Nutrition and prostate cancer

Prostate cancer will become an increasing burden on society

Prostate cancer is now the most common malignancy in Western men, accounting for 30% of newly diagnosed cancers, and it is the second leading cause of male cancer-related death. The burden of human suffering and the cost to society are expected to increase significantly in the coming decades due to increased life expectancy. The Canadian Cancer Society reports that an estimated 23,600 men will be diagnosed with prostate cancer in 2014 and that 4000 men will die from the disease. This represents 10% of all cancer deaths in men. The US Cancer society estimates for 2015 are about 220,800 new prostate cancer cases and 27,540 deaths. Statistics for the European Union are similar overall but are very interesting in that they show a very wide regional difference in mortality rates. In Mediterranean countries, prostate cancer mortality can account for as little as 4% of all cancer-related deaths in men whereas in Scandinavian countries it can be as high as 20%. This is where nutrition comes in to play. Poor diet has been consistently implicated as an important risk factor in prostate cancer.

Eat your vegetables, they are good for you!

Every parent has said it and many a child has protested. Yet parents do know best; epidemiological studies across European and North American populations consistently associate high life-time vegetable consumption with reduced risk of developing cancer and this is particularly true for prostate cancer. Unfortunately, a generation of people has been raised on high fat, carbohydrate and protein diet, low in fibre and plant-derived nutrients.

Prostate cancer develops slowly, with tumours that are already present in men below forty that grow to detectable size over a number of decades. These cancers usually start out as hormone-dependent tumours that respond to therapies that block androgen synthesis or androgen action, but progress to an androgen-independent state that is difficult to treat with conventional chemotherapeutic agents. These non-responsive tumours will eventually metastasize, resulting in the death of the patient. This slow path to malignancy provides valuable opportunities for effective chemopreventive dietary intervention. It is never too late to start eating healthy.

Broccoli, diindolylmethane and death of the prostate cancer cell

My laboratory at the INRS-Institut Armand-Frappier is very interested in understanding how natural compounds can kill prostate cancer cells. These are studies of a fundamental nature and have focussed on compounds found in vegetables of the Brassica family, such as broccoli, cauliflower and Brussels’ sprouts. They contain indole-3-carbinol, which in the stomach undergoes conversion to diindolylmethane (DIM). DIM is relatively non-toxic as it will kill prostate cancer cells at concentrations that do not affect normal prostate cells. In collaboration with professor StephenSafe at Texas A&M University, we have been testing a number of synthetic derivatives of DIM (named ring-DIMs), which have shown increased anticancer activity compared to native DIM. It is relatively well known how DIM exerts its anticancer effects and we expected that the synthetic ring- DIMs would act similarly, just more potently. This was not the case. Probing deeper into the machinery of the prostate cancer cell we found that the increased potency of the ring-DIMs is likely because they act on additional molecular pathways in the prostate cancer cell to trigger its death.

Significantly the ring-DIMs were effective against androgen-dependent as well as -independent prostate cancer cells. Tumour cells (and healthy cells for that matter) can die in several distinct ways, which include programmed cell death (apoptosis), uncontrolled cell death (necrosis) or by dissolving themselves into small components (autophagy). We found the ring-DIMs to trigger all three of these pathways. The question is: what is the trigger? We are currently trying to understand which molecular target or targets in the prostate tumour cell are initially activated to trigger ring-DIM-mediated cell death. Our various experiments have led us to the mitochondria, the energy producers of the cell, which appear to rapidly lose their function. On a deeper level, it appears that our most potent ring-DIM activates a certain kinase (an enzyme responsible for transferring signals that result in a cellular response) that may be a direct target. We have published the results of these studies in the journal Genes & Cancer.

Government policy and research funding

Governments can apply policies that stimulate the consumption of healthier foods (fresh produce, lean meats, cereals) and discourage that of highly processed and nutritionally questionable foods (fast food, foods with high sugar, fat and salt content). It can also improve the availability of fresh produce in remote areas, a problem that is very real in a country such as Canada, where a head of broccoli can cost upwards of $8,- in Canadian dollars in isolated communities… Also necessary is improved and more diversified funding for research on the potential anticancer effects of natural compounds, as research on natural compounds is neglected in comparison with drug and clinical research. It is often argued that natural compounds are not as interesting because they are usually less potent and do not have a specific cellular target. Untrue, because we know that highly selective anticancer agents can result in tumour resistance, whereas natural compounds (usually present in complex mixtures in food) have multiple targets and therefore can act via a diversity of anticancer mechanisms to inhibit tumour growth while making it harder for the tumour cells to adapt and develop resistance. Of course, we should see the consumption of natural compounds in the form of healthy foods mostly in the context of chemoprevention. A healthy diet nips cancerous cells in the bud before they can develop into full-blown tumours.

Bon appétit!

Dr Sanderson’s research is funded by the Canadian Institutes of Health Research (CIHR) and the Natural Sciences and Engineering Research Council of Canada (NSERC).


Thomas Sanderson, PhD Professor

INRS-Institut Armand-Frappier

Tel: 450 687 5010 ext 8819 


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