arimidex

[Guest guest]

>

> Bob I think your on to something here my Dr. when he sees new men

and checks there T levels if they are low on T and High on E2 he

treats the E2 first and there levels come back up. Can you post your

tests with the ranges. But my Dr. never started them on 1mgs.

> Phil

Phil,

My initial, very detailed message on this was #36231.

Extracting from that, we can see the following:

Mid-June, while on 10g/day of Androgel:

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

FSH 2.3 (Range 1.6-8.0 mIU/mL)

LH 2.2 (Range 1.5-9.3 mIU/mL)

Total T 562 (Range 260-1000 ng/dL)

Free Testosterone

% Free 1.1 (Range 1.0-2.7%)

Free 63.6 (Range 50.0-210.0 pg/mL)

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

Mid-July, first bloodwork ordered by my new urologist before changing

medication:

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

Estradiol 39 (Range 10-50 pg/mL)

Total T 687 (Range 241-827 ng/dL)

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

Mid-August, after 3 weeks on 1mg/day of Arimidex instead of 10g/day

of Androgel:

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

Estradiol 13 (Range 10-50 pg/mL)

Total T 617 (Range 241-827 ng/dL)

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

Tomorrow, I'll find out what my numbers are after being on this

regimen for two months, and I'll share that info with the group.

Bob

[Guest guest]

>

> Bob-

> Thanks for the clairification! My mind somehow skipped over

> the " primary's not working " part of your post. However, it points

my

> confusion in a different direction: why should the addition of

> testosterone (exogenous) make any difference in the final E2 levels

> as dictated by Arimidex. There must be some other mechanism going

on

> that I'm not aware of.

> Rich

Rich,

Maybe the answer is that we don't need to worry so much about

adjusting our E2 levels when our T is in the upper range of normal

without having to load ourselves up with exogenous testosterone.

Perhaps it's only when we are introducing TRT that our E2 levels make

such a big difference to the way some people feel. I'll run this by

my doctor tomorrow.

Here's how I understand things. As we age, the aromatization

mechanisms in our bodies grow more powerful and take away the natural

testosterone we produce (assuming, again, that we're not suffering

from primary hypogonadism instead of secondary). When we use the

brute force approach of throwing more and more T into our body, we're

trying to make sure that there's enough T left over after the

aromatization takes place. It's sort of like throwing a whole bowl

of spaghetti against the wall and hoping a bunch of it will stick

(that's our T), knowing that a huge amount will wind up on the floor

(that's our E2). The aromatization mechanisms make the wall

slippery, so that less and less of the spaghetti (the T) sticks.

Depending on what's happening, individually and uniquely, in each of

our bodies, differing amounts will wind up on the wall and on the

floor.

With TRT and Arimidex going on, it seems to become a real

juggling act to figure out what to do with adding exogenous T and

also not winding up with too much E2. This seems to me to be

evidenced empirically by a lot of the " juggling " experiences I read

about in this group. With TRT **plus** Arimidex, you've got your

natural production of T plus the added TRT which your body has to

deal with. Maybe our bodies just have a lot of difficulty handling

the overload, which could help explain the volatility in results that

some people report.

On the other hand, if you start taking the Arimidex before

taking T (or, in my case, getting off the T and switching to

Arimidex), everything seems so much simpler. The Arimidex interferes

with the aromatization mechanism, allowing our proverbial wall to

remain (or become) stickier than it would be otherwise. Existing T

production sticks to the wall better, leaving less E2 on the floor.

The brute force approach of throwing more and more T into the body

simply isn't needed, at least for those who are producing enough T on

their own.

It seems to me that the traditional TRT approach comes from a

very linear way of thinking. That is, if there's not enough T in the

body, add more T. Then if something else winds up messed up from

this (e.g., too much E2), do something else to fix that. It's hard

to think that we can make so many different adjustments at the same

time and expect it to come out just right.

How about thinking outside the box instead of in a linear

fashion? If somebody can produce plenty of T but it's getting

diverted into something else, why not attack the diversion problem

first? That way, we don't have to fill up the body with a whole

messy pot of spaghetti. It's so much simpler and cleaner.

Bob

[Guest guest]

>

> Bob - I would be interested in your pre-TRT conditions. I have

often wondered if I would fall into this category. My pre-TRT

conditions were:

>

> Total T = 180 ng/dl (260-1000)

> Free T = 40 (50-210)

> LH = 3.4 (1.5-9.3)

> Prolactin 4.6 (2-18)

> E2 = 30 - this gave me a T/E2 ratio of only 6

>

> Not clear whether I am primary or secondary - Uro thought

primary so we started TRT.

>

> How do we compare? -

>

> Arkansas

Arkansas:

I don't have numbers from several years ago when I was first

diagnosed with hypogonadism, but with low FSH and LH I was diagnosed

as secondary. The estradiol question wasn't even considered at that

time, so we went straight to TRT.

Bob

[Guest guest]

> It would seem yours is not pituitary based either, but strictly from

> high aromotase levels. Perhaps when we have TRT and arimidex its

quite

> different from natural T -E2-aromotase issues.

>

> If you don't mind my asking are you a bit overweight? Aromotase and

> fat correlate strongly. It tends to be overweight folks who can solve

> their T levels solely with arimidex.

Overweight is a good characterization. My BMI was way up there before

going for a lapband(laparascopic adjustable gastric band) a year ago.

Now, almost 100 pounds down, I'm knocking on the door of being

merely " overweight. "

Bob

[Guest guest]

Bob-

Thanks for the detailed explanation. I think I can follow your line

of reasoning...to a point. Believe me, I'm not trying to beat a dead

horse (or be dense on something that should make sense) but I still

have a problem with the dosage of Arimidex. Maybe the rules of the

game are different when you're not primary. Maybe with working testes

and HPA, somehow something suppresses the action of Arimidex for you,

otherwise, by all logic, you shouldn't -need- a dose of 1mg per day.

The same stuff thats capable of dropping a primary on TRT's E2 so low

that it takes a month to recover. The potency of Arimidex is there,

that's undeniable. Maybe your system only uses enough of it to drop

your levels to normal and flushes everything else out of the system,

but even so, why take that much to begin with. This is going to turn

out to be an itch I can't scratch, I know it. And since I'm also

taking the stuff, I have a vested interest in knowing everything it

does, or capable of doing if something goes wrong.

Rich

> >

> > Bob-

> > Thanks for the clairification! My mind somehow skipped over

> > the " primary's not working " part of your post. However, it points

> my

> > confusion in a different direction: why should the addition of

> > testosterone (exogenous) make any difference in the final E2

levels

> > as dictated by Arimidex. There must be some other mechanism going

> on

> > that I'm not aware of.

> > Rich

>

> Rich,

>

> Maybe the answer is that we don't need to worry so much about

> adjusting our E2 levels when our T is in the upper range of normal

> without having to load ourselves up with exogenous testosterone.

> Perhaps it's only when we are introducing TRT that our E2 levels

make

> such a big difference to the way some people feel. I'll run this

by

> my doctor tomorrow.

>

> Here's how I understand things. As we age, the aromatization

> mechanisms in our bodies grow more powerful and take away the

natural

> testosterone we produce (assuming, again, that we're not suffering

> from primary hypogonadism instead of secondary). When we use the

> brute force approach of throwing more and more T into our body,

we're

> trying to make sure that there's enough T left over after the

> aromatization takes place. It's sort of like throwing a whole bowl

> of spaghetti against the wall and hoping a bunch of it will stick

> (that's our T), knowing that a huge amount will wind up on the

floor

> (that's our E2). The aromatization mechanisms make the wall

> slippery, so that less and less of the spaghetti (the T) sticks.

> Depending on what's happening, individually and uniquely, in each

of

> our bodies, differing amounts will wind up on the wall and on the

> floor.

>

> With TRT and Arimidex going on, it seems to become a real

> juggling act to figure out what to do with adding exogenous T and

> also not winding up with too much E2. This seems to me to be

> evidenced empirically by a lot of the " juggling " experiences I read

> about in this group. With TRT **plus** Arimidex, you've got your

> natural production of T plus the added TRT which your body has to

> deal with. Maybe our bodies just have a lot of difficulty handling

> the overload, which could help explain the volatility in results

that

> some people report.

>

> On the other hand, if you start taking the Arimidex before

> taking T (or, in my case, getting off the T and switching to

> Arimidex), everything seems so much simpler. The Arimidex

interferes

> with the aromatization mechanism, allowing our proverbial wall to

> remain (or become) stickier than it would be otherwise. Existing T

> production sticks to the wall better, leaving less E2 on the

floor.

> The brute force approach of throwing more and more T into the body

> simply isn't needed, at least for those who are producing enough T

on

> their own.

>

> It seems to me that the traditional TRT approach comes from a

> very linear way of thinking. That is, if there's not enough T in

the

> body, add more T. Then if something else winds up messed up from

> this (e.g., too much E2), do something else to fix that. It's hard

> to think that we can make so many different adjustments at the same

> time and expect it to come out just right.

>

> How about thinking outside the box instead of in a linear

> fashion? If somebody can produce plenty of T but it's getting

> diverted into something else, why not attack the diversion problem

> first? That way, we don't have to fill up the body with a whole

> messy pot of spaghetti. It's so much simpler and cleaner.

>

> Bob

>

[Guest guest]

On Mon, 25 Sep 2006 23:19:42 -0000, you wrote:

>Bob-

>Thanks for the detailed explanation. I think I can follow your line

>of reasoning...to a point. Believe me, I'm not trying to beat a dead

>horse (or be dense on something that should make sense) but I still

>have a problem with the dosage of Arimidex. Maybe the rules of the

>game are different when you're not primary. Maybe with working testes

>and HPA, somehow something suppresses the action of Arimidex for you,

>otherwise, by all logic, you shouldn't -need- a dose of 1mg per day.

>The same stuff thats capable of dropping a primary on TRT's E2 so low

>that it takes a month to recover. The potency of Arimidex is there,

>that's undeniable. Maybe your system only uses enough of it to drop

>your levels to normal and flushes everything else out of the system,

>but even so, why take that much to begin with. This is going to turn

>out to be an itch I can't scratch, I know it. And since I'm also

>taking the stuff, I have a vested interest in knowing everything it

>does, or capable of doing if something goes wrong.

>Rich

>

I look at it differently than Bob. It's not that aromotization gets

stronger as we age. It's that most of us as we age get heavier.

Aromotase is concentrated in lipid cells. Hence as we get heavier we

get more aromotase, hence more E2.

People who lose their T levels for pituitary or primary reasons don't

have much T to convert to E2. People who put on considerable weight

and have healthy T production capabilities end up with higher E2

levels. Now E2 out competes T for many of the binding sites in the

body. hence high E2 robs the feel of healthy T levels. And this may

cause the body to produce less T if the FSH/LH feedback loops are

disrupted by the E2 binding.

These effects combine so that people who are overweight with high E2

levels and healthy HPG axis can get back to healthy T levels by simply

taking arimidex. Studies have shown a 200 to 300 point T boost is

possible with just arimidex .

Two thoughts here on why heavier doses don't effect people with

healthy HPG as much as those of us on TRT.

One, people for whom arimidex alone works tend to be much heavier and

have E2 levels and aromotase levels that are multiples of what thinner

people have. Hence a higher dose or more frequent dose is more

tolerable.

Two, natural T levels vary over the course of the day and can swing

as much as 400 points in an hour or so. Those of us on TRT have

comparatively steady state T levels throughout the day. I wonder if

this somehow effects aromotase levels as well. We're certainly doing a

lot more conversion than folks who have the usual spikes and valleys

of T levels.

>

>> >

>> > Bob-

>> > Thanks for the clairification! My mind somehow skipped over

>> > the " primary's not working " part of your post. However, it points

>> my

>> > confusion in a different direction: why should the addition of

>> > testosterone (exogenous) make any difference in the final E2

>levels

>> > as dictated by Arimidex. There must be some other mechanism going

>> on

>> > that I'm not aware of.

>> > Rich

>>

>> Rich,

>>

>> Maybe the answer is that we don't need to worry so much about

>> adjusting our E2 levels when our T is in the upper range of normal

>> without having to load ourselves up with exogenous testosterone.

>> Perhaps it's only when we are introducing TRT that our E2 levels

>make

>> such a big difference to the way some people feel. I'll run this

>by

>> my doctor tomorrow.

>>

>> Here's how I understand things. As we age, the aromatization

>> mechanisms in our bodies grow more powerful and take away the

>natural

>> testosterone we produce (assuming, again, that we're not suffering

>> from primary hypogonadism instead of secondary). When we use the

>> brute force approach of throwing more and more T into our body,

>we're

>> trying to make sure that there's enough T left over after the

>> aromatization takes place. It's sort of like throwing a whole bowl

>> of spaghetti against the wall and hoping a bunch of it will stick

>> (that's our T), knowing that a huge amount will wind up on the

>floor

>> (that's our E2). The aromatization mechanisms make the wall

>> slippery, so that less and less of the spaghetti (the T) sticks.

>> Depending on what's happening, individually and uniquely, in each

>of

>> our bodies, differing amounts will wind up on the wall and on the

>> floor.

>>

>> With TRT and Arimidex going on, it seems to become a real

>> juggling act to figure out what to do with adding exogenous T and

>> also not winding up with too much E2. This seems to me to be

>> evidenced empirically by a lot of the " juggling " experiences I read

>> about in this group. With TRT **plus** Arimidex, you've got your

>> natural production of T plus the added TRT which your body has to

>> deal with. Maybe our bodies just have a lot of difficulty handling

>> the overload, which could help explain the volatility in results

>that

>> some people report.

>>

>> On the other hand, if you start taking the Arimidex before

>> taking T (or, in my case, getting off the T and switching to

>> Arimidex), everything seems so much simpler. The Arimidex

>interferes

>> with the aromatization mechanism, allowing our proverbial wall to

>> remain (or become) stickier than it would be otherwise. Existing T

>> production sticks to the wall better, leaving less E2 on the

>floor.

>> The brute force approach of throwing more and more T into the body

>> simply isn't needed, at least for those who are producing enough T

>on

>> their own.

>>

>> It seems to me that the traditional TRT approach comes from a

>> very linear way of thinking. That is, if there's not enough T in

>the

>> body, add more T. Then if something else winds up messed up from

>> this (e.g., too much E2), do something else to fix that. It's hard

>> to think that we can make so many different adjustments at the same

>> time and expect it to come out just right.

>>

>> How about thinking outside the box instead of in a linear

>> fashion? If somebody can produce plenty of T but it's getting

>> diverted into something else, why not attack the diversion problem

>> first? That way, we don't have to fill up the body with a whole

>> messy pot of spaghetti. It's so much simpler and cleaner.

>>

>> Bob

>>

>

>

>

________________

I am human; nothing in humanity is alien to me.

Terence

[Guest guest]

Bob they miss the boat on your first test having a low LH and FSH can mean your

Secondary but if your cells are full of E2 your brain thinks it is T and stops

sending the LH and FSH to your testis.

Phil

rtolz <no_reply > wrote:

>

> Bob - I would be interested in your pre-TRT conditions. I have

often wondered if I would fall into this category. My pre-TRT

conditions were:

>

> Total T = 180 ng/dl (260-1000)

> Free T = 40 (50-210)

> LH = 3.4 (1.5-9.3)

> Prolactin 4.6 (2-18)

> E2 = 30 - this gave me a T/E2 ratio of only 6

>

> Not clear whether I am primary or secondary - Uro thought

primary so we started TRT.

>

> How do we compare? -

>

> Arkansas

Arkansas:

I don't have numbers from several years ago when I was first

diagnosed with hypogonadism, but with low FSH and LH I was diagnosed

as secondary. The estradiol question wasn't even considered at that

time, so we went straight to TRT.

Bob

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

Stay in the know. Pulse on the new .com. Check it out.

[Guest guest]

>You guys need to understand how low T and high E2 work. When the

cells are full of E2 the brain can't tell the difference. So it stops

sending the LH and FSH to the testis to make more T. So the bottom

line is when your E2 is high your brain thinks it's Testosterone.

Getting the E2 down your brain sees your T levels low and sends the

message to make more T this only works if your Testis work.

Phil

---That's absolutely my understanding as well

>

> Bob they miss the boat on your first test having a low LH and FSH

can mean your Secondary but if your cells are full of E2 your brain

thinks it is T and stops sending the LH and FSH to your testis.

> Phil

---If you think they missed the boat for not analyzing and

understanding the effect of the aromatization and the estradiol, I'm

in complete agreement with you.

Bob

[Guest guest]

>

> Bob-

> Thanks for the detailed explanation. I think I can follow your line

> of reasoning...to a point. Believe me, I'm not trying to beat a

dead

> horse (or be dense on something that should make sense) but I still

> have a problem with the dosage of Arimidex. Maybe the rules of the

> game are different when you're not primary. Maybe with working

testes

> and HPA, somehow something suppresses the action of Arimidex for

you,

> otherwise, by all logic, you shouldn't -need- a dose of 1mg per

day.

> The same stuff thats capable of dropping a primary on TRT's E2 so

low

> that it takes a month to recover. The potency of Arimidex is there,

> that's undeniable. Maybe your system only uses enough of it to drop

> your levels to normal and flushes everything else out of the

system,

> but even so, why take that much to begin with. This is going to

turn

> out to be an itch I can't scratch, I know it. And since I'm also

> taking the stuff, I have a vested interest in knowing everything it

> does, or capable of doing if something goes wrong.

> Rich

Rich,

As a matter of personal curiosity, I'll ask my doctor when I see

him in an hour or so how he deals with Arimidex with someone who's

primary.

Bob

[Guest guest]

>

> I look at it differently than Bob. It's not that aromotization gets

> stronger as we age. It's that most of us as we age get heavier.

> Aromotase is concentrated in lipid cells. Hence as we get heavier we

> get more aromotase, hence more E2.

I seem to recall reading that aromatase is associate both with

aging and with obesity. You are suggesting that the association with

aging is only because older people get heavier. Are you aware of any

studies that show that older people who do **not** get heavier do not

have an increase in aromatase action as they age?

>

> These effects combine so that people who are overweight with high E2

> levels and healthy HPG axis can get back to healthy T levels by

simply

> taking arimidex. Studies have shown a 200 to 300 point T boost is

> possible with just arimidex .

This certainly seems to be working in my case. I'll be curious

to see what happens as I continue to lose weight.

Bob

[Guest guest]

> >> >

> >> > Bob-

> >> > Thanks for the clairification! My mind somehow skipped over

> >> > the " primary's not working " part of your post. However, it

points

> >> my

> >> > confusion in a different direction: why should the addition of

> >> > testosterone (exogenous) make any difference in the final E2

> >levels

> >> > as dictated by Arimidex. There must be some other mechanism

going

> >> on

> >> > that I'm not aware of.

> >> > Rich

> >>

> >> Rich,

> >>

> >> Maybe the answer is that we don't need to worry so much

about

> >> adjusting our E2 levels when our T is in the upper range of

normal

> >> without having to load ourselves up with exogenous testosterone.

> >> Perhaps it's only when we are introducing TRT that our E2 levels

> >make

> >> such a big difference to the way some people feel. I'll run

this

> >by

> >> my doctor tomorrow.

> >>

> >> Here's how I understand things. As we age, the

aromatization

> >> mechanisms in our bodies grow more powerful and take away the

> >natural

> >> testosterone we produce (assuming, again, that we're not

suffering

> >> from primary hypogonadism instead of secondary). When we use

the

> >> brute force approach of throwing more and more T into our body,

> >we're

> >> trying to make sure that there's enough T left over after the

> >> aromatization takes place. It's sort of like throwing a whole

bowl

> >> of spaghetti against the wall and hoping a bunch of it will

stick

> >> (that's our T), knowing that a huge amount will wind up on the

> >floor

> >> (that's our E2). The aromatization mechanisms make the wall

> >> slippery, so that less and less of the spaghetti (the T)

sticks.

> >> Depending on what's happening, individually and uniquely, in

each

> >of

> >> our bodies, differing amounts will wind up on the wall and on

the

> >> floor.

> >>

> >> With TRT and Arimidex going on, it seems to become a real

> >> juggling act to figure out what to do with adding exogenous T

and

> >> also not winding up with too much E2. This seems to me to be

> >> evidenced empirically by a lot of the " juggling " experiences I

read

> >> about in this group. With TRT **plus** Arimidex, you've got

your

> >> natural production of T plus the added TRT which your body has

to

> >> deal with. Maybe our bodies just have a lot of difficulty

handling

> >> the overload, which could help explain the volatility in results

> >that

> >> some people report.

> >>

> >> On the other hand, if you start taking the Arimidex before

> >> taking T (or, in my case, getting off the T and switching to

> >> Arimidex), everything seems so much simpler. The Arimidex

> >interferes

> >> with the aromatization mechanism, allowing our proverbial wall

to

> >> remain (or become) stickier than it would be otherwise.

Existing T

> >> production sticks to the wall better, leaving less E2 on the

> >floor.

> >> The brute force approach of throwing more and more T into the

body

> >> simply isn't needed, at least for those who are producing enough

T

> >on

> >> their own.

> >>

> >> It seems to me that the traditional TRT approach comes from

a

> >> very linear way of thinking. That is, if there's not enough T

in

> >the

> >> body, add more T. Then if something else winds up messed up

from

> >> this (e.g., too much E2), do something else to fix that. It's

hard

> >> to think that we can make so many different adjustments at the

same

> >> time and expect it to come out just right.

> >>

> >> How about thinking outside the box instead of in a linear

> >> fashion? If somebody can produce plenty of T but it's getting

> >> diverted into something else, why not attack the diversion

problem

> >> first? That way, we don't have to fill up the body with a whole

> >> messy pot of spaghetti. It's so much simpler and cleaner.

> >>

> >> Bob

> >>

> >

> >

> >

>

>

> ________________

> I am human; nothing in humanity is alien to me.

> Terence

>

Agreed with your take on body fat, its one of the few things that

make some sense. At any rate, Bob had a lapband done and is down 100

lbs. If he keeps losing weight, he may drop down to a normal BMI, and

I'd be very curious to see if he can still keep taking 1mg doses of

Arimidex per day at that point.

Rich

[Guest guest]

On Tue, 26 Sep 2006 16:07:27 -0000, you wrote:

>Agreed with your take on body fat, its one of the few things that

>make some sense. At any rate, Bob had a lapband done and is down 100

>lbs. If he keeps losing weight, he may drop down to a normal BMI, and

>I'd be very curious to see if he can still keep taking 1mg doses of

>Arimidex per day at that point.

He should see some momentum from it as well. Because E2 leads to fat

accumulation. And aromotase leads to more E2.

SO less fat, means less aromotase means less E2. And with arimidex

even less.

It makes it easier to lose weight or at least fat - there is some

steroid muscle build up for most folks. A nice leaning process over

time - of the E2 is kept right. My theory anyway.

________________

I am human; nothing in humanity is alien to me.

Terence

[Guest guest]

On Tue, 26 Sep 2006 15:50:52 -0000, you wrote:

>> I look at it differently than Bob. It's not that aromotization gets

>> stronger as we age. It's that most of us as we age get heavier.

>> Aromotase is concentrated in lipid cells. Hence as we get heavier we

>> get more aromotase, hence more E2.

>

> I seem to recall reading that aromatase is associate both with

>aging and with obesity. You are suggesting that the association with

>aging is only because older people get heavier. Are you aware of any

>studies that show that older people who do **not** get heavier do not

>have an increase in aromatase action as they age?

I'm not aware of nay studies either way. But I do know most people put

on weight as they age.

For the flip side I've not seen any studies on aromotase and aging

that controlled for weight. It's just my theory.

In looking at this T stuff for a while there's a ton of studies I'd

sure like to see done. For one I suspect the bone density issues of

low T may result from low T meaning Low E. And the low Es cause the

bone density. It's just a theory but one I'd like to see. (I had bone

density issues. SOmetimes when my E2 gets low I feel a lot of the same

joint and bone pains I felt when the density issues were around.)

As you read this stuff you just realize how little medicine is really

looking t these issues. There's a million basic questions people don't

seem to know the answers to.

________________

I am human; nothing in humanity is alien to me.

Terence

[Guest guest]

On Tue, 26 Sep 2006 15:50:52 -0000, you wrote:

>> These effects combine so that people who are overweight with high E2

>> levels and healthy HPG axis can get back to healthy T levels by

>simply

>> taking arimidex. Studies have shown a 200 to 300 point T boost is

>> possible with just arimidex .

>

>

> This certainly seems to be working in my case. I'll be curious

>to see what happens as I continue to lose weight.

Best of luck. Keep exercising too.

________________

I am human; nothing in humanity is alien to me.

Terence

[Guest guest]

>

> Agreed with your take on body fat, its one of the few things that

> make some sense. At any rate, Bob had a lapband done and is down 100

> lbs. If he keeps losing weight, he may drop down to a normal BMI,

and

> I'd be very curious to see if he can still keep taking 1mg doses of

> Arimidex per day at that point.

> Rich

>

Just got back from my appointment. The doc certainly agrees that the

body fat is a major source of the aromatase problem. He doesn't

usually run into people who have gotten as good a hold on the obesity

problem as I have so doesn't have experience in what happens as I get

into normal BMI territory. His guess is that we won't have to change

very much at all, but we'll be monitoring things monthly.

As for this month's results, you may recall that last month my T was

up at 617. One month later, I'm at 826. This is with a range of 241-

827 ng/dL. My E2 is being retested, because the lab didn't use the

correct methodology as requested.

So, things are looking just hunky-dory for me. Doc says I'm the

champion among all his patients the way my T level has responded and

that I should thank my testicles. I said, " Thank you, thank you. "

One for each gonad.

I engaged him in a little bit of conversation to explore some of the

discussions we've been having here....

* This regimen of Arimidex instead of TRT is not for people whose

testicles don't work or whose HPG axis is nonresponsive. This is a

very small percentage of men (though probably a population that's well-

represented here in this group).

* He is vigorously against the use of Arimidex in conjunction with

TRT. He says that, especially for those who have been on lengthy TRT,

the HPG axis is messed up, and when you introduce Arimidex there's too

great a risk of E2 going too low, which will then introduce other

problems such as the risk of osteoporosis.

* He believes that high estrogen brings a high risk of prostate

cancer. As this becomes accepted by the medical community, he

suspects that most men in the future will be on Arimidex as a

prophylactic against prostate cancer.

Bob

[Guest guest]

>

> >

> > This certainly seems to be working in my case. I'll be

curious

> >to see what happens as I continue to lose weight.

>

> Best of luck. Keep exercising too.

>

>

Thanks. I'm in the gym at least 3 mornings a week: 10-15

minutes of cardio, 5-10 minutes of stretching and 30-45 minutes of

weights. I wanna' keep that lean muscle mass up and increasing.

There's no sense in becoming a flabby skinny person.

Bob

[Guest guest]

Sounds excellent. Your Doc is getting up on the issues and it's sounds

like you can talk with him!!

A few comments below:

On Tue, 26 Sep 2006 18:49:54 -0000, you wrote:

>So, things are looking just hunky-dory for me. Doc says I'm the

>champion among all his patients the way my T level has responded and

>that I should thank my testicles. I said, " Thank you, thank you. "

>One for each gonad.

>

>I engaged him in a little bit of conversation to explore some of the

>discussions we've been having here....

>

>* This regimen of Arimidex instead of TRT is not for people whose

>testicles don't work or whose HPG axis is nonresponsive. This is a

>very small percentage of men (though probably a population that's well-

>represented here in this group).

>

>* He is vigorously against the use of Arimidex in conjunction with

>TRT. He says that, especially for those who have been on lengthy TRT,

>the HPG axis is messed up, and when you introduce Arimidex there's too

>great a risk of E2 going too low, which will then introduce other

>problems such as the risk of osteoporosis.

You can go low. But I think before you start seeing osteoporosis

issues you'll see loss of libido and wood. The trick is moderation.

Very small amounts used carefully. I say this as someone who went

down that road from low T - 8 cracked ribs in two years.

>* He believes that high estrogen brings a high risk of prostate

>cancer. As this becomes accepted by the medical community, he

>suspects that most men in the future will be on Arimidex as a

>prophylactic against prostate cancer.

The research says this. How doe she put this together with his

reservations above?

________________

I am human; nothing in humanity is alien to me.

Terence

[Guest guest]

Bob-

One things for sure: if your testes can put out those levels of T,

you sure 'n hell never needed exogenous testosterone in the first

place. One for the books. Interesting Dr you got there (and you're

lucky - :-))

Rich

>

> > Agreed with your take on body fat, its one of the few things that

> > make some sense. At any rate, Bob had a lapband done and is down

100

> > lbs. If he keeps losing weight, he may drop down to a normal BMI,

> and

> > I'd be very curious to see if he can still keep taking 1mg doses

of

> > Arimidex per day at that point.

> > Rich

> >

>

> Just got back from my appointment. The doc certainly agrees that

the

> body fat is a major source of the aromatase problem. He doesn't

> usually run into people who have gotten as good a hold on the

obesity

> problem as I have so doesn't have experience in what happens as I

get

> into normal BMI territory. His guess is that we won't have to

change

> very much at all, but we'll be monitoring things monthly.

>

> As for this month's results, you may recall that last month my T

was

> up at 617. One month later, I'm at 826. This is with a range of

241-

> 827 ng/dL. My E2 is being retested, because the lab didn't use the

> correct methodology as requested.

>

> So, things are looking just hunky-dory for me. Doc says I'm the

> champion among all his patients the way my T level has responded

and

> that I should thank my testicles. I said, " Thank you, thank you. "

> One for each gonad.

>

> I engaged him in a little bit of conversation to explore some of

the

> discussions we've been having here....

>

> * This regimen of Arimidex instead of TRT is not for people whose

> testicles don't work or whose HPG axis is nonresponsive. This is a

> very small percentage of men (though probably a population that's

well-

> represented here in this group).

>

> * He is vigorously against the use of Arimidex in conjunction with

> TRT. He says that, especially for those who have been on lengthy

TRT,

> the HPG axis is messed up, and when you introduce Arimidex there's

too

> great a risk of E2 going too low, which will then introduce other

> problems such as the risk of osteoporosis.

>

> * He believes that high estrogen brings a high risk of prostate

> cancer. As this becomes accepted by the medical community, he

> suspects that most men in the future will be on Arimidex as a

> prophylactic against prostate cancer.

>

> Bob

>

[Guest guest]

On Tue, 26 Sep 2006 13:18:59 -0700 (PDT), you wrote:

>

> The other interesting thing I found was that while on the arimidex only

regiment, the men's LH for the most part doubled (~ 4 to 8).The resulting T

increased from 290 to 600.

Now that is interesting. SO phil is right- E2 convinces the HPG Axis

that it has enough T and so slows LH.

________________

I am human; nothing in humanity is alien to me.

Terence

[Guest guest]

>

> Now that is interesting. SO phil is right- E2 convinces the HPG Axis

> that it has enough T and so slows LH.

>

That's pretty much common knowledge, at least among the people

that know it. How's that for a self-contradicting statement?

Bob

[Guest guest]

On Tue, 26 Sep 2006 22:13:36 -0000, you wrote:

>

>>

>

>> Now that is interesting. SO phil is right- E2 convinces the HPG Axis

>> that it has enough T and so slows LH.

>>

>

> That's pretty much common knowledge, at least among the people

>that know it. How's that for a self-contradicting statement?

I'd hear it recently but I've never seen any science to support it.

I'm a verify kind of guy. We have lots of theories and assumptions

pass through here that don't stand up under closer scrutiny.

I was raised a scientist. I need the studies.

________________

I am human; nothing in humanity is alien to me.

Terence

[Guest guest]

.

>

> >* He believes that high estrogen brings a high risk of prostate

> >cancer. As this becomes accepted by the medical community, he

> >suspects that most men in the future will be on Arimidex as a

> >prophylactic against prostate cancer.

>

> The research says this. How doe she put this together with his

> reservations above?

>

His reservations on the use of Arimidex are in conjunction with TRT.

He seems to have few reservations when used without TRT.

Bob

[Guest guest]

.

>

> >* He believes that high estrogen brings a high risk of prostate

> >cancer. As this becomes accepted by the medical community, he

> >suspects that most men in the future will be on Arimidex as a

> >prophylactic against prostate cancer.

>

> The research says this. How doe she put this together with his

> reservations above?

>

His reservations on the use of Arimidex are in conjunction with TRT.

He seems to have few reservations when used without TRT.

Bob

[Guest guest]

>

> For sole Arimidex treatment is it important that the E2 is high to

begin with?

> sorry if I missed that part of this thread.

Well, I'm extrapolating here, because my doctor never put it

precisely that way, but what you say sounds generally true. Once you

use Arimidex, it will interfere with the conversion of T to E2, thus

allowing the T supply to increase, while the E2 supply decreases.

Bob

[Guest guest]

> >>

> >

> >> Now that is interesting. SO phil is right- E2 convinces the HPG

Axis

> >> that it has enough T and so slows LH.

> >>

> >

> > That's pretty much common knowledge, at least among the

people

> >that know it. How's that for a self-contradicting statement?

>

>

> I'd hear it recently but I've never seen any science to support it.

> I'm a verify kind of guy. We have lots of theories and assumptions

> pass through here that don't stand up under closer scrutiny.

>

> I was raised a scientist. I need the studies.

>

You need science? Well, I'm not going to read all the studies since

I seem to have been convinced of this even before the Arimidex has

proved it in practice for me, but here's a head start for you with

articles and abstracts on the web, all containing further references:

" Overall view of negative feedback inhibition by testosterone "

http://www.pumpedmag.com/articles/fall05/02text.htm

R J Santen, Is aromatization of testosterone to estradiol required

for inhibition of luteinizing hormone secretion in men?, J Clin

Invest. 1975 December; 56(6): 1555–1563.

http://www.pubmedcentral.nih.gov/botrender.fcgi?

blobtype=html & artid=333134

J. A. Schnorr2, M. J. Bray and J. D. Veldhuis, Aromatization

Mediates Testosterone's Short-Term Feedback Restraint of 24-Hour

Endogenously Driven and Acute Exogenous Gonadotropin-Releasing

Hormone-Stimulated Luteinizing Hormone and Follicle-Stimulating

Hormone Secretion in Young Men, The Journal of Clinical

Endocrinology & Metabolism Vol. 86, No. 6 2600-2606,

http://jcem.endojournals.org/cgi/content/full/86/6/2600. Search in

this abstract for " excessive estrogen delivery represses

gonadotropin secretion in the human "

See extensive list of abstracts on male hormone modulation at

http://www.lef.org/protocols/abstracts/abstr-txt/t-abstr-130.html