Common Names

  • DIM

For Patients & Caregivers

Diindolylmethane (DIM) may have anticancer effects, but this has not been studied in humans.

Diindolylmethane is a compound found in cruciferous vegetables including broccoli, cabbage, and cauliflower. It showed anticancer effects in laboratory and animal studies. However, human studies are limited.

  • Cancer Prevention
    Lab studies suggest anticancer activities. But evidence from human studies is lacking.

Rash, arthralgia, nausea, vomiting, headache and hot flashes have been reported.

DIM (and I3C) were shown to alter estrogen urinary metabolite profiles in women. However, their effects on breast cancer risk are unknown.

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For Healthcare Professionals


Diindolylmethane (DIM) is a metabolite of Indole-3-carbinol (I3C), a compound found in cruciferous vegetables including broccoli, cabbage and cauliflower. It is the most studied of all I3C metabolites and is thought to be superior to IC3 as a chemoprotective compound for breast cancer and prostate cancer (3). DIM demonstrated anti-proliferative effects in animal and cancer cell models through various mechanisms.
In contrast to I3C which has been used in over a dozen clinical trials, few studies have been published using DIM. In one study, daily supplementation with DIM led to changes in estrogen metabolism in post menopausal women with a history of early stage breast cancer (4); DIM supplementation, did not, however, have any effects in women with cervical cell abnormalities (13)
DIM’s effects have not been confirmed in cancer patients. Further studies are warranted.

Vegetables including broccoli, Brussels sprouts, cauliflower and cabbage (1)

  • Cancer prevention
  • Estrogen metabolism
  • Detoxification

Diindolylmethane (DIM), a metabolite of I3C, can induce apoptosis by modulating the expression of the Bax/Bcl-2. It demonstrated antiproliferative effects in animal and cancer cell models (1). It was also shown to inhibit invasion of normal tissue by cancer cells and to inhibit angiogenesis in cell culture models (5). Both DIM and I3C induce the activity of phase I and phase II enzymes involved in biotransformation and elimination of steroid hormones and carcinogens in vitro. Physiological concentrations of I3C and DIM induce cytochrome P450 enzymes in cancer cells in vitro. The increased CYP450 activity of these enzymes leads to increased metabolism of estrogen and degradation of estradiol needed for the growth of estrogen receptor-alpha positive cancer cells. DIM induces apoptosis in pancreatic cancer cells (6)and enhances the effect of erlotinib (7). In colon cancer and prostate cancer cells, DIM inhibits CDK activities (8) (9) and induces apoptosis by down regulating survivin (10) (11). DIM supplementation alters estrogen urinary metabolite profiles in women (4) and it has androgen-antagonistic effect (14). It also inhibits prostate cancer cells proliferation and induces apoptosis through Akt activation, NF-KB DNA binding, and androgen receptor phosphorylation (15).

Theoretically, DIM and I3C can induce cytochrome P450 1 enzyme and may reduce serum concentration of medications that it metabolizes.

DIM supplementation has been shown to alter estrogen urinary metabolites in women (4).

  1. Minich DM, Bland JS. A review of the clinical efficacy and safety of cruciferous vegetable phytochemicals. Nutr Rev 2007;65(6 Pt 1):259-267.
  2. Howells LM, Moiseeva EP, Neal CP et al. Predicting the physiological relevance of in vitro cancer preventive activities of phytochemicals. Acta Pharmacol Sin 2007;28(9):1274-1304.
  3. Bradlow HL. Review. Indole-3-carbinol as a chemoprotective agent in breast and prostate cancer. In Vivo 2008;22(4):441-445.
  4. Dalessandri KM, Firestone GL, Fitch MD, Bradlow HL, Bjeldanes LF.Pilot study: effect of 3,3’-diindolylmethane supplements on urinary hormone metabolites in postmenopausal women with a history of early-stage breast cancer. Nutr Cancer 2004;50(2), 161-167.
  5. Higdon JV, Delage B, Williams DE, Dashwood RH. Cruciferous vegetables and human cancer risk: epidemiologic evidence and mechanistic basis. Pharmacol Res 2007;55(3):224-236.
  6. Azmi AS, Ahmad A, Banerjee S et al. Chemoprevention of pancreatic cancer: characterization of Par-4 and its modulation by 3,3’ diindolylmethane (DIM). Pharm Res 2008;25(9):2117-2124.
  7. Ali S, Banerjee S, Ahmad A et al. Apoptosis-inducing effect of erlotinib is potentiated by 3,3’-diindolylmethane in vitro and in vivo using an orthotopic model of pancreatic cancer. Mol Cancer Ther 2008;7(6):1708-1719.
  8. Choi HJ, Lim DY, Park JH. Induction of G1 and G2/M cell cycle arrests by the dietary compound 3,3’-diindolylmethane in HT-29 human colon cancer cells. BMC Gastroenterol 2009;9(1):39.
  9. Chinnakannu K, Chen D, Li Y et al. Cell cycle-dependent effects of 3,3’-diindolylmethane on proliferation and apoptosis of prostate cancer cells. J Cell Physiol 2009;219(1):94-99.
  10. Bhatnagar N, Li X, Chen Y et al. 3,3’-Diindolylmethane Enhances the Efficacy of Butyrate in Colon Cancer Prevention through Down-Regulation of Survivin.Cancer Prev Res (Phila Pa) 2009;2(6):581-589.
  11. Rahman KM, Banerjee S, Ali S et al. 3,3’-Diindolylmethane enhances taxotere-induced apoptosis in hormone-refractory prostate cancer cells through survivin down-regulation. Cancer Res 2009;69(10):4468-4475.
  12. Reed GA, Sunega JM, Sullivan DK et al. Single-dose pharmacokinetics and tolerability of absorption-enhanced 3,3’-diindolylmethane in healthy subjects. Cancer Epidemiol Biomarkers Prev 2008;17(10):2619-2624.
  13. Castañon A, Tristram A, Mesher D, et al. Effect of diindolylmethane supplementation on low-grade cervical cytological abnormalities: double-blind, randomised, controlled trial. Br J Cancer. 2012 Jan 3;106(1):45-52.
  14. Le HT, Schaldach CM, Firestone GL, et al. Plant-derived 3,3’-Diindolylmethane is a strong androgen antagonist in human prostate cancer cells. J Biol Chem. 2003 Jun 6;278(23):21136-45.
  15. Bhuiyan MM, Li Y, Banerjee S, et al. Down-regulation of androgen receptor by 3,3’-diindolylmethane contributes to inhibition of cell proliferation and induction of apoptosis in both hormone-sensitive LNCaP and insensitive C4-2B prostate cancer cells. Cancer Res. 2006 Oct 15;66(20):10064-72.
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