Has anyone considered the fact that we can have a basic imbalance between the two forms of 5 alpha reductases? If some of us have, for example, a more active type 1 5 alpha reductase than type 2 from genetics, it may happen that during the use of finasteride there is a slight reduction in type 1 and a drastic reduction in type 2. This determines a type 1 hypertrophy that remains in suspension since type 2 is already less expressed in the base. The damage reported by most users is a type 1 expression. That is, an excess of DHT not suitable for receptors, an excess of neurosteroids that mess with the nervous system with mental fog and cognitive problems, anxiety, pain, muscle loss, rapid depletion of cortisol. In fact, free testosterone remains little because the overexpressed 5 alpha reductase of type 1 actually accelerates 3 processes: + conversion of T into DHT= - less anabolism for the reduction of free T; 2 greater conversion of progesterone into precursors of neurotransmitters = paradoxical reactions the brain is no longer able to manage the excess of dopamine, serotonin, gaba, noradrinephrine; 3 excessive conversion of cortisol into cortisone = diffuse pain. So, in my opinion, the basic superexpression of type 1 is exacerbated by the long suppression of type 2 and when the block ends type 2 remains subject to the prevalence of type 1 which continues to charge while type 2 removes matter from type 1a subtracting substantially more androgens because it converts T into DHT therefore a further reduction of circulating T with the effect of less anabolism and consequent symptoms related to this situation. The excessive activity of DHT causes a slowdown and/or blocking of the receptors by overload with the advancement of estrogen. For my part, an approach that modulates the activity of the two forms of the enzyme would be necessary even if there is no drug/product that lowers or modulates the activity of 5 alpha reductase type 1. What do you think?
