• Open Access

Systematic review: diet–gene interactions and the risk of colorectal cancer

Authors

  • V. Andersen,

    Corresponding author
    1. Institute of Regional Health Research, Faculty of Health Sciences, University of Southern Denmark, Odense, Denmark
    2. Medical Department, RHV Viborg, Viborg, Denmark
    • Medical Department, Hospital of Southern Jutland, Aabenraa, Denmark
    Search for more papers by this author
  • R. Holst,

    1. Institute of Regional Health Research, Faculty of Health Sciences, University of Southern Denmark, Odense, Denmark
    Search for more papers by this author
  • U. Vogel

    1. National Research Centre for the Working Environment, Copenhagen, Denmark
    Search for more papers by this author

  • This uncommissioned systematic review was subject to full peer-review.

Correspondence to:

Dr V. Andersen, Medical Department, Hospital of Southern Jutland, Kresten Philipsens Vej 15, 6200 Aabenraa, Denmark.

E-mail: vandersen@health.sdu.dk

Summary

Background

Diet contributes significantly to colorectal cancer (CRC) aetiology and may be potentially modifiable.

Aim

To review diet–gene interactions, aiming to further the understanding of the underlying biological pathways in CRC development.

Methods

The PubMed and Medline were systematically searched for prospective studies in relation to diet, colorectal cancer and genetics.

Results

In a meta-analysis, no interaction between NAT1 phenotypes and meat intake in relation to risk of CRC was found (P-value for interaction 0.95). We found a trend towards interaction between NAT2 phenotypes and meat intake in relation to risk of CRC. High meat intake was not associated with risk of CRC among carriers of the slow NAT2 phenotype, whereas NAT2 fast acetylators with high meat intake were at increased risk of CRC (OR = 1.25; 95% confidence interval (CI): 0.92–2.01) compared with slow acetylators with low meat intake (reference), P-value for interaction = 0.07. Low meat intake in the studied populations may influence the result. Interactions between meat, cruciferous vegetables, fibres, calcium, vitamins, and alcohol and ABCB1, NFKB1, GSTM1, GSTT1, CCND1, VDR, MGTM, IL10 and PPARG are suggested.

Conclusions

A number of interactions between genetic variation and diet are suggested, but the findings need replication in independent, prospective, and well-characterised cohorts before conclusions regarding the underlying biological mechanisms can be reached. When the above criteria are met, studies on diet–gene interactions may contribute valuable insight into the biological mechanisms underlying the role of various dietary items in colorectal carcinogenesis.

Ancillary