Re: Estradiol levels

[Guest guest]

Hi,

Hypogonadism can have many different causes, like head injury, or testicular

injury, or

some drug, or even a nasty fever or virus might do it.

It depends on your symptoms, do you have any symptoms of high estradiol, like

water

retention, bloating, sensitive nipples, hot flashes, etc....

Also that number for estradiol will continue to go up as you stay on TRT.

> Hi,

>

> I'm 26 and being treated for hypogonadism, cause is not yet know. I

> just recently had a karyotype to rule out Klinefelter's syndrome. My

> karyotype was 46,XY- normal male. I'm now going to schedule an MRI,

> to see if the cause is secondary. Since Klinefelter's is the number

> one cause for primary hypogonadism (not including the normal aging

> process), i was wondering if anyone else knows what might cause it?

> It may be idiopathic, right?

>

> ANYWAY- i'm self injecting Depo-testosterone 125 mg/ml weekly. My

> peak levels (3 days after injection) were Total- 953 (normal 189-

> 1111), Free- 273 (normal 37-240), Bioavail 561 (normal 98-615) i was

> told by me endo that " normal " ranges for testosterone were recently

> lowered.(which doesn't help me out, any...., however, my estradiol

> was

> 40 on a normal scale of 10-50. does anyone here think this is too

> high?

[Guest guest]

Hi and welcome yes your E2 Estradiol is to high are you having any problems with

ED do you still get morning wood. If not this is the high E2 doing this. You

can get it down using Indolplex/DIM but use this one it works for a lot of us

here use it.

http://www.ritecare.com/prodsheets/PHY-15336.html

Also get some Zinc/Copper and take it everyday.

http://www.myvitanet.com/zincop100cnt.html

Also ask your Dr. for Hcg do 250 IU's shot each of the two days before your T

shot. This will keep your testis working and give you a feeling of well being.

http://jcem.endojournals.org/cgi/content/abstract/90/5/2595

Your T levels are not to high you don't check T levels 3 days after a shot you

do the blood test the day you get the shot but do the test first.

You could get by on 100 mg. shots every week if your doing the Hcg also.

How do you feel. Your Dr. should not start you on T meds with out knowing why

you are low first along with and MRI you need this tested.

I will put the tests in a cut & paste below.

If you try the Indolplex/DIM get back to me and I will tell you how to take it

so you don't go to low.

pmgamer18@...

Also get the book " The Testosterone Syndrome " by Dr. Shippen.

How low were your levels before you started on TRT.

Phil

INITIAL LABWORK

Following a good Medical History, which laboratory assays should be

run as part of your initial hypogonadism workup? Following is my

list, but certainly other specialists in this area run expanded or

attenuated panels, per their experience and expertise. Of note,

there are several other tests which should be included to complete

the true comprehensive Anti-Aging Medicine workup (i.e.

homocysteine, fasting insulin, comprehensive thyroid study, etc.),

as this chapter is concerned solely with administering TRT. And as

always, the panel is tailored to the individual patient. Here they

are:

• Total Testosterone

• Bioavailable Testosterone (AKA " Free and Loosely Bound " )

• Free Testosterone (if Bioavailable T is unavailable)

• DHT

• Estradiol (specify the Extraction Method, or " sensitive " assay for

males)

• LH

• FSH

• Prolactin

• Cortisol

• Thyroid Panel

• CBC

• Comprehensive Metabolic Panel

• Lipid Profile

• PSA (if over 40)

• IGF-1 (if HGH therapy is being considered)

FOLLOW-UP LABS

Two weeks after initiating a transdermal, or five weeks after the

first IM injection:

• Total Testosterone

• Bioavailable Testosterone

• Free Testosterone (if Bioavailable T is still unavailable)

• Estradiol (specify the Extraction Method, or " sensitive " assay for

males)

• DHT (especially if patient is using a transdermal delivery system)

• FSH (3rd Generation—ultrasensitive assay this time)

• CBC

• Comprehensive Metabolic Panel

• Lipid Profile

• PSA (for more senior patients)

• IGF-1 (if GH Therapy has been initiated already)

boyyy77 <niu_guy@...> wrote:Hi,

I'm 26 and being treated for hypogonadism, cause is not yet know. I

just recently had a karyotype to rule out Klinefelter's syndrome. My

karyotype was 46,XY- normal male. I'm now going to schedule an MRI,

to see if the cause is secondary. Since Klinefelter's is the number

one cause for primary hypogonadism (not including the normal aging

process), i was wondering if anyone else knows what might cause it?

It may be idiopathic, right?

ANYWAY- i'm self injecting Depo-testosterone 125 mg/ml weekly. My

peak levels (3 days after injection) were Total- 953 (normal 189-

1111), Free- 273 (normal 37-240), Bioavail 561 (normal 98-615) i was

told by me endo that " normal " ranges for testosterone were recently

lowered.(which doesn't help me out, any...., however, my estradiol

was

40 on a normal scale of 10-50. does anyone here think this is too

high?

---------------------------------

[Guest guest]

Yes, very true, but here's the kicker:

When I was 24 my testosterone level (before HRT) was 240 on

their " normal " scale of 189-1111. I realize that the " normal " range

doesn't differentiate with specific age, and because of that 3

endocrinologists have INSISTED that I am COMPLETELY normal, despite

my

lack of facial hair and muscle mass, thin bones, and obesity in the

midsection. I mean hello, that screams hypogonadism right there!

So,

I've had 3 docs laugh in my face, the third one is treating me with

Testosterone only because he know's i'll go somewhere else if he

doesn't. SOOO-- because the docs see no problem, i am " self

diagnosing " I started with the karyotype which came back normal.

Should I do the MRI next, or what????? Someone please help me. How

do u find a doctor who cares when your bloodwork is showing you

have " normal " levels, even though they are not?

[Guest guest]

I have no use for Endo's they just are not good Dr.'s for low T. In the files

section at the home page is a file on finding a Dr. read it and tell me what

state you live in. Any Dr. will do as long as he knows about testing and

treating low T.

Go to this post number and read " My Current Best Thoughts on How To Administer

TRT for MEN- A Recipe for Success.

Message #14938 you need a Dr. like this one.

When you find a new Dr. call first and ask how many men do they treat for low T

and do they check for high E2 and if so do they use arimidex to get it down and

also if one has Secondary Hyp. do they treat it with Hcg. You will know when

you have found a good one.

Phil

boyyy77 <niu_guy@...> wrote:Yes, very true, but here's the kicker:

When I was 24 my testosterone level (before HRT) was 240 on

their " normal " scale of 189-1111. I realize that the " normal " range

doesn't differentiate with specific age, and because of that 3

endocrinologists have INSISTED that I am COMPLETELY normal, despite

my

lack of facial hair and muscle mass, thin bones, and obesity in the

midsection. I mean hello, that screams hypogonadism right there!

So,

I've had 3 docs laugh in my face, the third one is treating me with

Testosterone only because he know's i'll go somewhere else if he

doesn't. SOOO-- because the docs see no problem, i am " self

diagnosing " I started with the karyotype which came back normal.

Should I do the MRI next, or what????? Someone please help me. How

do u find a doctor who cares when your bloodwork is showing you

have " normal " levels, even though they are not?

---------------------------------

[Guest guest]

The issue is complicated because the doctors may well think they are

telling you the straight dope on low T. The problem is that the

current thinking of what is normal, or acceptable has changed a lot in

just the last few years. In my case I brought a copy of a 2002 paper

on hypogonadism to my MD. She actualy sat down and read much of it,

thanked me, took some notes and put me on androgel. I would start by

talking to your MD about your concerns, what you've learned and see

what they say. If they freak out about being caught behind the curve

just seek a new doctor. *Note levels aside a good doctor will take

into consideration your symptoms. Clearly if your in the middle of

the range or high symptoms won't matter so much. But if your low

normal and match up with lots of the symptoms she or he should act.

*My unmedical opinion.

> Yes, very true, but here's the kicker:

>

> When I was 24 my testosterone level (before HRT) was 240 on

> their " normal " scale of 189-1111. I realize that the " normal " range

> doesn't differentiate with specific age, and because of that 3

> endocrinologists have INSISTED that I am COMPLETELY normal, despite

> my

> lack of facial hair and muscle mass, thin bones, and obesity in the

> midsection. I mean hello, that screams hypogonadism right there!

> So,

> I've had 3 docs laugh in my face, the third one is treating me with

> Testosterone only because he know's i'll go somewhere else if he

> doesn't. SOOO-- because the docs see no problem, i am " self

> diagnosing " I started with the karyotype which came back normal.

> Should I do the MRI next, or what????? Someone please help me. How

> do u find a doctor who cares when your bloodwork is showing you

> have " normal " levels, even though they are not?

[Guest guest]

Are you saying that's all you use, or are you using those in

conjunction with T or HCG?

--- gin2c <no_reply > wrote:

> I use 1/2 Arimidex & 2 DIM 3 times a week. No noticable side

> effects. Lowered E2 to mid-range. " T " is in upper 1/4 of range.

>

> T:E2 ratio is 30:1 last tests. I prefer it higher. 50:1 seems great

>

> for me.

________________________________________________________________________________\

____

Need Mail bonding?

Go to the Q & A for great tips from Answers users.

http://answers./dir/?link=list & sid=396546091

[Guest guest]

Get the Arimidex and cut the 1mg. pill in half with a pill cutter then use a

single edge razor blaide to cut the halfs into 1/4's. Take 1/4 of a 1mg pill

every 3 days keep an eye out for some strong morning wood to start up. I use

this as a gauge to tell that my Estradiol is in the right level for me. Keep

taking the arimidex but if your wood stops this means you going to low. So stop

the arimidex until the wood comes back that day go back on it but do it every 5

days. I have use this gauge to keep my levels of Estradiol in the Zone and

blood work. Next time you test Estradiol do a test for men like this a

Sensitive test.

http://www.labcorp.com/datasets/labcorp/html/chapter/mono/sr012000.htm

Tom <indianawannabe04@...> wrote:

Does anyone have any comments, or can interpret qualitatively, these

results;

Tests done by Quest Diagnostics on an afternoon blood draw; on

androgel, and also 300 IU of HCG every 2-3days.

Some physicians do not trust the accuracy of the Quest testing, but;

Estrone " out of range " at 70 pg/ml vs. a reference range of < or = 68

Estradiol " out of range " at 42 pg/ml vs. a reference range of < or = 29

The numbers are a bit high, and correlate with symptoms: night sweats,

etc.

I notice a good result after 2 days of DIMS but could not tolerate the

GI problems.

I can get a prescription for Arimadex; my internist was somewhat

concerned that there would be mood swings? Does anyone have any

experience with these tests and problems at these levels?

My thanks to those of you who have written about these issues.

Regards, Tom

Co-Moderator " Don't believe anything you hear and only half of what you see. "

Phil

---------------------------------

Building a website is a piece of cake.

Small Business gives you all the tools to get online.

[Guest guest]

I don't remember what your bad reaction with arimidex was but the only one I

know of it bring down your Estradiol down to low. Most Dr.'s don't give this

out and the ones that do put men on way to high a dose of it. Most of the men

on this do well only taking .25mgs or 1/4 of a 1 mgs pill every 3 days. I and

others on the forums for low testosterone have been on this for yrs. not

problems. When I was on Indolplex/DIM and taking thyroid meds never has a

problem with the calcium in it I am on armour and it is said calcium with it

will make it not work. But my Dr. told me to take my armour and indolple/DIM at

different times so I never had a problem.

I hope you get this figured out high levels of Estradiol can mess one up.

Co-Moderator

Phil

> From: tomubl <ubl@...>

> Subject: Re: Estradiol Levels

>

> Date: Thursday, June 18, 2009, 7:57 AM

> My opinion, after a bad reaction to

> Arimidex, and after viewing all of the side effects and

> after reading tons of forums all over where women have died

> and all of the bad reactions.

>

> WE NEED AN ALTERNATIVE - WHICH TO THE BEST OF MY KNOWLEDGE

> DOESN'T EXIST.

>

> DIM treat existing E2.  BTW the Indoplex DIM everyone

> in here references is full of calcium and can bind other

> meds that you are taking.  Take the time to do a

> conflicts check and ask your GP if there is potential

> interference with any other med.

>

>

>

> > >

> > >   I am hearing that Arimidex is

> not approved for use in males and that a lot of insurance

> companies won't pay for it.  Is it expensive if I have

> to buy it on my own? 

> > >

> >

> > Arimidex is a product of Astra-Zenica and they have a

> patent on it in the US.  It is very expensive.

> >

> > Other countries (such as India) do not honor these

> patents and make a generic version, called anastrozole, and

> you can buy that online from offshore pharmacies.

> >

> > Compare these two pharmacies:  One sells the

> generic, and the other sells Astra-Zenica's patented

> version.

> >

> > http://www.alldaychemist.com/common_generic/Anastrozole.html

> >

> > http://www.inhousepharmacy.com/womens-hrt/arimidex.html

> >

>

>

>

>

> ------------------------------------

>

>

[Guest guest]

There are alternatives....got this from

http://forum.bodybuilding.com/archive/index.php/t-40724.html

Apparently Arimidex lowers iGF1 by 18% while letrozole raises it by 24%. For

muscle growth, letrozole is better...

The following 3 posts are copies of Zyglamail's posts on Elite,

3rd Generation Anti-E's

Everyone by now has heard of Arimidex/Liquidex(ie anastrozole) but there are a

couple others with slightly better estrogen suppression values as well as slight

differences in the way they affect the endocrine system.

The other two 3rd generation Anti-e's are letrozole(femara) and

exemestane(aromasin). Letrozole and anastrozole are aromatase inhibitors while

exemestane is considered an aromatase inactivator.

While all of these seem to exert an effect on our LH/FSH levels, some also have

an effect on IGF-1 levels as well. According to some studies for example,

anastrzole was shown to reduce IGF-1 levels by 18%(note 1), which is likely due

to reduced estrogen. Another abstract shows that letrozole actually increased

IGF-1 levels by an average of 24%(note 2).

Following are some detailed descriptions of the 3 products.

notes:

1. J Clin Endocrinol Metab 2000 Jul;85(7):2370-7

2. J Steroid Biochem Mol Biol 1997 Nov-Dec;63(4-6):261-7

Letrozole.

DESCRIPTION

Femara (letrozole tablets) for oral administration contain 2.5 mg of letrozole,

a nonsteroidal aromatase inhibitor (inhibitor of estrogen synthesis). It is

chemically described as 4,4'-(1H-1,2,4 -Triazol-1-ylmethylene) dibenzonitrile.

Letrozole is a white to yellowish crystalline powder, practically odorless,

freely soluble in dichloromethane, slightly soluble in ethanol, and practically

insoluble in water. It has a molecular weight of 285.31, empirical formula

C17H11N5 and a melting range of 184o C-185o C.

Femara (letrozole tablets) is available as 2.5 mg tablets for oral

administration.

Inactive Ingredients.

Colloidal silicon dioxide, ferric oxide, hydroxypropyl methylcellulose, lactose

monohydrate, magnesium stearate, maize starch, microcrystalline cellulose,

polyethylene glycol, sodium starch glycolate, talc, and titanium dioxide.

CLINICAL PHARMACOLOGY

Mechanism of Action

The growth of some cancers of the breast are stimulated or maintained by

estrogens. Treatment of breast cancer thought to be hormonally responsive (i.e.,

estrogen and/or progesterone receptor positive or receptor unknown) has included

a variety of efforts to decrease estrogen levels (ovariectomy, adrenalectomy,

hypophysectomy) or inhibit estrogen effects (antiestrogens and progestational

agents). These interventions lead to decreased tumor mass or delayed progression

of tumor growth in some women.

In postmenopausal women, estrogens are mainly derived from the action of the

aromatase enzyme, which converts adrenal androgens (primarily androstenedione

and testosterone) to estrone and estradiol. The suppression of estrogen

biosynthesis in peripheral tissues and in the cancer tissue itself can therefore

be achieved by specifically inhibiting the aromatase enzyme.

Letrozole is a nonsteroidal competitive inhibitor of the aromatase enzyme

system; it inhibits the conversion of androgens to estrogens. In adult nontumor-

and tumorbearing female animals, letrozole is as effective as ovariectomy in

reducing uterine weight, elevating serum LH, and causing the regression of

estrogen-dependent tumors. In contrast to ovariectomy, treatment with letrozole

does not lead to an increase in serum FSH. Letrozole selectively inhibits

gonadal steroidogenesis but has no significant effect on adrenal

mineralocorticoid or glucocorticoid synthesis.

Letrozole inhibits the aromatase enzyme by competitively binding to the heme of

the cytochrome P450 subunit of the enzyme, resulting in a reduction of estrogen

biosynthesis in all tissues. Treatment of women with letrozole significantly

lowers serum estrone, estradiol and estrone sulfate and has not been shown to

significantly affect adrenal corticosteroid synthesis, aldosterone synthesis, or

synthesis of thyroid hormones.

Pharmacokinetics

Letrozole is rapidly and completely absorbed from the gastrointestinal tract and

absorption is not affected by food. It is metabolized slowly to an inactive

metabolite whose glucuronide conjugate is excreted renally, representing the

major clearance pathway. About 90% of radiolabeled letrozole is recovered in

urine. Letrozole’s terminal elimination half-life is about 2 days and

steady-state plasma concentration after daily 2.5mg dosing is reached in 2-6

weeks. Plasma concentrations at steady-state are 1.5 to 2 times higher than

predicted from the concentrations measured after a single dose, indicating a

slight nonlinearity in the pharmacokinetics of letrozole upon daily

administration of 2.5mg. These steady-state levels are maintained over extended

periods, however, and continuous accumulation of letrozole does not occur.

Letrozole is weakly protein bound and has a large volume of distribution

(approximately 1.9 L/kg).

Metabolism and Excretion

Metabolism to a pharmacologically-inactive carbinol metabolite (4,

4'-methanol-bisbenzonitrile) and renal excretion of the glucuronide conjugate of

this metabolite is the major pathway of letrozole clearance. Of the radiolabel

recovered in urine, at least 75% was the glucuronide of the carbinol metabolite,

about 9% was two unidentified metabolites, and 6% was unchanged letrozole.

In human microsomes with specific CYP isozyme activity, CYP 3A4 metabolized

letrozole to the carbinol metabolite while CYP 2A6 formed both this metabolite

and its ketone analog. In human liver microsomes, letrozole strongly inhibited

CYP 2A6 and moderately inhibited CYP 2C19.

Special Populations

Pediatric, Geriatric and Race: In the study populations (adults ranging in age

from 35 to >80 years), no change in pharmacokinetic parameters was observed with

increasing age. Differences in letrozole pharmacokinetics between adult and

pediatric populations have not been studied. Differences in letrozole

pharmacokinetics due to race have not been studied.

Renal Insufficiency: In a study of volunteers with varying renal function

(24-hour creatinine clearance: 9-116 mL/min), no effect of renal function on the

pharmacokinetics of single doses of 2.5mg of Femara (letrozole tablets) was

found. In addition, in a study of 347 patients with advanced breast cancer,

about half of whom received 2.5mg Femara and half 0.5mg Femara, renal impairment

(calculated creatinine clearance: 20-50 mL/min) did not affect steady-state

plasma letrozole concentration.

Hepatic Insufficiency: In a study of subjects with varying degrees of

non-metastatic hepatic dysfunction (e.g., cirrhosis, Child-Pugh classification A

and , the mean AUC values of the volunteers with moderate hepatic impairment

were 37% higher than in normal subjects, but still within the range seen in

subjects without impaired function. Patients with severe hepatic impairment

(Child-Pugh classification C) have not been studied (see DOSAGE AND

ADMINISTRATION, Hepatic Impairment).

Drug/Drug Interactions

A pharmacokinetic interaction study with cimetidine showed no clinically

significant effect on letrozole pharmacokinetics. An interaction study with

warfarin showed no clinically significant effect of letrozole on warfarin

pharmacokinetics.

There is no clinical experience to date on the use of Femara in combination with

other anti-cancer agents.

Pharmacodynamics

In postmenopausal patients with advanced breast cancer, daily doses of 0.1 mg to

5 mg Femara suppress plasma concentrations of estradiol, estrone, and estrone

sulfate by 75%-95% from baseline with maximal suppression achieved within

two-three days. Suppression is dose-related, with doses of 0.5 mg and higher

giving many values of estrone and estrone sulfate that were below the limit of

detection in the assays. Estrogen suppression was maintained throughout

treatment in all patients treated at 0.5 mg or higher.

Letrozole is highly specific in inhibiting aromatase activity. There is no

impairment of adrenal steroidogenesis. No clinically-relevant changes were found

in the plasma concentrations of cortisol, aldosterone, 11-deoxycortisol,

17-hydroxy-progesterone, ACTH or in plasma renin activity among post-menopausal

patients treated with a daily dose of Femara 0.1 mg to 5 mg. The ACTH

stimulation test performed after 6 and 12 weeks of treatment with daily doses of

0.1, 0.25, 0.5, 1, 2.5, and 5 mg did not indicate any attenuation of aldosterone

or cortisol production. Glucocorticoid or mineralocorticoid supplementation is,

therefore, not necessary.

No changes were noted in plasma concentrations of androgens (androstenedione and

testosterone) among healthy postmenopausal women after 0.1, 0.5, and 2.5 mg

single doses of Femara or in plasma concentrations of androstenedione among

postmenopausal patients treated with daily doses of 0. 1 mg to 5 mg. This

indicates that the blockade of estrogen biosynthesis does not lead to

accumulation of androgenic precursors. Plasma levels of LH and FSH were not

affected by letrozole in patients, nor was thyroid function as evaluated by TSH

levels, T3 uptake, and T4 levels.

Captin Swole

06-27-2002, 07:25 PM

Exemestane.

DESCRIPTION

AROMASIN Tablets for oral administration contain 25 mg of exemestane, an

irreversible, steroidal aromatase inactivator. Exemestane is chemically

described as 6-methylenandrosta-1,4-diene-3, 17-dione. Its molecular formula is

C20H24O2.

The active ingredient is a white to slightly yellow crystalline powder with a

molecular weight of 296.41. Exemestane is freely soluble in N,

N-dimethylformamide, soluble in methanol, and practically insoluble in water.

Each AROMASIN Tablet contains the following inactive ingredients: mannitol,

crospovidone, polysorbate 80, hydroxypropyl methylcellulose, colloidal silicon

dioxide, microcrystalline cellulose, sodium starch glycolate, magnesium

stearate, simethicone, polyethylene glycol 6000, sucrose, magnesium carbonate,

titanium dioxide, methylparaben, and polyvinyl alcohol.

CLINICAL PHARMACOLOGY

Mechanism of Action

Breast cancer cell growth may be estrogen-dependent. Aromatase (exemestane) is

the principal enzyme that converts androgens to estrogens both in pre- and

postmenopausal women. While the main source of estrogen (primarily estradiol) is

the ovary in premenopausal women, the principal source of circulating estrogens

in postmenopausal women is from conversion of adrenal and ovarian androgens

(androstenedione and testosterone) to estrogens (estrone and estradiol) by the

aromatase enzyme in peripheral tissues. Estrogen deprivation through aromatase

inhibition is an effective and selective treatment for some postmenopausal

patients with hormone-dependent breast cancer.

Exemestane is an irreversible, steroidal aromatase inactivator, structurally

related to the natural substrate androstenedione. It acts as a false substrate

for the aromatase enzyme, and is processed to an intermediate that binds

irreversibly to the active site of the enzyme causing its inactivation, an

effect also known as “suicide inhibition.†Exemestane significantly lowers

circulating estrogen concentrations in postmenopausal women, but has no

detectable effect on adrenal biosynthesis of corticosteroids or aldosterone.

Exemestane has no effect on other enzymes involved in the steroidogenic pathway

up to a concentration at least 600 times higher than that inhibiting the

aromatase enzyme.

Pharmacokinetics

Following oral administration to healthy postmenopausal women, exemestane is

rapidly absorbed. After maximum plasma concentration is reached, levels decline

polyexponentially with a mean terminal half-life of about 24 hours. Exemestane

is extensively distributed and is cleared from the systemic circulation

primarily by metabolism. The pharmacokinetics of exemestane are dose

proportional after single (10 to 200 mg) or repeated oral doses (0.5 to 50 mg).

Following repeated daily doses of exemestane 25 mg, plasma concentrations of

unchanged drug are similar to levels measured after a single dose.

Pharmacokinetic parameters in postmenopausal women with advanced breast cancer

following single or repeated doses have been compared with those in healthy,

postmenopausal women. Exemestane appeared to be more rapidly absorbed in the

women with breast cancer than in the healthy women, with a mean tmax of 1.2

hours in the women with breast cancer and 2.9 hours in the healthy women. After

repeated dosing, the average oral clearance in women with advanced breast cancer

was 45% lower than the oral clearance in healthy postmenopausal women, with

corresponding higher systemic exposure. Mean AUC values following repeated doses

in women with breast cancer (75.4 ng•h/mL) were about twice those in healthy

women (41.4 ng•h/mL).

Absorption: Following oral administration of radiolabeled exemestane, at least

42% of radioactivity was absorbed from the gastrointestinal tract. Exemestane

plasma levels increased by approximately 40% after a high-fat breakfast.

Distribution: Exemestane is distributed extensively into tissues. Exemestane is

90% bound to plasma proteins and the fraction bound is independent of the total

concentration. Albumin and a1-acid glycoprotein both contribute to the binding.

The distribution of exemestane and its metabolites into blood cells is

negligible.

Metabolism and Excretion: Following administration of radiolabeled exemestane to

healthy postmenopausal women, the cumulative amounts of radioactivity excreted

in urine and feces were similar (42 ± 3% in urine and 42 ± 6% in feces over a

1-week collection period). The amount of drug excreted unchanged in urine was

less than 1% of the dose.

Exemestane is extensively metabolized, with levels of the unchanged drug in

plasma accounting for less than 10% of the total radioactivity. The initial

steps in the metabolism of exemestane are oxidation of the methylene group in

position 6 and reduction of the 17-keto group with subsequent formation of many

secondary metabolites. Each metabolite accounts only for a limited amount of

drug-related material. The metabolites are inactive or inhibit aromatase with

decreased potency compared with the parent drug. One metabolite may have

androgenic activity (see Pharmacodynamics: Other Endocrine Effects, below).

Studies using human liver preparations indicate that cytochrome P450 3A4 (CYP

3A4) is the principal isoenzyme involved in the oxidation of exemestane.

Special Populations

Geriatric: Healthy postmenopausal women aged 43 to 68 years were studied in the

pharmacokinetic trials. Age-related alterations in exemestane pharmacokinetics

were not seen over this age range.

Gender: The pharmacokinetics of exemestane following administration of a single,

25-mg tablet to fasted healthy males (mean age 32 years) were similar to the

pharmacokinetics of exemestane in fasted healthy postmenopausal women (mean age

55 years).

Race: The influence of race on exemestane pharmacokinetics has not been

evaluated.

Hepatic Insufficiency: The pharmacokinetics of exemestane have been investigated

in subjects with moderate or severe hepatic insufficiency (Childs-Pugh B or C).

Following a single 25-mg oral dose, the AUC of exemestane was approximately 3

times higher than that observed in healthy volunteers. (See PRECAUTIONS.)

Renal Insufficiency: The AUC of exemestane after a single 25-mg dose was

approximately 3 times higher in subjects with moderate or severe renal

insufficiency (creatinine clearance <35 mL/min/1.73 m2 ) compared with the AUC

in healthy volunteers (see PRECAUTIONS).

Pediatric: The pharmacokinetics of exemestane have not been studied in pediatric

patients.

Drug-Drug Interactions

Exemestane is metabolized by cytochrome P450 3A4 (CYP 3A4) and

aldoketoreductases. It does not inhibit any of the major CYP isoenzymes,

including CYP 1A2, 2C9, 2D6, 2E1, and 3A4. In a clinical pharmacokinetic study,

ketoconazole showed no significant influence on the pharmacokinetics of

exemestane. Although no other formal drug-drug interaction studies have been

conducted, significant effects on exemestane clearance by CYP isoenzymes

inhibitors appear unlikely. However, a possible decrease of exemestane plasma

levels by known inducers of CYP 3A4 cannot be excluded.

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.

[Guest guest]

>

> My opinion, after a bad reaction to Arimidex, and after viewing all

> of the side effects and after reading tons of forums all over where

> women have died and all of the bad reactions.

>

> WE NEED AN ALTERNATIVE - WHICH TO THE BEST OF MY KNOWLEDGE DOESN'T

> EXIST.

Hi,

there's aromasin...

which works but even through All Day Chemist is expensive...

arimidex and novaldex don't play well together...

but aromasin and novaldex do...

BUT... you can drive your e2 to low so you need to work up your dosages SLOW (it

takes a week for blood levels to stabilize with the stuff anyway)

then there's Letrozole(sp?) which is REALLY effective... almost to effective...

this is where the " research chemical " route makes sense since you can measure it

down to the drop.

[Guest guest]

Joe, I am not ignoring you, I have some major deadlines, plus i need to make a

reference back to another group i am involved in before i comment. It might be

helpful if you list some dietary and supplement sources of iron intake. Also

your phlebotomy frequency over the last year.

> > > >

> > > > I am hearing that Arimidex is not approved for use in males and that a

lot of insurance companies won't pay for it. Is it expensive if I have to buy

it on my own?

> > > >

> > >

> > > Arimidex is a product of Astra-Zenica and they have a patent on it in the

US. It is very expensive.

> > >

> > > Other countries (such as India) do not honor these patents and make a

generic version, called anastrozole, and you can buy that online from offshore

pharmacies.

> > >

> > > Compare these two pharmacies: One sells the generic, and the other sells

Astra-Zenica's patented version.

> > >

> > > http://www.alldaychemist.com/common_generic/Anastrozole.html

> > >

> > > http://www.inhousepharmacy.com/womens-hrt/arimidex.html

> > >

> >

>

[Guest guest]

So here is what I am on from a dietary perspective:

1000 UI of D with Calcium (I have a D deficiency)

B-Complex Vitamin (I am a vegan so I tend to get low B12 which you can only get

from meat)

1200 Omega 3

I am on a low fat vegan diet

For meds, I take:

liprinosil 10 mg for high blood pressure

clarinex 5mg for allergy

singulair 10 mg for allergy

testosterone shots.

I've had blood work done every 8 weeks since January but iron wasn't part of it.

I paid for a bunch of tests myself since my dr wouldn't do them. That included

the iron study.

> > > > >

> > > > > I am hearing that Arimidex is not approved for use in males and that

a lot of insurance companies won't pay for it. Is it expensive if I have to buy

it on my own?

> > > > >

> > > >

> > > > Arimidex is a product of Astra-Zenica and they have a patent on it in

the US. It is very expensive.

> > > >

> > > > Other countries (such as India) do not honor these patents and make a

generic version, called anastrozole, and you can buy that online from offshore

pharmacies.

> > > >

> > > > Compare these two pharmacies: One sells the generic, and the other

sells Astra-Zenica's patented version.

> > > >

> > > > http://www.alldaychemist.com/common_generic/Anastrozole.html

> > > >

> > > > http://www.inhousepharmacy.com/womens-hrt/arimidex.html

> > > >

> > >

> >

>

[Guest guest]

I do 10,000 IU's of Vit D. I use this there is 2000 IU's in a drop I put the

drops on the back of my hand and lick it off.

Bio D-Mulsion Forte

http://www.mccombsplanstore.com/prodinfo.asp?number=BIOD

You need more fat and protein in your diet to keep your CHOL up and this makes

hormones. You don't eat meat but you should know how to eat to keep your

protein levels up.

Co-Moderator

Phil

> From: noonanjg <jgnoonan@...>

> Subject: Re: Estradiol Levels

>

> Date: Thursday, June 18, 2009, 4:12 PM

> So here is what I am on from a

> dietary perspective:

>

> 1000 UI of D with Calcium  (I have a D deficiency)

> B-Complex Vitamin (I am a vegan so I tend to get low B12

> which you can only get from meat)

> 1200 Omega 3

> I am on a low fat vegan diet

>

> For meds, I take:

> liprinosil 10 mg for high blood pressure

> clarinex 5mg for allergy

> singulair 10 mg for allergy

> testosterone shots.

>

> I've had blood work done every 8 weeks since January but

> iron wasn't part of it.  I paid for a bunch of tests

> myself since my dr wouldn't do them.  That included the

> iron study.

>

>

>

> > > > > >

> > > > > >   I am hearing that

> Arimidex is not approved for use in males and that a lot of

> insurance companies won't pay for it.  Is it expensive

> if I have to buy it on my own? 

> > > > > >

> > > > >

> > > > > Arimidex is a product of Astra-Zenica

> and they have a patent on it in the US.  It is very

> expensive.

> > > > >

> > > > > Other countries (such as India) do not

> honor these patents and make a generic version, called

> anastrozole, and you can buy that online from offshore

> pharmacies.

> > > > >

> > > > > Compare these two pharmacies:  One

> sells the generic, and the other sells Astra-Zenica's

> patented version.

> > > > >

> > > > > http://www.alldaychemist.com/common_generic/Anastrozole.html

> > > > >

> > > > > http://www.inhousepharmacy.com/womens-hrt/arimidex.html

> > > > >

> > > >

> > >

> >

>

>

>

>

> ------------------------------------

>

>

[Guest guest]

Don't necessarily disagree with you......you have been at this MUCH longer than

I, but .....

Letrozole IS being used by men....

http://www.biogenesis.co.za/pi-femara.asp

Product Information

A potent aromatase inhibitor.

Femara® is the best known brand of a drug called Letrozole.

This is a potent and selective non-steroidal inhibitor of the Aromatase

(estrogen synthetase) system, which converts testosterone and adrenal androgens

to estrogens in peripheral tissue.

Femara is used in the treatment of advanced or locally advanced breast cancer,

and as adjuvant treatment in early breast cancer. In postmenopausal women the

dose is often 2.5mg daily by mouth.

However, Femara is also used by " aging " men, who want to reduce their conversion

of testosterone and adrenal hormones to estrogens. This is because it is quite

common for a 59-year old man to have more estrogen circulating (primarily as

estradiol), than a 54-year old woman!

It is thus believed that " skewed " estrogen ratios, possibly caused by toxins,

environmental factors and aging, play a major role in the formation of cancers

in both men and women, (particularly prostate, cervical and breast), and also

lead to other disturbances such as increased fat deposits etc.

Your estradiol, estrone and testosterone levels can be monitored using the

saliva test kit.

Although it's an unofficial use, an average of 1.25mg Femara, once or twice per

week is used by men who wish to see their estrogen levels decline, and their

free testosterone levels increase.

[Guest guest]

I am not saying men don't use it just saying what they said about it and going

to low. I have a big problem with high levels of Estradiol and yes I have been

trying to keep it in check for yrs. Thing is it changes all the time 8 weeks

ago I got by taking .25 mgs every 2 days labs come back to high 36 pg/ml I have

a low SHBG 20 so less is bound up for both Estradiol and Testosterone so now I

am doing .25 mgs everyday I don't like using it this much because some time in

the next few weeks I am going to go to low. If I catch this fast and stop

arimidex my levels will come back up fast in a few days.

Because Arimidx does not kill Aromatase it blocks it. When men take this potent

aromatase inhibitor. And go to low they can't come back up in days it's more

like weeks to months and it's very bad to be to low you get sore joint and

muscles, bone loss, ED, Brain Fog and the list goes on.

You can try this I can't say what dose to use or how often you take it. I don't

know anyone that staid on it.

I know some of the best Dr.'s that treat low testosterone Dr. , Shippen and

Dr. no and this Dr. just started a new forum go check it out ask him how he

feels about using this he will get back to you. Maybe he knows how to use this.

http://www.definitivemind.com/forums/forumdisplay.php?f=17

Also this is Dr. 's forum post to him see what he says he treats thousands

of men. Listen to this video he has out free it will not be out long so do

listen to this.

http://progressive.uvault.com/pd1005...ler/player.HTM

http://www.musclechatroom.com/forum/forumdisplay.php?f=2

Co-Moderator

Phil

> From: ihor <ihor43us@...>

> Subject: Re: Estradiol Levels

>

> Date: Thursday, June 18, 2009, 6:45 PM

> Don't necessarily disagree with

> you......you have been at this MUCH longer than I, but

> .....

>

> Letrozole IS being used by men....

>

> http://www.biogenesis.co.za/pi-femara.asp

>

> Product Information

> A potent aromatase inhibitor.

>

> Femara® is the best known brand of a drug called

> Letrozole.

>

> This is a potent and selective non-steroidal inhibitor of

> the Aromatase (estrogen synthetase) system, which converts

> testosterone and adrenal androgens to estrogens in

> peripheral tissue.

>

> Femara is used in the treatment of advanced or locally

> advanced breast cancer, and as adjuvant treatment in early

> breast cancer. In postmenopausal women the dose is often

> 2.5mg daily by mouth.

>

> However, Femara is also used by " aging " men, who want to

> reduce their conversion of testosterone and adrenal hormones

> to estrogens. This is because it is quite common for a

> 59-year old man to have more estrogen circulating (primarily

> as estradiol), than a 54-year old woman!

>

> It is thus believed that " skewed " estrogen ratios, possibly

> caused by toxins, environmental factors and aging, play a

> major role in the formation of cancers in both men and

> women, (particularly prostate, cervical and breast), and

> also lead to other disturbances such as increased fat

> deposits etc.

>

> Your estradiol, estrone and testosterone levels can be

> monitored using the saliva test kit.

>

> Although it's an unofficial use, an average of 1.25mg

> Femara, once or twice per week is used by men who wish to

> see their estrogen levels decline, and their free

> testosterone levels increase.

>

>

>

> ------------------------------------

>

>

[Guest guest]

On Thu, 18 Jun 2009 11:57:18 -0000, you wrote:

>My opinion, after a bad reaction to Arimidex, and after viewing all of the side

effects and after reading tons of forums all over where women have died and all

of the bad reactions.

>

>WE NEED AN ALTERNATIVE - WHICH TO THE BEST OF MY KNOWLEDGE DOESN'T EXIST.

>

>DIM treat existing E2. BTW the Indoplex DIM everyone in here references is

full of calcium and can bind other meds that you are taking. Take the time to

do a conflicts check and ask your GP if there is potential interference with any

other med.

For me, I do not see that much risk in arimidex. Of course you have

had a very strong reaction so your milage will vary.

My reading says to me that the doses we take are a very small fraction

of what women take. Women are prescribed this for breast cancer and

the aim is to shut down ALL E2 in the body while they try to kill the

tumors. Most of the side effects I see make sense as a result of so

totally shutting down E2. Men are seeking to get E2 into normal

healthy range.

Arimidex has a 48 hours half life and the enzyme bounces back quickly

so that when we overshoot you can return to your natural E2 level in 5

days of stopping. It also is milder than other available drugs - and

makes for an easier reduction as opposed to total shut down or

overshooting the mark as often.

The women tested for side effects are also doing chemo and coping with

cancer. So I believe the results will look worse than the risk for a

healthy man taking small moderate doses.

I am curious if maybe your strong reaction was from driving your E2

too low.

[Guest guest]

Phil: I bought the Indolplex DIM. The dosage on the bottle says one a day. Is

that correct?

> > > >

> > > > I am on Testosterone shots for low T.  I

> > have a 2mm Pituitary adenoma that I guess is causing all the

> > problems.  I received weekly shots of alternating

> > amounts.  It is a regimen of 1cc of 200 mg/ml one week

> > and then .5cc the following and then switching back. 

> > I've been on this for about 2 months.  I feel like

> > crap.  I am tired all the time.  My blood pressure

> > skyrocketed shortly after starting the shots.  I am on

> > bp meds now to control it.  I paid for a complete set

> > of blood work and there are weird readings all over the

> > place.  My E2 level is 79, my T level is 890.  My

> > CBC had several high readings, which my understanding is

> > that is normal.  Previous to this regimen, I was on 1cc

> > every week but my t level was 1600 so she went to the new

> > regimen.  I was really hoping to feel better but I

> > don't.  I have no interest in sex at all and couldn't

> > do it anyway if I was if you catch my drift.  I am so

> > frustrated.  I've gained 40lbs and just cannot loose

> > weight.  I went on a strict low fat vegan diet for 6

> > weeks and lost about 1 pound.  I am trying to exercise

> > but am just too exhausted to do much of anything although I

> > do try to do something for 30 minutes 3 times a week. 

> > I have a dr. appt coming up and don't know what to

> > ask.  I have high serum iron readings but low ferritin

> > levels (stored iron).  Any suggestions?

> > > >

> > >

> >

> >

> >

> >

> > ------------------------------------

> >

> >