Tuesday, May 11, 2010

Pancreatic cancer: Fat protects.....Carbs damage?

I've had stuff previously on sugar and cancer

Interesting to spot this abstract which - as far as I read it - indicates that intakes of available carbohydrate, glycemic load and sucrose are associated with elevated risks for pancreatic cancer, while fat - particularly saturated fat - intake is associated with diminished risks.

Available Carbohydrates, Glycemic Load, and Pancreatic Cancer: Is There a Link?

I haven't seen the full study (does anyone have it?) so I am not sure why the abstract finishes with the statement:

Rather than being causal, the short-term increase in pancreatic cancer risk associated with high available carbohydrate and low fat intake may be capturing dietary changes associated with subclinical disease.
So they are saying that subclinical pancreatic cancer makes you eat more carbs and less fat!

3 comments:

MJT said...

"So they are saying that subclinical pancreatic cancer makes you eat more carbs and less fat!"

I think that is what they are are saying (I also don't have the full article). A small pancreatic tumor can partially (or completely) block the pancreatic duct so there are less enzymes (including amylase for fat digestion) reaching the small bowel. There may also be mild pancreatitis. The patient, not tolerating fat very well, may switch to a higher percentage of carbohyrdrates in the diet.

Just a thought.

Anonymous said...

I'll second that. Couldn't pancreatic damage might modulate insulin release, altering appetite? Of course, it would be no surprise if the neolithic agents of disease were the culprit in the first place.

Chris D said...

http://www.mediafire.com/file/zk2jwinczlv/available-carbohydrates-glycemic-load-pancreatic-cancer.pdf

full text

"In conclusion, in this prospective study, an elevated risk of pancreatic cancer was associated with a high glycemic load and available carbohydrate intake only among participants with less than 4 years of follow-up. The association of total and saturated fat, in turn, was inversely associated with pancreatic cancer in the earlier, but not later, follow-up period. This finding suggests that participants who were diagnosed with incident pancreatic cancer earlier during follow-up may have been symptomatic at the time the food frequency questionnaire was completed, altering their diets to include more easily digestible carbohydrates and less fat. Future prospective studies examining recent diet and pancreatic cancer risk should consider the potential influence of preclinical disease on self-reported intake."