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| Main Author: | |
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| Format: | Recurso digital |
| Language: | English |
| Published: |
Zenodo
2026
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| Subjects: | |
| Online Access: | https://doi.org/10.5281/zenodo.19901062 |
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Table of Contents:
- <p><strong>Abstract</strong></p> <p><strong>Background</strong></p> <p>Endocrine models treat testosterone regulation as primarily hypothalamic–pituitary–gonadal signaling. <em>This excludes the continuous physiological fluxes required for steroidogenesis.</em></p> <p><br><strong>Objective</strong></p> <p>To define testosterone output as a perfusion-dependent constraint intersection and to integrate <em>chronic tadalafil-induced increases in total and free testosterone into the closed-system flux model.</em></p> <p><br><strong>Methods</strong></p> <p>Mechanistic synthesis. Inclusion required defined flux, mammalian conservation, and necessity for steroidogenesis. <em>Human tadalafil-only chronic studies demonstrating increased total/free testosterone were included. Non-causal explanations were eliminated.</em></p> <p><br><strong>Results</strong></p> <p>Tadalafil inhibits PDE5, elevates cGMP, produces sustained vasodilation, and increases microvascular perfusion to Leydig cells. This removes rate-limiting constraints on oxygen, substrate, and electron flux. Testosterone output rises when all steroidogenic fluxes remain non-zero. <em>Free testosterone further increases via reduced SHBG binding under improved metabolic signaling. SHBG itself declines as a secondary consequence of restored perfusion and metabolic flux. In post-androgen cessation states, SHBG elevation functions as a hepatic stabilizer of systemic constraint.</em></p> <p><br><strong>Conclusion</strong></p> <p>Testosterone is a dependent variable of systemic flux integrity. <em>Tadalafil increases testosterone by restoring perfusion-dependent flux continuity required for steroidogenesis. Endocrine output reflects constraint satisfaction, not isolated hormonal regulation.</em></p> <p> </p>