Vraag me af of ik het nu allemaal op een rijtje heb. Lijkt dit ergens op?
Week 1-13 HCG 250 IU 2x per week
Begrijp ik het goed dat je in dit geval er geen nolvadex naast hoeft te gebruiken?
T3 zou ik bijvoorbeeld 8 weken kunnen gebruiken. 1 week op 25 mcg, dan 6 weken op 50 mcg en nog een week op 25 mcg op het einde.
Dacht zelf aan t/m week 12, maar jij zegt nu t/m week 10. Dat houdt in dat ik week 11 en 12 trenbolone gebruik zonder T3 ernaast, ik dacht dat dat min of meer 'verplicht' was?
Zal na de T3 iig een paar weken ec(y) nemen.
bij deze dosis HCG heb je idd geen nolvadex nodig (tijdens de cycle)
T3 zou je ook tot aan je nakuur kunnen gebruiken, maar aangezien je al eindigd met korte esters, kom je dan direct in een catabole omgeving. wanneer je schildklier dan ook niet optimaal werkt, zou dit wellicht verkeerd uit kunnen vallen voor je. vandaar tot wk 10. meerdere studies geven namelijk aan dat de schildklier met 2 weken grotendeels weer functioneert.
T3 naast trenbolone is verstandig ivm negatief effect op de schildklier, maar zeker geen vereiste! maar het twee weken verlengen en het ondervangen met ECY zou ook nog kunnen idd
daarnaast verlaagd nolvadex serumlevels prolactin ook aanzienlijk ( aangezien dit je motivatie was voor t3 naast de trenbolone)
hier twee studies over tamoxifen inzake prolactin en progesterone..
Tamoxifen inhibition of estrogen receptor-alpha-negative mouse mammary tumorigenesis.Medina D, Kittrell FS, Hill J, Shepard A, Thordarson G, Brown P.
Baylor College of Medicine, Houston, TX 77030, USA.
dmedina@bcm.tmc.edu
Tamoxifen reduces the relative risk of breast cancer developing from specific premalignant lesions. Many breast cancers that arise after tamoxifen treatment are estrogen receptor-alpha (ER-alpha)-negative, although premalignant lesions such as atypical ductal hyperplasia are highly ER-alpha-positive. The p53 null mouse mammary epithelial transplant model is characterized by ER-alpha-positive premalignant lesions that give rise to both ER-alpha-positive and ER-alpha-negative tumors. Given this progression from ER-alpha-positive to ER-alpha-negative lesions, we tested the ability of tamoxifen to block or delay mammary tumorigenesis in several versions of this model. In groups 1 and 2, p53 null normal mammary epithelial transplants were maintained in virgin mice.
In groups 3 to 5, the p53 null and mammary transplants were maintained in mice continuously exposed to high levels of progesterone. In groups 6 and 7, transplants of the premalignant outgrowth line PN8a were maintained in virgin mice.
Tamoxifen blocked estrogen signaling in these mice as evidenced by decreases in progesterone-induced lateral branching and epithelial proliferation in the mammary epithelium. Tamoxifen did not alter the elevated levels of progesterone in the blood while significantly reducing the circulating level of prolactin. Tamoxifen reduced tumor incidence in p53 null normal mammary epithelial transplants maintained in virgin mice from 55% to 5% and in progesterone-stimulated mice from 81% to 21%. The majority of the resultant tumors were ER-alpha-negative. Tamoxifen also significantly delayed tumorigenesis in the ER-alpha-positive high premalignant line PN8a from 100% to 75%. These results show that tamoxifen delays the emergence of ER-alpha-negative tumors if given early in premalignant progression.
studie 2:
ABSTRACT: Breast carcinoma is the most common malignancy among women and it has a major impact on mortality. Studies of primary chemoprevention with tamoxifen have generated high expectations and considerable success rates.
The efficacy of lower doses of tamoxifen is similar to that seen with a standard dose of the drug, and there has been a reduction in healthcare costs and side effects.The immune reaction to monoclonal antibody Ki-67 (MIB-1) and the expression of estrogen receptors (1D5) and progesterone receptors (PgR 636) in breast carcinoma were studied in
patients treated with 10 mg of tamoxifen for a period of 14 days.A prospective randomized clinical trial was conducted with 38 patients divided into two groups: Group A: N = 20 (control group-without medication) and Group B: N = 18 (tamoxifen/10 mg/day for 14 days). All patients signed an informed consent term previously approved by both institutions. Patients underwent incisional biopsy before treatment and 14 days later a tumor tissue sample was obtained during surgical treatment. Positivity was quantitatively assessed, counting at least 1.000 cells per slide. For statistical data analysis, a Wilcoxon non-parametric test was used, and alpha was set at 5%.Both groups (A and B) were considered homogeneous regarding control variables. In Group A (control), there was no statistically significant reduction in Ki-67 (MIB-1) (p = 0.627), estrogen receptor (1D5) (p = 0.296) and progesterone receptor positivity (PgR 636) (p = 0.381).In Group B (tamoxifen 10 mg/day), the mean percentage of nuclei stained by Ki-67 (MIB-1) was 24.69% before and 10.43% after tamoxifen treatment. Mean percentage of nuclei stained by estrogen receptor (1D5) was 59.53% before and 25.99% after tamoxifen treatment.
Mean percentage of nuclei stained by progesterone receptor (PgR 636), was 59.34 before and 29.59% after tamoxifen treatment. A statistically significant reduction was found with the three markers (p < 0.001).
Tamoxifen significantly reduced monoclonal antibody Ki-67 (MIB-1), estrogen receptor (1D5) and progesterone receptor positivity (PgR 636) in the breast epithelium of carcinoma patients treated with a 10 mg dose of tamoxifen for 14 days.