Re: Re: Arimidex vs. DIM

January 9, 2007

I am trying the 0.25 mg ervery-other-day for six days and nothing on the

7th, then injection of 0.5 ml of 200mg/ml of Test. enanthate. So far I think

that this is OK. It is the first week that I have tried this and feel OK.

Other weeks I have gone too low and had to lay off for a while. I really

have to be careful and not go too far in one direction or the other.

Louis.

January 10, 2007

I feel this should work just keep on Eye on your morning wood going to low you

can 't get it up taking a pill.

Phil

louislarocque@... wrote:

I am trying the 0.25 mg ervery-other-day for six days and nothing on

the

7th, then injection of 0.5 ml of 200mg/ml of Test. enanthate. So far I think

that this is OK. It is the first week that I have tried this and feel OK.

Other weeks I have gone too low and had to lay off for a while. I really

have to be careful and not go too far in one direction or the other.

Louis.

January 10, 2007

I guess the other difference between the DIM an Arimidex is that the

Arimidex keeps your overall T level up as opposed to DIM.

Correct?

Louis

January 10, 2007

Arkansas,

So you are on 1/4 mg per injection. This does not seem like much at all.

Did you try other regimes before getting to this?

I am trying 0.25mg every-other-day for 6 days then nothing on the seventh,

then the injection of .5 ml of 200mg/ml enathate. I have yet to test but will

be doing so in a week. I feel OK but some days are tough.

Louis

January 10, 2007

I take 1/4th on the day I take my shot. Keep in mind that I usually get tested

on the last day or next to last of my 7 day cycle. So you would expect your E2

to go lower as your T goes lower. I do not have numbers on this regiment for the

peak value.

Arkansas

chis_az <chis_az@...> wrote:

How often are you on the 1/4 of arimidex dan?

Chris

> I am wondering what is the difference between the two?

>

> I currently use Arimidex. The pills are very small. I have found it

easy to

> go too low.

>

> Have people noticed any treatment differences? Is one easier to

dose than

> the other?

>

> Louis

>

January 11, 2007

No just getting E2 down brings up your T levels Free T goes up because getting

E2 down brings down SHBG.

Phil

louislarocque@... wrote:

I guess the other difference between the DIM an Arimidex is that the

Arimidex keeps your overall T level up as opposed to DIM.

Correct?

Louis

January 11, 2007

Yes I tried higher doses of arimidex and my E2 went offscale low. Through trial

and error, this value seems to be about right. I probably could doe 1/4 two

times a week and still be OK but I am trying to minimize cost and not take stuff

I don't have to. There is still some issues associated with long term use of

arimidex by men that are unknown. My theory is that if used in moderation (like

most things) will minimize the risk. Am I as horny as an 18 year old - no but I

can do what I need to do.

Arkansas

louislarocque@... wrote:

Arkansas,

So you are on 1/4 mg per injection. This does not seem like much at all.

Did you try other regimes before getting to this?

I am trying 0.25mg every-other-day for 6 days then nothing on the seventh,

then the injection of .5 ml of 200mg/ml enathate. I have yet to test but will

be doing so in a week. I feel OK but some days are tough.

Louis

January 11, 2007

Maybe I did not phrase my statement the way that I really meant it. I am

primary therefore do not really think in terms of the feedback mechanism, my

body cannot produce much T no matter what. Therefore the testosterone that is

injected either gets bound to SHBG or albumin or is in a free state or gets

converted to E2.

If I continue along this line of thought:

- If I take Arimidex then more T stays free instead of converting to E2,

when my free T is high

- If I was to use DIM then some fraction of my free T would end up as E2

then further converted to ....I forget exactly. The end result is a lower Total

T for a given injection.

I presently have very low SHBG (could be thyroid.....) and this complicates

things. For me to get a high Total T my free T may have to be relatively much

higher than most. I am not sure that I want to get it that high yet but if I

do my above reasoning is that the DIM will work a bit against me.

Any thought on my thinking on this?

Louis

January 11, 2007

So your saying this never happens Free T is bound to SHBG in a lot of men I have

talked to that had High SHBG and E2 with low Free T. Getting E2 down the SHBG

went down and the Free T come up. In this study SHBG came down.

http://jcem.endojournals.org/cgi/content/full/89/3/1174

Phil

chis_az <chis_az@...> wrote:

I think that's incorrect Phil.

Bringing down E2 usually increase total and free testosterone and it

does so independently of SHBG.

Reducing SHBG does not by any means automatically mean that SHBG will

be reduced.

The reason reducing E2 increase testosterone in basic terms is

because;

The hypothalamus cannot differentiate between testosterone and E2 and

the hypothalamus basis its negative feedback system on the total

steroid level (combined E2 DHT and Testosterone levels etc). When

you reduce E2, the hypothalamus assumes that there is too little

testosterone and so upregulates GnRH, this in turn upregulates LH-

end result- increased testosterone.

Although there are interactions between the hormones and SHBG, its

relationship is far less clear and not well understood and is less

linear than that of E2 and testosterone.

If reducing SHBG were as simple as reducing E2 then high SHBG would

be treated with arimidex, but it isn't.

In fact that is why there are medications such as Danazol.

> I guess the other difference between the DIM an Arimidex

is that the

> Arimidex keeps your overall T level up as opposed to DIM.

>

> Correct?

>

> Louis

>

January 11, 2007

On Thu, 11 Jan 2007 20:04:01 -0000, you wrote:

>

>The hypothalamus cannot differentiate between testosterone and E2 and

>the hypothalamus basis its negative feedback system on the total

>steroid level (combined E2 DHT and Testosterone levels etc).

Do you have a literature cite for that?

-----

" Anyone who has the power to make you believe absurdities has the

power to make you commit atrocities. " - Voltaire

January 11, 2007

On Fri, 12 Jan 2007 02:06:04 -0000, you wrote:

>The negative feedback/ system/ Hypothalamus simply cannot

>differentiate between the differing sex steroids.

I've read and listened to a lot of lectures on endocrinology and I've

not heard this before. I'd appreciate it if you could point me to

something on this.

-----

" Anyone who has the power to make you believe absurdities has the

power to make you commit atrocities. " - Voltaire

January 11, 2007

On Thu, 11 Jan 2007 19:59:58 EST, you wrote:

>Maybe I did not phrase my statement the way that I really meant it. I am

>primary therefore do not really think in terms of the feedback mechanism, my

>body cannot produce much T no matter what. Therefore the testosterone that is

>injected either gets bound to SHBG or albumin or is in a free state or gets

>converted to E2.

(Or converts to DHT)

-----

" Anyone who has the power to make you believe absurdities has the

power to make you commit atrocities. " - Voltaire

January 12, 2007

I can only go by what Arimidex and DIM did for me. My levels never changed

going from Arimidex to Indolplex/DIM and I got tested at the time every 4 weeks.

I don't know if you seen these but read for you self here are some likes I

have.

http://www.dimfaq.com/index.htm

This is a cut and paste from this link.

http://qualitycounts.com/fpdim.html

" DIM helps to eliminate active estrogen from the male body by promoting its

conversion into the " good " metabolites. These metabolites then free up

testosterone by bumping it off the testosterone-binding proteins. The end result

is a healthier balance of testosterone to estrogen and more free testosterone

circulating in the body. In scientific studies, high levels of testosterone and

low levels of estrogen have been linked to lean body mass, an efficient

fat-burning metabolism, and low abdominal obesity. Other benefits from

testosterone are improved mood, more interest in sex, and better physical

conditioning. In this chapter, we'll explore these issues in more detail. "

Phil

louislarocque@... wrote:

Maybe I did not phrase my statement the way that I really meant it. I

am

primary therefore do not really think in terms of the feedback mechanism, my

body cannot produce much T no matter what. Therefore the testosterone that is

injected either gets bound to SHBG or albumin or is in a free state or gets

converted to E2.

If I continue along this line of thought:

- If I take Arimidex then more T stays free instead of converting to E2,

when my free T is high

- If I was to use DIM then some fraction of my free T would end up as E2

then further converted to ....I forget exactly. The end result is a lower Total

T for a given injection.

I presently have very low SHBG (could be thyroid.....) and this complicates

things. For me to get a high Total T my free T may have to be relatively much

higher than most. I am not sure that I want to get it that high yet but if I

do my above reasoning is that the DIM will work a bit against me.

Any thought on my thinking on this?

Louis

January 12, 2007

Here is a cut & paste of some of what they said about SHBG doing down when E2

went down.

--------------------------------------------------------------------------------\

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

Mean serum SHBG levels decreased from 38 ± 12 to 34 ± 12 nmol/liter

--------------------------------------------------------------------------------\

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

Nothing works the same for eveyone but in my case and some others there SHBG

went down when E2 went down. And there Free T went way up. I had to lower my

dose of TRT just like the others did.

So let me restate my post to say " No just getting E2 down brings up your T

levels Free T goes up because getting E2 down (CAN) bring down SHBG. "

Phil

chis_az <chis_az@...> wrote:

Phil,

As far as I see it you have made an unfounded statement and you are

trying to substantiate such with a link that does not as far as I can

see say anything like what you are saying. Even if one link

supported such a notion it would not necessarily constitute proof,

even so I don't think the link supports you.

..

I said quote

Bringing down E2 usually increase total and free testosterone and it

does so independently of SHBG.

The reason reducing E2 increase testosterone in basic terms is

because;

The hypothalamus cannot differentiate between testosterone and E2 and

the hypothalamus basis its negative feedback system on the total

steroid level (combined E2 DHT and Testosterone levels etc). When

you reduce E2, the hypothalamus assumes that there is too little

testosterone and so upregulates GnRH, this in turn upregulates LH-

end result- increased testosterone.

unquote

Your report said quote

Anastrozole's effect on androgen production is likely directly

mediated by the reduction in estrogen production By reducing

estradiol synthesis (and hence estradiol's negative feedback on the

pituitary and hypothalamus) (30, 31, 32, 33), anastrozole appears to

stimulate pituitary LH secretion sufficiently to increase endogenous

testosterone.

unquote

Forgive me if I am wrong, but haven't you just produced a report that

has agreed with every word I have said?

Moving on to what you said……

Quote

So your saying this never happens Free T is bound to SHBG in a lot of

men I have

talked to that had High SHBG and E2 with low Free T. Getting E2 down

the SHBG

went down and the Free T come up. In this study SHBG came down.

Unquote

First of all you are putting words in my mouth and I think there is a

danger of completely misinterpreting what I am saying by doing that.

I am saying;

I agree that E2 is lowered by Arimidex and I agree that this tends in

most men to result in an increase in LH, total testosterone and free

testosterone. I believe it does so in the exact manner described in

the link you offered, Which is what I was saying anyway.. This says

nothing of arimidex's in relation to SHBG (If I am missing something

then I apologise- but I would need pointing to it).

In fact, does it say anywhere in that link/report that SHBG was

lowered?

Irrespective of that;

Can you show me serious substantiated evidence that SHBG is

significantly lowered with the use of arimidex?

I'm not sure you can, I'll be happy to look at it and alter my

thoughts if you can do that.

My position is this;

Arimidex's mechanism of action as far as I know is that described in

the report. I sated the same before you presented me the report.

I am not saying that SHBG is not affected by arimidex, but I am

saying that A) that is not the principle mechanism of action of

arimidex and the relationship between SHBG and androgens and

estrogens and other hormones is complex and not linear in the way you

have suggested.

Given the complexities involved I would not say that it is impossible

for SHBG to come down in some men with arimidex.. But what I am

saying is that A) I don't think SHBG will come down significantly in

many men who take arimidex and I don't think it is the medicine of

choice for the lowering of SHBG. Danazol is supposed to be far more

effective in that regard.

From what I have seen I think you might be making unfounded

statements or at the least overly simplistic statements that are not

uniformly true. If you can show me otherwise I'll be more than happy

to accept that.

> > I guess the other difference between the DIM an Arimidex

> is that the

> > Arimidex keeps your overall T level up as opposed to DIM.

> >

> > Correct?

> >

> > Louis

> >

January 12, 2007

Here are some cut & pastes from this link this is the first thing I ever read on

high E's in men and still to me the best.

http://www.griffinmedical.com/male_hormone_modulation_therapy.html

A more comprehensive study incorporating a different combination of

nutrients resulted in eight out of eight men experiencing increases in free

testosterone while levels of the undesirable SHBG declined in seven out of eight

men, compared to baseline. Estrogen and other blood parameters were not

significantly altered in this study.

One further complication of excess estrogen is that it increases the body's

production of sex hormone-binding globulin (SHBG). SHBG binds free testosterone

in the blood and makes it unavailable to cell receptor sites (51, 52, 55, 56).

Estrogen can also increase the production of SHBG, which binds the active

free testosterone into an inactive " bound testosterone. " Bound testosterone

cannot be picked up by testosterone receptors on cell membranes. For

testosterone to produce long-lasting, libido-enhancing effects, it must be kept

in the " free " form (not bound to SHBG) in the bloodstream. It is also necessary

to suppress excess estrogen because this hormone can compete for testosterone

receptor sites in the sex centers of the brain and the genitals.

As readers of Life Extension Magazine learned in late 1997, estrogen has been

identified as a primary culprit in the development of benign prostatic

hyperplasia (BPH). Estrogen has been shown to bind to SHBG in the prostate gland

and cause the proliferation of epithelial cells in the prostate (124, 182-184).

This is corroborated by the fact that as men develop benign prostate

enlargement, their levels of free testosterone plummet, although their estrogen

levels remain the same or are rising. As previously discussed, aging men tend to

convert their testosterone into estrogen. The published evidence shows that

higher serum levels of testosterone are not a risk factor for developing benign

prostate disease (8, 36, 41, 117-137).

Lifestyle Changes

Lifestyle changes (such as reducing alcohol intake) can produce a dramatic

improvement in the estrogen-testosterone balance, but many people need to use

aromatase-inhibiting agents to lower estrogen and to improve their liver

function to remove excess SHBG. Aromatase converts testosterone into estrogen

and can indirectly increase SHBG. SHBG binds to free testosterone and prevents

it from exerting its biochemical effects in the body.

Consider following some of the recommendations in the previous section to

inhibit aromatase because many of the same factors are involved in excess SHBG

activity.

As discussed already, a hormone that controls levels of free testosterone is

called SHBG. When testosterone binds to SHBG, it loses its biological activity

and becomes known as " bound testosterone, " as opposed to the desirable " free

testosterone. " As men age past age 45, SHBG's binding capacity increases almost

dramatically--by 40% on average--and coincides with the age-associated loss of

libido.

Some studies show that the decline in sexual interest with advancing age is

not always due to the amount of testosterone produced, but rather to the

increased binding of testosterone to globulin by SHBG. This explains why some

older men who are on testosterone replacement therapy do not report a long-term

aphrodisiac effect. That is, the artificially administered testosterone becomes

bound by SHBG and is not bioavailable to cellular receptor sites where it would

normally produce a libido-enhancing effect.

It should be noted that the liver also causes tes-tosterone to bind to

globulin. This liver-induced binding of testosterone is worsened by the use of

sedatives, antihypertensives, tranquilizers, and alcoholic beverages. The

overuse of drugs and alcohol could explain why some men do not experience a

libido-enhancing effect when consuming drugs and plant-based aphrodisiacs. An

interesting review entitled " How Desire Dies " (Nature, 381/6584, 1996) discusses

how frequently prescribed drugs, such as beta-blockers and antidepressants,

cause sexual dysfunction. Prescription drugs of all types have been linked to

inhibition of libido.

Logically, one way of increasing libido in older men would be to block the

testosterone-binding effects of SHBG. This would leave more testosterone in its

free, sexually activating form.

If all of the above fail to increase free testosterone and lower excess

estradiol, ask your doctor to prescribe the potent aromatase inhibiting drug

Arimidex (anastrozole) in the very low dose of 0.5 mg twice a week. Arimidex is

prescribed to breast cancer patients at the dose of 1-10 mg a day. Even at the

higher dose prescribed to cancer patients, side effects are rare. In the minute

dose of 0.5 mg twice a week, a man will see an immediate drop in estradiol

levels and should experience a rise in free testosterone to the optimal range.

Phil

chis_az <chis_az@...> wrote: The negative feedback/ system/

Hypothalamus simply cannot

differentiate between the differing sex steroids.

I have read this from many, many, many expert sources.

What shows this fact best of all is pathology.

If estradiol increases and testosterone and DHT remain the same, the

hypothalamus will be looking to reduce GnRH and in turn LH. If

estradiol and testosterone remain the same and DHT increases then

once again the hypothalamus will reduce GnRH and in turn LH.

For the most part you are looking at a three way balancing act. If

any of these three sex steroids increases GnRH and LH will be lowered

and you are looking at a negative feedback loop. (obviously if the

total level of sex steroids reaches a certain level you have complete

LH suppression and in these situations the above facts cannot be

readily seen in pathology)

A classic example of this balancing act going wrong and something

that shows how the sex steroids are not correctly differentiated by

the hypothalamus is seen in metabolic hypogoandism.

Often the individual has an inappropriately NORMAL LH given a low

testosterone level. Such individuals do not have any disease in the

testicles or pituitary. When such men have dynamic evocative tests

the HPTA shows a normal response and an increasing LH levels. Often

this results in endocrinologists incorrectly telling the patient that

they are not hypogondal because LH looks normal.

As we know with typical secondary hypogonadism we see lowered

gonadotropins. With testicular failure and typical primary

hypogonadism we see elevated gonadotropins.

In this case we see a normal LH DESPITE a low testosterone. This of

course should not happen, so why does it happen?

Because despite the fact that low testosterone and a working HPTA

should see increased LH in order to rectify the problem, there is an

inappropriately high level of estradiol- which the hypothalamus

cannot differentiate from testosterone- this tricks the hypothalamus

into thinking that there is enough testosterone when there is not and

as a result we have a our negative feedback problem and metabolic

hypogonadism.

I am going to get my copy of the Testosterone Syndrome by Eugene

Shippen and look at Chapter 5 on Estrogen, because I am sure that is

one source that cites this fact.

Hang on...I'll get the page an quote verbatim.....

Ok this almost explains the situation and is the best I have to hand

at present.

Quote

The mechanism of action is that the female hormone occupies some of

the hypothalamic receptors in the brain. The hypothalamus is tricked

into acting as if testosterone levels in the body are high, and so it

fails to send out the hormones that would tell the pituitary gland to

stimulate testosterone production in the gonads. This is a form of

the secondary hypogonadism that we discussed in the last chapter,

dependent now not upon a disease state or pharmaceutical side effects

or mere aging but purely upon an inappropriate high level of estrogen.

unquote

I would like to have a word for word source that I could cite for

you, but I don't keep these sources for such occasions, I just learn

what I need to for my own purposes.

Hopefully that covers it above well enough…

>

> >

> >The hypothalamus cannot differentiate between testosterone and E2

and

> >the hypothalamus basis its negative feedback system on the total

> >steroid level (combined E2 DHT and Testosterone levels etc).

>

> Do you have a literature cite for that?

> -----

> " Anyone who has the power to make you believe absurdities has the

> power to make you commit atrocities. " - Voltaire

>

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

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January 12, 2007

Are you two mixing apples and oranges? I think one situation is using arimidex

only and the affect has and the other is using arimidex while taking

testosterone externally. They both have radically different responses especially

related to LH.

Arkansas

chis_az <chis_az@...> wrote:

The negative feedback/ system/ Hypothalamus simply cannot