Endotoxin/LPS can cause spontaneous abortion by raising nitric oxide (NO)
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I am posting this study as a kind of a follow-up on the one I posted a few days ago showing that endotoxin/LPS can cause the dreaded and lethal “mad cow” disease all by itself, and without the need for infectious prions. Well, it sure seems like endotoxin rears its ugly head in pretty much any health condition medicine knows of. Now, we can add spontaneous abortion (SA) to the list of those conditions. SA is considered “idiopathic”, yet somehow linked to inflammation, hormones, age and metabolic status. Mainstream medicine says there are no known preventive of therapeutic for this condition, despite many animal studies demonstrating aspirin, progesterone, thyroid, vitamin E, etc to be able to prevent it and often stop it even after it is already underway. The study below shows that endotoxin, which is something every person is exposed to multiple times on a daily basis simply due to eating is perfectly capable of causing SA by itself. Interestingly, the known pro-inflammatory effects of endotoxin did not seem to be at play this time. Rather, it was the increase in NO (also a known effect of elevated endotoxin) that correlated well with the rates of SA in the animals subjected to endotoxin exposure. Considering how common chronic, low-grade endotoxemia is, it is not a too much of a leap of faith to conjecture that a good number of SA cases are of dietary/digestive origin. In terms of interventions, substances with known anti-NO effects include methylene blue, niacinamide, progesterone, and the amino acid lysine.
https://pubmed.ncbi.nlm.nih.gov/10442853/
“…In this report, we examined the involvement of the cytokines tumor necrosis factor (TNF)-alpha, interferon (IFN)-gamma, interleukin (IL)-4, and IL-10 as well as nitric oxide (NO) in the lipopolysaccharide (LPS)-induced experimental abortion model in BALB/c mice. Although in vivo administration of LPS in pregnant mice showed a 72% decrease of serum IL-10, no significant difference in serum TNF-alpha, IFN-gamma, and IL-4 levels, compared to controls, could be detected. At the same time, a correlation of fetal abortion and maternal splenomegaly with an important increase of NO synthesis in the serum was obtained. Simultaneous administration of LPS and aminoguanidine (AG; an inhibitor to NO synthase) rescued the LPS-induced fetal abortion, reduced maternal spleen weight to physiological levels, and decreased serum NO concentration to control levels. In vitro experiments showed that LPS directly induced NO production in primary placental cells and the TPOPHO-1 trophoblast cell line by stimulating the inducible isoform of NO synthase, which ultimately could be blocked by the NO synthase inhibitors AG and L-NAME. The results indicate that LPS, despite its beneficial involvement in intracellular infections, participates in inflammatory/autoimmune damage during pregnancy, leading to embryotoxicity, which is closely linked to the NO pathway.”