Angela Pfeiffer (41:48)
Yeah, yeah, absolutely. And I think to go deeper, too. So we have. You know, anyone in the SIBO realm should be very familiar. If not, please go get familiar with the reimagine studies coming out of cedar cyanide. They invented a sterile catheter, so when they go down and do the respiratory, it's not getting contaminated with anything as it's coming up and coming out of the oral cavity, too. Okay. So they're able to do really pristine studies on what is in the small intestine, and they're mapping out the small intestine for the first time in the last six years. Before that, we have digestive stool test. And forever, it is inferred that that Digestive stool test is representative of everything from nose to anus. It's the entire thing, guys. It's not. It's only large intestine. It's only large intestine. So we've got 20ft of small intestine. It's where it is so metabolically active you assimilate vitamins, minerals, macronutrients. So much is happening in that area. And then we've got your five feet of large intestine. They're on different planets. That is how we, we learned this at last year, 20 years ago. But for some reason it's interesting looking at studies where it's just like, yeah, no, it's everything. So they, lots of studies being done with reimagine. They're basically looking and comparing sibo patients versus non sibo patients. What they found was the proteobacteria is coming down and colonizing the upper small intestine. It's pushing down the firmicutes, which is fairly dominant in that area. Now in a stool test, we look at bacteroides and firmicutes as the two dominant phyla. Bacteroideides is a, is a pin drop in the small intestine. So we're looking at balance of that just again, we can't infer it all the way up the small intestine. So basically proteobacteria are coming in, they're pushing down firmicutes and then we've got lower diversity in the upper small intestine. It's competitive, lower diversity. You take an antibiotic, we've got, we've got firicides, among other bacteria, single cell bacteria, much more susceptible to the antibiotics, especially the broad spectrum. The second you're getting into Cipro, bactrum, metronidazole, neomycin, you are dropping the beneficial stuff greatly. But you have to, in their world, you have to because the gram negative bacteria, the proteobacteria have a double cell wall, harder to get to. Okay, so you're knocking down the beneficial stuff more. You're knocking down what is considered the more pathogenic. But then we all know what happens. The resistance stuff stays and the resistance stuff comes back up and takes the niche. Because it is pathogenic, it is better at coming back up and taking the niche. So in my view also, these recurrent antibiotics are dropping diversity more and just building more and more resistance in an area that we should be rebalancing and bringing back up into where it needs to be versus going after this with a kill, kill, kill. We need to look at recovery and rebalancing with the intestinal tract. We should not be looking at kill phases unless something's going to kill you. If that is a true infection, save your life. Antibiotics all the way. My God, thank God we have them. Thank God we have them. But this idea of, I'm dealing with chronic bloating, and I understand, it's so debilitating. This is not an easy thing to say at all. I know, but if the treatment isn't going to stick, why are we doing it? And what I hear from providers a lot is, well, this is just what we assume. A third of people are going to take an antibiotic and walk away. A third of people are going to need multiple antibiotics and probably get into, like, a recurrence. And a third aren't going to be helped by antibiotics. They have a stronger root cause. And I'm like, okay, so antibiotics out of the gate are having a negative effect on two thirds of that population. Why are we doing that? Right. And I kind of feel, too, if you have a patient that presents in one round of antibiotics and they go on their merry way and everything is fixed, I really question whether they had sibo. I just do. Where's the momentum? Where's the terrain? Reset. Did that antibiotic knock down something else? Did it happen to hit a parasite they had? Was it placebo? Did some people just get better? Cause I'm taking this, I'm better. Maybe that calms their brain down, thinking that I've got the treatment, I'm moving on. I don't know. But that just is such a. Knowing the mechanisms, how is that helping them recover?