Sulforaphane lowered markers linked to tumor growth in men with prostate cancer. Digest
Sulforaphane, a compound generated from precursors found in cruciferous vegetables, has attracted interest for its potential effects on cancer biology. Researchers tested whether a supplement designed to generate sulforaphane in the body could alter tumor-related markers in men with prostate cancer.
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The double-blind study randomly assigned 41 men with prostate cancer awaiting surgery to remove the prostate to receive either a daily placebo or a broccoli-derived supplement containing 240 mg of glucoraphanin plus myrosinase for four weeks. Together, these ingredients generate sulforaphane after consumption. Researchers then measured free fatty acids in blood and tumor tissue collected during surgery along with proteins involved in fatty acid production and tumor growth. In parallel, 40 mice genetically prone to developing prostate cancer received purified sulforaphane or a control for 16 weeks before researchers assessed tumor burden and many of the same biological changes measured in the human trial.
- In humans, the broccoli-derived supplement did not lower total free fatty acid levels in the blood or in tumor samples compared with placebo after four weeks.
- Compared with the placebo group, tumor samples from men who received the supplement had about 13% lower levels of two enzymes that help cancer cells make fatty acids, while a marker of how quickly cancer cells were multiplying was about 32% lower.
- Compared with mice given the control, sulforaphane reduced tumor burden by about 61%.
- Unlike the human trial, blood free fatty acid levels were about 30% lower in mice receiving sulforaphane.
- In mouse prostate tumors, sulforaphane also lowered levels of the same two enzymes that help cancer cells make fatty acids by about 46% and 31%, respectively. It also reduced another marker of how quickly cancer cells were multiplying by about 34% and increased a marker of programmed cell death by about 30%.
The researchers focused on fatty acid production because it is elevated in human prostate cancer and contributes to disease progression. However, the human findings suggest only a partial effect on this pathway. Although proteins involved in fatty acid production and cancer cell multiplication were lower, free fatty acid levels remained unchanged. That could reflect the short treatment period, differences in how mice and humans process sulforaphane, or differences between the precursor-based supplement and direct sulforaphane treatment. Sulforaphane may also affect tumor biology through additional pathways that were not directly examined in this study.
The main limitation is that the human trial was short and measured indirect signs of tumor activity rather than clinical cancer outcomes. It cannot show whether tumors became smaller, recurrence risk changed, or patients benefited after surgery. Nevertheless, the results suggest that sulforaphane-related interventions can influence prostate tumor biology, making larger and longer human studies a reasonable next step. In this clip, Dr. Jed Fahey describes sulforaphane's opposing effects on cancer.