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Jelisej
03-04-2013, 09:17 AM
Clomid For Men With Low Testosterone by Jeffrey Dach MD
Nice article about clomid with lot of studies and different reports from treatments.

Part 1:
Jeffrey Dach MD Bio-Identical Hormone Blog: Clomid For Men With Low Testosterone by Jeffrey Dach MD (http://jeffreydach.com/2012/06/18/clomid-for-men-with-low-testosterone-by-jeffrey-dach-md.aspx)

Part 2:
Jeffrey Dach MD Bio-Identical Hormone Blog: Clomid For Men With Low Testosterone, Part Two (http://jeffreydach.com/2013/03/01/clomid-for-men--with-low-testosterone-part-two.aspx)

Clomiphene Clomid Adverse Side Effects Part Three by Jeffrey Dach MD - Jeffrey Dach MD (http://jeffreydachmd.com/2013/04/clomiphene-clomid-adverse-side-effects-part-three/)

Fat Bill Dwyer
03-04-2013, 12:36 PM
Thanks again for some great case studies. I feel like I have improved my awareness of variances within HPTA suppression after reading them.

I do have a question though. What sensitized the bodybuilder's Hypothalamus to E2 so much? Obviously the AAS, but was it due to having long periods of high E2 from using heavily aromatizing compounds, or E2 rebound during a poor PCT?

Or did long periods of low E2 from using non-aromatizing compounds, or maybe being too aggresive with AIs upregulate E2 receptors in the hypothalamus?

Interested in anything you might know.

Jelisej
03-04-2013, 01:08 PM
Either I dont understand question properly or I dont know the answer :D. Not sure what you mean here: "What sensitized the bodybuilder's Hypothalamus to E2 so much?"
Now I know that majority of people who use AI to increase testosterone levels or because of high estrogen eventually end up with both low testosterone and low estrogen. Also guys who have been on TRT for years usually decrease AI dosage (to certain extent).

As why people get a high estrogen levels? Because aromatisation (decreased testicular function) lot of visceral fat etc... Envirometal factors, low adrenal output but also when cortisol goes to high it starts to aromatise (which practically does not happen so often, I think).

Fat Bill Dwyer
03-04-2013, 07:46 PM
I guess I misunderstood the article, so I read it again. This guy's problem was that too much test was aromatizing into E2. So it's not really a hypothalamus problem, it's an aromatase problem. Somewhere along the line he upregulated aromatase production and now his hypothalamus is responding properly to improper amounts of E2? Pretty much the same question, but with aromatase instead of hypothalamus.

Non-aromatizing compounds ran for a long time result in crashed test levels, and subsequently crashed E2 levels that would cause an increase in aromatase synthesis. Is this basically correct?

Crashing E2 with aromatase inhibitors would cause the same thing no?

What about test? I assume that more aromatase would also be synthesized in response to the test:E2 ratio getting too big. Is this true?

Obviously there's no research on what sort of compounds are more likely to cause this issue, but are there any decent theories, or bro-science?

Also I was wondering if you be able to help me with a few questions about aromatase. Wikipedia wasn't much help.

In what tissues is it synthesized?

What activates the gene that encodes it?

How long does aromatase "hang around" before it becomes inactive?

Thanks again bro.

O_RYAN_007
03-04-2013, 10:30 PM
Great articles J!

Jelisej
03-05-2013, 10:33 AM
Bill, from brains/body's point of view Estrogens are much more important than testosterone, and estrogens have more effect on neurotransmitters than for example testosterone. When hippotalamus senses that estrogen levels are insufficient it ramps up LH production from which testost. and estrogens (via aromatase) are made. Lh stimulates production of aromatase as well, (HCG does the same thing), endos say that aromatase also gets stored in fat tissue and as person tries to loses weight it relases and it makes job more difficult. Also reduced testicles functionality leads to more aromatisation.
Now, some endos said that there are other pathways of making estrogens, I dont know much about that; this is part of Dr Marianco's post: "In some men, the body may compensate by increasing production of estradiol via alternative pathways when its production via the aromatase enzyme is reduced excessively. Thus there may be a ceiling in reducing estradiol after which the body uses other pathways to produce estrogen. Also other estrogens may be produced when estradiol is reduced excessively. One can't also reduce estradiol excessively before the liver compensates by increasing cholesterol production."

part of certain hormones and their "signaling" to brain I dont understand to the point I could give any explanations; again part of Marianco's post:The sensitivity of each male to estradiol's effects will vary with the levels of other hormones, signals, and metabolic-nutritional status. For example, the estrogen signal, itself, may need adequate progesterone to stimulate the production of estrogen receptors. If hypothalamic-pituitary adrenal dysregulation is present, the estrogen signal is attenuated and symptoms of low estrogen may occur at higher levels. Additionally, thyroid hormone levels increase SHBG levels. The higher the SHBG, the higher the estradiol but less is free to function. Thus the estradiol signal is reduced despite the higher level. Once the other signal and metabolic-nutritional problems are addressed and signaling optimized in the other systems, the male may not have as large a negative effect from estradiol as prior to addressing the other problems first.


personaly, I think this signaling is just a fancy way of expaining things like: Changing one signal (as in testosterone) causes multiple downstream signaling changes in other systems. As long as one is ready to make the adjustments to thyroid hormone signaling and other signaling systems with TRT (such as estrogen signaling, adrenal signaling, nervous system, immune system, metabolism, nutrition, etc.), then one can avoid some complications with TRT, such as anxiety, fatigue, hypertension, insomnia, body aches, etc.

He could in other words say like: Testosterone downregulates thyroid releasing hormone production. In both cases we dont know what is mechanism of action, how does testosterone changes signaling of TRH or how test. downregulates TRH...

How long does aromatase "hang around"? Excellent question on which I never heard an meaningful answer. I would say its active life is long one, but it does have an end- for example people using non-sucidal (non-steroidal, reversible) AI like arimidex after a months of usage after they stop it experience "rebound effect" as lot of aromatase gets released (from arimidex) so their E2 goes high meaning that aromatase half-life is longer than arimidex's but I guess that lot of aromatse got "expired" otherwise their E2 levels would be even higher.

When crashing E2 one does not always have to have strong symptoms, obviously there would be some libido loss and erection quality loss (but if DHT is high eq may still be good enough altough "sensation" will be poor) and there would be some other effect on mood (estrogens stimulate serotonin a lot).
Worst thing with low estrogen is that it results in weak bones, and you cannot tell that until they start breaking.

As when one is on anabolics SHBG will be reduced (sometimes virtualy to zero) and in that cirmcustances less E2 is needed to do biological action (free estrogen- same as with free testosterone).

If using compounds that aromatise a lot one can use AI to try to control E2 as best as possible, in opposite scenario one can add DHEA as most of excessive DHEA will convert to estrogen. Tough side is that lot of DHEA may reduce ACTH signal which may reduce cortisol levels which is not really wanted.

But thing is any AAS cycle will affect endocrine system as whole and if any segment of it does not recover properly it will pose a problem some time in future. Adrenals will affect estrogen and tt levels, and thyroid levels. Thyroid will affect adrenals and sex hormones, sex hormone will affect adrenals and thyroid... So its hard to see bigger picture...

Don know if thats answer is what you asked for, you may ask again if I missed something, but mind you I'm just a random guy, not an expert...

Fat Bill Dwyer
03-05-2013, 12:10 PM
Thanks for the detailed answer. There is an abundance of information in there that put together a lot of things for me.

O_RYAN_007
03-05-2013, 06:14 PM
Bill, from brains/body's point of view Estrogens are much more important than testosterone, and estrogens have more effect on neurotransmitters than for example testosterone. When hippotalamus senses that estrogen levels are insufficient it ramps up LH production from which testost. and estrogens (via aromatase) are made. Lh stimulates production of aromatase as well, (HCG does the same thing), endos say that aromatase also gets stored in fat tissue and as person tries to loses weight it relases and it makes job more difficult. Also reduced testicles functionality leads to more aromatisation.
Now, some endos said that there are other pathways of making estrogens, I dont know much about that; this is part of Dr Marianco's post: "In some men, the body may compensate by increasing production of estradiol via alternative pathways when its production via the aromatase enzyme is reduced excessively. Thus there may be a ceiling in reducing estradiol after which the body uses other pathways to produce estrogen. Also other estrogens may be produced when estradiol is reduced excessively. One can't also reduce estradiol excessively before the liver compensates by increasing cholesterol production."

part of certain hormones and their "signaling" to brain I dont understand to the point I could give any explanations; again part of Marianco's post:The sensitivity of each male to estradiol's effects will vary with the levels of other hormones, signals, and metabolic-nutritional status. For example, the estrogen signal, itself, may need adequate progesterone to stimulate the production of estrogen receptors. If hypothalamic-pituitary adrenal dysregulation is present, the estrogen signal is attenuated and symptoms of low estrogen may occur at higher levels. Additionally, thyroid hormone levels increase SHBG levels. The higher the SHBG, the higher the estradiol but less is free to function. Thus the estradiol signal is reduced despite the higher level. Once the other signal and metabolic-nutritional problems are addressed and signaling optimized in the other systems, the male may not have as large a negative effect from estradiol as prior to addressing the other problems first.


personaly, I think this signaling is just a fancy way of expaining things like: Changing one signal (as in testosterone) causes multiple downstream signaling changes in other systems. As long as one is ready to make the adjustments to thyroid hormone signaling and other signaling systems with TRT (such as estrogen signaling, adrenal signaling, nervous system, immune system, metabolism, nutrition, etc.), then one can avoid some complications with TRT, such as anxiety, fatigue, hypertension, insomnia, body aches, etc.

He could in other words say like: Testosterone downregulates thyroid releasing hormone production. In both cases we dont know what is mechanism of action, how does testosterone changes signaling of TRH or how test. downregulates TRH...

How long does aromatase "hang around"? Excellent question on which I never heard an meaningful answer. I would say its active life is long one, but it does have an end- for example people using non-sucidal (non-steroidal, reversible) AI like arimidex after a months of usage after they stop it experience "rebound effect" as lot of aromatase gets released (from arimidex) so their E2 goes high meaning that aromatase half-life is longer than arimidex's but I guess that lot of aromatse got "expired" otherwise their E2 levels would be even higher.

When crashing E2 one does not always have to have strong symptoms, obviously there would be some libido loss and erection quality loss (but if DHT is high eq may still be good enough altough "sensation" will be poor) and there would be some other effect on mood (estrogens stimulate serotonin a lot).
Worst thing with low estrogen is that it results in weak bones, and you cannot tell that until they start breaking.

As when one is on anabolics SHBG will be reduced (sometimes virtualy to zero) and in that cirmcustances less E2 is needed to do biological action (free estrogen- same as with free testosterone).

If using compounds that aromatise a lot one can use AI to try to control E2 as best as possible, in opposite scenario one can add DHEA as most of excessive DHEA will convert to estrogen. Tough side is that lot of DHEA may reduce ACTH signal which may reduce cortisol levels which is not really wanted.

But thing is any AAS cycle will affect endocrine system as whole and if any segment of it does not recover properly it will pose a problem some time in future. Adrenals will affect estrogen and tt levels, and thyroid levels. Thyroid will affect adrenals and sex hormones, sex hormone will affect adrenals and thyroid... So its hard to see bigger picture...

Don know if thats answer is what you asked for, you may ask again if I missed something, but mind you I'm just a random guy, not an expert...

PCT is definitely a sensitive subject, and it seems as though everyone has their own protocols. What duration and what compounds/dosages would you recommend for a complete well rounded PCT?

Jelisej
03-07-2013, 09:24 AM
PCT is basically same thing as restart protocol only shorter (asuming person used HCG and did not allow E2 to goes out of control especuially at the end of cycle) I would say 8 weeks of SERM is enough (including tappering down), only in pct anti-cortisol may be included if neccesary.
This is my post about restart protocol from other thread:
He should run 13 weeks of 25mg of clomid every day or alternatively 50 mg every other day (some people react better on 50 mg every second day for some reason), then he should slowly start tappering down for another 4-8 weeks, (reducing on 75% for week or two, than 50% for couple of weeks, than 25% for week or two), in conjuction he should use AI (preferably irreversible/suicidal) like aromasin 12.5 mg 3X a week- he should run AI until 2-3 weeks after cesation of SERM.
Other thing he should eat mixed nuts every day (they will increase testicular sensitivity to LH- its actually same thing as tocco-8.
Vitamin d 1000 IU every day. (maybe more- up to 4000)
I'm not fan of DAA but in this situation its very helpful.
He should not exercise too much. Must get enough sleep.
Now, important thing is not just recovery of HPTA- but what is also target here- to create better "set point"- we are hoping that his "body" will accept normal/higher levels of TT rather than return to 300-400 ng/dl which is far below.

pman42
04-23-2013, 08:22 PM
Too bad Jelisej is no longer here, but I was wondering if anyone could shed some light on what he said here:


Now I know that majority of people who use AI to increase testosterone levels or because of high estrogen eventually end up with both low testosterone and low estrogen. Also guys who have been on TRT for years usually decrease AI dosage (to certain extent).

weekend
06-26-2013, 12:53 AM
alex is back! ^

pman42
07-14-2013, 12:26 AM
SO in a man with low testosterone and in whom clomid is acting as a sort of TRT, would one expect to see body composition changed associated with higher testosterone levels? i know that some people say you can't "feel" clomid like you can TRT

weekend
07-14-2013, 01:49 AM
I feel like I noticed changes.. Bloods 6 week post clomid at 50 mg for 5 weeks showed test at 1370 ng/dl (out of range) I'm sure it was higher in PCT and I was liftin hard for sure!

pman42
07-14-2013, 05:57 PM
right but it's always hard to tell right after a cycle because the gains can be coalescing. do you feel the clomid boosted things more than natural training?