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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone Side Effect Management
TRT Effect on 5 Alpha Reductase and Upstream Hormones- Cause of Low Mood and Anxiety?
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<blockquote data-quote="madman" data-source="post: 203879" data-attributes="member: 13851"><p><strong><em>Δ4 pathway</em></strong></p><p><strong>Progesterone, 17-OH-progesterone (17 OHP) </strong></p><p></p><p><em>One major finding of this study is that hCG/rFSH replacement stimulates and thus normalizes some important steroid hormones belonging to the Δ4 pathway of steroidogenesis in hypogonadotropic hypogonadal males.</em> <em><u>17-OHP levels were significantly decreased on treatment with testosterone, but not while the males were on gonadotropin replacement, indicating that a major proportion of this precursor steroid is produced in the gonads and requires gonadotropin stimulation for secretion</u>, while a minor part of it stems from other sources. It is likely that ACTH- stimulated production in the adrenal gland contributes to it.</em></p><p><em></em></p><p><em>17-OHP is recognized to have <u>anti-mineralocorticoid 15 and glucocorticoid potency 16,17, without direct androgenic properties</u>.</em> Since cross-reactivity among steroids is a recognized phenomenon, due to the high degree of homology at the DNA-binding domains of nuclear receptors within the steroid hormone receptor superfamily 18, the measured differences in serum 17-OHP concentrations may have clinical implications. <em><u>Surprisingly, progesterone serum levels in CHH males were decreased on both hCG+rFSH and testosterone substitution, when compared to controls, but the decrease was more pronounced on testosterone replacement</u>. <strong>This indicates that the gonadotropins used for replacement do enhance progesterone serum production in males, albeit to a lower extent than in healthy subjects.</strong> <u>The use of hCG instead of LH for CHH replacement may explain this phenomenon</u>. <u>Progesterone acts via intracellular progesterone receptors (PRs) A and B, thereby exerting classical genomic action. In addition, it has non-genomic effects</u>. <strong>In males, progesterone is involved in sperm capacitation/acrosome reaction, it influences LH receptor expression and subsequent testosterone biosynthesis in Leydig cells; it interacts with the GABAA receptor complex in the CNS, thereby eliciting effects on sleep, mood, and cognition, and also exert effects in adipose tissue and kidneys 19.</strong></em><strong><em> Progesterone is a high-affinity antagonist of the mineralocorticoid receptor (NR3C2; MR)15, thus eliciting anti-mineralocorticoid effects 20-23. Progesterone is able to transactivate the glucocorticoid receptor (NR3C1; GR) 16. A lack of progesterone and 17-OHP in men could therefore have an impact on water and electrolyte balance and systemic blood pressure regulation.</em></strong></p><p><strong></strong></p><p><strong></strong></p><p><strong></strong></p><p><strong></strong></p><p><strong></strong></p><p><strong>Figure 1 </strong></p><p><strong></strong></p><p><strong>Pathways of human androgen biosynthesis</strong></p><p></p><p><em>-The classic pathways, proceeding parallel for Δ5 and Δ4, convert steroidogenic precursors and lead to the formation of T, which can be further converted to DHT.</em></p><p><em></em></p><p><em>-The alternative pathway of T formation proceeds via androstenediol.</em></p><p><em></em></p><p><em>-The backdoor pathway proceeds via androstanediol to generate DHT.</em></p><p><em></em></p><p><em>-The 11-oxygenated C19 androgen pathway generates 11K T and 11 K DHT. The steroids measured in the present study are indicated in bold.</em></p><p><em></em></p><p><em>[ATTACH=full]15296[/ATTACH]</em></p></blockquote><p></p>
[QUOTE="madman, post: 203879, member: 13851"] [B][I]Δ4 pathway[/I] Progesterone, 17-OH-progesterone (17 OHP) [/B] [I]One major finding of this study is that hCG/rFSH replacement stimulates and thus normalizes some important steroid hormones belonging to the Δ4 pathway of steroidogenesis in hypogonadotropic hypogonadal males.[/I] [I][U]17-OHP levels were significantly decreased on treatment with testosterone, but not while the males were on gonadotropin replacement, indicating that a major proportion of this precursor steroid is produced in the gonads and requires gonadotropin stimulation for secretion[/U], while a minor part of it stems from other sources. It is likely that ACTH- stimulated production in the adrenal gland contributes to it. 17-OHP is recognized to have [U]anti-mineralocorticoid 15 and glucocorticoid potency 16,17, without direct androgenic properties[/U].[/I] Since cross-reactivity among steroids is a recognized phenomenon, due to the high degree of homology at the DNA-binding domains of nuclear receptors within the steroid hormone receptor superfamily 18, the measured differences in serum 17-OHP concentrations may have clinical implications. [I][U]Surprisingly, progesterone serum levels in CHH males were decreased on both hCG+rFSH and testosterone substitution, when compared to controls, but the decrease was more pronounced on testosterone replacement[/U]. [B]This indicates that the gonadotropins used for replacement do enhance progesterone serum production in males, albeit to a lower extent than in healthy subjects.[/B] [U]The use of hCG instead of LH for CHH replacement may explain this phenomenon[/U]. [U]Progesterone acts via intracellular progesterone receptors (PRs) A and B, thereby exerting classical genomic action. In addition, it has non-genomic effects[/U]. [B]In males, progesterone is involved in sperm capacitation/acrosome reaction, it influences LH receptor expression and subsequent testosterone biosynthesis in Leydig cells; it interacts with the GABAA receptor complex in the CNS, thereby eliciting effects on sleep, mood, and cognition, and also exert effects in adipose tissue and kidneys 19.[/B][/I][B][I] Progesterone is a high-affinity antagonist of the mineralocorticoid receptor (NR3C2; MR)15, thus eliciting anti-mineralocorticoid effects 20-23. Progesterone is able to transactivate the glucocorticoid receptor (NR3C1; GR) 16. A lack of progesterone and 17-OHP in men could therefore have an impact on water and electrolyte balance and systemic blood pressure regulation.[/I] Figure 1 Pathways of human androgen biosynthesis[/B] [I]-The classic pathways, proceeding parallel for Δ5 and Δ4, convert steroidogenic precursors and lead to the formation of T, which can be further converted to DHT. -The alternative pathway of T formation proceeds via androstenediol. -The backdoor pathway proceeds via androstanediol to generate DHT. -The 11-oxygenated C19 androgen pathway generates 11K T and 11 K DHT. The steroids measured in the present study are indicated in bold. [ATTACH type="full"]15296[/ATTACH][/I] [/QUOTE]
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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone Side Effect Management
TRT Effect on 5 Alpha Reductase and Upstream Hormones- Cause of Low Mood and Anxiety?
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