(19-05-2017, 11:04 AM)unezat Wrote: (19-05-2017, 04:22 AM)Lotus Wrote: Hi Uneza,
I'm not a fan of proprietary blends (I see conflict in mixed blends that counteract with NBE). Look into reishi extract and white peony extract (in place of saw palmetto and maca). The massage oils looks good, and breast massage has a big impact on the shape and foundation of the breasts. May I ask have you considered hrt?.
Hi Lotus
Thanks for your reply , no I dont want to go for HRT , I want to take effect with the natural herbs so thats why I have started natural herbs so you think SP and Maca will have to be replace those you have mentioned above ?
Regards
Uneza
Uneza,
Most phytoestrogens stimulate ER-b (estrogen receptor beta).....which is ok because ER-beta helps prevent (protect) against breast cancer. ER-alpha (estrogen receptor alpha) promotes linear breast growth, however, too much ER-a increases the chances (proliferation) of breast growth. So, no one should take 10-19 pills PM....ever.
Hops, red clover, fenugreek and PM are pro ER-a, and thus you choose only one for each per cycle (30 days). Finding an anti-androgen(s) that inhibits both types of 5 Alpha Reductase is imporatant. Reishi extract inhibits type I & type II @ 80-90%, saw palmetto inhibits type I & II but @ 32%. Testosterone takes multiple pathways...so there's a need to cut these pathways off before turning into DHT...which DHT destroys breast growth. I like reishi, green tea and fresh lemons wedges (in water) for taking down these pathways. Use SP if you already purchased it....3x per day. Maca has an indirect way of increasing testosterone.....via DHEA, it is in my opinion it happens through the adrenals (why it increases libidos in both men & women. For genetic males wanting breasts T needs to be from 0 ng/dL to 100 ng/mL (testosterone) for more female looking breasts, above 100 ng/dL and up to 250 ng/dL is possible but less likely to represent feminine breasts, rather moobs are more likely to be the outcome.
(24-06-2015, 04:51 AM)Lotus Wrote: Sertoli cells synthesize estradiol 17b from testosterone, and when testosterone is introduced with FSH (Follicle-stimulating hormone) it produces a 12 fold increase in E2 synthesis. And is markedly increased when cAMP (Cyclic adenosine monophosphate) is also added. Estrogen also triggers rapid activation of classical second messengers (cAMP, calcium, and inositol triphosphate). On another note, FSH and cAMP produce a 30 fold increase in aromatase, quite possibly making it the strongest aromatase.
Inhibit LH (luteinizing hormone) using black cohosh (nbe) Goserelin (pharma)
Stimulate FSH (follicle stimulating hormone) E2 or red clover, *(essential fatty acids)
Inhibit DHT in the liver/prostate. (reishi inhibits serum DHT @ 80%) dutas @93%, finasteride @70% and saw palmetto inhibits DHT @ 32% (combo's possible).
Inhibit adrenal DHT (calmodulin -via the calcium/calmodulin/CaMK pathway) (spiro or licorice root)
Urology. 2001 May;57(5):999-1005. Related Articles, Links
Tissue effects of saw palmetto and finasteride: use of biopsy cores for in situ quantification of prostatic androgens.
Marks LS, Hess DL, Dorey FJ, Luz Macairan M, Cruz Santos PB, Tyler VE.
Urological Sciences Research Foundation, Culver City, California, USA.
OBJECTIVES: To determine the effects of a saw palmetto herbal blend (SPHB) compared with finasteride on prostatic tissue androgen levels and to evaluate needle biopsies as a source of tissue for such determinations. METHODS: Prostate levels of testosterone and dihydrotestosterone (DHT) were measured on 5 to 10-mg biopsy specimens (18-gauge needle cores) in three groups of men with symptomatic benign prostatic hyperplasia: 15 men receiving chronic finasteride therapy versus 7 untreated controls; 4 men undergoing prostate adenomectomy to determine sampling variability (10 specimens each); and 40 men participating in a 6-month randomized trial of SPHB versus placebo, before and after treatment. RESULTS: Prostatic tissue DHT levels were found to be several times higher than the levels of testosterone (5.01 versus 1.51 ng/g), that ratio becoming reversed (1.05 versus 3.63 ng/g) with chronic finasteride therapy. The finasteride effect was statistically significant for both androgens (P <0.01), and little overlap of individual values between finasteride-treated and control patients was seen.
In the randomized trial, tissue DHT levels were reduced by 32% from 6.49 to 4.40 ng/g in the SPHB group (P <0.005), with no significant change in the placebo group. CONCLUSIONS: For control versus finasteride-treated men, the tissue androgen values obtained with needle biopsy specimens were similar-both for absolute values and the percentage of change-to those previously reported using surgically excised volumes of prostatic tissue. The quantification of prostatic androgens by assay of needle biopsies is thus feasible and offers the possibility of serial studies in individual patients. The SPHB-induced suppression of prostatic DHT levels, modest but significant in a randomized trial, lends an element of support to the hypothesis that inhibition of the enzyme 5-alpha reductase is a mechanism of action of this substance.
https://www.ncbi.nlm.nih.gov/pubmed/11337315