Thursday, 2 December 2010

What's the catch?

A quick reminder that the debate at Frank's is continuing with three more posts since I last mentioned it:

CATCH-3: Frank Davis adds his 2 cents to the discussion
CATCH-4: Chris Snowdon responds to Rich White and Frank Davis
CATCH-5: Frank Davis continues the discussion

To all those who have been commenting, I have been reading and I will try to reply to all your questions. Unfortunately, time has not been on my side recently, not least thanks to the inability of Britain's train operators, coach companies and taxi drivers to handle a dusting of snow in December.

9 comments:

  1. Dusting of snow?

    Where the hell do you live?

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  2. Near Gatwick, unfortunately. I had to hire a car in the end because the taxi firm considered the roads too dangerous. Soft Southern Jessies.

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  3. I thought you lived in Hove?

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  4. The discussions at Frank's place become more interesting by the day. As is usual with these things, the deeper you go, the more questions arise.

    It may be that we cannot arrive at a clear-cut resolution, but many matters will be resolved. For example, Relative Risk will be better understood among many other matters.

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  5. Hove is near enough to Gatwick for me to be stuck there for 7 hours.

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  6. Chris, how about looking into the recent work leading to a suggestion that lc in non smokers is a diferent disease to lc in smokers - something to do with different mutations apparently. To me this looks like a huge advance in understanding. A few people have commented on this and given links. Here is one

    http://www.montrealgazette.com/health/Lung+cancer+smokers+looks+different+than+smoker/3806044/story.html

    I'm surprised nobody other than Dave, possibly, has drawn the obvious prima facie conclusion that passive smoking does not increase the risk of lc. Otherwise around 1 in 6 to 1 in 10 of a reasonably large sample of non smokers with lc would have the smokers' variety. If tobacco smoke causes mutations, then passive smoking most likely would cause the same mutations as direct smoking.

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  7. Anon,

    I've seen it and it's very promising stuff, if true. It could be a way of finding out the truth about passive smoking once and for all. I don't know if they have the necessary records of previous subjects of SHS studies, but, if so, that would be the obvious place for someone to start. Would anyone risk funding such research, I wonder?

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  8. (cont'd) 2B.
    The claimed symptoms of tobacco “allergy” sound very much like classical anxiety reactions. These people are not faking symptoms. They are experiencing uncomfortable, distressing even, symptoms. And it is not intentional: Fear is getting the better of them. The critical point is that these physical symptoms are not being produced by the physical properties of an externality (e.g., SHS) but are psychologically medicated (i.e., psychogenic). The physical symptoms are therefore somatization (a physical manifestation) of fear. Another possibility is that persons experiencing allergic reactions for other [unknown] reasons will blame SHS if it is present. Others that have a variety of pangs, pokes, and pains will convince themselves that they are being “caused” by “dangerous” SHS.

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  9. (cont'd) 1B.
    Until the current crusade emphasizing secondhand smoke “danger”, “allergy” to tobacco smoke was unheard of. Allergies are typically reactions to particular proteins. There are proteins in the tobacco leaf but, once oxidized (burnt), there are none in tobacco smoke. Indeed, materialist research (e.g., immunological) can proceed. However, there is a major confounder in this circumstance. That the “allergy” claims began appearing post-SHS “danger” strongly suggests a psychological shift, i.e., psychogenic effects such as somatization.

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