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gjohnson5
New member
Here: http://www.elitefitness.com/articledata/efn/032906.html
I have also found research which does seem to indicate that anti estrogens have a negative effect on igf-1 since the release of estrogen seems to have almost a linear coorelation with estrogen levels. Some such as bigcat on bb.com suggest that allowing aromatization for maximum growth. But this would also seem to spur growth of breast tissue as well...
http://www.extremefitness.com/forum/archive/index.php/t-3578.html
Estrogen and GH/IGF-1
To date the most common explanation for why anti-estrogens may be
slightly counterproductive to growth in the sports literature has been
the suggestion that estrogen plays a role in the production of growth
hormone and IGF-1. IGF-1 (insulin like growth factor 1, formerly known
as somatomedin C) is of course an anabolic product released primarily in
the liver via GH stimulus. IGF-1 is responsible for the growth promoting
effects (increased nitrogen retention, cell proliferation) we associate
with growth hormone therapy. We do know that women have higher levels of
growth hormone than men, and also that GH secretion varies over the
course of the menstrual cycle in direct correlation with estrogen
levels[iv]. Estrogen is likewise often looked at as a key trigger in the
release of GH in women under normal physiological situations.
It is also suggested that the aromatization of androgens to estrogens in
men plays an important role in the release and production of GH and
IGF-1. This was evidenced by a 1993 study of hypogonadal men, comparing
the effects of testosterone replacement therapy on GH and IGF-1 levels
with and without the addition of tamoxifen[v]. When the anti-estrogen
tamoxifen was given, GH and IGF-1 levels were notably suppressed, while
both values were elevated with the administration of testosterone
enanthate alone. Another study has shown 300mg of testosterone enanthate
weekly (which elevated estradiol levels) to cause a slight IGF-1
increase in normal men, whereas 300mg weekly of nandrolone decanoate (a
poor substrate for aromatase that caused a lowering of estradiol levels
in this study) would not elevate IGF-1 levels[vi]. Yet another study
shows that GH and IGF-1 secretion is increased with testosterone
administration on males with delayed puberty, while dihydrotestosterone
(non-aromatizable) seems to suppress GH and IGF-1 secretion, presumably
due to its strong anti-estrogenic/gonadotropin suppressing action[vii].
All of these studies seem to support a direct, estrogen-dependant
mechanism for GH and/or IGF-1 release in men. It is difficult to say at
this point just how important estrogen is to IGF-1 production as it
relates to the promotion of anabolism in the steroid using athlete,
however it remains an interesting subject to investigate.
Glucose Utilization and Estrogen
Estrogen may play an even more vital role in promoting an anabolic state
by affecting glucose utilization in muscle tissue. This occurs via an
altering the level of available glucose 6-phosphate dehydrogenase. G6PD
is an important enzyme in the support anabolism, as it is directly tied
to the use of glucose for muscle growth and recuperation[viii] [ix].
During the period of regeneration after skeletal muscle damage, levels
of G6PD are shown to rise dramatically. G6PD enzyme plays a vital role
in what is known as the pentose phosphate pathway, and as such this rise
is believed to enhance the PPP related process in which nucleic acids
and lipids are synthesized in cells; fostering the repair of muscle tissue.
A 1980 study at the University of Maryland has shown that levels of
glucose 6-phosphate dehydrogenase rise after administration of
testosterone propionate, and further that the aromatization of
testosterone to estradiol is directly responsible for this increase.[x]
In this study neither dihydrotestosterone nor fluoxymesterone could
mimic the affect of testosterone propionate on levels of G6PD, an affect
that was also blocked by the addition of the potent anti-aromatase
4-hydroxyandrostenedione to testosterone. 17-beta estradiol
administration caused a similar increase in G6PD, which was not noticed
when its inactive estrogen isomer 17-alpha estradiol (unable to bind the
estrogen receptor) was given. An anti-androgen could also not block the
positive action of testosterone. This study provides one of the first
palatable explanations for a direct and positive effect of estrogen on
muscle tissue.
But there also appears to be science that femara actually can increase IGF-1
http://www.worldclassbodybuilding.c...rimindex-liquidex-aromisin-12982.html?t=12982
Aromsain is a nonreversible inhibitor, which means that it doesn't matter how much test you take,
it can not be diplaced as with arimidex/liquidex.
Once it does bind to the aromatase enzyme that's it ...no chance of estrogen.
Now the body continuely makes these enzymes,
so you have to take the aromsin continuely throughout the cycle as you would any other inhibitor.
This should be started a week before you start your cycle. You need that much time to totally saturate
your body
Arimidex or liquidex, can be displaced from the aromatase enzyme and then the testosterone can bind to it and make estrogen.
With Aromsain, this can't happen.
Femara (letrozole)
Dose: 2.5mgs/day
It is a nonsteroidal competitive inhibitor of the aromatase enzyme system.
Femara just leaves IGF-I intact, where as arimindex and liquidex lowers it.
Arimindex/Liquidex
Arimindex contain 1 mg of anastrozole, a non-steroidal aromatase inhibitor.
Liquidex is nothing more than anastrozole suspended in an oil base substraight
Anastrozole is a potent and selective non-steroidal aromatase inhibitor. It
significantly lowers serum estradiol concentrations.
These numbers are debateable but they still should be considered when choosing your inhibitor and such.
Femara - increases IGF-1 by 24%
Arimidex - decreases IGF-1 by 18%
Nolvadex - decreases IGF-1 by 23.5%
Aromasin - decreases IGF-1 by 23-24%
Elevated IGF-1 = means more growth
As you can see the help you get form these, the more that they detract from your gains.
Something to take in consideration.
I will look into the science of femara / letro to see if any studies have been conducted on IGF-1 levels...
I have also found research which does seem to indicate that anti estrogens have a negative effect on igf-1 since the release of estrogen seems to have almost a linear coorelation with estrogen levels. Some such as bigcat on bb.com suggest that allowing aromatization for maximum growth. But this would also seem to spur growth of breast tissue as well...
http://www.extremefitness.com/forum/archive/index.php/t-3578.html
Estrogen and GH/IGF-1
To date the most common explanation for why anti-estrogens may be
slightly counterproductive to growth in the sports literature has been
the suggestion that estrogen plays a role in the production of growth
hormone and IGF-1. IGF-1 (insulin like growth factor 1, formerly known
as somatomedin C) is of course an anabolic product released primarily in
the liver via GH stimulus. IGF-1 is responsible for the growth promoting
effects (increased nitrogen retention, cell proliferation) we associate
with growth hormone therapy. We do know that women have higher levels of
growth hormone than men, and also that GH secretion varies over the
course of the menstrual cycle in direct correlation with estrogen
levels[iv]. Estrogen is likewise often looked at as a key trigger in the
release of GH in women under normal physiological situations.
It is also suggested that the aromatization of androgens to estrogens in
men plays an important role in the release and production of GH and
IGF-1. This was evidenced by a 1993 study of hypogonadal men, comparing
the effects of testosterone replacement therapy on GH and IGF-1 levels
with and without the addition of tamoxifen[v]. When the anti-estrogen
tamoxifen was given, GH and IGF-1 levels were notably suppressed, while
both values were elevated with the administration of testosterone
enanthate alone. Another study has shown 300mg of testosterone enanthate
weekly (which elevated estradiol levels) to cause a slight IGF-1
increase in normal men, whereas 300mg weekly of nandrolone decanoate (a
poor substrate for aromatase that caused a lowering of estradiol levels
in this study) would not elevate IGF-1 levels[vi]. Yet another study
shows that GH and IGF-1 secretion is increased with testosterone
administration on males with delayed puberty, while dihydrotestosterone
(non-aromatizable) seems to suppress GH and IGF-1 secretion, presumably
due to its strong anti-estrogenic/gonadotropin suppressing action[vii].
All of these studies seem to support a direct, estrogen-dependant
mechanism for GH and/or IGF-1 release in men. It is difficult to say at
this point just how important estrogen is to IGF-1 production as it
relates to the promotion of anabolism in the steroid using athlete,
however it remains an interesting subject to investigate.
Glucose Utilization and Estrogen
Estrogen may play an even more vital role in promoting an anabolic state
by affecting glucose utilization in muscle tissue. This occurs via an
altering the level of available glucose 6-phosphate dehydrogenase. G6PD
is an important enzyme in the support anabolism, as it is directly tied
to the use of glucose for muscle growth and recuperation[viii] [ix].
During the period of regeneration after skeletal muscle damage, levels
of G6PD are shown to rise dramatically. G6PD enzyme plays a vital role
in what is known as the pentose phosphate pathway, and as such this rise
is believed to enhance the PPP related process in which nucleic acids
and lipids are synthesized in cells; fostering the repair of muscle tissue.
A 1980 study at the University of Maryland has shown that levels of
glucose 6-phosphate dehydrogenase rise after administration of
testosterone propionate, and further that the aromatization of
testosterone to estradiol is directly responsible for this increase.[x]
In this study neither dihydrotestosterone nor fluoxymesterone could
mimic the affect of testosterone propionate on levels of G6PD, an affect
that was also blocked by the addition of the potent anti-aromatase
4-hydroxyandrostenedione to testosterone. 17-beta estradiol
administration caused a similar increase in G6PD, which was not noticed
when its inactive estrogen isomer 17-alpha estradiol (unable to bind the
estrogen receptor) was given. An anti-androgen could also not block the
positive action of testosterone. This study provides one of the first
palatable explanations for a direct and positive effect of estrogen on
muscle tissue.
But there also appears to be science that femara actually can increase IGF-1
http://www.worldclassbodybuilding.c...rimindex-liquidex-aromisin-12982.html?t=12982
Aromsain is a nonreversible inhibitor, which means that it doesn't matter how much test you take,
it can not be diplaced as with arimidex/liquidex.
Once it does bind to the aromatase enzyme that's it ...no chance of estrogen.
Now the body continuely makes these enzymes,
so you have to take the aromsin continuely throughout the cycle as you would any other inhibitor.
This should be started a week before you start your cycle. You need that much time to totally saturate
your body
Arimidex or liquidex, can be displaced from the aromatase enzyme and then the testosterone can bind to it and make estrogen.
With Aromsain, this can't happen.
Femara (letrozole)
Dose: 2.5mgs/day
It is a nonsteroidal competitive inhibitor of the aromatase enzyme system.
Femara just leaves IGF-I intact, where as arimindex and liquidex lowers it.
Arimindex/Liquidex
Arimindex contain 1 mg of anastrozole, a non-steroidal aromatase inhibitor.
Liquidex is nothing more than anastrozole suspended in an oil base substraight
Anastrozole is a potent and selective non-steroidal aromatase inhibitor. It
significantly lowers serum estradiol concentrations.
These numbers are debateable but they still should be considered when choosing your inhibitor and such.
Femara - increases IGF-1 by 24%
Arimidex - decreases IGF-1 by 18%
Nolvadex - decreases IGF-1 by 23.5%
Aromasin - decreases IGF-1 by 23-24%
Elevated IGF-1 = means more growth
As you can see the help you get form these, the more that they detract from your gains.
Something to take in consideration.
I will look into the science of femara / letro to see if any studies have been conducted on IGF-1 levels...
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