Hello I want to hear the opinion of those who have more experience than me on the subject and I was instructed to post on the Over 35 lifter. If you need more information just ask for it. Any response is greatly appreciated.
Main symptom: No Libido
18yo 200lb 20%bf 6ft
Corticosteroids Treatment 18months ago No AAS history
So I went to see my Urologist. He told me Everything is fine. My prolactin is high because of some variation and my test is perfectly normal. The fucker also recommended me to go see a Sexual Psychologist and told me she would solve all of my problems. Seems like I am on my own again.
From What I know there are 4 options: -clomid -anastrozole -cabergoline -low dose of test
Im thinking of starting with the one I consider the most simple and lower risk that is Clomid. I would do it 300mg the first day and 50mg for a week. What are your thoughts?
Ok so maybe I do not understand thyroid labs very well, but wouldn't a lower value of TSH mean better thyroid function (assuming normal pituitary function). Higher values of TSH indicate hypothyroidism (but really a full thyroid panel is needed to make the diagnosis).
Lower TSH levels are a healthy sign, only if T3 and T4 are mid-range. Some have lower TSH because they are getting hyper, or they can have lower TSH because of a pituitary inadequacy. Test free T3, T4 [fT3, fT3].
Do you use iodized salt and eat sea food. Make sure that dietary iodine intake is reasonable.
Lower E and prolactin and see where things go. Note that SERMs should be used short term, not long term. You need to easy out of SERM use gradually and should be on AI, aromatase inhibitor, during and after.
Do not go near T for now, you are looking to make some changes for the better. Short term use of T can easily make things worse!
TSH secretion is suppressed by T4 and T3; the pituitary releases TSH when T3 & T4 are low, and TSH rises in response to low thyroid function. A TSH over 3.5 is seen in physiologic hypothyroidism. There are very few situations in which both TSH and T4/T3 are low.
Oh, but you may say that this lad has a high prolactin, and prolactin inhibits the secretion of TSH. Nope again, at least not in women:
Prolactin Suppresses GnRH but Not TSH Secretion G. Page-Wilsona, b, P.C. Smitha, C.K. Welta
aReproductive Endocrine Unit, Department of Medicine, Massachusetts General Hospital, and bHarvard Medical School, Boston, Mass., USA
Horm Res 2006;65:31-38 (DOI: 10.1159/000090377)
Background/Aims: In animal models, prolactin increases tuberoinfundibular dopamine turnover, which has been demonstrated to suppress both hypothalamic GnRH and pituitary TSH secretion. To test the hypothesis that prolactin suppresses GnRH and TSH secretion in women, as preliminary evidence that a short-feedback dopamine loop also operates in the human, the effect of hyperprolactinemia on GnRH and TSH secretion was examined. Methods: Subjects (n = 6) underwent blood sampling every 10 min in the follicular phase of a control cycle and during a 12-hour recombinant human prolactin (r-hPRL) infusion preceded by 7 days of twice-daily subcutaneous r-hPRL injections. LH and TSH pulse patterns and menstrual cycle parameters were measured. Results: During the 7 days of r-hPRL administration, baseline prolactin increased from 16.0 Â± 3.0 to 101.6 Â± 11.6 Âµg/l, with a further increase to 253.7 Â± 27.7 Âµg/l during the 12-hour infusion. LH pulse frequency decreased (8.7 Â± 1.0 to 6.0 Â± 1.0 pulses/12 h; p < 0.05) with r-hPRL administration, but there were no changes in LH pulse amplitude or mean LH levels. There were also no changes in TSH pulse frequency, mean or peak TSH. The decreased LH pulse frequency did not affect estradiol, inhibin A or B concentrations, or menstrual cycle length. Conclusion: These studies demonstrate that hyperprolactinemia suppresses pulsatile LH secretion but not TSH secretion and suggest that GnRH secretion is sensitive to hyperprolactinemia, but that TSH secretion is not. These data further suggest that the degree of GnRH disruption after 7 days of hyperprolactinemia is insufficient to disrupt menstrual cyclicity.
Probably off-topic for OP. And only loosely related to the above.
We do know that TSH and LH secretion are cross-coupled to some extent, as witnessed with [female] PCOS accompanied with hypothyroidism and high TSH levels. When treatment of the thyroid problem lowers TSH levels, LH levels can drop and many of the PCOS symptoms are reduced, in some cases.
We see that treating hypothyroidism can improve T levels [inferring more LH]; and increasing T with TRT can improve thyroid levels by increasing TSH [implying that TSH and thyroid hormones were low]. But that last example also has TRT pushing LH low, so the LH-TSH cross link would not seem to be possible. TRT may improve vitality and simply improve thyroid function.
These vague effects will always be there and make things less absolute.
as for """Conclusion: These studies demonstrate that hyperprolactinemia suppresses pulsatile LH secretion but not TSH secretion and suggest that GnRH secretion is sensitive to hyperprolactinemia, but that TSH secretion is not. These data further suggest that the degree of GnRH disruption after 7 days of hyperprolactinemia is insufficient to disrupt menstrual cyclicity. """
We know that hyperprolactinemia leads to many problems, including mental, sexual and loss of vitality. 7 days is not long enough to say that such long term changes cannot disrupt thyroid function and other functions. These 'systems' do not function in isolation from each other.