Nolvadex is a drug commonly referred to as an anti-estrogen. This would suggest less or no estrogen is produced due to the drug’s actions as in the case of Teslac. Actually, Nolvadex is an estrogen antagonist, meaning it competes with estrogen at estrogen receptor- sites. This prevents the active estrogen from entering its receptor and creating an estrogenic complex capable of activity. Since many AAS aromatize (covert to estrogen) to some degree, the control of feminizing side effects (males should pay attention here) is important. Males normally have a very low estrogen level. During AAS cycles, due to aromatization, estrogen levels rise considerably. This elevated estrogen level can cause feminizing side effects such as increased fat deposits, water retention, and gynecomastia (growth of breast gland tissue and painful tumors under the nipple). As a rule, it is more the ratio of androgens-to-estrogens than the simple increase in estrogen that actually initiates feminizing side effects.
It is important that the reader realizes that Nolvadex does not decrease estrogen production and that it simply blocks estrogen receptors. For this reason the sudden discontinuance of Nolvadex will allow the increased level of circulating estrogen to merge with the newly freed receptors and do feminine things to the body.
“Enter Proviron”. At the end of a steroid cycle, the body’s natural testosterone production can be impaired. Due to the aromatization of the AAS estrogen levels are significantly higher than normal and Nolvadex only helps by blocking the estrogen receptors. If an athlete abruptly ends an AAS protocol without regeneration of the HPTA under these conditions, much of the hard earned gains would disappear due to estrogen becoming the dominant hormone. So what did the boys (that didn’t want to be a girl) do?
Proviron is an anti-estrogen (*See “Proviron” for more info) that helps to prevent estrogen production while elevating androgen levels. During the last week of an AAS cycle, some male bodybuilders began a HCG protocol (*See HCG) and administered 25-mg Proviron/10-20-mg Novladex 1-2 times daily. This was commonly noted to almost completely suppress post-cycle estrogen and its activity. Since Nolvadex increases the body’s own testosterone production, as does HCG, much of the cycle gains were retained quite well. Nolvadex has a direct effect on the hypothalamus and therefore increases the release of Gonadotropic hormones to a minor degree. (The hormones that tell the Leydig cells in the testes to produce androgens such as testosterone are refereed to as Gonadotropics) Many added Clomid (*See Clomid) to their post-cycle stacks beginning 6-10 days after HCG and continued for the average reported two week duration. In most cases the result was athletes with normal (or above) sex drive and androgen production!
* High dosage use of Nolvadex can inhibit natural testosterone production. This is due to inhibition of enzymes needed for testosterone production by the testes.
Nolvadex was normally layered into any protocol utilizing high aromatizing steroids such as testosterone, Dianabol, or those that are progesterone receptor stimulators such as Anadrol-50. Those who were prone to high fat deposits, water retention, and gyno consistently reported inclusion of Nolvadex. Many are were to obtain excellent estrogenic activity suppression with only 10-mg daily while others noted the need for as much as 60-mg daily (20mg 3 times daily). The best results and guidelines were obtained by starting low and increasing dosages only when necessary.
It is important for the reader to realize that AAS must have some estrogen present in order to achieve their full positive potential effectiveness and provide the best commonly desired results. This is why many AAS lose their anabolic qualities when combined with anti-estrogens. It is also why Methandriol magnifies the effects of the same AAS. Those who used high anabolic/moderate-low androgenic steroids such as nandrolones, Primobolan, or Winstrol, and did not combine them with high aromatizing steroids (such as testosterone) often considered not using Nolvadex during cycles the best choice when increased mass was the primary intent.
Women who used Nolvadex usually did so because it aids in fat loss due to less estrogenic activity. I have yet to see a female compete whom was able to achieve truly cut legs with out it. Women athletes often combined 10-20mg of Nolvadex with 50-75mg Proviron daily for the last few weeks of dieting. Due to availability of Clenbuterol, Proviron dosages were reported lower as of late, at least in female fitness competitors. Women
should be aware that birth control is an estrogen and Novladex will block its effectiveness. Women have note irregular menstrual cycles, weaker menstrual bleeding, and sometimes skip periods all together during Nolvadex use. I know several women who use Nolvadex for this reason and can not say I disagree with their choice. After all, the use of progestin type birth control as a means of regulating or even stopping menstruation is becoming accepted in the medical circles at last.
A few athletes have experienced a paradox when using high dosages of Nolvadex. Instead of lowering estrogenic activity, it increased it. What happened was that the Adrenal glands went into over drive producing a pro-hormone called DHEA. DHEA is actually an adrenal androgen normally secreted in lower levels. As circulating levels increased enzymic factors came into play. Research shows DHEA readily converts into androstenedione, and to some extent, estrogens in males. (That sucks!) The female endocrine system usually favors testosterone production from converted DHEA or androstenedione. The newly formed estrogen then overwhelmed the estrogen receptors blocking the intended qualities of Novladex. In this case, Proviron, and especially Teslac where notably better choices.
*Gyno that fails to react to these drugs normally must be removed by surgery. DHT derivatives can cause increases endogenous estrogen production also in some individuals. Cytadren was a commonly co-administered drug with Nolvadex.
TAMOXIfin is effective in the treatment of metastatic breast cancer in women and men. In premenopausal women with metastatic breast cancer, TAMOXIPLEX is an alternative to oophorectomy or ovarian irradiation . Available evidence indicates that patients whose tumors are estrogen receptor positive are more likely to benefit from TAMOXIfin therapy .
Adjuvant Treatment of Breast Cancer
TAMOXIfin is indicated for the treatment of node-positive breast cancer in women following total mastectomy or segmental mastectomy, axillary dissection , and breast irradiation. In some TAMOXIPLEX adjuvant studies, most of the benefit to date has been in the subgroup with four or more positive axillary nodes.
TAMOXIfin is indicated for the treatment of axillary node-negative breast cancer in women following total mastectomy or segmental mastectomy, axillary dissection , and breast irradiation.
The estrogen and progesterone receptor values may help to predict whether adjuvant TAMOXIPLEX therapy is likely to be beneficial.
TAMOXIfin reduces the occurrence of contralateral breast cancer in patients receiving adjuvant TAMOXIPLEX therapy for breast cancer.
Ductal Carcinoma in Situ ( DCIS )
In women with DCIS, following breast surgery and radiation , TAMOXIfin is indicated to reduce the risk of invasive breast cancer (see BOXED WARNING at the beginning of the label). The decision regarding therapy with TAMOXIPLEX for the reduction in breast cancer incidence should be based upon an individual assessment of the benefits and risks of TAMOXIPLEX therapy.
Current data from clinical trials support five years of adjuvant TAMOXIPLEX therapy for patients with breast cancer.
Reduction in Breast Cancer Incidence in High Risk Women
TAMOXIfin is indicated to reduce the incidence of breast cancer in women at high risk for breast cancer. This effect was shown in a study of 5 years planned duration with a median follow-up of 4.2 years. Twenty-five percent of the participants received drug for 5 years. The longer-term effects are not known. In this study, there was no impact of tamoxifen on overall or breast cancer-related mortality