Missenger
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wtf?
Post-finasteride syndrome: An emerging clinical problem
The presence of side effects during pharmacological treatment is unfortunately a quite common problem. In this review, we focused our attention on adverse events related to 5 alpha-reductase (5α-R) inhibitors (i.e., finasteride and dutasteride), ...
www.ncbi.nlm.nih.gov
Dopamine/Serotonin dysregulation along with GABA would contribute to it. Finasteride is basically poison you can microdose for hair. Pharma has also sold lactic acid before as an anti-fungal cream, which is kind of funny to think about.Not only alterations in neuroactive steroid levels (Melcangi et al., 2014, 2016; Zorumski et al., 2013) but also changes in hippocampal neurogenesis have been related with depressive-like behaviors (Santarelli et al., 2003; Snyder et al., 2011). Altered hippocampal morphology and reduced hippocampal neurogenesis have been also reported in depressed patients (Hercher et al., 2009; Stockmeier et al., 2004). Interestingly, 6 days of finasteride administration in male C57BL/6N mice were able to decrease the hippocampal neurogenesis (Romer and Gass, 2010; Romer et al., 2010). Recent observations in a rat model have shown that 20 days of treatment induced a decrease of granule cell density in the granular layer of the dentate gyrus in rats showing depressive-like behavior one month after the end of finasteride treatment (Diviccaro et al., 2019) (Fig. 3).
In humans and experimental models, depression has been demonstrated to be associated with neuroinflammation (Yirmiya et al., 2015). Treatment with finasteride also affects this parameter (Fig. 3). Indeed, a significant increase in the number of astrocytes (i.e., cellular mediators of the inflammatory response) in the hilus of the dentate gyrus has been demonstrated one month after the end of the finasteride treatment (Diviccaro et al., 2019). This effect might be ascribed to the elevated levels of DHP observed one month after the end of the finasteride treatment in male rat hippocampus (Giatti et al., 2016). Indeed, in other experimental models, DHP has been demonstrated to increase GFAP gene expression in astrocytes (Melcangi et al., 1996). Reactive gliosis is associated with increased levels of proinflammatory molecules in the brain (Hostenbach et al., 2014; Wang et al., 2018). In agreement, finasteride treatment increased, immediately after the treatment, the expression of TNF-α in male rat hippocampus and, at the withdrawal, that of IL-1β (Diviccaro et al., 2019). It is important to note that both cytokines are increased in plasma of depressed patients and in the brain of animal models for depression (Cheng et al., 2018; Li et al., 2017; Todorovic and Filipovic, 2017; Wang et al., 2018). Dysregulation of the dopamine system may also contribute to major depressive disorders (Belujon and Grace, 2017; Felger, 2017; Grace, 2016). Therefore, in this context it is important to recall that androgens regulate the dopaminergic system in the brain (de Souza Silva et al., 2009; Kindlundh et al., 2004; Mitchell and Stewart, 1989). Interestingly, finasteride treatment (25 and 50 mg/kg for 14 days) inhibited open-field behaviors and reduced contents of dopamine and its metabolites in central nervous system (Li et al., 2018). In addition, finasteride treatment was also able to impair the signaling of dopamine (Devoto et al., 2012; Frau et al., 2016).
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