E and Free T are the major contributors to libido NOT DHT

General Discussion
#1

As I have been saying here. And all my experiments show this exactly. E2 screws eveything even if you have high T it will not help if your e2 is too high.

“There was no significant association between the Overall SF
score and DHT”

" Asignificant univariate association was observed between
SF Distress and higher total E2 only, which remained after
multivariable adjustment (model a). Using z-scored hormones (model b), the adjusted odds for being in a “higher
distress” group, compared with the reference group (no
distress), increased approximately 10% for eachSD increase in total E2. "

"Three main findings emerged from the current study. First,
T, and not E2 or DHT, was found to be related to Overall
SF in middle-aged and older European men. Second, there
was a T threshold for the relationship between total T,
Overall SF, and ED. Third, E2 was the only hormone associated with SF Distress. "

“We also found that total E2 was the only sex hormone
associated with SF Distress, even after adjusting for T levels, such that higher E2 levels were related to greater distress. This suggests that the observed effects of E2 are
independent of T.”

“implying that T
treatment is unlikely to provide beneficial effects for SF
Distress. A possible explanation for our findings is that
increasing levels of E2 may be associated with the development of depressed mood related to declining sexual
function in aging men.”

“Nonetheless, our finding is consistent with that of
Basaret al. (13) who showed that low total (and free) T
was associated with sexual symptoms of aging (e.g.impaired potency, ED), whereas E2 was positively correlated with the psychological symptoms (e.g.depressed,
irritable, anxious) of male aging. It is also noteworthy
in the current analyses that the association between E2
and SF Distress persisted after controlling for depression levels”

" If this is
the case, then it is feasible that higher and lower levels of
E2 would be associated with negative effects on sexual
activities and experience."

“In conclusion, using GC-MS, this study showed that T,
and not E2 or DHT, was associated with Overall SF in
middle-aged and older European men. E2 was the only sex
hormone related to SF Distress. Free T, but not total T, was
associated with ED or masturbation frequency in the fully
adjusted models. Moreover, there was a T threshold for
the relationship between total T, sexual function, and ED.
At total T concentrations less than or equal to 8 nmol/liter,
T was associated with worse sexual functioning, whereas
at total T levels over 8 nmol/liter, the relationship came to
a plateau. The magnitude of the observed associations was
modest, and the relationship between T and Overall SF did
not become stronger at higher levels of T”

Abstract
CONTEXT:

Limited data are available exploring the associations between sex hormones, multiple domains of sexual functioning, and sexual function-related distress in nonpatient samples in Europe.
OBJECTIVES:

The aim of the study was to investigate the relationships between serum testosterone (T), estradiol (E2), and dihydrotestosterone (DHT) and sexual function in a multicenter population-based study of aging in men.
DESIGN:

Using stratified random sampling, 2838 men aged 40-79 yr completed the European Male Ageing Study-Sexual Function Questionnaire and provided a blood sample for hormone measurements. T, E2, and DHT were measured using gas chromatography-mass spectrometry.
SETTING:

We conducted a community-based population survey in eight European centers.
MAIN OUTCOME MEASURES:

Self-reported sexual function (overall sexual function, sexual function-related distress, erectile dysfunction, masturbation) was measured.
RESULTS:

Total and free T, but not E2 or DHT, was associated with overall sexual function in middle-aged and older men. E2 was the only hormone associated with sexual function-related distress such that higher levels were related to greater distress. Free T levels were associated with masturbation frequency and erectile dysfunction in the fully adjusted models, such that higher T was associated with less dysfunction and greater frequency. Moreover, there was a T threshold for the relationship between total T, sexual function, and erectile dysfunction. At T concentrations of 8 nmol/liter or less, T was associated with worse sexual functioning, whereas at T levels over 8 nmol/liter, the relationship came to a plateau.
CONCLUSIONS:

These findings suggest that different hormonal mechanisms may regulate sexual functioning (T) vs. the psychological aspects (E2) of male sexual behavior. Moreover, there was a T threshold for overall sexual function such that at levels greater than 8 nmol/liter the relationship between T and sexual function did not become stronger.
Comment in

#2

To be honest, these types of posts are of questionable value. Posting this text does nothing to change anything about anyone’s condition. Not to mention posting excerpts without links to the papers they were pulled from.

Let real scientists, such as those involved in PFS research, do their job and help us find the answers. Playing armchair scientist lost its appeal years ago, especially now that we have scientific institutions involved.

#3

jcem.endojournals.org/content/ea … 6.full.pdf

The text comes from this paper.

This study was done with nearly 3000 people in which they tested all the important sexual hormones. So it is very important.

As for playing arm chair scientist. I think this is extremely important. The fact of the matter is that any institute studying this could do 100 expensive studies to rule out unrelated issues before they stumble upon the root cause. There are 1000;s of us here we need to all put our thinking caps on, research and test as much as we can. In terms of scientists and doctors fixing us. Most if us realize that 99 percent of doctors do not have a clue what is happening. How can we expect that scientists are going to head in the right direction with this important issue.

I have been to senior andrologists and he refused to even test free testosterone or estradiol. They simply looked at my body and said that I am fine. We have to take this into our own hands as we are the ones with the most motivation to fix this.

Mew even you admit that propecia changes the androgen to estrogen balance and I believe you got gyno. I am also feeling pain in nipples now after 5 years. We have to admit a loss of free T and an increase in E has horrible consiquences for a man.

Now in this study it says the higher the E the more sexual distress. Why does high e cause this. Is it because it block the testosterone receptor, reduces free t and down regulates the receptor hence lowering adiol g. My guess is yes.

#4

“Posting this text does nothing to change anything about anyone’s condition” :open_mouth:

#5

I agree with vincentv, we shouldn’t put all our eggs in one basket. There is no reason why we cant support the research and also investigate PFS ourselves.

#6

This forum should be used as a tool to organize and network to accomplish goals. We already have enough bullshit like this: viewtopic.php?f=27&t=4695&

#7

We know everyone here has low body temps. This would explain why we are having all sorts of problems with thyroid / adrenals. In the vast majority of people here it seems that fin throws of the T/E balance and this is one of the results of that. Along with of course loss of libido and loss of all the positive effects of high free testosterone levels.

Using changes in binding globulins to assess oral contraceptive compliance.
Westhoff CL, Petrie KA, Cremers S.
Source

Department of Obstetrics and Gynecology, Columbia University Medical Center, New York, NY 10032, USA. clw3@columbia.edu
Abstract
BACKGROUND:

Validity of oral contraceptive pill (OCP) clinical trial results depends on participant compliance. Ethinyl estradiol (EE2) induces increases in hepatic binding globulin (BG) levels. Measuring these BG increases may provide an effective and convenient approach to distinguish noncompliant from compliant OCP users in research settings. This analysis evaluated the usefulness of measuring increases in corticosteroid-, sex-hormone- and thyroxine-binding globulins (CBG, SHBG and TBG, respectively) as measures of OCP compliance.
METHODS:

We used frozen serum from a trial that compared ovarian suppression between normal-weight and obese women randomized to one of two OCPs containing EE2 and levonorgestrel (LNG). Based on serial LNG measurements during the trial, 17% of participants were noncompliant. We matched noncompliant participants with compliant participants by age, body mass index, ethnicity and OCP formulation. We measured CBG, SHBG and TBG levels and compared change from baseline to 3-month follow-up between the noncompliant and compliant participants. Construction of receiver operator characteristic (ROC) curves allowed comparison of various BG measures.
RESULTS:

Changes in CBG and TBG distinguished OCP noncompliant users from compliant users [area under the ROC curve (AUROC), 0.86 and 0.89, p<.01]. Changes in SHBG were less discriminating (AUROC 0.69)
CONCLUSIONS:

EE2-induced increases in CBG and TBG provide a sensitive integrated marker of compliance with an LNG-containing OCP.

Copyright © 2013 Elsevier Inc. All rights reserved.

#8

thyroid problem cause hairloss, and when i got pfs my real hairloss begen.
i didn’t know why because low t should+ more e, should give less hairloss.
it could explain it.

#9

Taken from
TRANSCORTIN: A CORTICOSTEROID-BINDING PROTEIN OF PLASMA.
III. THE EFFECTS OF VARIOUS STEROIDS * t

www.jci.org/articles/view/104216/pdf/render

Testosterone propionate, 1 7a-methyl- 19-nortestosterone, and 2a–methyl-dihydrotestosterone propionate were incapable of producing any significant
changes in the concentrations of transcortin or
17-OHCS. In addition, testosterone was not able
to prevent the changes in transcortin concentration
indtuced by estrogen therapy while the patient was
receiving large doses of testosterone.

Estrogens increase CBG, THBG and SHBG. This in turn makes you feel shit. In many aspects as we know. I believe CBG and THBG are increased due to the loss of anabolism which is caused by estrogen administration. I would guess the body has numerous mechanism to balance out the catabolic and the anabolic hormones, of course an imbalance on either side would potentially be fatal.

So in the study above we can see that administration of estradiol while on testosterone decreases the free cortisol in the body. Testosterone alone does not do this. To me this explains the other studies that I have posted which show that estrogen is the over riding factor in libido. You can have high testosterone but it will do nothing unless your estrogen is at an appropriate level. This is seen in a number of other studies.

The Relationships between Sex Hormones and Sexual Function in Middle-Aged and Older European Men -
Shows that estrogen is the overriding factor in causing sexual distress.

Measures of Bioavailable Serum Testosterone and
Estradiol and Their Relationships with Muscle Strength,
Bone Density, and Body Composition in Elderly Men -

Tells us that : “Serum SHBG concentrations were inversely related to lean” Men with high amounts of bound testosterone showed all the signs of aging such as decrease in fat free mass. We know that SHBG is one of the hormones that can increase with estradiol administraion.

Clinical Assisted Reproduction: Altered Balance Between the 5α-Reductase and Aromatase Pathways of Androgen Metabolism During Controlled Ovarian Hyperstimulation with Human Menopausal Gonadotropins

“Results: The levels of all steroids increased significantly from baseline during controlled ovarian hyperstimulation. Mean total testosterone levels increased from 0.29 ± 0.05 ng/mL to 0.58 ± 0.07 ng/mL after gonadotropin stimulation. Sex hormone-binding gonadotropin levels increased from 50 ± 16 nM to 73 ± 12 nM after gonadotropin stimulation. Estrone/androstenedione and estradiol/testosterone ratios, reflecting the aromatase pathway, increased whereas 3α-androstanediol glucuronide/androstenedione and 3α-androstanediol glucuronide/testosterone ratios, reflecting 5α-reductase activity, decreased.”

Another study shows us at least in men what HCG which is quite similar to HMG does to our hormonal profile.

“After HCG, spermatic venous E1 and E2 increased
strikingly: El, sixfold; and E2, eightfold. These responses were equal to or greater than changes observed
in any of the androgens, including T. The slight increase in the peripheral concentrations of E1 after HCG
support our conclusion that the major sources of El are
nontesticular. In contrast, the larger rise in peripheral
E2 after HCG (fourfold) also indicates that the testicular secretion of E2 is greater than E1.”

All of this can be seen in anedotal reports all over the internet. That is.

Steroids / Testosterone has little effect if estrogen levels are out. Estrogen will cancel out all of the positive effects of TRT.

My own personal experience corroborates this perfectly. I have been on TRT a few times. The first time I started HCG prior to starting TRT. I was on HCG at least a month before injecting T. When I started injecting T I felt pretty much nothing.

The second time I started injecting testosterone with no HCG at all. I felt great during the first week. Improvement of mood, energy, emotions, muscle. I really did feel great. But my libido has never been fixed by testosterone alone. My estrogen or some other metabolite seems to be too high to begin with so the only way I can get my libido back for limited periods of time is by reducing estrogen. I was able to get my libido back on TRT using ERASE. But VERY hard to stabilize. This cause of this needs to be further investigated.

This would all explain why the vast majority of us have low free T without LH and FSH going above range. Our bodies realize that more T will result in more E or another metabolite and this will make our condition worse. So our LH / FSH does not rise in response to low T.

#10

Around the time I crashed I had a phase of immense vertigo. When I went to the doctor he told me it was probably migraines, however interestingly enough he commented it’s a common symptom for women experiencing hormone fluctuations. He then joked that obviously wasn’t the case for me, being a 21 year old male. Could this have been synonymous with a mega spike in estrogen?

I’m going to experiment with low doses of Aromasin and see if I notice any improvement. I don’t want to obliterate my estrogen, just reduce it and hopefully knock my SHBG down as a consequence.

1 Like
#11

While I think that PFS has absolutely nothing to do with estrogen levels, I think it’s even more idiotic that a select few members here act like a dictators telling everyone over and over what they can and can’t think, do, say, etc…pretty narcissistic. I’ve received numerous emails from people saying the same thing. Factionizing the membership…its why so many people don’t even post or come here anymore.

Give the foundation you money and keep you mouth shut. All hail!

#12

moonman1 : I don’t really get the point of your post?

dannyfc : I have tried almost every anti estrogen. I only tried aromasin when I was recovering from TRT and I noticed that I felt more agression and improved mood. I did not notice any improvement in libido at that stage. I think my testosterone and estrogen were both very low then As I was shut down. I also recently tried ATD and I felt nothing despite T going up and E going down. It is said that ATD acts as an anti androgen. There are studies showing this. I did blood tests on ATD. T went from 5 to 6.4 9 (2.5 - 8) and e went from 39 to about 15 (11 - 40). It did nto feel much. But when I first took arimidex at low doses I thought my PFS days had finished. Libido came back stronger than ever. Felt lightening in my penis. Random woods, morning woods. I have been able to repeat this a few days. I have also repeated this with PES erase and low dose TRT.

Another factor is that I feel much worse when I eat any estrogenic foods. Soy, pumkin seeds, lycopene. They all make me feel like total crap. My PFS becomes much worse.

You should do your own testing and experementing and see what you can come up with.

The other thing that goes hand in hand with all this is that when on a very low dose of T. less than 10mg per day my testosterone got to mid range but my free e2 and e3 as measured by siliva testing went over range. I assume this is why my body is keeping free T low. If free T goes up even to normal range free e will be over range.

#13

vincentv,

I agree with you that estrogen is the major problem in PFS.

the best way to control estrogen is the excretion! not blocking! give a try! i´m almost recovering with this concept.

#14

How are you doing that? TMA and DIM Indol3?

Interestingly I have been on various anti estrogens recently. I tried letrozole and did blood tests. My T went over range and my estrogen was at some would call perfect range. I did not test my free testosterone. Probably still slightly low. But this makes me think there is another factor. Previously I thought the instability in benefits seen by blocking estrogen was due to an increase in free T leading to a further increase in free E which some people have experienced. But now this does not seem to be the case for me. I can lower estrogen but results are not consistent or stable. I have made almost full recoveries by blocking estrogen but this does not last long.

Also recently I have been experementing with phytoestrogens in foods. I can say that these make my pfs symptoms much much worse. Some foods can put me into a terrible state. On my last test I found my progesterone was over range, I just retested yesterday while not on any drugs. But some say progesterone can increase the bodies susceptibility to estrogen effects.

I also no testosterone plays a big part in this because when i quit TRT and my testosterone crashed my PFS got very bad. And when I inject testosterone I get improved mood, energy and appetite for 1 week then I feel worse on TRT depending on the dose. On a low dose of TRT my e2 and e3 go over range.

Please tell me how you are managing your estrogens? I think if I avoid food with any phytoestrogens I will feel not too bad but this is very very hard to do.

#15

vincentv,

May sound simple, but believe me, I’m feeling much better after I started this diet. I had diarrhea and poorly digested food for 5 years after finasteride, now its gone.

The concept is to have periods of fasting and following with this diet below. The most important is the vegetable juice that help eliminate toxins, helps to cleanse the liver.

I believe that every day our liver is bombarded with insulin, hormones and all that it processes, but can not excrete estrogen as before. This explains why many get worse after eating.

8:00AM
Organic juice of beets, carrots, kale, apples, broccoli. everything organic. Fiber is important, I’m doing with fiber. In the first week I made the juice without the fiber, then the fiber incorporated.

12:00PM
red meat, vegetables, potato.

18:00PM
Organic juice of beets, carrots, kale, apples, broccoli. everything organic. Fiber is important, I’m doing with fiber. In the first week I made the juice without the fiber, then the fiber incorporated.

18:00 to 23:00

fruits and vegetables. organic is best. only drink water between meals.

After two weeks I started dosing MACA each morning. For the first 5 years after the procecia, the herbs are working. A few months ago, I tried to use tribulus and the effect did not last three days. I’m much more aggressive day by day. good sign. Definitely the herbs are only working because the vegetable juice.

If you still have drugs in the liver because the half-life, may need more time to improve.

#16

After experimenting with Aromasin for about a month now, starting from low to very high doses, I’ve had no improvements in symptoms.

I don’t think estrogen is a problem. I think the T/E ratio is the crux of the issue, but that is skewed by high SHBG binding up free testosterone. With a SHBG level above 50, you’d need extremely low estrogen to compensate for the level of free testosterone available. And although estrogen is often linked to increases in SHBG, it’s not the only determinant. Insulin, age, and liver health also factor in.

I’ve looked around the internet and there are many cases of men with elevated SHBG with the exact same symptoms. It’s correlated with age, but there’s plenty of young guys as well. So far I’ve not seen one instance of someone being able to restore it back to normal levels (10-20 nmol) long term. TRT can reduce it by about 20-30% over a long-period, but it’s not enough and in the end is counter-intuitive if youre already producing enough test. Steroids such as Danazol, Winny and Proviron will bind to it temporarily, but this will be matched by a similar drop in testosterone. Supplements such as Boron, DiM, Nettle and Divanil all supposedly reduce it, but there’s little support for that and not to the extent required.

So where is the issue is that’s causing the elevation if not estrogen? SHBG is synthesised in the liver, but also the brain and testes. There’s definitely some dysfunction somewhere, or an adverse reaction that signaled abnormal production that never normalised. Cirrhosis leads to high concentrations, but clearly none of thus have that.

I read a post from a doctor that attributed it to inflammation and the GI tract. He claimed his patient’s SHBG fell from 70 to 20 once allergens had been identified. Overall I’m pretty stumped though.

#17

Thank you for your replies.

Regarding SHBG. Yes mine is high and free t is low. I have tried all the anti estrogens and they help to some degree. But it is not a cure all. And the effects usually fade and I start to see side effects. My tests with letrizole show that increased T and decreased E does not necessarily fix anything really. I got better morning wood.

The thing with this is tho. When I inject testosterone suddenly I get a rush and I start feeling more hungry and this will last a week and then i will feel worse after a week. If i could maintain those first week benefits I would be much better than I do now.

There are many unaswered questions. Why is SHBG too high? If SHBG goes to high there should be less estrogen right because there is less free t go convert to e? Or is there some other mechanism at play? Does low free t always mean low E?

If it was as simple as T / E we could just Inject T and take an anti estrogen and we should hit a sweet spot?

For those men with high SHBG maybe it is whatever it is that is causing high SHBG is also causing their problems.

But this is really confusing. To me it seems like it could be that one metabolite that is not usually tested is too high and this is messing us up? But then where is the source of this? Is it a hormone production issue or an excretion issue? Which organ is the root cause of this problem?