Prostate cancer prevention diet

Prostate cancer prevention

A recent prostate study showed that participants who consumed at least 10 portions of tomatoes weekly showed an 18% reduced risk of developing prostate cancer. The study concluded that a high intake of plant foods and tomato products, in particular, may help protect against prostate cancer.

Adherence to dietary and lifestyle recommendations and prostate cancer risk in the prostate testing for cancer and treatment (ProtecT) trial.

Er V, Lane JA, Martin RM, Emmett P, Gilbert R, Avery KN, Walsh E, Donovan JL, Neal DE, Hamdy FC, Jeffreys M
Cancer Epidemiol Biomarkers Prev. 2014 Oct; 23(10):2066-77.

Another study concluded that lycopene, green tea and potentially soy-containing products may be preventative.

Foods for prostate cancer prevention on a dinner plate with white fish, cherry tomatoes, and vegetables

A Mediterranean-style diet rich in monounsaturated fatty acids and vegetables and fruits and low in red meats also helps.

And daily sunshine exposure helps to build up vitamin D stores. In the ProtecT study, deficiency in vitamin D (circulating concentration <12 ng/ml) was associated with a greater risk of aggressive prostate cancer (higher grade or stage),

Foods to Avoid with prostate cancer

A recent meta-analysis of dietary factors and supplements and prostate cancer risk has concluded that foods to avoid are red and well-done meats, fat and milk should be limited.

Previously, the EPIC consortium found an increased prostate cancer risk with the highest quartiles of dairy protein, but no association with dietary fat (mostly using FFQs)., Data from the US Health Professionals study based on clinically detected cases found no association between calcium intake and localised prostate cancer (measured with FFQs) but a positive association with advanced disease.Conversely, calcium intake was related to an increased risk of localised disease with screen-detected cases in the US PLCO trial.

The evidence for a link between obesity and fatal prostate cancer is strengthening and energy intake might be on that causal pathway. An association between energy intake and advanced disease was shown in a meta-analysis for studies with disease stage with a combined odds ratio of 1.6 for advanced disease. In this study, there was no overall relationship between energy intake and prostate cancer nor heterogeneity in the risk of disease by stage (P=0.07); the association with advanced disease was positive (23% increase) but did not reach conventional statistical significance (95% CI 1.00–1.51).

The finding of weak evidence of heterogeneity in the association of vitamin D with risk between clinically and screen-detected disease may merit further investigation. The precision of estimates of foods consumed irregularly, such as oily fish, a good source of vitamin D, may be lower in food diaries than in questionnaires. Vitamin D levels are also related to sunlight exposure, making serological assessments more comprehensive. In the ProtecT study, deficiency in vitamin D (circulating concentration <12 ng/ml) was associated with a greater risk of aggressive prostate cancer (higher grade or stage), which would be more prevalent in clinically detected cases, but the recent meta-analysis does not support vitamin D supplementation, except for deficiency.

There was no association of overall diet (assessed using FFQs) and screen-detected prostate cancer in the US PCPT trial nor in the Swedish study., Food diary data from 133 prostate cancer cases also revealed no association with diet and prostate cancer, but a reduction with a Mediterranean-style diet rich in monounsaturated fatty acids and vegetables/fruits and low in red meats. A recent meta-analysis of adherence to a Mediterranean diet and overall cancer risk showed a 4% risk reduction for prostate cancer incidence.

The natural history of prostate cancer remains poorly understood, including the time points when dietary and environmental factors may influence disease development or progression. This study measured dietary intake prior to diagnosis and found no major associations with prostate cancer risk, yet migrant studies and international variation in prostate cancer incidence suggest that dietary or other environmental components contribute to disease risk. More recent evidence highlights a role of dietary factors in disease progression, for example, fat intake may influence prostate cancer mortality. Future studies will need to extend measurement of dietary intake across the life course, consider intermediary influences such as the insulin-like growth factor axis and examine the role of obesity, which increases the risk of aggressive prostate cancer, subsequent disease progression and mortality.

Conclusions

In summary, this large study revealed no strong evidence that prostate cancer risk is associated with dietary intake measured prior to diagnosis in middle-aged and older men.

Acknowledgments

We thank the participants and diary coding staff for their contributions, and Ms Vanessa Er and Dr Kate Northstone for analytical advice. Professor Sheila Rodwell (known professionally as Sheila Bingham) who died in 2009, established the Dietary Cohort Consortium as Director of the MRC Centre for Nutritional Epidemiology and Cancer. The authors’ responsibilities were JAL, SEO and TJK wrote the manuscript; PNA conducted the statistical analysis and all authors contributed to the interpretation of data and review of manuscript, including the final manuscript. None of the authors had a personal or financial conflict of interest. The sponsors had no role in study design, data collection, analysis and interpretation of results or the writing of the manuscript. Supported by the UK Medical Research Council and the Medical Research Council Population Health Sciences Research Network. The cohorts received funding from the British Heart Foundation; Cancer Research UK (grant number C8221/A19170); the Department of Health, UK; the Food Standards Agency, UK; the Medical Research Council, UK; the Stroke Association, UK and the WCRF. The ProtecT trial is funded by the UK National Institute for Health Research Health Technology Assessment Programme (projects 96/20/06 and 96/20/99) and the nested ProMPT study (Prostate Mechanisms of Progression and Treatment), funded by the National Cancer Research Institute (NCRI – formed by Cancer Research UK, the Medical Research Council and the Department of Health). DK is funded by the UK Medical Research Council (MC_UU_12019/1). The funding sources had no role in the study design, conduct, data collection, management, analysis and interpretation or preparation, review or approval of the article.

Footnotes

The authors declare no conflict of interest.

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Studied Nutrition and Physical Activity for Health at the University of Pittsburgh.