What Are Lipopolysaccharides and What’s Their Role in Endometriosis Growth and Pain?

Okay, so today I want to do another short episode, um, a bite-sized episode on lipopolysaccharides, because I talk about them so much, and I haven't done a dedicated episode on them, so I thought it would help [laughs] to do that.

Um, so lipopolysaccharides, known as LPS or endotoxins, so you might see them when you Google them or you're reading about something, you might see them come up as that.

They are toxins that are released from Gram-negative bacteria.

So bacteria can be Gram-positive or Gram-negative, and LPS come from Gram-negative.

In the overgrowths that have been seen in endo, a lot of them are Gram-negative, so we have higher levels of Gram-negative bacteria in our guts.

Now, LPS have been found at higher levels in the pelvic fluid and menstrual blood of people with endo, and they trigger specific inflammatory pathways that further endo growth and pain.

And actually, LPS are now thought to be an initial inflammatory mediator in endometriosis pathogenesis, so essentially, they think that they're one of the starting points of the development, the kind of inflammatory cascade that leads to its growth.

So where are these LPS coming from? Elevated levels of E.

coli, a Gram-negative bacteria, have been found in the gut microbiome, menstrual blood, vagina, and cervical and endometrial samples of people with endo, and researchers believe that the presence of E. coli is the cause of high levels of LPS that we see in the pelvic cavity of people with endo, as LPS break off E. coli bacteria, so they kind of float off [laughs] E. coli bacteria, essentially.

They, they make the bacteria, they're part of the walls that make the bacteria, and they kind of break off.

Now, they also think that the translocation from the gut to the pelvis is one of the key ways that E. coli and LPS are getting to this area, and translocation, um, of the, of LPS is the movement, simply the movement through the gut barrier into the bloodstream and the rest of the body.

So why might this be happening in the endo population? Well, many things can weaken the intestinal barrier, um, and this damage to the barrier lining is called intestinal permeability or leaky gut.

And intestinal permeability can be caused by, um, an unknown condition like celiac disease, which damages the small intestine.

Um, it can also come from food intolerances and sensitivities, so for example, if your, if your gut is continuously getting irritated by something, that can damage that lining.

It can also come from, uh, microbiome dysbiosis and repeated NSAID use, um, to name a few of the causes.

Now, I'm sure you've worked it out that all of these are pretty common in the endo community, right? A lot of us use NSAIDs.

Um, we know that we have microbiome dysbiosis in the research.

Uh, we know there's a high prevalence of celiac disease, and many of us do also have sensitivities, uh, food intolerances, et cetera.But another thing that causes intestinal permeability is SIBO, as SIBO increases LPS levels due to the amount of gram-negative bacteria that's found in SIBO, like E. coli and Klebsiella, which are the key bacteria in hydrogen-type SIBO.

Now, don't forget, the current research that we have estimates that 80 to 90% of us with endo have SIBO or intestinal methanogen overgrowth.

Annoyingly, we don't have stats on hydrogen sulfide yet.

I'm sure that will be coming in due course at some point.

But the high levels of LPS are one of the main causes of the intestinal permeability seen in SIBO, so the LPS damage that intestinal lining.

So now let's look at how LPS actually further endogrowth.

So what do they actually do? So E.

coli releases the LPS.