E. Kampman et al., Meat consumption, genetic susceptibility, and colon cancer risk: A United States multicenter case-control study, CANC EPID B, 8(1), 1999, pp. 15-24
Meat consumption may especially increase risk of colon cancer when the meat
is prepared at high temperatures and consumed by subjects with an inherite
d susceptibility to well-done meat. In this United States case-control stud
y, the association between meat consumption, genetic susceptibility, and co
lon canter risk was studied. Meat consumption data were available from a de
tailed diet history questionnaire and from questions about methods of prepa
ration. Molecular variants in the carcinogen-metabolizing genes NAT2 and GS
TM1 were determined in DNA extracted from WBCs, A total of 1542 cases and 1
860 population-based controls were included in these analyses.
The amount of red and white meat consumed was not associated with overall c
olon cancer risk. Processed meat consumption was weakly positively associat
ed with colon cancer risk in men only (odds ratio for highest versus lowest
quintile of intake = 1.4, 95% confidence interval = 1.0-1.9). The frequenc
y of fried, broiled, baked, or barbecued meat, use of drippings, and donene
ss of meat were not significantly associated with risk. The Mutagen Index,
as an estimate for exposure to mutagenic or carcinogenic substances, was sl
ightly positively associated with colon cancer risk in men (odds ratio = 1.
3, 95% confidence interval = 1.0-1.7). No significant associations with col
on cancer risk were observed for different NAT2 and GSTM1 gene variants. Th
e observed associations with processed meat and the Mutagen Index were stro
ngest for those with the intermediate or rapid NAT2 acetylator phenotype, A
ssociations were not markedly influenced by lack of the GSTM1 gene.
This study provides little support for an association between meat consumpt
ion and colon cancer risk but does provide some, albeit not strong, evidenc
e for a modifying effect of molecular variants of the NAT2 gene.