Hypothyroidism can cause low T and a shit ton of other problems.
I would also recommend you do a 4 point saliva cortisol test to see how your adrenal glands are doing, since if you have cortisol problems than TRT might actually make it worse.
Your estrogen is a little elevated, if you were on enanthate or cypionate I would tell you to inject smaller doses more frequently to lower estrogen. The elevation in estrogen could easily cause erectile and libido problems in some men.
Im on a daily dosage as it is 10ml of cyp ā¦ . . . the drs plan atm is to increase HCG to spike oestrogen more and then introduce an AI to try and conteract it ā¦
no erectile issues just no libido!
Cheers for replying
That makes no sense
Good luck with that, AIās canāt affect estrogen produced inside the testicles, AIās only affect estrogen through aromatization.
i think if the AI cancels out the aromatised estrogen ā¦ then by increasing the HCG will increase the left over levels of oestrogen so they dont go from being too high to being too low.
I do trust him hes not a shit doc , and i will have bloods taken again in 4 weeks, and we will go from there!
Would be interesting to know if you have a scientific reference to back this statement up.
@johann77
The endocrinologists donāt believe in data, but I think there is enough data. However, in STTM they may overestimate the significance of RT3 a bit
Iām happy mine have dropped it is now in range so I will not tackle it any more
Of course endocrinologists do care about data and evidence. Itās a different question if they are willing to constantly update their knowledge as science progresses.
@kratom_dumper
Let me very briefly explain why rT3 is meaningless for the diagnosis of thyroid disease:
The common understanding seems to be here that rT3 binds to thyroid receptors and block them.
In order for it to do so rT3
- needs to be transported into the cytoplasm from the extracellular space
- it needs to be shifted into the nucleus
- it needs to bind to the thyroid receptors
- and in order for it to block T3 it needs to bind and donāt let loose from the receptor (association versus disassociation)
-MCT8/10 transport T3 and T4 across the cellmembrane into the cytoplasm. There is no evidence that rT3 is also transported via this channels. Integrin type of membranetransporters transport rT3 into the cytoplasm for min genomic effects but with much less affinity/efficiency that T3 T4 is transported by MCTs. ā> what you measure as rT3 in plasma is not reflecting the intracellular concentration
- rT3 is not founded in the cell nucleus. Although rT3 is generated in the cytoplasm from T4, deionidase type 3 converts rT3 to T2.
- in times of excessive stress (starvation, infection, trauma) the intracellular ratio of T3 to rT3 is shifted towards rT3 (healthy ratio is about 8:1) and rT3 could get into the nucleus and block T3 from binding.
-however according to a study by Bolger and Jorgensen, rT3 has about 1% of affinity to the thyroid receptors compared to T3.
-and the the lower association is not compensated by a very low dissociation (resulting in a kind of covalent bond to the receptors which would block it)
In summary, measuring rT3 is pointless as itās only effect is lowering of the active T3. For the diagnosis of hypothyroidism T3 is sufficient.
A higher rT3 to T3 is a marker for stress (injury, infection, starvation) but meaningless for the diagnosis or treatment of thyroid disease.
The table in Bolger and Jorgensen
A schematic drawing of the fate and action of thyroid hormones
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Jan 2020 Bloodwork
Currently feeling at a steady 3/5 which is good but still 0 libido. Nothing wrong with the wood when needed , just very rarely used . . .
Doc changing protocol to little higher test with less HCG. See if we can bring back that libido
