New study on how estrogen affects male libido and fat accumulation

[Vash1986]

When I read this I was absolutely astonished:
http://www.theglobeandmail.com/life...a-big-role-in-mens-sex-drive/article14293730/
http://www.renalandurologynews.com/...n-men-on-testosterone-therapy/article/335894/

There are at least 5 more articles on the first page of google when you search:
"estrogen male libido"

...referring to this study:
http://www.nejm.org/doi/full/10.1056/NEJMoa1206168#t=articleTop
New England Journal of Medicine (2013;369:1011-1022)

Basically the study is based on 2 groups, one with various dosages of daily Tg gel, one with T gel + anastrozole 1mg/day.

The group on gel+anastrozole had estrogen almost totally suppressed: they had 2pg/ml, whereas the optimal level usually lies between 20-40pg/ml. In fact, the group which received 5g or 10g of Tgel without the AI had optimal E2 levels.

The results were pretty obvious: all guys with optimal T increased leg muscles and strength, and had good erectile function. But those with suppressed estrogen had lower sex drive and more fat accumulation.

Researchers concluded that estrogen plays an important role in fat accumulation, libido and bone density. Which we all know.

The brain-fucked article authors, instead, concluded that HIGH LEVELS OF ESTROGEN boost male libido, and that deficiency is likely to be the cause of lower libido. I think they should be denounced for misinformation. It's a scandal!

 

[Michael Scally MD]

The conclusion on every study to date regarding E2 & Libido has been the same. What is a scandal is the 'bro BS of the opposite.

 

[hardasnails1973]

Sorry,
But I am going to have to agree with Dr Scally on this one. From clinical evidence in pubmed there are no articles or studies as of now that actually support this claim. However, i am not rolling out evidence based approach may tell another story. Low e2 will not cause testosterone to function properly which may be why they lost mr happy in the morning. There is no direct correlation to just E2 levels alone to support its effect on libido.

 

[Vash1986]

From clinical evidence in pubmed there are no articles or studies as of now that actually support this claim.

Hello h.a.n. Which claim, exactly? I didn't make any claims, I just posted a study and was very unhappy with the way article authors interpreted the study. Not sure to which bro BS dr. Scally refers to, also.

 

[hardasnails1973]

Just saying there are no studies at this time clinically to support lowering estrogen increases libido. As we all know there may not have been a study conducted to even look at this subject. When doing research for my colleagues you find out that just because it does not exist in a study does not mean it not plausible.

 

[blazinshotguns]

No wonder I'm fat i take too much adex

 

[Vash1986]

Ah, now I understand, but I think we are speaking about different topics.
You mentioned
lowering estrogens = more libido

My point was that many of the authors of online articles quoting this study wrote something like "estrogens boost male libido" or even worse "high levels of estrogen boost libido". This is completely stupid... of course estrogen deficiency induced by AI or HPTA does crush libido, but this doesn't mean we boys need high levels for a libido boost.

Particularly, the article on www.renalandurologynews.com written by Jody A. Charnow is, in my opinion, a scandal.

 

[hardasnails1973]

Low e2 increases fatty liver. Estrogen is needed to signal production of phosphatdytial choline which is essential for proper functioning on transporting fat from the liver. I can provide clinical studies ..

 

[Vash1986]

No need for clinical studies! I do agree that low E2 is something that nobody would like, unless they had cancer.

 

[1erCru]

There are more than a few animal studies that show this. Basically the male rats without the ability to produce estrogen displayed no sexual interest at all. The reintroduction of estrogen reversed this behavior.

I can also concur that low estrogen is pretty awful. I think for a specific subset of men, " Andropause " involves a drop in both T and E, while for others ( maybe men with more body fat ) the drop primarily occurs in just T. If you maintain adequate E but lose T you will end up thinking E is the enemy. I think these studies are interesting and I'd wage the results will be verified over and over again as more studies are published.

 

[Vash1986]

Well, yes. I have seen many studies where elderly hypogonadal men have been given T + AI or T alone. The group with T alone had much better improvements in body composition and cognition.

But it's quite controverse anyway... there are also many studies demonstrating that aging men with low T get a boost with an AI.

In my case, I have varicocele and low-normal T (always < 400 ng/dL, sometimes < 300). I always noticed that adding HCG to my therapy or doing HCG monotherapy was a complete disaster. I become emotional, anxious, hungry, and also have a mild ED. It must be said that I never had those symptoms on T alone, even when I tested at 1100 ng/dL. I just get them with HCG, or tamoxifen. So I guess that for me Estrogen could be the enemy, although I'm not sure: labs have never shown higher E2 levels during HCG therapy.

 

[Sinister HellFire]

Sorry,
But I am going to have to agree with Dr Scally on this one. From clinical evidence in pubmed there are no articles or studies as of now that actually support this claim. However, i am not rolling out evidence based approach may tell another story. Low e2 will not cause testosterone to function properly which may be why they lost mr happy in the morning. There is no direct correlation to just E2 levels alone to support its effect on libido.

High E2 will inhibit the Hypothalamus and cause androgen depletion - so even if by rare chance one's libido isn't affected, their erectile function will be.
Having high E2 throws off the whole GABA/Glutamate balance...leading one to anxiety and depression. Whereas low E2 is the opposite and typically leads to not enough Glutamate or NMDA activity, and oxytocin/dopamine gets fucked up which leaves you numb and without any passion or sex drive.
So BULLSHIT when I hear high E2 or low e2 don't matter. They certainly do.
However one only needs very small amounts of estrogen to keep the proper groundwork / circuitry going.

 

[hardasnails1973]

I know hormone and neurotransmitters signaling very well. The original comment I did not disagree with. The fact is there is little studies to support it with in pub med. When dealing with well respected medical professionals you better have your shit together along with studies to back it up from well known journals . Im not talking bro science either. Sinister you try to present that to a team of doctors working on a case with out studies from journal's to back up your claim. They will eat you a live..again I am not arguing with you. Provide the evidence ..

 

[Vash1986]

I think that estrogen is still a little bit of a mistery. I know a guy who clearly has some kind of estrogen dominance: he has small shoulders, large hips, almost no body hair, chest fat at age 19. He also has bad anxiety. Nevertheless, he has boners all the day when he watches at girls. A friend of mine was also her girlfriend and she told me she saw him masturbate multiple times in a row and that he has a crazy libido.

And there are also several studies on aging men who benefit from estrogen in terms of cognition and bone density. Basically the studies had 2 control groups: one on T alone, one on T + AI.

And there is a friend of mine who always had a crazy libido. Once I asked him if he could do hormonal tests in the same lab I did them, to discover his secret, ahah! Well, it turned out to be:
Total T: 602 ng/dL (240-900)
DHT: 930 pg/mL (400-1200)
E2: 40 pg/mL (10-50)
SHBG: 27 nmol/L (15-60)

I was shocked because that was the time when I thought (thanks to bro-science) that optimal E2 was below 30 pg/mL. He is rock hard, powerlifter, never had body fat in his entire life, 6 pack from age 12 to 28. Jerks off 2 times a day and then bangs girlfriend.

On the other side there's me, and many other people that have written on this and other boards, that seem to be extremely sensitive to E2. I can tell you that adding arimidex to my HCG+T protocol changed my life. And you know what? My E2 was perfect, it was only 34 pg/mL, but still, it appears that it was too much for me.

By the way, my natural E2 levels, which I tested a few times, are normally between 15 and 25 pg/mL. Maybe that's why 34 was too much for me. I also have chest fat, even though I am not overweight.

Overall, the explanation I give to myself about this is that everybody has a different set point for optimal E2, and that it strongly correlates to DHT levels for balance. And that the studies on E2 function in men are bullshit because they use huge amounts of AI that totally crush estrogen levels.

 

[hardasnails1973]

Bio-individuality is what I have been stressing for close to a decade. What may work for one person may not work for others. Then you have people who are zebras in a horses world who are totally paradoxical to traditional science. I am one of those zebras. These are the cases who medical doctors refer out to me for further evaluations. Why I have to have my shit together, i dotted and T crossed when dealing with these cases. They do not care about Bro science they want to see the hard concrete evidence from research and clinical studies which are currently available.

 

[Sinister HellFire]

Bio-individuality is what I have been stressing for close to a decade. What may work for one person may not work for others. Then you have people who are zebras in a horses world who are totally paradoxical to traditional science. I am one of those zebras. These are the cases who medical doctors refer out to me for further evaluations. Why I have to have my shit together, i dotted and T crossed when dealing with these cases. They do not care about Bro science they want to see the hard concrete evidence from research and clinical studies which are currently available.

As well as I, there are so many factors and complexities in individuality. Going far beyond just hormones and going right down to what most would call "insignificant" enzymes. I mean there was even studies showing that pacific's have different ratios of hormones and the blacks generally have higher estrogen levels and DHT.

But perhaps it's the extra melanin/A-MSH that contributes seeing as these hormones stimulate the HPTA and lead to this "output". After all, the latest aphrodisiacs Or fairly new are melanocortin analogues~.

There has to be a criss-cross somewhere or in between.

Good to know you remember Me HAN.
http://www.ncbi.nlm.nih.gov/pubmed/15601582
http://www.nature.com/npp/journal/v25/n2/full/1395676a.html

The Role of Androgen Metabolism on Seizure Susceptibility
Variable effects of androgens may be due to actions of its metabolites. T is aromatized to estradiol (E2), which can have neuroexcitatory, proconvulsant or antiseizure effects (Frye & Rhodes, 2009a). T is metabolized by the 5α-reductase enzyme to dihydrotestosterone (DHT), which can decrease excitatory glutamatergic activity and be converted by 3α-hydroxysteroid dehydrogenase to 5α-androstane-3α,17α-diol (3α-diol), which has antiseizure effects. Notably, some antiepileptic drugs (AEDs) may alter the metabolism of T to E2, and/or DHT or 3α-diol (Herzog et al., 2004). Androgens’ modulation of seizures may occur as a result of the ratio of 5α-reduced to aromatized metabolites (Harden & Frye, 2007). Therefore, our work has focused on antiseizure effects of 3α-diol in female and male rodents.

http://www.ncbi.nlm.nih.gov/pubmed/16452668

The androgen 5alpha-dihydrotestosterone and its metabolite 5alpha-androstan-3beta, 17beta-diol inhibit the hypothalamo-pituitary-adrenal response to stress by acting through estrogen receptor beta-expressing neurons in the hypothalamus.
Lund TD1, Hinds LR, Handa RJ.
Author information

Abstract
Estrogen receptor beta (ERbeta) and androgen receptor (AR) are found in high levels within populations of neurons in the hypothalamus. To determine whether AR or ERbeta plays a role in regulating hypothalamo-pituitary-adrenal (HPA) axis function by direct action on these neurons, we examined the effects of central implants of 17beta-estradiol (E2), 5alpha-dihydrotestosterone (DHT), the DHT metabolite 5alpha-androstan-3beta, 17beta-diol (3beta-diol), and several ER subtype-selective agonists on the corticosterone and adrenocorticotropin (ACTH) response to immobilization stress. In addition, activation of neurons in the paraventricular nucleus (PVN) was monitored by examining c-fos mRNA expression. Pellets containing these compounds were stereotaxically implanted near the PVN of gonadectomized male rats. Seven days later, animals were killed directly from their home cage (nonstressed) or were restrained for 30 min (stressed) before they were killed. Compared with controls, E2 and the ERalpha-selective agonists moxestrol and propyl-pyrazole-triol significantly increased the stress induced release of corticosterone and ACTH. In contrast, central administration of DHT, 3beta-diol, and the ERbeta-selective compound diarylpropionitrile significantly decreased the corticosterone and ACTH response to immobilization. Cotreatment with the ER antagonist tamoxifen completely blocked the effects of 3beta-diol and partially blocked the effect of DHT, whereas the AR antagonist flutamide had no effect. Moreover, DHT, 3beta-diol, and diarylpropionitrile treatment significantly decreased restraint-induced c-fos mRNA expression in the PVN. Together, these studies indicate that the inhibitory effects of DHT on HPA axis activity may be in part mediated via its conversion to 3beta-diol and subsequent binding to ERbeta.

 

[Sinister HellFire]

I think that estrogen is still a little bit of a mistery. I know a guy who clearly has some kind of estrogen dominance: he has small shoulders, large hips, almost no body hair, chest fat at age 19. He also has bad anxiety. Nevertheless, he has boners all the day when he watches at girls. A friend of mine was also her girlfriend and she told me she saw him masturbate multiple times in a row and that he has a crazy libido.

And there are also several studies on aging men who benefit from estrogen in terms of cognition and bone density. Basically the studies had 2 control groups: one on T alone, one on T + AI.

And there is a friend of mine who always had a crazy libido. Once I asked him if he could do hormonal tests in the same lab I did them, to discover his secret, ahah! Well, it turned out to be:
Total T: 602 ng/dL (240-900)
DHT: 930 pg/mL (400-1200)
E2: 40 pg/mL (10-50)
SHBG: 27 nmol/L (15-60)

I was shocked because that was the time when I thought (thanks to bro-science) that optimal E2 was below 30 pg/mL. He is rock hard, powerlifter, never had body fat in his entire life, 6 pack from age 12 to 28. Jerks off 2 times a day and then bangs girlfriend.

On the other side there's me, and many other people that have written on this and other boards, that seem to be extremely sensitive to E2. I can tell you that adding arimidex to my HCG+T protocol changed my life. And you know what? My E2 was perfect, it was only 34 pg/mL, but still, it appears that it was too much for me.

By the way, my natural E2 levels, which I tested a few times, are normally between 15 and 25 pg/mL. Maybe that's why 34 was too much for me. I also have chest fat, even though I am not overweight.

Overall, the explanation I give to myself about this is that everybody has a different set point for optimal E2, and that it strongly correlates to DHT levels for balance. And that the studies on E2 function in men are bullshit because they use huge amounts of AI that totally crush estrogen levels.

And you know, then there's the skinny kids who clearly don't have any sign of high testosterone and act almost like girls who have ridiculous libidos - what sets that difference - it obviously isn't the masculnizing metabolites, because then E2 would be insignificant. Everyone who uses DHT-drugs and Aromatase Inhibitors combined (who also crush their E2 levels) have all the confidence in the world but no libido. lol

So it's VERY obvious that a small amount of estrogen necessary and is the driving force for libido...but the trick is this.
Testosterone crosses the blood brain barrier, estrogen (bioIdentical or otherwise) does NOT. Testosterone is needed Because it can cross the BBB THEN convert into estrogen.

Although some would argue about this - most evidence supports this notion.
I guess the question is maybe there are other things involved that interact in between.

Some of the science on Glutamate and Histamine being facillitators of sexual function seems to be sound on one end. But then again too much Glutamate I would presume would drive your stress response through the roof and cause cell death.

 

[Sinister HellFire]

And yet I've also heard of people with almost ZERO estrogen that have what they call normal or high libidos. How does this correlate...there must be something else to this - genetics or otherwise. Perhaps there is a certain amount of androgen or androgen receptor gene that is required to over ride the negative sides of low E2 and / or perhaps in these situations these people have a different definition of libido or just merely think it's normal.

Normal to one person is normal for them and not to another .....

But I could quibble about all kinds of other neurotransmitters or otherwise - but are these significant in comparison to the Psychology and Culture of the issue, person or persona???

 

[hardasnails1973]

I have use modulation of glutamate in a recent neurological case which revolved around excessive excitation resulting increased auditory hallucination of a young female. The sad part is that modern psychiatry does not look at glutamate, but rather since the child had what appeared to have schizo effective disorder they tampered up her anti psychotic drugs which had no effect. The shrink wanted to raise them, but parents said "hell not" The poor girl was a totally anhedonic since they trashed her dopamine levels by respiradol among a psychotic cocktail. By modulating the glutamate levels and examining the genetic profile showing highly expressive COMT GAD and few other snps it was obvious where the problem was. Removing gluten was huge in this case due to the GAD as gluten can increase GAD expression creating greater excitation. By using other modulating methods of modulating glutamate the auditory hallucinations decreased over a few week period.

Food for thought...
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3439647/

If you have excessive excitation then you are not going to be able to perform sexually.

Psychiatry in a nut shell.

You need to work on the breaking system of the brain or try to get your foot off the throttle before you burn out the motor.

Too many people are putting their foot in the throttle before making sure the brakes are working properly.

Also do not forget about acetyl choline plays a huge part in issues with libido
http://www.ncbi.nlm.nih.gov/pubmed/24561063

 

[Vash1986]

That's interesting stuff. But apart from removing gluten, I guess it's not easy to modulate glutamate.