Does Arimidex decrease estrone levels?

[maxzax]

Hey Guys,

Im wondering what the best way to combat overall estrogens would be. I tried 6-OXO and crashed after a week of using it. From the trials I've seen I think it only blocks the conversation from E1 (Estrone) to E2, thus increasing E1 significantly. That might of led to my system being worse off, due to the increase Estrone.

Does anyone know if 6-OXO raises LH levels, I've seen claims that in raises LH levels, but never any proof that it does.

The main reason Im looking for a aromatese inhibitor is my E2 is at 59 range of 10 -50, I am hopping if I could lower my E2 and over E levels lowered, I could get my pituitary working properly again.

Does anyone know if arimidex will decreases Estrone levels as well as Estradiol Levels?

Here's an interesting diagram of the hormone conversation process.

http://www.ceri.com/q_v7n2q3.htm

THanks
Max!!!

 

[jboldman]

of course

jb

 

[Millard]

Here's an interesting diagram of the hormone conversation process.

http://www.ceri.com/q_v7n2q3.htm

I'm not an 'arborist' or whatever you call those guys. But that is the most beautiful tree that I've ever seen

 

[jboldman]

I agree, whoever put that together deserves a medal!

jb

 

[maxzax]

Have you seen any studies or links you can provide me that show arimidex reduces estrone levels as well as estradiol, I been searching all over without much luck.

Thank you!!!
Max

of course

jb

 

[jboldman]

As you can see from that beautiful tree illustration, estrone only has two pathways with the major pathway being from estradiol via testosterone and the aromatase enzyme. Once the estradiol is reduced there would be a commensurate reduction in estrone. In post menopausal women a primary source of estrogen is via the aromatase pathway and arimidex reduces plasma estrone/estradiol by large numbers. Here is a study done on post-menopausal women were estrone was reduced by 81%.

jb

=================

J Clin Oncol. 2002 Feb 1;20(3):751-7. Related Articles, Links


Comment in:
J Clin Oncol. 2002 Jul 1;20(13):3039-40; author reply 3040.

Influence of letrozole and anastrozole on total body aromatization and plasma estrogen levels in postmenopausal breast cancer patients evaluated in a randomized, cross-over study.

Geisler J, Haynes B, Anker G, Dowsett M, Lonning PE.

Department of Oncology, Haukeland University Hospital, Bergen, Norway.

PURPOSE: To compare the effects of the two novel, potent, nonsteroidal aromatase inhibitors anastrozole and letrozole on total-body aromatization and plasma estrogen levels. PATIENTS AND METHODS: Twelve postmenopausal women with estrogen receptor-positive, metastatic breast cancer were treated with anastrozole 1 mg orally (PO) and letrozole 2.5 mg PO once daily, each given for a time interval of 6 weeks in a randomized sequence. Total-body aromatization was determined before treatment and at the end of each treatment period using a dual-label isotopic technique involving isolation of the metabolites with high-performance liquid chromatography. Plasma levels of estrone (E(1)), estradiol (E(2)), and estrone sulfate (E(1)S) were determined in samples obtained before each injection using highly sensitive radioimmunoassays. RESULTS: Pretreatment aromatase levels ranged from 1.68% to 4.27%. On-treatment levels of aromatase were detectable in 11 of 12 patients during treatment with anastrozole (mean percentage inhibition in the whole group, 97.3%) but in none of the 12 patients during treatment with letrozole (> 99.1% suppression in all patients; Wilcoxon, P =.0022, comparing the two drug regimens). Treatment with anastrozole suppressed plasma levels of E(1), E(2), and E(1)S by a mean of 81.0%, 84.9%, and 93.5%, respectively, whereas treatment with letrozole caused a corresponding decrease of 84.3%, 87.8% and 98.0%, respectively. The suppression of E(1) and E(1)S was found to be significantly better during treatment with letrozole compared with anastrozole (P =.019 and.0037, respectively). CONCLUSION: This study revealed letrozole (2.5 mg once daily) to be a more potent suppressor of total-body aromatization and plasma estrogen levels compared with anastrozole (1 mg once daily) in postmenopausal women with metastatic breast cancer.

 

[SWALE]

OOOHHHH! That IS a nice picture! It makes my heart go pitter-patter.

Unfortunately, we cannot extrapolate hormonal studies performed on females to males.

Here is what I have seen in my clinical practice: I lower Estradiol levels with Arimidex, to mid range. But Total Estrogens go up, sometimes to 50% over the top of their collective physiological range. Since Estradiol is going down, that means Estrone and/or Estriol is going up even more. I have not gathered enough labs to figure this out yet, but am working on it.

Analysis of the metabolic pathways would make one think this could not be true, as an AI inhibits both the conversion of Testosterone to Estradiol, AND androstenedione to Estrone. Also, the conversion of Estrone to Estradiol must be inhibited as well, because, as I have said, estradiol is going down while the rest are elevating. But obvioulsy the body is not willing to be ruled by intuitive thought from a lovely picture of the metabolic pathways.

I have never heard anyone else state what I just did, so do not know anyone I could go to for the purpose of comparing notes.

 

[jboldman]

Those are interesting results, perhaps shbg is lowered. Clearly arimidex decreases overall estradiol and clearly reducing estradiol must lead to lowered levels of estrone.
Here is a study done on 60 MEN on trt demonstarting a reduced level of estradiol after receiving arimidex.

jb

====================

Neurology. 2005 Jan 25;64(2):290-6. Related Articles, Links


The role of aromatization in testosterone supplementation: effects on cognition in older men.

Cherrier MM, Matsumoto AM, Amory JK, Ahmed S, Bremner W, Peskind ER, Raskind MA, Johnson M, Craft S.

Department of Psychiatry and Behavioral Sciences, University of Washington Medical School, Seattle, WA, USA. cherrier@u.washington.edu.

OBJECTIVE: To determine the contribution of conversion of testosterone (T) to estradiol on cognitive processing in a population of healthy older men who received T supplementation. METHODS: Sixty healthy, community-dwelling volunteers aged 50 to 90 years completed a randomized, double-blind, placebo-controlled study. Participants were randomized to receive weekly IM injections of 100 mg T enanthate plus daily oral placebo pill (T group, n = 20), 100 mg testosterone enanthate plus 1 mg daily of anastrozole, an aromatase inhibitor (oral pill), to block the conversion of T to estradiol (AT group, n = 19), or saline injection and placebo pill (placebo group, n = 21) for 6 weeks. Cognitive evaluations using a battery of neuropsychological tests were conducted at baseline, week 3 and week 6 of treatment, and after 6 weeks of washout. RESULTS: Circulating total T was increased from baseline an average of 238% in the T and AT treatment groups. Estradiol increased an average of 81% in the T group and decreased 50% in the AT group during treatment. Significant improvements in spatial memory were evident in the AT and T treatment groups. However, only the group with elevated estradiol levels (T group) demonstrated significant verbal memory improvement. CONCLUSION: In healthy older men, improvement in verbal memory induced by testosterone administration depends on aromatization of testosterone to estradiol, whereas improvement in spatial memory occurs in the absence of increases in estradiol.

 

[SWALE]

Thank you for that post, jb. I am adding it to my collection.

To address your particular point, if SHBG levels decrease, then all the E's would as well. I have lab printout after lab printout, from different labs around the country, so the result could not be the result of lab error. It is a real head scratcher, and surely complicates things for me and my patients.

Of note, the men who participated in this study were not reported to be hypogonadal.

I have never prescribed a full mg of Arimidex QD to any TRT patient. That resultant E levels would be too low to be healthy in the study group using the AI.

There is a lot of value in this study, though, as I see it. For instance, that is a whalloping increase in E at 100mg per week of TE. It also backs up why I use, usually, only 0.25mg EOD or ETD of Arimidex.

I got some hoots out of a crowd of docs when I delivered the very first lecture ever on hypogonadism at last year's Michigan Osteopathic Association Annual Convention, as I showed a couple of studies which relate males' superior spatial abilities ("except when determining the need to stop for directions") and females' superior verbal fluency skills ("well, they get much more practice at it"). Yup, I got away with saying that.

 

[jboldman]

 

[Endocrine_Supply]

Hey

How does Letrozole fall into this debacle? -ES

 

[maxzax]

Hi Swale and All,

It would be nice if you could figure out what exactly happens when arimidex is used. Does it only prevent the converstaion of E2 to E1 or does it block the conversation of Testosterone to E1 and E2.

What methods can be used to lower over Estrogen levels, or would elevated estrogen levels even be an issue when E2 is reduced?

My system crashed while using 6-OXO, which I believe only blocks the conversation from E1 to E2, so I was thinking of giving Arimidex a try.

Thanks!!!

OOOHHHH! That IS a nice picture! It makes my heart go pitter-patter.

Unfortunately, we cannot extrapolate hormonal studies performed on females to males.

Here is what I have seen in my clinical practice: I lower Estradiol levels with Arimidex, to mid range. But Total Estrogens go up, sometimes to 50% over the top of their collective physiological range. Since Estradiol is going down, that means Estrone and/or Estriol is going up even more. I have not gathered enough labs to figure this out yet, but am working on it.

Analysis of the metabolic pathways would make one think this could not be true, as an AI inhibits both the conversion of Testosterone to Estradiol, AND androstenedione to Estrone. Also, the conversion of Estrone to Estradiol must be inhibited as well, because, as I have said, estradiol is going down while the rest are elevating. But obvioulsy the body is not willing to be ruled by intuitive thought from a lovely picture of the metabolic pathways.

I have never heard anyone else state what I just did, so do not know anyone I could go to for the purpose of comparing notes.

 

[jboldman]

just look at the pretty tree, arimidex prevents the conversion of testosterone to estradiol, the rest should be clear.

jb

 

[SWALE]

Arimidex also prevents the conversion of androstenedione to estrone.

That is what is so puzzling. Why is it, if we are inhibiting the production of estrogens, and as demonstrated by lowered Estradiol levels, Total E's can remain at 50% over the top of physiological range??

 

[snipe]

My estrone went from 23 to 104 afer discontinuing Arimidex. (0.25mg. 3x/week)

Estradiol went from 12 to 52 but is not valid since the latter value was not obtained using the extraction method. (I will retest soon.)

My total E's went down form 180 to 100 after several weeks of I3C @400mg/day, and remained at 100 after discontinuing Arimidex.

I intend to stay off Adex, remain on I3C, and retest in about 6 weeks.

 

[jboldman]

Swale, are your tests showing this increase over a long period of time or short range? I believe that shbg is lowered by hcg and perhaps that would explain a short term increase.

jb

 

[SWALE]

I have never read anything with HCG and SHBG in the same sentence. Can you find what you read?

If SHBG goes down, so do total hormone levels.

 

[Millard]

I have never read anything with HCG and SHBG in the same sentence. Can you find what you read?

If SHBG goes down, so do total hormone levels.

I don't think hormone levels are directly related to SHBG.

If SHBG goes down, then free or active hormone levels go up. Which is why so many bodybuilders take drugs that bind to SHBG such as proviron and avoid supplements that purportedly increase SHBG such as soy isoflavones.

I don't know about HCG??

 

[Millard]

I don't think hormone levels are directly related to SHBG.

If SHBG goes down, then free or active hormone levels go up. Which is why so many bodybuilders take drugs that bind to SHBG such as proviron and avoid supplements that purportedly increase SHBG such as soy isoflavones.

I don't know about HCG??

One abstract that shows no change in SHBG in response to HCG...

Clin Endocrinol (Oxf). 1990 Feb;32(2):165-75.Related Articles, Links

[size=+1]Serum forms of testosterone in men after an hCG stimulation: relative increase in non-protein bound forms.[/size]

Cooke RR, McIntosh RP, McIntosh JG, Delahunt JW.

Department of Obstetrics and Gynaecology, Wellington School of Medicine, University of Otago, New Zealand.

A postulated function of steroid binding proteins in serum is to smooth changes in steroid levels. To test this, testosterone levels in six normal men were increased by injecting 6000 IU hCG i.m., and changes in serum forms of testosterone were measured. Blood was collected every 10 min for 2.5 h and then once a day for 4 days. By day 4 the mean serum testosterone level had risen to 178% +/- 13% (SEM) of a mean basal level (first five samples). This rise was less than that in free testosterone (221% +/- 18%), which was in turn less than the rise in the non-SHBG-bound fraction (255% +/- 19%). The concentrations of SHBG and albumin were constant. Thus, two putative bioactive fractions of testosterone, the free and non-SHBG-bound, increased to a greater extent than did total testosterone. Because the binding protein concentrations were constant, this implies they may act not as a buffer, but as an enhancer of active testosterone over this time interval.

 

[Millard]

Prepubertal boys show a decrease in SHBG in response to HCG - the researchers attribute it to increase in androgen levels.


Acta Endocrinol (Copenh). 1985 Jul;109(3):423-7.

[size=+1]Decrease in serum sex hormone binding globulin during human chorionic gonadotrophin stimulation in prepubertal boys.[/size]

Dunkel L.

Temporal relationships between steroidogenic and sex hormone binding globulin (SHBG) responses to hCG were studied in 27 prepubertal boys: 19 with incomplete testicular descent and 8 with hypogonadotrophic hypogonadism (HH). Nine of the boys with incomplete testicular descent were given a single im injection of hCG and blood samples were taken daily for 5 days. Six of them showed a slight decrease in SHBG concentration by day 5. All the other 18 boys were given four im injections of hCG on days 0, 4, 7 and 10. Blood was taken before each injection and on day 14. In the boys with incomplete testicular descent SHBG concentration decreased by day 14 (P less than 0.01). All the boys with HH had an impaired testosterone response to hCG, and SHBG levels did not decrease after hCG. In only 2 of these boys SHBG concentrations were greater than 10% below the basal by day 14. These boys, however, also had the highest testosterone responses of their group. Thus it appears that if testosterone increases in prepubertal boys, SHBG decreases.