Dietary Glucosinolate Intake, Polymorphisms in Selected Biotransformation Enzymes, and Risk of Prostate Cancer

Steinbrecher, Astrid; Rohrmann, Sabine; Timofeeva, Maria; Risch, Angela; Jansen, Eugène; Linseisen, Jakob

doi:10.1158/1055-9965.epi-09-0660

Cited by 53 publications

(40 citation statements)

References 26 publications

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“…The associations between gene polymorphisms and prostate cancer risk (main effects) were reported earlier [21][22] and are thus not shown here. The allele frequencies of the selected genetic variants in PCa cases and controls are shown in Table 2.…”

Section: Resultsmentioning

confidence: 76%

“…As a consequence, increased expression and metabolic activation of CYP1A1, CYP1A2 and CYP1B1 has been shown in benign prostatic hyperplasia (BPH) tissue 23,26 . In contrast, HCA carcinogens are known to be detoxified by gluathione Stransferases (GSTs) and possibly also NADPH-quinone oxidoreductase (NQO1) [22][23]25 .…”

Section: Discussionmentioning

confidence: 99%

“…In our EPIC-Heidelberg cohort, we previously have shown that polymorphisms of GSTM1, GSTT1, GSTP1, GSTA1, NQO1, GPX1, and GPX4 were not associated with PCa risk [21][22] .…”

Section: Discussionmentioning

confidence: 99%

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Heterocyclic Aromatic Amine [HCA] Intake and Prostate Cancer Risk: Effect Modification by Genetic Variants

Hemelrijck

Rohrmann

Steinbrecher

et al. 2012

Nutrition and Cancer

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The association between heterocyclic aromatic amine (HCA) intake and prostate cancer (PCa) risk may be modified by genetic variation in enzymes involved in HCA metabolism. We examined this question in a case-control study nested within the European Prospective Investigation into Cancer and Nutrition Heidelberg cohort. The study included 204 PCa cases and 360 matched controls. At baseline, participants provided dietary and lifestyle data and blood samples that were used for genotyping. Dietary HCA intake-2-amino-1-methyl-6-phenylimidazo [4,5-b] and 2-amino-3,4,8-dimethylimidazo [4,5-f]quinoxaline (DiMeIQx-was estimated using information on meat consumption, cooking methods, and browning degree. Risk estimates for gene × HCA interactions were calculated by unconditional logistic regression. We found inverse associations between PhIP, MeIQx, or DiMeIQx intake and PCa risk when having <2 deletions of the GSTT1 and GSTM1 genes (P(interaction): 0.03, 0.01, and 0.03, respectively), which is supported by analysis of darkly browned meat consumption data. Statistically significant effect modification of both HCA (DiMeIQx) and darkly browned meat intake and PCa risk was observed for allelic variants of MnSOD (rs4880) (P(interaction): 0.02). Despite limitations due to study size, we conclude that the association between HCA intake and PCa risk could be modified by polymorphisms of GSTT1, GSTM1, and MnSOD. AbstractThe association between heterocyclic aromatic amine (HCA) intake and prostate cancer (PCa) risk may be modified by genetic variation in enzymes involved in HCA metabolism.We examined this question in a case-control study nested within the European Prospective We found inverse associations between PhIP, MeIQx, or DiMeIQx intake and PCa risk when having <2 deletions of the GSTT1 and GSTM1 genes (P interaction : 0.03, 0.01, and 0.03, respectively), which is supported by analysis of darkly browned meat consumption data.Statistically significant effect modification of both HCA (DiMeIQx) and darkly browned meat intake and PCa risk was observed for allelic variants of MnSOD (rs4880) (P interaction :0.02). Despite limitations due to study size, we conclude that the association between HCA intake and PCa risk could be modified by polymorphisms of GSTT1, GSTM1, and MnSOD.3

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Section: Resultsmentioning

confidence: 76%

Section: Discussionmentioning

confidence: 99%

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Heterocyclic Aromatic Amine [HCA] Intake and Prostate Cancer Risk: Effect Modification by Genetic Variants

Hemelrijck

Rohrmann

Steinbrecher

et al. 2012

Nutrition and Cancer

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“…Interactions have also been shown between genes and diet in measures of DNA damage, 70 prostate cancer risk and levels of the glutathione s-transferase alpha. 71,72 Cognitive decline APOE has been identified as a susceptibility gene for Alzheimer's disease, with the e4 variant increasing risk for disease. The Risk Evaluation and Education for Alzheimer's Disease (commonly known as REVEAL) study examined how knowing APOE e4 status impacted behavior change in the adult offspring of parents with Alzheimer's disease.…”

Section: Cancermentioning

confidence: 99%

Nutrigenetics—Personalized Nutrition in the Genetic Age

Beckett¹,

Jones²,

Veysey³

et al. 2017

Exploratory Research and Hypothesis in Medicine

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Diet is an important modifiable determinant of disease, and it is becoming clear that diet and genetic risk factors are interactive in determining risk for diseases such as cardiovascular disease, diabetes and cancers. Advances in technology have improved our understanding of gene-nutrient interactions, and lead to the development of nutrigenetics, personalized nutrition based on genetics. While evidence is strong for some associations, others remain unclear. As such, the implementation of nutrigenetics remains controversial. While some argue it is not ready for clinical use, it has also been argued that nutrigenetics is unfairly held to a higher standard than traditional nutrition research. Despite the future promise of nutrigenetic testing for improving health outcomes, several barriers in science, technology, acceptance and ethics exist to its implementation. Gene-nutrient associations have been identified in a number of lifestyle-associated diseases, and better understanding of these relationships may lead to improved health outcomes. However, the success of nutrigenetics is not only dependent on the strength of the science, but in consumer acceptance and uptake. This narrative review provides an overview of the current landscape for nutrigenetics in relation to key disease states, and addresses the potential barriers to implementation.

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“…Other authors have demonstrated gene-diet-dependent effects on reduced DNA damage (Palli et al 2004), reduced prostate cancer risk (Steinbrecher et al 2010), and increased levels of GST alpha (Lampe et al 2000). These interactions among genotype, cruciferous vegetables, and lung cancer risk have also been confirmed in a systematic analysis (Lam et al 2009).…”

Section: Personalized Nutrition: If Not Now When?mentioning

confidence: 99%

Do we know enough? A scientific and ethical analysis of the basis for genetic-based personalized nutrition

et al. 2013

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This article discusses the prospects and limitations of the scientific basis for offering personalized nutrition advice based upon individual genetic information. Two divergent scientific positions are presented, with an ethical comment. The crucial question is whether the current knowledge base is sufficiently strong for taking an ethically responsible decision to offer personalized nutrition advice based upon gene-diet-health interaction. According to the first position, the evidence base for translating the outcomes of nutrigenomics research into personalized nutritional advice is as yet immature. There is also limited evidence that genotype-based dietary advice will motivate appropriate behavior changes. Filling the gaps in our knowledge will require larger and better randomized controlled trials. According to the second position, personalized nutrition must be evaluated in relation to generally accepted standard dietary advice-partly derived from epidemiological observations and usually not proven by clinical trials. With personalized nutrition, we cannot demand stronger evidence. In several specific cases of gene-diet interaction, it may be more beneficial for individuals with specific genotypes to follow personalized advice rather than general dietary recommendations. The ethical comment, finally, considers the ethical aspects of deciding how to proceed in the face of such uncertainty. Two approaches for an ethically responsible way forward are proposed. Arguing from a precautionary approach, it is suggested that personalized dietary advice should be offered only when there is strong scientific evidence for health effects, followed by stepwise evaluation of unforeseen behavioral and psychological effects. Arguing from theoretical and applied ethics as well as psychology, it is also suggested that personalized advice should avoid paternalism and instead focus on supporting the autonomous choice of each person.

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Dietary Glucosinolate Intake, Polymorphisms in Selected Biotransformation Enzymes, and Risk of Prostate Cancer

Cited by 53 publications

References 26 publications

Heterocyclic Aromatic Amine [HCA] Intake and Prostate Cancer Risk: Effect Modification by Genetic Variants

Heterocyclic Aromatic Amine [HCA] Intake and Prostate Cancer Risk: Effect Modification by Genetic Variants

Nutrigenetics—Personalized Nutrition in the Genetic Age

Do we know enough? A scientific and ethical analysis of the basis for genetic-based personalized nutrition

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