Document Detail


Intake of fatty acids and antioxidants and pancreatic cancer in a large population-based case-control study in the San Francisco Bay Area.
MedLine Citation:
PMID:  20104522     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
There are no well-established modifiable risk factors for pancreatic cancer except smoking. Some dietary factors have been associated with pancreatic cancer risk and require further study. We examined the associations among intake of specific fatty acids and antioxidants and risk of pancreatic cancer in a large population-based case-control study in the San Francisco Bay Area. Unconditional logistic regression models were used to compute odds ratios (ORs) and 95% confidence intervals (CI) as estimates of relative risk. Positive associations were observed for high levels of the 8 individual saturated fatty acids (4th vs. 1st quartile: ORs ranged from 1.6 to 2.6; all p(trend) < 0.01), monounsaturated palmitoleic and oleic fatty acids [OR = 1.6 (95% CI: 1.2-2.1) and 1.4 (95% CI: 1.1-1.9); both p(trend) < 0.01], and polyunsaturated linolenic acid [OR = 1.5 (95% CI: 1.1-2.0); p(trend) = 0.02]. Inverse associations were observed for high levels of gadolic acid [4th vs. 1st quartile: OR = 0.68 (95% CI: 0.50-0.92); p(trend) = 0.007] and omega-3 fatty acids [>or=0.85 g/day vs. 1st quartile: OR = 0.47 (95% CI: 0.25-0.90)]. An inverse association was also observed for high total intake of vitamin C [4th vs. 1st quartile: OR = 0.69 (95% CI: 0.51-0.94); p(trend) = 0.004] and of vitamin E [OR = 0.67 (95% CI: 0.49-0.92); p(trend) = 0.01]. Although similar decreased risks were also observed for high supplemental intake of these 2 vitamins (both p(trend) < 0.01), no association was observed for intake from food alone. These results support the hypotheses that a high intake of saturated and certain monounsaturated fatty acids may increase the risk of pancreatic cancer, whereas greater intake of omega-3 fatty acids, vitamins C and E may reduce the risk.
Authors:
Zhihong Gong; Elizabeth A Holly; Furong Wang; June M Chan; Paige M Bracci
Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  International journal of cancer. Journal international du cancer     Volume:  127     ISSN:  1097-0215     ISO Abbreviation:  Int. J. Cancer     Publication Date:  2010 Oct 
Date Detail:
Created Date:  2010-08-30     Completed Date:  2010-09-23     Revised Date:  2013-05-31    
Medline Journal Info:
Nlm Unique ID:  0042124     Medline TA:  Int J Cancer     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1893-904     Citation Subset:  IM    
Affiliation:
Department of Epidemiology and Biostatistics, School of Medicine, University of California San Francisco, San Francisco, CA 94118-1944, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Adenocarcinoma / epidemiology*,  prevention & control
Adult
Aged
Aged, 80 and over
Antioxidants / administration & dosage*
Case-Control Studies
Dietary Supplements*
Fatty Acids / administration & dosage*
Female
Follow-Up Studies
Humans
Male
Middle Aged
Pancreatic Neoplasms / epidemiology*,  prevention & control
Prognosis
San Francisco / epidemiology
Vitamins / administration & dosage*
Young Adult
Grant Support
ID/Acronym/Agency:
CA108370/CA/NCI NIH HHS; CA109767/CA/NCI NIH HHS; CA59706/CA/NCI NIH HHS; CA89726/CA/NCI NIH HHS; N01-PC-35136/PC/NCI NIH HHS; R01 CA059706-02/CA/NCI NIH HHS; R01 CA109767-01A1/CA/NCI NIH HHS; R03 CA089726-01/CA/NCI NIH HHS; R03 CA108370-01A1/CA/NCI NIH HHS; U55/CCR921930-02//PHS HHS
Chemical
Reg. No./Substance:
0/Antioxidants; 0/Fatty Acids; 0/Vitamins
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Ewing's sarcoma cells with CD57-associated increase of tumorigenicity and with neural crest-like dif...
Next Document:  Effects of estrogen on breast cancer development: Role of estrogen receptor independent mechanisms.