cvictorg
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This is what Dr Mariano said
http://www.definitivemind.com/forums/showthread.php?p=6830
MESO-Rx
Anabolic Steroids
Nolvadex for Low SHBG
- Thread starter James23
- Start date
This is what Dr Mariano said
http://www.definitivemind.com/forums/showthread.php?p=6830
Clown what a Psychiatrist says or believes is NOT a study!
Moreover apparently YOU CAN'T READ!
Locate a study where a low SHBG is the sole causation of SD. HIV patients with low TT and LOW SHBG obviously ARE NOT in that category.
Rest assured you won't locate one because their is NO SUCH ASSOCIATION, clown!
Read any of those "Endo texts" you keep referring to, because it's WELL established a HIGH SHBG and a reduced TT are causative factors for SD.
Where and how you contrive or extrapolate this crap is beyond reason.
Clown find a life outside the field of medicine, because your idea's (should anyone take them seriously) will undoubtedly lead to unnecessary "experimental" patient expenditures or worse yet, shit clown you may actually hurt someone with this garbage!
Moreover apparently YOU CAN'T READ!
Locate a study where a low SHBG is the sole causation of SD. HIV patients with low TT and LOW SHBG obviously ARE NOT in that category.
Rest assured you won't locate one because their is NO SUCH ASSOCIATION, clown!
Read any of those "Endo texts" you keep referring to, because it's WELL established a HIGH SHBG and a reduced TT are causative factors for SD.
Where and how you contrive or extrapolate this crap is beyond reason.
Clown find a life outside the field of medicine, because your idea's (should anyone take them seriously) will undoubtedly lead to unnecessary "experimental" patient expenditures or worse yet, shit clown you may actually hurt someone with this garbage!
Open a book, Dr. 1990. It's all there for you to read.
1.) There isn't a study for "low T" relating to SD, either. (Only clinical hypogonadism, something rarely seen even on the boards.)
2.) There isn't a study to show that Arimidex in the cases of high E2 alleviates SD.
3.) There are, however, studies that correlate T, FT and SHBG independently with respect to sexual function. In these studies, SHBG correlates uniquely with orgasm, irrespective of free testosterone levels. Owned.
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LMAO, more misapplied crap!
Lowered SHBG is associated with the following
1) Hyperandrogen states
2) Postinflammatory states with insulin resistance
3) Thyroid dysfunction
4) Abnormal ovarian functioning
Moreover of the FIVE genetic polymorphic SHBG regulatory coding regions which are known to lower SHBG, ALL but ONE has an ELEVATED testosterone level knuckle head!
However the involved SHBG "coding regions" are also involved in a variety of other biological, physiological and or metabolic functions.
Consequently, the congenital lowering of SHBG are often associated with SEPARATE disease processes which include; type II diabetes, PCOS, coronary artery disease, generalized ASCVD, breast cancer, endometrial cancer, infertility and lastly a lowered testosterone because of reduced enzymatic DHEA conversion.
Goodness since there are "several studies" which independently assert SHBG is an independent variable of SD regardless of TT levels POST IT, Clown!
Hint look in the index/reference section at the back of each chapter of the endocrinology text your using and locate the article they are citing and POST IT, clown,
Otherwise, again you don't know the difference between a chicken an egg or how either came about, lol!
Lowered SHBG is associated with the following
1) Hyperandrogen states
2) Postinflammatory states with insulin resistance
3) Thyroid dysfunction
4) Abnormal ovarian functioning
Moreover of the FIVE genetic polymorphic SHBG regulatory coding regions which are known to lower SHBG, ALL but ONE has an ELEVATED testosterone level knuckle head!
However the involved SHBG "coding regions" are also involved in a variety of other biological, physiological and or metabolic functions.
Consequently, the congenital lowering of SHBG are often associated with SEPARATE disease processes which include; type II diabetes, PCOS, coronary artery disease, generalized ASCVD, breast cancer, endometrial cancer, infertility and lastly a lowered testosterone because of reduced enzymatic DHEA conversion.
Goodness since there are "several studies" which independently assert SHBG is an independent variable of SD regardless of TT levels POST IT, Clown!
Hint look in the index/reference section at the back of each chapter of the endocrinology text your using and locate the article they are citing and POST IT, clown,
Otherwise, again you don't know the difference between a chicken an egg or how either came about, lol!
It doesn't matter. There's no study that shows men need estrogen for sex drive, either.
Interpretation.......James is unable to locate a SINGLE study which supports the "low SHBG/sexual dysfunction" garbage he's been preaching throughout this entire thread! What a clown!
I am still not sure what all the hubbub. The thread is entitled "Nolvadex for Low SHBG", and assuming that this means you are asking/probing as to whether not the application of this SERM will RAISE SHBG.?? But this is a good question with regard to my point on SHBG. Could it still be metabolized as a "Trash protein" in these cases!???
If you consider that SHBG most likely CAN NOT BE DELIVERED to cells requiring estrogen WHICH THE PARTICULAR SERM AFFECTS as ANTAGONIST, then of course SHBG will increase in serum as more will be available as an end result, at least temporarily.
An interesting note when examing is this. If you consider that different serms are agonist AND antagonist at different areas, then you have to wonder the REAL action by which serms are working. They are stated to work via Enzyme inhibition. If this were completely and simply true then WHY would different SERMS work DIFFERENTLY??!! Perhaps its a matter of more "customized" enzyme description and action that I am not technically astute to?? They almost appear to be affecting the RNA/or even DNA code at the intended receiving tissue cell - really..!
STILL this is exactly the proof of what I have been saying that what is present in serum HAS NOTHING TO DO with the VOLUME of quantities delivered/used/metabolized in any given time period. So really, any resulting decrease in estrogen metabolism would not be directly reflected in serum, and would be a reduction in activitiy X's-FOLD and DIRECTLY RELATED to which ever estrogen fed tissues the SERM is affecting. If serums CAN indeed by used on a snap shot as POTENTIAL INDICATORS, as I suspect, you could extrapolate. Still balance should be found sooner or later.
I suspect YOU/we are nothing more than the guinnie pigs for big pharma to see just how long it takes SERMS to KILL otherwise healthy individuals. Short of True AIS and any other similar REAL conditions/diseases, 99.6% of the guys being treated are on the hunt for a LAZY ROMAN SHORT SALE. I know I am..:drooling:
If you consider that SHBG most likely CAN NOT BE DELIVERED to cells requiring estrogen WHICH THE PARTICULAR SERM AFFECTS as ANTAGONIST, then of course SHBG will increase in serum as more will be available as an end result, at least temporarily.
An interesting note when examing is this. If you consider that different serms are agonist AND antagonist at different areas, then you have to wonder the REAL action by which serms are working. They are stated to work via Enzyme inhibition. If this were completely and simply true then WHY would different SERMS work DIFFERENTLY??!! Perhaps its a matter of more "customized" enzyme description and action that I am not technically astute to?? They almost appear to be affecting the RNA/or even DNA code at the intended receiving tissue cell - really..!
STILL this is exactly the proof of what I have been saying that what is present in serum HAS NOTHING TO DO with the VOLUME of quantities delivered/used/metabolized in any given time period. So really, any resulting decrease in estrogen metabolism would not be directly reflected in serum, and would be a reduction in activitiy X's-FOLD and DIRECTLY RELATED to which ever estrogen fed tissues the SERM is affecting. If serums CAN indeed by used on a snap shot as POTENTIAL INDICATORS, as I suspect, you could extrapolate. Still balance should be found sooner or later.
I suspect YOU/we are nothing more than the guinnie pigs for big pharma to see just how long it takes SERMS to KILL otherwise healthy individuals. Short of True AIS and any other similar REAL conditions/diseases, 99.6% of the guys being treated are on the hunt for a LAZY ROMAN SHORT SALE. I know I am..:drooling:
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There have been many studies showing a relationship between E2 and Libido. The experimental paradigm is difficult to explore, but following are some abstracts.
[P3-206] Hypogonadism with Estrogen Removal (HER): Effects of Androgens and Estrogens on Sexual Desire in Young Adult Men
BZ Leder, H Lee, EW Yu, S-AM Burnett-Bowie, JC Pallais, ML Webb, KE Wulczyn, AB Servais, JS Finkelstein. Massachusetts General Hospital, Boston, MA; Massachusetts General Hospital, Boston, MA.
Testosterone (T) is thought to be the primary hormonal regulator of libido/sexual desire (SD) in men.
Methods: To determine if SD is also regulated by estrogen (E), we recruited 2 cohorts of healthy men aged 20-50. All men received goserelin acetate (Zoladex?, AstraZeneca LP, 3.6 mg q4wk) to suppress endogenous T and E. Men in Cohort 1 (T/E+, n=198) were randomized to treatment with 1 of 5 doses of a T gel (AndroGel?, Abbott) daily for 16 weeks (G1-placebo; G2-1.25g; G3-2.5g; G4-5g; G5-10g). Men in Cohort 2 (T/E-, n=200) were randomized to the same T doses plus all men received anastrozole (Arimidex?, AstraZeneca LP, 1 mg/d) to block conversion of T to E. SD was assessed using both the International Index of Erectile Function (SD-M1) and a previously-validated question asking subjects to compare their sex drive now with baseline levels (-2=much less, -1=somewhat less, 0=the same, +1=somewhat more, +2=much more) (SD-M2).
Changes were assessed within the T/E- cohort to assess T effects and between cohorts to assess E effects. Specifically, if T has an independent effect on SD, subjects in the T/E- cohort who receive no or little testosterone replacement should experience decreased SD compared to those receiving higher doses (as E levels will be the same). Conversely, if E has an independent effect on SD, differences between the T/E+ and T/E- cohorts should be observed in Groups 2-5 but not G1 (because E levels should be similarly low in subjects in G1 of both cohorts but higher in G2-5 in the T/E+ cohort).
Results: Mean serum T levels in G1-5 were 43, 173, 346, 477, and 882 ng/dL in the T/E+ cohort and 34, 199, 329, 475, and 857 ng/dL in the T/E- cohort (P=NS at each dose between cohorts). SD declined more in men receiving placebo T than in the other T dose groups in both the T/E+ (P<0.005 vs G2, 3, 4 and 5 by SD-M1 and SD-M2) and the T/E- (P<0.02 vs G4 and G5 by SD-M1 and P<0.01 vs G3, 4, and 5 by SD-M2) cohorts. Aromatase inhibition further reduced SD in men receiving T gel (G2-5, P<0.0001 by both SD-M1 and SD-M2) but had no effect on SD in men receiving placebo T gel (G1, P=0.72 by SD-M1 and P=0.53 by SD-M2).
Conclusions: As expected, lowering T levels reduces SD in men. Surprisingly, S[exual]D[esire] is further reduced in men treated with an aromatase inhibitor to reduce E production. These results suggest that non-aromatizable androgens may be less effective than aromatizable androgens for hypogonadal men with low sexual desire.
Wibowo E, Schellhammer P, Wassersug RJ. Role of estrogen in normal male function: clinical implications for patients with prostate cancer on androgen deprivation therapy. J Urol 2011;185(1):17-23. Elsevier
PURPOSE: Patients with prostate cancer on androgen deprivation therapy with luteinizing hormone-releasing hormone agonists experience deleterious side effects, including sexual dysfunction, hot flashes and osteoporosis. Estrogen may relieve or reduce some of these side effects. We explore the role of estrogen in normal male function, emphasizing sexual interest and performance.
MATERIALS AND METHODS: We reviewed the literature on androgen deprivation therapy, estrogen and sexual function in males using PubMed(R) and other sources.
RESULTS: Estrogen receptors are present in tissues involved in sexual behavior including several brain centers and pelvic floor muscles. Exogenous estrogens can restore some sexual interest to greater than castrate level in castrated animals. This has also been reported for certain androgen deprived patients (eg voluntarily castrated men, male-to-female transsexuals) who take exogenous estrogens and others who are on high dose antiandrogens which increase endogenous estradiol levels. Estrogen also helps prevent hot flashes and bone mineral loss, which commonly occur with luteinizing hormone-releasing hormone agonist treatment. However, estrogen may cause gynecomastia and increases the risk of breast cancer. Thus, patients with prostate cancer should be informed about the pros and cons of estrogen therapy before starting androgen deprivation therapy. Based on these data estrogen is likely to have maximal benefits in men if initiated simultaneously with androgen deprivation therapy. Because estrogen autoregulates its own receptors, a constant dose of estrogen will not likely produce a constant serum concentration, suggesting that its effectiveness could be optimized if administered cyclically.
CONCLUSIONS: Prospective studies on the ability of parenteral estrogen to preserve sexual interest at greater than castrate level in patients with prostate cancer are warranted.
Simpson ER, Davis SR. Another role highlighted for estrogens in the male: Sexual behavior. Proceedings of the National Academy of Sciences 2000;97(26):14038-40. Another role highlighted for estrogens in the male: Sexual behavior
Models of lack of estrogen representation, whether they be failure of synthesis or insensitivity of response, have provided new, and in some respects counterintuitive, insights into the roles of estrogens in both males and females. Among the natural mutations, there is currently 1 man identified with a mutation of the estrogen receptor ? (ER?) and up to 10 individuals with mutations of the gene encoding aromatase, the enzyme responsible for estrogen biosynthesis. Of these, 2 are men. In addition, there are various mouse models involving targeted gene disruption. These include knock-outs of the ER? (?ERKO; ref. 1) and ER? (?ERKO; ref. 2) genes as well as the double ER? and ER? (??ERKO; ref. 3) knockout, in addition to the aromatase knockout (ArKO; refs. 4–6) mice. Analysis of the phenotypes resulting from these mutations has revealed various degrees and types of infertility in both male and female, depending on the mutation involved. Lipid and carbohydrate phenotypes involving increased adiposity with insulin resistance, hyperlipidemia and hyperleptinemia as well as disturbances in behavior patterns, both social and sexual, have also been described (6–8). These studies reveal that estrogens have more extensive roles in physiology than was previously thought, and moreover these are frequently of a non-sexually dimorphic nature. Indeed the traditional concepts of the terms estrogen and androgen are now challenged because the role of estradiol in the regulation of spermatogenesis (3, 9) is one that would more properly be classified as androgenic.
Ogawa S, Chester AE, Hewitt SC, et al. Abolition of male sexual behaviors in mice lacking estrogen receptors ? and ? (??ERKO). Proceedings of the National Academy of Sciences 2000;97(26):14737-41. Abolition of male sexual behaviors in mice lacking estrogen receptors ? and ? (??ERKO)
Male mice with a knockout of the estrogen receptor (ER)-? gene, a ligand-activated transcription factor, showed reduced levels of intromissions and no ejaculations whereas simple mounting behavior was not affected. In contrast, all components of sexual behaviors were intact in male mice lacking the novel ER-? gene. Here we measure the extent of phenotype in mice that lack both ER-? and ER-? genes (??ERKO). ??ERKO male mice did not show any components of sexual behaviors, including simple mounting behavior. Nor did they show ultrasonic vocalizations during behavioral tests with receptive female mice. On the other hand, reduced aggressive behaviors of ??ERKO mice mimicked those of single knockout mice of ER-? gene (?ERKO). They showed reduced levels of lunge and bite aggression, but rarely showed offensive attacks. Thus, either one of the ERs is sufficient for the expression of simple mounting in male mice, indicating a redundancy in function. Offensive attacks, on the other hand, depend specifically on the ER-? gene. Different patterns of natural behaviors require different patterns of functions by ER genes.
Carani C, Rochira V, Faustini-Fustini M, Balestrieri A, Granata AR. Role of oestrogen in male sexual behaviour: insights from the natural model of aromatase deficiency. Clin Endocrinol (Oxf) 1999;51(4):517-24. Role of oestrogen in male sexual behaviour: insights from the natural model of aromatase deficiency - Carani - 2001 - Clinical Endocrinology - Wiley Online Library
OBJECTIVE: In order to evaluate the role of oestrogens on human male sexual behaviour, the gender-identity, psychosexual orientation and sexual activity of a man with a congenital lack of oestradiol resulting from an inactivating mutation of the aromatase P450 gene was investigated. The psychosexual and sexual behavioural evaluations were performed before and during testosterone treatment and before oestradiol treatment, during three phases of different dosages of oestradiol treatment.
DESIGN: The study was performed before (phase A) and during (phase B) testosterone enanthate treatment (250 mg i.m. every 10 days, for 6 months), during testosterone withdrawal (phase C), and during each of the following transdermal oestradiol treatments: 50 microg twice a week for 6 months (phase D); 25 microg twice a week for 9 months (phase E), and 12.5 microg twice a week for 9 months (phase F).
MEASUREMENTS: Sexual behaviour was investigated by a sexological interview and by a 2-month self-reported daily diary performed during each phase of the protocol study. Furthermore, during each oestradiol treatment (phase C, D, E and F), a study of depression, anxiety trait and sexual behaviour was performed by the Beck Depression Inventory (BDI), the Spielberger Trait Anxiety Inventory (STAI) and the Golombok-Rust Inventory of Sexual Satisfaction (GRISS), respectively. Sexual orientation and gender-identity were evaluated by the BEM Sex Role Inventory (BSRI). Serum testosterone and oestradiol were measured during each phase of the study.
RESULTS: Before oestradiol treatment (phase C), serum oestradiol was undetectable, while it rose to 356.1, 88.1 and 55.1 pmol/l during phases D, E and F, respectively. Before any oestradiol treatment, during phase D, phase E and phase F serum testosterone was 18.13, 0.72, 14.3 and 18.51 nmol/l, respectively. The patient's gender-identity as assessed by BSRI and by the sexological interview was clearly male. The psychosexual orientation evaluated by BSRI, by the sexological interview and by the analysis of the self-filled diary was heterosexual. Relevant modification of the patient's sexual behaviour occurred only during oestrogen treatment. This was more evident during both phase E and phase F, and concerned the behavioural parameters with an increase of libido, frequency of sexual intercourse, masturbation and erotic fantasies. A reduction of BDI and STAI scores was detected during the oestrogen phases.
CONCLUSIONS: The study of the sexual behaviour in this man with aromatase deficiency suggests that oestrogens in humans do not affect gender-identity and sexual orientation but could have a role in male sexual activity.
There is no takeaway from this poor study except whoever was providing testosterone was not watching labs and doing TRT very poorly, if at all. And, the data is very suspect. T 1392 with 5 MG Transdermal AND T 187 with TC 200 MG BiWeekly - after stopping Oxandrolone.
Patient 1: "testosterone 5 mg once daily transdermally for 34 months"
Patient 2: "testosterone 5 mg once daily transdermally for 39 months"
Patient 3: "Testosterone cypionate was administered intramuscularly, initially 200 mg once monthly progressing to biweekly, for 41 months"
For three years plus, this caretaker did NOT question their dosing!!!
The conclusion is hardly warranted or supported: "First pass metabolism of orally administered oxandrolone may decrease hepatic synthesis of SHBG, allowing exogenously supplied testosterone to be excreted."
Are there any studies on T synthesis/degradation with varying SHBG levels? Also, what is being argued is the "Free Hormone Hypothesis," which continues to be controversial.
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I found the following in a quick file search.
Khosla S. Sex Hormone Binding Globulin: Inhibitor or Facilitator (or Both) of Sex Steroid Action? Journal of Clinical Endocrinology & Metabolism 2006;91(12):4764-6. http://jcem.endojournals.org/content/91/12/4764.full (Sex Hormone Binding Globulin: Inhibitor or Facilitator (or Both) of Sex Steroid Action?)
Khosla S. Sex Hormone Binding Globulin: Inhibitor or Facilitator (or Both) of Sex Steroid Action? Journal of Clinical Endocrinology & Metabolism 2006;91(12):4764-6. http://jcem.endojournals.org/content/91/12/4764.full (Sex Hormone Binding Globulin: Inhibitor or Facilitator (or Both) of Sex Steroid Action?)
(Doc, NOT to discount your incredible and informative post...!)
Well, perhaps this explains why I love it so much when SHE penetrates me and works over my prostate. Further, and as I get fatter, I seem to find myself speading my legs EVEN yelling, "more, harder, faster - FUK ME GUD U BITCH"....
Aromatase indeed.... And more proof the inherent dangers of obesity... :drooling:
Still, it leaves paradox, in that somehow the "Violator Proceedure" always tends to LIMP me right up.. Once there again, you have an acceptable hormone profile, arousal, desire - LIBIDO.....; and all to wind up with ineffective ED. At least for a few moments....
I am really starting to wonder how many times a temptuous woman can violate a mans as, and still have it "snap back into place"!?!?!?! How much is too much..?! WHERE IS THE LINE ??????????????? Do they know? Will THEY find out? Do I even care any more? Did I say that out loud....
BACK ON TRACK... Sorry I digressed as I again sherk my work duties with only the most astute power of procrastination... A POINT I think that this thread has currently taken, is the QUESTION of NORMAL Sex function in men with or without proper E2 actvity. Which the Doc elaborately, humbly, and causiously correct - as usual has offered plenty of proof that estrogens MAY INDEED be required in males for BOTH Libido AND "Function". And possibly even plenty of them, or just that normal function can possibly happen EVEN in the presence of many of them. I believe that terms like "desire, interest, performance, and activity" are used by many of the the citations. You can quickly of course further subset these into probably at least 3 REAL Major subsets.
1. Libido - Are ya horny? I know I know I am...
(the next two murk, and dont - depending, and given)
2. Can ya get it up? Sometimes I can, Sometimes I can't. I can tell you that I am living just as good a sex life as I ever had even with a "Part-time Loafer". Two quick points here little disgussed in real life. And perhaps it pertains to ones relation with their significant other. But I have found that I have just as rewarding a sex life with my wife even loafing (and I am referring to ME frogg'n her). I have found that with the right amount of lubricant, man can even have normal sex with a full on LIMP DIK. In an out even thru her Labia squeezin NUT..! I actually had the best three hours of sex ever I swear At some point in the last year soft the whole time.!!! FURTHER, (and the bonus), it has ONLY been through the action of my "LimPDiKiTus Maximus" that I have been empowered to make her cum through sex alone.!!! This has opened up a whole new chapter in our sex lives and bonding. A truth I have come to find is that MOST of them simply cant come with a fucking telephone pole lodged in them, OR at least it makes it harder for them. I somehow sadly personaly understand this too myself lately
. I used to get mad at her for not being able to cum from ANY form of stimulation when I was in there. Being able to fuck her with a soft dick has moved past this limitation in many ways, and expanded for both of us, now emmpowering even what was not possible in the past with a diamond cutter even..! A beast is now borne between us as now often, and on any given day, I'll see her eyes start to cross after ripping out the first two "hand operated/air cooled" nutz, as she starts to go into some new ballistic orgazmic mode I have rarely witness from the "operator end" - LOL
3. THIRD - is yur shit workin right (testosterone and Sperm production)? Really, the only corrolation I am starting to find in these three classifications which I selfishly and pompously PONTIFICATE, Is that there is little relation when it comes down to just want some pussy smeared all over your body, and from head to toe.. You can START to corrolate #1 and #3, but two appears left out MANY TIMES, in real life description and truth. I am not sure if the reason is most men wont admit ED and has left medical science blind unknowing of the carrot to chase, or that they just dont have to LIBIDO to "rub one off and in any given condition". You will DENOTE - There is no SERUM COUNT for libido... Some credit this to a "mental" Physchologican interaction which MAY supersede hormones. I dont discount the PHYSICAL brain hormones like Dopamine and dont go there now. I have actually come to believe the opposite, and opposite from what I used to; after quitting TRT for a while and finding myself a little more indifferent about my desires. Now also, just 200mgs per week tends to send me HORNIER than Ron Jeremy in a nut getting contest to which he would be awarded 100K for every time he could get one within a 24 hour perion... I can not over look the fact that I am softer and fatter than I have even been in my life... For those of you unfamilar and just stumbling onto a read, this equates to ultra high Estrogen activiy - usually.... It really makes me wonder if RAGE and SEXUAL DESIRE are not indeed inversly related.... And further, perhaps androgen associated RAGE makes for me that can fuk women with a rock pole for hours without themselves orgasming, and estrogen associated SEXUAL DESIRE makes for men which come like dumb monkeys and at the slightest touch... Again, if you look in the middle, you find the BALANCE. Hmmm... Is that just the proof....
** Again, about #2 not really being a truthful FAILURE as relating to #1 or #3. And Again, not discounting HORMONES ='s HORNS. Is this not the proof that actual physical Erectile Dysfunction MUST be only a function of Cardiovascular OR possibly Prostate physical condition (tying in some of my bullshit up top, or should I say in the bottom LOL)
POINTS:
- The relation of ED and prostate functioning is POORLY UNDERSTOOD short of having a prostate CANNIBALIZED by current medical standards. Then we KNOW you never get it up again really, and ORGAZM = Gone... I dare not go there in my mind for even a moment...!!!
- I wonder if Erectile Function COULD possibly be the BEST indicator of prostate cancer there could possibly be? If it were honestly discussed/addressed in society.??!!?? And if you could isolate Cardio away from the diagnosis equation by some QUALIFICATION of Physical testing... But ARE men able to have normal erections at the time of prostate cancer diagnosis I wonder?
- I wonder JUST how directly corrolated estrogen levels in men have to do with their ability to orgasm. Consider, orgasms without erection are not admitted OR discussed in society. IN FACT, I seem to recall reading in general propaganda when I was younger that a man MUST BE ERECT to ORGASM. Sadly, I have found to opposite...
- Just how much does estrogen COUNTER Prolactin?! While even finding that I could potentially orgasm 6-10 times in a day (if I wanted) with a loafer, and once on the hour, this does not resolve the REFRACTORY TIME ISSUE for men.!!! While you say any man can get a nut an hour for a day straight if they really try. REALISTICALLY, healthy erections in men prevent this, as we ALL KNOW that the more times we fuck with a normal wood, the more difficult it becomes to orgasm. This is not the case is the scenario of the estrogen laiden fat man sitting around "rubbing his floppy bean". Women can sit there and rub themselves till they simply cant stand the sensation of orgasm. I have found this in marital inquisition of late. Its not a matter of they came 6 times and ran out. It appears that if you imagine that "hot head" you sometimes get after good sex that you cant stand to have touched - this is the case for the orgasming woman all the time. I recently polled a guy that told me a story about a contest with his wife one night where he made her orgasm 60 times in a row!!! She regretted that he said.. LOL I wonder how much estrogen activity a man must sustain to defeat PROLACTIN and become multi-orgasmic truely.
- Is it polactin the renders a woman in the condition of "I'm just not gonno be able to get one tonight" ( Or perhaps she just cheated on me earlier - LOL). Seriously? And what does this say about a womans pregnancy cycle of hormone activity. The trimester the supposedly get "horny".? Was prolactin off the charts then? How does it relate to estrogen.?
- WHY HAS PORLACTIN NOT BEEN NOW IDENTIFIED AS THE CURSE OF MAN........?! Cant we let estrgoen off the hook for a while? Or is it easier to bash what we want to...? And PRETEND to know.
BBC3's CONCLUSION:
Its funny men try to tweak their hormones and lower the "percieved undesireables", when all along they are important. Some more than we realize. Balance always tend to prove key, as well as moderation - which is similar in action vs. result.
Sorry for the SEMI-Hijack. My little helper is work'n GOOOD today...
LIVE NOW My Friends. And Stay Thirsty....
Well, perhaps this explains why I love it so much when SHE penetrates me and works over my prostate. Further, and as I get fatter, I seem to find myself speading my legs EVEN yelling, "more, harder, faster - FUK ME GUD U BITCH"....
Aromatase indeed.... And more proof the inherent dangers of obesity... :drooling:Still, it leaves paradox, in that somehow the "Violator Proceedure" always tends to LIMP me right up.. Once there again, you have an acceptable hormone profile, arousal, desire - LIBIDO.....; and all to wind up with ineffective ED. At least for a few moments....
I am really starting to wonder how many times a temptuous woman can violate a mans as, and still have it "snap back into place"!?!?!?! How much is too much..?! WHERE IS THE LINE ??????????????? Do they know? Will THEY find out? Do I even care any more? Did I say that out loud....
BACK ON TRACK... Sorry I digressed as I again sherk my work duties with only the most astute power of procrastination... A POINT I think that this thread has currently taken, is the QUESTION of NORMAL Sex function in men with or without proper E2 actvity. Which the Doc elaborately, humbly, and causiously correct - as usual has offered plenty of proof that estrogens MAY INDEED be required in males for BOTH Libido AND "Function". And possibly even plenty of them, or just that normal function can possibly happen EVEN in the presence of many of them. I believe that terms like "desire, interest, performance, and activity" are used by many of the the citations. You can quickly of course further subset these into probably at least 3 REAL Major subsets.
1. Libido - Are ya horny? I know I know I am...
(the next two murk, and dont - depending, and given)
2. Can ya get it up? Sometimes I can, Sometimes I can't. I can tell you that I am living just as good a sex life as I ever had even with a "Part-time Loafer". Two quick points here little disgussed in real life. And perhaps it pertains to ones relation with their significant other. But I have found that I have just as rewarding a sex life with my wife even loafing (and I am referring to ME frogg'n her). I have found that with the right amount of lubricant, man can even have normal sex with a full on LIMP DIK. In an out even thru her Labia squeezin NUT..! I actually had the best three hours of sex ever I swear At some point in the last year soft the whole time.!!! FURTHER, (and the bonus), it has ONLY been through the action of my "LimPDiKiTus Maximus" that I have been empowered to make her cum through sex alone.!!! This has opened up a whole new chapter in our sex lives and bonding. A truth I have come to find is that MOST of them simply cant come with a fucking telephone pole lodged in them, OR at least it makes it harder for them. I somehow sadly personaly understand this too myself lately
. I used to get mad at her for not being able to cum from ANY form of stimulation when I was in there. Being able to fuck her with a soft dick has moved past this limitation in many ways, and expanded for both of us, now emmpowering even what was not possible in the past with a diamond cutter even..! A beast is now borne between us as now often, and on any given day, I'll see her eyes start to cross after ripping out the first two "hand operated/air cooled" nutz, as she starts to go into some new ballistic orgazmic mode I have rarely witness from the "operator end" - LOL3. THIRD - is yur shit workin right (testosterone and Sperm production)? Really, the only corrolation I am starting to find in these three classifications which I selfishly and pompously PONTIFICATE, Is that there is little relation when it comes down to just want some pussy smeared all over your body, and from head to toe.. You can START to corrolate #1 and #3, but two appears left out MANY TIMES, in real life description and truth. I am not sure if the reason is most men wont admit ED and has left medical science blind unknowing of the carrot to chase, or that they just dont have to LIBIDO to "rub one off and in any given condition". You will DENOTE - There is no SERUM COUNT for libido... Some credit this to a "mental" Physchologican interaction which MAY supersede hormones. I dont discount the PHYSICAL brain hormones like Dopamine and dont go there now. I have actually come to believe the opposite, and opposite from what I used to; after quitting TRT for a while and finding myself a little more indifferent about my desires. Now also, just 200mgs per week tends to send me HORNIER than Ron Jeremy in a nut getting contest to which he would be awarded 100K for every time he could get one within a 24 hour perion... I can not over look the fact that I am softer and fatter than I have even been in my life... For those of you unfamilar and just stumbling onto a read, this equates to ultra high Estrogen activiy - usually.... It really makes me wonder if RAGE and SEXUAL DESIRE are not indeed inversly related.... And further, perhaps androgen associated RAGE makes for me that can fuk women with a rock pole for hours without themselves orgasming, and estrogen associated SEXUAL DESIRE makes for men which come like dumb monkeys and at the slightest touch... Again, if you look in the middle, you find the BALANCE. Hmmm... Is that just the proof....
** Again, about #2 not really being a truthful FAILURE as relating to #1 or #3. And Again, not discounting HORMONES ='s HORNS. Is this not the proof that actual physical Erectile Dysfunction MUST be only a function of Cardiovascular OR possibly Prostate physical condition (tying in some of my bullshit up top, or should I say in the bottom LOL)
POINTS:
- The relation of ED and prostate functioning is POORLY UNDERSTOOD short of having a prostate CANNIBALIZED by current medical standards. Then we KNOW you never get it up again really, and ORGAZM = Gone... I dare not go there in my mind for even a moment...!!!
- I wonder if Erectile Function COULD possibly be the BEST indicator of prostate cancer there could possibly be? If it were honestly discussed/addressed in society.??!!?? And if you could isolate Cardio away from the diagnosis equation by some QUALIFICATION of Physical testing... But ARE men able to have normal erections at the time of prostate cancer diagnosis I wonder?
- I wonder JUST how directly corrolated estrogen levels in men have to do with their ability to orgasm. Consider, orgasms without erection are not admitted OR discussed in society. IN FACT, I seem to recall reading in general propaganda when I was younger that a man MUST BE ERECT to ORGASM. Sadly, I have found to opposite...
- Just how much does estrogen COUNTER Prolactin?! While even finding that I could potentially orgasm 6-10 times in a day (if I wanted) with a loafer, and once on the hour, this does not resolve the REFRACTORY TIME ISSUE for men.!!! While you say any man can get a nut an hour for a day straight if they really try. REALISTICALLY, healthy erections in men prevent this, as we ALL KNOW that the more times we fuck with a normal wood, the more difficult it becomes to orgasm. This is not the case is the scenario of the estrogen laiden fat man sitting around "rubbing his floppy bean". Women can sit there and rub themselves till they simply cant stand the sensation of orgasm. I have found this in marital inquisition of late. Its not a matter of they came 6 times and ran out. It appears that if you imagine that "hot head" you sometimes get after good sex that you cant stand to have touched - this is the case for the orgasming woman all the time. I recently polled a guy that told me a story about a contest with his wife one night where he made her orgasm 60 times in a row!!! She regretted that he said.. LOL I wonder how much estrogen activity a man must sustain to defeat PROLACTIN and become multi-orgasmic truely.
- Is it polactin the renders a woman in the condition of "I'm just not gonno be able to get one tonight" ( Or perhaps she just cheated on me earlier - LOL). Seriously? And what does this say about a womans pregnancy cycle of hormone activity. The trimester the supposedly get "horny".? Was prolactin off the charts then? How does it relate to estrogen.?
- WHY HAS PORLACTIN NOT BEEN NOW IDENTIFIED AS THE CURSE OF MAN........?! Cant we let estrgoen off the hook for a while? Or is it easier to bash what we want to...? And PRETEND to know.
BBC3's CONCLUSION:
Its funny men try to tweak their hormones and lower the "percieved undesireables", when all along they are important. Some more than we realize. Balance always tend to prove key, as well as moderation - which is similar in action vs. result.
Sorry for the SEMI-Hijack. My little helper is work'n GOOOD today...
LIVE NOW My Friends. And Stay Thirsty....
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Why do men lose their sex drives when they overdose their AI's? I see guy with test levels over 1000 who have no libido when they decrease their estrogen levels too much.
Doesnt this fly in the face of the idea that testosterone is all things male? If estrogen drives libido......
Doesnt this fly in the face of the idea that testosterone is all things male? If estrogen drives libido......
Well, perhaps that was all Kurt Cobain was trying to say in the lyrics, "everyone is GAY"... LOL I know every homosexual male out there belives this. LOL [)]
I know every homosexual male out there belives this. LOL [)]I'm actually 30 but I started TRT a few years ago.
I had a much better response to transdermal testosterone vs injections and this may be shbg related as individuals with shbg are "fast metabolizers" so it is more beneficial to have smaller daily doses than a large dump of testosterone via injection.
I had a much better response to transdermal testosterone vs injections and this may be shbg related as individuals with shbg are "fast metabolizers" so it is more beneficial to have smaller daily doses than a large dump of testosterone via injection.
Bottom line:
If you have normal TT, and subnormal (1/2 normal) SHBG, you will have twice the FT (4% of TT) of a normal male. Not disputed.
With twice the FT, you will have twice the E2. With twice the FT, you will have twice the rate of excretion. Not disputed.
This, for many men, especially young men, is a problem. The only consistent anomaly in cases of non-response to TRT (mood/libido) is when the body doesn't change expression of SHBG from the low-T to the normal-T state. The main complaint is a low to absent libido that can not be stabilized. Evidenced by countless anecdotes from males in the under 25 age group who fail to respond positively to TRT.
Studies show SHBG to have more responsibility than a simple inhibitor, but rather a both facilitator (SHBG-T entry into cell) and a signaling hormone itself (SHBG-R.) Not disputed.
Studies show SHBG to have indepenat action on glucose metabolism. Not disputed.
Low SHBG is a marker for multiple states of disease. Not disputed.
SHBG lowers when androgen levels are too high, to increase the rate of excretion. Not disputed.
SHBG increases in response to exercise. In healthy males, TT increases proportionality. Not disputed.
It is mind-blowing to hear doctors who would agree that any OTHER component of the endocrine system must be balanced, and point to normal ranges, age-appropriate ranges and "ideal" ranges ....
... and then excuse the primary transport and mediator of free to bound ratio, metabolism and excretion from being important!
SHBG has an average range and an ideal range (in proportion to other hormones) just like cortisol, testosterone, estrogen, prolactin or any other hormone discussed on this board.
We consider any obvious deficiency or excess to be a potential contributor to SD.
If you have normal TT, and subnormal (1/2 normal) SHBG, you will have twice the FT (4% of TT) of a normal male. Not disputed.
With twice the FT, you will have twice the E2. With twice the FT, you will have twice the rate of excretion. Not disputed.
This, for many men, especially young men, is a problem. The only consistent anomaly in cases of non-response to TRT (mood/libido) is when the body doesn't change expression of SHBG from the low-T to the normal-T state. The main complaint is a low to absent libido that can not be stabilized. Evidenced by countless anecdotes from males in the under 25 age group who fail to respond positively to TRT.
Studies show SHBG to have more responsibility than a simple inhibitor, but rather a both facilitator (SHBG-T entry into cell) and a signaling hormone itself (SHBG-R.) Not disputed.
Studies show SHBG to have indepenat action on glucose metabolism. Not disputed.
Low SHBG is a marker for multiple states of disease. Not disputed.
SHBG lowers when androgen levels are too high, to increase the rate of excretion. Not disputed.
SHBG increases in response to exercise. In healthy males, TT increases proportionality. Not disputed.
It is mind-blowing to hear doctors who would agree that any OTHER component of the endocrine system must be balanced, and point to normal ranges, age-appropriate ranges and "ideal" ranges ....
... and then excuse the primary transport and mediator of free to bound ratio, metabolism and excretion from being important!
SHBG has an average range and an ideal range (in proportion to other hormones) just like cortisol, testosterone, estrogen, prolactin or any other hormone discussed on this board.
We consider any obvious deficiency or excess to be a potential contributor to SD.
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cvictorg
New Member
Have you had your CRP measured?
$cally - $ex, $cience, & $tocks: Sex Hormone Binding Globulin (SHBG) Expression
$cally - $ex, $cience, & $tocks: Sex Hormone Binding Globulin (SHBG) Expression
I suspect it has been done, but I can't find anything. I will try to have it re-tested.
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