What is the interplay of SHBG with respect to the HPTA and Hypogonadism?

[anyman]

Despite studying for awhile, I am a bit puzzled as to the interplay of the Sex Hormone Binding Globulin (SHBG) on the HPTA and hypogonadism in general.

As I posted earlier, I obviously have low T as well as low FSH and LH. But--I also have what appears to be low SHBG (11 on a scale of 8-46).

I done some research, which appears to indicate that such explains my higher Estradiol (32) despite Low T (185-200 depending on the day). However, the rest of what I've found is all over the place. Can anyone make any sense out of all this?

 

[KSman]

It is [typically] elevated E that causes the liver to produce more SHMG. Your E2 at 32 is not high, not optimal either. SHBG does not drive the HPTA but reacts to it and the effects of aromatase. If one's SHBG is low, then low body fat could be a factor.

Changes in your HPTA and resultant T&E levels will then change the SHBG levels. Consider SHBG levels a result and not a cause.

Lower E will lower SHBG. Lower SHBG will lead to increased FT. An An AI will lower E. A SERM will increase LH and FSH which will increase T if the testes are responsive. However, that also leads to increased E as well and that E will also increase SHBG and offset some of the gains in FT that would otherwise be expected to come with the increase in TT. SERMs can have estrogenic side effects for some as they are estrogen compounds that are selective for some receptors, not for others and can activate some others as well. A few advocate the use of SERMs for some TRT benefits... for those who do not have side effects (only one way to find out). But those approaches cannot take T levels to the high end of normal range that seems to be needed in many cases to achieve results.

When you lower E2, there is less T converting to E, so more FT+TT left. Less SHBG is created which means that less FT becomes TT. So FT increases. And there is less competition from E at T receptors which can block the action of your FT. If you are on TRT, your T intake levels are fixed. If not on TRT, when you lower E, your HPTA will increase T production.

So with TRT and you lower E, you get less loss of T from T-->E conversion, SHBG goes down, FT goes up and the increased FT:E ratio allows the increased FT to get the job done at the T receptors. That is a lot of positive change factors.

If not on TRT and you lower E, you get the above positive factors and an increase in HL, FST and T.

When you lower E, this can help with fat loss and less fat means less aromatase conversion of T-->E.

See a pattern?

 

[hardasnails1973]

It is [typically] elevated E that causes the liver to produce more SHMG. Your E2 at 32 is not high, not optimal either. SHBG does not drive the HPTA but reacts to it and the effects of aromatase. If one's SHBG is low, then low body fat could be a factor.

Changes in your HPTA and resultant T&E levels will then change the SHBG levels. Consider SHBG levels a result and not a cause.

Lower E will lower SHBG. Lower SHBG will lead to increased FT. An An AI will lower E. A SERM will increase LH and FSH which will increase T if the testes are responsive. However, that also leads to increased E as well and that E will also increase SHBG and offset some of the gains in FT that would otherwise be expected to come with the increase in TT. SERMs can have estrogenic side effects for some as they are estrogen compounds that are selective for some receptors, not for others and can activate some others as well. A few advocate the use of SERMs for some TRT benefits... for those who do not have side effects (only one way to find out). But those approaches cannot take T levels to the high end of normal range that seems to be needed in many cases to achieve results. So as this vicious cycle continue it ends up burning out thyroid, adrenals, pancrease because cortisol and dhea lower shbg, as well does inuslin.

When you lower E2, there is less T converting to E, so more FT+TT left. Less SHBG is created which means that less FT becomes TT. So FT increases. And there is less competition from E at T receptors which can block the action of your FT. If you are on TRT, your T intake levels are fixed. If not on TRT, when you lower E, your HPTA will increase T production.

So with TRT and you lower E, you get less loss of T from T-->E conversion, SHBG goes down, FT goes up and the increased FT:E ratio allows the increased FT to get the job done at the T receptors. That is a lot of positive change factors.

If not on TRT and you lower E, you get the above positive factors and an increase in HL, FST and T.

When you lower E, this can help with fat loss and less fat means less aromatase conversion of T-->E.

See a pattern?

Could the body possible produce more shbg if the testosterone/estrogen is altered knowing that it has more estrogen and this may some how signal the liver to act as if there was too much estrogen in the body or if estrogen metabolism is altered through what ever means as estrogen that is being escorted out its being reciruculated back through the liver. How the hell does the liver distguish between e2, e1e3, or metabolitites and it just classifys them all as "estrogen" and causes more shbg to be released. When it comes to the body in terms of detoxfication estrogen is estrogen and there for the body is going to responds by possbly increasing shbg

 

[anyman]

Thanks, KSman- Very informative & interesting. I wonder about body fat as I'm not

overweight as I would characterize the term and am 6' and about 215 +/- with regular exercise. I could lose a good 15lbs from the middle, which the the same weight I gained once this T issue started. I am seeing a direct connection between these T issues and a sudden weight gain which I first ascribed to being over 40, but now am not so sure. I've increased cardio to try & compensate even though I much prefer weights. I do notice stagnation at the gym and possible regression if I am not careful. Damn this whole low T thing.....

Never realized this issue is so widespread and, worse still, on the rise. Such does not bode well for men and our species in general.

 

[hardasnails1973]

overweight as I would characterize the term and am 6' and about 215 +/- with regular exercise. I could lose a good 15lbs from the middle, which the the same weight I gained once this T issue started. I am seeing a direct connection between these T issues and a sudden weight gain which I first ascribed to being over 40, but now am not so sure. I've increased cardio to try & compensate even though I much prefer weights. I do notice stagnation at the gym and possible regression if I am not careful. Damn this whole low T thing.....

Never realized this issue is so widespread and, worse still, on the rise. Such does not bode well for men and our species in general.

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