BPH is a very common problem, apparently affecting more than 70%of men over 50. Ray has said in some email exchanges that prostatitis and BPH are linked with endotoxin. I was not able to find much published research on the topic but this new study finally makes that claim. What is more important, blocking the endotoxin "receptor" TLR4 may treat BPH and even prevent it from happening. Niacinamide and emodin are two of the most well-known TLR4 antagonists.
Of note is that the study also found strong associations between TLR4 expression and BMI, and PSA. So, endotoxin makes you fat and balloons your prostate.
LPS/TLR4 Signaling Enhances TGF-β Response Through Downregulating BAMBI During Prostatic Hyperplasia : Scientific Reports
Inhibition of TLR4 Signaling May Decrease BPH Chronic Inflammation, According to Study - BPH News
"...Novel therapeutic targeting of TLR4 signaling pathway may halt chronic inflammation leading to benign prostate hyperplasia (BPH), according to a study, “LPS/TLR4 Signaling Enhances TGF-β Response Through Downregulating BAMBI During Prostatic Hyperplasia,” published in the journal Scientific Reports."
"...The transforming growth factor-β1 (TGF-β1) cytokine is a strong extracellular inducer of EMT and it was shown to induce EMT phenotypes in prostatic epithelial cells. In follow-up studies, researchers found that TGF-β1 expression was increased with LPS treatment. LPS, short for lipopolysaccharide, is the major component of the outer membrane of Gram-negative bacteria. Researchers also observed that injection of LPS into rat prostates leads to an EMT phenotype."
"...Researchers analyzed TLR4 expression in BPH tissues with inflammation, and found it to be significantly higher, when compared to BPH tissues without inflammation. Correlation studies also suggested TLR4 expression (at the level of messenger RNA) associated with age, BMI, serum PSA levels, urgency and nocturia in the inflammatory group. In conclusion, these results suggest a link between prostatic hyperplasia and inflammation mediated by modulation of TGF-β induced EMT by LPS/TLR4 axis. Therefore, therapeutic targeting of TLR4 signaling may benefit BPH patients."
Of note is that the study also found strong associations between TLR4 expression and BMI, and PSA. So, endotoxin makes you fat and balloons your prostate.
LPS/TLR4 Signaling Enhances TGF-β Response Through Downregulating BAMBI During Prostatic Hyperplasia : Scientific Reports
Inhibition of TLR4 Signaling May Decrease BPH Chronic Inflammation, According to Study - BPH News
"...Novel therapeutic targeting of TLR4 signaling pathway may halt chronic inflammation leading to benign prostate hyperplasia (BPH), according to a study, “LPS/TLR4 Signaling Enhances TGF-β Response Through Downregulating BAMBI During Prostatic Hyperplasia,” published in the journal Scientific Reports."
"...The transforming growth factor-β1 (TGF-β1) cytokine is a strong extracellular inducer of EMT and it was shown to induce EMT phenotypes in prostatic epithelial cells. In follow-up studies, researchers found that TGF-β1 expression was increased with LPS treatment. LPS, short for lipopolysaccharide, is the major component of the outer membrane of Gram-negative bacteria. Researchers also observed that injection of LPS into rat prostates leads to an EMT phenotype."
"...Researchers analyzed TLR4 expression in BPH tissues with inflammation, and found it to be significantly higher, when compared to BPH tissues without inflammation. Correlation studies also suggested TLR4 expression (at the level of messenger RNA) associated with age, BMI, serum PSA levels, urgency and nocturia in the inflammatory group. In conclusion, these results suggest a link between prostatic hyperplasia and inflammation mediated by modulation of TGF-β induced EMT by LPS/TLR4 axis. Therefore, therapeutic targeting of TLR4 signaling may benefit BPH patients."