Testosterone, DHT, Estrogen Balance

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This thread is set up to foster an intelligent discussion of how a man's testosterone/dht/estrogen balance affects his hair loss and regrowth, and what natural substances can be used to modulate the levels of those hormones.

Just to start it off, here's an interesting article I found about using phytoestrogens to occupy estrogen receptor sites, and thus, modulate the negative effects of this hormone:

Estrogen, Testosterone, & Phytoestrogens
by Mike Falcon

As bodybuilders, there are words we love and words we hate. Valued words include testosterone, muscle mass, androgens, protein and Tylene Buck. Bad words and phrases? Impotence, testicular withering, dialysis, and "she's got a boyfriend.".

In a class by itself is the dreaded E-word. Estrogen is one of the most feared words in bodybuilding, and sadly, one of the most misunderstood. "The vast majority of bodybuilders don't understand the nature and role of estrogen or phytoestrogens," observes Tom Prince, 1997 USA champion. "They haven't investigated the nature of the phytoestrogens or attempted to determine how and why estrogen is produced...in men, as well as in women." Without a good overview, the average bodybuilder avoids anything that has, could have, or may contribute to the production of estrogen.

"That's a shame," says Dr. Eugene Shippen, M.D., a Reading, Pennsylvania internist and author (with William Fryer) of The Testosterone Syndrome: The Critical Factor for Energy, Health, & Sexuality ---Reversing the Male Menopause (publisher: M. Evans and Company, Inc., New York, NY. ISBN #0-87131-829-6). "Both testosterone and estrogen play vital roles in the healthy male's life overall." And in their sex lives and ability to build muscle mass. Shippen is an unabashed proponent of testosterone supplementation to cure a wide variety of ills, from lethargy to the slowly creeping (and rather creepy concept of) male menopause, which he re-terms metabolic andropause. The symptoms of metabolic andropause, as related in Dr. Shippen's book, bear an almost uncanny resemblance to overtraining and the overuse of anabolic steroids:

If you're overtraining or taking anabolic steroids, these indicators of metabolic andropause, testosterone deficiency, or an estrogen/testosterone imbalance may seem more than fleetingly familiar: Nervousness, insomnia, depression, antisocial tendencies, inability to concentrate, hot flashes, chilliness, increased pulse rate, headache, weakness, fatigue, muscle pains, decreased urinary flow force coupled with more frequent urinations, decrease in sexual interest and decreased erections.

What's most remarkable about this batch of symptoms is that while they are thoroughly contemporary and familiar to many advanced bodybuilders, Shippen notes that they were described by researchers over 50 years ago! Although Reader's Digest detailed testosterone therapies in the 1930s and Dutch scientists synthesized testosterone in 1935, testosterone therapy has been slow to gain widespread medical community acceptance.

Bodybuilders, however, generally know the value of this hormone. Optimal muscular development cannot occur without it. And we take androgens, testosterone precursors, boosters, elevators, and prohormones __ anything to increase testosterone. According to Shippen's book, that's relatively good news, but we can miss some essential modulating factors, which sometimes result in andropausal symptoms recurring.

These recurrences center on 3 primary reasons: the testosterone delivery systems; elevated estrogen levels; and non-optimal estrogen/testosterone ratios.

Pellet and patch delivery systems seem to provide slower testosterone elevation than injections, although the end result of useable free testosterone within the blood ---often just 2 to 3% of total serum testosterone --- is comparable. Slower delivery and buildup often avoids corresponding spikes in estrogen levels. "Some estrogen is good," notes Dr. Shippen, "and is essential for many male functions, including sexual activity. What would concern us is too much estrogen overall, and for most men that will be anything above 30 ng/dl, and the ratio of testosterone to estrogen within the blood." Anything outside a 12- or 20-to-one proportion, and estrogen's negative effects can surface, including increased coronary risk (precisely the opposite effect of increased estrogen in women).

How You May Modulate Estrogen Levels

Since estrogen is essential to men as well as to women, what can we do to optimize the relationship between testosterone and estrogen; and to minimize -- but not eliminate -- aromatization? Dr. Shippen points to a few contributing factors which we can control, and opens the door to soy protein and phytoestrogens:


The liver's P450 system is "a primary processing system that eliminates chemicals, hormones, drugs and metabolic waste products from the body," says Dr. Shippen in his book. "Among its many duties is the task of excreting excess estrogen from the body." Impair the P450 system and elevated estrogen may result. While aging itself results in larger amounts of aromatase (the enzyme that converts testosterone to estrogen), the P450 system can be compromised by a number of factors, including obesity, zinc deficiency, overuse of alcohol, and the ingestion of estrogen-enhancing food and some prescription drugs.

Obesity is the larger threat here, so don't let your powerlifting capabilities get in the way of your ability to control estrogen levels. Reduce excess bodyfat and you reduce your body's disposition to produce estrogen. Zinc is easily taken; Shippen suggests 50 to 100 mg per day, in 2 doses. Alcohol is a drug ingested in solution, pure and simple. A little alcohol may reduce inhibitions, but that decrease in sexual capability that comes on after "one too many" is quite likely due to the very nearly immediate increase in estrogen that alcohol induces.

Phytoestrogens, or the plant "version" of estrogen found in various edible foods, such as soy and soy protein, serve primarily as weak precursors to estrogen production. The isoflavones found in soy, for example, are similar in chemical structure to human estrogen, but Shippen notes that typically such estrogens have only about 1/500th the active effect of estradiol, the most active human estrogen.

"The fear of soy protein and phytoestrogens is absurd," says reigning USA champ Tom Prince."You need the proper receptor sites, and a significant amount of them, to produce estrogen in the body through ingestion of phytoestrogens."

Men have fewer estrogen receptors than do women. Additionally, there is a technique for manipulating these sites in men so that genuine estrogen is minimized: Shippen suggests that high levels of phytoestrogens compete with the female hormone for receptor sites, block its actions -- which can include some inhibition of pituitary functions -- and stimulate the P450 system in the liver to more actively process and excrete excess estrogen.

Susan Kleiner, Ph.D, RD, author of Power Eating, notes that phytoestrogens tend to overwhelm estrogen in competing at the receptor site level. "That's why we use phytoestrogens for both men and women who have hormonal-involved cancer," such as prostate or breast cancer. So, the process is absolutely clear: If you want to block estrogen, take moderate amounts of isoflavones.Soy protein is a great source of isoflavones, providing that you can find a soy protein that has the isoflavones in it. "Isoflavones can be found in soy protein, but not always, " advises Kleiner. "High heat or chemical processing can damage and deplete phytoestrogens and isoflavones. Some soy protein powders I had analyzed had no isoflavones whatsoever, even though the label touted their benefits. ."

There are 2 others dietary practices you can follow that alter estrogen production and uptake. Stop eating grapefruit. Shippen advises that for men in the "gray" zone it tends to inhibit the liver's breakdown of estrogen. Do, however, eat cruciferous vegetables, such as broccoli and cauliflower. They assist in estrogen burnoff (explaining their inclusion in Pinnacle's Chrysinex anti-aromatase formula of Chrysin and veggies).

Various drugs play roles in estrogen and testosterone production and uptake. Anti-inflammatories, including aspirin, ibuprophen (as found in AdvilTM and MidolTM), and acetaminophen (TylenolTM) inhibit the P450 estrogen elimination system, as do various antibiotics, antidepressants, antifungal agents, alcohol, amphetamines, marijuana, cocaine and high doses of vitamin E. Antifungal drugs, pesticides, some cancer chemotherapy drugs and DHEA "compete for testosterone cellular receptors or change metabolism indirectly," according to The Testosterone Dilemma. Thankfully, there are substances which may speed up the P450 system, decreasing estrogen levels, including vitamin K, niacin, TrazadoneTM, soy products, shellfish, and resveratrol (grape skin compound). High amounts of vitamin C may increase estrogen burnoff and testosterone production, says Dr. Shippen.


References:Eugene Shippen, M.D., & William Fryer: The Testosterone Syndrome: The Critical Factor for Energy, Health, & Sexuality -- Reversing the Male Menopause (IBSN# 0-87131-829-6). Publisher: M. Evans and Company, Inc. New York, NY. 1998. Highly recommended reading.
 
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indie85 said:
would applying topical estrogen to the hair be good? If that can be done.

I don't know, because I have no idea what estrogens role is in influencing hair follicles.

Someone here must know.
 
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indie85 said:
would applying topical estrogen to the hair be good? If that can be done.

I have no idea what estrogens role even is in influencing hair follicles.

Someone here must know.

From what I'm reading, men want to reduce estrogen levels by ingesting things that harmlessly bind to the estrogen receptors, and block estrogen from docking there.
 
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Gladly. Here's another one btw:

The Hypothalamus/Pituitary/Testes Axis

Hormones are the body's way of sending signals, or information from one part of the body to another. In a computer, electrons (electricity) act as the signal; in the body (which doesn't have wires!), the signals must be sent with chemicals, and that is the role of hormones. The term "HPT Axis" refers to the
interaction of the hypothalamus, pituitary, and testes (there are other axes as well). For the Leydig cells (the cells that produce Testosterone), Luteinizing hormone (LH) is released from the pituitary and it signals the Leydig cells to produce testosterone. Similarly, the pituitary releases FSH, and it tells the Sertoli cells to make sperm (as well as androgen-binding-protein). The pituitary is a gland that produces and stores a number of hormones, under the control of the hypothalamus. The hypothalamus might be considered to be the General (as in military), and the pituitary would be a Colonel under the General's command. The hypothalamus decides how the body's organs should operate, and the pituitary gives the actual "orders" to the target organs. Some of
the "signalling" hormones made or stored in the pituitary are:

Growth Hormone
IGF-I and IGF-II
Thyroid Stimulating Hormone (TSH)
Vasopressin (or Antidiuretic hormone)
Luteininzing Hormone (LH)
Follicle Stimulating Hormone (FSH)
Adrenocorticotropic Hormone (ACTH)

The hypothalamus and the pituitary are very close together, and are located at the base of the brain. Just as the pituitary uses hormones to signal the target organ (testes, thyroid, etc) to do something, the hypothalamus uses other hormones to signal the pituitary to do its job.

Some of these "Hypothalamic Releasing Factors" are (along with the pituitary hormones affected):

Hypothalamic Hormone: Regulates:
Gonadotropin Releasing Hormone LH, FSH
Growth Hormone Releasing Hormone GH
Thyrotropin Releasing Hormone TSH
Corticotropin Releasing Hormone ACTH

But how does the hypothalamus know when its commands have been carried out? By what's called a "feedback loop". Just as a General relies on reports from the field, the hypothalamus must monitor the results of its commands. The hypothalamus has sensors (receptors) to determine the levels of the chemicals (hormones) produced by the target organs. For our purposes, we will examine only one feedback loop, the one involving the testes.

The hypothalamus has both androgen (Male hormone) receptors and estrogen (female hormone) receptors. This is important and if you are not already aware estrogen is the female hormone and is required by men albeit but in much smaller amounts.

When the level of either hormone gets too high, the receptors become more highly activated, and the hypothalamus stops sending Gonadotropin Releasing Hormone to the pituitary. The pituitary, in turn, stops sending LH and FSH to the testes. Thus, the signal is, "stop producing testosterone (and sperm)". The important thing to note here is that Estrogen occupies the same receptors that Testosterone does and fools the hypothalamus into thinking there is enough Testosterone. Elevated levels of the female hormone will suppress the axes into lowering Testosterone production. The Testosterone to Estrogen ratio will plummet and all the problems associated with it will begin take hold.

From here: http://www.propeciasideeffects.com/inde ... age403.htm
 

Bryan

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Erik D said:
I have no idea what estrogens role even is in influencing hair follicles.

Someone here must know.

The available evidence indicates that estrogen stimulates the growth of balding scalp hair follicles.
 
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What would the effect of Soy Isoflavones be on the hair growth process?

Same for Beta Sitosterol?

The reason I ask, is that they're both reputed to occupy estrogen receptor sites.
 

Bryan

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Erik D said:
What would the effect of Soy Isoflavones be on the hair growth process?

Same for Beta Sitosterol?

The reason I ask, is that they're both reputed to occupy estrogen receptor sites.

I can't answer that question, and I wouldn't be at all surprised if nobody else can, either, not even doctors and scientists. The reason for that is that these natural substances (like soy derivatives, and various other products) can have very complex interactions with estrogen receptors, and even alter gene expression in complex and unpredictable ways.

For example, even the FDA-approved estrogen receptor-blocker drug Tamoxiphen has paradoxical effects of its own, because it has an estrogen ANTAGONISTIC effect in the female breast (which is why it's used in breast cancer), but has an estrogen AGONIST effect in certain other female tissues. Considering how the study of the effect of even real estrogen on human scalp hair growth is still in its relative infancy, I would be simply astonished if the effects of these various other substances like soy and beta sitosterol had ever been tested for their specific effects on estrogen receptors in human hair follicles.
 

bubka

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the website if full of crap, i don't see any references to any scientific studies on their claims, it this were a high school paper it would get an "F"
 

Bryan

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bubka said:
the website if full of crap, i don't see any references to any scientific studies on their claims, it this were a high school paper it would get an "F"

Indeed. Notice how they are STILL, to this very day, trying to get people to believe that estrogen is a negative factor in male pattern baldness, despite the increasing evidence to the contrary (like that brand-new study showing that the same estrogen-blocker used years ago by Smart et al to grow hair on mice doesn't work at all on the human scalp). They just LOVE to try to sell "Super-Miraforte" to all their readers, as a supposed anti-estrogen supplement! :)
 

purecontrol

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The biggest thing here is that all estrogen is not created equal, studies showing that it is good involves the Beta while studies showing it is bad shows the Alpha.

Another consideration is that bad estrogen will increase the amount and number of Androgen Receptors, this is a reason why some people don't benefit from finasteride as much as others or not at all.

If you have far less DHT but higher levels of test with high Androgen Receptor number and sensativity then you end up in the same boat that you were in before.

The fronteir will to modulate estrogen metabolites so that you have an optimal level in order to keep AR numbers as low as possible in the dermis, hair folicle, ect while keeping an optimal amount in the muscle.

Alpha estrogen has been linked to numerous types of cancers in both men and women.

Another thing to consider is that all of the polyphenols ie herbal antioxidants act as anti-estrogens but with a slight estrogen effect, when you have proper estrogen metabolites it will act as an antioxidant as well.


DIM and I3C both act to keep excess estrogen and androgens that are not being taken up to where it needs to be ie muscle ect and flushes it out, the body will work in a priority system where the cells that need the androgens or estrogens the most will have the highest degree of them, but once they have come to a certain saturation point you end up with more and more estrogen and androgens that are free to go around the body and attach to other cells that would normally not see that much estrogen or androgens.

In this case there is an excess of over spill, so that scalp ect get even more of what it is not supposed to.

Next DIM and I3C work to increase proper estrogen metabolism, so that you have more estrogen that act as an anti-oxidant and a weaker estrogen. This reverses the effects of the Alpha estrogen which has been show to cause cancer and hair loss.

Finally DIM and I3C work as a weak anti-androgen in estrogen sensative areas.


Note that I3C when metabolised by the body produces DIM. If that is not enough DIM it's self has strong anti-oxidant effects.

The answer here is much much more in the middle of the road rather than one side or another.
 

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purecontrol said:
The biggest thing here is that all estrogen is not created equal, studies showing that it is good involves the Beta while studies showing it is bad shows the Alpha.

Dude, what in the Sam Hell are you talking about?

purecontrol said:
Another consideration is that bad estrogen will increase the amount and number of Androgen Receptors, this is a reason why some people don't benefit from finasteride as much as others or not at all.

Reference or citation, please.

I think you're making this sh*t up as you go along.
 

harold

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In looking for info on the relative strengths of various antiandrogens I was interested to see that estrogen actually has a pretty decent affinity for the androgen receptor and is actually capable of eliciting a fair bit of response from the androgen receptor. As are powerful antiandrogens such as cyproterone acetate. It has forced me to think of these hormones/compounds as weaker stimulators of the AR rather than as antagonists. Which is not really news but I guess I was shocked to see that if you had no androgens in your systm and you then added a whole bunch of cyproterone acetate or even estradiol in all probability you would be worse off than if you had none.
Interestingly flutamide seemed to have no ability to stimulate androgenic transcription whereas the far more potent antiandrogen hydroxyflutamide did in high enough doses. The problem is that you need about 30 times as much flutamide to get the equivalent effect of a given amount of hydroxyflutamide. The upshot being that you are probably better off having a drug which is a weak to moderate agonist of the AR but has a high binding affinity than a pure antiandrogen with a weak affinity at the end of the day.
All of this makes sense when you consider that men on finasteride can usually maintain pretty much all their hair with more testosterone in their scalp and less DHT. Even testosterone could be viewed as a "weak antiandrogen" when compared to DHT. If all this is true then it is interesting to see just how much AR activity is needed to have a significant impact on hairloss and that it seems hair is actually quite resistant to at least some stimulus. Maybe. :)
hh
 

Bryan

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harold said:
In looking for info on the relative strengths of various antiandrogens I was interested to see that estrogen actually has a pretty decent affinity for the androgen receptor and is actually capable of eliciting a fair bit of response from the androgen receptor.

Yeah, but that depends on what you mean by "response". Do you mean a true ANDROGENIC response, or something else?

harold said:
As are powerful antiandrogens such as cyproterone acetate. It has forced me to think of these hormones/compounds as weaker stimulators of the AR rather than as antagonists. Which is not really news but I guess I was shocked to see that if you had no androgens in your systm and you then added a whole bunch of cyproterone acetate or even estradiol in all probability you would be worse off than if you had none.

I can't really quite go along with that. It seems to me that it shows a true biphasic effect, not an overall weak androgenic effect. Some of these "antiandrogens" like cyproterone acetate (and possibly other ones like flutamide and RU58841) do have ANTI-androgenic effects at low-to-moderate concentrations, but begin to show a PRO-androgenic effect at much higher concentrations.

harold said:
Interestingly flutamide seemed to have no ability to stimulate androgenic transcription whereas the far more potent antiandrogen hydroxyflutamide did in high enough doses. The problem is that you need about 30 times as much flutamide to get the equivalent effect of a given amount of hydroxyflutamide. The upshot being that you are probably better off having a drug which is a weak to moderate agonist of the AR but has a high binding affinity than a pure antiandrogen with a weak affinity at the end of the day.

Well, the relative concentrations of the two would be an important factor, too.

harold said:
All of this makes sense when you consider that men on finasteride can usually maintain pretty much all their hair with more testosterone in their scalp and less DHT. Even testosterone could be viewed as a "weak antiandrogen" when compared to DHT.

You know, that was actually the rationale that Durk Pearson & Sandy Shaw used in their book "Life Extension" to justify the use of topically-applied testosterone to fight male pattern baldness! :)

harold said:
If all this is true then it is interesting to see just how much AR activity is needed to have a significant impact on hairloss and that it seems hair is actually quite resistant to at least some stimulus. Maybe. :)

Good point, although I also suspect that the timing of the androgen suppression or withdrawal is important, too. I think stopping it well before balding starts to get advanced requires less androgen reduction than waiting untill balding is well on its way.
 

docj077

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Bryan said:
purecontrol said:
The biggest thing here is that all estrogen is not created equal, studies showing that it is good involves the Beta while studies showing it is bad shows the Alpha.

Dude, what in the Sam Hell are you talking about?
He's referring to the estrogen receptor subtypes.
 

Bryan

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docj077 said:
Bryan said:
purecontrol said:
The biggest thing here is that all estrogen is not created equal, studies showing that it is good involves the Beta while studies showing it is bad shows the Alpha.

Dude, what in the Sam Hell are you talking about?
He's referring to the estrogen receptor subtypes.

Then what was that bit about "all estrogen is not created equal"?
 
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