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From the publication:

Mounting evidence shows that low, rather than high, T[estosterone] levels favor prostate inflammation and that hyperestrogenism also may play a role. Considering all these data, we postulate that BPH results from the actions of multiple factors occurring together or at different time points, which can reinforce and favor their mutual detrimental effects. The initial steps in this process are likely to occur early in life with an overt or subclinical prostatitis, probably influenced by infectious agents. The resulting prostatic inflammation could be amplified and maintained by metabolic derangements occurring in such conditions as MetS [metabolic syndrome]. Low T and the relative hyperestrogenism secondary to MetS [metabolic syndrome] could further exacerbate the immune process, leading to a chronic inflammation. When prostatitis becomes chronic, a number of cytokines are produced that act in the tissue to maintain the pathological condition. On the other hand, several growth factors are secreted, and their elevated concentrations lead to prostate remodeling and enlargement. The resulting mechanical obstruction and inflammatory damage are the basis of BPH and its associated urinary symptoms.


In addition, treating hypogonadism, which frequently accompanies MetS, not only is not detrimental for the prostate, but also could even be a therapeutic resource for relieving urinary symptoms and limiting the inflammatory process in the prostate.


The apparent contradiction of these results with the success of 5-alpha reductase inhibitors in treating LUTS merits closer investigation. Undoubtedly, treatment with 5-alpha reductase inhibitors results in a prostate volume decrease, which in turn translates into an improvement in LUTS. Nonetheless, it should be kept in mind that studies assessing intraprostatic androgen levels have linked 5-alpha reductase inhibition with a decrease in DHT and an increase in T.

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