Patrick Arnold SERM's not all they are cut out to be

Patrick Arnold SERM's not all they are cut out to be

Source: Patrick Arnold SERM's not all they are cut out to be

SERM stands for selective estrogen receptor modulator. Also known as estrogen receptor agonist/ antagonists (or anti-estrogens), these drugs are used by bodybuilders to block the estrogenic effects of anabolic steroids and/or to help stimulate the production of natural testosterone after a steroid cycle. Examples of SERMs are tamoxifen (Nolvadex), clomiphene (Clomid), and raloxifene (Evista).

These drugs work at the estrogen receptor to block the effects of estrogen in certain areas of the body (such as the central nervous system and breast) while in other parts of the body (bone, liver) they act as active estrogens. Their antagonist properties at the breast make them useful in avoiding or treating anabolic steroid induced gynecomastia, while at the hypothalamus/pituitary the anti-estrogen action helps to block the suppressive effect of estrogens upon luteinizing hormone production (and hence testosterone production).

Lately, some people have explored using SERMs as an alternative to testosterone replacement therapy. Indeed they do work to stimulate testosterone production in most males and they can restore healthy levels to guys who have lower than normal testosterone blood readings. The question is however, are you getting the full biological effect of testosterone when you are taking a SERM?

This is an interesting question since it has been observed by many SERM users that the subjective physical response one gets from a SERM often does not correlate with the measured substantial increase in circulating testosterone. In other words, you don’t feel the same when your blood testosterone is doubled by taking a SERM as compared to when it is doubled by a testosterone injection or testosterone gel. Why is that?

There are some theories. Number one, SERMs may act as estrogen antagonists in the brain and it is well known that many of the effects of testosterone upon libido and mood are due to its local conversion to DHT as well as estrogen (estradiol) in the CNS. Therefore blocking the effects of estrogen upon key levels of the brain may blunt the psychological response one would expect from testosterone.

SERMs also are known to act as estrogen agonists (active estrogens) in the liver. This can have a couple of relevant effects. First of all, estrogens strongly promote the production of sex hormone binding globulin (SHBG). This protein circulates in your blood and irreversibly binds to sex hormones such as testosterone, rendering them inactive. So with a SERM you may have high total testosterone levels but actual bioactive testosterone may not be so high.

Another consequence of SERM estrogen agonist action in the liver is suppression of IGF-1 production. IGF-1 is a systemic hormone responsible for whole body anabolism and it is produced in the liver under the positive influence of growth hormone, as well as other hormones such as insulin, thyroid hormone, and androgens. Estrogens on the other hand suppress IGF-1 production in the liver. In a recent study* it was directly demonstrated that administration of either tamoxifen or raloxifene to males increased LH and testosterone levels (as expected). However they also significantly reduced circulating IGF-1 production. Given the fact that it is well demonstrated that exogenous administration of testosterone increases IGF-1 levels in the blood you begin to see that this may be a big part of the SERM testosterone mystery. Systemic IGF-1 levels may not do much for contractile muscle tissue growth but they can lead to overall body composition changes and increases in bodyweight. The difference between the suppressed IGF-1 state (compared to control) of the SERM user to the heightened IGF-1 state (compared to control) of the exogenous testosterone user may indeed be quite profound.

In conclusion, I suspect that once all this information is considered and digested by people then the use of SERMs may go out of favor as an alternative to testosterone replacement therapy. It is my personal opinion that carefully titrated estrogen control via use of an aromatase inhibitor (perhaps combined with a proven natural testosterone elevator such as D-Aspartic Acid) may be a smarter way to achieve the end goal of natural testosterone elevation.

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This article of Patrick's is quite compelling and he touches on a few relevant points I've questioned.

SERMs tank my sex drive. I certainly do not feel as if my testosterone is going up when I take a SERM. I feel incredibly shut down and completely disinterested in sex. That includes a potent resveratrol-based natural SERM.

I had to dial back my dose of Sustain Alpha gel to just one pump because any AI/SERM-like action and I have no sex drive.

I have often wondered if I'm alone on this.

I wonder why nothing is mentioned about combating SHBG with Nettle et al?

As Pat wants people to buy his Testforce product, one could reason that this is just marketing: Eric Potratz cautioned against Serm use also. Impossible for me to know the truth as I'm not a chemist so I have to go with the 'accepted wisdom'. But it's also good to question that, also.

yea PA doesnt care for serms or sarms

Quote:

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Originally Posted by BoneDaddy

I wonder why nothing is mentioned about combating SHBG with Nettle et al?

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Bro law was that Nettle was great in PCT, then it wasn't. Now it is:) except in lower dosages, i.e. 500mgs ed, not megadoses. More info at Datbtrue. Also a thanks to BBG for clearing up the confusion for me.

In all honesty, I found his Testforce product to be a good one. All the DAA benefits without diarrhea, but one always has to follow the money and question if selling products is the underlying motive.

Quote:

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Originally Posted by BoneDaddy

I wonder why nothing is mentioned about combating SHBG with Nettle et al?

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SHBG doesn't only free up test; it also increases the amount of E2 released, which is already going to be elevated from the SERM. You'd need to take an AI to deal with the further increase in E2. Also, increasing SHBG is partially how a SERM works and modulating it may actually be counter productive to the end goal.

It's a shame we'll probably never get to see what Eric was working on with regard to his plan for a complete solution on natural male hormone optimization.

Quote:

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Originally Posted by Rodja

SHBG doesn't only free up test; it also increases the amount of E2 released, which is already going to be elevated from the SERM. You'd need to take an AI to deal with the further increase in E2. Also, increasing SHBG is partially how a SERM works and modulating it may actually be counter productive to the end goal.

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But if you don't (shock, horror) use a Serm?

Quote:

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Originally Posted by markam

But if you don't (shock, horror) use a Serm?

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What about it?

Quote:

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Originally Posted by Rodja

SHBG doesn't only free up test; it also increases the amount of E2 released, which is already going to be elevated from the SERM. You'd need to take an AI to deal with the further increase in E2. Also, increasing SHBG is partially how a SERM works and modulating it may actually be counter productive to the end goal.

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Excellent point. I knew modulating SHBG also affected E2, but I wasn't aware of the Serm aspect of it. Thanks.

Quote:

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Originally Posted by Rodja

What about it?

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Need to do some more research :)

To simplify things- SERM cheats brain into thinking that there is not enough estrogens, so it raises testosterone to get more estrogens (via aromatisation). So advantage of SERM over AI as PCT is that it works much faster, also as Rodja said SERMS raise SHBG a bit which helps recovery process as after any serious cycle SHBG will be virtualy reduced to zero.
IMO best option is SERM+ little bit of AI- lot of people are doing mistake and overdose SERMS, as sometime with too high dose you get opposite effect.
Now, fact is that raising testosterone with SERM or AI dont yield same benefits as with natural or even exogenous test, and also TT:E and TT:SHBG (levels of free test.) ratio is important- and also (IMO) testosterone effect on wellbeing is bit overated.

Quote:

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Originally Posted by Jelisej

To simplify things- SERM cheats brain into thinking that there is not enough estrogens, so it raises testosterone to get more estrogens (via aromatisation). So advantage of SERM over AI as PCT is that it works much faster, also as Rodja said SERMS raise SHBG a bit which helps recovery process as after any serious cycle SHBG will be virtualy reduced to zero.
IMO best option is SERM+ little bit of AI- lot of people are doing mistake and overdose SERMS, as sometime with too high dose you get opposite effect.
Now, fact is that raising testosterone with SERM or AI dont yield same benefits as with natural or even exogenous test, and also TT:E and TT:SHBG ratio is important- and also (IMO) testosterone effect on wellbeing is bit overrated.

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now, what's a little bit when it comes to an AI on pct?

cheers!

Quote:

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Originally Posted by longBallLima

now, what's a little bit when it comes to an AI on pct?

cheers!

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Thats a good question. Depends from person to person, I would say as a rough guide somewhere between 37.5 -75 g of aromasin/exemestane per week, 37.5 would be sufficient for majority of healthy guys 9asuming that their E2 was under control during cycle), and 75 for guys with a lot of aromatisation- but again, this is my rough estimation based on not insufficient evidence, to be honest.

Quote:

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Originally Posted by Jelisej

Thats a good question. Depends from person to person, I would say as a rough guide somewhere between 37.5 -75 g of aromasin/exemestane per week, 37.5 would be sufficient for majority of healthy guys 9asuming that their E2 was under control during cycle), and 75 for guys with a lot of aromatisation- but again, this is my rough estimation based on not insufficient evidence, to be honest.

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gotcha, thanks!

Interesting....I know my SHBG came back elevated just last week. It has been months since I stopped the use of a SERM but have to think it played a role in the elevated number.

Similar to Freepress it has tanked my sex drive which is never fun. Did not use SA this time which was a mistake. I usually feel great on SA after a few days...

To those that have skim read the first post, here is the most relevant part:

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This is an interesting question since it has been observed by many SERM users that the subjective physical response one gets from a SERM often does not correlate with the measured substantial increase in circulating testosterone. In other words, you don’t feel the same when your blood testosterone is doubled by taking a SERM as compared to when it is doubled by a testosterone injection or testosterone gel. Why is that?

There are some theories. Number one, SERMs may act as estrogen antagonists in the brain and it is well known that many of the effects of testosterone upon libido and mood are due to its local conversion to DHT as well as estrogen (estradiol) in the CNS. Therefore blocking the effects of estrogen upon key levels of the brain may blunt the psychological response one would expect from testosterone.

SERMs also are known to act as estrogen agonists (active estrogens) in the liver. This can have a couple of relevant effects. First of all, estrogens strongly promote the production of sex hormone binding globulin (SHBG). This protein circulates in your blood and irreversibly binds to sex hormones such as testosterone, rendering them inactive. So with a SERM you may have high total testosterone levels but actual bioactive testosterone may not be so high.

Another consequence of SERM estrogen agonist action in the liver is suppression of IGF-1 production. IGF-1 is a systemic hormone responsible for whole body anabolism and it is produced in the liver under the positive influence of growth hormone, as well as other hormones such as insulin, thyroid hormone, and androgens. Estrogens on the other hand suppress IGF-1 production in the liver. In a recent study* it was directly demonstrated that administration of either tamoxifen or raloxifene to males increased LH and testosterone levels (as expected). However they also significantly reduced circulating IGF-1 production. Given the fact that it is well demonstrated that exogenous administration of testosterone increases IGF-1 levels in the blood you begin to see that this may be a big part of the SERM testosterone mystery. Systemic IGF-1 levels may not do much for contractile muscle tissue growth but they can lead to overall body composition changes and increases in bodyweight. The difference between the suppressed IGF-1 state (compared to control) of the SERM user to the heightened IGF-1 state (compared to control) of the exogenous testosterone user may indeed be quite profound.

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Worrying?

Quote:

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Originally Posted by milehighguy

Interesting....I know my SHBG came back elevated just last week. It has been months since I stopped the use of a SERM but have to think it played a role in the elevated number.

Similar to Freepress it has tanked my sex drive which is never fun. Did not use SA this time which was a mistake. I usually feel great on SA after a few days...

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If it has been over 3 months that you used SERMS than SHBG would be down by now- its probably mixture of few things, 1. liver is responsible for clearing up SHBG 2. Your testosterone levels are below what it should be- you may be low on other hormones that oppose SHBG (DHT, GH,) 3. If you dont get no insulin spikes that may contribute to problem (insulin lowers SHBG a lot- for example, people with diabetes whose insulin is high have very low SHBG which is one of reasons why their TT is low).

PA owns supplement company and says serms are bad, go figure
Eric also owns supplement company and doesn't like serms, go figure

i wouldn't imagine supplement company owners who have otc pct products recommending serms, it would take money out of their pockets

This is small part of post written by Dr. Mariano, and it may be interesting for some guys:
Tamoxifen (I would prefer this to Clomiphene due to the visual changes that can occur with Clomiphene) is a weak estrogen. This blocks the stronger estrogens from being sensed by the brain. This then causes the brain to release more Luteinizing Hormone to stimulate testosterone production, leading to estrogen production. The increase in testosterone would have the effects listed previously. The problem is that Tamoxifen also blocks estrogen. This leads to lower estrogen signaling activity. Estrogen helps control norepinephrine by increasing serotonin and dopamine production. Estrogen is also needed to improve sensitivity to testosterone by increasing testosterone receptor production. Estrogen is also important in generating energy, motivation, drive, competitiveness, sex drive (libido). Estrogen (particularly in women) is important for neuron growth and memory. The loss of estrogen signaling, depending on the balance with testosterone, may lead to negative effects. If testosterone production is driven high enough, then perhaps this would improve things overall. This is particularly true in men. However, in women, this may not occur and destabilization of the system and dysfunction may occur instead. This is why many women do not like treatment with Tamoxifen or Arimidex for breast cancer.

Quote:

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Originally Posted by sandman

PA owns supplement company and says serms are bad, go figure
Eric also owns supplement company and doesn't like serms, go figure

i wouldn't imagine supplement company owners who have otc pct products recommending serms, it would take money out of their pockets

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I understand what you're saying, but I wouldn't presume their opinions are wrong, necessarily.