I would like some perspective on my labs as I try to make some decisions. I recently got some labs back which once again showed some low-T and wonky thyroid. I have had these wonky labs for at least 7 years with little to no treatment (some T4 for a while). My pcp is open to TRT but wants me to get a sleep study first (to rule out sleep apnea). He doesn't see a need to treat thyroid at this point. I have an appointment with a urologist but wondering if that is going to be a waste of time based on what I keep reading. Do these labs suggest primary or secondary hypogonadism? Should I try to get thyroid treated first? Would these numbers suggest trt treatment? I am posting here because I am wanting to educate myself on TRT. I have made several lifestyle changes over the past few years with little difference (lost weight, started lifting, clean diet, eliminate xenoestrogens, consistent 8 hrs of sleep, etc).
You are primary as your LH is high and FSH on the top end.
Prolactin is just over the top end.
Would be wise to have estradiol and SHBG tested.
Unfortunately, you had your FT tested using an inaccurate assay the piss poor direct immunoassay!
Keep in mind that although TT is important to know FT is what truly matters as it is the active unbound fraction of testosterone responsible for the positive effects.
The only way to know where your FT truly sits is to have it tested using the most accurate assays such as the gold standard Equilibrium Dialysis or Ultrafiltration (next best).
Regardless with a TT in the 300s, your FT would be absurdly low.
You definitely would benefit from trt.
The hardest part will be finding a knowledgeable doctor when it comes to up-to-date treatment.
Keep in mind that although having healthy hormones is critical to men's overall health that thyroid/adrenal health will have a significant impact.
4.Why does testosterone deficiency occur?
Testosterone production primarily occurs in the Leydig cells of the testis and is regulated by the hypothalamic-pituitary-gonadal axis (HPG, Figure 1).17 For normal testosterone production, gonadotropin-releasing hormone (GnRH) is released in a pulsatile manner from the hypothalamus. GnRH stimulates the production and release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) from the anterior pituitary. LH stimulates testosterone production by the Leydig cells in the testis. The HPG axis is regulated by a negative feedback loop whereby high levels of testosterone send a feedback signal (via estradiol and testosterone) to both the pituitary and the hypothalamus to inhibit ongoing testosterone production.17 This pathway is essential for testosterone production and any disruptions can cause downstream effects and inhibit the production of testosterone.
Clinical TD results when the body fails to produce adequate levels of testosterone. If there is an intrinsic failure at the level of the testis to produce testosterone, it is termed primary hypogonadism. By contrast, if there is a hormonal/gonadotropin signaling problem within the brain (hypothalamus or pituitary), it is considered secondary hypogonadism.
Primary hypogonadism results in low levels of testosterone but high levels of gonadotropins (LH, FSH). The brain is trying to amplify its signal to the testis to produce testosterone. Secondary hypogonadism is a result of a neural signaling deficiency and clinically manifests with low levels of testosterone and low or normal levels of gonadotropins. A combined pattern of primary and secondary hypogonadism is common. TD or hypogonadism occurs as men age due to several factors including a decrease in Leydig cell size, reduced Leydig cell sensitivity to LH, increases in systemic estrogen levels, and a diminution of GnRH pulsatility.18,19 Multiple medications and medical conditions are also responsible for TD (Table 2).