Can a single dose of .25mg Arimidex crash my E2?

[JCUSN]

I’m on HCG monotherapy. Mostly for fertility, but also loving the testosterone boost.

My doctor decided to put me on 1000iu 3x per week.

I started feeling sensitive (not painful) nipples. They aren’t sore, they’re just sensitive and they’re very hard often. No tissue growth.
I also noticed my penis not being as “full” as usual, even though I take daily 5mg Cialis. It just appears shriveled a bit.

I just took a .25mg Arimidex (1mg pill split into 4 pieces with pill cutter).

I know this might sound crazy, but there’s no way that single dose would crash my E2 right? I took labs yesterday, but no results yet, and I was foolish and jumped the gun taking the .25mg dose. Will I be fine, or did I screw myself?

 

[Systemlord]

I also noticed my penis not being as “full” as usual, even though I take daily 5mg Cialis. It just appears shriveled a bit.

This is either a self fulfilling prophecy (mindfu**** yourself) or you indeed crushed your E2 levels. In either case, the result is the same,, you screwed yourself either way.

I started feeling sensitive (not painful) nipples.

This is to be expected starting out on any hormone therapy, you jumped the gun and are paying for it.

The fear of gyno screwed with your head and caused you to make rash decision to start anastrozole.

Live and learn.

In my experience, 0.050 anastrozole at a tenth of that dose can crush my E2 levels. Response to anastrozole comes down to individual tolerance.

 

[JCUSN]

This is either a self fulfilling prophecy (mindfu**** yourself) or you indeed crushed your E2 levels. In either case, the result is the same,, you screwed yourself either way.


This is to be expected starting out on any hormone therapy, you jumped the gun and are paying for it.

The fear of gyno screwed with your head and caused you to make rash decision to start anastrozole.

Live and learn.

In my experience, 0.050 anastrozole at a tenth of that dose can crush my E2 levels. Response to anastrozole comes down to individual tolerance.

These were symptoms I was experiencing BEFORE I took the .25mg anastrozole. I took the .25mg about an hour ago. I don’t really feel any different.

I took anastrozole years ago while on a full TRT protocol and it didn’t crash me. So I don’t think I’m any sort of hyper-responder…but that’s when I was on a full TRT protocol.

 

[Seagal]

I’m on HCG monotherapy. Mostly for fertility, but also loving the testosterone boost.

My doctor decided to put me on 1000iu 3x per week.

I started feeling sensitive (not painful) nipples. They aren’t sore, they’re just sensitive and they’re very hard often. No tissue growth.
I also noticed my penis not being as “full” as usual, even though I take daily 5mg Cialis. It just appears shriveled a bit.

I just took a .25mg Arimidex (1mg pill split into 4 pieces with pill cutter).

I know this might sound crazy, but there’s no way that single dose would crash my E2 right? I took labs yesterday, but no results yet, and I was foolish and jumped the gun taking the .25mg dose. Will I be fine, or did I screw myself?

I bet you didn't crash your E2, whatever that means. Looking forward to your lab results!

 

[JCUSN]

I bet you didn't crash your E2, whatever that means. Looking forward to your lab results!

You don’t know what it means to crash one’s E2??

Looking forward to my labs coming back too!

 

[Seagal]

You don’t know what it means to crash one’s E2??

Looking forward to my labs coming back too!

I meant there is hysteria about this. Some men seem to be very sensitive to it. I once made an experiment with anastrozol with my E2 result at 13 and I still felt well. And I could feel the effects of anastrozol increasing and decreasing.
How do you feel? Observe Analyse ....

 

[JCUSN]

I meant there is hysteria about this. Some men seem to be very sensitive to it. I once made an experiment with anastrozol with my E2 result at 13 and I still felt well. And I could feel the effects of anastrozol increasing and decreasing.
How do you feel? Observe Analyse ....

Well, I only took the .25mg a couple hours ago. So far I feel totally fine. If anything, my nipples feel “sensitive” again lol. But could be nothing.

 

[Systemlord]

These were symptoms I was experiencing BEFORE I took the .25mg anastrozole. I took the .25mg about an hour ago. I don’t really feel any different.

For some, there is a delayed response in the lowering of estrogen and feeling the effects of low estrogen. You could say the same for testosterone.

 

[Seagal]

Well, I only took the .25mg a couple hours ago. So far I feel totally fine. If anything, my nipples feel “sensitive” again lol. But could be nothing.

Relax and expect the ana can only improve your nipples.

 

[JCUSN]

For some, there is a delayed response in the lowering of estrogen and feeling the effects of low estrogen. You could say the same for testosterone.

After doing a bit more reading…it seems adex only goes after “aromataze enzyme.” So does that mean it doesn’t actually reduce my current E2 in my body? The way I read it, it will only prevent further production of E2, not diminish the current E2. Is that correct, or am I totally misunderstanding?

 

[Systemlord]

After doing a bit more reading…it seems adex only goes after “aromataze enzyme.” So does that mean it doesn’t actually reduce my current E2 in my body?

The majority of estrogen comes from aromatase enzymes. So by blocking aromatase enzymes, your estrogen will decrease.

You're creating some estrogen within the testicles using hCG.

 

[BadassBlues]

It's never a good idea to take an AI if you're not on TRT. By disabling the enzyme, you are preventing the conversion of the substrate to the product (Testosterone to Estradiol / Androstenedione to Estrone). No conversion, no estrogen. TRT provides enough of the substrate to replenish the product after the AI has been eliminated (around 50 hours). It takes significantly more time to regain estrogen balance after an AI if you are relying on natural, or even HCG induced testosterone levels.

Function​

[edit]
Aromatase is localized in the endoplasmic reticulum where it is regulated by tissue-specific promoters that are in turn controlled by hormones, cytokines, and other factors. It catalyzes the last steps of estrogen biosynthesis from androgens (specifically, it transforms androstenedione to estrone and testosterone to estradiol). These steps include three successive hydroxylations of the 19-methyl group of androgens, followed by simultaneous elimination of the methyl group as formate and aromatization of the A-ring.

Pharmacokinetics/Pharmacodynamics (Arimidex)​

Absorption​

Well absorbed; extent of absorption not affected by food

Metabolism​

Extensively hepatic (~85%) via N-dealkylation, hydroxylation, and glucuronidation; primary metabolite (triazole) inactive

Excretion​

Feces; urine (urinary excretion accounts for ~10% of total elimination, mostly as metabolites)

Onset of Action​

Onset of estradiol reduction: 70% reduction after 24 hours; 80% after 2 weeks of therapy

Time to Peak​

Plasma: ~2 hours without food; 5 hours with food

Duration of Action​

Duration of estradiol reduction: 6 days

Half-Life Elimination​

~50 hours


In the end however, you will bounce back. And as Systemlord stated above, lesson learned...

You might consider adding DIM to your protocol.

 

[JCUSN]

It's never a good idea to take an AI if you're not on TRT. By disabling the enzyme, you are preventing the conversion of the substrate to the product (Testosterone to Estradiol / Androstenedione to Estrone). No conversion, no estrogen. TRT provides enough of the substrate to replenish the product after the AI has been eliminated (around 50 hours). It takes significantly more time to regain estrogen balance after an AI if you are relying on natural, or even HCG induced testosterone levels.

Function​

[edit]
Aromatase is localized in the endoplasmic reticulum where it is regulated by tissue-specific promoters that are in turn controlled by hormones, cytokines, and other factors. It catalyzes the last steps of estrogen biosynthesis from androgens (specifically, it transforms androstenedione to estrone and testosterone to estradiol). These steps include three successive hydroxylations of the 19-methyl group of androgens, followed by simultaneous elimination of the methyl group as formate and aromatization of the A-ring.

Pharmacokinetics/Pharmacodynamics (Arimidex)​

Absorption​

Well absorbed; extent of absorption not affected by food

Metabolism​

Extensively hepatic (~85%) via N-dealkylation, hydroxylation, and glucuronidation; primary metabolite (triazole) inactive

Excretion​

Feces; urine (urinary excretion accounts for ~10% of total elimination, mostly as metabolites)

Onset of Action​

Onset of estradiol reduction: 70% reduction after 24 hours; 80% after 2 weeks of therapy

Time to Peak​

Plasma: ~2 hours without food; 5 hours with food

Duration of Action​

Duration of estradiol reduction: 6 days

Half-Life Elimination​

~50 hours


In the end however, you will bounce back. And as Systemlord stated above, lesson learned...

You might consider adding DIM to your protocol.

Is this really saying that it reduces estradiol by 70% after just 24 hours? So if you have an E2 of 20, and you take .25mg of adex, you’ll have an E2 of only 6? That can’t be correct.

 

[BadassBlues]

Is this really saying that it reduces estradiol by 70% after just 24 hours? So if you have an E2 of 20, and you take .25mg of adex, you’ll have an E2 of only 6? That can’t be correct.

Those are the actual pharmacokinetics of the drug. And yes, you could crash your estrogen down to 6. At one-point years ago when I was taking Arimidex daily, my E2 labs showed a level of 6 at one point. That prompted me to lower the dose and dosing schedule. I stopped using AI's a long time ago. I now take DIM to balance my estrogens.

 

[JCUSN]

Those are the actual pharmacokinetics of the drug. And yes, you could crash your estrogen down to 6. At one-point years ago when I was taking Arimidex daily, my E2 labs showed a level of 6 at one point. That prompted me to lower the dose and dosing schedule. I stopped using AI's a long time ago. I now take DIM to balance my estrogens.

But I’ve taken one single dose…one…of .25mg. You said you were taking it daily. Doesn’t that make a big difference? I’ve taken one single dose of .25mg, and I’m not taking another.

I will def research more on DIM instead!
Do you have a recommended dose?

 

[BadassBlues]

But I’ve taken one single dose…one…of .25mg. You said you were taking it daily. Doesn’t that make a big difference? I’ve taken one single dose of .25mg, and I’m not taking another.

I will def research more on DIM instead!

Absolutely. The dosage and frequency definitely have to be factored in. I just wanted to show the actual facts of the drug and the mechanism of action as that seemed to be in question. I highly doubt you are going to feel any ill effects of a single .25 dose.

As to DIM, DIM works differently and has more of a balancing effect on all estrogens. In men it has a very positive effect on prostate health. It also has an effect on the less desirable estrogens. Most people are aware of the 3 basic estrogen types, Estradiol, Estrone and Estriol. There are just a few more than that:

Estrogen
Estradiol (E2)	100	506 ± 20	+++	12–19	100
Estrone (E1)	11 ± 8	490 ± 22	+++	?	20
Estriol (E3)	10 ± 4	468 ± 30	+++	8–18	3
Estetrol (E4)	0.5 ± 0.2	?	Inactive	?	1
17α-Estradiol	4.2 ± 0.8	?	?	?	?
2-Hydroxyestradiol	24 ± 7	285 ± 8	+b	31–61	28
2-Methoxyestradiol	0.05 ± 0.04	101	Inactive	?	130
4-Hydroxyestradiol	45 ± 12	?	?	?	?
4-Methoxyestradiol	1.3 ± 0.2	260	++	?	9
4-Fluoroestradiola	180 ± 43	?	+++	?	?
2-Hydroxyestrone	1.9 ± 0.8	130 ± 9	Inactive	110–142	8
2-Methoxyestrone	0.01 ± 0.00	103 ± 7	Inactive	95–100	120
4-Hydroxyestrone	11 ± 4	351	++	21–50	35
4-Methoxyestrone	0.13 ± 0.04	338	++	65–92	12
16α-Hydroxyestrone	2.8 ± 1.0	552 ± 42	+++	7–24	<0.5
2-Hydroxyestriol	0.9 ± 0.3	302	+b	?	?
2-Methoxyestriol	0.01 ± 0.00	?	Inactive	?	4

Multiple therapeutic and preventive effects of 3,3′-diindolylmethane on cancers including prostate cancer and high grade prostatic intraepithelial neoplasia - PMC

Cruciferous vegetables belong to the plant family that has flowers with four equal-sized petals in the pattern of a crucifer cross. These vegetables are an abundant source of dietary phytochemicals, including glucosinolates and their hydrolysis ...

www.ncbi.nlm.nih.gov

DIM has effects on estrogen in two ways: affecting estrogen metabolism and regulating ER activity. For its metabolic effects, DIM can increase the conversion of E2 into 2-hydroxyestrone (2-OHE), a “good” estrogenic metabolite with anti-estrogenic and anti-proliferative properties[79],[80] while decreasing the conversion of E2 into 4-hydroxyestrone (4-OHE) or 16-α-hydroxyestrone (16-α-OHE), both “bad” estrogenic metabolites that can increase cell proliferation[80]. DIM also increases urinary 16-α-OHE levels in postmenopausal women[78]. For its effects on ER, DIM can inhibit the transcription of estrogen-responsive genes stimulated by E2, and increase ERα protein degradation [40],[45],[82].

DIM's effects on androgen, androgen receptor (AR) and prostate-specific antigen (PSA)​

The male sex hormones, androgens mainly including testosterone and DHT, mediate their effects by binding to AR, forming androgen-receptor complex in cytoplasm and then translocating into the nucleus. The complex in the nucleus then binds to a DNA segment in androgen-responsive genes, the androgen response element, to regulate gene transcription. By turning the genes on or off, androgen and AR help direct the development of male sexual characteristics. In prostate cancer, androgen and AR are critical in oncogenesis and cancer growth[35],[59],[73],[75].

It has been shown in in vitro[29],[31]-[33] and in vivo studies[26],[57] that DIM has an anti-androgen effect which downregulates AR and PSA. In androgen-dependent LNCaP cells, DIM suppresses cell proliferation, inhibits DHT stimulation of DNA synthesis and endogenous PSA transcription and suppresses androgen-induced AR translocation into the nucleus[81]. Similar effects of DIM were observed in PC-3 cells only when these cells were co-transfected with a wild-type androgen receptor expression plasmid[82].

DIM results in cell cycle arrest in androgen-sensitive LNCaP cells and androgen-insensitive C4-2B cells not only by affecting cell cycle regulatory molecules including cdks and their inhibitors but also by downregulating AR[31]. In the same cell lines, DIM was found to promote cell cycle arrest and cause apoptosis that may be associated with effects on Akt and AR signaling pathways by affecting Akt/FOXO3a/GSK-3β/β-catenin signaling[46]. In a separate study, the same research group found that B-DIM's anti-androgenic effects were associated with inhibition of AR phosphorylation, AR expressions and AR nuclear translocation, leading to the down-regulation of AR target genes[32]. The anti-androgen effect from DIM is not associated with prostate cancer cell's androgen status[29]. The results of structural modeling studies showed that DIM is remarkably similar in conformational geometry and surface charge distribution to an established synthetic AR antagonist[81]. These observations provide rationales for DIM in treating hormone-sensitive, but more importantly hormone-refractory prostate cancer by using DIM alone or combining with other therapeutics[3

 

[JCUSN]

Absolutely. The dosage and frequency definitely have to be factored in. I just wanted to show the actual facts of the drug and the mechanism of action as that seemed to be in question. I highly doubt you are going to feel any ill effects of a single .25 dose.

As to DIM, DIM works differently and has more of a balancing effect on all estrogens. In men it has a very positive effect on prostate health. It also has an effect on the less desirable estrogens. Most people are aware of the 3 basic estrogen types, Estradiol, Estrone and Estriol. There are just a few more than that:

Estrogen
Estradiol (E2)	100	506 ± 20	+++	12–19	100
Estrone (E1)	11 ± 8	490 ± 22	+++	?	20
Estriol (E3)	10 ± 4	468 ± 30	+++	8–18	3
Estetrol (E4)	0.5 ± 0.2	?	Inactive	?	1
17α-Estradiol	4.2 ± 0.8	?	?	?	?
2-Hydroxyestradiol	24 ± 7	285 ± 8	+b	31–61	28
2-Methoxyestradiol	0.05 ± 0.04	101	Inactive	?	130
4-Hydroxyestradiol	45 ± 12	?	?	?	?
4-Methoxyestradiol	1.3 ± 0.2	260	++	?	9
4-Fluoroestradiola	180 ± 43	?	+++	?	?
2-Hydroxyestrone	1.9 ± 0.8	130 ± 9	Inactive	110–142	8
2-Methoxyestrone	0.01 ± 0.00	103 ± 7	Inactive	95–100	120
4-Hydroxyestrone	11 ± 4	351	++	21–50	35
4-Methoxyestrone	0.13 ± 0.04	338	++	65–92	12
16α-Hydroxyestrone	2.8 ± 1.0	552 ± 42	+++	7–24	<0.5
2-Hydroxyestriol	0.9 ± 0.3	302	+b	?	?
2-Methoxyestriol	0.01 ± 0.00	?	Inactive	?	4

Multiple therapeutic and preventive effects of 3,3′-diindolylmethane on cancers including prostate cancer and high grade prostatic intraepithelial neoplasia - PMC

Cruciferous vegetables belong to the plant family that has flowers with four equal-sized petals in the pattern of a crucifer cross. These vegetables are an abundant source of dietary phytochemicals, including glucosinolates and their hydrolysis ...

www.ncbi.nlm.nih.gov

DIM has effects on estrogen in two ways: affecting estrogen metabolism and regulating ER activity. For its metabolic effects, DIM can increase the conversion of E2 into 2-hydroxyestrone (2-OHE), a “good” estrogenic metabolite with anti-estrogenic and anti-proliferative properties[79],[80] while decreasing the conversion of E2 into 4-hydroxyestrone (4-OHE) or 16-α-hydroxyestrone (16-α-OHE), both “bad” estrogenic metabolites that can increase cell proliferation[80]. DIM also increases urinary 16-α-OHE levels in postmenopausal women[78]. For its effects on ER, DIM can inhibit the transcription of estrogen-responsive genes stimulated by E2, and increase ERα protein degradation [40],[45],[82].

DIM's effects on androgen, androgen receptor (AR) and prostate-specific antigen (PSA)​

The male sex hormones, androgens mainly including testosterone and DHT, mediate their effects by binding to AR, forming androgen-receptor complex in cytoplasm and then translocating into the nucleus. The complex in the nucleus then binds to a DNA segment in androgen-responsive genes, the androgen response element, to regulate gene transcription. By turning the genes on or off, androgen and AR help direct the development of male sexual characteristics. In prostate cancer, androgen and AR are critical in oncogenesis and cancer growth[35],[59],[73],[75].

It has been shown in in vitro[29],[31]-[33] and in vivo studies[26],[57] that DIM has an anti-androgen effect which downregulates AR and PSA. In androgen-dependent LNCaP cells, DIM suppresses cell proliferation, inhibits DHT stimulation of DNA synthesis and endogenous PSA transcription and suppresses androgen-induced AR translocation into the nucleus[81]. Similar effects of DIM were observed in PC-3 cells only when these cells were co-transfected with a wild-type androgen receptor expression plasmid[82].

DIM results in cell cycle arrest in androgen-sensitive LNCaP cells and androgen-insensitive C4-2B cells not only by affecting cell cycle regulatory molecules including cdks and their inhibitors but also by downregulating AR[31]. In the same cell lines, DIM was found to promote cell cycle arrest and cause apoptosis that may be associated with effects on Akt and AR signaling pathways by affecting Akt/FOXO3a/GSK-3β/β-catenin signaling[46]. In a separate study, the same research group found that B-DIM's anti-androgenic effects were associated with inhibition of AR phosphorylation, AR expressions and AR nuclear translocation, leading to the down-regulation of AR target genes[32]. The anti-androgen effect from DIM is not associated with prostate cancer cell's androgen status[29]. The results of structural modeling studies showed that DIM is remarkably similar in conformational geometry and surface charge distribution to an established synthetic AR antagonist[81]. These observations provide rationales for DIM in treating hormone-sensitive, but more importantly hormone-refractory prostate cancer by using DIM alone or combining with other therapeutics[3

Fantastic info and fantastic news I likely won’t feel ill effects on my dose.

One thing though…does it matter than I’m on HCG only? I read that the E2 levels raised by HCG are “different” than by testosterone. I couldn’t make much sense out of it.

I will certainly be getting some DIM tomorrow to take along with my HCG monotherapy.

 

[BadassBlues]

Fantastic info and fantastic news I likely won’t feel ill effects on my dose.

One thing though…does it matter than I’m on HCG only? I read that the E2 levels raised by HCG are “different” than by testosterone. I couldn’t make much sense out of it.

I will certainly be getting some DIM tomorrow to take along with my HCG monotherapy.

The simple answer is that HCG is an LH analog and stimulates the testes to make testosterone.

TRT is the process of putting an exogenous substance (exogenous)
into a body.

The difference is that HCG stimulates your own testosterone production and TRT by means of injection, topical and now oral route bypasses that process and is given directly into the body to utilize.

That is a very short and basic answer, if you want more details, please let me know.

 

[JCUSN]

The simple answer is that HCG is an LH analog and stimulates the testes to make testosterone.

TRT is the process of putting an exogenous substance (exogenous)
into a body.

The difference is that HCG stimulates your own testosterone production and TRT by means of injection, topical and now oral route bypasses that process and is given directly into the body to utilize.

That is a very short and basic answer, if you want more details, please let me know.

So does a compound like adex or DIM still help to lower E2 if that E2 is generated by means of HCG monotherapy? Or do those compounds only address E2 if the E2 spikes were caused by exogenous testosterone injections?

 

[Belekas]

I had a bottle of DIM long time but never used it. Yesterday popped 100mg. What dose you on @BadassBlues ? How long u've been on? Also no hair shedding as I've read some folks get that. Im not on TRT but interested in its effects.