SHBG Crawling Up

My SHBG has been crawling up since I experimented for two weeks with clomid in May.
Then it jumped from 32 to 43, I’ve been taking caber also in this period. Then I stopped the clomid, continued with caber and started metformin as well and SHBG has gone up to 48, and two weeks later after the 48 measurement now is 50.

In this time frame I also lost 10kg with disciplined dieting, exercise and metformin.

What could be the reason for this SHBG increase and do you think it will continue?

To be honest I finally plan to start TRT until end of December the latest unless the doc doesn’t come up with another idea, but he is a great TRT proponent(not an endo from sick care)

Increase in SHBG is directly induced by the clomiphene. If you plan to run TRT then it doesn’t particularly matter either way

I know clomiphene increases it but it continued to rise for months after I’ve stopped clomiphene so looks there is something else

Cabergoline is described to increase SHBG, at least in woman for which it is used to treat PCOS.

Bromocriptine appears to have less of an impact on SHBG, but is also a weaker dopamine agonist and less effective in reducing prolactin. But maybe worth a try.

In my case it makes sense that cabergoline has increased SHBG since it is the only drug I used for all this time. But I could not find any information on internet about this.
I’m not switching to bromo because I plan to start TRT in the next month or January at most.

The caber managed to increase my testosterone to 500 but this is nearly not enough for me according to the symptoms and free T now with the latest SHBG is like 8.8 ng/dl

I’m not sure for how long I need to stay on the caber for the prolactin not to jumb back again even on TRT

Ahhh misread, didn’t notice the caber part

Don’t think it’s the caber, though it could be as it has been seen in literature. SHBG naturally fluctuates based on a variety of parameters… I wouldn’t worry about it

If you are able to control prolactin and thereby increase T with bromo without increasing SHBG than this could make a difference in free T.

Here are the links, not sure if you have access for the first one
https://www.fertstert.org/article/S0015-0282(16)58563-X/pdf

https://www.researchgate.net/publication/5580977_Quality_of_life_in_women_with_microprolactinoma_treated_with_dopamine_agonists

Resistance to caber had also been described
https://academic.oup.com/jcem/article/86/11/5256/2849382

Further readings

@johann77 I will take a look but to be honest I dont want to mess with bromo.

I know it has more side effects and It was very difficult for me to stop feeling paranoid with caber, it took me like 3 months. And I’m not resistant to caber because it decreased my prolactin a lot.

I will discuss with the doctor but I have no more mental strength to experiment with drugs. I want to start testosterone and start feeling better.

Wouldn’t worry about it. I’ve seen some of the better docs say to never try to lower shbg. Take more T if needed and be happy your shbg isn’t low.

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Sure fully understand. Hope you are doing better soon!

What just came to my mind.

Closely monitore prolactin on TRT. Nor sure if you actually have a micro or macroadenoma at your pituitary, but case reports exist on TRT induced excarbations of prolactin in this setup.

https://www.endocrine-abstracts.org/ea/0007/ea0007p288

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@johann77 That sucks I’ve heard it.
For many people T decrease prolactin but for some increase it. Doctors seem to not know why.

I had NMR no adenoma but I have empty sella. Which nobody can tell this empty sella how it plays and what does it cause.

I guess you know that already so for whatever its worth.
Also i can only restate the literature as its far away from biochemistry and i have zero experience in this field.

Anyway here is what the literature says

It seems that empty sella is present in about 20% of the population (based on autopsy) and in the majority of the cases doesnt cause any clinical symptoms. Potential implications can be hypopituitarism, hyperprolactinemia and cushing disease (high cortisol).
Empty sella can be primary eg due to intracranial hypertension (can apparently caused by sleep apnea) or secondary eg infection, trauma.

These are also interesting reads/links

Again apologizes if you know already

@johann77 Thanks for the literature. Just read the first study. Turns out 1/5 of empty sella subjects have hyperprolactemia. I was wondering why my prolactin was elevated but only slightly. The other suspect was the very subtle form of hypothiroidism to which you did not agree and my TSH > 1.5 but it is not that much more.

Im not sure if the empty sella presses the channel trough which the dopamine flows, the turkish saddle was called I think. But what I do know is my FSH really suck and ACTH seems low to me - 17-20 where the upper range is 60.

Are you an endocrinologist?

Are you waiting for Dr to prescribe you the TRT ? Why the wait ?

Im not waiting for prescription I will do it without prescription. Im waiting for a remote consultation from overseas to clarify the details like protocol, thyroid supplementation and possibly something for the adrenals.
Also I need to free sperm, but I took some antibiotics so need to wait a little more.
Trust me I want to start yesterday already…

Well just an FYI , stay away from caber unless absolutely necessary and it doesn’t seem like you absolutely need it . Just my two cents , and protocol etc will be how u feel , nobodies going to be able to give u correct protocol . The free sperm thing , ok I get that :+1:t2: Get it done and get to it . You’ve been saying your going to start for 6 months bud . Test is great , stop loading up on other shit drugs !!

No I am no clinician, i am a biochemist.

Everything you describe, the slightly evelated prolactin, the lowish ACTH and FSH is consisted with a diagnosis of hypopituitarism due to a pituitary defect (the empty stella syndrom).

I think what you need is some more diagnostics like a ACTH and GH stimulation test and then proper hormone replacement, maybe not only TRT.
Did you also get a basal GH (growth hormone) measured? In the context of a hypopituitarism the regulatory feedback T3 to TSH is also disturbed in a sense that TSH release is reduced. So you were actually correct in your suspicion that the thyroid hormones could be out of the optimum, but as long as T3 is ok, TSH release might still be sufficient. TSH deficiency in the context of hypopituitarism is described to be the least frequent finding.

Let me see if I can find some time to read up on things. But again I am no clinician and I can only provide food for thought on finding the root cause of your situation and potential treatment options.