As mentioned in:
"Foods/Supplements-Vitamins: Cruciferous Phytochemicals -  Introduction"
... cruciferous phytochemicals are initially in glucosinolate form. To activate the chemical, the glucose structure must be removed via the myrosinase enzyme. Indole-3-carbinol [I3C] is the active component of the glucosinolate glucobrassicin.
In the low pH stomach environment, I3C converts to a number of chemicals, one of which is DIM. We know little about the rest. Are they all helpful - are any harmful? In any case, I3C is unstable in the stomach & does not survive as such.
About 16 years ago there seems to have been a clash of egos. Dr. Michael A. Zeligs was promoting his patented form of bioavailable DIM, while Life Extension [LEF] was selling products containing I3C but not DIM. In the January 2002 issue of the LEF magazine, we find :
"I3C vs DIM"
"Who is Michael Zeligs, and why is he saying negative things about I3C?"
Eventually, DIM found its way into LEF products - in combination with I3C.
I found the case for I3C to be weak. It didn't help that DIM was thought to be the active factor in some studies. DIM studies (Zeligs' version) showed promising results. & even now, I can't name another metabolite of I3C.
But many years have passed since I began using DIM, so here is a quick review of the 69 papers that PubMed returns on a <prostate "Indole-3-carbinol"> search. Unfortunately, many of the hits are not I3C-specific.
For those interested only in the conclusion, skip to , a review paper that might have been written by Dr. Zeligs himself.
 A cell study used I3C & DIM at 20% of the I3C weight. Results seem to have been identical. Implication: one needs a lot more I3C to do the job, & this might be due to DIM being the active agent.
 "Studies in prostate cancer models and cells have concluded that both I3C and DIM inhibit prostate carcinogenesis, decrease cell proliferation, increase apoptosis and induce G1 cell cycle arrest (Chinni et al., 2001; Nachshon-Kedmi et al., 2004b; Garikapaty et al., 2006; Hsu et al., 2006; Souli et al., 2008; Vivar et al., 2009; Fares et al., 2010). While both I3C and DIM have been established as chemopreventive agents, there is growing evidence that the acid condensation products, such as DIM, have distinct targets and greater bioactivity. For example, DIM was more effective at lower concentrations than I3C in inducing apoptosis in prostate cancer cells (Garikapaty et al., 2006). Furthermore, DIM has been shown to be more effective than I3C at down regulating the Akt survival pathway in prostate cancer cells (Garikapaty et al., 2006). While I3C and DIM have the potential to be therapeutic and chemopreventative phytochemicals, the complete mechanisms by which they induce the anti-carcinogenic properties is not well understood."
"The chemopreventive effects of DIM are well–established and have been linked to proliferation/survival events and the induction of apoptosis (reviewed in (Banerjee et al., 2012). Despite this intense study, the precise molecular mechanisms by which DIM inhibits proliferation and induces apoptosis remains unclear. Here we show for the first time that DIM, but not I3C, inhibits HDAC activity in cancer cells. This inhibition of HDACs by DIM is associated with an up-regulation of the cell cycle regulator p21 in prostate cancer cells. We further show that DIM induces the down regulation of HDAC2 which is a protein that is upregulated in prostate cancers and associated with decreased patient survival ..."
 "I3C significantly inhibited telomerase activity and hTERT mRNA expression in LNCaP and PC3 cells. Combination of I3C and DES enhanced the inhibitory effect on telomerase activity, gene expression, and cell viability. These results implied that I3C and DES combined might help in prostate cancer treatment."
 "In vivo pharmacodynamics of indole-3-carbinol in the inhibition of prostate cancer in transgenic adenocarcinoma of mouse prostate (TRAMP) mice: involvement of Nrf2 and cell cycle/apoptosis signaling pathways."
 "Indole-3-carbinol inhibits prostate cancer cell migration via degradation of beta-catenin."
 "Broccoli-derived phytochemicals indole-3-carbinol and 3,3'-diindolylmethane exerts concentration-dependent pleiotropic effects on prostate cancer cells ..."
"We ... demonstrated that an inhibitory effect of DIM and I3C on cell growth involves inhibition of insulin-like growth factor-1 receptor expression. More importantly, we showed that differences in efficacies and mechanisms existed between DIM and I3C. These included differences in effective concentrations, a differential effect on androgen receptor binding, and a differential effect on xenobiotic metabolic pathway ..."
"We also showed that some cellular pathways are not likely to be affected by DIM or I3C when circulating concentration of orally ingested DIM or I3C is considered. Based on our results, a model for cancer protective effects of DIM and I3C was proposed."
 "Indole-3-carbinol (I3C) exhibits inhibitory and preventive effects on prostate tumors in mice."
 "Indole-3-carbinol mediated cell cycle arrest of LNCaP human prostate cancer cells requires the induced production of activated p53 tumor suppressor protein."
 "BRCA1 and BRCA2 as molecular targets for phytochemicals indole-3-carbinol and genistein in breast and prostate cancer cells."
 "Indole-3-carbinol inhibition of androgen receptor expression and downregulation of androgen responsiveness in human prostate cancer cells."
 "Indole-3-carbinol induces a G1 cell cycle arrest and inhibits prostate-specific antigen production in human LNCaP prostate carcinoma cells."
 "Akt inactivation is a key event in indole-3-carbinol-induced apoptosis in PC-3 cells."
 "Indole-3-carbinol (I3C) induced cell growth inhibition, G1 cell cycle arrest and apoptosis in prostate cancer cells."
 (2008 - U.S. - Review)
"Assessment of the oral use of indole-3-carbinol (I3C) as a chemoprotective compound has not sufficiently considered the chemical instability of I3C. This review addresses the question of whether I3C is directly active in its own right or only serves as a precursor, with all of the biological responses coming from reaction products arising in culture media and in the presence of stomach acid. Because of the rapid conversion of I3C into its dimer. diindolylmethane (DIM), and trimers very little circulating I3C is present following oral use to effect a biological response. Reports of toxicity associated with oral use of I3C relate to unfavorable enzyme induction, which can be attributed to non-DIM reaction products. Because DIM provides a predictable, safer response than the mélange of compounds derived from I3C DIM should be regarded as the chemoprotective compound of choice."
"In light of ... cumulative and recent evidence on the conversion of I3C to DIM in cell culture, peritoneal fluid, and with oral use, and in view of substantial direct activity seen with DIM, there is no longer a case for considering I3C to be directly active. In view of the evidence that non-DIM digestive products from I3C are associated with greater enzyme induction than DIM, questions of safety surround the chronic use of I3C as a dietary supplement. The fact that one month human use of 400 mg/day of I3C showed induction of CYP1A2 does not indicate safety for chronic I3C use, since CYP1A2 is now known to be a source of 4- hydroxyestrogen . The documented increase in carcinogenic 4-hydroxyestrogen following oral use of I3C in animals and humans should discourage the use of I3C as an acceptable chemopreventive supplement. Based on evidence of bioavailability, clinical studies, and studies showing reduced 4-hydroxyestrogen production with absorption-enhanced DIM, DIM supplementation is a promising alternative to the use of I3C. One must keep in mind that because of its greater initial availability, all of the initial studies in our and other laboratories were carried out with I3C. These promising studies lead to further work showing the advantages of using DIM, a dimer of I3C, as the drug of choice."
Forget about I3C - my next post will deal with DIM:
"Foods/Supplements-Vitamins: Cruciferous Phytochemicals -  3,3'-Diindolylmethane [DIM]"