Absolutely. The dosage and frequency definitely have to be factored in. I just wanted to show the actual facts of the drug and the mechanism of action as that seemed to be in question. I highly doubt you are going to feel any ill effects of a single .25 dose.
As to DIM, DIM works differently and has more of a balancing effect on all estrogens. In men it has a very positive effect on prostate health. It also has an effect on the less desirable estrogens. Most people are aware of the 3 basic estrogen types, Estradiol, Estrone and Estriol. There are just a few more than that:
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DIM has effects on estrogen in two ways: affecting estrogen metabolism and regulating ER activity. For its metabolic effects, DIM can increase the conversion of E2 into 2-hydroxyestrone (2-OHE), a “good” estrogenic metabolite with anti-estrogenic and anti-proliferative properties
[79],
[80] while decreasing the conversion of E2 into 4-hydroxyestrone (4-OHE) or 16-α-hydroxyestrone (16-α-OHE), both “bad” estrogenic metabolites that can increase cell proliferation
[80]. DIM also increases urinary 16-α-OHE levels in postmenopausal women
[78]. For its effects on ER, DIM can inhibit the transcription of estrogen-responsive genes stimulated by E2, and increase ERα protein degradation
[40],
[45],
[82].
DIM's effects on androgen, androgen receptor (AR) and prostate-specific antigen (PSA)
The male sex hormones, androgens mainly including testosterone and DHT, mediate their effects by binding to AR, forming androgen-receptor complex in cytoplasm and then translocating into the nucleus. The complex in the nucleus then binds to a DNA segment in androgen-responsive genes, the androgen response element, to regulate gene transcription. By turning the genes on or off, androgen and AR help direct the development of male sexual characteristics. In prostate cancer, androgen and AR are critical in oncogenesis and cancer growth
[35],
[59],
[73],
[75].
It has been shown in in vitro
[29],
[31]-
[33] and in vivo studies
[26],
[57] that DIM has an anti-androgen effect which downregulates AR and PSA. In androgen-dependent LNCaP cells, DIM suppresses cell proliferation, inhibits DHT stimulation of DNA synthesis and endogenous PSA transcription and suppresses androgen-induced AR translocation into the nucleus
[81]. Similar effects of DIM were observed in PC-3 cells only when these cells were co-transfected with a wild-type androgen receptor expression plasmid
[82].
DIM results in cell cycle arrest in androgen-sensitive LNCaP cells and androgen-insensitive C4-2B cells not only by affecting cell cycle regulatory molecules including cdks and their inhibitors but also by downregulating AR
[31]. In the same cell lines, DIM was found to promote cell cycle arrest and cause apoptosis that may be associated with effects on Akt and AR signaling pathways by affecting Akt/FOXO3a/GSK-3β/β-catenin signaling
[46]. In a separate study, the same research group found that B-DIM's anti-androgenic effects were associated with inhibition of AR phosphorylation, AR expressions and AR nuclear translocation, leading to the down-regulation of AR target genes
[32]. The anti-androgen effect from DIM is not associated with prostate cancer cell's androgen status
[29]. The results of structural modeling studies showed that DIM is remarkably similar in conformational geometry and surface charge distribution to an established synthetic AR antagonist
[81]. These observations provide rationales for DIM in treating hormone-sensitive, but more importantly hormone-refractory prostate cancer by using DIM alone or combining with other therapeutics
[3
