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rundled
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Date Joined Jan 2001
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   Posted 1/19/2001 10:35 AM (GMT -4)    Quote This PostAlert An Admin About This Post.
I recently came across this reference to IC3s instability and poor shelf life. I have never read anything before indicating this about IC3 and was wondering if anyone knows of a references to support these claims?

http://www3.netrition.com/estrogen_factor_page.html

Excerpt from above link:

Since indole-3-carbinol (I3C) is capable of neutralizing excess estrogen and promoting its excretion, some supplement companies have incorporated I3C into their proprietary prohormone formulas. This, however, isnt effective. First, I3C is highly unstable and has a poor shelf life. Odds are good that any supplement containing this substance doesnt have much to begin with, and even less by the time a consumer purchases it. In addition, I3C, as noted, isnt the active chemical anyway; its instead, DIM. I3C is converted into DIM through a process involving gastric hydrochloric acid (HCL). If a person is deficient in HCL, as commonly occurs in the elderly, I3C wont effectively convert into DIM. In contrast to I3C, DIM is highly stable, doesnt need any conversion in stomach acid, and is by far the most active phytochemical in promoting the synthesis of good, protective estrogens such as 2-hydroxyestrone.

::While it is true that I3C is unstable in weak acids and that it is converted in the GI tract to several chemicals which are the active beneficial components, it is misleading to state that taking it orally is not effective or that sealed capsules containing it are ineffective because it has deteriorated on the shelf. Furthermore, while most of the research has been done on its DIM metabolite, this is not the only active conversion product. Therefore, it is better to take I3C in a stable form and let it get converted to the several potentially beneficial products (including DIM) within the GI tract.
If one wishes to gain the added benefit from DIM directly then taking that more expensive supplement would also make sense.

Here is a reference which supports some of this.

Pharmacol Toxicol 1999 Feb;84(2):59-65
Modulation of drug-metabolising enzyme expression by condensation products of indole-3-ylcarbinol, an inducer in cruciferous vegetables.
Vang O, Frandsen H, Hansen KT, Nielsen JB, Andersen O
Department of Life Sciences and Chemistry, Roskilde University, Denmark.

Indole-3-ylcarbinol (13C) is formed during processing of cruciferous vegetables and is suggested to be one of the modulators of drug-metabolising enzymes. Indole-3-ylcarbinol is a far less efficient inducer of hepatic enzymes after parenteral than after oral administration, due to formation of active metabolites in the gastrointestinal tract. As indole-3-ylcarbinol is unstable in weakly acidic aqueous solutions, non-active condensation products may be formed from indole-3-ylcarbinol, that cannot be transformed to the active products when reaching the stomach. The purpose of the present study was to test the ability of the condensation products formed at a pH corresponding to that of fresh vegetable juice to modulate the metabolism of xenobiotics. Indole-3-ylcarbinol was incubated in vitro at room temperature in the dark at pH 5.5 and samples taken at various times, for oral administration to rats and for chemical analysis. Indole-3-ylcarbinol was rapidly transformed into various oligomeric products. The 7-ethoxyresorufin O-deethylase activities (marker of cytochrome Cytochrome P450 1A enzymes, CYP1A) in liver, kidney and colon increased with the duration of the in vitro condensation period whereas the formation of 6beta-, 15beta- and and 2alpha-hydroxytestosterone was not affected significantly, indicating no effect on CYP2C11 or CYP3A enzymes. The hepatic metabolism of the food mutagen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP). was increased by indole-3-ylcarbinol condensation products and the 4-OH-PhIP/N-OH-PhIP ratio was decreased due to a significantly increased formation of the proximate genotoxic metabolite. N-OH-PhIP. The activities of DT-diaphorase and glutathione S-transferase were not changed significantly in the rat organs. These experiments clearly indicate that indole-3-ylcarbinol is not the definitive CYP1A inducer and that indole-3-ylcarbinol at near-neutral pH, is transformed to compounds that are inducers by themselves or may be further converted into inducing compounds in the rat stomach. Also, the enzyme inducing potency of indole-3-ylcarbinol containing vegetable juice is apparently enhanced by incubation in vitro before the intake.
PMID: 10068148, UI: 99165517

Here is a clinical trial which shows that I3C is effective orally.

Gynecol Oncol 2000 Aug;78(2):123-9
Placebo-controlled trial of indole-3-carbinol in the treatment of CIN.
Bell MC, Crowley-Nowick P, Bradlow HL, Sepkovic DW, Schmidt-Grimminger D, Howell P, Mayeaux EJ, Tucker A, Turbat-Herrera EA, Mathis JM
Department of Obstetrics and Gynecology, Louisiana State University Medical Center-Shreveport, 1501 Kings Highway, Shreveport, Louisiana, 71130-3932, USA.

OBJECTIVE: Most precancerous lesions of the cervix are treated with surgery or ablative therapy. Chemoprevention, using natural and synthetic compounds, may intervene in the early precancerous stages of carcinogenesis and prevent the development of invasive disease. Our trial used indole-3-carbinol (I-3-C) administered orally to treat women with CIN as a therapeutic for cervical CIN.
METHODS: Thirty patients with biopsy proven CIN II-III were randomized to receive placebo or 200, or 400 mg/day I-3-C administered orally for 12 weeks. If persistent CIN was diagnosed by cervical biopsy at the end of the trial, loop electrocautery excision procedure of the transformation zone was performed. HPV status was assessed in all patients.
RESULTS: None (0 of 10) of the patients in the placebo group had complete regression of CIN. In contrast 4 of 8 patients in the 200 mg/day arm and 4 of 9 patients in the 400 mg/day arm had complete regression based on their 12-week biopsy. This protective effect of I-3-C is shown by a relative risk (RR) of 0.50 ((95% CI, 0. 25 to 0.99) P = 0.023) for the 200 mg/day group and a RR of 0.55 ((95% CI, 0.31 to 0.99) P = 0.032) for the 400 mg/day group. HPV was detected in 7 of 10 placebo patients, in 7 of 8 in the 200 mg/day group, and in 8 of 9 in the 400 mg/day group.
CONCLUSIONS: There was a statistically significant regression of CIN in patients treated with I-3-C orally compared with placebo. The 2/16 alpha-hydroxyestrone ratio changed in a dose-dependent fashion. Copyright 2000 Academic Press.
Publication Types:
Clinical trial
Randomized controlled trial
PMID: 10926790, UI: 20387250::

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