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Aromasin experiences?

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The recent research onthis compound suggests that it does not negatively impact igf-1 levels or cholesterol. I'm curious about everyone's experiences with it, and the cost the benefits ratio when compaired to letrozol.
 
O ordered some from P n' P my last cycle when I had gyno problems and saw zero results with it. Surprisingly, as I think P n' P is a good company. My advice is try and get the real shit or some generics, and skip the liquied versions.
 
Good Broly, I would assume the "Recent Study" to which you refer had women as the test subjects. In refering to the male population, I would hazard a guess that since 85% to 95% whole body aromatization suppression is achieved, in men, that would greatly impact cholesterol levels since cholesterol is so important in maintaining our proper levels. I may be shooting blanks here, but I'd still be concerned with my cholesterol levels.

PART OF PRODUCT INSERT WITH SOME IMPLICATIONS FOR BB'ers
Pharmacodynamics

Effect on Estrogens:
Multiple doses of exemestane ranging from 0.5 to 600 mg/day were administered to postmenopausal women with advanced breast cancer. Plasma estrogen (estradiol, estrone, and estrone sulfate) suppression was seen starting at a 5-mg daily dose of exemestane, with a maximum suppression of at least 85% to 95% achieved at a 25-mg dose. Exemestane 25 mg daily reduced whole body aromatization (as measured by injecting radiolabeled androstenedione) by 98% in postmenopausal women with breast cancer. After a single dose of exemestane 25 mg, the maximal suppression of circulating estrogens occurred 2 to 3 days after dosing and persisted for 4 to 5 days.

Effect on Corticosteroids:
In multiple-dose trials of doses up to 200 mg daily, exemestane selectivity was assessed by examining its effect on adrenal steroids. Exemestane did not affect cortisol or aldosterone secretion at baseline or in response to ACTH at any dose. Thus, no glucocorticoid or mineralocorticoid replacement therapy is necessary with exemestane treatment.

Other Endocrine Effects:
Exemestane does not bind significantly to steroidal receptors, except for a slight affinity for the androgen receptor (0.28% relative to dihydrotestosterone). The binding affinity of its 17-dihydrometabolite for the androgen receptor, however, is 100-times that of the parent compound. Daily doses of exemestane up to 25 mg had no significant effect on circulating levels of testosterone, androstenedione, dehydroepiandrosterone sulfate, or 17-hydroxy-progesterone. Increases in testosterone and androstenedione levels have been observed at daily doses of 200 mg or more. A dose-dependent decrease in sex hormone binding globulin (SHBG) has been observed with daily exemestane doses of 2.5 mg or higher. Slight,
nondose-dependent increases in serum lutenizing hormone (LH) and follicle-stimulating hormone (FSH) levels have been observed even at low doses as a consequence of feedback at the pituitary level.

PEACE
:garza:
 
I've used aromasin at 12.5mg MWF while on 500mg test EW. My LDL didn't really change much from the pre-cycle levels, my HDL went from 74 to 46. My estradiol fell to 6 pg/ml which is considerably below the reference range of 10 to 50.
 
thx9000 said:
I've used aromasin at 12.5mg MWF while on 500mg test EW. My LDL didn't really change much from the pre-cycle levels, my HDL went from 74 to 46. My estradiol fell to 6 pg/ml which is considerably below the reference range of 10 to 50.

Interesting. Which brand did you use?
 
thx9000 said:
I've used aromasin at 12.5mg MWF while on 500mg test EW. My LDL didn't really change much from the pre-cycle levels, my HDL went from 74 to 46. My estradiol fell to 6 pg/ml which is considerably below the reference range of 10 to 50.

To me it seems that HDL levels dropping from 74 to 46 is significant. It more than a 50% decrease. What happened to your LDL levels and total cholesterol?

I have read that aromasin doesn't effect your lipid profile. But if you have a significant decrease in estrogen, the lipid profile should be effected.
 
buckwheat1 said:
To me it seems that HDL levels dropping from 74 to 46 is significant. It more than a 50% decrease. What happened to your LDL levels and total cholesterol?

I have read that aromasin doesn't effect your lipid profile. But if you have a significant decrease in estrogen, the lipid profile should be effected.

To me too!

LDL went from 123 to 131. Total went from 189 to 199. Yup, E is important for keeping LDL down and HDL up. My E level was not healthy.
 
Funny, because Arimidex didn't cause my joints to hurt. But Femear did big time! And it killed my sexual desires too.
 
my personal experience was with a liquid version from a research outfit, and I found it borderline effective and therefore much less cost effective than femara
 
BodyByFinaplix said:
The recent research onthis compound suggests that it does not negatively impact igf-1 levels or cholesterol. I'm curious about everyone's experiences with it, and the cost the benefits ratio when compaired to letrozol.


I will tell you in a few weeks if you can wait. I have the Chinese generics from S.B.C. I have heard very good things about them over at VIP which is why I bought these over upjohn. That ... and the price. lol.

Here is a recent study you would probably like to see. Utler posted this a while back. The studies prior to 2004 showed mixed results. However the studies that were done recently have showed that arimidex and letrozole DO affect lipid profiles and Aromasin doesn't.

Ann Oncol. 2004 Feb;15(2):211-7. Related Articles, Links


The effect of exemestane on serum lipid profile in postmenopausal women with metastatic breast cancer: a companion study to EORTC Trial 10951, 'Randomized phase II study in first line hormonal treatment for metastatic breast cancer with exemestane or tamoxifen in postmenopausal patients'.

Atalay G, Dirix L, Biganzoli L, Beex L, Nooij M, Cameron D, Lohrisch C, Cufer T, Lobelle JP, Mattiaci MR, Piccart M, Paridaens R.

Jules Bordet Institute, Brussels, Belgium.

BACKGROUND: The impact of aromatase inhibitors (AIs) on non-cancer-related outcomes, which are known to be affected by oestrogens, has become increasingly important in postmenopausal women with hormone-dependent breast cancer. So far, data related to the effect of AIs on lipid profile in postmenopausal women is scarce. This study, as a companion substudy of an EORTC phase II trial (10951), evaluated the impact of exemestane, a steroidal aromatase inactivator, on the lipid profile of postmenopausal metastatic breast cancer (MBC) patients. PATIENTS AND METHODS: The EORTC trial 10951 randomised 122 postmenopausal breast cancer patients to exemestane (E) 25 mg (n = 62) or tamoxifen (T) 20 mg (n = 60) once daily as a first-line treatment in the metastatic setting. Exemestane showed promising results in all the primary efficacy end points of the trial (response rate, clinical benefit rate and response duration), and it was well tolerated with low incidence of serious toxicity. As a secondary end point of this phase II trial, serum triglycerides (TRG), high-density lipoprotein cholesterol (HDL), total cholesterol (TC), lipoprotein a (Lip a), and apolipoproteins (Apo) B and A1 were measured at baseline and while on therapy (at 8, 24 and 48 weeks) to assess the impact of exemestane and tamoxifen on serum lipid profiles. Of the 122 randomised patients, those who had baseline and at least one other lipid assessment are included in the present analysis. The patients who received concomitant drugs that could affect lipid profile are included only if these drugs were administered throughout the study treatment. Increase or decrease in lipid parameters within 20% of baseline were considered as non-significant and thus unchanged. RESULTS: Seventy-two patients (36 in both arms) were included in the statistical analysis. The majority of patients had abnormal TC and normal TRG, HDL, Apo A1, Apo B and Lip a levels at baseline. Neither exemestane nor tamoxifen had adverse effects on TC, HDL, Apo A1, Apo B or Lip a levels at 8, 24 and 48 weeks of treatment. Exemestane and tamoxifen had opposite effects on TRG levels: exemestane lowered while tamoxifen increased TRG levels over time. There were too few patients with normal baseline TC and abnormal TRG, HDL, Apo A1, Apo B and Lip a levels to allow for assessment of E's impact on these subsets. The atherogenic risk determined by Apo A1:Apo B and TC:HDL ratios remained unchanged throughout the treatment period in both the E and T arms. CONCLUSIONS: Overall, exemestane has no detrimental effect on cholesterol levels and the atherogenic indices, which are well-known risk factors for coronary artery disease. In addition, it has a beneficial effect on TRG levels. These data, coupled with E's excellent efficacy and tolerability, support further exploration of its potential in the metastatic, adjuvant and chemopreventive setting.
 
Mavy said:
I will tell you in a few weeks if you can wait. I have the Chinese generics from S.B.C. I have heard very good things about them over at VIP which is why I bought these over upjohn. That ... and the price. lol.

Here is a recent study you would probably like to see. Utler posted this a while back. The studies prior to 2004 showed mixed results. However the studies that were done recently have showed that arimidex and letrozole DO affect lipid profiles and Aromasin doesn't.

Ann Oncol. 2004 Feb;15(2):211-7. Related Articles, Links


The effect of exemestane on serum lipid profile in postmenopausal women with metastatic breast cancer: a companion study to EORTC Trial 10951, 'Randomized phase II study in first line hormonal treatment for metastatic breast cancer with exemestane or tamoxifen in postmenopausal patients'.

Atalay G, Dirix L, Biganzoli L, Beex L, Nooij M, Cameron D, Lohrisch C, Cufer T, Lobelle JP, Mattiaci MR, Piccart M, Paridaens R.

Jules Bordet Institute, Brussels, Belgium.

BACKGROUND: The impact of aromatase inhibitors (AIs) on non-cancer-related outcomes, which are known to be affected by oestrogens, has become increasingly important in postmenopausal women with hormone-dependent breast cancer. So far, data related to the effect of AIs on lipid profile in postmenopausal women is scarce. This study, as a companion substudy of an EORTC phase II trial (10951), evaluated the impact of exemestane, a steroidal aromatase inactivator, on the lipid profile of postmenopausal metastatic breast cancer (MBC) patients. PATIENTS AND METHODS: The EORTC trial 10951 randomised 122 postmenopausal breast cancer patients to exemestane (E) 25 mg (n = 62) or tamoxifen (T) 20 mg (n = 60) once daily as a first-line treatment in the metastatic setting. Exemestane showed promising results in all the primary efficacy end points of the trial (response rate, clinical benefit rate and response duration), and it was well tolerated with low incidence of serious toxicity. As a secondary end point of this phase II trial, serum triglycerides (TRG), high-density lipoprotein cholesterol (HDL), total cholesterol (TC), lipoprotein a (Lip a), and apolipoproteins (Apo) B and A1 were measured at baseline and while on therapy (at 8, 24 and 48 weeks) to assess the impact of exemestane and tamoxifen on serum lipid profiles. Of the 122 randomised patients, those who had baseline and at least one other lipid assessment are included in the present analysis. The patients who received concomitant drugs that could affect lipid profile are included only if these drugs were administered throughout the study treatment. Increase or decrease in lipid parameters within 20% of baseline were considered as non-significant and thus unchanged. RESULTS: Seventy-two patients (36 in both arms) were included in the statistical analysis. The majority of patients had abnormal TC and normal TRG, HDL, Apo A1, Apo B and Lip a levels at baseline. Neither exemestane nor tamoxifen had adverse effects on TC, HDL, Apo A1, Apo B or Lip a levels at 8, 24 and 48 weeks of treatment. Exemestane and tamoxifen had opposite effects on TRG levels: exemestane lowered while tamoxifen increased TRG levels over time. There were too few patients with normal baseline TC and abnormal TRG, HDL, Apo A1, Apo B and Lip a levels to allow for assessment of E's impact on these subsets. The atherogenic risk determined by Apo A1:Apo B and TC:HDL ratios remained unchanged throughout the treatment period in both the E and T arms. CONCLUSIONS: Overall, exemestane has no detrimental effect on cholesterol levels and the atherogenic indices, which are well-known risk factors for coronary artery disease. In addition, it has a beneficial effect on TRG levels. These data, coupled with E's excellent efficacy and tolerability, support further exploration of its potential in the metastatic, adjuvant and chemopreventive setting.

Thanks BRO. It looks like it's going to be exemestane for me from now on. The last cycle I used femera, my HDL went to 15mg/dl. Very un-cool.

PEACE
:garza:
 
boogersnax said:
Thanks BRO. It looks like it's going to be exemestane for me from now on. The last cycle I used femera, my HDL went to 15mg/dl. Very un-cool.

PEACE
:garza:


I am curious what other drugs were part of your cycle. Usually it is the AAS components that decimate the HDL, the anti-a's contribute to some degree by lowering estrogen, however, when dosed appropriately the estrogen still stays in a healthy physiological range and as such, the anti-a's are not the primary root cause of the HDL problem.
 
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