Rich said was a slur based on his own misreading of the study.

    • richwhite09 says:

      “As Rich is not replying”
      What? I did reply, I even pointed out your mistake that you just picked up on…
      I notice your new technique – instead of replying to the comment, start a new thread so i don’t get notified of a reply. Great. Anyway, it’s a blatant lie i haven’t replied, because i did and everyone can see it.
      “What Rich has done is look at table 1 which shows higher smoking prevalence in Japan and confused that with cigarette consumption. ”
      Actually that’s not what i’ve done, i actually wrote out more than once just for you Chris that the Japanese were smoking more cigarettes than Wynder noted.
      “and he’s picking an entirely different time period.”
      Oh, not the study period then?
      “without including the following passage which explains why higher prevalence of cigarette smoking and lung cancer were discrepant “for the same period of time” ie. there is a time-lag between smoking initiation and lung cancer.”
      Then it wouldn’t be discrepant.
      The more this goes on, the more comical it becomes. Every entry just becomes another excuse for you to just try to engage in an argument with me and ignore everything else. Get in on the discussion Chris, or leave, you’re obviously not here for much of a reason.

      • richwhite09 says:

        On the “Rich is not replying” point, I specifically said on this topic, not in general.
        To say i’m not replying and then just list all the points i’ve already replied to, well, what more is there to be said? I’ll repeat myself:
        “The more this goes on, the more comical it becomes. Every entry just becomes another excuse for you to just try to engage in an argument with me and ignore everything else. Get in on the discussion Chris, or leave, you’re obviously not here for much of a reason.”

  47. cjsnowdon says:

    Rich White: “Only epidemiology and statistics exist to link smoking to cancer.”
    Rich White: ” i’m not prepared to discuss the epidemiology endlessly, I stated at the start of this CATCH entry that it isn’t getting us anywhere.”
    Doesn’t look like we have much room for debate then. I damned if I’m going to talk about these animal experiments again (‘there’s never been one that worked…except this one… and this one.. and this one… etc.)
    I’ll let Rich and this mysterious stranger discuss their admiration for that renowned scientific expert Nightlight. If we’ve got to the stage where the main source of evidence is an internet chat-room I think it’s time to empty the ash-trays and switch out the lights.
    PS.
    (Rich White, CATCH-10: “To clarify something, i don’t think i’ve provided ‘evidence’ from a web forum or chat room. I have used them a couple of times just to point out they’re well circulated suggestions, but never as active evidence. I wouldn’t ever do that and would reject anyone else doing so too.”)

  48. cjsnowdon says:

    Rich White: “Only epidemiology and statistics exist to link smoking to cancer.”
    Rich White: ” i’m not prepared to discuss the epidemiology endlessly, I stated at the start of this CATCH entry that it isn’t getting us anywhere.”
    Doesn’t look like we have much room for debate then. I damned if I’m going to talk about these animal experiments again (‘there’s never been one that worked…except this one… and this one.. and this one… etc.)
    I’ll let Rich and this mysterious stranger discuss their admiration for that renowned scientific expert Nightlight. If we’ve got to the stage where the main source of evidence is an internet chat-room I think it’s time to empty the ash-trays and switch out the lights.
    PS.
    (Rich White, CATCH-10: “To clarify something, i don’t think i’ve provided ‘evidence’ from a web forum or chat room. I have used them a couple of times just to point out they’re well circulated suggestions, but never as active evidence. I wouldn’t ever do that and would reject anyone else doing so too.”)

    • richwhite09 says:

      “If we’ve got to the stage where the main source of evidence is an internet chat-room I think it’s time to empty the ash-trays and switch out the lights. ”
      By the rationale you’re implying, nothing here must be relevant because it’s a blog.
      The main source of evidence is actual evidence posted on a forum. There’s a difference.
      “I’ll let Rich and this mysterious stranger discuss their admiration for that renowned scientific expert Nightlight”
      Nightlight is a theoretical physiciat qualified in quantum physics. Scientific expert is a pretty correct defintion.
      And if the only response you have to the points he raised, complete with scientific links and references, is, well, nothing, and if you can’t look at the statements on their own merit then you shouldn’t be involved in a debate, especially one as demanding and complex as smoking.
      “(‘there’s never been one that worked…except this one… and this one.. and this one… etc.)”
      Ok Chris, whatever. If you think rats and mice generally engineered to develop cancer count as evidence of a successful experiment, that’s fine. If you think tobacco suddenly began affecting them in 2004 with no basis, that’s up to you.
      “Rich White: “Only epidemiology and statistics exist to link smoking to cancer.”
      Rich White: ” i’m not prepared to discuss the epidemiology endlessly, I stated at the start of this CATCH entry that it isn’t getting us anywhere.”
      Doesn’t look like we have much room for debate then”
      How wrong you are. What everyone else is managing to do is look beyond that for reasons the correlation from epidemiology exists. The only reason we don’t have much room for debate is because you’re point blank refusing to discuss anything beyond ‘but look at this statistic…’ Rose has put endless quotations with references up on each and every CATCH entry, highlighting that there is a big chasm in tobacco research and there’s much we don’t know that goes against TC mantra. This post in itself was to extend the discussion beyond epidemiology – not to say it doesn’t exist, but to look at the smoking issue as a whole. Apparently you’re incapable of doing that, and your absolute refusal to even attempt to talk about the points Nightlight, and others, and in fact this entire post (besides Wynder) just acts as a very thin veil covering up the fact you don’t know as much as you think you do on this topic, nor do you know how to talk about it when it moves beyond statistics.
      Chris, these brattish and bullying posts aren’t getting you anywhere and they’re not getting the debate anywhere. If you seriously can’t respond to things, don’t post at all. There’s plenty of people (read: everyone else) who can, and want to talk about the issue in its entirety.

  49. richwhite09 says:

    “If we’ve got to the stage where the main source of evidence is an internet chat-room I think it’s time to empty the ash-trays and switch out the lights. ”
    By the rationale you’re implying, nothing here must be relevant because it’s a blog.
    The main source of evidence is actual evidence posted on a forum. There’s a difference.
    “I’ll let Rich and this mysterious stranger discuss their admiration for that renowned scientific expert Nightlight”
    Nightlight is a theoretical physiciat qualified in quantum physics. Scientific expert is a pretty correct defintion.
    And if the only response you have to the points he raised, complete with scientific links and references, is, well, nothing, and if you can’t look at the statements on their own merit then you shouldn’t be involved in a debate, especially one as demanding and complex as smoking.
    “(‘there’s never been one that worked…except this one… and this one.. and this one… etc.)”
    Ok Chris, whatever. If you think rats and mice generally engineered to develop cancer count as evidence of a successful experiment, that’s fine. If you think tobacco suddenly began affecting them in 2004 with no basis, that’s up to you.
    “Rich White: “Only epidemiology and statistics exist to link smoking to cancer.”
    Rich White: ” i’m not prepared to discuss the epidemiology endlessly, I stated at the start of this CATCH entry that it isn’t getting us anywhere.”
    Doesn’t look like we have much room for debate then”
    How wrong you are. What everyone else is managing to do is look beyond that for reasons the correlation from epidemiology exists. The only reason we don’t have much room for debate is because you’re point blank refusing to discuss anything beyond ‘but look at this statistic…’ Rose has put endless quotations with references up on each and every CATCH entry, highlighting that there is a big chasm in tobacco research and there’s much we don’t know that goes against TC mantra. This post in itself was to extend the discussion beyond epidemiology – not to say it doesn’t exist, but to look at the smoking issue as a whole. Apparently you’re incapable of doing that, and your absolute refusal to even attempt to talk about the points Nightlight, and others, and in fact this entire post (besides Wynder) just acts as a very thin veil covering up the fact you don’t know as much as you think you do on this topic, nor do you know how to talk about it when it moves beyond statistics.
    Chris, these brattish and bullying posts aren’t getting you anywhere and they’re not getting the debate anywhere. If you seriously can’t respond to things, don’t post at all. There’s plenty of people (read: everyone else) who can, and want to talk about the issue in its entirety.

  50. Anonymous says:

    Thanks for your replies.
    Anon above — I skimmed the article — not sure what your point was.
    From the link – “The theory invokes non-parametric structural equations models as a formal and meaningful language for defining causal quantities, formulating causal assumptions, testing identifiability, and ex-plicating many concepts used in causal discourse. These include: randomization,intervention, direct and indirect effects, confounding, counterfactuals, and attribution.”
    Yes, we “approach” being able to talk about causality in the complex world of health stats by using more scientific methods such as randomization, intervention, including more effects, etc… That in itself is not news – although having a comprehensive language to talk about these things may be a contribution. Personally, I think the future lies in models and concepts that will eventually be derived from complexity theory – I don’t think we’re ready for the “language” because we don’t understand all the concepts yet. JMO. (And Frank partly hit on this in his last post, I believe)
    Before I forget again, I meant to credit Rose with providing so many of the research citations that have influenced my own thinking. I bow to your tireless efforts, Rose.
    The problem that I see is that both the internal and external environments are terribly complex. Chris asks for the one confounder that will explain LC “better” than smoking. But life isn’t like that. For example, CDC acknowledges that LC cases clustering along the coasts of the U.S. is at least partly due to shipyard employment. I don’t recall if they explain this further, but I assume they mean exposures to asbestos, and diesel – exposures that I imagine would have been particularly acute during the WWII period (and that women would have experienced later than men). Prior to that period, railroads probably accounted for similar exposures (mostly for men). After that period, radioactive exposures… Things change. Meanwhile, we have other things going on, like the aforementioned dietary changes (e.g., wrt to type of grain consumption). And then add in the puzzle of human genetic make-up. Even the best multi-factorial analyses can’t hope to account for even a tiny fraction of all of the potential internal and external effects and confounding variables.
    And yet, we take these sledgehammers – hit the problem over the head, and pretend we are doing brain surgery. As a health statistician, I get really depressed when someone just doesn’t understand what we can and cannot tell with these sorts of stats. It’s only the roughest of hints. Measures of association simply can’t tell you any more than that. No matter how many times you recite “correlation doesn’t imply causation” and then go on to ignore what you’ve just recited, correlation STILL doesn’t imply causation.
    The real tragedy of the smoking – LC theory is that after 60 years, it has brought us no closer to a prevention or cure for LC. If smoking cessation was a strong preventive for LC (and it doesn’t seem to be, as these days as evidence of such an effect is quickly disappearing – as LC rates for ex-smokers reach or exceed those of smokers – also note the randomized trials that failed) perhaps the theory would have some use. The theory has also not led to a cure or vaccine (just as the smoking – cervical cancer theory led nowhere, but the HPV causing cervical cancer and throat cancer theory did quickly lead somewhere useful).
    Ahhh… just read Chris’s “dodging all the issues” reply. The main source of “evidence is an internet chat room”? Noooo… the venue of discussion is an internet chat room (much like this discussion). The “evidence” is in the references and the logic. And I must say I’m disappointed. Am I the “mysterious stranger? Jeezy-peezy Chris — this is the internet. Ideas live and die on their merit. Would it help if I gave you my name? Why? Is your name supposed to mean something to me? Are you less a mysterious stranger to me because you have a name? Yes, Chris, I’ve had many discussions with Nightlight and I admire his intellect. I mean no disrespect, but your refusal to engage doesn’t fill me with the same admiration.
    GDF

  51. Anonymous says:

    Thanks for your replies.
    Anon above — I skimmed the article — not sure what your point was.
    From the link – “The theory invokes non-parametric structural equations models as a formal and meaningful language for defining causal quantities, formulating causal assumptions, testing identifiability, and ex-plicating many concepts used in causal discourse. These include: randomization,intervention, direct and indirect effects, confounding, counterfactuals, and attribution.”
    Yes, we “approach” being able to talk about causality in the complex world of health stats by using more scientific methods such as randomization, intervention, including more effects, etc… That in itself is not news – although having a comprehensive language to talk about these things may be a contribution. Personally, I think the future lies in models and concepts that will eventually be derived from complexity theory – I don’t think we’re ready for the “language” because we don’t understand all the concepts yet. JMO. (And Frank partly hit on this in his last post, I believe)
    Before I forget again, I meant to credit Rose with providing so many of the research citations that have influenced my own thinking. I bow to your tireless efforts, Rose.
    The problem that I see is that both the internal and external environments are terribly complex. Chris asks for the one confounder that will explain LC “better” than smoking. But life isn’t like that. For example, CDC acknowledges that LC cases clustering along the coasts of the U.S. is at least partly due to shipyard employment. I don’t recall if they explain this further, but I assume they mean exposures to asbestos, and diesel – exposures that I imagine would have been particularly acute during the WWII period (and that women would have experienced later than men). Prior to that period, railroads probably accounted for similar exposures (mostly for men). After that period, radioactive exposures… Things change. Meanwhile, we have other things going on, like the aforementioned dietary changes (e.g., wrt to type of grain consumption). And then add in the puzzle of human genetic make-up. Even the best multi-factorial analyses can’t hope to account for even a tiny fraction of all of the potential internal and external effects and confounding variables.
    And yet, we take these sledgehammers – hit the problem over the head, and pretend we are doing brain surgery. As a health statistician, I get really depressed when someone just doesn’t understand what we can and cannot tell with these sorts of stats. It’s only the roughest of hints. Measures of association simply can’t tell you any more than that. No matter how many times you recite “correlation doesn’t imply causation” and then go on to ignore what you’ve just recited, correlation STILL doesn’t imply causation.
    The real tragedy of the smoking – LC theory is that after 60 years, it has brought us no closer to a prevention or cure for LC. If smoking cessation was a strong preventive for LC (and it doesn’t seem to be, as these days as evidence of such an effect is quickly disappearing – as LC rates for ex-smokers reach or exceed those of smokers – also note the randomized trials that failed) perhaps the theory would have some use. The theory has also not led to a cure or vaccine (just as the smoking – cervical cancer theory led nowhere, but the HPV causing cervical cancer and throat cancer theory did quickly lead somewhere useful).
    Ahhh… just read Chris’s “dodging all the issues” reply. The main source of “evidence is an internet chat room”? Noooo… the venue of discussion is an internet chat room (much like this discussion). The “evidence” is in the references and the logic. And I must say I’m disappointed. Am I the “mysterious stranger? Jeezy-peezy Chris — this is the internet. Ideas live and die on their merit. Would it help if I gave you my name? Why? Is your name supposed to mean something to me? Are you less a mysterious stranger to me because you have a name? Yes, Chris, I’ve had many discussions with Nightlight and I admire his intellect. I mean no disrespect, but your refusal to engage doesn’t fill me with the same admiration.
    GDF

  52. Anonymous says:

    Thanks for your replies.
    Anon above — I skimmed the article — not sure what your point was.
    From the link – “The theory invokes non-parametric structural equations models as a formal and meaningful language for defining causal quantities, formulating causal assumptions, testing identifiability, and ex-plicating many concepts used in causal discourse. These include: randomization,intervention, direct and indirect effects, confounding, counterfactuals, and attribution.”
    Yes, we “approach” being able to talk about causality in the complex world of health stats by using more scientific methods such as randomization, intervention, including more effects, etc… That in itself is not news – although having a comprehensive language to talk about these things may be a contribution. Personally, I think the future lies in models and concepts that will eventually be derived from complexity theory – I don’t think we’re ready for the “language” because we don’t understand all the concepts yet. JMO. (And Frank partly hit on this in his last post, I believe)
    Before I forget again, I meant to credit Rose with providing so many of the research citations that have influenced my own thinking. I bow to your tireless efforts, Rose.
    The problem that I see is that both the internal and external environments are terribly complex. Chris asks for the one confounder that will explain LC “better” than smoking. But life isn’t like that. For example, CDC acknowledges that LC cases clustering along the coasts of the U.S. is at least partly due to shipyard employment. I don’t recall if they explain this further, but I assume they mean exposures to asbestos, and diesel – exposures that I imagine would have been particularly acute during the WWII period (and that women would have experienced later than men). Prior to that period, railroads probably accounted for similar exposures (mostly for men). After that period, radioactive exposures… Things change. Meanwhile, we have other things going on, like the aforementioned dietary changes (e.g., wrt to type of grain consumption). And then add in the puzzle of human genetic make-up. Even the best multi-factorial analyses can’t hope to account for even a tiny fraction of all of the potential internal and external effects and confounding variables.
    And yet, we take these sledgehammers – hit the problem over the head, and pretend we are doing brain surgery. As a health statistician, I get really depressed when someone just doesn’t understand what we can and cannot tell with these sorts of stats. It’s only the roughest of hints. Measures of association simply can’t tell you any more than that. No matter how many times you recite “correlation doesn’t imply causation” and then go on to ignore what you’ve just recited, correlation STILL doesn’t imply causation.
    The real tragedy of the smoking – LC theory is that after 60 years, it has brought us no closer to a prevention or cure for LC. If smoking cessation was a strong preventive for LC (and it doesn’t seem to be, as these days as evidence of such an effect is quickly disappearing – as LC rates for ex-smokers reach or exceed those of smokers – also note the randomized trials that failed) perhaps the theory would have some use. The theory has also not led to a cure or vaccine (just as the smoking – cervical cancer theory led nowhere, but the HPV causing cervical cancer and throat cancer theory did quickly lead somewhere useful).
    Ahhh… just read Chris’s “dodging all the issues” reply. The main source of “evidence is an internet chat room”? Noooo… the venue of discussion is an internet chat room (much like this discussion). The “evidence” is in the references and the logic. And I must say I’m disappointed. Am I the “mysterious stranger? Jeezy-peezy Chris — this is the internet. Ideas live and die on their merit. Would it help if I gave you my name? Why? Is your name supposed to mean something to me? Are you less a mysterious stranger to me because you have a name? Yes, Chris, I’ve had many discussions with Nightlight and I admire his intellect. I mean no disrespect, but your refusal to engage doesn’t fill me with the same admiration.
    GDF

    • Anonymous says:

      Thank you GDF
      Just doing my civic duty.
      I kept hoping that a proper qualified plant biologist would take over,but when one didn’t, I just had to try my best.
      Glad that I have been of some use, however limited.
      It could take decades to sort this all out.
      Rose

    • Anonymous says:

      I do not have a specific point on the subject. I’m not an expert in statistics. I’m an economist, but I’m not an expert in econometrics (I did several courses in statistics on my post graduation in economics, but I consider myself an ignoramus on this subject). My concern is about methodology and philosophy of science. Nevertheless, I thought this article shows very clearly the difficulties in dealing with the idea of causality in statistics.

  53. richwhite09 says:

    “As Rich is not replying”
    What? I did reply, I even pointed out your mistake that you just picked up on…
    I notice your new technique – instead of replying to the comment, start a new thread so i don’t get notified of a reply. Great. Anyway, it’s a blatant lie i haven’t replied, because i did and everyone can see it.
    “What Rich has done is look at table 1 which shows higher smoking prevalence in Japan and confused that with cigarette consumption. ”
    Actually that’s not what i’ve done, i actually wrote out more than once just for you Chris that the Japanese were smoking more cigarettes than Wynder noted.
    “and he’s picking an entirely different time period.”
    Oh, not the study period then?
    “without including the following passage which explains why higher prevalence of cigarette smoking and lung cancer were discrepant “for the same period of time” ie. there is a time-lag between smoking initiation and lung cancer.”
    Then it wouldn’t be discrepant.
    The more this goes on, the more comical it becomes. Every entry just becomes another excuse for you to just try to engage in an argument with me and ignore everything else. Get in on the discussion Chris, or leave, you’re obviously not here for much of a reason.

  54. richwhite09 says:

    “As Rich is not replying”
    What? I did reply, I even pointed out your mistake that you just picked up on…
    I notice your new technique – instead of replying to the comment, start a new thread so i don’t get notified of a reply. Great. Anyway, it’s a blatant lie i haven’t replied, because i did and everyone can see it.
    “What Rich has done is look at table 1 which shows higher smoking prevalence in Japan and confused that with cigarette consumption. ”
    Actually that’s not what i’ve done, i actually wrote out more than once just for you Chris that the Japanese were smoking more cigarettes than Wynder noted.
    “and he’s picking an entirely different time period.”
    Oh, not the study period then?
    “without including the following passage which explains why higher prevalence of cigarette smoking and lung cancer were discrepant “for the same period of time” ie. there is a time-lag between smoking initiation and lung cancer.”
    Then it wouldn’t be discrepant.
    The more this goes on, the more comical it becomes. Every entry just becomes another excuse for you to just try to engage in an argument with me and ignore everything else. Get in on the discussion Chris, or leave, you’re obviously not here for much of a reason.

  55. Anonymous says:

    WRT to the Wynder stuff — (not that it matters really)
    Chris posted:
    [Rich said] Chris has said the researchers of the 1950s were honest. But really? Wynder said: “The age adjusted mortality rates for laryngeal cancer during 1955 are higher in US White[s] than in the Japanese. These differences can be partially explained by the higher levels of cigarette and alcohol consumption in the US” even though his own tables demonstrated the Japanese smoked more.
    [Chris replied] Er, no. Figure 1 of that study shows that Americans consumed more than 3 times as many cigarettes than the Japanese in 1950 and consistently smoked more cigarettes throughout the whole period of the study (1920-1985). And Figure 4 shows that Americans drunk more alcohol, which is also a major risk factor for laryngeal. So who’s being ‘dishonest’ here?
    Actually, although I think Rich may have over-reached (i.e., I don’t think Wynder was mistaken, I think he just didn’t offer the complete stats – for the entire time period and all groups), I also think that Wynder even confused himself as he states in the Discussion —
    “Still there are some discrepancies in the international
    trends and differences in cancer mortality that conflict
    with what is currently known about the risk factors of
    specific malignancies. Laryngeal cancer rates in Japanese
    males are lower than in the US, and surprisingly are declining, despite their relatively high levels of cigarette
    smoking”
    But again, time to move past the sledgehammer.
    GDF

  56. Anonymous says:

    WRT to the Wynder stuff — (not that it matters really)
    Chris posted:
    [Rich said] Chris has said the researchers of the 1950s were honest. But really? Wynder said: “The age adjusted mortality rates for laryngeal cancer during 1955 are higher in US White[s] than in the Japanese. These differences can be partially explained by the higher levels of cigarette and alcohol consumption in the US” even though his own tables demonstrated the Japanese smoked more.
    [Chris replied] Er, no. Figure 1 of that study shows that Americans consumed more than 3 times as many cigarettes than the Japanese in 1950 and consistently smoked more cigarettes throughout the whole period of the study (1920-1985). And Figure 4 shows that Americans drunk more alcohol, which is also a major risk factor for laryngeal. So who’s being ‘dishonest’ here?
    Actually, although I think Rich may have over-reached (i.e., I don’t think Wynder was mistaken, I think he just didn’t offer the complete stats – for the entire time period and all groups), I also think that Wynder even confused himself as he states in the Discussion —
    “Still there are some discrepancies in the international
    trends and differences in cancer mortality that conflict
    with what is currently known about the risk factors of
    specific malignancies. Laryngeal cancer rates in Japanese
    males are lower than in the US, and surprisingly are declining, despite their relatively high levels of cigarette
    smoking”
    But again, time to move past the sledgehammer.
    GDF

  57. Anonymous says:

    WRT to the Wynder stuff — (not that it matters really)
    Chris posted:
    [Rich said] Chris has said the researchers of the 1950s were honest. But really? Wynder said: “The age adjusted mortality rates for laryngeal cancer during 1955 are higher in US White[s] than in the Japanese. These differences can be partially explained by the higher levels of cigarette and alcohol consumption in the US” even though his own tables demonstrated the Japanese smoked more.
    [Chris replied] Er, no. Figure 1 of that study shows that Americans consumed more than 3 times as many cigarettes than the Japanese in 1950 and consistently smoked more cigarettes throughout the whole period of the study (1920-1985). And Figure 4 shows that Americans drunk more alcohol, which is also a major risk factor for laryngeal. So who’s being ‘dishonest’ here?
    Actually, although I think Rich may have over-reached (i.e., I don’t think Wynder was mistaken, I think he just didn’t offer the complete stats – for the entire time period and all groups), I also think that Wynder even confused himself as he states in the Discussion —
    “Still there are some discrepancies in the international
    trends and differences in cancer mortality that conflict
    with what is currently known about the risk factors of
    specific malignancies. Laryngeal cancer rates in Japanese
    males are lower than in the US, and surprisingly are declining, despite their relatively high levels of cigarette
    smoking”
    But again, time to move past the sledgehammer.
    GDF

    • richwhite09 says:

      “although I think Rich may have over-reached (i.e., I don’t think Wynder was mistaken, I think he just didn’t offer the complete stats – for the entire time period and all groups)”
      I quite possibly did. In loose discussions such as this i’m not accustomed to making sure each and every word has been checked and triple checked in case someone ignores the entire post to pick up on a slight linguistics nuance. I did try to balance this with another post on this page where I said to move beyond the terminology of ‘honest’, ‘dishonest’, but that was also ignored.
      Of course, the entire crux of my argument was the flimsy nature of the evidence on offer. Most people, as you have accurately demonstrated with the post i’m replying to now, have grasped this. Unsurprisingly, the one person who hasn’t is the very same person unwilling to engage in debate with the points on offer.

  58. richwhite09 says:

    On the “Rich is not replying” point, I specifically said on this topic, not in general.
    To say i’m not replying and then just list all the points i’ve already replied to, well, what more is there to be said? I’ll repeat myself:
    “The more this goes on, the more comical it becomes. Every entry just becomes another excuse for you to just try to engage in an argument with me and ignore everything else. Get in on the discussion Chris, or leave, you’re obviously not here for much of a reason.”

  59. richwhite09 says:

    On the “Rich is not replying” point, I specifically said on this topic, not in general.
    To say i’m not replying and then just list all the points i’ve already replied to, well, what more is there to be said? I’ll repeat myself:
    “The more this goes on, the more comical it becomes. Every entry just becomes another excuse for you to just try to engage in an argument with me and ignore everything else. Get in on the discussion Chris, or leave, you’re obviously not here for much of a reason.”

  60. Anonymous says:

    So if you cant connect the end points,theres no proof of causation!
    As Ive read they cant prove smoking causes cancer unless another element is in the mix like radon,asbestos etc!
    The weakness of the first hand theory makes the second hand theory IMPOSSIBLE……..Then we have 3rd hand insanity…..
    My opinion is until the anti-tobacco agenda is destroyed and public trust and integrity returns to research and science we shall all suffer….with probably trillions of dollars wasted worldwide on research that produces absolutely nothing.

  61. Anonymous says:

    So if you cant connect the end points,theres no proof of causation!
    As Ive read they cant prove smoking causes cancer unless another element is in the mix like radon,asbestos etc!
    The weakness of the first hand theory makes the second hand theory IMPOSSIBLE……..Then we have 3rd hand insanity…..
    My opinion is until the anti-tobacco agenda is destroyed and public trust and integrity returns to research and science we shall all suffer….with probably trillions of dollars wasted worldwide on research that produces absolutely nothing.

  62. Anonymous says:

    So if you cant connect the end points,theres no proof of causation!
    As Ive read they cant prove smoking causes cancer unless another element is in the mix like radon,asbestos etc!
    The weakness of the first hand theory makes the second hand theory IMPOSSIBLE……..Then we have 3rd hand insanity…..
    My opinion is until the anti-tobacco agenda is destroyed and public trust and integrity returns to research and science we shall all suffer….with probably trillions of dollars wasted worldwide on research that produces absolutely nothing.

    • richwhite09 says:

      “Then we have 3rd hand insanity…..”
      We also have 4th hand insanity now.
      “As Ive read they cant prove smoking causes cancer unless another element is in the mix like radon,asbestos etc!”
      They haven’t proven it then either. Actually dogs exposed to radon get lung cancer; dogs exposed to radon and tobacco smoke get much less lung cancer.
      I think what you’ve read is just that people exposed to radon and asbestos get lung cancer, and some/a lot smoke too, and that’s then used as causation. Although it’s quite an obvious point that if we have 2 things with definite causation, adding something else in and claiming the 3rd thing is the responsible agent is quite ridiculous.

  63. richwhite09 says:

    “although I think Rich may have over-reached (i.e., I don’t think Wynder was mistaken, I think he just didn’t offer the complete stats – for the entire time period and all groups)”
    I quite possibly did. In loose discussions such as this i’m not accustomed to making sure each and every word has been checked and triple checked in case someone ignores the entire post to pick up on a slight linguistics nuance. I did try to balance this with another post on this page where I said to move beyond the terminology of ‘honest’, ‘dishonest’, but that was also ignored.
    Of course, the entire crux of my argument was the flimsy nature of the evidence on offer. Most people, as you have accurately demonstrated with the post i’m replying to now, have grasped this. Unsurprisingly, the one person who hasn’t is the very same person unwilling to engage in debate with the points on offer.

  64. richwhite09 says:

    “although I think Rich may have over-reached (i.e., I don’t think Wynder was mistaken, I think he just didn’t offer the complete stats – for the entire time period and all groups)”
    I quite possibly did. In loose discussions such as this i’m not accustomed to making sure each and every word has been checked and triple checked in case someone ignores the entire post to pick up on a slight linguistics nuance. I did try to balance this with another post on this page where I said to move beyond the terminology of ‘honest’, ‘dishonest’, but that was also ignored.
    Of course, the entire crux of my argument was the flimsy nature of the evidence on offer. Most people, as you have accurately demonstrated with the post i’m replying to now, have grasped this. Unsurprisingly, the one person who hasn’t is the very same person unwilling to engage in debate with the points on offer.

  65. richwhite09 says:

    “Then we have 3rd hand insanity…..”
    We also have 4th hand insanity now.
    “As Ive read they cant prove smoking causes cancer unless another element is in the mix like radon,asbestos etc!”
    They haven’t proven it then either. Actually dogs exposed to radon get lung cancer; dogs exposed to radon and tobacco smoke get much less lung cancer.
    I think what you’ve read is just that people exposed to radon and asbestos get lung cancer, and some/a lot smoke too, and that’s then used as causation. Although it’s quite an obvious point that if we have 2 things with definite causation, adding something else in and claiming the 3rd thing is the responsible agent is quite ridiculous.

  66. richwhite09 says:

    “Then we have 3rd hand insanity…..”
    We also have 4th hand insanity now.
    “As Ive read they cant prove smoking causes cancer unless another element is in the mix like radon,asbestos etc!”
    They haven’t proven it then either. Actually dogs exposed to radon get lung cancer; dogs exposed to radon and tobacco smoke get much less lung cancer.
    I think what you’ve read is just that people exposed to radon and asbestos get lung cancer, and some/a lot smoke too, and that’s then used as causation. Although it’s quite an obvious point that if we have 2 things with definite causation, adding something else in and claiming the 3rd thing is the responsible agent is quite ridiculous.

  67. Anonymous says:

    Rich I was just thinking that too,I was going to add just change the smoking inclusion to oxygen or argon or carbon dioxide or etc……..those things are in the atmosphere in great qunatities that everyone is exposed to 24/7 and if I remember correctly tobacco smoke is nearly 90% of the normal atmospheric gases,but of course it would be as all organic materials that burn basically give off the same amounts….hense our atmosphere is whats been burned in it for a billion years………
    Excuse typos my laptop caught a soda pop earlier……..not good

  68. Anonymous says:

    Rich I was just thinking that too,I was going to add just change the smoking inclusion to oxygen or argon or carbon dioxide or etc……..those things are in the atmosphere in great qunatities that everyone is exposed to 24/7 and if I remember correctly tobacco smoke is nearly 90% of the normal atmospheric gases,but of course it would be as all organic materials that burn basically give off the same amounts….hense our atmosphere is whats been burned in it for a billion years………
    Excuse typos my laptop caught a soda pop earlier……..not good

  69. Anonymous says:

    Rich I was just thinking that too,I was going to add just change the smoking inclusion to oxygen or argon or carbon dioxide or etc……..those things are in the atmosphere in great qunatities that everyone is exposed to 24/7 and if I remember correctly tobacco smoke is nearly 90% of the normal atmospheric gases,but of course it would be as all organic materials that burn basically give off the same amounts….hense our atmosphere is whats been burned in it for a billion years………
    Excuse typos my laptop caught a soda pop earlier……..not good

  70. Anonymous says:

    Catch 17
    As noted by GDF in his comments, the inclusion of a “recovery” period in many of the animal experiments may have compromised the integrity of the data. There is some evidence to suggest that a similar phenomena may be occurring in the human population.
    The last numerical data I looked at suggested there were 45.3 million current smokers in the US, and 45.7 million former smokers. Those are figures for 2006. The ALA put the figures at 45 million current smokers, 51 million former smokers in 2008. And, although the numbers vary according to the source, the phenomena (where former smokers exceed current smokers) appears to be a fairly recent development in the US.
    A chart prepared by the CDC, based on 2006 data, shows the break down of LC prevalence in the various smoking categories: 20.9% current smokers, 61.2% former Smokers, 17.9% never smokers.
    Source: http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5644a2.htm
    This means that there were far more former smokers (almost three times as many) diagnosed with lung cancer than current smokers, despite a similar sized population. And, in turn, it suggests that the relative risk of contracting (and eventually dying from) lung cancer is greater among former smokers than current smokers. In addition, it intimates that, as far as lung cancer is concerned, there is little benefit in quitting; a seemingly absurd proposition if we accept that LC is, in fact, caused by smoking.
    Given the number of animal studies conducted in an effort to show that smoking causes LC and the relatively fewer number that have actually produced worthwhile data, I find the evidence underwhelming and inconclusive. That, of course, is opinion, not fact.
    I would also like to point out that despite the seemingly high risk (1 in 10 smokers developing LC), the real significance of those numbers appears to have been overlooked. Even when the death rate is reduced to 1 in 5, it still means that 80% to 90% of smokers do not die from lung cancer.
    Is it really realistic to infer that smoking is the cause of lung cancer when only 10% of those exposed to the risk actually succumb to the disease? Why have there been no further studies to determine why only 10% of smokers are likely to expire from LC?
    I would opine that, given recent studies which suggest that LC among never smoker smokers and current smokers may be two entirely different diseases, that comparing lung cancer rates between the two may be somewhat akin to comparing apples and oranges.
    And, one last point. I’ve found this debate to be highly informative. It is not enhanced, however, by personal attacks. Please keep it civil, and continue to debate the merits of the argument, rather than questioning the motivation or integrity of those engaged in the debate.
    Matt Todd,
    aka The Old Rambler

  71. Anonymous says:

    Catch 17
    As noted by GDF in his comments, the inclusion of a “recovery” period in many of the animal experiments may have compromised the integrity of the data. There is some evidence to suggest that a similar phenomena may be occurring in the human population.
    The last numerical data I looked at suggested there were 45.3 million current smokers in the US, and 45.7 million former smokers. Those are figures for 2006. The ALA put the figures at 45 million current smokers, 51 million former smokers in 2008. And, although the numbers vary according to the source, the phenomena (where former smokers exceed current smokers) appears to be a fairly recent development in the US.
    A chart prepared by the CDC, based on 2006 data, shows the break down of LC prevalence in the various smoking categories: 20.9% current smokers, 61.2% former Smokers, 17.9% never smokers.
    Source: http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5644a2.htm
    This means that there were far more former smokers (almost three times as many) diagnosed with lung cancer than current smokers, despite a similar sized population. And, in turn, it suggests that the relative risk of contracting (and eventually dying from) lung cancer is greater among former smokers than current smokers. In addition, it intimates that, as far as lung cancer is concerned, there is little benefit in quitting; a seemingly absurd proposition if we accept that LC is, in fact, caused by smoking.
    Given the number of animal studies conducted in an effort to show that smoking causes LC and the relatively fewer number that have actually produced worthwhile data, I find the evidence underwhelming and inconclusive. That, of course, is opinion, not fact.
    I would also like to point out that despite the seemingly high risk (1 in 10 smokers developing LC), the real significance of those numbers appears to have been overlooked. Even when the death rate is reduced to 1 in 5, it still means that 80% to 90% of smokers do not die from lung cancer.
    Is it really realistic to infer that smoking is the cause of lung cancer when only 10% of those exposed to the risk actually succumb to the disease? Why have there been no further studies to determine why only 10% of smokers are likely to expire from LC?
    I would opine that, given recent studies which suggest that LC among never smoker smokers and current smokers may be two entirely different diseases, that comparing lung cancer rates between the two may be somewhat akin to comparing apples and oranges.
    And, one last point. I’ve found this debate to be highly informative. It is not enhanced, however, by personal attacks. Please keep it civil, and continue to debate the merits of the argument, rather than questioning the motivation or integrity of those engaged in the debate.
    Matt Todd,
    aka The Old Rambler

  72. Anonymous says:

    Catch 17
    As noted by GDF in his comments, the inclusion of a “recovery” period in many of the animal experiments may have compromised the integrity of the data. There is some evidence to suggest that a similar phenomena may be occurring in the human population.
    The last numerical data I looked at suggested there were 45.3 million current smokers in the US, and 45.7 million former smokers. Those are figures for 2006. The ALA put the figures at 45 million current smokers, 51 million former smokers in 2008. And, although the numbers vary according to the source, the phenomena (where former smokers exceed current smokers) appears to be a fairly recent development in the US.
    A chart prepared by the CDC, based on 2006 data, shows the break down of LC prevalence in the various smoking categories: 20.9% current smokers, 61.2% former Smokers, 17.9% never smokers.
    Source: http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5644a2.htm
    This means that there were far more former smokers (almost three times as many) diagnosed with lung cancer than current smokers, despite a similar sized population. And, in turn, it suggests that the relative risk of contracting (and eventually dying from) lung cancer is greater among former smokers than current smokers. In addition, it intimates that, as far as lung cancer is concerned, there is little benefit in quitting; a seemingly absurd proposition if we accept that LC is, in fact, caused by smoking.
    Given the number of animal studies conducted in an effort to show that smoking causes LC and the relatively fewer number that have actually produced worthwhile data, I find the evidence underwhelming and inconclusive. That, of course, is opinion, not fact.
    I would also like to point out that despite the seemingly high risk (1 in 10 smokers developing LC), the real significance of those numbers appears to have been overlooked. Even when the death rate is reduced to 1 in 5, it still means that 80% to 90% of smokers do not die from lung cancer.
    Is it really realistic to infer that smoking is the cause of lung cancer when only 10% of those exposed to the risk actually succumb to the disease? Why have there been no further studies to determine why only 10% of smokers are likely to expire from LC?
    I would opine that, given recent studies which suggest that LC among never smoker smokers and current smokers may be two entirely different diseases, that comparing lung cancer rates between the two may be somewhat akin to comparing apples and oranges.
    And, one last point. I’ve found this debate to be highly informative. It is not enhanced, however, by personal attacks. Please keep it civil, and continue to debate the merits of the argument, rather than questioning the motivation or integrity of those engaged in the debate.
    Matt Todd,
    aka The Old Rambler

  73. Anonymous says:

    Thank you GDF
    Just doing my civic duty.
    I kept hoping that a proper qualified plant biologist would take over,but when one didn’t, I just had to try my best.
    Glad that I have been of some use, however limited.
    It could take decades to sort this all out.
    Rose

  74. Anonymous says:

    Thank you GDF
    Just doing my civic duty.
    I kept hoping that a proper qualified plant biologist would take over,but when one didn’t, I just had to try my best.
    Glad that I have been of some use, however limited.
    It could take decades to sort this all out.
    Rose

  75. Anonymous says:

    west2
    Some bits I’ve found on Diabetes, if they are any use.
    Diabetes
    “Giving up smoking leads to a sharp increase in the risk of developing type-2 diabetes, according to media reports.
    Quitters face an almost doubled risk of developing diabetes in their first three smoke-free years.
    In the first three years after giving up, new quitters were 91 per cent more likely to develop diabetes”
    “Patients should, however, be made aware of the risk and advised to consider countermeasures, particularly for heavy smokers, they said”
    http://www.gponline.com/News/article/976970/Behind-Headlines-diabetes-linked-quitting-smoking/
    Quite so, but what countermeasures?
    Silent Killer: Big Rise In Diabetes
    “There has been an alarming rise in the number of diabetes cases in the UK – prompting a stark warning from health experts.
    The number of people suffering from the condition rose by 167,000 since last year, bringing the total number to 2.5 million.
    The latest increase is more than double the 2006 to 2007 rise of 83,000
    In England, a 6.4% increase means the number of people with diabetes has passed two million for the first time.”
    http://news.sky.com/skynews/Home/Health/Diabetes-Silent-Killer-Numbers-On-The-Rise/Article/200810315124260
    Prepare to be ostracised, all you smokers of England
    June 11, 2007
    “The organisation Ash hopes that four million people, or almost 40 per cent of smokers, will stop because of the ban. When smokers find they must enter the kingdom of chavdom, expect that figure to rise.
    It is estimated that more than 46,000 people quit as a result of the smoking ban in Scotland. In some areas, the initial “quit rates” were as high as 69 per cent.”
    http://www.timesonline.co.uk/tol/comment/columnists/guest_contributors/article1913299.ece
    Eeek!
    Quitting smoking and diabetes risk
    “This study found that smokers and recent quitters had a greater risk of diabetes compared to those who had never smoked, but that three years after quitting this risk had reduced.
    The suggestion that this is because quitters are more likely to gain weight is logical, but it cannot be proven by this cohort study”
    http://www.nhs.uk/news/2010/01January/Pages/Quitting-smoking-and-diabetes-risk.aspx
    So not the weight gain then.
    “Despite the statement in the introduction that cigarette smoking is consistently identified as a risk factor for incident diabetes, the issue is far from established, and several studies (2,3) indicate smoking may partly protect (women) against diabetes.
    Indeed, in a part of the ARIC cohort, adjusted subjects with isolated impaired glucose tolerance, a prediabetic state more prone to diabetes, were less likely to smoke than those with normal or impaired fasting glucose (4).
    In most studies concerned, the group which subsequently developed diabetes had fewer smokers than those who did not develop.”
    http://www.annals.org/content/152/1/10.abstract/reply#annintmed_el_124005
    Rose

  76. Anonymous says:

    west2
    Some bits I’ve found on Diabetes, if they are any use.
    Diabetes
    “Giving up smoking leads to a sharp increase in the risk of developing type-2 diabetes, according to media reports.
    Quitters face an almost doubled risk of developing diabetes in their first three smoke-free years.
    In the first three years after giving up, new quitters were 91 per cent more likely to develop diabetes”
    “Patients should, however, be made aware of the risk and advised to consider countermeasures, particularly for heavy smokers, they said”
    http://www.gponline.com/News/article/976970/Behind-Headlines-diabetes-linked-quitting-smoking/
    Quite so, but what countermeasures?
    Silent Killer: Big Rise In Diabetes
    “There has been an alarming rise in the number of diabetes cases in the UK – prompting a stark warning from health experts.
    The number of people suffering from the condition rose by 167,000 since last year, bringing the total number to 2.5 million.
    The latest increase is more than double the 2006 to 2007 rise of 83,000
    In England, a 6.4% increase means the number of people with diabetes has passed two million for the first time.”
    http://news.sky.com/skynews/Home/Health/Diabetes-Silent-Killer-Numbers-On-The-Rise/Article/200810315124260
    Prepare to be ostracised, all you smokers of England
    June 11, 2007
    “The organisation Ash hopes that four million people, or almost 40 per cent of smokers, will stop because of the ban. When smokers find they must enter the kingdom of chavdom, expect that figure to rise.
    It is estimated that more than 46,000 people quit as a result of the smoking ban in Scotland. In some areas, the initial “quit rates” were as high as 69 per cent.”
    http://www.timesonline.co.uk/tol/comment/columnists/guest_contributors/article1913299.ece
    Eeek!
    Quitting smoking and diabetes risk
    “This study found that smokers and recent quitters had a greater risk of diabetes compared to those who had never smoked, but that three years after quitting this risk had reduced.
    The suggestion that this is because quitters are more likely to gain weight is logical, but it cannot be proven by this cohort study”
    http://www.nhs.uk/news/2010/01January/Pages/Quitting-smoking-and-diabetes-risk.aspx
    So not the weight gain then.
    “Despite the statement in the introduction that cigarette smoking is consistently identified as a risk factor for incident diabetes, the issue is far from established, and several studies (2,3) indicate smoking may partly protect (women) against diabetes.
    Indeed, in a part of the ARIC cohort, adjusted subjects with isolated impaired glucose tolerance, a prediabetic state more prone to diabetes, were less likely to smoke than those with normal or impaired fasting glucose (4).
    In most studies concerned, the group which subsequently developed diabetes had fewer smokers than those who did not develop.”
    http://www.annals.org/content/152/1/10.abstract/reply#annintmed_el_124005
    Rose

  77. Anonymous says:

    west2
    Some bits I’ve found on Diabetes, if they are any use.
    Diabetes
    “Giving up smoking leads to a sharp increase in the risk of developing type-2 diabetes, according to media reports.
    Quitters face an almost doubled risk of developing diabetes in their first three smoke-free years.
    In the first three years after giving up, new quitters were 91 per cent more likely to develop diabetes”
    “Patients should, however, be made aware of the risk and advised to consider countermeasures, particularly for heavy smokers, they said”
    http://www.gponline.com/News/article/976970/Behind-Headlines-diabetes-linked-quitting-smoking/
    Quite so, but what countermeasures?
    Silent Killer: Big Rise In Diabetes
    “There has been an alarming rise in the number of diabetes cases in the UK – prompting a stark warning from health experts.
    The number of people suffering from the condition rose by 167,000 since last year, bringing the total number to 2.5 million.
    The latest increase is more than double the 2006 to 2007 rise of 83,000
    In England, a 6.4% increase means the number of people with diabetes has passed two million for the first time.”
    http://news.sky.com/skynews/Home/Health/Diabetes-Silent-Killer-Numbers-On-The-Rise/Article/200810315124260
    Prepare to be ostracised, all you smokers of England
    June 11, 2007
    “The organisation Ash hopes that four million people, or almost 40 per cent of smokers, will stop because of the ban. When smokers find they must enter the kingdom of chavdom, expect that figure to rise.
    It is estimated that more than 46,000 people quit as a result of the smoking ban in Scotland. In some areas, the initial “quit rates” were as high as 69 per cent.”
    http://www.timesonline.co.uk/tol/comment/columnists/guest_contributors/article1913299.ece
    Eeek!
    Quitting smoking and diabetes risk
    “This study found that smokers and recent quitters had a greater risk of diabetes compared to those who had never smoked, but that three years after quitting this risk had reduced.
    The suggestion that this is because quitters are more likely to gain weight is logical, but it cannot be proven by this cohort study”
    http://www.nhs.uk/news/2010/01January/Pages/Quitting-smoking-and-diabetes-risk.aspx
    So not the weight gain then.
    “Despite the statement in the introduction that cigarette smoking is consistently identified as a risk factor for incident diabetes, the issue is far from established, and several studies (2,3) indicate smoking may partly protect (women) against diabetes.
    Indeed, in a part of the ARIC cohort, adjusted subjects with isolated impaired glucose tolerance, a prediabetic state more prone to diabetes, were less likely to smoke than those with normal or impaired fasting glucose (4).
    In most studies concerned, the group which subsequently developed diabetes had fewer smokers than those who did not develop.”
    http://www.annals.org/content/152/1/10.abstract/reply#annintmed_el_124005
    Rose

    • Anonymous says:

      Could this be the answer?
      Regulation of insulin activity
      “Although experts cannot agree on the precise mechanism though which vitamin B3 affects blood sugar regulation and function of the hormone insulin, the vitamin has repeatedly been shown to be involved in insulin metabolism and blood sugar regulation.
      Some (but by no means all) researchers support the idea of a “glucose tolerance factor” (GTF) molecule that includes vitamin B3 and must be present for optimal insulin activity.”
      http://whfoods.org/genpage.php?tname=nutrient&dbid=83
      “But a lapse of niacin research during and after World War 11 gave the pharmaceutical companies a voice of unquestioned authority over the new practicing clinicians who had no real experience with niacin deficiency cases and had not lived through events of the Pellagra years in the South, indeed did not recognize the symptoms of pellagra.”
      http://www.orthomed.org/resources/papers/cleadiab.htm
      Or this?
      Coenzyme Q10
      Coenzyme Q10 is a compound that occurs naturally in the body, and may be able to help with carbohydrate metabolism.
      It is has been proven that animals suffering from diabetes are coenzyme Q10 deficient.
      Clinical trials using coenzyme Q10 suggest that supplementation may significantly lower blood sugar levels. Coenzyme Q10 also oxygenates the blood, and therefore may be able to help in some cases of diabetic retinopathy”
      http://www.diabetes.co.uk/vitamins-supplements.html
      CTRI wins patent for using tobacco as medicine
      “New Delhi (PTI): Tobacco will now be used for manufacturing cancer and cardiac drugs with the Central Tobacco Research Institute (CTRI) bagging the patent for ‘solanesol’ — a medicinal substance extracted from tobacco.
      Solanesol, a white crystalline powder derived from tobacco’s green leaf, has curative effects against cardiac insufficiency, muscular dystrophy, anaemia, cancer, diabetes, high blood pressure, asthma and liver injury.
      “Many pharmaceutical companies have approached us for carrying out clinical trials for the usage of solanesol as anti-cancer and anti-diabetic drugs,” CTRI Director V Krishna Murthy told PTI.”
      http://www.hinduonnet.com/thehindu/holnus/008200802171223.htm
      Or this?
      Carbon Monoxide Reverses Diabetic Gastric Problem In Mice, Study Suggests
      “ScienceDaily (June 6, 2009) — Mayo Clinic researchers have shown that very low doses of inhaled carbon monoxide in diabetic mice reverses the condition known as gastroparesis or delayed stomach emptying, a common and painful complication for many diabetic patients. The findings will be presented on June 1 at Digestive Disease Week in Chicago.
      “This is a significant finding, as it shows that loss of the enzyme that makes carbon monoxide is the actor in this process and that it provides us with a clear approach toward a possible new therapy for this condition,” says Gianrico Farrugia, M.D., Mayo Clinic gastroenterologist and lead investigator on the study.”
      http://www.sciencedaily.com/releases/2009/06/090601182653.htm
      Cups of coffee can ward off diabetes . . .
      DRINKING coffee can substantially reduce the risk of developing diabetes, scientists have discovered.
      A major study involving more than 14,000 people in Finland, which has the highest rate of coffee consumption in the world, has revealed that those who drink most have the lowest incidence of adult-onset or type 2 diabetes.
      When people drank three to four cups of coffee a day, their risk of developing diabetes fell by 29 per cent for women and 27 per cent for men.
      “Coffeeholics” who drank very large amounts of coffee — ten or more cups a day — were even less likely to suffer from the disease: such high consumption reduced the risk by 79 per cent for women and 55 per cent for men.”
      http://www.timesonline.co.uk/tol/news/uk/health/article1042229.ece
      Only 10 cups? … amateurs
      Medicine: Vitamin Powwow
      Monday, Sep. 29, 1941
      “All For One. Keynote of the meeting was sounded by Dr. Conrad Elvehjem of Wisconsin (originator of nicotinic-acid treatment for pellagra), who said: “Many of the deficiency diseases . . . are multiple deficiencies.”
      “For specific vitamins do not invariably cure specific diseases; they all work together.”
      http://www.time.com/time/magazine/article/0,9171,766161-1,00.html
      Rose

  78. Anonymous says:

    Could this be the answer?
    Regulation of insulin activity
    “Although experts cannot agree on the precise mechanism though which vitamin B3 affects blood sugar regulation and function of the hormone insulin, the vitamin has repeatedly been shown to be involved in insulin metabolism and blood sugar regulation.
    Some (but by no means all) researchers support the idea of a “glucose tolerance factor” (GTF) molecule that includes vitamin B3 and must be present for optimal insulin activity.”
    http://whfoods.org/genpage.php?tname=nutrient&dbid=83
    “But a lapse of niacin research during and after World War 11 gave the pharmaceutical companies a voice of unquestioned authority over the new practicing clinicians who had no real experience with niacin deficiency cases and had not lived through events of the Pellagra years in the South, indeed did not recognize the symptoms of pellagra.”
    http://www.orthomed.org/resources/papers/cleadiab.htm
    Or this?
    Coenzyme Q10
    Coenzyme Q10 is a compound that occurs naturally in the body, and may be able to help with carbohydrate metabolism.
    It is has been proven that animals suffering from diabetes are coenzyme Q10 deficient.
    Clinical trials using coenzyme Q10 suggest that supplementation may significantly lower blood sugar levels. Coenzyme Q10 also oxygenates the blood, and therefore may be able to help in some cases of diabetic retinopathy”
    http://www.diabetes.co.uk/vitamins-supplements.html
    CTRI wins patent for using tobacco as medicine
    “New Delhi (PTI): Tobacco will now be used for manufacturing cancer and cardiac drugs with the Central Tobacco Research Institute (CTRI) bagging the patent for ‘solanesol’ — a medicinal substance extracted from tobacco.
    Solanesol, a white crystalline powder derived from tobacco’s green leaf, has curative effects against cardiac insufficiency, muscular dystrophy, anaemia, cancer, diabetes, high blood pressure, asthma and liver injury.
    “Many pharmaceutical companies have approached us for carrying out clinical trials for the usage of solanesol as anti-cancer and anti-diabetic drugs,” CTRI Director V Krishna Murthy told PTI.”
    http://www.hinduonnet.com/thehindu/holnus/008200802171223.htm
    Or this?
    Carbon Monoxide Reverses Diabetic Gastric Problem In Mice, Study Suggests
    “ScienceDaily (June 6, 2009) — Mayo Clinic researchers have shown that very low doses of inhaled carbon monoxide in diabetic mice reverses the condition known as gastroparesis or delayed stomach emptying, a common and painful complication for many diabetic patients. The findings will be presented on June 1 at Digestive Disease Week in Chicago.
    “This is a significant finding, as it shows that loss of the enzyme that makes carbon monoxide is the actor in this process and that it provides us with a clear approach toward a possible new therapy for this condition,” says Gianrico Farrugia, M.D., Mayo Clinic gastroenterologist and lead investigator on the study.”
    http://www.sciencedaily.com/releases/2009/06/090601182653.htm
    Cups of coffee can ward off diabetes . . .
    DRINKING coffee can substantially reduce the risk of developing diabetes, scientists have discovered.
    A major study involving more than 14,000 people in Finland, which has the highest rate of coffee consumption in the world, has revealed that those who drink most have the lowest incidence of adult-onset or type 2 diabetes.
    When people drank three to four cups of coffee a day, their risk of developing diabetes fell by 29 per cent for women and 27 per cent for men.
    “Coffeeholics” who drank very large amounts of coffee — ten or more cups a day — were even less likely to suffer from the disease: such high consumption reduced the risk by 79 per cent for women and 55 per cent for men.”
    http://www.timesonline.co.uk/tol/news/uk/health/article1042229.ece
    Only 10 cups? … amateurs
    Medicine: Vitamin Powwow
    Monday, Sep. 29, 1941
    “All For One. Keynote of the meeting was sounded by Dr. Conrad Elvehjem of Wisconsin (originator of nicotinic-acid treatment for pellagra), who said: “Many of the deficiency diseases . . . are multiple deficiencies.”
    “For specific vitamins do not invariably cure specific diseases; they all work together.”
    http://www.time.com/time/magazine/article/0,9171,766161-1,00.html
    Rose

  79. Anonymous says:

    Could this be the answer?
    Regulation of insulin activity
    “Although experts cannot agree on the precise mechanism though which vitamin B3 affects blood sugar regulation and function of the hormone insulin, the vitamin has repeatedly been shown to be involved in insulin metabolism and blood sugar regulation.
    Some (but by no means all) researchers support the idea of a “glucose tolerance factor” (GTF) molecule that includes vitamin B3 and must be present for optimal insulin activity.”
    http://whfoods.org/genpage.php?tname=nutrient&dbid=83
    “But a lapse of niacin research during and after World War 11 gave the pharmaceutical companies a voice of unquestioned authority over the new practicing clinicians who had no real experience with niacin deficiency cases and had not lived through events of the Pellagra years in the South, indeed did not recognize the symptoms of pellagra.”
    http://www.orthomed.org/resources/papers/cleadiab.htm
    Or this?
    Coenzyme Q10
    Coenzyme Q10 is a compound that occurs naturally in the body, and may be able to help with carbohydrate metabolism.
    It is has been proven that animals suffering from diabetes are coenzyme Q10 deficient.
    Clinical trials using coenzyme Q10 suggest that supplementation may significantly lower blood sugar levels. Coenzyme Q10 also oxygenates the blood, and therefore may be able to help in some cases of diabetic retinopathy”
    http://www.diabetes.co.uk/vitamins-supplements.html
    CTRI wins patent for using tobacco as medicine
    “New Delhi (PTI): Tobacco will now be used for manufacturing cancer and cardiac drugs with the Central Tobacco Research Institute (CTRI) bagging the patent for ‘solanesol’ — a medicinal substance extracted from tobacco.
    Solanesol, a white crystalline powder derived from tobacco’s green leaf, has curative effects against cardiac insufficiency, muscular dystrophy, anaemia, cancer, diabetes, high blood pressure, asthma and liver injury.
    “Many pharmaceutical companies have approached us for carrying out clinical trials for the usage of solanesol as anti-cancer and anti-diabetic drugs,” CTRI Director V Krishna Murthy told PTI.”
    http://www.hinduonnet.com/thehindu/holnus/008200802171223.htm
    Or this?
    Carbon Monoxide Reverses Diabetic Gastric Problem In Mice, Study Suggests
    “ScienceDaily (June 6, 2009) — Mayo Clinic researchers have shown that very low doses of inhaled carbon monoxide in diabetic mice reverses the condition known as gastroparesis or delayed stomach emptying, a common and painful complication for many diabetic patients. The findings will be presented on June 1 at Digestive Disease Week in Chicago.
    “This is a significant finding, as it shows that loss of the enzyme that makes carbon monoxide is the actor in this process and that it provides us with a clear approach toward a possible new therapy for this condition,” says Gianrico Farrugia, M.D., Mayo Clinic gastroenterologist and lead investigator on the study.”
    http://www.sciencedaily.com/releases/2009/06/090601182653.htm
    Cups of coffee can ward off diabetes . . .
    DRINKING coffee can substantially reduce the risk of developing diabetes, scientists have discovered.
    A major study involving more than 14,000 people in Finland, which has the highest rate of coffee consumption in the world, has revealed that those who drink most have the lowest incidence of adult-onset or type 2 diabetes.
    When people drank three to four cups of coffee a day, their risk of developing diabetes fell by 29 per cent for women and 27 per cent for men.
    “Coffeeholics” who drank very large amounts of coffee — ten or more cups a day — were even less likely to suffer from the disease: such high consumption reduced the risk by 79 per cent for women and 55 per cent for men.”
    http://www.timesonline.co.uk/tol/news/uk/health/article1042229.ece
    Only 10 cups? … amateurs
    Medicine: Vitamin Powwow
    Monday, Sep. 29, 1941
    “All For One. Keynote of the meeting was sounded by Dr. Conrad Elvehjem of Wisconsin (originator of nicotinic-acid treatment for pellagra), who said: “Many of the deficiency diseases . . . are multiple deficiencies.”
    “For specific vitamins do not invariably cure specific diseases; they all work together.”
    http://www.time.com/time/magazine/article/0,9171,766161-1,00.html
    Rose

  80. richwhite09 says:

    Just found this article, thought it was quite appropriate for this debate
    Proving the Danger of Active Smoking
    I will begin by noting that around 60 million people are said to have died in 2004. Of this number, 603,000 is around one per cent. Most governments are incapable of collecting even the more obvious vital statistics. Probably most African governments have no idea how many people die of diseases like tuberculosis or malaria – and these are direct causes of death. Probably, they have no real idea of how many people are born or die every year. Expecting there to be reliable statistics about passive smoking – which is only said to be a cause of other causes of death – from even a minority of the 192 countries surveyed requires heroic faith in the honesty and competence of people notorious for their incompetence and dishonesty. Indeed, the Report does not claim reliable statistics. It admits that
    [f]or countries without survey data about second-hand smoke, exposure was modelled. [p.3 of the Report]
    That is, the figures were guessed. Anyone who has followed the debate over “climate change” will know that facts derived from computer modelling are at best doubtful.
    But, numbers aside, I really doubt if there is reason to suppose that passive smoking is a cause of other causes of death. Even for active smoking, the evidence of harm is rather weak.It seems reasonable to say that inhaling large amounts of vegetable smoke does the lungs no good. But it is very hard to say what long-term harm it does. Once we look beyond the propagandistic claim that smoking is the biggest preventable cause of fatal illnesses, we see only a mass of conjectures. Because we have been able to observe their entire progress, we know the causes of tuberculosis and malaria. We have been able to gather data and make and test hypotheses. We are not in this position where heart disease and lung cancer are concerned. These appear to have long preparatory stages, during which no symptoms are shown. Tracing them back to any particular cause has not so far been possible.
    After sixty years of research into the effect of active smoking, the best anyone has found are possible correlations. They are no more than possible correlations because they are based on three inherently weak methods of investigation.
    First, there are cohort studies. Two groups of people are taken, the only significant difference between them being that one is comprised of smokers and the other is not. These groups are then followed through life, and periodically questioned, and their rates of cancer in old age are compared. This method is unreliable because people often lie about their behaviour, or are not able to keep accurate records of it. Unlike with tuberculosis and malaria, direct observation is replaced by questionnaire research. Also, it is possible for other important variables to be overlooked.
    Second, there are case studies. Here, people who already have cancer are asked whether they smoked in the past, and how heavily. This method is still more unreliable. There are the same problems of evidence based on self-reporting, and there is the same possibility that other variables may be ignored. There is the further problem that not everyone asked will agree to answer questions about past lifestyle. The result is a biassed sample.
    Third, there are ecologic studies. Here, exposure is estimated to a possible cause of illness, and then matched against incidence of the illness. When plainly stated, this method is obviously defective. No individuals are approached or tested. All that happens is that large statistics are brought together to see what emerges. Imagine this possible case:
    In London three people per 100,000 die of lung diseases. In Teheran, 12 people per 100,000 die of lung diseases. In Iran, lead is allowed in petrol, but not in Britain. From this, we conclude that lead in petrol increases deaths from lung disease by up to 400 per cent.

  81. richwhite09 says:

    Just found this article, thought it was quite appropriate for this debate
    Proving the Danger of Active Smoking
    I will begin by noting that around 60 million people are said to have died in 2004. Of this number, 603,000 is around one per cent. Most governments are incapable of collecting even the more obvious vital statistics. Probably most African governments have no idea how many people die of diseases like tuberculosis or malaria – and these are direct causes of death. Probably, they have no real idea of how many people are born or die every year. Expecting there to be reliable statistics about passive smoking – which is only said to be a cause of other causes of death – from even a minority of the 192 countries surveyed requires heroic faith in the honesty and competence of people notorious for their incompetence and dishonesty. Indeed, the Report does not claim reliable statistics. It admits that
    [f]or countries without survey data about second-hand smoke, exposure was modelled. [p.3 of the Report]
    That is, the figures were guessed. Anyone who has followed the debate over “climate change” will know that facts derived from computer modelling are at best doubtful.
    But, numbers aside, I really doubt if there is reason to suppose that passive smoking is a cause of other causes of death. Even for active smoking, the evidence of harm is rather weak.It seems reasonable to say that inhaling large amounts of vegetable smoke does the lungs no good. But it is very hard to say what long-term harm it does. Once we look beyond the propagandistic claim that smoking is the biggest preventable cause of fatal illnesses, we see only a mass of conjectures. Because we have been able to observe their entire progress, we know the causes of tuberculosis and malaria. We have been able to gather data and make and test hypotheses. We are not in this position where heart disease and lung cancer are concerned. These appear to have long preparatory stages, during which no symptoms are shown. Tracing them back to any particular cause has not so far been possible.
    After sixty years of research into the effect of active smoking, the best anyone has found are possible correlations. They are no more than possible correlations because they are based on three inherently weak methods of investigation.
    First, there are cohort studies. Two groups of people are taken, the only significant difference between them being that one is comprised of smokers and the other is not. These groups are then followed through life, and periodically questioned, and their rates of cancer in old age are compared. This method is unreliable because people often lie about their behaviour, or are not able to keep accurate records of it. Unlike with tuberculosis and malaria, direct observation is replaced by questionnaire research. Also, it is possible for other important variables to be overlooked.
    Second, there are case studies. Here, people who already have cancer are asked whether they smoked in the past, and how heavily. This method is still more unreliable. There are the same problems of evidence based on self-reporting, and there is the same possibility that other variables may be ignored. There is the further problem that not everyone asked will agree to answer questions about past lifestyle. The result is a biassed sample.
    Third, there are ecologic studies. Here, exposure is estimated to a possible cause of illness, and then matched against incidence of the illness. When plainly stated, this method is obviously defective. No individuals are approached or tested. All that happens is that large statistics are brought together to see what emerges. Imagine this possible case:
    In London three people per 100,000 die of lung diseases. In Teheran, 12 people per 100,000 die of lung diseases. In Iran, lead is allowed in petrol, but not in Britain. From this, we conclude that lead in petrol increases deaths from lung disease by up to 400 per cent.

  82. richwhite09 says:

    Just found this article, thought it was quite appropriate for this debate
    Proving the Danger of Active Smoking
    I will begin by noting that around 60 million people are said to have died in 2004. Of this number, 603,000 is around one per cent. Most governments are incapable of collecting even the more obvious vital statistics. Probably most African governments have no idea how many people die of diseases like tuberculosis or malaria – and these are direct causes of death. Probably, they have no real idea of how many people are born or die every year. Expecting there to be reliable statistics about passive smoking – which is only said to be a cause of other causes of death – from even a minority of the 192 countries surveyed requires heroic faith in the honesty and competence of people notorious for their incompetence and dishonesty. Indeed, the Report does not claim reliable statistics. It admits that
    [f]or countries without survey data about second-hand smoke, exposure was modelled. [p.3 of the Report]
    That is, the figures were guessed. Anyone who has followed the debate over “climate change” will know that facts derived from computer modelling are at best doubtful.
    But, numbers aside, I really doubt if there is reason to suppose that passive smoking is a cause of other causes of death. Even for active smoking, the evidence of harm is rather weak.It seems reasonable to say that inhaling large amounts of vegetable smoke does the lungs no good. But it is very hard to say what long-term harm it does. Once we look beyond the propagandistic claim that smoking is the biggest preventable cause of fatal illnesses, we see only a mass of conjectures. Because we have been able to observe their entire progress, we know the causes of tuberculosis and malaria. We have been able to gather data and make and test hypotheses. We are not in this position where heart disease and lung cancer are concerned. These appear to have long preparatory stages, during which no symptoms are shown. Tracing them back to any particular cause has not so far been possible.
    After sixty years of research into the effect of active smoking, the best anyone has found are possible correlations. They are no more than possible correlations because they are based on three inherently weak methods of investigation.
    First, there are cohort studies. Two groups of people are taken, the only significant difference between them being that one is comprised of smokers and the other is not. These groups are then followed through life, and periodically questioned, and their rates of cancer in old age are compared. This method is unreliable because people often lie about their behaviour, or are not able to keep accurate records of it. Unlike with tuberculosis and malaria, direct observation is replaced by questionnaire research. Also, it is possible for other important variables to be overlooked.
    Second, there are case studies. Here, people who already have cancer are asked whether they smoked in the past, and how heavily. This method is still more unreliable. There are the same problems of evidence based on self-reporting, and there is the same possibility that other variables may be ignored. There is the further problem that not everyone asked will agree to answer questions about past lifestyle. The result is a biassed sample.
    Third, there are ecologic studies. Here, exposure is estimated to a possible cause of illness, and then matched against incidence of the illness. When plainly stated, this method is obviously defective. No individuals are approached or tested. All that happens is that large statistics are brought together to see what emerges. Imagine this possible case:
    In London three people per 100,000 die of lung diseases. In Teheran, 12 people per 100,000 die of lung diseases. In Iran, lead is allowed in petrol, but not in Britain. From this, we conclude that lead in petrol increases deaths from lung disease by up to 400 per cent.

    • richwhite09 says:

      (cont’d…)
      Such a claim should never be made or accepted. It takes no account of any other differences between London and Teheran – the climate, the amount of industry in each city, the age and racial profile of each city, the standards of medical treatment, and so forth. The only advantage of ecologic studies is that, assuming the underlying statistics are themselves grounded in reality, they do reveal correlations.
      But, whether strong or weak, correlation is not the same as cause. Correlations may inspire hypotheses about cause, but do not themselves establish cause. Saying, on the basis of any of the three methods, that smoking causes cancer is about as valid as claiming that, because most drivers who crash their cars have eaten bread that day, bread causes motor accidents.
      http://www.lewrockwell.com/orig7/gabb5.1.1.html

  83. richwhite09 says:

    (cont’d…)
    Such a claim should never be made or accepted. It takes no account of any other differences between London and Teheran – the climate, the amount of industry in each city, the age and racial profile of each city, the standards of medical treatment, and so forth. The only advantage of ecologic studies is that, assuming the underlying statistics are themselves grounded in reality, they do reveal correlations.
    But, whether strong or weak, correlation is not the same as cause. Correlations may inspire hypotheses about cause, but do not themselves establish cause. Saying, on the basis of any of the three methods, that smoking causes cancer is about as valid as claiming that, because most drivers who crash their cars have eaten bread that day, bread causes motor accidents.
    http://www.lewrockwell.com/orig7/gabb5.1.1.html

  84. richwhite09 says:

    (cont’d…)
    Such a claim should never be made or accepted. It takes no account of any other differences between London and Teheran – the climate, the amount of industry in each city, the age and racial profile of each city, the standards of medical treatment, and so forth. The only advantage of ecologic studies is that, assuming the underlying statistics are themselves grounded in reality, they do reveal correlations.
    But, whether strong or weak, correlation is not the same as cause. Correlations may inspire hypotheses about cause, but do not themselves establish cause. Saying, on the basis of any of the three methods, that smoking causes cancer is about as valid as claiming that, because most drivers who crash their cars have eaten bread that day, bread causes motor accidents.
    http://www.lewrockwell.com/orig7/gabb5.1.1.html

  85. Anonymous says:

    I agree Matt — and I think it’s a real problem for the smoking > LC argument that smoking cessation is failing to reduce risk (note — cessation is more often coerced these days — which brings the situation closer to the randomized trials that failed). Back in the day when folks self-selected to stop smoking — more often the folks who didn’t “need” (due to genetic variation, vitamin deficiency, other exposures – whatever) to smoke were those who stopped. These folks would have LC risks similar to non-smokers – which might look like risk reduction for that group. The lack of risk reduction we’re seeing now (as smokers who need to smoke, don’t) lends support to a medicinal view of smoking. The failure of cessation theories is backing the smoking > LC group into the corner of 1 cigarette >LC or ETS > LC. Eventually this becomes absurd and destroys the statistical basis on which the argument was originally founded.
    @ west2
    I find the psychological aspects of smoking inbteresting as well. I recall reading Peter Kramer’s “Listening to Prozac” in which he remarked on new Prozac users reported feelings of “feeling like themselves”. He questioned how a person could feel more like themselves with a substance than without. It’s an odd effect. I find that without caffeine I experience headaches. However, without smoking I experience no obvious physical difference effects — but I experience the subtle feeling of not feeling like myself. It’s an odd thing — and I suspect it’s a mix of effects. What I do know — is that even if I were not “smoking” I would still be a “smoker”
    I hope it is clear to those who support the smoking > LC argument that we (I, at least) are not denying this connection because it is convenient — but rather that the argument (IMO)has led nowhere. Like the drunk who keeps looking for the keys under the lamp post (measuring only the things that are easy to measure and trying to make them fit) we need to expand the ideas around the study of LC. I would think this is especially pertinient to the non-smokers who contract LC. Continued harping on smoking > LC is certainly not helping them either.
    Another thought — I also agree with Frank that smoking is not just one thing. There are many, many patterns to how and what people smoke. That’s an interesting area as well.

  86. Anonymous says:

    I agree Matt — and I think it’s a real problem for the smoking > LC argument that smoking cessation is failing to reduce risk (note — cessation is more often coerced these days — which brings the situation closer to the randomized trials that failed). Back in the day when folks self-selected to stop smoking — more often the folks who didn’t “need” (due to genetic variation, vitamin deficiency, other exposures – whatever) to smoke were those who stopped. These folks would have LC risks similar to non-smokers – which might look like risk reduction for that group. The lack of risk reduction we’re seeing now (as smokers who need to smoke, don’t) lends support to a medicinal view of smoking. The failure of cessation theories is backing the smoking > LC group into the corner of 1 cigarette >LC or ETS > LC. Eventually this becomes absurd and destroys the statistical basis on which the argument was originally founded.
    @ west2
    I find the psychological aspects of smoking inbteresting as well. I recall reading Peter Kramer’s “Listening to Prozac” in which he remarked on new Prozac users reported feelings of “feeling like themselves”. He questioned how a person could feel more like themselves with a substance than without. It’s an odd effect. I find that without caffeine I experience headaches. However, without smoking I experience no obvious physical difference effects — but I experience the subtle feeling of not feeling like myself. It’s an odd thing — and I suspect it’s a mix of effects. What I do know — is that even if I were not “smoking” I would still be a “smoker”
    I hope it is clear to those who support the smoking > LC argument that we (I, at least) are not denying this connection because it is convenient — but rather that the argument (IMO)has led nowhere. Like the drunk who keeps looking for the keys under the lamp post (measuring only the things that are easy to measure and trying to make them fit) we need to expand the ideas around the study of LC. I would think this is especially pertinient to the non-smokers who contract LC. Continued harping on smoking > LC is certainly not helping them either.
    Another thought — I also agree with Frank that smoking is not just one thing. There are many, many patterns to how and what people smoke. That’s an interesting area as well.

  87. Anonymous says:

    I agree Matt — and I think it’s a real problem for the smoking > LC argument that smoking cessation is failing to reduce risk (note — cessation is more often coerced these days — which brings the situation closer to the randomized trials that failed). Back in the day when folks self-selected to stop smoking — more often the folks who didn’t “need” (due to genetic variation, vitamin deficiency, other exposures – whatever) to smoke were those who stopped. These folks would have LC risks similar to non-smokers – which might look like risk reduction for that group. The lack of risk reduction we’re seeing now (as smokers who need to smoke, don’t) lends support to a medicinal view of smoking. The failure of cessation theories is backing the smoking > LC group into the corner of 1 cigarette >LC or ETS > LC. Eventually this becomes absurd and destroys the statistical basis on which the argument was originally founded.
    @ west2
    I find the psychological aspects of smoking inbteresting as well. I recall reading Peter Kramer’s “Listening to Prozac” in which he remarked on new Prozac users reported feelings of “feeling like themselves”. He questioned how a person could feel more like themselves with a substance than without. It’s an odd effect. I find that without caffeine I experience headaches. However, without smoking I experience no obvious physical difference effects — but I experience the subtle feeling of not feeling like myself. It’s an odd thing — and I suspect it’s a mix of effects. What I do know — is that even if I were not “smoking” I would still be a “smoker”
    I hope it is clear to those who support the smoking > LC argument that we (I, at least) are not denying this connection because it is convenient — but rather that the argument (IMO)has led nowhere. Like the drunk who keeps looking for the keys under the lamp post (measuring only the things that are easy to measure and trying to make them fit) we need to expand the ideas around the study of LC. I would think this is especially pertinient to the non-smokers who contract LC. Continued harping on smoking > LC is certainly not helping them either.
    Another thought — I also agree with Frank that smoking is not just one thing. There are many, many patterns to how and what people smoke. That’s an interesting area as well.

    • richwhite09 says:

      “I would think this is especially pertinient to the non-smokers who contract LC. Continued harping on smoking > LC is certainly not helping them either. ”
      This is the most criminal thing about TC. There was a news report the other day of a lifelong non-smoker who developed lung cancer. She was shocked, naturally, but actually said she didn’t know non-smokers could get lung cancer – that’s how much non-smokers are being failed by the medical community. I wish I had bookmarked the story now, i didn’t think i’d be referencing it again though

  88. richwhite09 says:

    “I would think this is especially pertinient to the non-smokers who contract LC. Continued harping on smoking > LC is certainly not helping them either. ”
    This is the most criminal thing about TC. There was a news report the other day of a lifelong non-smoker who developed lung cancer. She was shocked, naturally, but actually said she didn’t know non-smokers could get lung cancer – that’s how much non-smokers are being failed by the medical community. I wish I had bookmarked the story now, i didn’t think i’d be referencing it again though

  89. richwhite09 says:

    “I would think this is especially pertinient to the non-smokers who contract LC. Continued harping on smoking > LC is certainly not helping them either. ”
    This is the most criminal thing about TC. There was a news report the other day of a lifelong non-smoker who developed lung cancer. She was shocked, naturally, but actually said she didn’t know non-smokers could get lung cancer – that’s how much non-smokers are being failed by the medical community. I wish I had bookmarked the story now, i didn’t think i’d be referencing it again though

  90. Anonymous says:

    Forgot to sign that last post — it was me (aka mysterious stranger)
    GDF

  91. Anonymous says:

    Forgot to sign that last post — it was me (aka mysterious stranger)
    GDF

  92. Anonymous says:

    Forgot to sign that last post — it was me (aka mysterious stranger)
    GDF

  93. Anonymous says:

    Rich — within the last 2 years my two best friends and another very good friend have all been diagnosed with cancer (none of them LC). All are in their mid 50’s. Two never smokers and one ex-smoker (quit 28 years ago). One of the never smokers has recently taken up smoking after surgery, chemo, radiation, and repeat) . She said she always wanted to smoke — and now “what the hell?”. All three have expressed how surprised they were at the diagnoses because they “did what they were supposed to do”. It’s only anecdotal — not evidence of anything – but is part of my own motivation for trying to understand cancer better.

  94. Anonymous says:

    Rich — within the last 2 years my two best friends and another very good friend have all been diagnosed with cancer (none of them LC). All are in their mid 50’s. Two never smokers and one ex-smoker (quit 28 years ago). One of the never smokers has recently taken up smoking after surgery, chemo, radiation, and repeat) . She said she always wanted to smoke — and now “what the hell?”. All three have expressed how surprised they were at the diagnoses because they “did what they were supposed to do”. It’s only anecdotal — not evidence of anything – but is part of my own motivation for trying to understand cancer better.

  95. Anonymous says:

    Rich — within the last 2 years my two best friends and another very good friend have all been diagnosed with cancer (none of them LC). All are in their mid 50’s. Two never smokers and one ex-smoker (quit 28 years ago). One of the never smokers has recently taken up smoking after surgery, chemo, radiation, and repeat) . She said she always wanted to smoke — and now “what the hell?”. All three have expressed how surprised they were at the diagnoses because they “did what they were supposed to do”. It’s only anecdotal — not evidence of anything – but is part of my own motivation for trying to understand cancer better.

    • richwhite09 says:

      “All three have expressed how surprised they were at the diagnoses because they “did what they were supposed to do””
      That’s not unheard of. We had the same thing in my family, my nan died of bone cancer and there was no reason given. She smoked 5 silk cut a day, and besides being such a small amount she got the ‘wrong’ cancer for it to be smoking-related. It seems that beyond drinkers and smokers, there is very little doctors say about what causes someone’s cancer. Which is part of the reason I stated to Chris earlier in the debate that it’s simply not possible to say the smoking/cancer link is conclusive and that all other areas have been investigated, because they simply haven’t – there’s too much we don’t know about the disease yet.

  96. Anonymous says:

    Darn! That was me again – GDF

  97. Anonymous says:

    Darn! That was me again – GDF

  98. Anonymous says:

    Darn! That was me again – GDF

  99. Anonymous says:

    Stigma, shame, and blame experienced by patients with lung cancer:qualitative study
    “Doctors as well as friends and family seemed to assume that a patient’s lung cancer was caused by smoking even if he or she had stopped smoking years ago or never smoked.
    One man, despite never smoking, recalled negative attitudes at the hospital when he had his operation:
    “I think cancer does have a stigma attached to it. . . I think all lung cancer patients are stigmatised because of smoking. . . When I went to see an oncologist for further treatments because I’d had an operation and I’d had half of my left lung removed, I asked them what he thought had caused it and he just laughed and said,
    “That’s obvious, through smoking.”
    And my wife who was with me at the time, and we’ve been together since we were 14, she just said, “Well he’s never smoked.”
    So right away what annoyed me as well as that, on my medical records I’m classed as a smoker and every time I ever went for review after that they would ask me, “Are you still smoking?” because that’s down there.
    And no matter how I told them, I’d say, “Look I don’t want that on there, I never smoked,”
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC428516/
    Words fail me.
    Rose

  100. Anonymous says:

    Stigma, shame, and blame experienced by patients with lung cancer:qualitative study
    “Doctors as well as friends and family seemed to assume that a patient’s lung cancer was caused by smoking even if he or she had stopped smoking years ago or never smoked.
    One man, despite never smoking, recalled negative attitudes at the hospital when he had his operation:
    “I think cancer does have a stigma attached to it. . . I think all lung cancer patients are stigmatised because of smoking. . . When I went to see an oncologist for further treatments because I’d had an operation and I’d had half of my left lung removed, I asked them what he thought had caused it and he just laughed and said,
    “That’s obvious, through smoking.”
    And my wife who was with me at the time, and we’ve been together since we were 14, she just said, “Well he’s never smoked.”
    So right away what annoyed me as well as that, on my medical records I’m classed as a smoker and every time I ever went for review after that they would ask me, “Are you still smoking?” because that’s down there.
    And no matter how I told them, I’d say, “Look I don’t want that on there, I never smoked,”
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC428516/
    Words fail me.
    Rose

  101. Anonymous says:

    Stigma, shame, and blame experienced by patients with lung cancer:qualitative study
    “Doctors as well as friends and family seemed to assume that a patient’s lung cancer was caused by smoking even if he or she had stopped smoking years ago or never smoked.
    One man, despite never smoking, recalled negative attitudes at the hospital when he had his operation:
    “I think cancer does have a stigma attached to it. . . I think all lung cancer patients are stigmatised because of smoking. . . When I went to see an oncologist for further treatments because I’d had an operation and I’d had half of my left lung removed, I asked them what he thought had caused it and he just laughed and said,
    “That’s obvious, through smoking.”
    And my wife who was with me at the time, and we’ve been together since we were 14, she just said, “Well he’s never smoked.”
    So right away what annoyed me as well as that, on my medical records I’m classed as a smoker and every time I ever went for review after that they would ask me, “Are you still smoking?” because that’s down there.
    And no matter how I told them, I’d say, “Look I don’t want that on there, I never smoked,”
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC428516/
    Words fail me.
    Rose

  102. Anonymous says:

    I do not have a specific point on the subject. I’m not an expert in statistics. I’m an economist, but I’m not an expert in econometrics (I did several courses in statistics on my post graduation in economics, but I consider myself an ignoramus on this subject). My concern is about methodology and philosophy of science. Nevertheless, I thought this article shows very clearly the difficulties in dealing with the idea of causality in statistics.

  103. Anonymous says:

    I do not have a specific point on the subject. I’m not an expert in statistics. I’m an economist, but I’m not an expert in econometrics (I did several courses in statistics on my post graduation in economics, but I consider myself an ignoramus on this subject). My concern is about methodology and philosophy of science. Nevertheless, I thought this article shows very clearly the difficulties in dealing with the idea of causality in statistics.

  104. Anonymous says:

    Medicine: Making Cigarettes Safe?
    1957
    “Dr. Wynder told the American Association for Cancer Research, meeting in Chicago, that the villain is not present in tobacco leaves in their natural, unburned state.
    His research team proved this by extracting tar from cigarette tobacco without burning it: the resulting substance produced virtually no cancers when painted on the backs of mice.
    But batches of the same tobacco were burned at varying temperatures, and the tars extracted. Tar from the lower-temperature-burning ranges (560° to 720° C.) produced few or no cancers. From 800° to 880° C. the number of cancers increased.
    Conclusion: evidently, the cancer-causing agent is the result of high-temperature combustion.”
    “Tentative Conclusion. Could the original substance from which the cancer agent is formed be pinned down and removed from the tobacco? Wynder & Co. closed in on a natural waxy substance that is known to coat the tobacco leaf. In the wax are “aliphatic hydrocarbons.” which, burned at high temperatures, produce “polycyclic hydrocarbons,” and these in turn can cause cancer.
    Working with the University of Toronto’s Chemist George Wright, the researchers washed tobacco in hot hexane, which dissolves the wax. They extracted the wax and burned it alone.
    The resulting tar proved to be at least ten times as cancer-potent as ordinary tar from whole tobacco: in five months all mice painted with a 5% solution from tests at 880° had papillomas (precursors of cancer), and 27% had full-blown cancer.
    The tar from the wax contained all the cancer agents now known to exist in small amounts in cigarette tar, but Dr. Wynder doubts that these substances are the only cause of the lung-cancer increase, suspects there are others in the tar.”
    http://www.time.com/time/magazine/article/0,9171,824810,00.html
    Destructive distillation again?
    Duvatrienediol, alkanes, and fatty acids in cuticular wax of tobacco leaves of various physiological maturity
    4,8,13-Duvatriene-1,3-diol found in the leaf wax of Nicotiana tabacum was of highest concentration in the wax from young leaves, and quantitatively decreased in importance with leaf age.
    Tobacco plants in flower had less duvatrienediol than those that were less mature; however, the total wax content did not change with leaf age.
    Air drying leaves reduced the duvatrienediol concentration”
    http://tinyurl.com/29hzpck
    “Production of leaf surface lipid and duvatrienediol was affected by soil conditions or amount of N fertilizer.
    Leaf surface lipid and duvatrienediol decreased during curing of tobacco leaves, the change in the latter being more drastic”
    http://eurekamag.com/keyword/d/293/duvatrienediol.php
    I daresay that’s what all that aging after curing is about.
    Rose

  105. Anonymous says:

    Medicine: Making Cigarettes Safe?
    1957
    “Dr. Wynder told the American Association for Cancer Research, meeting in Chicago, that the villain is not present in tobacco leaves in their natural, unburned state.
    His research team proved this by extracting tar from cigarette tobacco without burning it: the resulting substance produced virtually no cancers when painted on the backs of mice.
    But batches of the same tobacco were burned at varying temperatures, and the tars extracted. Tar from the lower-temperature-burning ranges (560° to 720° C.) produced few or no cancers. From 800° to 880° C. the number of cancers increased.
    Conclusion: evidently, the cancer-causing agent is the result of high-temperature combustion.”
    “Tentative Conclusion. Could the original substance from which the cancer agent is formed be pinned down and removed from the tobacco? Wynder & Co. closed in on a natural waxy substance that is known to coat the tobacco leaf. In the wax are “aliphatic hydrocarbons.” which, burned at high temperatures, produce “polycyclic hydrocarbons,” and these in turn can cause cancer.
    Working with the University of Toronto’s Chemist George Wright, the researchers washed tobacco in hot hexane, which dissolves the wax. They extracted the wax and burned it alone.
    The resulting tar proved to be at least ten times as cancer-potent as ordinary tar from whole tobacco: in five months all mice painted with a 5% solution from tests at 880° had papillomas (precursors of cancer), and 27% had full-blown cancer.
    The tar from the wax contained all the cancer agents now known to exist in small amounts in cigarette tar, but Dr. Wynder doubts that these substances are the only cause of the lung-cancer increase, suspects there are others in the tar.”
    http://www.time.com/time/magazine/article/0,9171,824810,00.html
    Destructive distillation again?
    Duvatrienediol, alkanes, and fatty acids in cuticular wax of tobacco leaves of various physiological maturity
    4,8,13-Duvatriene-1,3-diol found in the leaf wax of Nicotiana tabacum was of highest concentration in the wax from young leaves, and quantitatively decreased in importance with leaf age.
    Tobacco plants in flower had less duvatrienediol than those that were less mature; however, the total wax content did not change with leaf age.
    Air drying leaves reduced the duvatrienediol concentration”
    http://tinyurl.com/29hzpck
    “Production of leaf surface lipid and duvatrienediol was affected by soil conditions or amount of N fertilizer.
    Leaf surface lipid and duvatrienediol decreased during curing of tobacco leaves, the change in the latter being more drastic”
    http://eurekamag.com/keyword/d/293/duvatrienediol.php
    I daresay that’s what all that aging after curing is about.
    Rose

  106. Anonymous says:

    Medicine: Making Cigarettes Safe?
    1957
    “Dr. Wynder told the American Association for Cancer Research, meeting in Chicago, that the villain is not present in tobacco leaves in their natural, unburned state.
    His research team proved this by extracting tar from cigarette tobacco without burning it: the resulting substance produced virtually no cancers when painted on the backs of mice.
    But batches of the same tobacco were burned at varying temperatures, and the tars extracted. Tar from the lower-temperature-burning ranges (560° to 720° C.) produced few or no cancers. From 800° to 880° C. the number of cancers increased.
    Conclusion: evidently, the cancer-causing agent is the result of high-temperature combustion.”
    “Tentative Conclusion. Could the original substance from which the cancer agent is formed be pinned down and removed from the tobacco? Wynder & Co. closed in on a natural waxy substance that is known to coat the tobacco leaf. In the wax are “aliphatic hydrocarbons.” which, burned at high temperatures, produce “polycyclic hydrocarbons,” and these in turn can cause cancer.
    Working with the University of Toronto’s Chemist George Wright, the researchers washed tobacco in hot hexane, which dissolves the wax. They extracted the wax and burned it alone.
    The resulting tar proved to be at least ten times as cancer-potent as ordinary tar from whole tobacco: in five months all mice painted with a 5% solution from tests at 880° had papillomas (precursors of cancer), and 27% had full-blown cancer.
    The tar from the wax contained all the cancer agents now known to exist in small amounts in cigarette tar, but Dr. Wynder doubts that these substances are the only cause of the lung-cancer increase, suspects there are others in the tar.”
    http://www.time.com/time/magazine/article/0,9171,824810,00.html
    Destructive distillation again?
    Duvatrienediol, alkanes, and fatty acids in cuticular wax of tobacco leaves of various physiological maturity
    4,8,13-Duvatriene-1,3-diol found in the leaf wax of Nicotiana tabacum was of highest concentration in the wax from young leaves, and quantitatively decreased in importance with leaf age.
    Tobacco plants in flower had less duvatrienediol than those that were less mature; however, the total wax content did not change with leaf age.
    Air drying leaves reduced the duvatrienediol concentration”
    http://tinyurl.com/29hzpck
    “Production of leaf surface lipid and duvatrienediol was affected by soil conditions or amount of N fertilizer.
    Leaf surface lipid and duvatrienediol decreased during curing of tobacco leaves, the change in the latter being more drastic”
    http://eurekamag.com/keyword/d/293/duvatrienediol.php
    I daresay that’s what all that aging after curing is about.
    Rose

    • Anonymous says:

      You can’t burn what is no longer there.
      So Wynders experiment was pointless on anything but young, green tobacco.
      On reflection, another reason that they might have only experimented on the extracted “tar”, is that it was already known that nicotine oxidized to nicotinic acid, because they were already putting it in the bread.
      Voluntarily from 1938 and later by law.
      Effectiveness of Food Fortification in the United States : The Case of Pellagra

      Click to access 727.pdf


      “Nicotinic acid was first made by the oxidation of nicotine and Whiffens operate a commercial process in this country starting with tobacco.
      Later they were supplied with nicotine by the British Nicotine Company and continued the oxidation.
      Finally – before the Second World War – they found they were unable to compete with manufacturers starting from quinoline and picoline although it could be made directly from tobacco waste, from pyridine, some other coal tar bases, nicotine, anabasine, nor-nicotine or mixed tobacco alkaloids.
      The U.S. Department of Agriculture sponsored work aimed to make nicotine compete, as early as 1942, but although a new catalytic oxidation process was developed quinoline was still the cheapest source of nicotinic acid.
      Comparative costs were published in 1951 by Coal Tar Products of Philadelphia”

      Click to access 00000711.pdf


      Rose

      • richwhite09 says:

        Rose, I mentioned already I’m considering updating my book following the information from this debate. Your posts have been very informative, especially on nicotine and niacin, and I want to use some of your information in my chapters on nicotine and the health benefits of smoking. Would you mind dropping me an email to discuss it and for me to start collating some of your evidence and references?(my email is richwhite[at]smokescreens.org – replace the [at] with @, i have to type it like this now to avoid being inundated with spam)

  107. richwhite09 says:

    “All three have expressed how surprised they were at the diagnoses because they “did what they were supposed to do””
    That’s not unheard of. We had the same thing in my family, my nan died of bone cancer and there was no reason given. She smoked 5 silk cut a day, and besides being such a small amount she got the ‘wrong’ cancer for it to be smoking-related. It seems that beyond drinkers and smokers, there is very little doctors say about what causes someone’s cancer. Which is part of the reason I stated to Chris earlier in the debate that it’s simply not possible to say the smoking/cancer link is conclusive and that all other areas have been investigated, because they simply haven’t – there’s too much we don’t know about the disease yet.

  108. richwhite09 says:

    “All three have expressed how surprised they were at the diagnoses because they “did what they were supposed to do””
    That’s not unheard of. We had the same thing in my family, my nan died of bone cancer and there was no reason given. She smoked 5 silk cut a day, and besides being such a small amount she got the ‘wrong’ cancer for it to be smoking-related. It seems that beyond drinkers and smokers, there is very little doctors say about what causes someone’s cancer. Which is part of the reason I stated to Chris earlier in the debate that it’s simply not possible to say the smoking/cancer link is conclusive and that all other areas have been investigated, because they simply haven’t – there’s too much we don’t know about the disease yet.

  109. richwhite09 says:

    On the tumour suppression/self-medication theme, I thought this was a good place for this comment.
    I have just looked at the news report from Vancouver posted on this board a few times about lung cancer in smokers being different to non smokers (http://www.montrealgazette.com/health/Lung+cancer+smokers+looks+different+than+smoker/3806044/story.html)
    The article doesn’t seem to give the study name, and it quickly goes into just talking about screening methods for LC. But it does say, of the results, that:
    “Tumours in those who had never smoked actually had twice as many genetic abnormalities, or DNA mutations, as those who were current or former smokers, according to the research presented Tuesday at an American Association of Cancer Research conference in Philadelphia.”
    This seems to be in perfect keeping with the posts already made, about the ‘recovery period’ in animal studies and the tumour-suppression effects of tobacco smoke. It’s not possible to state with certainty until i read the actual study, but the part mentioned in the press (above) says that non-smokers’ tumours had twice the levels of DNA mutations, which does tie in perfectly with the suggestion of the protective effect of smoke.
    Rather than hail this as a breakthrough of a ‘new disease’, perhaps the medical community should be doing what has already been suggested and conduct research into why only 10% of smokers get LC and what, if any, biological variations they naturally have compared to either smokers who don’t get the disease or non-smokers.
    The more studies and evidence that gets posted in this debate, the more it seems science is laying out the benefits of smoking. Yet at the same time it’s working very hard to demonise it. I wonder if the balance will reverse at some point if and when the evidence becomes overwhelming.

  110. richwhite09 says:

    On the tumour suppression/self-medication theme, I thought this was a good place for this comment.
    I have just looked at the news report from Vancouver posted on this board a few times about lung cancer in smokers being different to non smokers (http://www.montrealgazette.com/health/Lung+cancer+smokers+looks+different+than+smoker/3806044/story.html)
    The article doesn’t seem to give the study name, and it quickly goes into just talking about screening methods for LC. But it does say, of the results, that:
    “Tumours in those who had never smoked actually had twice as many genetic abnormalities, or DNA mutations, as those who were current or former smokers, according to the research presented Tuesday at an American Association of Cancer Research conference in Philadelphia.”
    This seems to be in perfect keeping with the posts already made, about the ‘recovery period’ in animal studies and the tumour-suppression effects of tobacco smoke. It’s not possible to state with certainty until i read the actual study, but the part mentioned in the press (above) says that non-smokers’ tumours had twice the levels of DNA mutations, which does tie in perfectly with the suggestion of the protective effect of smoke.
    Rather than hail this as a breakthrough of a ‘new disease’, perhaps the medical community should be doing what has already been suggested and conduct research into why only 10% of smokers get LC and what, if any, biological variations they naturally have compared to either smokers who don’t get the disease or non-smokers.
    The more studies and evidence that gets posted in this debate, the more it seems science is laying out the benefits of smoking. Yet at the same time it’s working very hard to demonise it. I wonder if the balance will reverse at some point if and when the evidence becomes overwhelming.

  111. richwhite09 says:

    On the tumour suppression/self-medication theme, I thought this was a good place for this comment.
    I have just looked at the news report from Vancouver posted on this board a few times about lung cancer in smokers being different to non smokers (http://www.montrealgazette.com/health/Lung+cancer+smokers+looks+different+than+smoker/3806044/story.html)
    The article doesn’t seem to give the study name, and it quickly goes into just talking about screening methods for LC. But it does say, of the results, that:
    “Tumours in those who had never smoked actually had twice as many genetic abnormalities, or DNA mutations, as those who were current or former smokers, according to the research presented Tuesday at an American Association of Cancer Research conference in Philadelphia.”
    This seems to be in perfect keeping with the posts already made, about the ‘recovery period’ in animal studies and the tumour-suppression effects of tobacco smoke. It’s not possible to state with certainty until i read the actual study, but the part mentioned in the press (above) says that non-smokers’ tumours had twice the levels of DNA mutations, which does tie in perfectly with the suggestion of the protective effect of smoke.
    Rather than hail this as a breakthrough of a ‘new disease’, perhaps the medical community should be doing what has already been suggested and conduct research into why only 10% of smokers get LC and what, if any, biological variations they naturally have compared to either smokers who don’t get the disease or non-smokers.
    The more studies and evidence that gets posted in this debate, the more it seems science is laying out the benefits of smoking. Yet at the same time it’s working very hard to demonise it. I wonder if the balance will reverse at some point if and when the evidence becomes overwhelming.

  112. Anonymous says:

    Quitting and the recovery period
    The anti-smokers always clam that quitting reduces the likelihood of lung cancer. Doll’s ‘Doctors study’ appears to show a much lower LC risk for ex-smokers and I think this is the main source for the claim.
    But on closer inspection, all is not as it appears.
    The British Doctors study began with a questionnaire sent to all British doctors in 1951. Follow up questionnaires and papers were published at intervals for 50 years.
    From his 1994 paper – “Mortality in relation to smoking: 40 years’ observations on male British doctors” – http://www.bmj.com/content/309/6959/901.full
    “Deaths that occurred in the year that a repeat questionnaire was sent out were related to the reply to the previous questionnaire. (This helps limit the effects of disease on smoking.) Otherwise non-smokers and continuing smokers were analysed in the category in which they last described themselves. The same is true for former smokers, except that they were classed as having stopped smoking for progressively longer periods as each year passed.”
    From his final 2004 paper – “Mortality in relation to smoking: 50 years’ observations on male British doctors” – http://www.bmj.com/content/328/7455/1519.full.pdf
    “The 1951 study has now continued for much longer than originally anticipated, as the doctors did indeed prove easy to follow, and they provided further information about any changes in their smoking habits along the way (in 1957, 1966, 1971, 1978,and 1991). A final questionnaire was sent out in 2001.”
    What this means is that if someone sent off the questionnaire and promptly quit, they would have to live long enough to fill out the next questionnaire which could be between 5 and 13 years later. Only then would their subsequent death be recorded as an ex-smoker death. I other words they could (at worst) have been categorised as a current smoker at death even if they had given up 13 years earlier.
    Receiving the original 1951 questionnaire would have been a very strong incentive to quit. And my impression is that the quit rate was very high in the early years. Intriguingly though, the lung cancer death rate amongst his doctors rose from 15 per annum (1951-1954) to 24 per annum (1954-1956 – Doll’s second follow up paper). Though I should point out that there were few doctors over 80 who responded to the 1951 questionnaire. Which means that some increase was to be expected due to the aging study population.
    Hammond and Horn’s study of 1958 doesn’t mention ex-smokers. But once again, many of their smokers would have quit during the period and as far as I can see, they did not reclassify any as ex-smokers.
    Tony

  113. Anonymous says:

    Quitting and the recovery period
    The anti-smokers always clam that quitting reduces the likelihood of lung cancer. Doll’s ‘Doctors study’ appears to show a much lower LC risk for ex-smokers and I think this is the main source for the claim.
    But on closer inspection, all is not as it appears.
    The British Doctors study began with a questionnaire sent to all British doctors in 1951. Follow up questionnaires and papers were published at intervals for 50 years.
    From his 1994 paper – “Mortality in relation to smoking: 40 years’ observations on male British doctors” – http://www.bmj.com/content/309/6959/901.full
    “Deaths that occurred in the year that a repeat questionnaire was sent out were related to the reply to the previous questionnaire. (This helps limit the effects of disease on smoking.) Otherwise non-smokers and continuing smokers were analysed in the category in which they last described themselves. The same is true for former smokers, except that they were classed as having stopped smoking for progressively longer periods as each year passed.”
    From his final 2004 paper – “Mortality in relation to smoking: 50 years’ observations on male British doctors” – http://www.bmj.com/content/328/7455/1519.full.pdf
    “The 1951 study has now continued for much longer than originally anticipated, as the doctors did indeed prove easy to follow, and they provided further information about any changes in their smoking habits along the way (in 1957, 1966, 1971, 1978,and 1991). A final questionnaire was sent out in 2001.”
    What this means is that if someone sent off the questionnaire and promptly quit, they would have to live long enough to fill out the next questionnaire which could be between 5 and 13 years later. Only then would their subsequent death be recorded as an ex-smoker death. I other words they could (at worst) have been categorised as a current smoker at death even if they had given up 13 years earlier.
    Receiving the original 1951 questionnaire would have been a very strong incentive to quit. And my impression is that the quit rate was very high in the early years. Intriguingly though, the lung cancer death rate amongst his doctors rose from 15 per annum (1951-1954) to 24 per annum (1954-1956 – Doll’s second follow up paper). Though I should point out that there were few doctors over 80 who responded to the 1951 questionnaire. Which means that some increase was to be expected due to the aging study population.
    Hammond and Horn’s study of 1958 doesn’t mention ex-smokers. But once again, many of their smokers would have quit during the period and as far as I can see, they did not reclassify any as ex-smokers.
    Tony

  114. Anonymous says:

    Quitting and the recovery period
    The anti-smokers always clam that quitting reduces the likelihood of lung cancer. Doll’s ‘Doctors study’ appears to show a much lower LC risk for ex-smokers and I think this is the main source for the claim.
    But on closer inspection, all is not as it appears.
    The British Doctors study began with a questionnaire sent to all British doctors in 1951. Follow up questionnaires and papers were published at intervals for 50 years.
    From his 1994 paper – “Mortality in relation to smoking: 40 years’ observations on male British doctors” – http://www.bmj.com/content/309/6959/901.full
    “Deaths that occurred in the year that a repeat questionnaire was sent out were related to the reply to the previous questionnaire. (This helps limit the effects of disease on smoking.) Otherwise non-smokers and continuing smokers were analysed in the category in which they last described themselves. The same is true for former smokers, except that they were classed as having stopped smoking for progressively longer periods as each year passed.”
    From his final 2004 paper – “Mortality in relation to smoking: 50 years’ observations on male British doctors” – http://www.bmj.com/content/328/7455/1519.full.pdf
    “The 1951 study has now continued for much longer than originally anticipated, as the doctors did indeed prove easy to follow, and they provided further information about any changes in their smoking habits along the way (in 1957, 1966, 1971, 1978,and 1991). A final questionnaire was sent out in 2001.”
    What this means is that if someone sent off the questionnaire and promptly quit, they would have to live long enough to fill out the next questionnaire which could be between 5 and 13 years later. Only then would their subsequent death be recorded as an ex-smoker death. I other words they could (at worst) have been categorised as a current smoker at death even if they had given up 13 years earlier.
    Receiving the original 1951 questionnaire would have been a very strong incentive to quit. And my impression is that the quit rate was very high in the early years. Intriguingly though, the lung cancer death rate amongst his doctors rose from 15 per annum (1951-1954) to 24 per annum (1954-1956 – Doll’s second follow up paper). Though I should point out that there were few doctors over 80 who responded to the 1951 questionnaire. Which means that some increase was to be expected due to the aging study population.
    Hammond and Horn’s study of 1958 doesn’t mention ex-smokers. But once again, many of their smokers would have quit during the period and as far as I can see, they did not reclassify any as ex-smokers.
    Tony

  115. Anonymous says:

    Catch 17
    Epidemiology has been shown to be less than effective in proving causality than some claim. One case in point is the relationship between smoking and cervical cancer.
    In 2004, the Surgeon General of the US added uterine cervical cancer to the list of those for which evidence was allegedly sufficient to conclude a causal relationship between smoking and the disease. Health Canada used the claim to justify the addition of cervical cancer to their list of smoking related diseases. Their 2007 SAMMEC report claims that 126 of 382 deaths (34.7%) from cervical cancer were caused by smoking.
    However, by September, 2009, the Canadian Cancer Society (and Health Canada) was claiming that all cervical cancer was caused by persistent HPV infection with high risk types of the virus. “Nearly all cervical cancers are caused by persistent high-risk HPV infection. High-risk types of HPV are considered known cancer-causing agents. About 70% of cervical cancers are associated with high-risk HPV type 16 and 18. Other high-risk types of HPV are associated with the other 30% of cervical cancers.”
    So, despite a seemingly strong statistical correlation between cervical cancer and smoking, it was eventually determined that smoking was not a cause of that particular cancer. The fact that more women who developed or died from cervical cancer were smokers was inconsequential; a false lead.
    The growing evidence linking LC and HPV has also been largely ignored in North America and the UK, as has been noted in previous comments.
    For epidemiology to be effective in developing hypotheses as to the cause and effect of various risk factors on disease incidence, it must be constantly re-appraised and re-evaluated in light of new information and circumstances. That hasn’t happened in the case of smoking and LC.
    And, as noted in other comments, all lung cancer victims are stigmatized by the statistical association with smoking. Even more criminal, however, is the fact that lung cancer research is so grossly underfunded compared to other types, thanks largely to the association with smoking.
    From the Lung Cancer Alliance: “Sad. Lung cancer patients continue to be “blamed” whether they smoked or not. The public is not even aware that nearly 80% of new lung cancer patients have never smoked or already quit. Public health policy has been focused almost solely on tobacco cessation. While this is a critical component which LCA strongly supports, tobacco cessation alone will not eliminate lung cancer. Lung cancer in never smokers is the sixth biggest cancer killer.”
    Matt Todd
    aka The Old Rambler

  116. Anonymous says:

    Catch 17
    Epidemiology has been shown to be less than effective in proving causality than some claim. One case in point is the relationship between smoking and cervical cancer.
    In 2004, the Surgeon General of the US added uterine cervical cancer to the list of those for which evidence was allegedly sufficient to conclude a causal relationship between smoking and the disease. Health Canada used the claim to justify the addition of cervical cancer to their list of smoking related diseases. Their 2007 SAMMEC report claims that 126 of 382 deaths (34.7%) from cervical cancer were caused by smoking.
    However, by September, 2009, the Canadian Cancer Society (and Health Canada) was claiming that all cervical cancer was caused by persistent HPV infection with high risk types of the virus. “Nearly all cervical cancers are caused by persistent high-risk HPV infection. High-risk types of HPV are considered known cancer-causing agents. About 70% of cervical cancers are associated with high-risk HPV type 16 and 18. Other high-risk types of HPV are associated with the other 30% of cervical cancers.”
    So, despite a seemingly strong statistical correlation between cervical cancer and smoking, it was eventually determined that smoking was not a cause of that particular cancer. The fact that more women who developed or died from cervical cancer were smokers was inconsequential; a false lead.
    The growing evidence linking LC and HPV has also been largely ignored in North America and the UK, as has been noted in previous comments.
    For epidemiology to be effective in developing hypotheses as to the cause and effect of various risk factors on disease incidence, it must be constantly re-appraised and re-evaluated in light of new information and circumstances. That hasn’t happened in the case of smoking and LC.
    And, as noted in other comments, all lung cancer victims are stigmatized by the statistical association with smoking. Even more criminal, however, is the fact that lung cancer research is so grossly underfunded compared to other types, thanks largely to the association with smoking.
    From the Lung Cancer Alliance: “Sad. Lung cancer patients continue to be “blamed” whether they smoked or not. The public is not even aware that nearly 80% of new lung cancer patients have never smoked or already quit. Public health policy has been focused almost solely on tobacco cessation. While this is a critical component which LCA strongly supports, tobacco cessation alone will not eliminate lung cancer. Lung cancer in never smokers is the sixth biggest cancer killer.”
    Matt Todd
    aka The Old Rambler

  117. Anonymous says:

    Catch 17
    Epidemiology has been shown to be less than effective in proving causality than some claim. One case in point is the relationship between smoking and cervical cancer.
    In 2004, the Surgeon General of the US added uterine cervical cancer to the list of those for which evidence was allegedly sufficient to conclude a causal relationship between smoking and the disease. Health Canada used the claim to justify the addition of cervical cancer to their list of smoking related diseases. Their 2007 SAMMEC report claims that 126 of 382 deaths (34.7%) from cervical cancer were caused by smoking.
    However, by September, 2009, the Canadian Cancer Society (and Health Canada) was claiming that all cervical cancer was caused by persistent HPV infection with high risk types of the virus. “Nearly all cervical cancers are caused by persistent high-risk HPV infection. High-risk types of HPV are considered known cancer-causing agents. About 70% of cervical cancers are associated with high-risk HPV type 16 and 18. Other high-risk types of HPV are associated with the other 30% of cervical cancers.”
    So, despite a seemingly strong statistical correlation between cervical cancer and smoking, it was eventually determined that smoking was not a cause of that particular cancer. The fact that more women who developed or died from cervical cancer were smokers was inconsequential; a false lead.
    The growing evidence linking LC and HPV has also been largely ignored in North America and the UK, as has been noted in previous comments.
    For epidemiology to be effective in developing hypotheses as to the cause and effect of various risk factors on disease incidence, it must be constantly re-appraised and re-evaluated in light of new information and circumstances. That hasn’t happened in the case of smoking and LC.
    And, as noted in other comments, all lung cancer victims are stigmatized by the statistical association with smoking. Even more criminal, however, is the fact that lung cancer research is so grossly underfunded compared to other types, thanks largely to the association with smoking.
    From the Lung Cancer Alliance: “Sad. Lung cancer patients continue to be “blamed” whether they smoked or not. The public is not even aware that nearly 80% of new lung cancer patients have never smoked or already quit. Public health policy has been focused almost solely on tobacco cessation. While this is a critical component which LCA strongly supports, tobacco cessation alone will not eliminate lung cancer. Lung cancer in never smokers is the sixth biggest cancer killer.”
    Matt Todd
    aka The Old Rambler

  118. Anonymous says:

    You can’t burn what is no longer there.
    So Wynders experiment was pointless on anything but young, green tobacco.
    On reflection, another reason that they might have only experimented on the extracted “tar”, is that it was already known that nicotine oxidized to nicotinic acid, because they were already putting it in the bread.
    Voluntarily from 1938 and later by law.
    Effectiveness of Food Fortification in the United States : The Case of Pellagra

    Click to access 727.pdf


    “Nicotinic acid was first made by the oxidation of nicotine and Whiffens operate a commercial process in this country starting with tobacco.
    Later they were supplied with nicotine by the British Nicotine Company and continued the oxidation.
    Finally – before the Second World War – they found they were unable to compete with manufacturers starting from quinoline and picoline although it could be made directly from tobacco waste, from pyridine, some other coal tar bases, nicotine, anabasine, nor-nicotine or mixed tobacco alkaloids.
    The U.S. Department of Agriculture sponsored work aimed to make nicotine compete, as early as 1942, but although a new catalytic oxidation process was developed quinoline was still the cheapest source of nicotinic acid.
    Comparative costs were published in 1951 by Coal Tar Products of Philadelphia”

    Click to access 00000711.pdf


    Rose

  119. Anonymous says:

    You can’t burn what is no longer there.
    So Wynders experiment was pointless on anything but young, green tobacco.
    On reflection, another reason that they might have only experimented on the extracted “tar”, is that it was already known that nicotine oxidized to nicotinic acid, because they were already putting it in the bread.
    Voluntarily from 1938 and later by law.
    Effectiveness of Food Fortification in the United States : The Case of Pellagra

    Click to access 727.pdf


    “Nicotinic acid was first made by the oxidation of nicotine and Whiffens operate a commercial process in this country starting with tobacco.
    Later they were supplied with nicotine by the British Nicotine Company and continued the oxidation.
    Finally – before the Second World War – they found they were unable to compete with manufacturers starting from quinoline and picoline although it could be made directly from tobacco waste, from pyridine, some other coal tar bases, nicotine, anabasine, nor-nicotine or mixed tobacco alkaloids.
    The U.S. Department of Agriculture sponsored work aimed to make nicotine compete, as early as 1942, but although a new catalytic oxidation process was developed quinoline was still the cheapest source of nicotinic acid.
    Comparative costs were published in 1951 by Coal Tar Products of Philadelphia”

    Click to access 00000711.pdf


    Rose

  120. richwhite09 says:

    Rose, I mentioned already I’m considering updating my book following the information from this debate. Your posts have been very informative, especially on nicotine and niacin, and I want to use some of your information in my chapters on nicotine and the health benefits of smoking. Would you mind dropping me an email to discuss it and for me to start collating some of your evidence and references?(my email is richwhite[at]smokescreens.org – replace the [at] with @, i have to type it like this now to avoid being inundated with spam)

  121. richwhite09 says:

    Rose, I mentioned already I’m considering updating my book following the information from this debate. Your posts have been very informative, especially on nicotine and niacin, and I want to use some of your information in my chapters on nicotine and the health benefits of smoking. Would you mind dropping me an email to discuss it and for me to start collating some of your evidence and references?(my email is richwhite[at]smokescreens.org – replace the [at] with @, i have to type it like this now to avoid being inundated with spam)

  122. Anonymous says:

    Catch 17
    I hope that no one minds me making a rather frivolous comment.
    I was watching ‘Strictly…’ tonight. After the conclusion, an amusing thought came into my mind.
    Suppose that, in say 30 years time, someone was doing a thesis on ‘physical fitness and co-ordination in old age’ and came across this info in a newspaper that a certain ‘Anne Whitcomb’ who was in her late sixties, got through to the fifth round in an important dancing contest on the BBC – thus showing that age is no barrier to physical fitness and co-ordination. And, to further confirm this claim, pointed out that in a previous year, another old person, this time a male, John Sargeant, also got through to the fifth round – in fact, he might have gone further if it were not that he withdrew voluntarily.
    What is wrong with the conclusions? I mean, there is no doubt that the Great British Public obviously voted EN MASSE for these old people and therefore these old people must have been among the best dancers, mustn’t they?
    We, here and now, know that the those conclusions are hopelessly wrong. We know that there were two (and possibly more) factors which confounded the votes; one was the ‘sympathy’ vote (very possibly the votes of the older generation), and, two, there was ‘the glee factor’ – being the peculiar human trait of gaining pleasure from ‘upsetting the apple cart’. But, surely, the ‘sympathy’ voters and ‘the glee factor’ voters must have been a very small minority of the voters? In thirty years time, people would think that, wouldn’t they? But we, HERE AND NOW, know how powerful these factors are.
    Thus, people looking at statistics originating from the 50s and 60s might disregard the smogs of those times. But those of us who experienced these smogs know better. We remember arriving home from walking home from work and our mothers saying, “Good Heavens, you’re filthy!” and looking into a mirror and seeing a blackish, yellowish face looking back at us. The ‘stinkers’ who complain about the smell of tobacco smoke on their clothes know nothing about dirt and smells! My father was a miner. Before the gov passed a law requiring baths to be available at pits, he used to come home from work ‘black as up chimney’ and needed to take a bath every day (filled by kettle, by the way). And he smoked as well (woodbines)! But he managed to live until he was 76, at which time he had a stroke. No doubt the Surgeon General of the USA would say that he would not have had the stroke had he not smoked! “It was that last cigarette, just before he fell over; that was what brought on the stroke! It was smoking what killed him!” That is, essentially, what she has just gone on record as saying.
    Anyone who lived through the smogs knows how awful they were. People died in their thousands directly as a result of the smogs. Not to have taken this into account when compiling statistics about that time is truly incomprehensible.
    A confounding factor may have a HUGE influence.
    I hope that this is not too frivolous.
    Finally, can I re-iterate whosit’s (daren’t go back to check name!) call for the eradication of abuse? I can say to Frank Davis, “Frank, your facts are wrong” – I do not have to say, “Frank, YOU STUPID BUGGER, your facts are wrong”.
    As I said earlier – at the beginning of this debate, we were scratching the surface. Now we are getting below the surface. Let us continue to pursue the subject. We have loads of time.

  123. Anonymous says:

    Catch 17
    I hope that no one minds me making a rather frivolous comment.
    I was watching ‘Strictly…’ tonight. After the conclusion, an amusing thought came into my mind.
    Suppose that, in say 30 years time, someone was doing a thesis on ‘physical fitness and co-ordination in old age’ and came across this info in a newspaper that a certain ‘Anne Whitcomb’ who was in her late sixties, got through to the fifth round in an important dancing contest on the BBC – thus showing that age is no barrier to physical fitness and co-ordination. And, to further confirm this claim, pointed out that in a previous year, another old person, this time a male, John Sargeant, also got through to the fifth round – in fact, he might have gone further if it were not that he withdrew voluntarily.
    What is wrong with the conclusions? I mean, there is no doubt that the Great British Public obviously voted EN MASSE for these old people and therefore these old people must have been among the best dancers, mustn’t they?
    We, here and now, know that the those conclusions are hopelessly wrong. We know that there were two (and possibly more) factors which confounded the votes; one was the ‘sympathy’ vote (very possibly the votes of the older generation), and, two, there was ‘the glee factor’ – being the peculiar human trait of gaining pleasure from ‘upsetting the apple cart’. But, surely, the ‘sympathy’ voters and ‘the glee factor’ voters must have been a very small minority of the voters? In thirty years time, people would think that, wouldn’t they? But we, HERE AND NOW, know how powerful these factors are.
    Thus, people looking at statistics originating from the 50s and 60s might disregard the smogs of those times. But those of us who experienced these smogs know better. We remember arriving home from walking home from work and our mothers saying, “Good Heavens, you’re filthy!” and looking into a mirror and seeing a blackish, yellowish face looking back at us. The ‘stinkers’ who complain about the smell of tobacco smoke on their clothes know nothing about dirt and smells! My father was a miner. Before the gov passed a law requiring baths to be available at pits, he used to come home from work ‘black as up chimney’ and needed to take a bath every day (filled by kettle, by the way). And he smoked as well (woodbines)! But he managed to live until he was 76, at which time he had a stroke. No doubt the Surgeon General of the USA would say that he would not have had the stroke had he not smoked! “It was that last cigarette, just before he fell over; that was what brought on the stroke! It was smoking what killed him!” That is, essentially, what she has just gone on record as saying.
    Anyone who lived through the smogs knows how awful they were. People died in their thousands directly as a result of the smogs. Not to have taken this into account when compiling statistics about that time is truly incomprehensible.
    A confounding factor may have a HUGE influence.
    I hope that this is not too frivolous.
    Finally, can I re-iterate whosit’s (daren’t go back to check name!) call for the eradication of abuse? I can say to Frank Davis, “Frank, your facts are wrong” – I do not have to say, “Frank, YOU STUPID BUGGER, your facts are wrong”.
    As I said earlier – at the beginning of this debate, we were scratching the surface. Now we are getting below the surface. Let us continue to pursue the subject. We have loads of time.

  124. Anonymous says:

    Catch 17
    I hope that no one minds me making a rather frivolous comment.
    I was watching ‘Strictly…’ tonight. After the conclusion, an amusing thought came into my mind.
    Suppose that, in say 30 years time, someone was doing a thesis on ‘physical fitness and co-ordination in old age’ and came across this info in a newspaper that a certain ‘Anne Whitcomb’ who was in her late sixties, got through to the fifth round in an important dancing contest on the BBC – thus showing that age is no barrier to physical fitness and co-ordination. And, to further confirm this claim, pointed out that in a previous year, another old person, this time a male, John Sargeant, also got through to the fifth round – in fact, he might have gone further if it were not that he withdrew voluntarily.
    What is wrong with the conclusions? I mean, there is no doubt that the Great British Public obviously voted EN MASSE for these old people and therefore these old people must have been among the best dancers, mustn’t they?
    We, here and now, know that the those conclusions are hopelessly wrong. We know that there were two (and possibly more) factors which confounded the votes; one was the ‘sympathy’ vote (very possibly the votes of the older generation), and, two, there was ‘the glee factor’ – being the peculiar human trait of gaining pleasure from ‘upsetting the apple cart’. But, surely, the ‘sympathy’ voters and ‘the glee factor’ voters must have been a very small minority of the voters? In thirty years time, people would think that, wouldn’t they? But we, HERE AND NOW, know how powerful these factors are.
    Thus, people looking at statistics originating from the 50s and 60s might disregard the smogs of those times. But those of us who experienced these smogs know better. We remember arriving home from walking home from work and our mothers saying, “Good Heavens, you’re filthy!” and looking into a mirror and seeing a blackish, yellowish face looking back at us. The ‘stinkers’ who complain about the smell of tobacco smoke on their clothes know nothing about dirt and smells! My father was a miner. Before the gov passed a law requiring baths to be available at pits, he used to come home from work ‘black as up chimney’ and needed to take a bath every day (filled by kettle, by the way). And he smoked as well (woodbines)! But he managed to live until he was 76, at which time he had a stroke. No doubt the Surgeon General of the USA would say that he would not have had the stroke had he not smoked! “It was that last cigarette, just before he fell over; that was what brought on the stroke! It was smoking what killed him!” That is, essentially, what she has just gone on record as saying.
    Anyone who lived through the smogs knows how awful they were. People died in their thousands directly as a result of the smogs. Not to have taken this into account when compiling statistics about that time is truly incomprehensible.
    A confounding factor may have a HUGE influence.
    I hope that this is not too frivolous.
    Finally, can I re-iterate whosit’s (daren’t go back to check name!) call for the eradication of abuse? I can say to Frank Davis, “Frank, your facts are wrong” – I do not have to say, “Frank, YOU STUPID BUGGER, your facts are wrong”.
    As I said earlier – at the beginning of this debate, we were scratching the surface. Now we are getting below the surface. Let us continue to pursue the subject. We have loads of time.

    • richwhite09 says:

      Re: Catch 17
      “Finally, can I re-iterate whosit’s (daren’t go back to check name!) call for the eradication of abuse? I can say to Frank Davis, “Frank, your facts are wrong” – I do not have to say, “Frank, YOU STUPID BUGGER, your facts are wrong”.”
      That was the Old Rambler.
      And you’re very true. I’m quite bemused how it’s quickly turned into me having to defend my actual personal character, I wasn’t quite prepared for that.
      But your post is very good, and it’s extremely ‘curious’ that the studies didn’t take any air pollution into account. I said in this main entry that if there truly was no bias in Doll’s study, he wouldn’t have just focused on smoking – at least not until the second or third study after a link had became unavoidable after all confounders in the first study. But no, he just went straight for the smokers. And it’s no surprise he found what he did. With such a huge amount of smokers there would be have been a strong correlation to just about anything.

    • Anonymous says:

      Re: Catch 17
      “I can say to Frank Davis, “Frank, your facts are wrong” – I do not have to say, “Frank, YOU STUPID BUGGER, your facts are wrong”.
      Better yet I can say “Frank, your facts are wrong, and this is why”
      But Frank is never wrong, so I don’t.
      *smiles winningly at Frank
      I remember the smogs, I did have an article on the exact toxicity of the Great London Smog, sadly the link no longer works.
      But I remember that the ph of the air was said to be the same as lemon juice and visibility down to a yard in some areas.
      Secret plot to play down risks of air pollution
      “Official documents unearthed by a scientific historian reveal that the Medical Research Council (MRC), which had just begun to establish the link between lung cancer and smoking, was asked to modify public statements about air pollution after intervention from the Government”
      http://www.independent.co.uk/news/uk/politics/secret-plot-to-play-down-risks-of-air-pollution-610356.html
      The government had insisted that all the clean coal be sent for export, leaving the public burning sulphurous coal.
      “What is now attracting interest are the political implications of the Great London Smog.
      First, there were no immediate answers to the problem. But it was necessary to reassure – or fool – the general public into believing that the Government was doing something.
      In a statement that could easily have come from the “Yes Minister” television series, a British Government minister, Harold Macmillan, said: “We cannot do very much, but we can seem to be very busy – and that is half the battle nowadays”.
      Second, the Government decided that two million cheap “smog masks” should be issued to people with heart and respiratory problems. The Government knew that the masks were useless but, again, it gave the impression that something was being done.
      By the way, an American tobacco company offered to donate 100,000 masks that used a novel filter technology designed for cigarettes.
      The Government rejected the offer because it feared that the company would use the gift in its advertising campaign: “this cigarette filter is so good it could keep out London smog”.
      Third, the real shocker has been the Government’s policy to underestimate the number of people killed. The official line was that the fog was simply killing off the frail elderly, who were going to die anyway; the Great London Smog simply speeded up the process.
      We now know that some medical experts within the Ministry of Health were troubled about this claim. Too many people were dying to whom this explanation would not normally apply: middle aged people and babies.
      The Ministry of Health then claimed that there was a ‘flu epidemic which had also contributed to the high number of deaths. This was another lie because there is no evidence that there was a ‘flu epidemic.”
      http://www.keithsuter.com/2008/12/27/archive-article-killed-by-a-london-fog-6-dec-02/
      James Repace reminded me.
      “More people died in 2002 from passive smoking at work in the UK than were killed by the Great London smog of 1952”
      James Repace
      http://news.bbc.co.uk/1/hi/health/2925633.stm
      I’ve done a little research.
      Air Pollution and The Great London Smog
      http://tinyurl.com/36ldm8u
      Rose

  125. junican says:

    Damn! That was from Junican.

  126. junican says:

    Damn! That was from Junican.

  127. junican says:

    Damn! That was from Junican.

  128. Anonymous says:

    FOR FRANK–Technical Note
    Frank,
    I’ve added the “CATCH” debate to FORCES news page. If you can find the time, could you please add the “catch” tag to all of the relevant contributions, because I’ve provided the FORCES link according to that tag.
    The discussion is, of course, entirely relevant to FORCES, so I had to add something on it.
    Also, if Frank or any of the participants feel that I’ve misrepresented something in my blurb, just let me know, and I’ll do my best to correct it. I’ve presumed in the title that the “CATCH” debate is done for now, so correct me if there are going to be further contributions. It’s late, and there may even be a typo in there that I’ve missed.
    http://forces.org/News_Portal/news_viewer.php?id=2117
    -WS

  129. Anonymous says:

    FOR FRANK–Technical Note
    Frank,
    I’ve added the “CATCH” debate to FORCES news page. If you can find the time, could you please add the “catch” tag to all of the relevant contributions, because I’ve provided the FORCES link according to that tag.
    The discussion is, of course, entirely relevant to FORCES, so I had to add something on it.
    Also, if Frank or any of the participants feel that I’ve misrepresented something in my blurb, just let me know, and I’ll do my best to correct it. I’ve presumed in the title that the “CATCH” debate is done for now, so correct me if there are going to be further contributions. It’s late, and there may even be a typo in there that I’ve missed.
    http://forces.org/News_Portal/news_viewer.php?id=2117
    -WS

  130. Anonymous says:

    FOR FRANK–Technical Note
    Frank,
    I’ve added the “CATCH” debate to FORCES news page. If you can find the time, could you please add the “catch” tag to all of the relevant contributions, because I’ve provided the FORCES link according to that tag.
    The discussion is, of course, entirely relevant to FORCES, so I had to add something on it.
    Also, if Frank or any of the participants feel that I’ve misrepresented something in my blurb, just let me know, and I’ll do my best to correct it. I’ve presumed in the title that the “CATCH” debate is done for now, so correct me if there are going to be further contributions. It’s late, and there may even be a typo in there that I’ve missed.
    http://forces.org/News_Portal/news_viewer.php?id=2117
    -WS

  131. richwhite09 says:

    Re: Catch 17
    “Finally, can I re-iterate whosit’s (daren’t go back to check name!) call for the eradication of abuse? I can say to Frank Davis, “Frank, your facts are wrong” – I do not have to say, “Frank, YOU STUPID BUGGER, your facts are wrong”.”
    That was the Old Rambler.
    And you’re very true. I’m quite bemused how it’s quickly turned into me having to defend my actual personal character, I wasn’t quite prepared for that.
    But your post is very good, and it’s extremely ‘curious’ that the studies didn’t take any air pollution into account. I said in this main entry that if there truly was no bias in Doll’s study, he wouldn’t have just focused on smoking – at least not until the second or third study after a link had became unavoidable after all confounders in the first study. But no, he just went straight for the smokers. And it’s no surprise he found what he did. With such a huge amount of smokers there would be have been a strong correlation to just about anything.

  132. richwhite09 says:

    Re: Catch 17
    “Finally, can I re-iterate whosit’s (daren’t go back to check name!) call for the eradication of abuse? I can say to Frank Davis, “Frank, your facts are wrong” – I do not have to say, “Frank, YOU STUPID BUGGER, your facts are wrong”.”
    That was the Old Rambler.
    And you’re very true. I’m quite bemused how it’s quickly turned into me having to defend my actual personal character, I wasn’t quite prepared for that.
    But your post is very good, and it’s extremely ‘curious’ that the studies didn’t take any air pollution into account. I said in this main entry that if there truly was no bias in Doll’s study, he wouldn’t have just focused on smoking – at least not until the second or third study after a link had became unavoidable after all confounders in the first study. But no, he just went straight for the smokers. And it’s no surprise he found what he did. With such a huge amount of smokers there would be have been a strong correlation to just about anything.

  133. Frank Davis says:

    Re: FOR FRANK–Technical Note
    Thanks. Super-busy right now, but will do.
    Frank

  134. Frank Davis says:

    Re: FOR FRANK–Technical Note
    Thanks. Super-busy right now, but will do.
    Frank

  135. Anonymous says:

    Re: Catch 17
    “I can say to Frank Davis, “Frank, your facts are wrong” – I do not have to say, “Frank, YOU STUPID BUGGER, your facts are wrong”.
    Better yet I can say “Frank, your facts are wrong, and this is why”
    But Frank is never wrong, so I don’t.
    *smiles winningly at Frank
    I remember the smogs, I did have an article on the exact toxicity of the Great London Smog, sadly the link no longer works.
    But I remember that the ph of the air was said to be the same as lemon juice and visibility down to a yard in some areas.
    Secret plot to play down risks of air pollution
    “Official documents unearthed by a scientific historian reveal that the Medical Research Council (MRC), which had just begun to establish the link between lung cancer and smoking, was asked to modify public statements about air pollution after intervention from the Government”
    http://www.independent.co.uk/news/uk/politics/secret-plot-to-play-down-risks-of-air-pollution-610356.html
    The government had insisted that all the clean coal be sent for export, leaving the public burning sulphurous coal.
    “What is now attracting interest are the political implications of the Great London Smog.
    First, there were no immediate answers to the problem. But it was necessary to reassure – or fool – the general public into believing that the Government was doing something.
    In a statement that could easily have come from the “Yes Minister” television series, a British Government minister, Harold Macmillan, said: “We cannot do very much, but we can seem to be very busy – and that is half the battle nowadays”.
    Second, the Government decided that two million cheap “smog masks” should be issued to people with heart and respiratory problems. The Government knew that the masks were useless but, again, it gave the impression that something was being done.
    By the way, an American tobacco company offered to donate 100,000 masks that used a novel filter technology designed for cigarettes.
    The Government rejected the offer because it feared that the company would use the gift in its advertising campaign: “this cigarette filter is so good it could keep out London smog”.
    Third, the real shocker has been the Government’s policy to underestimate the number of people killed. The official line was that the fog was simply killing off the frail elderly, who were going to die anyway; the Great London Smog simply speeded up the process.
    We now know that some medical experts within the Ministry of Health were troubled about this claim. Too many people were dying to whom this explanation would not normally apply: middle aged people and babies.
    The Ministry of Health then claimed that there was a ‘flu epidemic which had also contributed to the high number of deaths. This was another lie because there is no evidence that there was a ‘flu epidemic.”
    http://www.keithsuter.com/2008/12/27/archive-article-killed-by-a-london-fog-6-dec-02/
    James Repace reminded me.
    “More people died in 2002 from passive smoking at work in the UK than were killed by the Great London smog of 1952”
    James Repace
    http://news.bbc.co.uk/1/hi/health/2925633.stm
    I’ve done a little research.
    Air Pollution and The Great London Smog
    http://tinyurl.com/36ldm8u
    Rose

  136. Anonymous says:

    Re: Catch 17
    “I can say to Frank Davis, “Frank, your facts are wrong” – I do not have to say, “Frank, YOU STUPID BUGGER, your facts are wrong”.
    Better yet I can say “Frank, your facts are wrong, and this is why”
    But Frank is never wrong, so I don’t.
    *smiles winningly at Frank
    I remember the smogs, I did have an article on the exact toxicity of the Great London Smog, sadly the link no longer works.
    But I remember that the ph of the air was said to be the same as lemon juice and visibility down to a yard in some areas.
    Secret plot to play down risks of air pollution
    “Official documents unearthed by a scientific historian reveal that the Medical Research Council (MRC), which had just begun to establish the link between lung cancer and smoking, was asked to modify public statements about air pollution after intervention from the Government”
    http://www.independent.co.uk/news/uk/politics/secret-plot-to-play-down-risks-of-air-pollution-610356.html
    The government had insisted that all the clean coal be sent for export, leaving the public burning sulphurous coal.
    “What is now attracting interest are the political implications of the Great London Smog.
    First, there were no immediate answers to the problem. But it was necessary to reassure – or fool – the general public into believing that the Government was doing something.
    In a statement that could easily have come from the “Yes Minister” television series, a British Government minister, Harold Macmillan, said: “We cannot do very much, but we can seem to be very busy – and that is half the battle nowadays”.
    Second, the Government decided that two million cheap “smog masks” should be issued to people with heart and respiratory problems. The Government knew that the masks were useless but, again, it gave the impression that something was being done.
    By the way, an American tobacco company offered to donate 100,000 masks that used a novel filter technology designed for cigarettes.
    The Government rejected the offer because it feared that the company would use the gift in its advertising campaign: “this cigarette filter is so good it could keep out London smog”.
    Third, the real shocker has been the Government’s policy to underestimate the number of people killed. The official line was that the fog was simply killing off the frail elderly, who were going to die anyway; the Great London Smog simply speeded up the process.
    We now know that some medical experts within the Ministry of Health were troubled about this claim. Too many people were dying to whom this explanation would not normally apply: middle aged people and babies.
    The Ministry of Health then claimed that there was a ‘flu epidemic which had also contributed to the high number of deaths. This was another lie because there is no evidence that there was a ‘flu epidemic.”
    http://www.keithsuter.com/2008/12/27/archive-article-killed-by-a-london-fog-6-dec-02/
    James Repace reminded me.
    “More people died in 2002 from passive smoking at work in the UK than were killed by the Great London smog of 1952”
    James Repace
    http://news.bbc.co.uk/1/hi/health/2925633.stm
    I’ve done a little research.
    Air Pollution and The Great London Smog
    http://tinyurl.com/36ldm8u
    Rose

  137. Anonymous says:

    Understood. Got it. Thanks for the reply.
    -WS

  138. Anonymous says:

    Understood. Got it. Thanks for the reply.
    -WS

  139. Anonymous says:

    Understood. Got it. Thanks for the reply.
    -WS

  140. Anonymous says:

    Most vitamins are not synthesised by the human body, we depend on dietary uptake, so a lot points to diet.
    The biochemistry of the human body and it’s variation in individuals is something which needs to be looked at. Some hormones e.g. cortisol, varies greatly in a space of 24 hrs; others (e.g. Thyroid hormones) depend on positive/negative feedbacks; and so on.
    Then we have individuals affected by chronic conditions e.g. diabetics, which have altered biochemical processes. And so on.
    Molecular biology provides great tools to investigate and manipulate DNA but it is only a small part of the full picture.

  141. Anonymous says:

    Most vitamins are not synthesised by the human body, we depend on dietary uptake, so a lot points to diet.
    The biochemistry of the human body and it’s variation in individuals is something which needs to be looked at. Some hormones e.g. cortisol, varies greatly in a space of 24 hrs; others (e.g. Thyroid hormones) depend on positive/negative feedbacks; and so on.
    Then we have individuals affected by chronic conditions e.g. diabetics, which have altered biochemical processes. And so on.
    Molecular biology provides great tools to investigate and manipulate DNA but it is only a small part of the full picture.

  142. Anonymous says:

    I agree with the points made above. I’m not interested in “liar, liar, pants on fire” discussions either.
    I don’t know that much about the great London smog — but I would think that it wouldn’t be a really important epidemiological factor for explaining differential LC rates unless it was affecting smokers unequally with non-smokers. That is, it wouldn’t account for different rates of LC if everyone was experiencing the same fog (although it could account for a general increase – which may be important if you don’t think there were real differences). Or are you making a case that some group of people smoked more because of this smog?
    Or is the argument simply that Doll (who was working there) had reason to point the finger elsewhere? (That is, it’s simply an argument about Doll’s motivation?) Can someone clarify this point for me?
    Meanwhile, I’m thinking we should just continue the discussion on the next thread that Frank so kindly set up for continuing the discussion? That way we don’t have to check multiple threads?
    GDF

  143. Anonymous says:

    I agree with the points made above. I’m not interested in “liar, liar, pants on fire” discussions either.
    I don’t know that much about the great London smog — but I would think that it wouldn’t be a really important epidemiological factor for explaining differential LC rates unless it was affecting smokers unequally with non-smokers. That is, it wouldn’t account for different rates of LC if everyone was experiencing the same fog (although it could account for a general increase – which may be important if you don’t think there were real differences). Or are you making a case that some group of people smoked more because of this smog?
    Or is the argument simply that Doll (who was working there) had reason to point the finger elsewhere? (That is, it’s simply an argument about Doll’s motivation?) Can someone clarify this point for me?
    Meanwhile, I’m thinking we should just continue the discussion on the next thread that Frank so kindly set up for continuing the discussion? That way we don’t have to check multiple threads?
    GDF

  144. Anonymous says:

    I agree with the points made above. I’m not interested in “liar, liar, pants on fire” discussions either.
    I don’t know that much about the great London smog — but I would think that it wouldn’t be a really important epidemiological factor for explaining differential LC rates unless it was affecting smokers unequally with non-smokers. That is, it wouldn’t account for different rates of LC if everyone was experiencing the same fog (although it could account for a general increase – which may be important if you don’t think there were real differences). Or are you making a case that some group of people smoked more because of this smog?
    Or is the argument simply that Doll (who was working there) had reason to point the finger elsewhere? (That is, it’s simply an argument about Doll’s motivation?) Can someone clarify this point for me?
    Meanwhile, I’m thinking we should just continue the discussion on the next thread that Frank so kindly set up for continuing the discussion? That way we don’t have to check multiple threads?
    GDF

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