The stronger form of estrogen (estradiol) can be converted into the weaker form (estriol) without using drugs. Estriol is considered to be a more desirable form of estrogen; it is less active than estradiol, so when it occupies the estrogen receptor it effectively blocks estradiol’s strong “grow” signals.
Using a natural substance, such as Diindolylmethane – a stable indole found in cruciferous vegetables – researchers were able to increase the conversion of estradiol to estriol by 50% in 12 healthy people. Next, they tested the natural substance in female mice prone to developing breast cancer. The incidence of cancer and the number of tumors fell significantly. This substance was Indole-3-carbinol (IC3) or DIM (diindolylmethane), phytochemicals isolated from cruciferous vegetables (broccoli, cauliflower, Brussels sprouts, turnips, kale, green cabbage and mustard seed). Additionally, the level of an estrogen metabolite associated with breast and endometrial cancer (16-alpha-hydroxyestrone) fell.
In 1997, researchers at Strang Cancer Research Laboratory at Rockefeller University discovered that when DIM (diindolylmethane) changes “strong” estrogen to “weak” estrogen, it stops human cancer cells from growing and provokes the cells to self-destruct (apoptosis). Subsequent studies done at the University of California at Berkeley show that DIM (diindolylmethane) inhibits some human breast cancer cells from growing by as much as 90% in culture. Growth arrest does not depend on estrogen receptors.
16-alpha-hydroxyestrone (16OHE) and 2-hydroxyestrone (2OHE) are metabolites of estrogens. 2OHE is biologically inactive, while 16OHE is biologically active meaning that, like estradiol, it can send those “grow” signals. In cases of breast cancer, the bad 16OHE is often elevated and the good 2OHE is decreased. Interestingly, cancer-causing chemicals change the metabolism of estrogen so that 16OHE is elevated. Studies show that people who take DIM not only have beneficial increases in estriol, they also have beneficial increases in 2OHE.
Low levels of the 2OHE have been linked to breast cancer (in both women and men), uterine cancer, cervical cancer and lupus. An immune disorder that affects mostly women, lupus appears related to estrogen metabolism.
Diindolylmethane is generally much more effective than I3C and less expensive. In the mid-1990s it was determined that IC3 was biologically inactive until converted to DIM (diindolylmethane), which in humans occurs in the digestive tract. 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 won’t effectively convert into DIM. In contrast to I3C, diindolylmethane is highly stable, doesn’t need any conversion in stomach acid, and is by far the most active phytochemical in promoting the synthesis of protective 2OHE. However, DIM is poorly absorbed unless “absorption enhanced” in some way. Please look for such wording on any DIM product you consider purchasing. It is generally agreed that 300mg of IC3 converts to 30-40mg of DIM (diindolylmethane).
As little as 0.5- 2mg mg/kg body weight/day of DIM has been demonstrated as an effective dose. The usual dosage of diindolylmethane for women is 100 – 200mg per day taken with food. When used for weight loss, the dosage used has been up to 400mg per day. It is used in association with carbohydrate restriction and exercise. The usual dosage of DIM for men is 200 – 400 mg per day taken with food. For men involved in a plan of muscular development and/or fat loss, the dose of DIM could be increased to 400 – 500mg per day.
More importantly from an anabolic point of view, the level of free testosterone rises in the blood with use of diindolylmethane. The mechanism behind this is that 2-hydroxy estrogens have a greater binding affinity for the blood proteins that “lock up” testosterone in the blood. Thus, these plasma binding proteins instead latch on to 2-hydroxy, leaving greater levels of free testosterone, including that produced through the use of supplemental prohormones.
The 2-hydroxy estrogens promoted by usage also increase testosterone synthesis through another mechanism. Estrogen, even more than testosterone itself, incurs a negative hormonal feedback loop to the pituitary gland, where the rate-limiting gonadotropin for testosterone synthesis, luteinizing hormone (LH) is synthesized and released. What this means is that high blood levels of estrogen, as may occur through aromatization of free testosterone, turn off the release of LH from the pituitary gland. This leads to a vicious biochemical cycle characterized by an imbalance between testosterone and estrogen in favor of the latter. These events, however, are nullified by 2-hydroxy, which doesn’t provide the negative feedback message to the pituitary induced by estrogen. The net effect is greater testosterone synthesis in the Leydig cells of the testes, as well as lower levels of bad estrogen and all the effects that go with it.