I accidentally took too much Arimidex...did I screw myself!?

[Vitamin_C]

maybe something will come out one day that changes this but right now i stand by. we have one study on rats which we cannot just say thats applicable to humans. There are several studies on men using letrozole and anastrozole for gyno treatment and no one became permanantly dysfunctional.

I have over used arimidex and aromasin in the past. Arimidex is the devil that shit will destroy you. Aromasin is much friendlier in my experience. Now I run 250 mg of test enanthate once per week and no ai. My trough is around 1200 ng/dl and estrogen is within the normal range. Im hoping i can slowly back off, I know this is high but it keeps things balanced for me now. If i try to run 100mg of test per week i have low estrogen symptoms.

I believe I read one of those studies, males were treated with 1mg of Arimidex per day for months and there were no adverse events reported. That is a hefty dose, I crashed my E2 at 1.25mg a week to 5 and it didn't come back up to therapeutic ranges until a few months later. I couldn't imagine how low for how long these dudes in that study were, they had to have been <0 for quite some time. As far as Crislers theory of endocrine disruption, the evidence just isn't there. There are countless numbers of bodybuilders who crash their E2 either accidentally or for shows AND in literature with male patients, you would much more about this issue if this were the case just as you see about PFS but you just don't at all. Also, countless amounts of women who have used this drug in mega-doses for breast cancer. Crisler also still prescribes Arimidex without hesitation, but won't prescribe Finasteride.

Correct me if I am wrong, but Estrogen modulates the release of dopamine, so if Estrogen wasn't doing its job, wouldn't we see fluctuations in values such as prolactin? particularly increase prolactin due to a decrease in dopamine?

 

[nurselyfe]

I believe I read one of those studies, males were treated with 1mg of Arimidex per day for months and there were no adverse events reported. That is a hefty dose, I crashed my E2 at 1.25mg a week to 5 and it didn't come back up to therapeutic ranges until a few months later. I couldn't imagine how low for how long these dudes in that study were, they had to have been <0 for quite some time. As far as Crislers theory of endocrine disruption, the evidence just isn't there. There are countless numbers of bodybuilders who crash their E2 either accidentally or for shows, you would much more about this issue if this were the case. Also, countless amounts of women who have used this drug in mega-doses for breast cancer...

The males who have used it were not on TRT. Anastrazole cannot touch testicular E2, which is why they did not crash as it only lowers E2 by 50-60%.

Was that E2 reading on the sensitive test or non sensitive ROCHE method where the lowest it reports E2 is "<5"

Also, women who use it 1mg a day sometimes develop epigenetic silencing of the ERa on tumor cells so their growth is now hormone independent - making them more aggressive and harder to treat.

 

[Vitamin_C]

The males who have used it were not on TRT. Anastrazole cannot touch testicular E2, which is why they did not crash as it only lowers E2 by 50-60%.

Was that E2 reading on the sensitive test or non sensitive ROCHE method where the lowest it reports E2 is "<5"

Also, women who use it 1mg a day sometimes develop epigenetic silencing of the ERa on tumor cells so their growth is now hormone independent - making them more aggressive and harder to treat.

A 50-60% reduction in mens E2 would be a significant crash as males have lower amounts of E2 compared to women. Say a man's sensitive E2 was 18, he's now around 9 for a substantial amount of time. I will try to find the study but I remember reading it and these men were on 1mg/day for a substantial amount of time. If estrogen wasn't doing its thing in the body after crash, we would see fluctuations in prolactin as estrogen modulates dopamine release which modulates prolactin.

If estrogen is modulating dopamine which is keeping prolactin levels in check, what is saying its not doing what its supposed to do anywhere else (nocturnal erections etc).

 

[nurselyfe]

A 50-60% reduction in mens E2 would be a significant crash as males have lower amounts of E2 compared to women. Say a man's sensitive E2 was 18, he's now around 9 for a substantial amount of time. I will try to find the study but I remember reading it and these men were on 1mg/day for a substantial amount of time. If estrogen wasn't doing its thing in the body after crash, we would see fluctuations in prolactin as estrogen modulates dopamine release which modulates prolactin.

9 is still not "crashed" to zero. Which is what i did. I know the studiest you are talking about and no ones E2 dropped to zero because no one was on TRT. And dopamine is not the only way prolactin is modulated.

Was your E2 test sensitive or non

 

[Vitamin_C]

9 is still not "crashed" to zero. Which is what i did. I know the studiest you are talking about and no ones E2 dropped to zero because no one was on TRT. And dopamine is not the only way prolactin is modulated.

Was your E2 test sensitive or non

When I crashed my E2? All my tests have been sensitive, I was at 5 at the lowest in August, a month later I was at 9, a month later I was at 26 and my latest one I was at 21. My current symptoms are anxiety and joint popping, libido is good, erections are good when I'm not anxious, but I didn't start getting bad anxiety till I started reading about the "permanent" theoretical E2 stuff which really ramped up my anxiety so I started researching through pubmed at my university (I am a doctoral student) and I just couldn't find good data to support this. I also exhaustively searched the web on bodybuilding sites where many dudes have crashed their E2 on accident or purposely lower their E2 for bodybuilding shows and couldn't find any feedback that supports this either, but you can find a lot on PFS. A lot of anxiety symptoms will mirror low E2 symptoms as well, same with hypoadrenal.

 

[Vitamin_C]

When I crashed my E2? All my tests have been sensitive, I was at 5 at the lowest in August, a month later I was at 9, a month later I was at 26 and my latest one I was at 21. Are you theorizing you need to be at zero for a while in order for this to happen? My current symptoms are anxiety and joint popping, libido is good, erections are good when I'm not anxious, but I didn't start getting bad anxiety till I started reading about the "permanent" theoretical E2 stuff which really ramped up my anxiety so I started researching through pubmed at my university (I am a doctoral student) and I just couldn't find good data to support this. I also exhaustively searched the web on bodybuilding sites where many dudes have crashed their E2 on accident or purposely lower their E2 for bodybuilding shows and couldn't find any feedback that supports this either, but you can find a lot on PFS. A lot of anxiety symptoms will mirror low E2 symptoms as well, same with hypoadrenal.

 

[nurselyfe]

When I crashed my E2? All my tests have been sensitive, I was at 5 at the lowest in August, a month later I was at 9, a month later I was at 26 and my latest one I was at 21. My current symptoms are anxiety and joint popping, libido is good, erections are good when I'm not anxious, but I didn't start getting bad anxiety till I started reading about the "permanent" theoretical E2 stuff which really ramped up my anxiety so I started researching through pubmed at my university (I am a doctoral student) and I just couldn't find good data to support this. I also exhaustively searched the web on bodybuilding sites where many dudes have crashed their E2 on accident or purposely lower their E2 for bodybuilding shows and couldn't find any feedback that supports this either, but you can find a lot on PFS. A lot of anxiety symptoms will mirror low E2 symptoms as well, same with hypoadrenal.

Ive crashed my E2 to low numbers plenty of times. I had the same symptoms as you. Always recovered fine within a week of cessation of arimidex. You'll be okay. I bet if you raised your T dose a smidge or took DHEA you'd feel a lot better.

The difference here is that I had my E2 suppressed to 0 for a long period of time. Now I 110% have permanent side effects. No issues with adrenals or thyroid. I feel the exact same way PFS sufferers do, but it's with the estrogen receptor.

 

[Vitamin_C]

I’m gonna PM you nurselyfe

 

[Vitamin_C]

there are couple of guys here and few on other board that didn't have an improvement in symptoms even though their e2 levels returned. same thing as guys with post finasteride symptoms got fu**ed for life after finasteride with insensetivity to dht. I have messages in my inbox on this forum and another trt forum from guys asking me what did I do to improve and how long did it took. there is nothing in medical literature on this because anastrozole is breast cancer drug and was made to fight breast cancer.. the usage of AIs in trt is off-label

That's true, but wouldn't there be reports of women who are insensitive to estrogen after using mega doses of Arimidex for years? Low E2 with women has very similar side effects as with men, there would be robust data and reports from women about this.

"from guys asking me what did I do to improve and how long did it took"

So whats the answer lol? spill the beans

 

[at15]

wow these subjects took arimidex 1 mg daily for 16 weeks with trt doses of testosterone!

http://www.nejm.org/doi/full/10.1056/NEJMoa1206168

looks like all the anastrozole subjects are close to 0 on the sensitive test

 

[Vitamin_C]

wow these subjects took arimidex 1 mg daily for 16 weeks with trt doses of testosterone!

http://www.nejm.org/doi/full/10.1056/NEJMoa1206168

looks like all the anastrozole subjects are close to 0 on the sensitive test

Yep, I've read a similar study. These dudes were seriously suppressed, 7mg a week is a female breast cancer dose, and women take that dose for years potentially.

 

[at15]

Yep, I've read a similar study. These dudes were seriously suppressed, 7mg a week is a female breast cancer dose, and women take that dose for years potentially.

must have been absolutely brutal, wish we could talk to the guys now ask them how long to recover.

 

[nurselyfe]

wow these subjects took arimidex 1 mg daily for 16 weeks with trt doses of testosterone!

http://www.nejm.org/doi/full/10.1056/NEJMoa1206168

looks like all the anastrozole subjects are close to 0 on the sensitive test

So you're saying i'm lying that i have permanent physical side effects? All starting when I crashed my e2 to 0 multiple times? I had the thickest head of hair before this and now I have severely thinned out hair and hair loss that is only speeding up, dry skin, dry scalp, lost all my veins, no sebum production, lower blood pressure, cold hands and feet, severe water retention, can't get a pump anymore when they used to feel like my muscles were bursting out of my skin.

Sounds like hypothyroid a bit right? TSH, T4, T3 all normal. Getting a more comprehensive work up and will gladly share my results but i'm certain it's not that. I can't take SERMS because they make me feel way worse. Anytime my E2 goes up gene expression is permanently silenced further.

Ive never had any other medical problems. Don't take any other medications. I was perfectly healthy before this.

 

[at15]

i dont think your lying about whats happening with your body but im confident its not from taking anastrozole. there is something else going on here. I mean just a few months ago in july you told us e2 sensitive was 89 so its not like you were crashed out 24/7. then august you said my joints feel a lot more lubricated than normal. Serious question, do you have other OCD symptoms in your life? If im reading correctly you just went on a testosterone cycle when you were 20, then came off on 120mg trt. I would come off everything cold turkey give your body 6 months to come back to normal and re-assess.

 

[simeoni]

If I have understood correctly nurselyfe is mainly basing his theory in this animal study: http://www.sciencedirect.com/science/article/pii/0018506X81900180

Im not really sure if this backs up nurselyfe's theory. Here's what Im seeing from the full study:

- The rats with long term estrogen deprivation (35 days) did show a diminished response to combined estrogen and progesterone therapy. They did not show a similiar response in their behavioral patterns that was seen in the short term group - that was deprived for 5 days.

- They did not see a decrease in the number of E2 receptors. Decrease in progestin receptors was observed.

Here are few quotes from the full study: "Estrogen deprivation for a prolonged period (35 days) resulted in adecline in the effectiveness of subsequent estrogen treatment in activatingboth proceptive and receptive behaviors, and in stimulating cytoplasmicprogestin receptor in the PIT and POA-MBH. This decline in the effectivenessof E, was not accompanied by a reduction in the amount ofestrogen receptor translocated into PIT and POA-MBH cell nuclei afterE, treatment."

"One explanation for thereduced behavioral effect of combined E, and progesterone treatmentin long-term OVX animals might therefore be a decline in the effectivenessof estrogen in stimulating progestin receptor synthesis in the POAMBH.The present results are consistent with this idea. However, itwould be premature to conclude that a change in the sensitivity of theprogestin receptor system is the only factor involved."

"One explanation for thereduced behavioral effect of combined E, and progesterone treatmentin long-term OVX animals might therefore be a decline in the effectivenessof estrogen in stimulating progestin receptor synthesis in the POAMBH.The present results are consistent with this idea. However, itwould be premature to conclude that a change in the sensitivity of theprogestin receptor system is the only factor involved."

"These observations indicate that other central nervous estrogen-dependentfactors, besides the induction of PR,, become desensitizedduring long-term estrogen deprivation. The change in overall behavioralsensitivity to estrogen + progesterone therapy which occursafter gonadectomy probably reflects contributions from these factors aswell as from PR, synthesis."

Ok. So based on this rat study from 1981 there was an observable change in their behavior after a prolonged estrogen deprivation. From what I understand this study does not come to the conclusion that the cause of this was the desensitization of estrogen receptors.

Im not saying that it cannot happen. I would just like to know how does nurselyfe come to that conclusion based on this study?

 

[Vitamin_C]

If I have understood correctly nurselyfe is mainly basing his theory in this animal study: http://www.sciencedirect.com/science/article/pii/0018506X81900180

Im not really sure if this backs up nurselyfe's theory. Here's what Im seeing from the full study:

- The rats with long term estrogen deprivation (35 days) did show a diminished response to combined estrogen and progesterone therapy. They did not show a similiar response in their behavioral patterns that was seen in the short term group - that was deprived for 5 days.

- They did not see a decrease in the number of E2 receptors. Decrease in progestin receptors was observed.

Here are few quotes from the full study: "Estrogen deprivation for a prolonged period (35 days) resulted in adecline in the effectiveness of subsequent estrogen treatment in activatingboth proceptive and receptive behaviors, and in stimulating cytoplasmicprogestin receptor in the PIT and POA-MBH. This decline in the effectivenessof E, was not accompanied by a reduction in the amount ofestrogen receptor translocated into PIT and POA-MBH cell nuclei afterE, treatment."

"One explanation for thereduced behavioral effect of combined E, and progesterone treatmentin long-term OVX animals might therefore be a decline in the effectivenessof estrogen in stimulating progestin receptor synthesis in the POAMBH.The present results are consistent with this idea. However, itwould be premature to conclude that a change in the sensitivity of theprogestin receptor system is the only factor involved."

"One explanation for thereduced behavioral effect of combined E, and progesterone treatmentin long-term OVX animals might therefore be a decline in the effectivenessof estrogen in stimulating progestin receptor synthesis in the POAMBH.The present results are consistent with this idea. However, itwould be premature to conclude that a change in the sensitivity of theprogestin receptor system is the only factor involved."

"These observations indicate that other central nervous estrogen-dependentfactors, besides the induction of PR,, become desensitizedduring long-term estrogen deprivation. The change in overall behavioralsensitivity to estrogen + progesterone therapy which occursafter gonadectomy probably reflects contributions from these factors aswell as from PR, synthesis."

Ok. So based on this rat study from 1981 there was an observable change in their behavior after a prolonged estrogen deprivation. From what I understand this study does not come to the conclusion that the cause of this was the desensitization of estrogen receptors.

Im not saying that it cannot happen. I would just like to know how does nurselyfe come to that conclusion based on this study?

We have something better in humans , women on Arimidex for years for breast cancer therapy , years of suppression, not months. A finding like this in humans would be a breakthrough .

 

[Vitamin_C]

I found a few cases of estrogen insensitivity issues, but none of them were involving arimidex use as it is congenital disease. With the MASSIVE amounts of women and bodybuilders using arimidex, there are no cases of this happening.
https://en.wikipedia.org/wiki/Estrogen_insensitivity_syndrome


In all cases, estrogen was ELEVATED because it was not binding to receptors. Adex also poorly crosses into the blood-brain barrier and CNS. In the study with the sisters, their SHBG levels were low due to estrogens effects on the liver. So its looking like common themes among people that have this are elevated E2 and low SHBG.

"Impaired negative feedback by estrogen on the hypothalamic-pituitary-gonadal (HPG) axis would account for the elevated estradiol and gonadotropin levels" meaning if you had estrogen sensitivity issues you would have elevated E2 just as the tiny few who have this.

I also find it fascinating that the first male in this link still had normal sexual functioning, further demonstrating how absolutely complex libido and erections are...

If you think you have this, have your doc prescribe you some estrogen and see if you get gyno or other high E2 symptoms like they did in the case study.

 

[nurselyfe]

i dont think your lying about whats happening with your body but im confident its not from taking anastrozole. there is something else going on here. I mean just a few months ago in july you told us e2 sensitive was 89 so its not like you were crashed out 24/7. then august you said my joints feel a lot more lubricated than normal. Serious question, do you have other OCD symptoms in your life? If im reading correctly you just went on a testosterone cycle when you were 20, then came off on 120mg trt. I would come off everything cold turkey give your body 6 months to come back to normal and re-assess.

Yeah E2 sensitive was 89. But I crashed it 3 times before that AT ZERO, and 2 times after. Each crash, I felt permanently
worse and worse. Then when I took Nolvadex in late august my life went completely down hill. Things got really bad in terms of anxiety, libido, depression and more intense low E2 symptoms. I didn't put two and two together.

2 weeks after that, I did my 60mg dose on thursday. Couldn't remember on friday if I did my thursday ahot, that's how bad the brain fog is (imagine being in an accelerated Nursing program with that), and did a 40mg shot on friday. That night and saturday I had such bad anxiety and more low E2 symptoms.

2 weeks ago I took 25mg of clomid because I saw it helped someone with post finasteride syndrome. It did the same thing that nolvadex did. I was bed ridden for a week. Also made me permanently worse.

Lets get this straight. I've used nolvadex and clomid before, never had a bad reaction to them. Helped me recover well after my first cycle. Also, Please do no tell me low estrogen and high estrogen symptoms are the same. They are night and day for me. I've been on TRT for 3 years, I know this by now. I never had issues.

No OCD symptoms ever. Coming off would only do me more harm. I don't respond to HCG and SERMS only make me worse. I'm already depressed and have anxiety and muscle wastage. I need to fix the underlying issue here before I do anything drastic. I'm not okay with my potentially making myself worse.

 

[nurselyfe]

I found a few cases of estrogen insensitivity issues, but none of them were involving arimidex use as it is congenital disease. With the MASSIVE amounts of women and bodybuilders using arimidex, there are no cases of this happening.
https://en.wikipedia.org/wiki/Estrogen_insensitivity_syndrome


In all cases, estrogen was ELEVATED because it was not binding to receptors. Adex also poorly crosses into the blood-brain barrier and CNS. In the study with the sisters, their SHBG levels were low due to estrogens effects on the liver. So its looking like common themes among people that have this are elevated E2 and low SHBG.

"Impaired negative feedback by estrogen on the hypothalamic-pituitary-gonadal (HPG) axis would account for the elevated estradiol and gonadotropin levels" meaning if you had estrogen sensitivity issues you would have elevated E2 just as the tiny few who have this.

I also find it fascinating that the first male in this link still had normal sexual functioning, further demonstrating how absolutely complex libido and erections are...

If you think you have this, have your doc prescribe you some estrogen and see if you get gyno or other high E2 symptoms like they did in the case study.

I'm also on TRT so i'm artificially controlling my E2 levels. My HPTA is not since it is shut down.

 

[Vitamin_C]

I'm also on TRT so i'm artificially controlling my E2 levels. My HPTA is not since it is shut down.

But theoretically, E2 would pool and increase with each shot because it is not being absorbed by the receptor, that is why the congenital estrogen insufficiency patients all had very high E2. Also, estrogen increases SHBG, so if estrogen is not working on the cells you would see very low SHBG https://www.ncbi.nlm.nih.gov/pubmed/10439005

Also, I went through nursing school, I know how daunting it is, I am in school for my DNP currently. If you are surviving nursing school, you are doing fine man. I'm not saying you aren't struggling, but anxiety can manifest some nasty physical and mental symptoms.