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Estrogen Is NOT Needed For Either Muscle Or Bone Growth / Anabolism

Discussion in 'Scientific Studies' started by haidut, Jan 16, 2019.

  1. haidut

    haidut Member

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    I have had my eye on posting this study for at least 3 years now but something more important always came up, so I kept putting it off. However, the recent thread posted on the forum about how estrogen is "essential" for health convinced me it is way overdue that I post something on this topic, as I promised in the post below.
    Estrogen Is Absolutely Critical For Men
    I am sure by now all forum users are aware of the mainstream medical claim that estrogen is absolutely "essential" for bone health. The increased incidence of osteomalacia/osteopenia and osteoporosis after menopause are explained as due to deficiency of estrogen and millions of women are put on HRT with estrogen in the hope that their bones will recover. Peat mentioned tongue in cheek several times in his articles that doctors conveniently ignore the fact that estrogen potently stimulates prolactin release, and the latter is one of the most potent bone catabolic hormones. However, direct evidence showing estrogen is not needed for bone health is sparse, possibly because of the complete taboo of attacking the dogma of estrogen's role in bone health.
    In addition to the purported "benefits" of estrogen for bone health, a similar myth circulates in sports and bodybuilding circles. Part of that myth is illustrated in the thread above - i.e. that without estrogen men and women get fat and and their muscles cannot grow. Bodybuilders seem especially affected by that myth, illustrated by the design of cycles and PCT regimens so that estrogen is left untouched during a cycle and only partially inhibited during PCT in order to preserve its "benefits". I think some of that myth stems from the usage of both an AAS and estrogen in combination in the livestock industry in order to maximize growth. However, even the livestock studies clearly explain that the contribution of estrogen to growth of the animal is mostly in the form of fat and water retention, not muscle.
    Anyways, I hope that the study below will give the estrogen-backers some food for thought. It showed directly that estrogen is not needed for muscle or bone growth, and anabolic effects of steroids on muscle/bone to be the same without estrogen. Actually, the increase in muscle mass and the decrease in fat mass was augmented when the androgen was combined with inhibiting estrogen synthesis (5% bigger muscle growth and 12% bigger fat loss). The reason I like the study so much is that it went a step further than other estrogen-blocking experiments. One of the steroids used to increase bone/muscle growth was Trenbolone. For those who do not know, trenbolone is not only devoid of estrogenic effects, it is actually a potent progestin with 3-4 times stronger effect at PR than progesterone itself. It is also about 50% more potent agonist at AR than even DHT. The combination of potent progestogenic and androgenic effects, combined with the fact that trenbolone cannot be aromatized, results in one of the most potent anti-estrogenic chemicals known. These potent anti-estrogenic effects were the reason why the orally bioavailable version of trenbolone known as R1881 was studied as treatment for advanced/terminal breast cancer back in the 1960s and 1970s.
    Metribolone - Wikipedia
    "...Metribolone (developmental code name R1881), also known as methyltrienolone, is a synthetic and orally active anabolic–androgenic steroid (AAS) and a 17α-alkylated nandrolone (19-nortestosterone) derivative which was never marketed for medical use but has been widely used in scientific research as a hot ligand in androgen receptor (AR) ligand binding assays (LBAs) and as a photoaffinity label for the AR.[1][2][3] It was investigated briefly for the treatment of advanced breast cancer in women in the late 1960s and early 1970s but was found to produce signs of severe hepatotoxicity at very low dosages, and its development was subsequently discontinued."

    So, not only did the study use a potent androgenic and anti-estrogenic steroid like trenbolone but it also combined it with an aromatase inhibitor (AI). And what do you think the negative effects of this complete blockade of estrogen on bone/muscle health were? None. Nada. Zilch. To make matters worse for the estrogen-backers, the AI drug (anastrozole, AN) used was administered in an absolutely massive dose, equivalent to 10mg-15mg daily for a human. For comparison, most bodybuilders use 0.5mg-1mg daily even in severe cases of estrogen elevations resulting in gyno and even lactation. At a dose of 10mg-15mg daily, AN will tank estrogen levels by more than 90%.
    Finally, and perhaps most tellingly, trenbolone by itself led to only a non-significant reductions in fat mass. However, adding the AI to trenbolone resulted in significant fat reduction of 31% compared to untreated animals, and the fat mass in the trenbolone + AI group was about 7%-9% lower than even the control (healthy) group. So much for "blocking estrogen will make us fat" myth...

    EDIT (1/18/19): If even that evidence again estrogen is enough, here is the sister thread I posted a few days after this one showing that blocking estrogen signalling in the brain was shockingly anabolic for both muscle and bones in females.
    Blocking Estrogen In Brain Strikingly Anabolic For Female Muscles / Bones

    EDIT (1/19/2019): Another forum user posted a human study on effects of AI drugs on bone health. Hidden in that study was a gem quote that the group receiving only an AI had both increases in muscle mass and decreases in fat mass, and it was the only group that experienced these effects. Testosterone administration on its own or the placebo group saw no such benefits. Perfect corroboration of the study below. :):
    Estrogen Is NOT Needed For Either Muscle Or Bone Growth / Anabolism

    @AretnaP @Wagner83 @Lokzo @RisingSun @jb116 @tankasnowgod @opethfeldt

    Influence of aromatase inhibition on the bone-protective effects of testosterone. - PubMed - NCBI
    "...Both androgens and estrogens influence skeletal development and maintenance in males.(1, 2) In older men, hypogonadism [i.e., low circulating total/bioavailable testosterone (T)] is associated with reduced BMD (3, 4) and increased fracture risk (5), despite elderly men experiencing an elevated estradiol (E2)/T ratio within the circulation(6); suggesting that bone loss in hypogonadal men results primarily from a T deficiency. Within this population, T administration dose-dependently improves BMD, with physiologic T replacement therapy providing modest enhancement of bone mass and higher-than-replacement T required for more robust musculoskeletal and lipolytic results.(7, 8) However, it remains unclear whether the skeletal protection induced by T administration occurs directly, via androgen-mediated actions, or indirectly, via estrogen-mediated actions that occur following the gonadal and/or tissue-specific aromatization of T to E2. (9) For example, we previously demonstrated that supraphysiologic T administration dramatically increases circulating and intraskeletal androgen concentrations and completely prevents bone loss in ORX rats, without altering circulating or intraskeletal E2 concentrations.(10, 11) In addition, several clinical studies have reported that elderly men experience very minimal to no bone loss following pharmacologic aromatase inhibition, despite reductions in circulating E2 ranging from 30-50%. (12-14) Interestingly, administration of either dihydrotestosterone (DHT, a potent non-aromatizable androgenic metabolite of T) (15) or trenbolone (a synthetic non-estrogenic, non-aromatizable androgen) (16) completely prevents ORX-induced bone loss in skeletally-mature rodents, providing further evidence that elevated systemic and/or skeletal-specific E2 is not required for androgen induced bone maintenance or that only a very minimal threshold concentration of E2 may be required for bone health in adult males(5)."

    "...µCT analysis of the distal femur indicated that cancellous BV/TV was 25% lower in ORX animals compared with SHAMs (p < 0.001, Figure 1) and AN co-administration did not alter this effect. This difference was characterized by a 20% reduction in Tb.N (p < 0.001) and a 20% increase in Tb.Sp (p < 0.01), with no difference in Tb.Th. Both TE and TREN completely prevented cancellous bone loss, with BV/TV being 23-35% higher than ORX animals (p < 0.01, Table 2). Ultimately, all cancellous bone variables in androgen treated animals were maintained at the level of SHAMs, with no differences resulting from co-administration of AN."

    "...Cancellous (medullary) vBMD was ~20% lower at the distal femoral metaphysis and at the femoral neck in ORX animals compared with SHAMs (p < 0.001, Table 3); AN co-administration did not alter this effect. Both TE and TREN administration completely prevented these reductions, with cancellous vBMD values being 21-26% higher at the distal femoral metaphysis (p < 0.01) and 22-30% higher at the femoral neck compared with ORX animals (p < 0.01) and not different than SHAMs (Table 3). AN co-administration did not alter these androgen induced effects."

    "...LABC mass was 45% lower in ORX and ORX+AN animals compared with SHAMs (p < 0.001, Supplemental Table 1). Conversely, LABC mass in TE and TREN animals was 38-42% greater than SHAMs (p < 0.001) and >2.5 times larger than ORX animals (p < 0.001), a result that was not inhibited by AN coadministration. Retroperitoneal fat mass was 22-24% higher in ORX and ORX+AN animals compared with SHAMs (p < 0.05, Supplemental Table 1). All androgen treatments prevented the ORX-induced increase in retroperitoneal fat mass, with fat mass being 33% lower in ORX+TE (p < 0.01), 23% lower in ORX+TE+AN (p < 0.05), 19% lower in ORX+TREN (non-significant), and 31% lower in ORX+TREN+AN animals (p < 0.01)."
     
  2. aguilaroja

    aguilaroja Member

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    The action of testosterone and trenbolone in combination suggests there is more to muscle bulk, and function, than "inhibition" of myostatin protein.
    Testosterone and trenbolone enanthate increase mature myostatin protein expression despite increasing skeletal muscle hypertrophy and satellite cel... - PubMed - NCBI
    "Testosterone and trenbolone administration increased muscle fCSA [skeletal muscle fibre cross-sectional area] and satellite cell number without increasing myonuclei number, and increased Mstn[myostatin] protein levels."
     
  3. OP
    haidut

    haidut Member

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    I agree, and here is another interesting study that discusses differential effects of T and trenbolone on muscle growth.
    Transcriptional regulation of myotrophic actions by testosterone and trenbolone on androgen-responsive muscle. - PubMed - NCBI
     
  4. Cameron

    Cameron Member

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    This is why I've always wondered why some don't use aromosin for after cycle or just standalone PED? do you believe in the estrogen rebound theory? specially with an already anti estrogenic diet with liver carrot? Dhea and preg while using aromasin could create the additional steroid pathway aromasin to block pathways to estrogen and keep a pathway toward test and 5ar steroids with it's half life maybe used 10mg every other day
     
  5. boxers

    boxers Member

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    I feel best with my Estrogen a bit high (70 area). Previously when taking AI and keeping my e2 low was just a mess, horrible libido, joint pain. etc

    Since I stopped using an AI to keep my e2 around 15-30 and let it rise to 70 range. my Morning wood has returned.

    Crushing estrogen is a bad idea. We need eatrogen
     
  6. Fractality

    Fractality Member

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  7. baccheion

    baccheion Member

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    What are the associated testosterone and DHT levels? What testosterone:estradiol ratio does 70 represent?
     
  8. tankasnowgod

    tankasnowgod Member

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    Excellent study. This part especially caught my eye-

    When I went looking for the studies in the "Estrogen is critical for men" thread, I found the following study was the basis for the claim that "Estrogen reduces fat, especially belly fat"- Gonadal steroids and body composition, strength, and sexual function in men. - PubMed - NCBI

    In the study, they used Goserelin Acetate on all the male subjects, in order to suppress endogenous Testosterone and Estrogen production. It works well for that, but guess what else it suppresses? Progesterone!

    Goserelin Acetate (Zoladex®) - For Women | OncoLink

    "About: Goserelin Acetate (Zoladex®) - For Women
    While estrogen and progesterone may not actually cause breast cancer, they are necessary for the cancer to grow in some breast cancers. Estrogen and progesterone are female hormones produced by the ovaries. The production of these hormones can be stopped by surgically removing the ovaries or through medication therapy. A hormone called luteinizing hormone, which is produced by the pituitary gland, stimulates production of estrogen and progesterone by the ovaries. LHRH agonists stop the production of luteinizing hormone by the pituitary gland. This reduces the production of estrogen and progesterone. The cancer cells may then grow more slowly or stop growing altogether. Goserelin acetate is a type of LHRH agonist."

    After giving all men Goserelin Acetate, they were split into groups that got various amounts of Testosterone (og, 1.25 g, 2.5 g, 5 g, or 10 g daily), and each of those groups were split into two, one getting the AI anastrozole, and the other nothing.

    Not surprisingly, the groups that got the largest dose of Testosterone fared better in terms of strength, minimizing fat gain, and subjective scores about sex life. Those that didn't get Anastrozole gained less bodyfat than those getting the same level of Testosterone that did. The researchers conclude from this that Estrogen can prevent fat gain.

    But again..... Estrogen isn't the only thing that Anastrozole inhibits. What else does it suppress? That's right, Progesterone!

    Short-term anastrozole therapy reduces Ki-67 and progesterone receptor expression in invasive breast cancer: a prospective, placebo-controlled, dou... - PubMed - NCBI

    Obviously, I think drawing the conclusion that "Estrogen prevents bodyfat" from a study that used both Goserelin Acetate and Anastrozole together is flawed. A better conclusion might be that it's better to use an aromatase inhibitor that does not suppress progesterone or androgen production.
     
  9. tankasnowgod

    tankasnowgod Member

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    Which AI were you using?
     
  10. Iceman2016

    Iceman2016 Member

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    Why do so many people have libido issues, joint problems, etc when estrogen formation is inhibited by anti aromatases such as anastrozle, letrozole, etc? Obviously we can't say the experiences of so many people are just psychosomatic, can we? In other words, there must be some (many?) essential, beneficial effects of estrogens on the male body that are negated when people lower estrogen levels too low.

    I remember having conversations with a few doctors when Proscar (finasteride) first came out to treat BPH. These doctors were adamant that DHT only caused acne, hairloss, and other negative effects and that after puberty, only testosterone was needed to maintain general male health.

    Despite the studies posted showing the various clear negative effects of estrogen in a number of situations, could making the same broad sweeping statements about estrogen being evil and unnecessary for male health be treading down the same path as the doctors mentioned above?
     
  11. baccheion

    baccheion Member

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    Maybe it results in less acetylcholine, oxytocin, etc? Estrogen protects against bone loss (osteoclast formation). Without enough, more calcium and fat-soluble vitamins are required. Estrogen also aids in the absorption of calcium.
     
  12. Douglas Ek

    Douglas Ek Member

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    Really nice find. Always thought that the body had sort of jing jang chemicals. I cant see estrogen basically having any potential good benefits for any animal since to me it sounds like a stress hormone. A hormone that increases fat deposits feels like a hormone where it’s purpose is to stock up energy for an emergency or energy for carrying a child in their body. Reducing estrogen with AI would in that case lower body fat since it tells the body hey we dont need to store fat for emergency we can channel it to building muscles. I think building muscle is the last thing the body prioritise after survival so reducing all stress hormones like estrogen, cortisol and even serotonin, prolactin which seems tied into the whole estrogen to prepare for child birth etc keep em low and the body will realize ok we can build muscles. Thyroid also fit in nicely to this type of thinking since its basically your metabolism knob and if you don’t eat the anabolic way and eat enough energy to support energy production and beyond that your body dont see any reason to funnel it towards anabolic processes like muscle building and eating to little energy (glucose) where the body has to breakdown tissue and supply its own energy and store some as fat incase of emergency cortisol and estrogen does just that. Its so straight forward and makes perfect logical sense and still science today just got it so wrong. We can sit here on a forum discuss these principles so easily while science cant even figure it out. Jesus christ its sad
    In the end its just as simple as energy and anabolism having enough surplus of energy and catabolism being low on energy breaking down. Such easy concept but still so many got it wrong.
     
  13. Regina

    Regina Member

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    :thumbsup: Idealabs Trenbone
     
  14. Douglas Ek

    Douglas Ek Member

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    Short for tremendous boner
     
  15. RisingSun

    RisingSun Member

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    Great find @haidut

    The common practice is to NOT give a prophylactic dose of AI when replacing testosterone until we know for sure what is the aromatization rate of the patient.

    I’ve had more people complain of low E2 sides than when it’s in the upper range: libido loss, joints cracking.

    I haven’t monitered anyone long enough on either high E2 or low E2 to know what are the broader and longer term effects on bone mineral density and other physical parameters, so this study is very helpful in that sense.

    I would be vigilant on two aspects:

    - the study involving TREN can’t be bluntly interpreted as to whether complete blockade of E2 is beneficial, as TREN is also a strong progesterone receptor agonist, so there is more to it.

    - NOBODY should be taking oral tren aka methyltrienolone, it’s one of the most liver toxic AAS out there.
    I know you are not advocating for it, just want to set the record straight for everyone reading this.


    Other than that, the study showing that supraphysiological doses of bioidentical androgens accompanied by E2 blockade cause no bone loss is very interesting.

    Thank you
     
  16. RisingSun

    RisingSun Member

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    Like all 19-nor, it’s a hit or miss, depending on the tren dose and the test dose.

    Libido increase is reported in 99,99% of cases, however erection capacity is very often impaired
     
  17. Lokzo

    Lokzo Member

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    Exactly right. Most guys feel terrible with low E, as you've pointed out. I experience the exact same effects as you mentioned.
     
  18. RisingSun

    RisingSun Member

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  19. rei

    rei Member

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    If you strongly and artificially inhibit estrogen you need to ensure through raising other hormones that a balance is maintained. Trenbelone seems to take care of some of the necessary effects of estrogen. It is ridiculous to think that estrogen is completely undesirable and should be minimized at all times.
     
  20. OP
    haidut

    haidut Member

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    Thanks for the comments. I think the issues with libido and joints from AI depend heavily on the AI used. The *zoles like the one used in this study seem to be the worst. Lower dose exemestane (5mg-6mg) which seems to achieve about 60% reduction in estrogen levels (both E1 and E2) has not been associated with such complaints. Maybe it is due to the fact that exemestane metabolizes into 6-methylene-boldenone and boldenone has been shown to improve joint health and libido even in people taking AI. The non-steroidal *zoles have no such side benefit.
    And yes, definitely not recommending using R1881 or any other 17-alpha-methylated steroid. Among the most hepatotoxic chemicals. Second worst are the 7-alpha methylated ones (trestolone, mibolerone, etc), third-worst are the 2-oxa (oxandrolone), and perhaps the least dangerous (but still worthy of caution) are the 1-alpha and 2-alpha methylated ones (Proviron, drostanolone). For the record, even Proviron has reports of liver toxicity, leaving drostanolone as probably the only synthetic, FDA-approved, AAS without known liver toxicity. The studies on breast cancer with drostanolone back in the 1960s used 50mg-100mg daily with no serious side effects, which is still a huge dose considering the steroid is just 2a-methyl-DHT. So, in more acceptable doses similar to the ones for Proviron (10mg-20mg daily) it should be relatively safe.
     
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