I think I get it. What was argued in other threads was that T3 would eventually drop down as well since T4 "runs out"? Doesn't seem to be the case (yet).
I received more results today and would really appreciate your input. I have experienced a scary increase in Cystatin C and therefore a drop in eGFR in just 45 which seem to match the increase in HGH dosage. From googling around a bit I was able to find some info on hypothyroidism, high TSH and T4 treatment all affecting cystatin c and creatinine making them possibly unreliable markers in people with thyroid disorders or people who possibly use HGH.
eGFR went from 88 to 64 in 45 days.... Am I running into trouble here? I believe I see a downwards trend as increased the HGH dosage. Beginning of July is when I ramped up the GH dosage to 12 IUs per day. Before that I didn't go over 3-4IUs. Will getting on T4 decrease my cystatin C or do I have to back off everything and go back to the drawing board?
Date | 10 months ago | 45 days ago | Today |
Cystatin C (ref range <1.2 mg/l) | 0.93 mg/l | 0.98 mg/l | 1.25 mg/l |
eGFR (CysC, CKD-EPI) (>90 ml) | 95.46 ml | | 64.23 ml/min/1,73m2 |
Creatinine (64-111 μmol/l) | 89 μmol/l | | |
eGFR (Crea, CKD-EPI) | 98.28 ml | | |
| | | |
I'd need to know a lot more about your base-line bloodwork values, other drugs, training, and rule out any medical condition. I'll be honest bro, it'd be more work than I can give you my time and effort for here to give you proper advice. And I'm not pitching you on shit, while it's the sort of thing I do deal with with clients, I don't think I want take any ProM guys at this time.
Is TSH supposed to increase when someone takes a high dose of HGH or was his TSH likely already that high?
So the high TSH is a reason to
not administer Synthroid/Levothyroxine, because the "pull" from GH in cells & tissues to convert f/T4 to active f/T3 is also already getting this "push" on the thyroid from high TSH (in response to reduced blood T4, that does not reflect the increased cell/tissue peripheral activity) to secrete more T4 (reflecting, as mentioned, enhanced thyroid function).
It should also be noted that if exogenous androgen is being used, there are also AAS effects on thyroid function that result in
even more peripheral T3 activity. Basically, and this reflects their anabolic potency, thyroxine-binding globulin (TBG) is suppressed by AAS, resulting in decreased total T4 serum levels and increased resin uptake of
T3
& T4.
As you can imagine, all of this increased T3 activity by combined AAS & rhGH is more than sufficient for some additional lipolysis.
Rather than trying to play whack-a-mole with bloodwork values, take the simple tack and just treat symptoms if they even exist.
The symptoms of hypothyroidism to watch for would be:
- dry and scaly skin
- sensitivity to cold
- brittle hair and nails
- slow movements and thoughts
- depression
- Only if not using Clen, muscle cramps may be considered as an additional symptom
There are other symptoms of hypothyroidism; however, they are easily confused with primary effects of rhGH and/or AAS use.