If the thought of eating servings of broccoli and cabbage every day does not appeal to you, then you should read this post to learn why you should grin and bear it.

Multiple recent studies continue to document diindolylmethane (DIM) as one of the most effective phytonutrients in the prevention and treatment of breast, prostate, colon and pancreatic cancers. DIM is the compound found in cruciferous vegetables that regulates hormone balance and cell behavior.

“In a study published in the May 1, 2008 Biochemical Pharmacology Journal, researchers report having previously shown that DIM is able to stop tumors from establishing their own blood supply (angiogenesis) in cultured endothelial cells in rodents. In this study, they demonstrated that DIM reduces the level of hypoxia-inducible factor (HIF)-1alpha in hypoxic tumor cell lines, as well as HIF-1 transcriptional activity. Moreover, the level of oxygen in tumor cells was increased. This study is the first to show that DIM can decrease the accumulation and activity of the key angiogenesis regulatory factor, HIF-1alpha, in hypoxic tumor cells.

The April 22, 2008 Pharmaceutical Research reports that prostrate apoptosis response-4 (Par-4) is a unique pro-apoptotic protein that selectively induces apoptosis in prostate cancer cells. Apoptosis is the planned appropriate death of cells without which cells may exhibit excess proliferation. Researchers sought to identify the functional significance of Par-4 in pancreatic cancer. Results revealed that low doses of the B-DIM (the most bioavailable formulation of DIM) induced Par-4 in pancreatic cancer cells. DIM reduced cancer cell viability and caused cell growth inhibition and apoptosis.

The Cancer Letter, March 28, 2008 reports that the interaction between the chemokine receptor and its unique ligand is known to mediate the progression and metastasis of breast, prostate and other cancers. Organs to which these cancers metastasize secrete the particular ligand which binds to the chemokine receptor on the surface of primary cancer cells. This process subsequently stimulates the invasive properties of the cancer cells and attracts them to the preferred organ sites of metastases. The researchers found that DIM down-regulates both the ligand and the receptor in breast cancer cells as well as in ovarian cancer cells at the transcriptional level and in an estrogen-independent manner. They demonstrated that the potential of cells for chemotaxis and invasion is inhibited by DIM. Furthermore, they showed that DIM down-regulates the chemokine receptor under hypoxia and the ligand under estradiol-inducing conditions. The data suggest that one mechanism whereby DIM protects against breast, ovarian, and possibly other cancers is through the repression of this mechanism, thereby lowering the invasive and metastatic potential of these cells.

From the March 15, 2008 Cancer Research comes a study reporting that platelet-derived growth factor-D (PDGF-D) is a newly recognized growth factor known to regulate many cellular processes, including cell proliferation, transformation, invasion, and angiogenesis. Recent studies have shown that PDGF-D and its receptor are expressed in prostate tumor tissues, suggesting that PDGF-D plays an important role in the development and progression of prostate cancer. Researchers found that PDGF-D was significantly inhibited by B-DIM. This correlated with decreased cell proliferation and invasion. B-DIM also inhibited the tube formation of human umbilical vein endothelial cells. They concluded that B-DIM could serve as an efficient preventative and/or therapeutic agent in prostate cancer.

Molecular Cancer Therapeutics February, 2008, reports a study of human breast cancer cell lines to understand the mechanisms of DIM. In vitro experiments were done with breast cancer cell lines. Researchers found that DIM inhibited the growth of all four breast cancer cell lines. Because two of the cell lines over expressed Her-2 and two of the lines lacked estrogen receptors, these were studied further. In both cell lines, DIM appeared to induce expression of p27 protein before the loss of cell viability and apoptosis. DIM induced p27 transcript expression within 6 hours. DIM also induced nuclear localization of p27 in both cell lines. In one of the cell lines, DIM induced a decrease in phosphorylation. Researchers concluded that DIM modulates p27 through transcription, prolongation of protein half-life, and nuclear localization. These effects appear to be independent of Her-2, or estrogen receptor status.

The January, 2008 Journal of Nutrition finds that because recurrent or chronic inflammation has been implicated in the development of a variety of human cancers, researchers examined the anti-inflammatory effects of DIM and the underlying mechanisms using lipopolysaccharides (LPS) stimulated macrophages. DIM significantly decreased the release of nitric oxide, prostaglandin E2, tumor necrosis factor alpha, interleukin-6 and IL-1beta cells treated with LPS. DIM inhibited LPS induced increases in protein levels of inducible NO synthase. The messenger RNA levels of phospholipase A2 decreased, whereas neither COX 2 protein nor transcript was altered. Researchers concluded that DIM inhibits LPS induced release of pro-inflammatory mediators in macrophages.”

It is possible to purchase DIM supplements, but I am not aware of any good research that demonstrates that you get the same positive effects as you would if you ate the actual vegetable.

DIM is nature’s hormone modulator and you need to consume it. So, go ahead and enjoy your broccoli.

Joel T Nowak MA, MSW