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  1. #1
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    Joes Unsponsored Log

    Hey guys,

    A lot of you already know me from my previous log over in one of the sponsor sub-forums.

    Unfortunately we have since parted ways, but I didnt want to let you guys down who have been following the content, so I will continue here!

    For those of you that dont know me - my name is Joe, Im based in the UK and am an online physique & health coach by trade.

    In here I will share personal updates, my podcasts, articles and all other content.

    Thanks guys, I hope you enjoy!


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  2. #2
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    Well this is a surprise to see you not with them anymore. Hopefully everything is fine and well.

    I've always followed your log over there, will follow this one also, Joe.

  3. #3
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    Quote Originally Posted by TripleOvertime View Post
    Well this is a surprise to see you not with them anymore. Hopefully everything is fine and well.

    I've always followed your log over there, will follow this one also, Joe.
    I was surprised also man, but it is what it is, onwards we go! Appreciate the follow my brother.


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  4. #4
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    Will be following. Great log.

  5. #5
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    Quote Originally Posted by malfeasance View Post
    Will be following. Great log.
    Thank you sir...

    - - - Updated - - -

    USING ANDROGENS TO MEDIATE ESTROGENIC SIDE EFFECTS VIA CONTROLLING YOUR A:E RATIO.
    There is a tonne of confusion in here on this premise, so heres a basic breakdown.
    So firstly, cotrolling estrogenic effects with androgens, vs. actual anti-estrogenic actions - whats the difference?
    Selective estrogen receptor modulators (SERMS) are both antagonistic and agonistic at the estrogen receptor. They are anti-estrogenic where they are antagonistic, such as the breast.
    Aromatase inhibitors (AIs) are anti-estrogens. By direct mechanism, they reduce serum estrogen by inhibiting the aromatase pathway action.
    Now... onto androgens.
    Dihydrotestosterone (DHT) has SOME anti-aromatase activity, but really not much. NOTE: this applies to DHT only, not all 5-AR compounds/DHT derivatives.
    So how do we use androgens to balance estrogenic side effects outside of DHT only?
    Many AAS have been studied and utilised in the treatment of breast cancer (including testosterone). When androgen receptor binding at the breast is greater than estrogen receptor binding, this will prevent proliferation of breast tissues.
    Typical AAS used for this purpose are masteron, proviron, epistane and winstrol, but all androgens can be utilised.
    Simply, increasing your A:E ratio by introducing non-aromatising will counteract estrogenic side effects via the drugs action at the androgen receptor, NOT due to any anti-estrogenic factors.
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  6. #6
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    I'll be following along

  7. #7
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    Quote Originally Posted by TheShadow View Post
    Thank you sir...

    - - - Updated - - -

    USING ANDROGENS TO MEDIATE ESTROGENIC SIDE EFFECTS VIA CONTROLLING YOUR A:E RATIO.
    There is a tonne of confusion in here on this premise, so heres a basic breakdown.
    So firstly, cotrolling estrogenic effects with androgens, vs. actual anti-estrogenic actions - whats the difference?
    Selective estrogen receptor modulators (SERMS) are both antagonistic and agonistic at the estrogen receptor. They are anti-estrogenic where they are antagonistic, such as the breast.
    Aromatase inhibitors (AIs) are anti-estrogens. By direct mechanism, they reduce serum estrogen by inhibiting the aromatase pathway action.
    Now... onto androgens.
    Dihydrotestosterone (DHT) has SOME anti-aromatase activity, but really not much. NOTE: this applies to DHT only, not all 5-AR compounds/DHT derivatives.
    So how do we use androgens to balance estrogenic side effects outside of DHT only?
    Many AAS have been studied and utilised in the treatment of breast cancer (including testosterone). When androgen receptor binding at the breast is greater than estrogen receptor binding, this will prevent proliferation of breast tissues.
    Typical AAS used for this purpose are masteron, proviron, epistane and winstrol, but all androgens can be utilised.
    Simply, increasing your A:E ratio by introducing non-aromatising will counteract estrogenic side effects via the drugs action at the androgen receptor, NOT due to any anti-estrogenic factors.
    huh. I have been wondering about this. I have been using masteron when needed but did not understand how it prevented estrogen sides. I just knew it did.

  8. #8
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    Following
    All characters appearing in this work are fictitious. Any resemblance to real persons, living or dead, is purely coincidental.

  9. #9
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    Photos upon waking this morning @ 220.4lbs


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  10. #10
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    Height?

  11. #11
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    Quote Originally Posted by malfeasance View Post
    Height?
    511


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  12. #12
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    That's a very solid weight for that height. What is your competition weight?

  13. #13
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    Quote Originally Posted by malfeasance View Post
    That's a very solid weight for that height. What is your competition weight?
    Thank you. I began lifting at this same height at 125lbs! Last time I was contest lean I was 180ish, but Ive put on at lease 10lbs of tissue since then.


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  14. #14
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    243 men received either testosterone or placebo and took the Cognitive Reflection Test.

    Scores were reduced in men receiving testosterone, suggesting a mechanism by which testosterone reduces decision making and judgement.

    I think of all future research on AAS, the deleterious psychological effects will likely be the most worrisome.

    https://www.researchgate.net/publica...lection_in_Men


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  15. #15
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    Pretty cool study on using trenbolone instead of testosterone in hormone replacement settings.




    The rats received 2 mg/kg/day of trenbolone! The equivalent of me taking 200mg of tren base every single day. These doses are meaningless for the most part when comparing to our situation however, due to the huge physiological differences between rats and humans.




    In 6 weeks, rats taking trenbolone noted...

    - decreased fat mass

    - increased lean mass

    - reduced serum triglycerides, HDL and LDL

    - benign prostate hyperplasia

    - no evidence of adverse cardiac or hepatic effects was observed




    Hopefully these studies give way for human studies in the future. I am especially interested in the tissue-selective androgenic activity of AAS like tren and their propensity to reduce some risks of long-term TRT, just like we are hoping with new-generation SARMS.




    https://www.ncbi.nlm.nih.gov/pubmed/25554582
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