New Research Suggests The Conversion Of Testosterone To Estrogen In The Brain Is Crucial For Male Se

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TheBeard

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My guess is -
It’s a pathological incoherent sex drive, perceived taboos and depravity to get aroused, even this state of arousal is somewhat flaccid because it’s driven more by stress hormones.
It’s a survival mode sex drive. It’s an energy disorder underlying it all, an extremely attractive grown woman is maximizing her energy levels, it’s becomes a stressor for some men to match her energy levels, her general tissue capacitance has a higher capacity to maintain energy ,basically what stress is -something in the environment requires you to expend energy to overcome/resolve/solve/match and connect with it. The woman in question signals greater fitness and she selects males that can match it for the most part.
Depravity is a form of lowering energy in another which brings the victim to the energetic level of the abuser even if it’s only temporary.

A child as metabolically coherent as they are must still develop the growth to maximize energy capacitance in all tissues and organs therefore they are weaker than most adults, even adults in a low energy state like paedophiles have more general energy capacitance hence their predatory behavior toward kids and not more coherently energetic adults ,obviously some tissues within a paedophile have less capacity for energetic storage like the prefrontal cortex, a child’s prefrontal cortex is still developing, the paedophile construes this similarity as attraction when in reality it’s "dysfunction" and rigidity of the adult brain, pathological, it’s also the predator knowing/sensing the most powerful aspect of the brain in a child is not formed yet and acting in a predatory manner.
It almost like the paedophile is hijacking the preferred process of coherent energy and symmetry in its early stages because once fully grown the paedophiles are rejected and overpowered, it’s predatory without question.

Exactly my thoughts, thanks for writing this.
 

sladerunner69

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Oh yes, this is why heavy doses of AIs (or even light doses for some) kill a man’s libido as Estrogen sensitizes the androgen receptors, which then uptakes dht to act on that desire. And the balance of these hormones, amongst others, is extremely delicate. Good study!

So then how does one increase brain estrogen delicately enough to get the optimal result?
 

JoeKool

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Hey @sladerunner69 hows things going?

I approach this issue differently, as my experience with pfs showed me. I look at it as a receptor question, not the actual hormones.

For example, look at dopamine and subultiamine :

“This nootropic actually reduces the release of dopamine in the prefrontal cortex. When dopamine levels are reduced, the amount of dopamine receptors increases as part of a compensatory system.”

How does Sulbutiamine affect Dopamine Receptors?

Evidence for a modulatory effect of sulbutiamine on glutamatergic and dopaminergic cortical transmissions in the rat brain - ScienceDirect

Role of the Synthetic B1 Vitamin Sulbutiamine on Health

The first link isn’t a study but sums up its benefits, the second link is a study showing the d1 receptors increase.

So my opinion is, you repair and increase the number of said receptors which will improve the effects of hormones on your body.

I'm sure you saw this study in your PFS research but blocking DHT with finasteride increased ARs:

Immunohistochemical Evaluation of Androgen Receptor and Nerve Structure Density in Human Prepuce from Patients with Persistent Sexual Side Effects after Finasteride Use for Androgenetic Alopecia

So is there a way to block estrogen, say twice a week for 8 weeks, then let it return to staved ARs improve your 'receptivity' to it? I'm not sure but you see my thought process & some supplement use in my past may have shown that but I wasn't cognitive of it back then.
 

schultz

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All of those are metrics of desire. I did agree that estrogen is partially involved in sexual desire, as the abstract itself states. Unfortunately, the popular press article talks about estrogen being crucial for sexual "behavior" and behavior to most people means performance - i.e. they are commonly used to mean the same thing in language.
"...Scientists have uncovered an enzyme that appears to play a key role in regulating sexual behavior in males. Their new research, published in the journal Endocrinology, found that selectively disrupting the enzyme aromatase in the brains of male mice led to a sharp decrease in sexual behavior."
Synonyms of behavior | Thesaurus.com

I am not a native English speaker, so maybe I am reading too much into this, but when I read the popular press article this is the overall message I got - i.e. lower your estrogen and your sex life will suffer.
Aside from that problem of semantics, my other other problem with studies like that is that decrease in sexual desire is not based on any standard. What is "optimal" sexual desire? Is it wanting it all the time, once daily, once every other day, only when provoked, etc? So, the popular press article is worded to suggest that estrogen is crucial for male sexual health, when all the study showed is a reduction in sexual interest. That matches the findings of the human studies I referenced but those human studies did not get complaints from the men that their sexual lives were negatively affected. What if low estrogen leads to a state where sexual activity occurs only when stimulated? Is that good or bad? Is the 50% decrease in sexual desire the study found a good or a bad thing? There is no standard based on which one can judge those changes.

Btw, the study I posted is the study the popular press article discusses. It is not an arbitrary study I dug up.
Brain Aromatase and the Regulation of Sexual Activity in Male Mice

Good points. When Ray mentioned it (I think it was a recent podcast, possibly one of the ones you were involved in) he didn't say it was crucial (I'm not saying he thinks it is or isn't), just that there was an effect from estrogen via aromatization in the brain (I am really butchering this, so I encourage people to find the quote for themselves).

And you're right, the article suggests it's critical for libido, when we don't really know that. Maybe it's critical to a degree, or maybe not at all? The animals didn't have a 100% reduction. The article states a 50% reduction and that they just weren't chasing the females around (my goats do this... It's a bit rapey and it is very agitating to the females when they are not in heat to be constantly chased and mounted... Usually I shoot the male with a rock and slingshot. Don't judge me!)

Ray has hinted that kids go through puberty earlier via the influence of estrogen when they are under stress and that it's sort of a survival mechanism. Reproduction needs to occur earlier as the person may not live long, and reproduction is the most important thing. Perhaps someone under stress of some sort has increased brain aromatase which triggers a greater need for immediate copulation?

How much were you taking? I think all AI drugs in higher doses affect the upstream steroids like pregnenolone/progesterone. There are several reports on this forum and also on bodybuilding websites that adding pregnenolone, or pregnenolone/DHEA, or progesterone, or progesterone/DHEA resolves the sexual desire issues despite the very low estrogen levels as a result of the AI drug. Despite the claims of pharma companies, I don't know of any AI drug that is selective only for the aromatase enzyme. They are all "promiscuous", similarly to the drug finasteride that is now known to be a lot more than a "selective" 5-AR inhibitor.

The idea that they are not selective seems to dovetail with the many case reports on PubMed showing bizarre side effects from taking high doses of various AI's. I've seen it discussed in papers but it's not really talked about openly. And one of the times I saw it talked about was because they wanted to use the non-specific nature of one of these drugs as a way to design a new drug.
 

haidut

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Ray has hinted that kids go through puberty earlier via the influence of estrogen when they are under stress and that it's sort of a survival mechanism. Reproduction needs to occur earlier as the person may not live long, and reproduction is the most important thing. Perhaps someone under stress of some sort has increased brain aromatase which triggers a greater need for immediate copulation?

Yep, exactly this. Earlier puberty, more children per couple, earlier menopause, heavy smoking by both sexes are reliable signs of suboptimal health/environment.

As far as the AI being non-selective:
https://www.accessdata.fda.gov/drugsatfda_docs/label/2004/020541s015.pdf
"...Other Endocrine Effects: In multiple daily dosing trials with 5 and 10 mg, thyroid stimulating hormone (TSH) was measured; there was no increase in TSH during the administration of ARIMIDEX. ARIMIDEX does not possess direct progestogenic, androgenic, or estrogenic activity in animals, but does perturb the circulating levels of progesterone, androgens, and estrogens."

Also, vitamin D has been shown to remove the muscle/joint pain in AI users, which strongly suggests the low estrogen is not the cause of these side effects as vitamin D is itself anti-estrogenic.
High-Dose Vitamin D May Ease Joint Pain from Arimidex

Vitamin D also has progesterone receptor (PR) activating properties, which corroborates the idea that the disturbance of AI in some steroid pathway (possibly the progesterone one, but definitely NOT the estrogen one) is behind the side effects. Checkout the writeup and the studies in the Calcirol thread below.
Calcirol - Liquid Vitamin D3
 
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Drareg

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As much as knockout mousse models can be useful in a particular context it’s important to take them with a grain of salt IMO.

The complexity of genetic interactions is extremely difficult to control, once again the establishment language gives the impression of extreme precision like the marketed effects of SSRI’s and the like, this isn’t the case.
A similar issue is present with the "genes" for eye color.

From the gospel of PR for big business-
Knockout mouse - Wikipedia


"While knockout mouse technology represents a valuable research tool, some important limitations exist. About 15 percent of gene knockouts are developmentally lethal, which means that the genetically altered embryos cannot grow into adult mice. This problem is often overcome through the use of conditional mutations. The lack of adult mice limits studies to embryonic development and often makes it more difficult to determine a gene's function in relation to human health. In some instances, the gene may serve a different function in adults than in developing embryos.

Knocking out a gene also may fail to produce an observable change in a mouse or may even produce different characteristics from those observed in humans in which the same gene is inactivated. For example, mutations in the p53 gene are associated with more than half of human cancers and often lead to tumours in a particular set of tissues. However, when the p53 gene is knocked out in mice, the animals develop tumours in a different array of tissues.

There is variability in the whole procedure depending largely on the strain from which the stem cells have been derived. Generally cells derived from strain 129 are used. This specific strain is not suitable for many experiments (e.g., behavioural), so it is very common to backcross the offspring to other strains. Some genomic loci have been proven very difficult to knock out. Reasons might be the presence of repetitive sequences, extensive DNA methylation, or heterochromatin. The confounding presence of neighbouring 129 genes on the knockout segment of genetic material has been dubbed the "flanking-gene effect".[6] Methods and guidelines to deal with this problem have been proposed.[7][8]

Another limitation is that conventional (i.e. non-conditional) knockout mice develop in the absence of the gene being investigated. At times, loss of activity during development may mask the role of the gene in the adult state, especially if the gene is involved in numerous processes spanning development. Conditional/inducible mutation approaches are then required that first allow the mouse to develop and mature normally prior to ablation of the gene of interest.

Another serious limitation is a lack of evolutive adaptations in knockout model that might occur in wild type animals after they naturally mutate. For instance, erythrocyte-specific coexpression of GLUT1 with stomatin constitutes a compensatory mechanism in mammals that are unable to synthesize vitamin C".
 
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b555

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Yep, exactly this. Earlier puberty, more children per couple, earlier menopause, heavy smoking by both sexes are reliable signs of suboptimal health/environment.

As far as the AI being non-selective:
https://www.accessdata.fda.gov/drugsatfda_docs/label/2004/020541s015.pdf
"...Other Endocrine Effects: In multiple daily dosing trials with 5 and 10 mg, thyroid stimulating hormone (TSH) was measured; there was no increase in TSH during the administration of ARIMIDEX. ARIMIDEX does not possess direct progestogenic, androgenic, or estrogenic activity in animals, but does perturb the circulating levels of progesterone, androgens, and estrogens."

Also, vitamin D has been shown to remove the muscle/joint pain in AI users, which strongly suggests the low estrogen is not the cause of these side effects as vitamin D is itself anti-estrogenic.
High-Dose Vitamin D May Ease Joint Pain from Arimidex

Vitamin D also has progesterone receptor (PR) activating properties, which corroborates the idea that the disturbance of AI in some steroid pathway (possibly the progesterone one, but definitely NOT the estrogen one) is behind the side effects. Checkout the writeup and the studies in the Calcirol

or just stop using an ai.
I have zero gyno, all my hair, lean and awesome energy all from stop caring about high e2.
 

Drareg

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@Hans posted this article and it’s interesting with this thread discussion in mind.

Is it a possibility that testosterone saturated cells are not allowing DHT to bind in this mouse model ?

It’s interesting to think about testosterone being converted to estrogen in coherent amounts to allow DHT to bind, estrogen limits testosterone from saturating the cell? Obviously estrogen saturation is not good, there is a dynamic ratio at work, estrogen also limits an increase in metabolic state when the environment isn’t providing the energetic resources, the question is if DHT and testosterone are in a coherent ratio to allow for binding and the environment has all your needs metabolically speaking is estrogen as important? It would be an interesting study, it’s like the PUFA studies on mice, their metabolism speeds up and they became deficient in B vitamins because of the rat chow.


The study only briefly mentions DHT in the conclusion, it’s reasonable to ask why they didn’t measure bound DHT, the quote below calls for it.

"The lack of sexual behavior in castrated control mice following E2 treatment indicates that systemically delivered E2 alone is not sufficient to stimulate male sexual behavior. Control mice treated with either T or a combination of T and E2 showed robust sexual activity."

The truth on DHT: what the research shows » MENELITE
 

Hans

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@Hans posted this article and it’s interesting with this thread discussion in mind.

Is it a possibility that testosterone saturated cells are not allowing DHT to bind in this mouse model ?

It’s interesting to think about testosterone being converted to estrogen in coherent amounts to allow DHT to bind, estrogen limits testosterone from saturating the cell? Obviously estrogen saturation is not good, there is a dynamic ratio at work, estrogen also limits an increase in metabolic state when the environment isn’t providing the energetic resources, the question is if DHT and testosterone are in a coherent ratio to allow for binding and the environment has all your needs metabolically speaking is estrogen as important? It would be an interesting study, it’s like the PUFA studies on mice, their metabolism speeds up and they became deficient in B vitamins because of the rat chow.


The study only briefly mentions DHT in the conclusion, it’s reasonable to ask why they didn’t measure bound DHT, the quote below calls for it.

"The lack of sexual behavior in castrated control mice following E2 treatment indicates that systemically delivered E2 alone is not sufficient to stimulate male sexual behavior. Control mice treated with either T or a combination of T and E2 showed robust sexual activity."

The truth on DHT: what the research shows » MENELITE
That might very well be true. According to this study:
"Estrogens, possibly in conjunction with DHT, facilitate patterns of male sexual behavior including mounting and ejaculatory reflexes. Thus, at the level of the brain, testosterone per se may not be essential for masculine sex behavior, although a combination of DHT plus estrogen seems to be important to optimize adult male sexuality"
 

haidut

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or just stop using an ai.
I have zero gyno, all my hair, lean and awesome energy all from stop caring about high e2.

Nobody has argued that everybody should be using an AI. The discussion here is IF somebody is using an AI what side effects can be expected and if those are actually due to low estrogen or something else. It is nice that you are in this position of no gyno and good hair, but your approach to "stop caring about high e2" is hardly applicable to say menopausal women (high risk of breast cancer), an overweight person, males with gyno, or really any person with with a chronic condition like diabetes, cancer, CVD, Alzheimer, autism, depression, etc where high estrogen is known to be involved.
 
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schultz

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x2

how can we achieve this

I am completely guessing here, but I feel like DHEA taken orally would do this. I know when I took 15mg a day (the DMSO Pansterone) my libido was sky-high to the point of affecting my day to day life in a negative way. Hard to concentrate on work and regular life things when you're thinking about sex non-stop. I also noticed, for the first time in my life, my nipple was slightly itchy or something. I don't remember the feeling exactly but I think it was high estrogen from the DHEA. So I had crazy high libido and an itchy nipple lol. Then the forum sort of realized that the DHEA in DMSO was quite a bit more potent than we originally thought, so 15mg was no longer recommended. A friend of mine had the same experience with this early Pansterone. He takes T now and says his libido was a lot higher with the DHEA.
 

skycop00

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I am completely guessing here, but I feel like DHEA taken orally would do this. I know when I took 15mg a day (the DMSO Pansterone) my libido was sky-high to the point of affecting my day to day life in a negative way. Hard to concentrate on work and regular life things when you're thinking about sex non-stop. I also noticed, for the first time in my life, my nipple was slightly itchy or something. I don't remember the feeling exactly but I think it was high estrogen from the DHEA. So I had crazy high libido and an itchy nipple lol. Then the forum sort of realized that the DHEA in DMSO was quite a bit more potent than we originally thought, so 15mg was no longer recommended. A friend of mine had the same experience with this early Pansterone. He takes T now and says his libido was a lot higher with the DHEA.
Yes same here. I use the pansterone and then simply DHEA stand alone liposomal and its very predictable that my desire and drive increase. I have a stronger desire and faster applied to scrotum. Simply 5mg. I am on T replacement and the addition of DHEA and Pregnenolone supports me in many ways. No hcg required. No atrophy etc.
 

sladerunner69

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Yes same here. I use the pansterone and then simply DHEA stand alone liposomal and its very predictable that my desire and drive increase. I have a stronger desire and faster applied to scrotum. Simply 5mg. I am on T replacement and the addition of DHEA and Pregnenolone supports me in many ways. No hcg required. No atrophy etc.

Is there a liposomal form of dhea? I have never seen it talked about here around the forum.
 
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