Max
Are you on TRT if not you crashed because you took to much and went past the window for a go level.
Here are some links I have or is it better to cut & paste I am new to this group.
http://www.medibolics.com/ArimidexBoostsTestosterone.htm
Study Shows That Arimidex Boosts Testosterone
Estrogen suppression in males: metabolic effects.
J Clin Endocrinol Metab 2000 Jul;85(7):2370-7 (ISSN: 0021-972X)
Mauras N; O'Brien KO; Klein KO; Hayes V
nmauras@nemours.org.
We have shown that testosterone (T) deficiency per se is associated with marked catabolic effects on protein, calcium metabolism, and body composition in men independent of changes in GH or insulin-like growth factor I production. It is not clear,,however, whether estrogens have a major role in whole body anabolism in males. We investigated the metabolic effects of selective estrogen suppression in the male using a potent aromatase inhibitor, Arimidex (Anastrozole). First, a dose-response study of 12 males (mean age, 16.1 +/- 0.3 yr) was conducted, and blood withdrawn at baseline and after 10 days of oral Arimidex given as two different doses (either 0.5 or 1 mg) in random order with a 14-day washout in between. A sensitive estradiol (E2) assay showed an approximately 50% decrease in E2
concentrations with either of the two doses; hence, a 1-mg dose was selected for other studies. Subsequently, eight males (aged 15-22 yr; four adults and four late pubertal) had isotopic infusions of [(13)C]leucine and (42)Ca/(44)Ca, indirect calorimetry, dual energy x-ray absorptiometry, isokinetic dynamometry, and growth factors measurements performed before and after 10 weeks of daily doses of Arimidex. Contrary to the effects of T withdrawal, there were no significant changes in body composition (body mass index, fat mass, and fat-free mass) after estrogen suppression or in rates of protein synthesis or degradation; carbohydrate, lipid, or protein oxidation; muscle strength; calcium kinetics; or bone growth factors concentrations. However, E2 concentrations decreased 48% (P = 0.006), with
no significant change in mean and peak GH concentrations, but with an 18% decrease in plasma insulin-like growth factor I concentrations. There was a 58% increase in serum T (P = 0.0001), sex hormone-binding globulin did not change, whereas LH and FSH concentrations increased (P < 0.02, both). Serum bone markers, osteocalcin and bone alkaline phosphatase concentrations, and
rates of bone calcium deposition and resorption did not change. In conclusion, these data suggest that in the male 1) estrogens do not contribute significantly to the changes in body composition and protein
synthesis observed with changing androgen levels; 2) estrogen is a main regulator of the gonadal-pituitary feedback for the gonadotropin axis; and 3) this level of aromatase inhibition does not negatively impact either kinetically measured rates of bone calcium turnover or indirect markers of bone calcium turnover, at least in the short term. Further studies will provide valuable information on whether timed aromatase inhibition can be useful in increasing the height potential of pubertal boys with profound
growth retardation without the confounding negative effects of gonadal androgen suppression.
And this one.
http://tinyurl.com/2s292
1: J Clin Endocrinol Metab. 2004 Mar;89(3):1174-80. Related Articles, Links
Effects of aromatase inhibition in elderly men with low or borderline-low serum testosterone levels.
Leder BZ, Rohrer JL, Rubin SD, Gallo J, Longcope C.
Endocrine Unit, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114, USA.
As men age, serum testosterone levels decrease, a factor that may contribute to some aspects of age-related physiological deterioration. Although androgen replacement has been shown to have beneficial effects in frankly hypogonadal men, its use in elderly men with borderline hypogonadism is controversial. Furthermore, current testosterone replacement methods have important limitations. We investigated the ability of the orally administered aromatase inhibitor, anastrozole, to increase endogenous testosterone production in 37 elderly men (aged 62-74 yr) with screening serum testosterone levels less than 350 ng/dl. Subjects were randomized in a double-blind fashion to the following 12-wk oral regimens: group 1: anastrozole 1 mg daily (n = 12); group 2: anastrozole 1 mg twice weekly (n = 11); and group 3: placebo daily (n = 14). Hormone levels, quality of life (MOS Short-Form Health Survey), sexual function (International Index of Erectile Function), benign prostate hyperplasia severity (American Urological Association Symptom Index Score), prostate-specific antigen, and measures of safety were compared among groups. Mean +/- SD bioavailable testosterone increased from 99 +/- 31 to 207 +/- 65 ng/dl in group 1 and from 115 +/- 37 to 178 +/- 55 ng/dl in group 2 (P < 0.001 vs. placebo for both groups and P = 0.054 group 1 vs. group 2). Total testosterone levels increased from 343 +/- 61 to 572 +/- 139 ng/dl in group 1 and from 397 +/- 106 to 520 +/- 91 ng/dl in group 2 (P < 0.001 vs. placebo for both groups and P = 0.012 group 1 vs. group 2). Serum estradiol levels decreased from 26 +/- 8 to 17 +/- 6 pg/ml in group 1 and from 27 +/- 8 to 17 +/- 5 pg/ml in group 2 (P < 0.001 vs. placebo for both groups and P = NS group 1 vs. group 2). Serum LH levels increased from 5.1 +/- 4.8 to 7.9 +/- 6.5 U/liter and from 4.1 +/- 1.6 to 7.2 +/- 2.8 U/liter in groups 1 and 2, respectively (P = 0.007 group 1 vs. placebo, P = 0.003 group 2 vs. placebo, and P = NS group 1 vs. group 2). Scores for hematocrit, MOS Short-Form Health Survey, International Index of Erectile Function, and American Urological Association Symptom Index Score did not change. Serum prostate-specific antigen levels increased in group 2 only (1.7 +/- 1.0 to 2.2 +/- 1.5 ng/ml, P = 0.031, compared with placebo). These data demonstrate that aromatase inhibition increases serum bioavailable and total testosterone levels to the youthful normal range in older men with mild hypogonadism. Serum estradiol levels decrease modestly but remain within the normal male range. The physiological consequences of these changes remain to be determined.
Publication Types:
Clinical Trial
Randomized Controlled Trial
PMID: 15001605 [PubMed - indexed for MEDLINE]
Here is what has worked for a lot of guys I have talked to get some Indolopex with DIM. Take the cialis every 72 hrs and if your not on TRT take a half of a Indolopex/DIM when you start getting rock hard wood in the morning your E2 has come down to the window so keep taking it if the wood goes away stop the pill until it comes back the go back on half of what you started with keep doing this until you find the dose that keeps you in the window. If you are on TRT start on 1 pill a day if in 2 weeks you have nothing than take the max 2 pills.
It has to be Indolplex with DIM this is the only one we have had good luck with. I buy this one.
http://www.ritecare.com/prodsheets/PHY-15336.html
The guys in the UK have gotten it from 3 different brand names and it is working for them.
If your DHT is high this beings it down it has got mine down form 145 to 99 still high but better.
http://www.dimfaq.com/index.htm
A cut and paste on lower DHT.
http://www.lef.org/whatshot/2003_05.html#i3cb
Indole-3-carbinol byproduct acts as antiandrogen to halt prostate cancer cell growth
In a study funded in part by the National Institutes of Health, to be published in the June 6 2003 issue of the Journal of Biological Chemistry, University of California, Berkeley researchers have found that a digestive product of indole-3-carbinol, which occurs naturally in broccoli and other cruciferous vegetables, halts the growth of prostate cancer cells in vitro. The compound, 3,3-diindolymethane (DIM), inhibits androgenic hormones that fuel prostate cancer growth. Although androgen is important for the normal development of the prostate, it is believed to be involved in the early stages of prostate cancer.
The researchers administered DIM to androgen dependent and androgen independent prostate cancer cells and found that androgen-dependent cells experienced a 70 percent reduction in growth compared to those that did not receive the compound. Androgen-independent prostate cancer cells were not affected by DIM. The scientists went on to discover that DIM inhibited dihydrotestosterone, the primary androgenic hormone that is believed to be the culprit in prostate cancer. Dihydrotesterone stimulates prostate specific antigen, or PSA, which is elevated in prostate cancer. When DIM was administered to the androgen-dependent prostate cancer cells, PSA levels dropped.
A study of the molecular structure of DIM showed that it is similar to the androgen-blocking drug Casodex. Lead author Hien Le, PhD, explained, DIM works by binding to the same receptor that DHT uses, so it's essentially blocking the androgen from triggering the growth of the cancer cells."
Principle researcher and professor nutritional sciences and toxicology at UC Berkeley's College of Natural Resources, Leonard Bjeldanes, summarized, "As far as we know, this is the first plant-derived chemical discovered that acts as an antiandrogen. This is of considerable interest in the development of therapeutics and preventive agents for prostate cancer."
-D Dye
May 16, 2003
If doing this does not work then you need to see a Uro.
Phil