Περίληψη:
Coffee and tea contain numerous antimutagenic and antioxidant components
and high levels of caffeine that may protect against colorectal cancer
(CRC). We investigated the association between coffee and tea
consumption and CRC risk and studied potential effect modification by
CYP1A2 and NAT2 genotypes, enzymes involved in the metabolization of
caffeine. Data from 477,071 participants (70.2% female) of the European
Investigation into Cancer and Nutrition (EPIC) cohort study were
analyzed. At baseline (1992-2000) habitual (total, caffeinated and
decaffeinated) coffee and tea consumption was assessed with dietary
questionnaires. Cox proportional hazards models were used to estimate
adjusted hazard ratio’s (HR) and 95% confidence intervals (95% CI).
Potential effect modification by genotype-based CYP1A2 and NAT2 activity
was studied in a nested case-control set of 1,252 cases and 2,175
controls. After a median follow-up of 11.6 years, 4,234 participants
developed CRC (mean age 64.78.3 years). Total coffee consumption (high
vs. non/low) was not associated with CRC risk (HR 1.06, 95% CI
0.95-1.18) or subsite cancers, and no significant associations were
found for caffeinated (HR 1.10, 95% CI 0.97-1.26) and decaffeinated
coffee (HR 0.96, 95% CI 0.84-1.11) and tea (HR 0.97, 95% CI
0.86-1.09). High coffee and tea consuming subjects with slow CYP1A2 or
NAT2 activity had a similar CRC risk compared to non/low coffee and tea
consuming subjects with a fast CYP1A2 or NAT2 activity, which suggests
that caffeine metabolism does not affect the link between coffee and tea
consumption and CRC risk. This study shows that coffee and tea
consumption is not likely to be associated with overall CRC.
What’s new? Coffee and tea contain numerous compounds that may protect
against colorectal cancer (CRC). In this study of more than 475,000
participants over more than a decade, the authors investigated whether
coffee or tea consumption is associated with an altered risk of
developing CRC. They also asked whether genetic variations in two
enzymes involved in caffeine metabolism (CYP1A2 and NAT2) might affect
this risk. They conclude that neither consumption patterns, nor genetic
differences in caffeine metabolism, appear to have a significant impact
on CRC risk.
Συγγραφείς:
Dik, Vincent K.
Bueno-de-Mesquita, H. B(as)
Van Oijen, Martijn
G. H.
Siersema, Peter D.
Uiterwaal, Cuno S. P. M.
Van Gils,
Carla H.
Van Duijnhoven, Fraenzel J. B.
Cauchi, Stephane and
Yengo, Loic
Froguel, Philippe
Overvad, Kim
Bech, Bodil H.
and Tjonneland, Anne
Olsen, Anja
Boutron-Ruault, Marie-Christine
and Racine, Antoine
Fagherazzi, Guy
Kuehn, Tilman
Campa,
Daniele
Boeing, Heiner
Aleksandrova, Krasimira
Trichopoulou,
Antonia
Peppa, Eleni
Oikonomou, Eleni
Palli, Domenico and
Grioni, Sara
Vineis, Paolo
Tumino, Rosaria
Panico, Salvatore
and Peeters, Petra H. M.
Weiderpass, Elisabete
Engeset, Dagrun
and Braaten, Tonje
Dorronsoro, Miren
Chirlaque, Maria-Dolores
and Sanchez, Maria-Jose
Barricarte, Aurelio
Zamora-Ros, Raul and
Argueelles, Marcial
Jirstroem, Karin
Wallstroem, Peter and
Nilsson, Lena M.
Ljuslinder, Ingrid
Travis, Ruth C.
Khaw,
Kay-Tee
Wareham, Nick
Freisling, Heinz
Licaj, Idlir and
Jenab, Mazda
Gunter, Marc J.
Murphy, Neil
Romaguera-Bosch,
Dora
Riboli, Elio
