Par contre, ses choix diététiques vont jouer un rôle
Can creatine supplementation form carcinogenic heterocyclic amines in humans?
Renato Tavaresdos Santos Pereira The Journal of Physiology 2015 593 Issue 14
Creatine supplementation has been associated with increased cancer risk. In fact, there is evidence indicating that creatine and/or creatinine are important precursors of carcinogenic heterocyclic amines (HCAs).
The present study aimed to investigate the acute and chronic effects of low- and high-dose creatine supplementation on the formation of carcinogenic HCAs (i.e., PhIP, 8-MeIQx, IFP, and 4,8-DiMeIQx) in healthy humans. This was a non-counterbalanced single-blind crossover study divided in two phases, in which low- and high-dose creatine protocols were tested. After acute (1 day) and chronic supplementation (30 days), the HCAs 2-Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP), 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (8-MeIQx), 2-amino-(1,6-dimethylfuro[3,2-e]imidazo[4,5-b])pyridine (IFP) and 2-amino-3,4,8-trimethylimidazo[4,5-f]quinoxaline (4,8-DiMeIQx) were assessed through a newly developed HPLC–MS/MS method. Dietary HCAs intake and blood and urinary creatinine were also evaluated.
Out of 576 assessments performed (from 149 urine samples), only 9 (3 from creatine and 6 from placebo) showed quantifiable levels of HCAs (8-MeIQx: n = 3; 4,8-DiMeIQx: n = 2; PhIP: n = 4). Individual analyses revealed that diet rather than creatine supplementation was the main responsible factor for HCA formation in these cases.
This study provides compelling evidence that both low and high doses of creatine supplementation, given either acutely or chronically, did not cause increases in the carcinogenic HCAs PhIP, 8-MeIQx, IFP, 4,8-DiMeIQx in healthy subjects. These findings challenge the long-existing notion that creatine supplementation could potentially increase the risk of cancer by stimulating the formation of these mutagens.