Nov. 3, 2025
SIBO Part I: Clinical Presentation
Dr. Navin Kumar, gastroenterologist and RTL co-founder, joins guest-host Ally Scheve to discuss the clinical presentation of Small Intestinal Bacterial Overgrowth (SIBO) in this three-part series. In this episode, they discuss the pathophysiology of SIBO, how bacteria in the small intestine lead to GI symptoms, and the risk factors for developing SIBO.
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WEBVTT
00:05.262 --> 00:10.670
[SPEAKER_00]: I am Ali Shivie, a current third year medical student, Harvard, and a recent member of the RTL team.
00:11.231 --> 00:22.588
[SPEAKER_00]: Today, we will be talking about small intestinal bacterial overgrowth, also known as CBO, and increasingly discussed and diagnosed condition in the primary care office and gastroenterology clinic.
00:23.189 --> 00:30.780
[SPEAKER_00]: I have with me Dr. Kumar, a gastroenterologist at Brigham and Women's Hospital, and of course one of our fearless leaders of RTL.
00:31.013 --> 00:37.179
[SPEAKER_01]: Thank you so much, Ali, it's so great to be back recording with you, and especially on such a hot topic as Sebo.
00:37.599 --> 00:48.170
[SPEAKER_01]: I also want to thank you for all your outstanding work and bringing back our RTL handouts along with your cold medical student Hannah Shapiro, who is also a third year student at Harvard Medical School.
00:49.091 --> 00:56.498
[SPEAKER_01]: And if I may have the honor as it's been a little bit, so I'd love to say our token line here, let's go ahead and run the list.
00:56.866 --> 00:58.989
[SPEAKER_00]: And as always, let's start with a case.
00:59.630 --> 01:12.668
[SPEAKER_00]: Ms. R is a 45-year-old female with a history of obesity, status posts ruined why gastric bypass, who presents to primary care clinic with two months of worsening bloating, flatulence, and diarrhea.
01:13.209 --> 01:18.036
[SPEAKER_00]: She reports abdominal distension is present upon waking up in worsens after meals.
01:18.676 --> 01:21.140
[SPEAKER_00]: She's concerned that she might have underlying seabough.
01:21.681 --> 01:24.865
[SPEAKER_00]: Dr. Kumar, can you first explain what seabough is?
01:24.997 --> 01:39.129
[SPEAKER_01]: Absolutely, so CBO or small intestinal bacterial overgrowth is a condition in which bacteria proliferate in the small intestine, which at otherwise be a largely sterile environment, where you do not have very much bacteria at all.
01:39.490 --> 01:54.463
[SPEAKER_01]: So we can contrast that with the colon, which is full of bacteria, and think about how, if these bacteria or other species take resonance more proximally in the small intestine, how those bacteria can produce a variety of symptoms for patients dealing with this condition.
01:54.697 --> 01:55.741
[SPEAKER_00]: that totally makes sense.
01:56.162 --> 02:01.602
[SPEAKER_00]: So how does the overgrowth of bacteria cause the symptoms our patient is experiencing?
02:01.717 --> 02:03.540
[SPEAKER_01]: That's an excellent question, Ali.
02:03.620 --> 02:13.414
[SPEAKER_01]: And the way I think about this, when I'm teaching or even when I'm in clinic and talking to my own patients, is that there's three main pathways for bacterial overgrowth of a small intestine to cause symptoms.
02:13.754 --> 02:20.023
[SPEAKER_01]: So the first one is that the small intestinal bacteria that are in this area of the digestive tract where they shouldn't be.
02:20.063 --> 02:30.238
[SPEAKER_01]: End up breaking down the foods and the nutrients from a recently ingested meal, right, because the first thing that happens after the food empties from the stomach is that it gets into the small intestine.
02:30.218 --> 02:36.089
[SPEAKER_01]: And normally, those nutrients would be broken down and completely absorbed in the small intestine.
02:36.209 --> 02:40.537
[SPEAKER_01]: But when there's bacteria there, the bacteria actually break down these nutrients.
02:41.038 --> 02:44.965
[SPEAKER_01]: And in the process of breaking down these products, they release gas.
02:45.325 --> 02:53.340
[SPEAKER_01]: And that gas leads to the classic symptoms of abdominal bloating, cramping, distension, as well as flatulence.
02:53.320 --> 03:00.353
[SPEAKER_01]: So the first mechanism is from the bacteria breaking down the food products and releasing gas.
03:00.894 --> 03:14.299
[SPEAKER_01]: Now the second pathway that I think about is how the small intestinal bacteria, which again are not in the location that they should be, they can actually take up residents right along the
03:14.279 --> 03:18.864
[SPEAKER_01]: and as they line up on the mucosal surfaces, they can interfere with absorption.
03:19.385 --> 03:40.489
[SPEAKER_01]: In these cases, what typically happens is a watery diarrhea ensues because the unabsorbed substances that would have otherwise been absorbed, but instead of remaining in the lumen because they're not getting absorbed, being blocked by this bacteria that are lying to mucosum, those unabsorbed substances draw water into the intestinal tract, ala azimatic diarrhea.
03:40.469 --> 03:52.401
[SPEAKER_01]: So in even more severe cases, you don't only have an osmotic diarrhea, but you can also get stiatoria because it's a small intestinal bacteria actually disrupt the absorption of fats.
03:52.881 --> 04:03.252
[SPEAKER_01]: So some patients would see, though, actually complain more of stiatoria where they see oil droplets in the stool or they have the classic very difficult to flush stool from the toilet bowl of stiatoria.
04:03.272 --> 04:09.598
[SPEAKER_01]: So think about what is happening at the mecoso level in terms of absorption and how that
04:09.578 --> 04:10.679
[SPEAKER_01]: Stateria.
04:11.581 --> 04:26.480
[SPEAKER_01]: And the third pathway, and this is typically only in extreme cases, but these same small intestinal bacteria that are competing for nutrients and potentially interfering with absorption at the level of the mecosa, they can actually lead to vitamin and mineral deficiencies.
04:26.560 --> 04:36.312
[SPEAKER_01]: So what can happen is that these bacteria can absorb B12 for themselves and take that away essentially steal it from the host and cause B12 deficiency.
04:36.292 --> 04:43.523
[SPEAKER_01]: This can also happen with iron deficiency as well, where the bacteria are consuming the iron that was ingested.
04:43.563 --> 04:47.950
[SPEAKER_01]: And instead of the host being able to absorb that iron, the bacteria take it for themselves.
04:48.411 --> 04:55.161
[SPEAKER_01]: And then, inversely, it's an interesting phenomenon, as some of these bacteria actually produce folate.
04:55.141 --> 05:00.569
[SPEAKER_01]: And so they can raise the levels of folate above assay when measured from the blood.
05:00.910 --> 05:13.690
[SPEAKER_01]: So a little pearl to share is that if you have a patient who has clinical signs or symptoms of seabull, let's say they have the abdominal gas to mention in diarrhea, you may also see this hallmark sign
05:13.670 --> 05:25.605
[SPEAKER_01]: on labs where they have B12 deficiency because the CBO is stealing the B12 from the host and then high folate levels often greater than assay because they are producing folate.
05:25.625 --> 05:33.516
[SPEAKER_01]: So I always, if the patients happen to have had recent and email labs with a B12 in folate, I look to look at those because it fits that pattern.
05:33.996 --> 05:39.964
[SPEAKER_01]: Low B12, high folate, I'm thinking, okay, my index is suspicion for this being CBO is even higher.
05:39.944 --> 05:41.568
[SPEAKER_00]: that's a great pearl.
05:41.929 --> 05:55.725
[SPEAKER_00]: So now that we understand the pathophysiology explaining why the concentration of symptoms of sebo occurs, who actually gets sebo and are there any risk factors for developing this disease?
05:55.705 --> 05:56.667
[SPEAKER_01]: Yes, for sure.
05:56.687 --> 06:03.278
[SPEAKER_01]: So the overarching theme, as with any proliferation of bacteria in any part of the body, is altered motility.
06:03.899 --> 06:09.930
[SPEAKER_01]: So the most common cause of altered GI motility, as we all know, is IBS or Errol Balsendrum.
06:10.531 --> 06:14.177
[SPEAKER_01]: And that's why there's such a significant overlap between IBS and SIBO.
06:14.698 --> 06:20.869
[SPEAKER_01]: Actually, recent data and literature shows that up to a third of patients who have IBS,
06:20.849 --> 06:24.634
[SPEAKER_01]: also had SIBO based on data obtained from those patients.
06:25.035 --> 06:33.747
[SPEAKER_01]: So there's a very high overlap between IBS and SIBO, and that's largely driven by the altered GI motility that is characteristic of IBS.
06:34.127 --> 06:50.350
[SPEAKER_01]: There are also other diseases that affect gut motility that we should also consider in patients who are at risk for SIBO, and that includes conditions such as diabetes, mellitus, radiation
06:50.330 --> 07:02.425
[SPEAKER_01]: That's a bigger box and some are more common than others, but it's always important to just consider what is the underlying motility of my patients digests of tract and does that put them at risk for sebo.
07:02.806 --> 07:03.787
[SPEAKER_00]: That makes sense.
07:03.807 --> 07:05.990
[SPEAKER_00]: It peristelsus is not consistent.
07:06.190 --> 07:11.617
[SPEAKER_00]: This provides an excellent environment for bacteria to stay in one place and replicate.
07:11.697 --> 07:12.658
[SPEAKER_01]: Right exactly.
07:12.899 --> 07:19.527
[SPEAKER_01]: And then stasis can occur not just because of altered motility, but also due to anatomical variation.
07:19.507 --> 07:25.013
[SPEAKER_01]: And that's true for the patient that you described, this M, who has a history of a ruin-wide gastric bypass.
07:25.453 --> 07:33.001
[SPEAKER_01]: And so with the ruin-wide gastric bypass, there is this formation of a blind pouch within the newly altered GI tract.
07:33.281 --> 07:39.728
[SPEAKER_01]: And within that blind pouch, there is stasis and hence an increased risk for bacteria to proliferate in that area.
07:40.309 --> 07:44.613
[SPEAKER_01]: Another example would be stasis due to an illule structure in Crohn's disease.
07:44.993 --> 07:49.378
[SPEAKER_01]: We already mentioned Crohn's disease as a
07:49.358 --> 08:02.056
[SPEAKER_01]: But also, if there is a narrowing, stool is not going to travel through that area as readily, and so that decrease in motility and also just stasis from hanging above the structure can lead to increased risk for seabull.
08:02.356 --> 08:08.545
[SPEAKER_01]: Another common, actually fairly common cause that I found in my patients is identifying a small ball of diverticula.
08:08.725 --> 08:14.573
[SPEAKER_01]: We think about diverticula is primarily in a large intestine, but it can also be present in the small intestine.
08:14.553 --> 08:29.811
[SPEAKER_01]: And you can imagine if there's an outpouching in the small intestine that almost shields is shielded from the natural transit through the lumen, bacteria can proliferate in that little outpouching within the small intestine, so the bacteria like to hang out there as well.
08:29.791 --> 08:49.605
[SPEAKER_01]: So, we talked mainly about stasis in this segment, but the other anatomical variants to consider our fishulas, so think about fishulizing Crohn's disease, where you're connecting the large intestine to the small intestine and how bacteria can move retrograde from the large to the small intestine via the fishula.
08:49.585 --> 09:12.640
[SPEAKER_01]: Or also, many patients who have had surgery such as a right-hemi-collectomy, they will lose the Iliocicle valve that otherwise prevents back flow or reflux of calonic contents into the small intestine, so loss of that valve will allow bacteria to directly flow upwards from the large intestine to the small intestine and cause sebo in those patients.
09:13.025 --> 09:18.233
[SPEAKER_00]: great review of other comorbidities we should be thinking about when Cibo is on the differential.
09:18.975 --> 09:23.762
[SPEAKER_00]: I've also heard about there being a risk of Cibo when there is long-term PPI use.
09:24.183 --> 09:26.387
[SPEAKER_00]: What is the mechanism behind this relationship?
09:26.807 --> 09:39.488
[SPEAKER_01]: Right, so as you can imagine, Stomach asks is one of the GI defenses against bacterial growth that the lower pH is actually an environment in which bacteria do not grow well in.
09:39.653 --> 09:50.829
[SPEAKER_01]: And so when patients are put on long-term PPI, the reduction in stomach acid impairs this host defense and allows bacteria to grow more proxmoly in the small intestine.
09:51.570 --> 10:00.463
[SPEAKER_01]: So it's important to think about Cibo and your patients who are on long-term PPI and coming to you with symptoms like bloating or diarrhea.
10:00.781 --> 10:12.300
[SPEAKER_01]: And then also it can occur outside of PPIUs in patients who have extensive atrophic gastritis where they've lost or damaged many of their pridal cells from an autoimmune process.
10:12.881 --> 10:21.355
[SPEAKER_01]: The lack of pridal cells producing acid will lead to this again low acid state that can put them at risk for bacterial overgrowth.
10:21.689 --> 10:29.997
[SPEAKER_00]: So to review, we've identified altered GI motility, altered anatomy, and low stomach acid production, as causes for SIBO.
10:30.658 --> 10:32.980
[SPEAKER_00]: Are there any other categories we should be considering?
10:33.541 --> 10:37.865
[SPEAKER_01]: Yes, there are two more risk factors for SIBO that we should generally be aware of.
10:37.905 --> 10:41.128
[SPEAKER_01]: The first big bucket is anyone with immunodeficiency.
10:41.689 --> 10:49.637
[SPEAKER_01]: So things we think about here, our patients with CV, ID, or common variable immune deficiency, IGA deficiency,
10:49.617 --> 11:03.833
[SPEAKER_01]: or HIV or AIDS, just the general risk factor of being a amino deficient will of course put these patients at higher risk for any type of bacterial proliferation and that includes that bacterial proliferation within the small intestine.
11:04.274 --> 11:11.642
[SPEAKER_01]: The second category includes patients who have altered bile or digestive enzyme composition.
11:11.622 --> 11:20.277
[SPEAKER_01]: So the main disorder is that we think about in this category, our patients with cirrhosis, as well as patients with chronic pancreatitis.
11:20.397 --> 11:32.517
[SPEAKER_01]: Both of these patient categories cirrhosis and chronic pancreatitis have this issue with altered bile digestive enzyme composition, which can lead to the proliferation of bacteria in the small intestine.
11:32.632 --> 11:33.293
[SPEAKER_00]: fantastic.
11:33.873 --> 11:42.863
[SPEAKER_00]: We covered a lot today in terms of understanding why CBO happens, why patients present with the symptoms they do, and who might be at risk.
11:43.623 --> 11:47.547
[SPEAKER_00]: Before we go, can you summarize the most important takeaways for our listeners?
11:47.707 --> 11:48.428
[SPEAKER_01]: Yes, absolutely.
11:48.448 --> 11:50.410
[SPEAKER_01]: Let's do three key takeaways here.
11:50.470 --> 12:01.862
[SPEAKER_01]: So the first key takeaway is just understanding that CBO or small intestinal bacterial overgrowth is due to a pathological increase in the amount of bacteria in the small bowel.
12:01.842 --> 12:09.552
[SPEAKER_01]: which otherwise should be a sterile environment and contrast that with the colon which we discussed earlier is full of bacteria.
12:09.973 --> 12:14.539
[SPEAKER_01]: So the issue is when these bacteria start proliferating in the small intestine where they shouldn't be.
12:15.079 --> 12:29.318
[SPEAKER_01]: The second main takeaway that I'd like to share is that these small that intestinal bacteria can produce a variety of symptoms, but the main ones are due to increased gas
12:29.298 --> 12:47.221
[SPEAKER_01]: and the combination of the increased gas production and the decreased mucosal absorption could lead to the classic symptoms of bloating, abdominis comfort, and diarrhea, which is usually a watery diarrhea due to osmotic diarrhea from the osmolites remaining in the intestine as opposed to me absorbed.
12:47.801 --> 12:53.989
[SPEAKER_01]: But then as we talked about earlier, there are instances where patients will present more with stateria due to fat elabsorption.
12:54.307 --> 13:12.130
[SPEAKER_01]: And my last key takeaway is that the major risk factor for Sivo is altered motility in the GI tract, and that's most commonly due to IBS, but also consider abnormal anatomy, whether that be strictures, or officializing disease, or small intestinal diverticula, or post-surgical, such as Ruin Y, or
13:12.110 --> 13:25.691
[SPEAKER_01]: or loss of illicycle valve, and then also the gastric hypochlorhydria, which basically means a low-assid state, which can be due to long-term PPIUs, or excessive atrophic gastritis, lean to bridal cell death.
13:26.031 --> 13:35.586
[SPEAKER_01]: So those are the main risk factors that I want you to think about when you're seeing patients who you believe may have seabough, because it gives you an sense of why they're presenting with this condition at this time.
13:35.903 --> 13:39.714
[SPEAKER_00]: Thank you, Dr. Kumar, for all your CBO insights into our audience.
13:39.774 --> 13:43.605
[SPEAKER_00]: We hope you enjoyed the first episode of our three part series on CBO.
13:44.066 --> 13:47.617
[SPEAKER_00]: We will be back soon to discuss CBO diagnosis and treatment.
13:48.178 --> 13:48.920
[SPEAKER_01]: Thank you so much, Alie.
13:48.941 --> 13:52.852
[SPEAKER_01]: You were an awesome guest host, and thank you again for helping to resurrect.
13:53.413 --> 14:01.978
[SPEAKER_01]: Our handouts will definitely have one for this episode, and like Alie said, we're looking forward to coming back to discuss the next two episodes on CBO and diagnosis of the treatment.
00:05.262 --> 00:10.670
[SPEAKER_00]: I am Ali Shivie, a current third year medical student, Harvard, and a recent member of the RTL team.
00:11.231 --> 00:22.588
[SPEAKER_00]: Today, we will be talking about small intestinal bacterial overgrowth, also known as CBO, and increasingly discussed and diagnosed condition in the primary care office and gastroenterology clinic.
00:23.189 --> 00:30.780
[SPEAKER_00]: I have with me Dr. Kumar, a gastroenterologist at Brigham and Women's Hospital, and of course one of our fearless leaders of RTL.
00:31.013 --> 00:37.179
[SPEAKER_01]: Thank you so much, Ali, it's so great to be back recording with you, and especially on such a hot topic as Sebo.
00:37.599 --> 00:48.170
[SPEAKER_01]: I also want to thank you for all your outstanding work and bringing back our RTL handouts along with your cold medical student Hannah Shapiro, who is also a third year student at Harvard Medical School.
00:49.091 --> 00:56.498
[SPEAKER_01]: And if I may have the honor as it's been a little bit, so I'd love to say our token line here, let's go ahead and run the list.
00:56.866 --> 00:58.989
[SPEAKER_00]: And as always, let's start with a case.
00:59.630 --> 01:12.668
[SPEAKER_00]: Ms. R is a 45-year-old female with a history of obesity, status posts ruined why gastric bypass, who presents to primary care clinic with two months of worsening bloating, flatulence, and diarrhea.
01:13.209 --> 01:18.036
[SPEAKER_00]: She reports abdominal distension is present upon waking up in worsens after meals.
01:18.676 --> 01:21.140
[SPEAKER_00]: She's concerned that she might have underlying seabough.
01:21.681 --> 01:24.865
[SPEAKER_00]: Dr. Kumar, can you first explain what seabough is?
01:24.997 --> 01:39.129
[SPEAKER_01]: Absolutely, so CBO or small intestinal bacterial overgrowth is a condition in which bacteria proliferate in the small intestine, which at otherwise be a largely sterile environment, where you do not have very much bacteria at all.
01:39.490 --> 01:54.463
[SPEAKER_01]: So we can contrast that with the colon, which is full of bacteria, and think about how, if these bacteria or other species take resonance more proximally in the small intestine, how those bacteria can produce a variety of symptoms for patients dealing with this condition.
01:54.697 --> 01:55.741
[SPEAKER_00]: that totally makes sense.
01:56.162 --> 02:01.602
[SPEAKER_00]: So how does the overgrowth of bacteria cause the symptoms our patient is experiencing?
02:01.717 --> 02:03.540
[SPEAKER_01]: That's an excellent question, Ali.
02:03.620 --> 02:13.414
[SPEAKER_01]: And the way I think about this, when I'm teaching or even when I'm in clinic and talking to my own patients, is that there's three main pathways for bacterial overgrowth of a small intestine to cause symptoms.
02:13.754 --> 02:20.023
[SPEAKER_01]: So the first one is that the small intestinal bacteria that are in this area of the digestive tract where they shouldn't be.
02:20.063 --> 02:30.238
[SPEAKER_01]: End up breaking down the foods and the nutrients from a recently ingested meal, right, because the first thing that happens after the food empties from the stomach is that it gets into the small intestine.
02:30.218 --> 02:36.089
[SPEAKER_01]: And normally, those nutrients would be broken down and completely absorbed in the small intestine.
02:36.209 --> 02:40.537
[SPEAKER_01]: But when there's bacteria there, the bacteria actually break down these nutrients.
02:41.038 --> 02:44.965
[SPEAKER_01]: And in the process of breaking down these products, they release gas.
02:45.325 --> 02:53.340
[SPEAKER_01]: And that gas leads to the classic symptoms of abdominal bloating, cramping, distension, as well as flatulence.
02:53.320 --> 03:00.353
[SPEAKER_01]: So the first mechanism is from the bacteria breaking down the food products and releasing gas.
03:00.894 --> 03:14.299
[SPEAKER_01]: Now the second pathway that I think about is how the small intestinal bacteria, which again are not in the location that they should be, they can actually take up residents right along the
03:14.279 --> 03:18.864
[SPEAKER_01]: and as they line up on the mucosal surfaces, they can interfere with absorption.
03:19.385 --> 03:40.489
[SPEAKER_01]: In these cases, what typically happens is a watery diarrhea ensues because the unabsorbed substances that would have otherwise been absorbed, but instead of remaining in the lumen because they're not getting absorbed, being blocked by this bacteria that are lying to mucosum, those unabsorbed substances draw water into the intestinal tract, ala azimatic diarrhea.
03:40.469 --> 03:52.401
[SPEAKER_01]: So in even more severe cases, you don't only have an osmotic diarrhea, but you can also get stiatoria because it's a small intestinal bacteria actually disrupt the absorption of fats.
03:52.881 --> 04:03.252
[SPEAKER_01]: So some patients would see, though, actually complain more of stiatoria where they see oil droplets in the stool or they have the classic very difficult to flush stool from the toilet bowl of stiatoria.
04:03.272 --> 04:09.598
[SPEAKER_01]: So think about what is happening at the mecoso level in terms of absorption and how that
04:09.578 --> 04:10.679
[SPEAKER_01]: Stateria.
04:11.581 --> 04:26.480
[SPEAKER_01]: And the third pathway, and this is typically only in extreme cases, but these same small intestinal bacteria that are competing for nutrients and potentially interfering with absorption at the level of the mecosa, they can actually lead to vitamin and mineral deficiencies.
04:26.560 --> 04:36.312
[SPEAKER_01]: So what can happen is that these bacteria can absorb B12 for themselves and take that away essentially steal it from the host and cause B12 deficiency.
04:36.292 --> 04:43.523
[SPEAKER_01]: This can also happen with iron deficiency as well, where the bacteria are consuming the iron that was ingested.
04:43.563 --> 04:47.950
[SPEAKER_01]: And instead of the host being able to absorb that iron, the bacteria take it for themselves.
04:48.411 --> 04:55.161
[SPEAKER_01]: And then, inversely, it's an interesting phenomenon, as some of these bacteria actually produce folate.
04:55.141 --> 05:00.569
[SPEAKER_01]: And so they can raise the levels of folate above assay when measured from the blood.
05:00.910 --> 05:13.690
[SPEAKER_01]: So a little pearl to share is that if you have a patient who has clinical signs or symptoms of seabull, let's say they have the abdominal gas to mention in diarrhea, you may also see this hallmark sign
05:13.670 --> 05:25.605
[SPEAKER_01]: on labs where they have B12 deficiency because the CBO is stealing the B12 from the host and then high folate levels often greater than assay because they are producing folate.
05:25.625 --> 05:33.516
[SPEAKER_01]: So I always, if the patients happen to have had recent and email labs with a B12 in folate, I look to look at those because it fits that pattern.
05:33.996 --> 05:39.964
[SPEAKER_01]: Low B12, high folate, I'm thinking, okay, my index is suspicion for this being CBO is even higher.
05:39.944 --> 05:41.568
[SPEAKER_00]: that's a great pearl.
05:41.929 --> 05:55.725
[SPEAKER_00]: So now that we understand the pathophysiology explaining why the concentration of symptoms of sebo occurs, who actually gets sebo and are there any risk factors for developing this disease?
05:55.705 --> 05:56.667
[SPEAKER_01]: Yes, for sure.
05:56.687 --> 06:03.278
[SPEAKER_01]: So the overarching theme, as with any proliferation of bacteria in any part of the body, is altered motility.
06:03.899 --> 06:09.930
[SPEAKER_01]: So the most common cause of altered GI motility, as we all know, is IBS or Errol Balsendrum.
06:10.531 --> 06:14.177
[SPEAKER_01]: And that's why there's such a significant overlap between IBS and SIBO.
06:14.698 --> 06:20.869
[SPEAKER_01]: Actually, recent data and literature shows that up to a third of patients who have IBS,
06:20.849 --> 06:24.634
[SPEAKER_01]: also had SIBO based on data obtained from those patients.
06:25.035 --> 06:33.747
[SPEAKER_01]: So there's a very high overlap between IBS and SIBO, and that's largely driven by the altered GI motility that is characteristic of IBS.
06:34.127 --> 06:50.350
[SPEAKER_01]: There are also other diseases that affect gut motility that we should also consider in patients who are at risk for SIBO, and that includes conditions such as diabetes, mellitus, radiation
06:50.330 --> 07:02.425
[SPEAKER_01]: That's a bigger box and some are more common than others, but it's always important to just consider what is the underlying motility of my patients digests of tract and does that put them at risk for sebo.
07:02.806 --> 07:03.787
[SPEAKER_00]: That makes sense.
07:03.807 --> 07:05.990
[SPEAKER_00]: It peristelsus is not consistent.
07:06.190 --> 07:11.617
[SPEAKER_00]: This provides an excellent environment for bacteria to stay in one place and replicate.
07:11.697 --> 07:12.658
[SPEAKER_01]: Right exactly.
07:12.899 --> 07:19.527
[SPEAKER_01]: And then stasis can occur not just because of altered motility, but also due to anatomical variation.
07:19.507 --> 07:25.013
[SPEAKER_01]: And that's true for the patient that you described, this M, who has a history of a ruin-wide gastric bypass.
07:25.453 --> 07:33.001
[SPEAKER_01]: And so with the ruin-wide gastric bypass, there is this formation of a blind pouch within the newly altered GI tract.
07:33.281 --> 07:39.728
[SPEAKER_01]: And within that blind pouch, there is stasis and hence an increased risk for bacteria to proliferate in that area.
07:40.309 --> 07:44.613
[SPEAKER_01]: Another example would be stasis due to an illule structure in Crohn's disease.
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[SPEAKER_01]: We already mentioned Crohn's disease as a
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[SPEAKER_01]: But also, if there is a narrowing, stool is not going to travel through that area as readily, and so that decrease in motility and also just stasis from hanging above the structure can lead to increased risk for seabull.
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[SPEAKER_01]: Another common, actually fairly common cause that I found in my patients is identifying a small ball of diverticula.
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[SPEAKER_01]: We think about diverticula is primarily in a large intestine, but it can also be present in the small intestine.
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[SPEAKER_01]: And you can imagine if there's an outpouching in the small intestine that almost shields is shielded from the natural transit through the lumen, bacteria can proliferate in that little outpouching within the small intestine, so the bacteria like to hang out there as well.
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[SPEAKER_01]: So, we talked mainly about stasis in this segment, but the other anatomical variants to consider our fishulas, so think about fishulizing Crohn's disease, where you're connecting the large intestine to the small intestine and how bacteria can move retrograde from the large to the small intestine via the fishula.
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[SPEAKER_01]: Or also, many patients who have had surgery such as a right-hemi-collectomy, they will lose the Iliocicle valve that otherwise prevents back flow or reflux of calonic contents into the small intestine, so loss of that valve will allow bacteria to directly flow upwards from the large intestine to the small intestine and cause sebo in those patients.
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[SPEAKER_00]: great review of other comorbidities we should be thinking about when Cibo is on the differential.
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[SPEAKER_00]: I've also heard about there being a risk of Cibo when there is long-term PPI use.
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[SPEAKER_00]: What is the mechanism behind this relationship?
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[SPEAKER_01]: Right, so as you can imagine, Stomach asks is one of the GI defenses against bacterial growth that the lower pH is actually an environment in which bacteria do not grow well in.
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[SPEAKER_01]: And so when patients are put on long-term PPI, the reduction in stomach acid impairs this host defense and allows bacteria to grow more proxmoly in the small intestine.
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[SPEAKER_01]: So it's important to think about Cibo and your patients who are on long-term PPI and coming to you with symptoms like bloating or diarrhea.
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[SPEAKER_01]: And then also it can occur outside of PPIUs in patients who have extensive atrophic gastritis where they've lost or damaged many of their pridal cells from an autoimmune process.
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[SPEAKER_01]: The lack of pridal cells producing acid will lead to this again low acid state that can put them at risk for bacterial overgrowth.
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[SPEAKER_00]: So to review, we've identified altered GI motility, altered anatomy, and low stomach acid production, as causes for SIBO.
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[SPEAKER_00]: Are there any other categories we should be considering?
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[SPEAKER_01]: Yes, there are two more risk factors for SIBO that we should generally be aware of.
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[SPEAKER_01]: The first big bucket is anyone with immunodeficiency.
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[SPEAKER_01]: So things we think about here, our patients with CV, ID, or common variable immune deficiency, IGA deficiency,
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[SPEAKER_01]: or HIV or AIDS, just the general risk factor of being a amino deficient will of course put these patients at higher risk for any type of bacterial proliferation and that includes that bacterial proliferation within the small intestine.
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[SPEAKER_01]: The second category includes patients who have altered bile or digestive enzyme composition.
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[SPEAKER_01]: So the main disorder is that we think about in this category, our patients with cirrhosis, as well as patients with chronic pancreatitis.
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[SPEAKER_01]: Both of these patient categories cirrhosis and chronic pancreatitis have this issue with altered bile digestive enzyme composition, which can lead to the proliferation of bacteria in the small intestine.
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[SPEAKER_00]: fantastic.
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[SPEAKER_00]: We covered a lot today in terms of understanding why CBO happens, why patients present with the symptoms they do, and who might be at risk.
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[SPEAKER_00]: Before we go, can you summarize the most important takeaways for our listeners?
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[SPEAKER_01]: Yes, absolutely.
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[SPEAKER_01]: Let's do three key takeaways here.
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[SPEAKER_01]: So the first key takeaway is just understanding that CBO or small intestinal bacterial overgrowth is due to a pathological increase in the amount of bacteria in the small bowel.
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[SPEAKER_01]: which otherwise should be a sterile environment and contrast that with the colon which we discussed earlier is full of bacteria.
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[SPEAKER_01]: So the issue is when these bacteria start proliferating in the small intestine where they shouldn't be.
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[SPEAKER_01]: The second main takeaway that I'd like to share is that these small that intestinal bacteria can produce a variety of symptoms, but the main ones are due to increased gas
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[SPEAKER_01]: and the combination of the increased gas production and the decreased mucosal absorption could lead to the classic symptoms of bloating, abdominis comfort, and diarrhea, which is usually a watery diarrhea due to osmotic diarrhea from the osmolites remaining in the intestine as opposed to me absorbed.
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[SPEAKER_01]: But then as we talked about earlier, there are instances where patients will present more with stateria due to fat elabsorption.
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[SPEAKER_01]: And my last key takeaway is that the major risk factor for Sivo is altered motility in the GI tract, and that's most commonly due to IBS, but also consider abnormal anatomy, whether that be strictures, or officializing disease, or small intestinal diverticula, or post-surgical, such as Ruin Y, or
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[SPEAKER_01]: or loss of illicycle valve, and then also the gastric hypochlorhydria, which basically means a low-assid state, which can be due to long-term PPIUs, or excessive atrophic gastritis, lean to bridal cell death.
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[SPEAKER_01]: So those are the main risk factors that I want you to think about when you're seeing patients who you believe may have seabough, because it gives you an sense of why they're presenting with this condition at this time.
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[SPEAKER_00]: Thank you, Dr. Kumar, for all your CBO insights into our audience.
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[SPEAKER_00]: We hope you enjoyed the first episode of our three part series on CBO.
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[SPEAKER_00]: We will be back soon to discuss CBO diagnosis and treatment.
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[SPEAKER_01]: Thank you so much, Alie.
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[SPEAKER_01]: You were an awesome guest host, and thank you again for helping to resurrect.
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[SPEAKER_01]: Our handouts will definitely have one for this episode, and like Alie said, we're looking forward to coming back to discuss the next two episodes on CBO and diagnosis of the treatment.