Novaldex and gains

This is a no brainer if you are gyno prone, take the Nolvadex. The issue is the anabolic effect of the estrogen and the concommitant rise in circulating igf-1. There has been evidence that localized igf-1 may be more important than systemic igf-1 in terms of anabolism although there is still a contribution from circulating igf-1. In your case, the risk of gyno would certainly outweigh the minor differences possible in your results.

jb

Very well put jboldman.

I would use 10mg of nolvadex ed. That keeps gyno symptoms at bay for me as I too am gyno prone. If this isn't sufficient then up the dose to 20mg ed. No sense in using more than necessary.

Likewise good point.

jb

Posted by: jboldman

This is a no brainer if you are gyno prone, take the nolvadex. The issue is the anabolic effect of the estrogen and the concommitant rise in circulating igf-1. There has been evidence that localized igf-1 may be more important than systemic igf-1 in terms of anabolism although there is still a contribution from circulating igf-1. In your case, the risk of gyno would certainly outweigh the minor differences possible in your results.

jb

There's more to estrogen anabolic properties than IGF-1. There are 3 processes aside from IGF-1 which, supossedly, make estrogen anabolic:

1) Estrogen upgrades androgen receptors
2) Estrogen mediates glucose metabolisms
3) Estrogen promotes water retention, which, in turn, is anabolic

This, at least, is what BigCat has stated several times.
However, even if this is true, at what price? At the price of a bigger HPT Axis suppression? Would that HPTA supression be more catabolic than estrogen is anabolic?
That's the big question, pal!

Posted by: neurotic

There's more to estrogen anabolic properties than IGF-1. There are 3 processes aside from IGF-1 which, supossedly, make estrogen anabolic:

1) Estrogen upgrades androgen receptors
2) Estrogen mediates glucose metabolisms
3) Estrogen promotes water retention, which, in turn, is anabolic

This, at least, is what BigCat has stated several times.
However, even if this is true, at what price? At the price of a bigger HPT Axis suppression? Would that HPTA supression be more catabolic than estrogen is anabolic?
That's the big question, pal!

Were not talking about aromatose inhibitors, its nolvadex, estrogen will still be circulating

To say that estrogens upregulate the androgen receptor in human skeletal muscle is a stretch. Estrogens work via the estrogen receptor, except for a few poorly characterized non genomic actions, and some possible actions by direct binding to the androgen receptor in the prostate. Estrogen receptor mRNA was only just recently discovered in human skeletal muscle (1). Prior to that, it was believed that human skeletal muscle lacked the estrogen receptor (2). So it is really premature to start ascribing anabolic effects to estrogen in humans that may or may not even exist in animals and certainly have never been demonstrated in humans

There is also evidence that we have discussed here at length that estrogens may have a negative impact on muscle recovery:

"More recently, investigations into the potential effect of estrogen on muscle damage have explored the possible role that estrogen may play in the inflammatory response following muscle damage. In light of these studies, it may be suggested that if estrogen inhibits the vital inflammatory response process associated with the muscle damage and repair cycle, it has a negative role in restoring normal muscle function after muscle damage has occurred."(3)

Normal cellular hydration may be important for GH release and glucose uptake, but there is no evidence that estrogen induced edema enhances these effects.

It is important here to distinguish one person's speculation from what is documented in the scientific literature. There is nothing wrong with theorizing, like Big Cat is doing; I do it all the time. But readers must realize that is all it is: speculation.

If I had to choose between a possible loss in gains versus a good chance of developing gyno, based on the published scientific research I'm with jboldman: It's a no brainer.

(1) Med Sci Sports Exerc 2003 Mar;35(3):439-43

Estrogen receptor alpha mRNA in human skeletal muscles.

Lemoine S, Granier P, Tiffoche C, Rannou-Bekono F, Thieulant ML, Delamarche P.

(2) Prog Clin Biol Res 1984;142:261-90

Studies on steroid receptors in human and rabbit skeletal muscle - clues to the understanding of the mechanism of action of anabolic steroids.

Gustafsson JA, Saartok T, Dahlberg E, Snochowski M, Haggmark T, Eriksson E

(3) Sports Med 2002;32(2):103-23

Exercise-induced muscle damage and the potential protective role of estrogen.

Kendall B, Eston R.

I think jb and Nandi pretty much nailed it. Weight gains from estrogen are merely fluid and strength gains are from leverage due to the fluid. If you are gyno prone, please use a SERM or an anti-aromatase when using aromatizing drugs.

Posted by: Nandi12

To say that estrogens upregulate the androgen receptor in human skeletal muscle is a stretch. Estrogens work via the estrogen receptor, except for a few poorly characterized non genomic actions, and some possible actions by direct binding to the androgen receptor in the prostate. Estrogen receptor mRNA was only just recently discovered in human skeletal muscle (1). Prior to that, it was believed that human skeletal muscle lacked the estrogen receptor (2). So it is really premature to start ascribing anabolic effects to estrogen in humans that may or may not even exist in animals and certainly have never been demonstrated in humans

There is also evidence that we have discussed here at length that estrogens may have a negative impact on muscle recovery:

"More recently, investigations into the potential effect of estrogen on muscle damage have explored the possible role that estrogen may play in the inflammatory response following muscle damage. In light of these studies, it may be suggested that if estrogen inhibits the vital inflammatory response process associated with the muscle damage and repair cycle, it has a negative role in restoring normal muscle function after muscle damage has occurred."(3)

Normal cellular hydration may be important for GH release and glucose uptake, but there is no evidence that estrogen induced edema enhances these effects.

It is important here to distinguish one person's speculation from what is documented in the scientific literature. There is nothing wrong with theorizing, like Big Cat is doing; I do it all the time. But readers must realize that is all it is: speculation.

If I had to choose between a possible loss in gains versus a good chance of developing gyno, based on the published scientific research I'm with jboldman: It's a no brainer.

(1) Med Sci Sports Exerc 2003 Mar;35(3):439-43

Estrogen receptor alpha mRNA in human skeletal muscles.

Lemoine S, Granier P, Tiffoche C, Rannou-Bekono F, Thieulant ML, Delamarche P.

(2) Prog Clin Biol Res 1984;142:261-90

Studies on steroid receptors in human and rabbit skeletal muscle - clues to the understanding of the mechanism of action of anabolic steroids.

Gustafsson JA, Saartok T, Dahlberg E, Snochowski M, Haggmark T, Eriksson E

(3) Sports Med 2002;32(2):103-23

Exercise-induced muscle damage and the potential protective role of estrogen.

Kendall B, Eston R.

Then if it's not because of aromatization why is Testosterone still Kinf of the Road when it comes to bulking muscle mass?

If I were to take an anti-estrogen while on a steroids cycle, could I use the same anti-e as a post-cycle therapy?

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Then if it's not because of aromatization why is testosterone still Kinf of the Road when it comes to bulking muscle mass?

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Testosterone is FAR from being the best steroid for adding muscle mass. Deca is twice as anabolic and MENT is 10 times more anabolic. This means that in castrated animals, it takes 10 times as much testosterone as it does MENT to maintain body mass:

Body weight in monkeys receiving testosterone (light shading) or MENT (dark shading). Administered doses of each androgen are indicated in milligrams per day on the abscissa. Body weight is expressed as a percentage of the baseline relative to values in intact animals before initiation of drug therapy. Actual baseline body weights in these animals were 4.8 � 0.6 kg for the testosterone group and 5.6 � 1.1 kg for the MENT group. Values are the mean � SEM (n = 6/group). 

Posted by: Nandi12

Testosterone is FAR from being the best steroid for adding muscle mass. Deca is twice as anabolic and MENT is 10 times more anabolic. This means that in castrated animals, it takes 10 times as much testosterone as it does MENT to maintain body mass:

Body weight in monkeys receiving testosterone (light shading) or MENT (dark shading). Administered doses of each androgen are indicated in milligrams per day on the abscissa. Body weight is expressed as a percentage of the baseline relative to values in intact animals before initiation of drug therapy. Actual baseline body weights in these animals were 4.8 � 0.6 kg for the testosterone group and 5.6 � 1.1 kg for the MENT group. Values are the mean � SEM (n = 6/group).

Why would nandrolone be more anabolic than testosterone when testosterone has more androgen receptor affinity binding? How can you know that nandrolone anabolic properties aren't largely dependant upon progestins activity at the estrogen receptor sites? In fact, the bloating from nandrolone should be attributed to progestenic/estrogenic activity, shouldn't it?

Posted by: Nandi12

Testosterone is FAR from being the best steroid for adding muscle mass. Deca is twice as anabolic and MENT is 10 times more anabolic. This means that in castrated animals, it takes 10 times as much testosterone as it does MENT to maintain body mass:

Body weight in monkeys receiving testosterone (light shading) or MENT (dark shading). Administered doses of each androgen are indicated in milligrams per day on the abscissa. Body weight is expressed as a percentage of the baseline relative to values in intact animals before initiation of drug therapy. Actual baseline body weights in these animals were 4.8 � 0.6 kg for the testosterone group and 5.6 � 1.1 kg for the MENT group. Values are the mean � SEM (n = 6/group).

How can you know that nandrolone anabolic properties aren't largely mediated by progestins activity at the estrogen receptor sites? In fact, the bloating from nandrolone should be attributed to progestenic/estrogenic activity, shouldn't it?

quote:

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Why would nandrolone be more anabolic than testosterone when testosterone has more androgen receptor affinity binding? How can you know that nandrolone anabolic properties aren't largely dependant upon progestins activity at the estrogen receptor sites? In fact, the bloating from nandrolone should be attributed to progestenic/estrogenic activity, shouldn't it?

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Receptor binding affinity has very little to do with how anabolic something is. The set of genes activated by a particular steroid determines its biological profile. This is why drugs with very low AR binding affinity like oxandrolone can be highly anabolic. See the next issue of Mind and Muscle for an in depth look at this.

Progestins aren't anabolic, neither is estrogen. If they were women on the pill would be huge.

Bloating from nandrolone comes primarily from the fact that 19-nortestosterone and its derivatives bind strongly to the mineralocorticoid receptor. That and the fact that androgens themselves cause Na retention.

Nandy12:

So if AR binding affinity doesn't determine how anabolic a steroid is, could we have a strongly anabolic steroid which wouldn't cause no baldness or BHP whatsoever?
If estrogen or AR binding aren't that important, could we take nolvadex and Proscar/Saw Pametto during a cycle to prevent side effects without hindering our gains?
I know that BigCat is completely against this, he says that if you are going to do so don't ever bother taking steroides, however if estrogen/AR binding are not that important it might be a wise thing to do, especially if you are prone to gyno and hairloss.

quote:

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So if AR binding affinity doesn't determine how anabolic a steroid is, could we have a strongly anabolic steroid which wouldn't cause no baldness or BHP whatsoever?

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First, binding affinity can effect the potency of a steroid, but a strong binding affinity is not essential for potency, either anabolic or androgenic. I was not clear in emphasising this earlier.

In truth, not enough is known about how steroids cause prostate growth or baldness to say definitively. But go back and look at the study about MENT:

Its anabolic/androgenic ratio is so high that a dosage that maintains muscle mass in castrated monkeys is barely enough to even maintain prostate weight, much less cause the prostate to enlarge. This can be seen by comparing figures 4 and 5. But bodybuilders take dosages much higher than those required simply to maintain body weight, so MENT "abuse" would lead to prostate enlargement. This is the case with all of the commonly used AAS: their anabolic/androgenic ratio is not high enough so that prostate enlargement can be avoided at the dosages used by bodybuilders. There are experimental compounds I've seen discussed with anabolic/androgenic ratios as high as 25 to 1. Something like that could probably be used to build muscle with no effect on the prostate.

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If estrogen or AR binding aren't that important, could we take nolvadex and Proscar/Saw Pametto during a cycle to prevent side effects without hindering our gains?

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Here again, just not enough is known. My original point is that if a person had to decide between a high liklihood of getting gyno versus a possible but unproven effect on gains, I would do everything possible to avoid gyno, and take the risk of a possible loss in some gains.

quote:

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I know that BigCat is completely against this, he says that if you are going to do so don't ever bother taking steroides

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IMO that is an extreme position. I would experiment and see. You are going to make gains using nolva and/or proscar. Countless bodybuilders do. There is nothing wrong with making a potential compromise (and there may not even be a compromise) to help preserve health. That is just common sense.