Anyone tried berberine?

Hello guys,
As im really scared to try anything new, i wanted to check, if anyone else tried this supplement before?
If not, i have already bought a bottle, and im willing to give it a try (So afraid to crash again :()

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I tried it it’s meant to be good for digestion wasn’t really on it for long enough to see any noticeable improvements. Why do you want to try it out? Just be careful.

Tried for 6 months, no difference.

Hey @Xorack, please fill out the survey.

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I really don’t think its useful … still taking Lupron and maybe I wont stop it.

Just curious, have you tried stopping lupron? And if yes what happened when you stopped?

@silentpain89 @Xorack, it has been 3 months since you are registered. I assume that you have symptoms at least for 3 months. So… What is/are your excuse(s) to not fill out the survey ? If no, could you kindly do that ASAP, as it certainly the easiest way to help yourself and community. Thank you.

Because I still taking an AA and its written, to complete the survey you must have stopped AA at least 3 months before. I shouldn’t be here because of that.
I stopped AA in the past and the pain was unbearable.

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I tried, it’s AMPK activator and can improve erection quality, but I stopped taking it once I found the studies that show berberine is inducing muscle wastage.

It is concerning to me that a 2019 study found Berberine is a 5ARi in vitro and in vivo. I’ve been using it daily for blood glucose control and have felt a bit off. I’m now planning to only use it occasionally. Maybe it’s similar to the Turmeric situation where it’s not as strong as Finasteride, but it can still noticably inhibit 5ARi and bring back mild sides.

Berberine Improves Benign Prostatic Hyperplasia via Suppression of 5 Alpha Reductase and Extracellular Signal-Regulated Kinase in Vivo and in Vitro
“Benign prostate hyperplasia (BPH) is a common disease in elderly men, characterized by proliferated prostate and urinary tract symptoms. The hormonal cascade starting by the action of 5-alpha-reductase (5AR) is known to be one of the pathways responsible for the pathogenesis of BPH. Present investigation evaluated the capacity of berberine (BBR), a nature-derived compound abundant in Coptis japonica, in testosterone-induced BPH rats. Experimental BPH was induced by inguinal injection with testosterone propionate (TP) for 4 weeks. BBR or finasteride, a 5AR inhibitor as positive control, was treated for 4 weeks during BPH. BPH induced by TP evoked weight gaining and histological changes of prostate and BBR treatment improved all the detrimental effects not only weight reduction and histological changes but also suppression of prostate-specific antigen (PSA), which is elevated during BPH. Additionally, BBR suppressed TP-associated increase of 5AR, androgen receptor (AR) and steroid coactivator-1 (SRC-1), the key factors in the pathogenesis of BPH. To evaluate the underlying molecular mechanisms responsible for beneficial effects of BBR, we investigated whether these effects were associated with the mitogen-activated protein kinase pathway. BPH induced by TP showed increased phosphorylation of extracellular signal-regulated kinase (ERK), whereas this was suppressed by BBR treatment. On the other hand, c-jun-N-terminal kinase (JNK) and p38 mitogen-activated protein kinase was not changed in BPH rats. In in vitro study using RWPE-1 cells, a human prostate epithelial cell line. TP increased cell proliferation and BPH-related key factors such as PSA, AR, and 5AR in RWPE-1 cells, and those factors were significantly decreased in the presence of BBR. Furthermore, these proliferative effects in RWPE-1cells were attenuated by treatment with U0126, an ERK inhibitor, confirming BBR can relieve overgrowth of prostate via ERK-dependent signaling. The cotreatment of U0126 and BBR did not affect the change of 5AR nor proliferation compared with U0126 alone, suggesting that the effect of BBR was dependent on the action of ERK. In conclusion, this study shows that BBR can be used as a therapeutic agent for BPH by controlling hyperplasia of prostate through suppression of ERK mechanism.”