I think you will find your answer in the reference section of that last link. I 
think just reading those two, fairly brief sections, at that link will give you 
a feel for the current work being done in animal models and a fuller 
appreciation of this area of research as going beyond epidemiological, 
correlational studies. None of this says anything about the issue of the most 
recent correlational study and its inappropriate description using causal 
language. I am only addressing what seemed to be the assumption of the thread 
that all work on this link has been correlational. Clearly, it has gone beyond 
that point. I would also say that correlational research, correctly 
interpreted, as with the risks calculated by Christopher Green, can be quite 
useful in distinguishing between statistical significance and real world 
significance. They do use the word "possible" as is appropriate in ongoing 
biological research but these possibilities are based on past and ongoing 
empirical research in animal models. They also distinguish between a simple 
causal model (alcohol causes cancer) which they don't find evidence of and a 
more complicated and nuanced model (which, of course, will not fit within the 
bounds of a parenthetical statement).



To give you a flavor of their review, here is a bit from the introduction (all 
emphases mine):



"The exact mechanism(s) of ethanol-associated carcinogenesis, however, have 
remained obscure, as ethanol itself is not a carcinogen (Ketcham et al., 1963).



Multiple mechanisms are involved in alcohol-associated cancer development, 
including the effect of acetaldehyde (AA), the first metabolite of ethanol 
oxidation, the induction of cytochrome P-4502E1 (CYP2E1) leading to the 
generation of reactive oxygen species (ROS), and enhanced procarcinogen 
activation, as well as the modulation of cellular regeneration and nutritional 
deficiencies. Since it is far beyond the scope of this review to discuss all 
factors of alcohol-associated carcinogenesis in detail, major emphasis is laid 
on genetic and nutritional aspects.



In addition, it is primarily focused on major general pathogenetic mechanisms 
and to a lesser degree on tissue specific ethanol actions. For more details see 
recent review articles (Seitz et al., 2003, 2004; Stickel et al., 2002; 
Salaspuro, 2003)."



Rick



Dr. Rick Froman, Chair

Division of Humanities and Social Sciences Box 3055

x7295

[email protected]

http://tinyurl.com/DrFroman



Proverbs 14:15 "A simple man believes anything, but a prudent man gives thought 
to his steps."





-----Original Message-----
From: Paul Brandon [mailto:[email protected]]
Sent: Friday, February 27, 2009 10:53 AM
To: Teaching in the Psychological Sciences (TIPS)
Subject: Re: [tips] BBC NEWS | Health | Drink a day increases cancer risk



The key word here is "possible".

There are many speculations in the literature about possible

mechanisms for ethanol as a carcinogen that are consistent with

biological knowledge.

The question is whether there are any experimental demonstrations of

the _magnitude_ of these effects in vivo; even in animal models?



On Feb 27, 2009, at 7:25 AM, Rick Froman wrote:



> Since the assumption of this thread seems to be that all research on the link 
> between alcohol and cancer is correlational and epidemiological, I thought I 
> would do a Google Scholar search on alcohol and cancer and see what is out 
> there. What was out there was approximately 814,000 hits. Of course these 
> could all be correlational studies (and many are probably duplicates) so I 
> clicked on the second one in the list and found an interesting article on 
> possible biological mechanisms (http://www.ncbi.nlm.nih.gov/pubmed/2686698). 
> I also found a link to a review of studies of alcohol and cancer as early as 
> 1986 (http://www.ncbi.nlm.nih.gov/pubmed/3035901). The last line of the 
> abstract was, "Animal models are needed in which effects of ethanol on 
> carcinogenesis can be consistently demonstrated and which can then be used to 
> examine mechanisms".  I thought it unlikely that no experimental work had 
> ensued in the intervening years. Indeed, a 2004 review article is available 
> full text on the web at: 
> http://alcalc.oxfordjournals.org/cgi/content/full/39/3/155 that includes 
> sections on Animal Models and Possible Biological Mechanisms. The reference 
> list of the article has links to many related articles available in full-text.





Paul Brandon

Emeritus Professor of Psychology

Minnesota State University, Mankato

[email protected]





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