3rd Week of TRT...Feel tired and unmotivated.......
- Thread starter Alpin
- Start date
Megatron28
Moderator
In the way I described in my message.
Megatron28
Moderator
I like it when you speak sense Megatron. It's a damn shame what Optimus did to you in the last movie.Although, I would suspect that his E2 levels should be better off at 160mg/wk than what he was producing endogenously. If his adex dose for monotherapy didn't crush his E2, I doubt that (unless he has a problem with his feedback loop; dumping excess estrogen into his system) he'd totally crush it if at the same dose. Then again, .25mg EOD is a tad high for that dose of test.
I would really like to see labs as well.
Apollon: (Sorry, didn't feel like doing a multi-quote
Just a hunch given monotherapy didn't completely jackhammer your estradiol into the ground...
I know guys who have done adex mono-therapy and they can take a buttload of the stuff without crushing their E2. But as soon as they start injecting test cyp they can't tolerate nearly as much. The same adex dose crashes their E2.
Alpin
New member
What do I do then if I'm running T 160 mg/7days in one weekly shot and E3D 350 i.u. Human Chorionic Gonadotropin (HCG) ?
they are both bound to raise E2...
Prescription label says take 2 half milligram tabs twice per week...
So that's 1 mg...
I'm doing 0.25 mg EOD (0.75 mg/week total dose)
If taken E3D it is 0.5 mg/week
they are both bound to raise E2...
Prescription label says take 2 half milligram tabs twice per week...
So that's 1 mg...
I'm doing 0.25 mg EOD (0.75 mg/week total dose)
If taken E3D it is 0.5 mg/week
Megatron28
Moderator
Below is an excerpt from the following study. We all know that when we are on testosterone replacement therapy (TRT) we cannot tolerate anything near the doses of arimidex used in this study. But these men who were not taking test tolerated it well. See the parts I bolded. The whole thing can be read using the following link.
Aromatase inhibitors in men: effects and therapeutic options
Reproductive Biology and Endocrinology : RB&E
BioMed Central
Aromatase inhibitors in men: effects and therapeutic options
Willem de Ronde and Frank H de Jong
Effects of aromatase inhibition on luteinizing hormone release and testosterone production
It is well known from experimental evidence and from clinical observations that estradiol has powerful effects on gonadotropin release in men. Modulation of plasma estradiol levels within the male physiological range is associated with strong effects on plasma levels of LH through an effect at the level of the pituitary gland [32]. Lowering estradiol levels, by administering an aromatase inhibitor, is associated with an increase in levels of LH, follicle-stimulating hormone (FSH) and testosterone [28,29]. Aromatase inhibitors, therefore, have been suggested as a tool to increase testosterone levels in men with low testosterone levels. Due to their mode of action the use of aromatase inhibitors is limited to men with at least some residual function of the hypothalamo-pituitary-gonadal axis. Therefore aromatase inhibitors have been tested in older men suffering from so-called late-onset hypogonadism or partial androgen deficiency. Aging in men is associated with a gradual decline of total and free testosterone levels [33] as a result of combined testicular and hypothalamic dysfunction. The decline of testosterone levels has been implicated in the pathogenesis of physical frailty in older men. Androgen treatment, therefore, has been advocated for older men with signs and symptoms of androgen deficiency and unequivocally low plasma testosterone levels [34,35].
Aromatase inhibitors may be an attractive alternative for traditional testosterone substitution in elderly men because these compounds can be administered orally once daily and may result in physiological 24 h testosterone profiles. Additionally, misuse of aromatase inhibitors is unlikely since testosterone levels will not be stimulated to vastly supraphysiological levels. A small, controlled study demonstrated that anastrozole in a dose of 1 mg daily during 12 weeks will result in doubling of the mean bioavailable testosterone level in older men [36]. A more recent study also showed a moderate but significant effect of aromatase inhibition on estradiol and testosterone levels in older men [37]. Treatment with atamestane 100 mg once daily resulted in a 40% increase in total testosterone levels after 36 weeks. However, no beneficial effects were seen on muscle strength, body composition or quality-of-life scores. A similar increase of testosterone levels in the absence of effects on body composition and strength was reported in a study, in which elderly men with borderline low levels of serum testosterone were treated with anastrozole during 1 year [38]. There is a number of possible explanations for the lack of a clear treatment effect. First of all, the numbers of studied subjects were relatively small. Moreover, the mean baseline testosterone levels in the treated groups were in, or only slightly below, the normal range for young adult men and the relative increase in testosterone levels may have been too small. It has been suggested that men with the lowest baseline testosterone levels benefit most from testosterone substitution [39]. Finally, the decreased levels of estradiol may have affected the expected rise in lean body mass [38]. These observations outline a serious limitation of the use of aromatase inhibitors in older men; the stimulating effect on testosterone levels may be too weak, especially in the men with the lowest baseline testosterone levels who would potentially benefit most.
Aromatase inhibitors in men: effects and therapeutic options
Reproductive Biology and Endocrinology : RB&E
BioMed Central
Aromatase inhibitors in men: effects and therapeutic options
Willem de Ronde and Frank H de Jong
Effects of aromatase inhibition on luteinizing hormone release and testosterone production
It is well known from experimental evidence and from clinical observations that estradiol has powerful effects on gonadotropin release in men. Modulation of plasma estradiol levels within the male physiological range is associated with strong effects on plasma levels of LH through an effect at the level of the pituitary gland [32]. Lowering estradiol levels, by administering an aromatase inhibitor, is associated with an increase in levels of LH, follicle-stimulating hormone (FSH) and testosterone [28,29]. Aromatase inhibitors, therefore, have been suggested as a tool to increase testosterone levels in men with low testosterone levels. Due to their mode of action the use of aromatase inhibitors is limited to men with at least some residual function of the hypothalamo-pituitary-gonadal axis. Therefore aromatase inhibitors have been tested in older men suffering from so-called late-onset hypogonadism or partial androgen deficiency. Aging in men is associated with a gradual decline of total and free testosterone levels [33] as a result of combined testicular and hypothalamic dysfunction. The decline of testosterone levels has been implicated in the pathogenesis of physical frailty in older men. Androgen treatment, therefore, has been advocated for older men with signs and symptoms of androgen deficiency and unequivocally low plasma testosterone levels [34,35].
Aromatase inhibitors may be an attractive alternative for traditional testosterone substitution in elderly men because these compounds can be administered orally once daily and may result in physiological 24 h testosterone profiles. Additionally, misuse of aromatase inhibitors is unlikely since testosterone levels will not be stimulated to vastly supraphysiological levels. A small, controlled study demonstrated that anastrozole in a dose of 1 mg daily during 12 weeks will result in doubling of the mean bioavailable testosterone level in older men [36]. A more recent study also showed a moderate but significant effect of aromatase inhibition on estradiol and testosterone levels in older men [37]. Treatment with atamestane 100 mg once daily resulted in a 40% increase in total testosterone levels after 36 weeks. However, no beneficial effects were seen on muscle strength, body composition or quality-of-life scores. A similar increase of testosterone levels in the absence of effects on body composition and strength was reported in a study, in which elderly men with borderline low levels of serum testosterone were treated with anastrozole during 1 year [38]. There is a number of possible explanations for the lack of a clear treatment effect. First of all, the numbers of studied subjects were relatively small. Moreover, the mean baseline testosterone levels in the treated groups were in, or only slightly below, the normal range for young adult men and the relative increase in testosterone levels may have been too small. It has been suggested that men with the lowest baseline testosterone levels benefit most from testosterone substitution [39]. Finally, the decreased levels of estradiol may have affected the expected rise in lean body mass [38]. These observations outline a serious limitation of the use of aromatase inhibitors in older men; the stimulating effect on testosterone levels may be too weak, especially in the men with the lowest baseline testosterone levels who would potentially benefit most.
Megatron28
Moderator
Best bet is to get labs and see where your E2 is at. You need really frequent lab work in the beginning to get dialed in. Keep in mind that your TT is nowhere near peak levels after only three weeks.
Austin1
New member
Hang in there. 3 weeks is nothing. Give your protocol time. It's not uncommon to feel down while your serum stabilizes.
halfwit
I like turtles.
Very interesting. There must be an additional component that is shut off when exogenous testosterone is introduced then. That is the only explanation that makes sense to me on why estradiol levels would be higher with monotherapy than as part of a testosterone replacement therapy (TRT) protocol. I'm going to need to do some homework on this as it seems very counter-intuitive to me.
Thanks for the link and info mang. I wonder if the men taking 1mg of adex ED had serious problems with low E2 then? That's just so much Aromatase inhibitor (AI), I can't see them being okay at that dose... Unless there's some sort of other pathway as I mentioned above that is closed when exogenous test is involved that would somehow shunt away the additional adex that would drop E2 below an optimal or healthy range. I have some homework to do on this now!
Spunkey71
New member
After being on this site for a short period of time now and reading posts as well as the studies that everyone posts I feel as though my IQ has risen some, it is nice to have found a place where so many very knowledgeable people are willing to share their experiences and wisdom with others!
Megatron28
Moderator
I can't explain it either Halfwit, other than guessing the feedback loop must remain open on adex alone and it closes when you add exogenous test???
I have a friend who was trying to get his wife pregnant and got diagnosed with secondary hypogonadism. He was put on something like 1mg of adex a day. When I heard that I thought he was in for all sorts of problems.
But he tolerated it very well. It got his TT up around 500-600. And his E2 was in the normal range. He ended up getting his wife pregnant and then switched over to test cyp.
On test cyp he could barely tolerate any Adex. He was so surprised since he was using so much before. Now .25mg a week -- he was on a something like 80mg or 100mg a week -- was crashing his E2. His TT was up in the 700-800 range if I remember right. He got to the point where he wanted to get on a dose of test where he could avoid needing to use an Aromatase inhibitor (AI).
So one day he is going through Aromatase inhibitor (AI) like it is skittles and then when he introduced test cyp he could hardly tolerate any of it.
Also, for what it is worth, even with similar TT levels, he preferred how he felt when he was using Test Cyp. Even though adex increased his TT and made him feel better, it wasn't the same as taking test.
I have a friend who was trying to get his wife pregnant and got diagnosed with secondary hypogonadism. He was put on something like 1mg of adex a day. When I heard that I thought he was in for all sorts of problems.
But he tolerated it very well. It got his TT up around 500-600. And his E2 was in the normal range. He ended up getting his wife pregnant and then switched over to test cyp.
On test cyp he could barely tolerate any Adex. He was so surprised since he was using so much before. Now .25mg a week -- he was on a something like 80mg or 100mg a week -- was crashing his E2. His TT was up in the 700-800 range if I remember right. He got to the point where he wanted to get on a dose of test where he could avoid needing to use an Aromatase inhibitor (AI).
So one day he is going through Aromatase inhibitor (AI) like it is skittles and then when he introduced test cyp he could hardly tolerate any of it.
Also, for what it is worth, even with similar TT levels, he preferred how he felt when he was using Test Cyp. Even though adex increased his TT and made him feel better, it wasn't the same as taking test.
Alpin
New member
Why did he give up 500-600 ng/dl Natty T.T. for a life of injects ?
Did he do a sleep study ?
bushleaguechew
Junior Bodybuilder
Not everyone has sleep apnea and not everyone feels fine on 500-600.
Megatron28
Moderator
Yes. He has a cpap.
You missed what I wrote. He was hypogonadal. He got to 500-600 TT on adex mono-therapy.
Like I wrote. Even though adex alone gave him TT in the 500-600 range he feels better being in the same range from injecting test. Think about clomid. It increases your TT too, but how many guys report not feeling "right" on it. Apparently, where you get your TT from makes a difference.
You have done clomid, adex mono-therapy, and test cyp Apollon. Did you feel the same on each of this at the same TT level? Or does one work better for you?
halfwit
I like turtles.
That's a pretty sound theory. I remember reading studies on obese men taking an Aromatase inhibitor (AI) to help restore TT levels, but flipped when I saw the doses of adex they were feeding to them. There must be something else that triggers the negative feedback loop than just estrogen spiking. Man, every time I feel I have a grasp on this stuff - I learn something new that has me reevaluate how it all fits in together.
I need an owner's manual for the human body, or at least a schematic or something!
Alpin
New member
Never did clomid...
Nolva was ok at 20 mg/day for 2 months. Adex E3D was a little better decent, I too was in Natty 594 ng/dl range with it.
HCG felt great when I first went on it. Test E felt best there after.
Problem is no Endo will believe that a person feels better on a certain medication...even though they are at the same T. level with either/or. They will absolutely say it is psychological.
Megatron28
Moderator
My friend's endo believed it.
Alpin
New member
He's lucky.
