[caption id="attachment_319" align="alignnone" width="300"] My degree of shredded is thanks to Aromatase inhibition and estrogen blockage. Notice the cut THROUGH the nipple? No Gyno here![/caption]

By Todd Lee M.D.

Hyperlinked words are in blue. Click them to learn more about them:)

Estrogen Blockers

Estrogen blockers are a frequently misused term. Most people use the term ‘Estrogen blocker’ and ‘Anti-estrogen’ interchangeably but they are not the same.  A blocker is a form of anti-estrogen but there is another form, Aromatase inhibitors.

[caption id="attachment_704" align="alignleft" width="525"] This shows how estrogen blockers (SERMs) bind to some receptors and block them, but in the uterus activates them! Good thing us guys don't have a uterus![/caption]

Estrogen blocker literally means to block the estrogen from binding to the receptor and therefore only SERMS or Selective Estrogen Receptor Modulators are estrogen blockers. It does not mean to stop estrogen from being produced or to remove it from the system. To stop estrogen from being created by the aromatase enzyme from testosterone you need an aromatase inhibitor (AI), not an estrogen blocker.

Tamoxifen, prescription name Nolvadex, is my absolute favorite prescription estrogen blocker or SERM. It offers several advantages over its competing compound Clomid, even for PCT. It’s not a scheduled controlled substance but possession of a prescription drug is illegal without a script.

[caption id="attachment_705" align="alignnone" width="444"] Cut and Dry superiority over the class? Only if you don't have a Uterus! Also, the way it facilitates bone growth is through muscle growth.[/caption]

Is It Bad To Have a Ton of Estrogen?

Yes! But estrogen has its uses, it is great for a ton of different reasons but too much and we get side effects.  Estrogen helps you build muscle 2 different ways. There are 2 different estrogen receptors on the muscle cells: ER alpha and ER beta.  Estrogen binding to the Alpha receptor has a function like MGF as it causes satellite cells to migrate. Binding of estrogen to ER beta causes IGF-1 to be released; these two things are the key to muscle growth.

One Pump Chump? Here Is The Fix!

Sexually you want some estrogen.  With no estrogen you have no sex drive. Period.  Almost as important, estrogen levels determine how long you can last in bed. More estrogen =  More sexual endurance.  Now, the last part is hard to scientifically prove but if your estrogen is really really low and you look super dry and inhuman than women are less likely to find you attractive.  For all these reasons it's important to have some estrogen.

Estrogen also increases HDL which indirectly lowers LDL, making estrogen important for your cardiovascular health!

TOO MUCH estrogen results in fat gain, water storage, whining, prostate cancer and high blood pressure. So you want SOME estrogen but not a lot.  This is why the blend of estrogen blockers and Aromatase inhibitors  in Thor's Hammer and Todd Lee M.D. Test booster are Ideal!

Estrogen Blockade

The reason why people want an estrogen blocker is usually to combat the side effect of gynecomastia. But this is a day late and a dollar short. All your doing is blocking the estrogen receptor on the breast and preventing the breast from growing. It will reduce breast size but why wait until you have a boob?

[caption id="attachment_706" align="alignleft" width="471"] This applies to any steroid hormone. In the case of SERM: this does happen in the liver and uterus but NOT in the breast! So bikini competitors get smaller boobs AND increased risk of uterine cancer when thy listen to their coaches who 'Prescribe' tamoxifen![/caption]

Tamoxifen has the special ability to decrease the size of breast tumors, which means in us male bodybuilders, when you DO have a nodule beneath your nipple, it is the drug which clears that up. It doesn't stop the pain though, an AI like Arimidex works best for that.

Why do I say this is a day late and a dollar short?

[caption id="attachment_707" align="alignleft" width="239"] Aromatase inhibitors prevent the estrogen from being formed from testosterone in the first place. All estrogen blockers do is decrease the damage estrogen does![/caption]

You developed the gyno because the aromatase enzyme converted your testosterone, boldenone, deca or D-Bol into estrogen at a rate of 20%. That means if you take 1000 mg testosterone a week but don't take an AI, you're really getting 600 mg testosterone and 200 mg estrogen, and 200 mg DHT. Now, you get gyno from having more estrogen than a pregnant girl and block the receptor on the breast with the tamoxifen. This does not prevent the estrogen from binding somewhere else! For this reason I think AIs are FAR FAR FAR more important than a SERM while on cycle or post cycle. This is why I developed my original test booster and improved it with Thor's Hammer.

Why are the SERMS so much more popular than A.I.s?

Why do turkeys drown when it rains? Because their stupid. Unfortunately, the guys who are the ‘experts’ on the forums have a 1/10 in necessary knowledge. They seem smart because they know more than the majority of the population who have a 0/10 in knowledge in the fields of Endocrinology, Andrology, Gynecology, Pharmacology,  Anabolic Pharmacology, and Biochemistry. Most practicing physicians fail Biochemistry in Medical School and use their points from other classes to drag them through to barely pass.  

Then Why Use Nolvadex and Not an A.I.?

You wouldn’t. You would add a SERM like Tamoxifen to a cycle if you had break through gyno your AI could not stop from forming. Additionally, Tamoxifen is a SELECTIVE estrogen receptor MODULATOR. This means it binds to some estrogen receptors and activates them!

One example of this is in the liver. Tamoxifen works like estrogen in the liver and increases HDL (good cholesterol) which will scavenge LDL (bad cholesterol) and this it is good for protecting you from heart disease while on cycle. Since my favorite AI, Arimidex (Anastrazole), is not harmful to HDL like other AIs are this combination is the best prescription way to combat estrogen. I used two AIs and two Estrogen receptor blockers   when I designed Thor's Hammer and TLMD Test Booster!  This makes them WAY better than just using a test booster! 

On Cycle Therapy, Post Cycle Therapy

Most internet ‘experts’ think that a SERM is a good OCT (On Cycle Therapy) and PCT (Post Cycle Therapy) and that clomid is the best for PCT. This is completely and totally untrue. Clomid does act like Tamoxifen as a SERM, but unlike Tamoxifen it isn’t beneficial to your HDL. Clomid causes a decrease, not increase in LH like Tamoxifen and clomid causes blindness in some men.

So why does every Tom, Dick,and ‘I got my education on the internet’ Harry think that clomid is better? Because clomid was so bad when it was developed for breast cancer the only thing they could get FDA approval for ‘on label’ use was male infertility.  (On label means insurance will pay for the script to be filled and the doctor is unlikely to lose a lawsuit for prescribing it). Since Tamoxifen sales are so good for breast cancer they never got FDA approval for it to be on label for male infertility, despite it being better than clomid in every way. Even the price of Tamox is superior when you consider 40 mg of Tamoxifen gives better testosterone increase than 150 mg Clomid.

As I said, for OCT, the most important thing to control your estrogen level is to stop your testosterone and other wet anabolics from being DEGRADED down to estrogen from test. For that, you want a mild AI or a low low dose of a strong AI For instance, Letrozole is so strong that a half dose (1.25 mg) every 3 days is ideal and when used all by itself, results in 4x normal testosterone levels, while using it as prescribed (2.5mg/day) only results in 2x normal testosterone increase.

How do the A.I.s and the SERMs Increase Testosterone?

[caption id="attachment_695" align="alignleft" width="386"] Details the relationship of visceral fat converting testosterone to estrogen, and estrogens inhibition on testosterone production. Blocking the estrogen receptors on the pituitary is how Tamoxifen (NOT CLOMID) increases natural testosterone production and using Arimidex (AI) stops that new testosterone from being DEGRADED to estrogen. [/caption]

Well, the whole point of OCT and PCT is to maintain or restore natural testosterone production. IT IS NOT to decrease estrogen. The reason you flip a light switch is to turn the lights on, not to change the orientation of the switch!

Remember how I said an A.I. stops aromatase from converting your testosterone to estrogen? Well BOOM, there you go.  By not degrading test to estrogen, you have more test! It’s common sense.

Also, the main way you get shutdown of the HTPA (hypothalamic pituitary axis) is estrogen binds to the pituitary and stops LH release. Tamoxifen stops this and causes THE OPPOSITE effect of estrogen, it actually stimulates the pituitary to release more, not less LH.

LH is the hormone which tells your testicles to make more testosterone. So not only does Tamoxifen block estrogen induced shut down, it REVERSES it, generating more testosterone! See, selective modulator!

Clomid on the other hand does not do this. It, like estrogen, still decreases LH output just not to the same extent. See, it’s garbage. Shame on anyone who ever uses Clomid for PCT after reading this and a doctor who prescribes this for PCT over Tamoxifen needs to learn what he’s doing.

Who am I kidding, I have never met another doctor who knew what OCT or PCT even was. Most, even their endocrinologists, Suck royally at their jobs. It's sad. I had to explain what tamoxifen and hcg was to the guy who used to prescribe me Androgel in 2008. I had to draw him a picture on how estrogen blockade would increase LH output.  

Summary

[caption id="attachment_711" align="alignnone" width="582"] HRT: birth control, Estrogen The combination of 2 A.I.s and 4 SERMs in Thor's Hammer will function closer to the Ideal SERM hypothesized on the right.[/caption]

Nolvadex/Tamoxifen is the best estrogen blocker, better than Clomid. BUT you may actually want an AI, not an estrogen blocker.  A.I.s stop your anabolics and testosterone from being ruined by conversion to estrogen. All an estrogen blocker does is help you control the side effects of too much estrogen. Estrogen blockers are the bandaid and AIs are the cure... and the prevention.

The exception is if you want to use Tamoxifen post cycle to enhance your natural testosterone production (you most certainly do) and you can use Tamoxifen to protect your arteries from anabolics through their increase to your HDL. Clomid does neither of these extra effects and is the Danny Devito to Tamoxifen’s Schwarzenegger.

Make sure if you're buying illegal drugs you know what you're doing. If any of this information is new to you, I would suggest you use a simpler legal alternative.

 AI/SERM Combination Products!

Both Thor's Hammer / Todd Lee MD Test Booster Combo Pack modulate your estrogen receptors AND stop conversion of testosterone to estrogen and they are legal. Both contain 2 A.I.s (mild) and estrogen receptor modulators. Either is great for OCT or PCT  and they of course boost natural testosterone production similar to HCG, increase the testosterone (androgen) receptor, increase natural GH release similar to GHRP-6 and CJC -1295, and these products stimulate the testes to produce natural testosterone and the pituitary to release LH (which indirectly causes testosterone release). It also has other ingredients to facilitate erections like viagra and blood flow to your whole body giving you an awesome pump in the gym like Cialis or Viagra would.

Thor's Hammer and TLMD Test booster are legal and do not require any specialized knowledge to use, just take them as the label says. These  products  are the best legal approach at maximizing your natural testosterone.  Protecting your natural testosterone production from shut down if your on cycle and restoring your natural production to normal post cycle should always be your only real concern from using anabolics. And with Thor's Hammer and TLMD Test Booster I have mitigated those risks and increased the effectiveness of the cycle you are already on if your on cycle. 

References

http://www.ncbi.nlm.nih.gov/pubmed/14759718

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Fortunati N, Raineri M, Cignetti A, Hammond GL, Frairia R. Control of the membrane sex hormone-binding globulin-receptor (SHBG-R) in MCF-7 cells: effect of locally produced SHBG. Steroids. 63(5-6):282-4, 1998

Fazzari A, Catalano MG, Comba A, Becchis M, Raineri M, Frairia R, Fortunati N. The control of progesterone receptor expression in MCF-7 breast cancer cells: effects of estradiol and sex hormone-binding globulin (SHBG). Mol Cell Endocrinol. 172(1-2):31-6, 2001

Försti A, Jin Q, Grzybowska E, Söderberg M, Zientek H, Sieminska M, etal. Sex hormone-binding globulin polymorphisms in familial and sporadic breast cancer. Carcinogenesis. 23(8):1315-20, 2002

Catalano MG, Comba A, Fazzari A, Benedusi-Pagliano E, Sberveglieri M, Revelli A, et al. Sex steroid binding protein receptor (SBP-R) is related to a reduced proliferation rate in human breast cancer. Breast Cancer Res Treat. 42(3):227-34, 1997

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Fortunati N, Fissore F, Fazzari A, Berta L, Benedusi-Pagliano E, Frairia R. Biological relevance of the interaction between sex steroid binding protein and its specific receptor of MCF-7 cells: effect on the estradiol-induced cell proliferation. J Steroid Biochem Mol Biol. 45(5):435-44, 1993

Khan HN, Rampaul R, Blamey RW: Management of physiological gynaecomastia with tamoxifen. Breast. Feb;13(1):61-5, 2004

Lawrence SE, Faught KA, Vethamuthu J, Lawson ML: Beneficial effects of raloxifene and tamoxifen in the treatment of pubertal gynecomastia. J Pediatr. Jul;145(1):71-6, 2004

Parte P, Balasinor N, Gill-Sharma MK, Maitra A, Juneja HS: Temporal effect of tamoxifen on cytochrome P450 side chain cleavage gene expression and steroid concentration in adult male rats. J Steroid Biochem Mol Biol. Nov;82(4-5):349-58, 2002

Hanavadi S, Banerjee D, Monypenny IJ, Mansel RE. The role of tamoxifen in the management of gynaecomastia. Breast. 15(2):276-80, 2006

MacNab MW, Tallarida RJ, Joseph R. An evaluation of tamoxifen as a partial agonist by classical receptor theory–an explanation of the dual action of tamoxifen. Eur J Pharmacol. 103(3-4):321-6, 1984

Vandekerckhove P, Lilford R, Vail A, Hughes E: Clomiphene or tamoxifen for idiopathic oligo/asthenospermia. Cochrane Database Syst Rev. (2):CD000151, 2000

Disclaimer

Nothing in this article or on this site should be considered medical advice or as an endorsement to violate any law of the country in which you reside.  The information given is for fun and entertainment purposes only.  All claims are 100% dependent upon proper diet and exercise.  Please consult a medical practitioner prior to any diet and exercise program.