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How do you reckon your thyroid function is perfect? Quite sure nobody's is. I think you'll find that most of the methods preached on this forum at improving thyroid should improve true testosterone. I use the term True as I have had high testosterone before with limited effects that you would suspect to come along with it.Hi, I eat liver regulary, I take t3+t4, my cholesterol was high before i started using thyroid so I think my cholesterol is fine. My testicles are not in pain.
What else could it be? I eat 2300-2700 calories per day. If I eat more I get fat, I'm very sedentary, I tried eating 3200 calories per day for weeks but I didn't "feel" any better
I don't feel bad in any way, however, I feel not as masculine as I should.
Good for you. Just think over time good thyroid function should yield favorable results regarding high testosteroneI think my thyroid works perfect because my hypothyroid symptoms are gone.
Pregnenolone steal syndrome. Google low testosterone high cortisol. Look into the transcription factors for minerals - enzymes, Iodine, zinc, magnesium being huge for enzymatic processes
I drink 1,5 L of milk and some water on top of that.
Water restriction could induce the upregulation of the CYP3A4 enzyme in the liver.
This enzyme seems to be able to convert cholesterols into oxysterols (25-hydroxycholesterol and 4β-hydroxycholesterol).
Moreover, these oxysterols are known to be ligands for the Liver X Receptor (LXR). What is interesting is that the LXR seems to be involved in testosterone synthesis in testis:
Liver X Receptor: A Cardinal Target for Atherosclerosis and Beyond
"Initially, this receptor was identified in tissue obtained from a rat liver, with no known endogenous ligands, and was named LXR. Later, LXR was termed an ‘adopted’ nuclear receptor with the discovery of oxysterols as endogenous ligands for this receptor."Another hypothetical reasoning:
"The cardinal functions of the testis are testosterone production and spermatogenesis. Leydig and Sertoli cells are testicular cells. Leydig cells secrete testosterone, while Sertoli cells provide structural and nutritional support for developing germ cells.
Furthermore, Leydig cells express LXRα, while Sertoli cells LXRβ, whereas germ cells express both LXRs. LXRα regulates basal testosterone synthesis and is involved in the control of germ cell apoptosis. In contrast, LXRβ controls lipid metabolism in Sertoli cells by regulating cholesterol export, as well as germ cell proliferation. Moreover, both LXRs together regulate ligand-induced steroidogenesis, fatty acid metabolism and, surprisingly, the retinoic acid signaling pathway in the testis."
"Moreover, both LXRs together regulate ligand-induced steroidogenesis, fatty acid metabolism and, surprisingly, the retinoic acid signaling pathway in the testis."
- the enzyme CYP11A1, also called CYP450scc, is in charge of converting cholesterol: "P450scc is a mitochondrial enzyme that catalyzes conversion of cholesterol to pregnenolone. This is the first reaction in the process of steroidogenesis in all mammalian tissues that specialize in the production of various steroid hormones. " (wikipedia)
- It seems like the transcription factor NFAT5 could have a link with this enzyme, RNA-Seq analysis of high NaCl-induced gene expression:
- "Categories of NFAT5 Target Genes Upregulated after Adaptation to High NaCl, but Not after as Little as 24 h of High NaCl.
- Steroid hormones. Cyp11a1 protein localizes to the mitochondrial inner membrane and catalyzes the conversion of cholesterol to pregnenolone, the first and rate-limiting step in the synthesis of the steroid hormones."
- NFAT5 is upregulated during water restriction.