HRT Protocols

Bigger Stronger Leaner Competitive Bodybuilding
1

Greetings.

I am one of the fortysomething club who thankfully am not hypogonodal.

However, many of my friends and acquantances who are around my age are experiencing that “decline” (don’t know how to explain someone else’s description!)

There seems to be a couple of camps with regards to partial or complete shutdown of the body’s natural endogenouse testosterone system with the intake of exogenous test.

camp 1: The first camp says that once you take a certain threshold of test (say 50 mg), your natural system is 100% shutdown.

camp 2: The second camp says that the body’s natural test system is nothing more than a typical analog feedback control system; i.e. as levels of test rise or fall, the governing command signals to the testes (LH, FSH) rise and fall in proportion. The argument here is that exogenous T is exactly the same as endogenous T and the body can’t tell the difference.

Question: Say a person has an output of T that is 50% of normal range. Would supplementing with 50% exogenous T reduce this person’s natural output of 50% down or would it stay the same?

Though I am not hypogonodal and don’t suffer from T issues, I AM hypothyroidal and take small amounts of levoxyl and cytomel everyday to keep me in the normal range. Every bloodtest results I see, I see my baseline thyroid natural output (which wasn’t enough) not changing in the presence of exogenous thyroid.

It would appear the replacement of “only what is needed to reach normal” doesn’t effect my thyroid control system. I suspect the same with the testosterone system (and thus am a member of camp 2), but would like to know other’s technical opinions.

2

[quote]buffd_samurai wrote:
Greetings.

I am one of the fortysomething club who thankfully am not hypogonodal.

However, many of my friends and acquantances who are around my age are experiencing that “decline” (don’t know how to explain someone else’s description!)

There seems to be a couple of camps with regards to partial or complete shutdown of the body’s natural endogenouse testosterone system with the intake of exogenous test.

camp 1: The first camp says that once you take a certain threshold of test (say 50 mg), your natural system is 100% shutdown.

camp 2: The second camp says that the body’s natural test system is nothing more than a typical analog feedback control system; i.e. as levels of test rise or fall, the governing command signals to the testes (LH, FSH) rise and fall in proportion. The argument here is that exogenous T is exactly the same as endogenous T and the body can’t tell the difference.

Question: Say a person has an output of T that is 50% of normal range. Would supplementing with 50% exogenous T reduce this person’s natural output of 50% down or would it stay the same?

Though I am not hypogonodal and don’t suffer from T issues, I AM hypothyroidal and take small amounts of levoxyl and cytomel everyday to keep me in the normal range. Every bloodtest results I see, I see my baseline thyroid natural output (which wasn’t enough) not changing in the presence of exogenous thyroid.

It would appear the replacement of “only what is needed to reach normal” doesn’t effect my thyroid control system. I suspect the same with the testosterone system (and thus am a member of camp 2), but would like to know other’s technical opinions. [/quote]

Unfortunately you can’t just top up your testosterone levels in order to get to normal or high normal. Your body wants to stay at a certain homeostatic level based on a number of different factors; testosterone, estradiol, LH, prolactin, etc… which can negatively affect the feedback loop. If you’re at 50% and add another 50 to try and get to 100, your body will down regulate in order to stay at a level where all the other factors dictate it’s balance.

I can imagine it also depends on whether you’re primary or secondarily hypogonadal as well. If you’re primary your testicles aren’t properly responding to LH in order to make more testosterone, so the feedback inhibition may be less if you’re adding more exogenous testosterone, thus making it easier to top up I’d think.

Being primary hypogonadal is also a relative term I believe determined by the desired testosterone level you are trying to achieve. If you’re aiming towards high normal levels of testosterone but can only achieve mid-range levels by manipulating estradiol, prolactin, and LH, then it’s possible you could define yourself as being hypogonadal still.

I don’t believe in only looking at numbers. You should be looking for efficacy based on optimal values like how you feel and things like muscle mass, body fat, mood, stress tolerance, cholesterol, lipid values etc…

I think it’s also important to look at circadian rythyms and it’s effects on testosterone production. If you’re taking an exogenous source with a half life of approx a week like testosterone enanthate, it changes the feedback look differently than if you were going to be taking say… a very short half life testosterone like suspension, only in the mornings.

I’m not sure if there’s been much research done on this for HRT but with other steroids like Dianabol, taking an only morning dose protocol compared to throughout the day results in different levels of feedback inhibition. Bill Roberts has theorized about this.

Many people try to increase both endogenous T and exogenous at the same time trying to get the best of both worlds. They’ll take anti-estrogens(Arimidex), dopaminergics(Dostinex), and LH increasing drugs(HCG), to increase exogenous production, then fill in the remaining gap with exogenous T, like enanthate injections or Androgel.

Hopefully that sort of answered your question. I’m still learning about this stuff so any one else can chime in to correct or add to what I’ve said.

3

I agree with Camp 1. Within 2 weeks of starting 5 grams/daily of Testim I started to shut down and my total testosterone levels fell to less than what I started with without the Testim indicating I was totally shutdown.

4

[quote]deadlifter405 wrote:
I agree with Camp 1. Within 2 weeks of starting 5 grams/daily of Testim I started to shut down and my total testosterone levels fell to less than what I started with without the Testim indicating I was totally shutdown.[/quote]

Well, not really, unless I’m missing something you’re trying to say. Just because your levels fell to less than what it was before you started Testim does not mean you are completely shut down; it could mean your body’s natural system has compensated to the extra T by lowering LH, and over time of continuously taking the Testim, your body will eventually come to equilibrium.

Thanks, however, for your experience. If you guys don’t mind, I would like to forward them to my old geezer collegues to continue our rather interesting discussion about all this.

5

[quote]Bri Hildebrandt wrote:
buffd_samurai wrote:
Greetings.

I am one of the fortysomething club who thankfully am not hypogonodal.

However, many of my friends and acquantances who are around my age are experiencing that “decline” (don’t know how to explain someone else’s description!)

There seems to be a couple of camps with regards to partial or complete shutdown of the body’s natural endogenouse testosterone system with the intake of exogenous test.

camp 1: The first camp says that once you take a certain threshold of test (say 50 mg), your natural system is 100% shutdown.

camp 2: The second camp says that the body’s natural test system is nothing more than a typical analog feedback control system; i.e. as levels of test rise or fall, the governing command signals to the testes (LH, FSH) rise and fall in proportion. The argument here is that exogenous T is exactly the same as endogenous T and the body can’t tell the difference.

Question: Say a person has an output of T that is 50% of normal range. Would supplementing with 50% exogenous T reduce this person’s natural output of 50% down or would it stay the same?

Though I am not hypogonodal and don’t suffer from T issues, I AM hypothyroidal and take small amounts of levoxyl and cytomel everyday to keep me in the normal range. Every bloodtest results I see, I see my baseline thyroid natural output (which wasn’t enough) not changing in the presence of exogenous thyroid.

It would appear the replacement of “only what is needed to reach normal” doesn’t effect my thyroid control system. I suspect the same with the testosterone system (and thus am a member of camp 2), but would like to know other’s technical opinions.

Unfortunately you can’t just top up your testosterone levels in order to get to normal or high normal. Your body wants to stay at a certain homeostatic level based on a number of different factors; testosterone, estradiol, LH, prolactin, etc… which can negatively affect the feedback loop. If you’re at 50% and add another 50 to try and get to 100, your body will down regulate in order to stay at a level where all the other factors dictate it’s balance.

I can imagine it also depends on whether you’re primary or secondarily hypogonadal as well. If you’re primary your testicles aren’t properly responding to LH in order to make more testosterone, so the feedback inhibition may be less if you’re adding more exogenous testosterone, thus making it easier to top up I’d think.

Being primary hypogonadal is also a relative term I believe determined by the desired testosterone level you are trying to achieve. If you’re aiming towards high normal levels of testosterone but can only achieve mid-range levels by manipulating estradiol, prolactin, and LH, then it’s possible you could define yourself as being hypogonadal still.

I don’t believe in only looking at numbers. You should be looking for efficacy based on optimal values like how you feel and things like muscle mass, body fat, mood, stress tolerance, cholesterol, lipid values etc…

I think it’s also important to look at circadian rythyms and it’s effects on testosterone production. If you’re taking an exogenous source with a half life of approx a week like testosterone enanthate, it changes the feedback look differently than if you were going to be taking say… a very short half life testosterone like suspension, only in the mornings.

I’m not sure if there’s been much research done on this for HRT but with other steroids like Dianabol, taking an only morning dose protocol compared to throughout the day results in different levels of feedback inhibition. Bill Roberts has theorized about this.

Many people try to increase both endogenous T and exogenous at the same time trying to get the best of both worlds. They’ll take anti-estrogens(Arimidex), dopaminergics(Dostinex), and LH increasing drugs(HCG), to increase exogenous production, then fill in the remaining gap with exogenous T, like enanthate injections or Androgel.

Hopefully that sort of answered your question. I’m still learning about this stuff so any one else can chime in to correct or add to what I’ve said.[/quote]

You have made an excellent point about primary versus secondary hypogonadism. My opinion: I agree that if the issue is with the 'nads, then “topping off” with some extra T might not effect the original mechanism. If one had a doctor willing to monitor the levels over a period of time, the eventual dialing in to what “topping off” really means to an individual can be determined.

If you don’t mind, I would like to forward your words to my pals in order to give them some more thoughts to consider for the next time we have our discussions.

6

[quote]buffd_samurai wrote:
You have made an excellent point about primary versus secondary hypogonadism. My opinion: I agree that if the issue is with the 'nads, then “topping off” with some extra T might not effect the original mechanism. If one had a doctor willing to monitor the levels over a period of time, the eventual dialing in to what “topping off” really means to an individual can be determined.

If you don’t mind, I would like to forward your words to my pals in order to give them some more thoughts to consider for the next time we have our discussions. [/quote]

I don’t think it’s ever either 100% primary or secondary, more like shades of grey. I don’t think the testes are 100% desensitized to LH in primary cases, they just aren’t sufficient to maintain optimal ranges, no matter how high you increase LH. You may still be getting some kind of increase however small it is. So in a primary case you may have only 25%(made up for use as an example) less endogenous T with exogenous therapy as opposed to perhaps 75% shutdown with a secondary case. This is more conjecture though, and not based on any specific research studies.

Yeah go ahead, forward it to your pals. I have no problems with that. Just glad to help. :slight_smile:

7

Let me offer some follow-up evidence then. After 3 months of Testim 10 grams/day, first month was 5 grams, I had a skin reaction and my endo switched me to Androgel. Within 5 days I crashed hard and got sent for a blood test. It came back at 70 ng/dl vs. my original 227 ng/dl without any HRT. I believe that 70 ng/dl was all the Androgel I was able to absorb through my thick skin and I was shutdown.

In time, I might have recovered back to near my original 227 ng/dl level, with 70 of it being the Androgel, but I’m much happier having been switched to Test Cypionate.

[quote]buffd_samurai wrote:
deadlifter405 wrote:
I agree with Camp 1. Within 2 weeks of starting 5 grams/daily of Testim I started to shut down and my total testosterone levels fell to less than what I started with without the Testim indicating I was totally shutdown.

Well, not really, unless I’m missing something you’re trying to say. Just because your levels fell to less than what it was before you started Testim does not mean you are completely shut down; it could mean your body’s natural system has compensated to the extra T by lowering LH, and over time of continuously taking the Testim, your body will eventually come to equilibrium.

Thanks, however, for your experience. If you guys don’t mind, I would like to forward them to my old geezer collegues to continue our rather interesting discussion about all this. [/quote]

8

[quote]deadlifter405 wrote:
Let me offer some follow-up evidence then. After 3 months of Testim 10 grams/day, first month was 5 grams, I had a skin reaction and my endo switched me to Androgel. Within 5 days I crashed hard and got sent for a blood test. It came back at 70 ng/dl vs. my original 227 ng/dl without any HRT. I believe that 70 ng/dl was all the Androgel I was able to absorb through my thick skin and I was shutdown.

In time, I might have recovered back to near my original 227 ng/dl level, with 70 of it being the Androgel, but I’m much happier having been switched to Test Cypionate.

buffd_samurai wrote:
deadlifter405 wrote:
I agree with Camp 1. Within 2 weeks of starting 5 grams/daily of Testim I started to shut down and my total testosterone levels fell to less than what I started with without the Testim indicating I was totally shutdown.

Well, not really, unless I’m missing something you’re trying to say. Just because your levels fell to less than what it was before you started Testim does not mean you are completely shut down; it could mean your body’s natural system has compensated to the extra T by lowering LH, and over time of continuously taking the Testim, your body will eventually come to equilibrium.

Thanks, however, for your experience. If you guys don’t mind, I would like to forward them to my old geezer collegues to continue our rather interesting discussion about all this.

[/quote]

That’s very interesting. I’ve heard of others having the same problem. I’m wondering if that phenomenon is more common with the gels as opposed to injections.

I think it’s more important to observe real life case studies, rather than logic and how things “should work”.

9

I’m mentally trying to puzzle through the factors involved here.

I think there are cases where camp 1 will be correct and where camp 2 will be correct.

If it is low because your body is limiting your production for some reason, then upping it is likely to limit production more… to keep the total at the same level.

It is is low because you can’t produce enough, or it’s used up too quickly, then having more may not run into the limit that your body is willing to tolerate.

Sound plausible? Time to go do some research…

10

[quote]vroom wrote:
I’m mentally trying to puzzle through the factors involved here.

I think there are cases where camp 1 will be correct and where camp 2 will be correct.

If it is low because your body is limiting your production for some reason, then upping it is likely to limit production more… to keep the total at the same level.

It is is low because you can’t produce enough, or it’s used up too quickly, then having more may not run into the limit that your body is willing to tolerate.

Sound plausible? Time to go do some research…[/quote]

Vroom: It sounds plausible to me! I am also trying to mentally put some pieces together here.

Let’s take my thyroid case for an example of the second case you mentioned. I’m producing alot of TSH, but not enough thyroid. I am producing some, but not enough to be considered really normal, and not enough to prevent me from experiencing the hypothyroidism that I did. My endo put me through a test where they injected me with something sort of like TSH and then monitored my thyroid response over a period of 1 hour. I think blood was drawn every 15 minutes.
So, I then take a “starting” dose of levoxyl and cytomel, and come back for more blood tests after a period of about a couple of months. After a couple months, I go back in, draw more blood, endo adjusts the dosage, then do it all over again.
Eventually my endo dialed in the correct dosage for me. I take just enough to be in the normal zone and clearly I am not effecting my own production terribly.

So, in this case, it is my thyroid which is the problem. Similiarly, if the testes are the culprit with folks suffering from low T, then I believe the above protocol would work in the same manner. It requires alot of blood work for real feedback. I think a similiar test of injection with HCG and monitoring of the T levels in the blood over a period of hours would determine whether or not it is the end organ within the “factory” that is the culprit. If it is, then “topping off” concept might work.

Bri brings up a good concept as well with regards to the circadian rhythm. If “topping off” is the protocol of choice, the next difficult step is determining how to top off at the right time. This might simply be impossible with the raw materials currently available.

However, I wonder (for the case of “topping off”)if Testosterone suspension at topping off doses in the morning would be the best solution.

Thanks for the discussion! This is great!

11

What I’m curious about… is whether estrogen mimics have fooled our bodies into thinking their sex hormone levels are high enough… when really they aren’t.

I hope it’s not going off topic, but here’s an interesting article on how easily this might happen to us… and how it may even contribute to insulin resistance as well.

Diabetes from a Plastic? Estrogen mimic provokes insulin resistance

[i]
Exposure to small amounts of an ingredient in polycarbonate plastic may increase a person’s risk of diabetes, according to a new study in mice.

The synthetic chemical called bisphenol-A is used to make dental sealants, sturdy microwavable plastics, linings for metal food-and-beverage containers, baby bottles, and numerous other products. When consumed, the chemical can mimic the effects of estrogen. Previous tests had found that bisphenol-A can leach into food and water and that it’s widely prevalent in human blood.

The newfound contribution of the chemical to insulin resistance, a precursor to diabetes, might partially explain the global epidemic of that disease, says Angel Nadal of Miguel Hernandez University of Elche in Spain, who led the new study.

The finding is a “wake-up call” for public health researchers who are concerned by the prevalence of diabetes, comments developmental biologist Frederick vom Saal of the University of Missouri-Columbia.

Earlier test-tube studies had suggested that bisphenol-A makes pancreatic cells secrete the glucose-regulating hormone insulin. To investigate this effect in live animals, Nadal and his colleagues injected adult male mice with pure corn oil or with oil containing either bisphenol-A or an equal amount of the natural female sex hormone estradiol. Animals received as many as eight shots over 4 days.

Within 30 minutes of an injection, animals receiving either the sex hormone or bisphenol-A had abnormally low concentrations of glucose in their blood, Nadal’s team reports in the January Environmental Health Perspectives. The chemicals acted on recently discovered estrogen receptors on pancreatic cells’ surfaces to boost the cells’ secretion of insulin, the researchers determined.

Repeated exposure to either bisphenol-A or the natural estrogen over several days produced insulin resistance, a pre-diabetic state in which tissues lose their sensitivity to normal concentrations of insulin, Nadal’s group says. Estrogen receptors in the pancreatic-cell nucleus appear to contribute to this gradual effect.

So, receptors both in the cell nucleus and on the surface could contribute to insulin resistance and diabetes, Nadal says.

This risk could add to or elucidate already documented health effects of bisphenol-A. Animal studies have suggested that exposure to the chemical early in life causes obesity, says Ana M. Soto of Tufts University School of Medicine in Boston.

Furthermore, bisphenol-A exposure might contribute to gestational diabetes in women, in whom insulin resistance often increases during pregnancy, says Jerry Heindel of the National Institute of Environmental Health Sciences in Research Triangle Park, N.C.

Inside cells’ nuclei, bisphenol-A is less potent than the natural sex hormone, says vom Saal. But the new work shows that at the surface of pancreatic cells, the compounds have the same potency, he notes. Doses of bisphenol-A considered by the Environmental Protection Agency to have no adverse effect led to insulin resistance in the mouse study.
[/i]
It is a mouse study, which means it may not apply, either in whole or in part, but then again, we just don’t know, do we?

What other crap are we ingesting every day?

12

[quote]vroom wrote:
What I’m curious about… is whether estrogen mimics have fooled our bodies into thinking their sex hormone levels are high enough… when really they aren’t.

I hope it’s not going off topic, but here’s an interesting article on how easily this might happen to us… and how it may even contribute to insulin resistance as well.

Diabetes from a Plastic? Estrogen mimic provokes insulin resistance

[i]
Exposure to small amounts of an ingredient in polycarbonate plastic may increase a person’s risk of diabetes, according to a new study in mice.

The synthetic chemical called bisphenol-A is used to make dental sealants, sturdy microwavable plastics, linings for metal food-and-beverage containers, baby bottles, and numerous other products. When consumed, the chemical can mimic the effects of estrogen. Previous tests had found that bisphenol-A can leach into food and water and that it’s widely prevalent in human blood.

The newfound contribution of the chemical to insulin resistance, a precursor to diabetes, might partially explain the global epidemic of that disease, says Angel Nadal of Miguel Hernandez University of Elche in Spain, who led the new study.

The finding is a “wake-up call” for public health researchers who are concerned by the prevalence of diabetes, comments developmental biologist Frederick vom Saal of the University of Missouri-Columbia.

Earlier test-tube studies had suggested that bisphenol-A makes pancreatic cells secrete the glucose-regulating hormone insulin. To investigate this effect in live animals, Nadal and his colleagues injected adult male mice with pure corn oil or with oil containing either bisphenol-A or an equal amount of the natural female sex hormone estradiol. Animals received as many as eight shots over 4 days.

Within 30 minutes of an injection, animals receiving either the sex hormone or bisphenol-A had abnormally low concentrations of glucose in their blood, Nadal’s team reports in the January Environmental Health Perspectives. The chemicals acted on recently discovered estrogen receptors on pancreatic cells’ surfaces to boost the cells’ secretion of insulin, the researchers determined.

Repeated exposure to either bisphenol-A or the natural estrogen over several days produced insulin resistance, a pre-diabetic state in which tissues lose their sensitivity to normal concentrations of insulin, Nadal’s group says. Estrogen receptors in the pancreatic-cell nucleus appear to contribute to this gradual effect.

So, receptors both in the cell nucleus and on the surface could contribute to insulin resistance and diabetes, Nadal says.

This risk could add to or elucidate already documented health effects of bisphenol-A. Animal studies have suggested that exposure to the chemical early in life causes obesity, says Ana M. Soto of Tufts University School of Medicine in Boston.

Furthermore, bisphenol-A exposure might contribute to gestational diabetes in women, in whom insulin resistance often increases during pregnancy, says Jerry Heindel of the National Institute of Environmental Health Sciences in Research Triangle Park, N.C.

Inside cells’ nuclei, bisphenol-A is less potent than the natural sex hormone, says vom Saal. But the new work shows that at the surface of pancreatic cells, the compounds have the same potency, he notes. Doses of bisphenol-A considered by the Environmental Protection Agency to have no adverse effect led to insulin resistance in the mouse study.
[/i]
It is a mouse study, which means it may not apply, either in whole or in part, but then again, we just don’t know, do we?

What other crap are we ingesting every day?[/quote]

I have read that we even absorb this shit from the steering wheels of cars. Its everywhere!
Good post, Vroom!

H2

13

I think it’s important to realize estrogen is important for male function just as much as testosterone is. It all depends on the range. Men can suffer from low estrogen which can be just as bad or worse than high estrogen. I think it’s hardly ever looked at, even less that testosterone due to the stereotypes that exist.

After a lot of experimentation I think I may have been having problems with low estrogen. I tend to feel better when taking supplements and food that increase estrogens like a high fat diet, copper, and possibly soy. A negative reaction to zinc may signify a low estrogen problem as well.

I remember a number of years ago seemingly doing well when I was eating around 50-100 grams a day of soy. I soon stopped eating soy after a number of negative articles here on T-Nation. This was probably around 7 years ago. It could have all been coincidence. I’ll have to try another trial to see if I have the same effect as I did before.

I’m going to be having a doctor’s appt at a men’s clinic shortly that specialized in testosterone therapy, so perhaps I’ll be able to finally be able to test my estradiol levels. I couldn’t convince other doctors to understand the significance of it’s implication on health. I’d like to get my adrenal status checked as well since I think that may be a factor with my health issues.

14

[quote]Bri Hildebrandt wrote:
I think it’s important to realize estrogen is important for male function just as much as testosterone is. It all depends on the range. Men can suffer from low estrogen which can be just as bad or worse than high estrogen. I think it’s hardly ever looked at, even less that testosterone due to the stereotypes that exist.

After a lot of experimentation I think I may have been having problems with low estrogen. I tend to feel better when taking supplements and food that increase estrogens like a high fat diet, copper, and possibly soy. A negative reaction to zinc may signify a low estrogen problem as well.

I remember a number of years ago seemingly doing well when I was eating around 50-100 grams a day of soy. I soon stopped eating soy after a number of negative articles here on T-Nation. This was probably around 7 years ago. It could have all been coincidence. I’ll have to try another trial to see if I have the same effect as I did before.

I’m going to be having a doctor’s appt at a men’s clinic shortly that specialized in testosterone therapy, so perhaps I’ll be able to finally be able to test my estradiol levels. I couldn’t convince other doctors to understand the significance of it’s implication on health. I’d like to get my adrenal status checked as well since I think that may be a factor with my health issues.[/quote]

Alas I think it is a consensus that when getting T levels checked via bloodwork, the following parameters should be checked (not in any order of priority):

  1. Total T
  2. Free T
  3. Estrodiol
  4. Prolactin
  5. LH
  6. Perhaps TSH, T3, and T4 though this would really probably be considered a different issue.

I’m sure many HRT or smart steroid users have some ideas of other parameters to check; this is just my list based upon my understanding of the subject.

My question based upon Vroom’s post: would measuring estrodiol level be enough to measure estrogenic effects of environmental estrogens? Or do these “Xeno-estrogens” not show up as estrodiol but still have a potent estrogenic effect? If the later, would consistent use of estrogen agonists such as clomid or novaldex really protect the male organism from these?

I believe some of these topics have been discussed in other posts or articles before; I am going to do my research today.

15

Unfortunately, it looks pretty complex. For example, things like soy and I3C appear to be able to moderate the effects of estrogen (estradiol) in some situations.

Soy apparently is a phytoestrogen which can “get in the way” of stronger estrogens. I3C on the other hand seems to steer estrogen production towards forms that are less strong than estradiol.

Xenoestrogens, unlike phytoestrogens, are not always as easily eliminated from the body.

The following site deals with estrogen from a woman’s point of view (as most of them do actually) with respect to breast cancer, but it talks about xenoestrogens and things – it might be a bit over the top though.

An interesting page on calcium D-glucarate. I wonder if it would an effect on estrogen receptors on the prostrate, as it apparently does in breast tissue? Anyway, it appears to be a detoxicant though it may work on hormones in general.

Very interestingly, many sunscreens contains what are apparently xenoestrogenic substances as well. Another site (not the one I’m linking to) discusses that the absorption of these things through the skin could lead to concentrations that are much higher than nature estrogens (though they may be weaker). I’m looking at my own suncscreen and it contains these products… hmmm.

http://www.anapsid.org/cnd/hormones/estrogen4.html

There are also sites which claim all of this is hype and that we don’t need to worry about any of it. Then there are sites showing how fish and reptiles are suffering from gender-bender situations due to artificial estrogens in the environment.

Something that caught my attention was the concept of estrogenic implants being given to cattle to help them gain weight…

I don’t know if there is any ability for the estrogens to be bioavailable through consumption. Here the government of Canada discusses the issue… and doesn’t really conclude much of anything.

http://www.foodsafetynetwork.ca/en/article-details.php?a=3&c=10&sc=78&id=308

Wikipedia has a page that discussions xenoestrogens.

More questions than answers out of all my reading so far, I’m afraid. Here’s an article Cy wrote back near the end of 2001.

http://www.T-Nation.com/readTopic.do?id=459845

16

[quote]buffd_samurai wrote:
Alas I think it is a consensus that when getting T levels checked via bloodwork, the following parameters should be checked (not in any order of priority):

  1. Total T
  2. Free T
  3. Estrodiol
  4. Prolactin
  5. LH
  6. Perhaps TSH, T3, and T4 though this would really probably be considered a different issue.

I’m sure many HRT or smart steroid users have some ideas of other parameters to check; this is just my list based upon my understanding of the subject.

My question based upon Vroom’s post: would measuring estrodiol level be enough to measure estrogenic effects of environmental estrogens? Or do these “Xeno-estrogens” not show up as estrodiol but still have a potent estrogenic effect? If the later, would consistent use of estrogen agonists such as clomid or novaldex really protect the male organism from these?

I believe some of these topics have been discussed in other posts or articles before; I am going to do my research today.
[/quote]

Some other useful tests:

Bioavailable testosterone (slightly different than free)
DHT (Important for sexual function)
SHBG
FSH
Cortisol
CBC
Lipid profile
PSA

DHEA and progesterone are sometimes checked as well. Testosterone, cortisol, estradiol, prolactin, and T3/T4 are all inter-related. If you top up T and are deficient in cortisol or T3/T4 you may not feel better, therefore it’s important to get a fuller picture of what’s going on in the body.

A lot of the symptoms are similar as well. Depression, fatigue, and sexual dysfunction may be caused by a number of different disease states.

I’ve read that eating soy can directly increase estradiol levels as measured by blood essays. I’m not sure about the other estrogens or other stuff that may be happening as well. There could be both pro-estrogenic and anti-estrogenic functions to a lot of these phytoestrogen compounds.