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skwood
05-29-2002, 10:57 AM
Does anyone know what the proper dosage is for Anastrozole (generic Arimidex)?

Thanks - Skwood

mbstrong
05-29-2002, 11:30 AM
.25 or .50 it all depends on your body. You will have to play around with it to find out what works for you.

th1rty6
05-29-2002, 12:16 PM
Hey, I've got some on the way too (liquidex). I've read in some other posts that taking too much will make your estrogen levels too low because some level of estrogen is necessary. How do you know if the dose you're taking is too high? Is there some telltale physical sign? (nipples shrivel up and fall off, etc) Seriously, we all know what happens if you have too much estrogen. What are the symptoms of not having enough?

CJ Buff
05-29-2002, 01:13 PM
I found with 500mg of Sustanon .25mg/ed wasn't enough on my next cycle I am gonna try .5/ed and if that doesn't keep the bloat down I will up doseage to 1mg/ed... Everyone is different, if you're taking .5/eod and you still have soft nips and water retention then up it... Just go with trial and error, that's the only way to know what works for U...

CJ;)

CoachK On Roids
05-29-2002, 01:52 PM
I normally use .25mgs ed, but I've never exceeded 700mgs of test a week. I use .5mgs ed if also using D-bol.

BStrongBwell*
05-29-2002, 02:27 PM
yep, you have to play with it...the doseages that is :D ...some guys can get away with .25EOD. If you suppress estrogen too much, you'll rob your gains.

Superfrk
05-29-2002, 04:08 PM
I have not found that estrogen plays to big a role in growth. I personally have used 1mg -2mg of armidex ED while on a cycle. I still had very good gains and yes I may / may not have had better gains with out it who knows, I am sure I would have had some more water gains and such as well. I do know that throught the cycle and at the end of the cycle I was muchy more pleased with the results. I have also ran armidex by its self and accualy lost fat and gained some quality muscle. I have been trying to figure out why I made the gains and this is what I think happened. Armidex has an effect on FSH. FSH can only occure if the FS protein is present, so armidex must have a role in incressing this FS protein that isn produced by the body. FS protein has been found to block the protein that carries out the effects of the Myostatin gene. There have been geneticaly engineered mice that produced more FS protein, They have about 4 times the muscle mass of non egineered mice. The reson we are not seeing this is because armidex also lowers IGF-1. Either way I am shareing this with you to show that armidex may have some properties that would compensate for any lack of gains caused by lower estrogen,if indeed estrogen does play a role in gains- Superfrk

Superfrk
05-29-2002, 04:13 PM
Estrogen suppression in males: metabolic effects.

Mauras N, O'Brien KO, Klein KO, Hayes V

Nemours Research Programs at the Nemours Children's Clinic, Jacksonville, Florida 32207, USA. 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.

Publication Types:
Clinical trial

Superfrk
05-29-2002, 04:15 PM
Building the best mouse trap using estrogen reducing drugs.
By: Superfrk
Chapter one: The research
About 5 years ago scientist at Johns Hopkins created mice that had been genetically altered to be super mice by turning off a growth regulating gene called myostatin. More recently they have created another batch of super mice. Unlike the first group of mice that had their gene for myostatin turned off, this set of mice have normally working myostatin genes. This time the scientist altered the mice by tweaking production of three different proteins that have the effect of blocking the myostatin gene.
Before we continue I think it is important that we understand how myostatin works. Myostatin is a negative regulator of skeletal muscle mass. In other words it limits the amount of muscle we are able to produce. So by blocking it we could literally take the brakes off of new muscle growth. There were three groups of mice one group was engineered to produce more of the protein follistatin. Another group was engineered to produce excess amounts of mutant activin II receptors. While the last group was engineered to have myostatin propeptide. While all three groups showed increased muscle mass, the group that produced more of the protein follistatin had the best results which resulted in one mouse that exhibited average muscle weights 261 percent greater than the control animals.
We will mainly be dealing with the protein follistatin so lets learn a little more about it.
FOLLISTATIN (FS) is a single chain, glycosylated protein that inhibits FSH secretion. Although similar in function to inhibins in suppressing pituitary FSH secretion, it is structurally distinct from the previously characterized family of inhibins and activins. It was first isolated in 1987 from follicular fluid and has since been shown to exist as a number of different molecular mass isoforms (MW 32–44 kDa). Aside from microheterogeneity, originating from glycosylation differences, alternate messenger RNA splicing results in the translation of two isoforms containing 288 or 315 (+signal sequence) amino acids. Each isoform also can be processed posttranslationally by proteolytic cleavage. Though the distribution of FS isoforms may differ in follicular fluid and serum, both forms have been shown to inhibit FSH secretion .
O.k. now that we have all the research out of the way and as a treat for making you guys read all this mumbo jumbo. I will get to the point and show you how we can make this all come together to work for us.
As some of you guys already know clomid and armidex have both been shown to incress FSH levels. In fact this is the reson we use them to jump start our HTPA after a cycle is over. Here is a line from above that is very important to us. FOLLISTATIN (FS) is a single chain, glycosylated protein that inhibits FSH secretion. What this is saying is that with out FOLLISTATIN (FS) you can not produce FSH, so this means that armidex and clomid both help to increase (FS) in order to have an effect on FSH levels. Why is this so important? Because the group that produced more of the protein follistatin had the best results which resulted in one mouse that exhibited average muscle weights 261 percent greater than the control animals.
So basically what I am saying is that armidex and clomid are capable of blocking the myostatin gene. Now the problem with armidex is that it also decreases the production of the growth factor IGF-1. This is why we are not seeing super size gains with armidex, ( I have noticed that gains seem better with Fina when I have used it with armidex though). The draw back with clomid is we do not take it for long enough and that it will not work in highly anabolic situations such as that of being on a cycle.

skwood
05-29-2002, 05:49 PM
Great Info, Thanks!

Skwood

BStrongBwell*
05-30-2002, 08:59 AM
That's a nice read suprfrk. I'm still a little skeptical on suppressing estrogen to that degree though. The first study used a pretty small group and looks like it was more geared toward measuring bone density loss, and the second study was done using mice, so what those studies say is really interesting, but not exactly conclusive IMO. If you happen to run across any more stuff, I'd like to keep up w/it. Like most of the assumptions we make on bodybuilding science, it's based partly on definitive studies, but mostly on trial and error and on making logical deductions from studies with strong but maybe not definitive results like those.