CLASH

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@RisingSun @Douglas Ek
Thanks for the responses.
This has been my experience to some extent. After using the hormone in very low doses, over a period of time there starts to be some negative effects. I havent tried DHEA, but i’ve found this to be the case with progesterone and pregnenolone. The best I can get away with is using them at most
2-3x/week on non-consecutive days and even then I still get some side effects (this is at very low doses btw; progesterone 3mg, and pregnenolone less than 6-8mg). I dont think I would want to try anything stronger than the parent compounds or synthetics.
 

LCohen

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As Peat said once - estrogen is the hormone of new beginnings, of growth and replacement. So, great for short periods if facing issues like wounds, burns, bone damage/break, etc. But not something you want to get stuck in for longer as continually erasing what was built (high cell turnover) is basically the hallmark of cancer.

Never heard this. Good statement.

This may explain how transgenders regrow hair?

Since the baldness strongly associated with fibrosis of the scalp. I think it reforms collagen/fibrosis stuff, going on scalp. It shifts to growth and replacement.

Instead of silly anti-androgenic explanation, that makes more sense. Still not a desirable thing.
 
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@RisingSun @Douglas Ek
Thanks for the responses.
This has been my experience to some extent. After using the hormone in very low doses, over a period of time there starts to be some negative effects. I havent tried DHEA, but i’ve found this to be the case with progesterone and pregnenolone. The best I can get away with is using them at most
2-3x/week on non-consecutive days and even then I still get some side effects (this is at very low doses btw; progesterone 3mg, and pregnenolone less than 6-8mg). I dont think I would want to try anything stronger than the parent compounds or synthetics.

What have your sides been?
 
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haidut

haidut

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Never heard this. Good statement.

This may explain how transgenders regrow hair?

Since the baldness strongly associated with fibrosis of the scalp. I think it reforms collagen/fibrosis stuff, going on scalp. It shifts to growth and replacement.

Instead of silly anti-androgenic explanation, that makes more sense. Still not a desirable thing.

The transgenders usually get a combination treatment of progesterone + estrogen. They almost never get estrogen only due to health risks of pure estrogen therapy and more importantly because estrogen on its own does not produce the femininity most MTF patients want. So, I think it is the progesterone that is responsible for hair regrowth. Estrogen is more for wounds and the connective tissue it forms becomes scar. So estrogen actually promotes fibrosis instead of reversing it. Progesterone, testosterone and DHT are anti-fibrotic.
 
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haidut

haidut

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I’m interested to know more details. E.g. respective percent of men and women that dropped out. Also what the rate of erectile dysfunction was... thinking about sex 24x7 is very different from sexual ability.

No sexual dysfunction reported, to the contrary actually. Mostly women were tested because it was designed as a breast cancer drug but the pro-sexual effects are notorious in both sexes. The Russians took note of those US studies in the 1960s and developed a drostanolone mix they called Proloteston. It was used for cancer and sexual dysfunction in BOTH men and women. As I mentioned, Google for "drostanolone libido" or "drostanolone sex". DHT is the main driver of male sexuality so it is quite expected that a DHT derivative will have these effects.
DHT Is The Primary Driver Of Male Sexual Activity And Is Crucial For Male Orgasm
 

boxers

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How is your total T? High estrogen may give you good libido but that does not mean it is the optimal way to do it. High T with E2 in the bottom 25% also gives people great libido. This is the phenotype 20yo males have, together with higher progesterone.
High dose Masteron (drostanolone) is notorious for turning people into sexually berserk rhinos yet it crushes E2 (and E1) below detectable levels. In fact, about 20% of the people on whom drostanolone was tested back in the 1960s dropped out of the trials due to excessive libido. They could just not do anything except think about sex 24x7.
So, libido is probably not the best metric of estrogen's healthiness, and there are arguably healthier ways to achieve it. According to the study above even bone health can be perfectly maintained by non-aromatizable steroids like DHT or trenbolone, even when adding an AI.
Estrogen is THE primordial growth hormone. Growth, as in uncontrolled, de-differentiating type. The bad kind, the kind that kills if left unchecked for too long. I don't think estrogen should be crushed, but most people probably produce and carry around way more than what they need for optimal health. Increased peripheral aromatization is one of the earliest biomarkers of aging/disease.
Just my 2c.

My total test is 1000, e2 was 47. It was 70 but when i switched to daily injections it dropped a bit

I have experimented with anastrozole and aromasin
 

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Hold your horses:

After 12 months, we found AI treatment was associated with lower lumbar spine BMD compared to TT and placebo group. Our results confirm previous reports that aromatization of T to E is important for the male skeleton. For example, a previous 12‐month study in older hypogonadal men treated with AI also showed lower lumbar spine BMD compared to placebo (Burnett‐Bowie et al., 2009). Although previous studies of older men have shown that T treatment increases lumbar spine BMD (Amory et al., 2004; Leder, 2007), we were unable to find a significant difference between the TT and placebo groups, perhaps because small sample size. We speculate that the increase in lumbar spine BMD in placebo could be attributed to oral calcium and vitamin D intake. Indeed, daily intake of 500 mg calcium and 700 IU vitamin D for 1 year by men >65 years increased BMD in lumbar spine (Dawson‐Hughes et al., 1997).Our findings support the notion that sufficient E levels in older men is an important contributor to bone density (Falahati‐Nini et al., 2000; Gennari et al., 2003; Amory et al., 2004; Rodriguez‐Tolra et al., 2013; Argoud et al., 2014).
 
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haidut

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Hold your horses:

After 12 months, we found AI treatment was associated with lower lumbar spine BMD compared to TT and placebo group. Our results confirm previous reports that aromatization of T to E is important for the male skeleton. For example, a previous 12‐month study in older hypogonadal men treated with AI also showed lower lumbar spine BMD compared to placebo (Burnett‐Bowie et al., 2009). Although previous studies of older men have shown that T treatment increases lumbar spine BMD (Amory et al., 2004; Leder, 2007), we were unable to find a significant difference between the TT and placebo groups, perhaps because small sample size. We speculate that the increase in lumbar spine BMD in placebo could be attributed to oral calcium and vitamin D intake. Indeed, daily intake of 500 mg calcium and 700 IU vitamin D for 1 year by men >65 years increased BMD in lumbar spine (Dawson‐Hughes et al., 1997).Our findings support the notion that sufficient E levels in older men is an important contributor to bone density (Falahati‐Nini et al., 2000; Gennari et al., 2003; Amory et al., 2004; Rodriguez‐Tolra et al., 2013; Argoud et al., 2014).

We already discussed anastrozole earlier in this thread. That drug depletes progesterone and likely has other negative effects, so its effects on bones cannot be ascribed to depletion of estrogen only. This is supported by the fact that exemestane either has no negative effects on BMD or in some cases can actually improve it.
Differential profile of letrozole and exemestane on bone turnover markers in vinylcyclohexene diepoxide treated ovotoxic female mice. - PubMed - NCBI
Exemestane's 17-hydroxylated metabolite exerts biological effects as an androgen. - PubMed - NCBI
"...Aromatase inhibitors (AI) are being evaluated as long-term adjuvant therapies and chemopreventives in breast cancer. However, there are concerns about bone mineral density loss in an estrogen-free environment. Unlike nonsteroidal AIs, the steroidal AI exemestane may exert beneficial effects on bone through its primary metabolite 17-hydroexemestane. "

Btw, you forgot to quote the most important portion of your study. In other words, only AI administration BOTH increased muscle mass and decreased fat mass. Corroborates perfectly the study in the original post. :):
"...Although LBM increased in both of the intervention groups, it only reached statistical significance in the AI group in which LBM increased by (1.2 ± 0.6 kg) at 12 months. Similarly, the reduction in FM was only significant in men on AI (1.8 ± 0.6 kg) at 12 months. However, across groups, these changes were not statistically significant (Table 2)."
 
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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)."
Nice post, thanks.
I think evidence like this while dissecting the chicanery of, for example that rouzier video, which as Peat has mentioned, is trickery with word play demonstrates just how much estrogen has been blown out of proportion for decades as far as its importance is concerned and how much its danger has been hidden. Now the very entity that's been pushing it is trying to [probably] monopolize the antithesis to estrogen to fix diseases. So which is it?! lol
 
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haidut

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Nice post, thanks.
I think evidence like this while dissecting the chicanery of, for example that rouzier video, which as Peat has mentioned, is trickery with word play demonstrates just how much estrogen has been blown out of proportion for decades as far as its importance is concerned and how much its danger has been hidden. Now the very entity that's been pushing it is trying to [probably] monopolize the antithesis to estrogen to fix diseases. So which is it?! lol

I think you hit the nail on the head. The medical industry does not even have to respond to contradictions any more. They can publish two studies back to back, one claiming estrogen is good for muscle and one that it is bad. And if anybody asks what this nonsense is all about the answer always is "are you a doctor?". If you are not then you are not owed an explanation. If you are a doctor then...well...you know better than to rock the boat or you will be quickly summoned for a quick "re-education" session on how residency, funding, and career progression work in this world :):
We are already seeing this with serotonin. Pharma companies continue to push the view that serotonin is great and SSRI sales are at an all-time high. At the same time, Pfizer is advancing the anti-serotonin drug terguride through multiple human trials showing it treats a number of "incurable" conditions like heart failure, pulmonary hypertension, and possibly even cystic fibrosis for which the story is still that their cause is "unknown".
It really does not bode well for the future of this world. Such state of absolute deception either has to be maintained regardless of the cost, or if the public wakes up...well I think you can imagine what the outcome will be if people realize their doctor, the most sacred profession, has been killing them for more than century and quite on purpose.
 
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How is your total T? High estrogen may give you good libido but that does not mean it is the optimal way to do it. High T with E2 in the bottom 25% also gives people great libido. This is the phenotype 20yo males have, together with higher progesterone.
High dose Masteron (drostanolone) is notorious for turning people into sexually berserk rhinos yet it crushes E2 (and E1) below detectable levels. In fact, about 20% of the people on whom drostanolone was tested back in the 1960s dropped out of the trials due to excessive libido. They could just not do anything except think about sex 24x7.
So, libido is probably not the best metric of estrogen's healthiness, and there are arguably healthier ways to achieve it. According to the study above even bone health can be perfectly maintained by non-aromatizable steroids like DHT or trenbolone, even when adding an AI.
Estrogen is THE primordial growth hormone. Growth, as in uncontrolled, de-differentiating type. The bad kind, the kind that kills if left unchecked for too long. I don't think estrogen should be crushed, but most people probably produce and carry around way more than what they need for optimal health. Increased peripheral aromatization is one of the earliest biomarkers of aging/disease.
Just my 2c.
Is 11ng/dl too low?
 
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I think a low dose of aromasin 5mg and maybe low dose proviron like 5-10mg. Androsterone be good to instead of proviron and transfermal DHEA & Preg low dose aswell ofc. Like @haidut mentioned so many times lowering the dose of most steroids is a good way to not get the suppresive effects and also minimize/prevent hepatotoxicity. From the mentioned above proviron might be the only weak hepatoxic aas mentioned but I doubt that in the doses Ive mentioned its very small as people use it in 100mg + and barely then get liver problems. But I still believe that combination of low dose aromasin and proviron would sky rocket your own testosterone production since they are completely active in those low doses with minimim suppressive effects and would reduce both estrogen, SHBG and cortisol by a lot. Obviously consuming lots of sugars on these steroids to prime for the extra need and prevent cortisol release.
Do you think low dose androsterone/DHEA/pregnenolone etc. has the potential to cure baseline levels even when not taking them or would you have to stay on them? That’s what I’m wondering
 
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What about studies regarding humans and mice that because of genetics produce no aromatase at all.... don’t such studies pin-point an essential role for estrogen in bone health and libido? I think one can likely get away with no estrogen and higher dht for a temporary treatment, but seeking to do so permanently it would create damage.
 
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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
I’m sort of toying with that theory. Did you check your DHT to go along with the low vs high estrogen?
 
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haidut

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What about studies regarding humans and mice that because of genetics produce no aromatase at all.... don’t such studies pin-point an essential role for estrogen in bone health and libido? I think one can likely get away with no estrogen and higher dht for a temporary treatment, but seeking to do so permanently it would create damage.

Look at my comment 7 steps above this one. Do you see the human study Lokzo posted? So, giving an AI to human males resulted in both muscle mass increase AND fat decrease. It corroborates perfectly the study with trenbolone and AI. What more evidence do you need? Not sure how genetic mutants provide better evidence than the one above.
 

tankasnowgod

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What about studies regarding humans and mice that because of genetics produce no aromatase at all.... don’t such studies pin-point an essential role for estrogen in bone health and libido? I think one can likely get away with no estrogen and higher dht for a temporary treatment, but seeking to do so permanently it would create damage.

I don't believe so. Here's a case study where they look at both a brother and sister that were born with Aromatase deficeincy-

Aromatase deficiency in male and female siblings caused by a novel mutation and the physiological role of estrogens

Here is what they state about the brother-

"He was sexually fully mature and had macroorchidism. The plasma concentrations of testosterone (2015 ng/dL), 5 alpha-dihydrotestosterone (125 ng/dL), and androstenedione (335 ng/dL) were elevated; estradiol and estrone levels were less than 7 pg/mL. Plasma FSH and LH concentrations were more than 3 times the mean value. Plasma PRL was low; serum insulin-like growth factor I and GH-binding protein were normal"

His testosterone is elevated higher than even what men on TRT generally achieve. His plasma FSH and LH are 3 times normal. His state is no doubt due to high androgens, low estrogen, and other hormones that are likely very low, or very high. He may also be suffering from various vitamin and nutrient deficiencies that would not affect a normal person, similar to how Burr's rats displayed nutrient deficiencies due to their elevated metabolism from eating a diet "deficient" in "essential" fatty acids.
 
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Effects of Exemestane and Tamoxifen Treatment on Bone Texture Analysis Assessed by TBS in Comparison With Bone Mineral Density Assessed by DXA in Women With Breast Cancer

https://www.sciencedirect.com/science/article/pii/S1094695013000401


Bone loss with exemestane. All I’m taking away from the more I read here is that crushing e is bad, and you can bypass the negatives of the crush by upping dht, but I see no reason to believe this gives any credence to somehow being superior to keeping e in the body at a comfortable level of not too high and not too low. Exemestane which presumably does not effect progesterone has common bone pain and joint pain side effects, so it looks like this idea that the studies showing damage from various ‘zole’ ai being because of lack of progesterone rather than lack of e is invalid.
 
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I don't believe so. Here's a case study where they look at both a brother and sister that were born with Aromatase deficeincy-

Aromatase deficiency in male and female siblings caused by a novel mutation and the physiological role of estrogens

Here is what they state about the brother-

"He was sexually fully mature and had macroorchidism. The plasma concentrations of testosterone (2015 ng/dL), 5 alpha-dihydrotestosterone (125 ng/dL), and androstenedione (335 ng/dL) were elevated; estradiol and estrone levels were less than 7 pg/mL. Plasma FSH and LH concentrations were more than 3 times the mean value. Plasma PRL was low; serum insulin-like growth factor I and GH-binding protein were normal"

His testosterone is elevated higher than even what men on TRT generally achieve. His plasma FSH and LH are 3 times normal. His state is no doubt due to high androgens, low estrogen, and other hormones that are likely very low, or very high. He may also be suffering from various vitamin and nutrient deficiencies that would not affect a normal person, similar to how Burr's rats displayed nutrient deficiencies due to their elevated metabolism from eating a diet "deficient" in "essential" fatty acids.

You left out the good part about his bones.

“The height of the brother was 204 cm (+3.7 SD) with eunuchoid skeletal proportions, and the weight was 135.1 kg (+2.1 SD). He was sexually fully mature and had macroorchidism. The plasma concentrations of testosterone (2015 ng/dL), 5 alpha-dihydrotestosterone (125 ng/dL), and androstenedione (335 ng/dL) were elevated; estradiol and estrone levels were less than 7 pg/mL. Plasma FSH and LH concentrations were more than 3 times the mean value. Plasma PRL was low; serum insulin-like growth factor I and GH-binding protein were normal. The bone age was 14 yr at a chronological age of 24 3/12 yr. Striking osteopenia was noted at the wrist. Bone mineral densitometric indexes of the lumbar spine (cancellous bone) and distal radius (cortical bone) were consistent with osteoporosis; the distal radius was -4.7 SD below the mean value for age- and sex-matched normal men; indexes of bone turnover were increased. Hyperinsulinemia, increased serum total and low density lipoprotein cholesterol, and triglycerides and decreased high density lipoprotein cholesterol were detected.”
 
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https://www.sciencedirect.com/science/article/pii/S1094695013000401

Bone loss with exemestane. All I’m taking away from the more I read here is that crushing e is bad, and you can bypass the negatives of the crush by upping dht, but I see no reason to believe this gives any credence to somehow being superior to keeping e in the body at a comfortable level of not too high and not too low. Exemestane which presumably does not effect progesterone has common bone pain and joint pain side effects, so it looks like this idea that the studies showing damage from various ‘zole’ ai being because of lack of progesterone rather than lack of e is invalid.

Who said anything about crushing estrogen? I said several times in this thread that dropping it very low is not desirable but the current situation where most people carry more of it than they need for health is definitely not desirable. This thread is more about the (wrong) perception that we should not worry about estrogen and leave it along, and most of that sentiment stems from the continued advertising from Pharma and doctors that "estrogen is good so here is your estrogen patch".
 
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Who said anything about crushing estrogen? I said several times in this thread that dropping it very low is not desirable but the current situation where most people carry more of it than they need for health is definitely not desirable. This thread is more about the (wrong) perception that we should not worry about estrogen and leave it along, and most of that sentiment stems from the continued advertising from Pharma and doctors that "estrogen is good so here is your estrogen patch".

I must have misinterpreted the title of the thread to mean estrogen is of no use to bone health.
 

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