j. wrote:According to this study, pregnenolone can make prostate cancer worse.
Pregnenolone stimulates LNCaP prostate cancer cell growth via the mutated androgen receptor.
Pregnenolone (P(5)), a common precursor of many steroids, is present in the blood of normal adult men at concentrations of 1-3 nM. In vitro, P(5) was found to stimulate LNCaP-cell proliferation 7-8-fold at a physiological concentration (2 nM), and 3-4-fold at a subphysiological concentration (0.2 nM). Growth stimulation at the 2-nM concentration was comparable with that of the androgen, dihydrotestosterone at its physiological concentration (0.5 nM; 9-10-fold increase in cell number). To determine whether P(5) or its metabolites were mediating this growth response, LNCaP cells were incubated with [3H]P(5) and high-performance liquid chromatography (HPLC) was performed. After a 48-h exposure, two unidentified metabolites were detected. Although, the P(5) metabolites slightly increased LNCaP-cell growth in vitro, their effect was significantly less than P(5) alone, suggesting that the growth stimulation was mediated by P(5) itself. We further showed that P(5) sustained its proliferative activity in vivo and stimulated the growth of LNCaP-tumor xenografts in intact male SCID mice as well as in castrated animals. In order to determine whether P(5) was binding to a specific site in LNCaP cells, receptor binding studies were performed. Scatchard analysis predicted for a single class of binding sites with K(d)=1.4 nM. Studies were performed to determine the effects of P(5) on transcription mediated by wild-type and LNCaP androgen receptors. P(5) was shown to activate transcription through the LNCaP androgen receptor (AR), but not the wild-type AR. This implies that P(5) most likely stimulates LNCaP-cell proliferation through binding to the cellular mutated AR present in LNCaP cells. We have also demonstrated that drugs designed to be antagonists of the androgen, progesterone and estrogen receptors, and one of our novel compounds designed to be an inhibitor of androgen synthesis, were potent inhibitors of the AR-mediated transcriptional activity induced by P(5), and were able to inhibit LNCaP-cell proliferation. These findings suggest that some prostate cancer patients who appear to become hormone-independent may have tumors which are stimulated by P(5) via a mutated AR and that these patients could benefit from treatment with antiestrogens, antiprogestins, or with some of our novel androgen synthesis inhibitors.
jag2594 wrote: In a ray peat interview he talks about how male pattern baldness was not associated with androgens that everyone seems to think, but with estrogen and prolactin. Estradiol is converted from Testosterone, and high prolactin and pituitary tumors need estrogen. Pregnenolone being the precursor to all steroids, will be convert into the disease causing hormones that cause cancer.
jyb wrote:Doesn't the pregnelonone conversion depend on diet and metabolism?
jyb wrote:jag2594 wrote: In a ray peat interview he talks about how male pattern baldness was not associated with androgens that everyone seems to think, but with estrogen and prolactin. Estradiol is converted from Testosterone, and high prolactin and pituitary tumors need estrogen. Pregnenolone being the precursor to all steroids, will be convert into the disease causing hormones that cause cancer.
Doesn't the pregnelonone conversion depend on diet and metabolism?
Isadora wrote:Anyway, the study mentions pregnenolone in one's own body producing the cancer-causing metabolites. Maybe the supplemental kind doesn't cascade into P5, one can always hope, right? I don't know, I'm very skeptical at this point of all these hormones. And the fast paced level of new discoveries related to them is not good news, in my book. What isn't yet known could kill us, too. I will stop all experiments with this, "face lifting" effect and other such mundane goodies aren't worth it.
jyb wrote:Not saying you're wrong but that's just one study. You can also find recent studies showing PUFAs are wonderful.
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