University of Oulu

Beynon, R.A., Richmond, R.C., Santos Ferreira, D.L., Ness, A.R., May, M., Smith, G.D., Vincent, E.E., Adams, C., Ala-Korpela, M., Würtz, P., Soidinsalo, S., Metcalfe, C., Donovan, J.L., Lane, A.J., Martin, R.M., and (2019), Investigating the effects of lycopene and green tea on the metabolome of men at risk of prostate cancer: The ProDiet randomised controlled trial. Int. J. Cancer, 144: 1918-1928.

Investigating the effects of lycopene and green tea on the metabolome of men at risk of prostate cancer : the ProDiet randomised controlled trial

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Author: Beynon, Rhona A.1,2; Richmond, Rebecca C.1,2; Santos Ferreira, Diana L.1,2;
Organizations: 1Population Health Sciences, Bristol Medical School, University of Bristol, Bristol, United Kingdom
2Medical Research Council Integrative Epidemiology Unit at the University of Bristol, Bristol, United Kingdom
3The National Institute for Health Research (NIHR) Bristol Biomedical Research Centre, Upper Maudlin Street, Bristol, United Kingdom
4School of Cellular and Molecular Medicine, University of Bristol, Bristol, United Kingdom
5Computational Medicine, University of Oulu and Biocenter Oulu, Oulu, Finland
6NMR Metabolomics Laboratory, School of Pharmacy, University of Eastern Finland, Kuopio, Finland
7Systems Epidemiology, Baker Heart and Diabetes Institute, Melbourne, Victoria, Australia
8Department of Epidemiology and Preventive Medicine, School of Public Health and Preventive Medicine, Faculty of Medicine, Nursing and Health Sciences, The Alfred Hospital, Monash University, Melbourne, Victoria, Australia
9Research Programs Unit, Diabetes and Obesity, University of Helsinki, Helsinki, Finland
10Nightingale Health Ltd., Helsinki, Finland
11Bristol Randomised Trials Collaboration, School of Social and Community Medicine, University of Bristol, Bristol, United Kingdom
Format: article
Version: published version
Access: open
Online Access: PDF Full Text (PDF, 1 MB)
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Language: English
Published: John Wiley & Sons, 2019
Publish Date: 2019-07-05


Lycopene and green tea consumption have been observationally associated with reduced prostate cancer risk, but the underlying mechanisms have not been fully elucidated. We investigated the effect of factorial randomisation to a 6‐month lycopene and green tea dietary advice or supplementation intervention on 159 serum metabolite measures in 128 men with raised PSA levels (but prostate cancer‐free), analysed by intention‐to‐treat. The causal effects of metabolites modified by the intervention on prostate cancer risk were then assessed by Mendelian randomisation, using summary statistics from 44,825 prostate cancer cases and 27,904 controls. The systemic effects of lycopene and green tea supplementation on serum metabolic profile were comparable to the effects of the respective dietary advice interventions (R² = 0.65 and 0.76 for lycopene and green tea respectively). Metabolites which were altered in response to lycopene supplementation were acetate [β (standard deviation difference vs. placebo): 0.69; 95% CI = 0.24, 1.15; p = 0.003], valine (β: −0.62; −1.03, −0.02; p = 0.004), pyruvate (β: −0.56; −0.95, −0.16; p = 0.006) and docosahexaenoic acid (β: −0.50; −085, −0.14; p = 0.006). Valine and diacylglycerol were lower in the lycopene dietary advice group (β: −0.65; −1.04, −0.26; p = 0.001 and β: −0.59; −1.01, −0.18; p = 0.006). A genetically instrumented SD increase in pyruvate increased the odds of prostate cancer by 1.29 (1.03, 1.62; p = 0.027). An intervention to increase lycopene intake altered the serum metabolome of men at risk of prostate cancer. Lycopene lowered levels of pyruvate, which our Mendelian randomisation analysis suggests may be causally related to reduced prostate cancer risk.

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Series: International journal of cancer
ISSN: 0020-7136
ISSN-E: 1097-0215
ISSN-L: 0020-7136
Volume: 144
Issue: 8
Pages: 1918 - 1928
DOI: 10.1002/ijc.31929
Type of Publication: A1 Journal article – refereed
Field of Science: 3122 Cancers
Funding: This work has been supported by Cancer Research UK (CRUK) (ref: C11046/A10052) and the UK National Institute for Health Research (NIHR) Health Technology Assessment (HTA) Programme, HTA 96/20/99; ISRCTN20141297. Further information available at: RAB is funded by a Wellcome Trust 4-year studentship (WT099874MA). RCR is funded by CRUK (grant number: C18281/A19169). EEV is funded by an RD Lawrence Fellowship from Diabetes UK (grant number: 17/0005587). RMM is supported by CRUK (C18281/A19169). RB, DDSF, RCR, EEV, CA, MAK and RMM work in a Unit that receives funds from the University of Bristol and the UK Medical Research Council (MC_UU_12013/1, MC_UU_12013/5). AL and CM work in a unit that receives National Institute for Health Research CTU Support Funding. PW is supported by the Academy of Finland (312476 and 312477) and the Novo Nordisk Foundation (15998). MAK was supported by the Sigrid Juselius Foundation, Finland.
Copyright information: © 2018 The Authors. International Journal of Cancer published by John Wiley & Sons Ltd on behalf of UICC. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.