Is GnRH suppression hurting us?

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I think about that as well. Who knows what that did or could have done to my system.
I wouldn't sweat it. Not saying there's zero risk, but keep in mind the FDA has approved this class of drugs to be given at much higher doses. And in the case of gonadorelin, it is a bioidentical hormone that's already approved for use in infusion pumps to treat hypogonadism. Taking it should in theory be analogous to TRT: replacing something that's normally there but missing.
 
Makes me wonder if something like enclomiphene would be a better long term to keep all the bodies systems active. I’d like to hear from men that have used this after a while.
I did just ask Dr. Saya to give us a report on enclomiphene after he's accumulated some experience with it; Defy recently started offering this drug.

What troubles me is that the clinical trial results apparently were lackluster, which is why the FDA didn't grant approval yet.


Nice! How is defy able to offer this?

Another option is Natesto. Very short half-life, doesn't shut down the hpta. I was going to get on it, but not available in canada until next year due to some quality issues.
 
I wouldn't sweat it. Not saying there's zero risk, but keep in mind the FDA has approved this class of drugs to be given at much higher doses. And in the case of gonadorelin, it is a bioidentical hormone that's already approved for use in infusion pumps to treat hypogonadism. Taking it should in theory be analogous to TRT: replacing something that's normally there but missing.
are you speaking of triptorelin?
 
As another poster said, you may on to something Cataceous.

My rudimentary understanding is that the body cannot distinguish exogenous/synthetic testosterone from natural testosterone. If that is the case, why didn‘t I suffer from low libido and blunted emotions when I was younger with levels of T that probably exceeded my TRT? Maybe the lack of GnRH is one major contributing factor.
 
As another poster said, you may on to something Cataceous.

My rudimentary understanding is that the body cannot distinguish exogenous/synthetic testosterone from natural testosterone. If that is the case, why didn‘t I suffer from low libido and blunted emotions when I was younger with levels of T that probably exceeded my TRT? Maybe the lack of GnRH is one major contributing factor.
that could be it or maybe it’s the durnial rhythm or that we are boosting levels too high. So many things at play
 
Indeed. A frustrating thought is that we may control enough variables to do well when they are set right, but we lack the knowledge to make the correct adjustments.
It’s one of the biggest hurdles I have with trt. The constant thought of what if I’m hurting myself in the long run. I know studies say xyz but for the most part trt is far from optimal even though guys like to throw that word around. But if you feel great compared to low t it’s worth it.
 
It’s one of the biggest hurdles I have with trt. The constant thought of what if I’m hurting myself in the long run. I know studies say xyz but for the most part trt is far from optimal even though guys like to throw that word around. But if you feel great compared to low t it’s worth it.
An interesting parallel is illustrated by my father, a Type 1 diabetic. If he didn't take insulin he'd be dead. And in spite of being far from optimized a lot of the time—blood sugar-wise—he has done quite well after almost a half-century of treatment. The point is that even non-optimized TRT is probably beneficial overall, particularly if lab work is ok.
 
An interesting parallel is illustrated by my father, a Type 1 diabetic. If he didn't have insulin he'd be dead. And in spite of being far from optimized a lot of the time—blood sugar-wise—he has done quite well after almost a half-century of treatment. The point is that even non-optimized TRT is probably beneficial overall, particularly if lab work is ok.
Yes I think I’ve finally accepted that lol. My last natural reading was 168. I’m 37 I literally never had depression. And at that level the world felt so dark. My body hurt so bad. I’m back on and I think after 11 years of trying to avoid trt I’m committed mentally.

trt hasn’t been easy for me. It lowers my already low normal cortisol and the only way I’ve been able to be on trt is with super low dose ssri. Again not optimal but better then being off
 
Here's a cross-reference for those interested in this thread who haven't seen my related post:
 
Yes I think I’ve finally accepted that lol. My last natural reading was 168. I’m 37 I literally never had depression. And at that level the world felt so dark. My body hurt so bad. I’m back on and I think after 11 years of trying to avoid trt I’m committed mentally.

trt hasn’t been easy for me. It lowers my already low normal cortisol and the only way I’ve been able to be on trt is with super low dose ssri. Again not optimal but better then being off
Hey Charlie. Do you work out? Proper workouts I mean.
 
@Cataceous


I didn't post the full study here because it's behind a paywall. However, it's available through Sci-Hub and I strongly recommend you read it for the detailed numbers and tables.

In post-menopausal Chinese women, follicle stimulating hormone was inversely correlated with fatty liver and all the other markers of metabolic syndrome - most worrisome was an increase in insulin resistance. This is not definitive with regard to men on TRT, but it makes you wonder what's going on with men who have completely suppressed FSH long term.

Anything that can increase HOMA-IR is a major red flag to me.
 
@Cataceous


I didn't post the full study here because it's behind a paywall. However, it's available through Sci-Hub and I strongly recommend you read it for the detailed numbers and tables.

In post-menopausal Chinese women, follicle stimulating hormone was inversely correlated with fatty liver and all the other markers of metabolic syndrome - most worrisome was an increase in insulin resistance. This is not definitive with regard to men on TRT, but it makes you wonder what's going on with men who have completely suppressed FSH long term.

Anything that can increase HOMA-IR is a major red flag to me.
Of course I'd like to think that there are benefits in having normal FSH, particularly now that treatment with GnRH has given me this. The study's authors acknowledge that "we cannot draw a causal relationship between FSH and NAFLD because the nature of this study is cross-sectional." In the detailed discussion they say:

Follicle-stimulating hormone may be associated with NAFLD risk partly through its relationship to abdominal obesity. In a study mainly recruiting Caucasian and African-American women, obesity significantly attenuated the rise of FSH after the final menstrual period. The same trend was observed in our Asian population. Another study also found that weight loss led to increases in FSH among overweight and obese postmenopausal women. Some may think that E2 is involved in this association. In postmenopausal women, E2 secretion shifts from the ovary to a compensatory source in fat. It is reasonable to deduce that FSH decreases because more E2 is secreted in obese women and E2 is positively associated with obesity. However, in postmenopausal women after adjustment for E2, changes in FSH were still associated with changes in weight and NAFLD, which suggests that adiposity-related factors other than E2 may be associated with FSH. Moreover, it is controversial whether E2 is negatively or positively associated with NAFLD in postmenopausal women.
 

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Of course I'd like to think that there are benefits in having normal FSH, particularly now that treatment with GnRH has given me this. The study's authors acknowledge that "we cannot draw a causal relationship between FSH and NAFLD because the nature of this study is cross-sectional." In the detailed discussion they say:

Follicle-stimulating hormone may be associated with NAFLD risk partly through its relationship to abdominal obesity. In a study mainly recruiting Caucasian and African-American women, obesity significantly attenuated the rise of FSH after the final menstrual period. The same trend was observed in our Asian population. Another study also found that weight loss led to increases in FSH among overweight and obese postmenopausal women. Some may think that E2 is involved in this association. In postmenopausal women, E2 secretion shifts from the ovary to a compensatory source in fat. It is reasonable to deduce that FSH decreases because more E2 is secreted in obese women and E2 is positively associated with obesity. However, in postmenopausal women after adjustment for E2, changes in FSH were still associated with changes in weight and NAFLD, which suggests that adiposity-related factors other than E2 may be associated with FSH. Moreover, it is controversial whether E2 is negatively or positively associated with NAFLD in postmenopausal women.
If FSH suppression is potentially having negative health consequences for men on TRT, would the solution not be to just take exogenous FSH?
 
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If FSH suppression is potentially having negative health consequences for men on TRT, would the solution not be to just take exogenous FSH?
That's certainly an option, albeit a fairly expensive one. Might as well go with HMG to get some LH in there too. I seriously considered this option while casting about for ways to get the benefits of hCG without the problems.

I'm not yet convinced about the relevance of this FSH study to men. One source puts normal FSH for postmenopausal women at 25.8-134.8 mIU/mL. This is really high compared to both adult men and premenopausal women.
 
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