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      learn Microneedling

      technique to create small wounds in skin to activate collagen production and hair growth

      learn Mesotherapy

      technique to inject very small amounts of beneficial chemicals into the scalp

      learn Exosomes

      Microscopic delivery system that sends growth-promoting signals to hair follicles

      learn PP405

      mitochondrial pyruvate carrier (MPC) inhibitor by Pelage in early trials

      learn Saw Palmetto

      a natural and far less effective alternative to Finasteride

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      research A SIBO-Mediated Etiology for a Subset of Post-Finasteride Syndrome Cases: Investigating Gut-Derived Toxins

      February 2026 in “Zenodo (CERN European Organization for Nuclear Research)”
      This theoretical paper suggests a novel gut-centric cause for a subset of Post-Finasteride Syndrome (PFS) cases, which are not fully explained by androgen deprivation. It hypothesizes that a chronic overgrowth of hydrogen sulphide (H₂S)-producing bacteria in the small intestine acts as a systemic mitochondrial toxin. This condition may create a dysbiotic feedback loop that perpetuates the epigenetic silencing initially triggered by finasteride exposure. The paper proposes that this acquired metabolic dysfunction, driven by gut-derived toxins, could explain the persistence of PFS symptoms and highlights the small intestinal microbiome as a potential therapeutic target.

      research A SIBO-Mediated Etiology for a Subset of Post-Finasteride Syndrome Cases: Investigating Gut-Derived Toxins

      February 2026 in “Zenodo (CERN European Organization for Nuclear Research)”
      This theoretical paper suggests a novel gut-centric cause for a subset of Post-Finasteride Syndrome (PFS) cases, which are not fully explained by androgen deprivation. It hypothesizes that a chronic overgrowth of hydrogen sulphide (H₂S)-producing bacteria in the small intestine acts as a systemic mitochondrial toxin. This condition may create a dysbiotic feedback loop that perpetuates the epigenetic silencing initially triggered by finasteride exposure. The paper proposes that this acquired metabolic dysfunction, driven by gut-derived toxins, could explain the persistence of PFS symptoms and highlights the small intestinal microbiome as a potential therapeutic target.

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