In this episode of Dr. Ruscio Radio, the doc and Susan discuss how stress can negatively impact your microbiota and what to do about it.
If you need help with stress or your microbiota, please click here
Dr. R’s Fast Facts
- Stress has been shown to cause:
- Leaky gut
- Enhanced gut immunity, short term
- Decreased gut immunity, aka immunosuppression, long term – which correlates with increased risk of infection
- Decreased intestinal mucous membrane which is likely why stress causes the decreased immunity and leaky gut mentioned above
- Decreased blood flow to the intestinal tract
- Suppression of stomach acid secretion
- Slowing of stomach and small intestinal motility
- A real life example of how this plays out… chronic stress causes adrenal fatigue and SIBO
- Stress can worsen IBS and IBD
- Stress can negatively affect the gut microbiota and can be pro-inflammatory; these changes can then be corrected by antibiotics
- Bacteria in the gut help prevent over activation of the HPA axis, and human clinical trials show probiotics can decrease stress hormones and improve mood
- Probiotic bacteria help stimulate GI motility, which might be why they help with SIBO
Obesity and the microbiota…..4:10
Negative impacts of stress on the gut…..8:35
Real world example – Sue…..10:57
Microbiota stress piece…..15:33
Probiotics and SIBO…..25:02
Diet and lifestyle solutions…..32:25
What to do when diet and lifestyle changes do not work…..36:33
Susan’s IBD/parasite story…..37:46
(4:10) “This suggests that in humans the changes in gut microbiota are an association with rather than the cause of obesity.” http://www.ncbi.nlm.nih.gov/pubmed/26474235
IBS is estimated to effect 15% of the United States population, http://www.ncbi.nlm.nih.gov/pubmed/1889716 and 11% of the world http://www.ncbi.nlm.nih.gov/pubmed/24523597. However, 75% of IBS may go undiagnosed because patients with IBS do not see their doctor for a diagnosis. This means the actual percentage of people with IBS might be much, much higher. http://www.ncbi.nlm.nih.gov/pubmed/10983480
How does stress factor into this? It has been well documented that stress does make IBS worse http://www.ncbi.nlm.nih.gov/pubmed/25339801. And we just detailed Sue’s case wherein stress, caused SIBO which then manifests as IBS. So Sue’s case can be quite common.
More on stress and your microbiota
(15:49) Stress has been documented to worsen irritable bowel syndrome and inflammatory bowel disease. http://www.ncbi.nlm.nih.gov/pubmed/20372115 / http://www.ncbi.nlm.nih.gov/pubmed/25339801
Stress has also been shown to cause us to make poor food choices http://www.ncbi.nlm.nih.gov/pubmed/24123563, craving food both high in fat and carbs.
(16:49) College students have decreased levels of lactobacilli during periods of exam stress when compared to their non-stressed peers. http://www.ncbi.nlm.nih.gov/pubmed/18023961. These findings have been affirmed by other researchers also, http://www.ncbi.nlm.nih.gov/pubmed/24997038
(18:55) When mice were exposed to just two hours of social stress, their microbiota shifted, including a reduction in lactobacilli. http://www.ncbi.nlm.nih.gov/pubmed/25028050
(19:08) The stress hormones released, as part of stress, might be a key reason for the negative effects from stress. It has also been shown that injection stress hormones can fuel the growth of potentially dangerous bacteria in the gut.
http://www.ncbi.nlm.nih.gov/pubmed/10497953 / http://www.ncbi.nlm.nih.gov/pubmed/19884332
(19:37) Stress, motility and an inflammatory microbiota?
After exposure to social stress mice experience a shift in their microbiota that increased inflammation. If these mice where then exposed to stress again, more inflammation occurred. However, if these mice were treated with antibiotics before being exposed to stress again, no inflammation! http://www.ncbi.nlm.nih.gov/pubmed/21040780
Similar findings have been document by others. http://www.ncbi.nlm.nih.gov/pubmed/23236381
(22:43) So do we want no bacteria?
Mice that have no bacteria in their guts (known as germfree mice) have been shown to be more sensitive to stress; specifically their HPA axis responds more to stress than normal mice. http://www.ncbi.nlm.nih.gov/pubmed/15133062
(23:57) Bacterial stress relief
We discussed how mice with no bacteria in their guts (aka germfree mice) are more sensitive to stress. Does this mean probiotics might be able to help with stress? Yes! Randomized control trials have found probiotics can alleviate depression, anger, hostility and anxiety, while also decreasing stress hormone levels. http://www.ncbi.nlm.nih.gov/pubmed/20974015 /http://www.ncbi.nlm.nih.gov/pubmed/25862297 /http://www.ncbi.nlm.nih.gov/pubmed/21983070
- (29:52) Germfree mice do not have healthy intestinal motility but when we add bacteria back into the guts of these mice we see their motility improve. http://www.ncbi.nlm.nih.gov/pubmed/2752868
- (30:21) LPS, bind to receptors known as toll-like receptors, which then stimulate the nerves of your gut to keep things moving. http://www.ncbi.nlm.nih.gov/pubmed/22732731. It’s almost as if bacteria flip the switch in your gut to keep things moving. http://www.ncbi.nlm.nih.gov/pubmed/7926490
(34:23) Stress and lifestyle
Dan Buettner wrote a book entitled Thrive: Finding Happiness the Blue Zones Way:
You shouldn’t sacrifice your friends, hobbies and time in nature to research health because these are proven tools that will improve your health and well-being. I know it’s tough, I’ve been there – but don’t lose your grip on these important fundamentals of good health. To say it simply make sure you don’t neglect the life you’re trying to improve by becoming healthier.
“Don’t make yourself miserable in attempts to be healthy.”
Something to consider – Is a healthy person with a neglected life any better off than an ill person with a rich and fulfilling life? Chris Kresser and I recently recorder a podcast where we discussed this, the audio with transcript is available here
Right click on link and ‘Save As’
Stress and Your Microbiota
Welcome to Dr. Ruscio Radio, discussing the cutting edge in health, nutrition, and functional medicine. To make sure you’re up to date on this and other important topics, visit DrRuscio.com and sign up to receive weekly updates. That’s D-R-R-U-S-C-I-O.com.
The following discussion is for educational purposes only and is not intended to diagnose or treat any disease. Please do not apply any of this information without first speaking with your doctor.
Now, let’s head to the show!
Dr. Michael Ruscio: Hey, everyone. I just wanted to give you your fast facts for today’s episode on stress and the microbiota.
Stress has been shown to cause leaky gut (1), in the short term, enhanced gut immunity (1), and in the long term, suppressed gut immunity, which also correlates with an increased risk of infection (1). Stress has also been shown to cause a decrease in the intestinal mucous membrane (1), decreased bloodflow to the intestinal tract, suppression of stomach acid (1), and slowing of stomach and small intestinal motility (1).
We go through a real-world example of how this plays out using a case named Susan where chronic stress then tips her into having SIBO and adrenal fatigue.
Stress has been documented to worsen the symptoms associated with IBS and also to worsen IBD, or inflammatory bowel disease.
Stress has been shown to decrease lactobacillus species in the gut in both human and animal models.
And in animal studies, we review a couple of fascinating ones that show that stress can induce a proinflammatory shift in the microbiota, and then antibiotics can actually undo this proinflammatory shift in the microbiota. There’s a little more context that we go through in the episode, but that’s essentially the piece there.
Bacteria in the gut help prevent overactivation of the HPA axis, or bacteria in the gut help you handle stress better, if you will. And maybe even more importantly, human clinical trials have shown probiotics can decrease stress hormone levels and also improve mood.
We also cite some very interesting animal data mechanisms that show that probiotics help stimulate gastrointestinal motility, or the migratory motor complex, which might be why probiotics help with SIBO.
That’s it. We’ll now jump into the show.
DR: Hey, folks. Welcome to Dr. Ruscio Radio. This is Dr. Ruscio. I am with here with the lovely Susan McCauley. Hey, Susan.
Susan McCauley: Hey, Dr. R. What’s going on?
DR: Not a whole lot. Just plugging away on the microbiota eBook, which has pretty much become my life lately, and so I wanted to talk about stress and stress’ impact on the microbiota today, so I thought we could jump in and do that.
SM: Stress is one of my all-time favorite topics because what I tell people is that everything else could be perfect—you could be eating the most cleanest diet ever, you could be sleeping, you could be working out—but if you’re stressed out, it’s going to cancel everything out.
DR: Yeah, I think you’re 100 percent correct. And with the microbiota, it’s certainly very exciting, and I think we’re going to see some new probiotics and some new testing and maybe even a few new novel and, hopefully, safe drugs being developed from all the microbiota research that is occurring right now. But I think if we look at the literature with a discerning eye, we see that a whole heck of a lot of microbiota improvements can happen if you just address diet and lifestyle factors. So let’s definitely give a good rundown on stress and the microbiota.
Obesity and the microbiota
DR: But before we do that, I just quickly wanted to highlight a study that I put out a few days ago on my Facebook page. It’ll also go out on our Friday edition of one of the upcoming newsletters where I go through the research highlights, but this was a study that… it was a review paper, and you know my thoughts on review papers. I’m a huge advocate of review papers because I think looking at review papers, either systemic reviews or systemic reviews with meta-analyses, help prevent us from being misled because one study could be a little off the mark. It could have a poor design or a poor selection process or just have been an outlier, and so we can be misled by one study, but looking at reviews gives us a better aggregate opinion on what the data at large show.
So there was a review paper published that essentially concluded that the changes seen in the microbiota are an association rather than the cause of obesity (1). In the eBook, essentially you’ll read about one page and you’ll get an overview on what we know about obesity and the microbiota very concisely, but I think this study really encapsulates that nicely, and, of course, it being a review, that’s kind of what review papers are supposed to do anyway. They’re supposed to examine the existing evidence and give you a short synopsis on that. So this paper is firming up what I’m starting to believe, which is with obesity, to a large extent, a lot of the changes that we see in the microbiota are reactive to the obesity state itself rather than causing the obesity state. And we see some of this with some of the clinical trials where we use fecal transplant therapy in things like overweight, metabolic syndrome, and type 2 diabetes, and the results there have been very dismal. There’s only really been one paper looking at metabolic syndrome and type 2 diabetes, and the results there were you could have a better result by taking berberine for two weeks than you could by doing an FMT for your diabetes.
I hate to burst a bubble here, but I just want to give people the truth on how strongly causal the microbiota might be in driving obesity. It doesn’t mean that we don’t have treatments for obesity, and it doesn’t mean that there are not favorable ways we can modulate the gut to help with weight loss, but I think it’s important that people understand what the research is really showing rather than getting swept up into all the excitement about the microbiota and then turning every condition into a potential treatment through the microbiota.
SM: Right. We’re kind of narrowing it down what comes first, the chicken or the egg. It’s like the obesity comes first, and that probably causes the changes to the microbiome.
DR: Right, and I think that’s what we’re seeing.
SM: And it makes so much more sense.
DR: Exactly. Just quickly, and then I want to get on to the stress piece, but the animal data really seem to show this type of association, but as you’ve heard me say and people have heard me harp on, we can’t put all of our eggs in the animal basket, because what happens in an animal model may not really be viable in a human model.
With that, let’s transition now to stress because toward the end of this dialogue about stress and the microbiota, there are a few animal studies I want to talk about, and I just want to make the note now that while, yes, I certainly prefer human studies, sometimes we can’t do stuff to humans ethically, so it’s interesting to be able to see if we expose rats to stress what happens to their microbiota. Sometimes these things really can’t be ethically done to humans, but we can garner some mechanisms from animal data—and this is a really important point—then cross-reference that with human interventional studies and see if we can start to firm up a clinical recommendation.
And I apologize if people can hear a leaf blower in the background. It is the bane of my existence, leaf blowers. I can hear it. It’s driving me crazy. Hopefully people can’t hear it too bad.
SM: It’s funny. You used to hear a lot of lawnmowers in my neighborhood, not so much anymore with the drought.
DR: Right, yeah. That’s the one good thing about the drought, I guess.
SM: Yeah, and only leaf blowers are left.
SM: So on to stress!
Negative impacts of stress on the gut
DR: There are a number of negative impacts stress can have on the gut, and I’m sure people have heard some of these to a greater or lesser extent—and we’ll put a list of these in the transcript along with supporting references—but stress can cause leaky gut (1). Stress can cause enhanced gut immunity in the short term (1) but decreased gut immunity in the long term (1). So long-term stress can cause immunosuppression. Short-term stress seems to upregulate the immune system, which kind of makes sense from an evolutionary perspective.
SM: Oh, total sense, because when we have some acute stressor, we need to upregulate our immune system to combat that, but when it’s over a long period of time, we’re just not evolved for that.
DR: Exactly. We also see a decreased intestinal mucous membrane, or decrease in the thickness of the intestinal mucous membrane (1), which is probably why we see the decreased immunity and the leaky gut that we mentioned previously. Part of the mechanism for that is probably the decreased mucosal membrane that’s associated with long-term stress. We see decreased bloodflow to the gut. We also see suppression in stomach acid secretion (1), so you secrete less hydrochloric acid, and we see slowing of stomach and small intestinal motility (1).
That’s not an exhaustive list, but certainly we know that through multiple parameters prolonged stress is going to have a negative effect on your gut.
SM: And that’s evolutionary as well, is that our bodies are geared for acute stress, and so all of our resources are going to combat that acute stress. That’s why we don’t digest food as fast. All the energy for hormone production and reproduction—all that gets put aside to take care of the acute stressor.
DR: Right. It’s kind of like the concept of the pregnenolone steal, where your body starts to divert adrenal hormone precursors toward stress hormone production instead of toward steroid hormone production, like testosterone, estrogen, and progesterone. Exactly.
DR: Because those hormones, the stress hormones, are more important for short-term survival, and of course, survival takes precedence over procreation.
SM: Over everything!
DR: Right, yeah.
Real-world example – Sue
DR: So just to kind of tie together some of those examples, let’s walk through a real-world example.
Let’s say we have Sue, and Sue is in her early 30s. She’s been living kind of a high-stress lifestyle for a while. She just finished her master’s degree. Right on the heels of that, she got married and they decided to move to the suburbs, so now she has a longer commute to work. She still wants to be able to exercise, she still wants to be able to spend time with her husband, but she’s finding it very challenging to do all of that—to keep up her six-days-a-week exercise routine, spend time with her husband, decorate the house and do all those things—in addition to her commute. So she starts sleeping a little bit less. She shaves about an hour or so off of her sleep to fit everything in. And she doesn’t realize this, but she’s now put her body under more stress than it can tolerate, so she starts to notice she’s not sleeping as well. She’s tossing and turning. She’s waking up 45 minutes before her alarm goes off, unable to fall back to sleep. She’s tired during the day. She starts noticing that she’s having some chronic muscle pulls and joint pain. And then a few months later, she starts noticing she’s having some bloating, and she’s not going to the bathroom every day.
What’s happening is the additional stress of the commute combined with less sleep is now putting her body, again, into a stress response, into a chronic stress response. She went over her acceptable stress load, and now these things—like exercise that could be beneficial—are now actually being detrimental. And what’s happening underneath the surface there is she’s going into adrenal fatigue, and that adrenal fatigue is causing her to have low blood sugar at night. That low blood sugar at night is causing her not to be able to sleep well, and it’s also causing her to be tired during the day and may also cause her to have cravings. And that stress is also suppressing stomach acid production and motility, both of which open the door wide open for SIBO, so she starts having bacterial overgrowth. The immune system is somewhat suppressed, not able to clean out the bacterial overgrowth in addition to the lack of acid and the lack of motility, so now she forms SIBO and adrenal fatigue.
And what I would add onto this—because this is what I typically see in the clinic—is Sue reads an article that makes her think that she has adrenal fatigue and that really resonates with her, and she is impressed by the concept of HPA axis dysfunction and starts taking some herbal supplements to help reconnect her HPA axis or fix her HPA axis. And that works well for a couple of months, and then a few months later, she’s back to square one, not really sure what to do.
That’s how these things play out in the real world, and the real solution to Sue’s problem is, A, the proper diagnosis and treatment of SIBO in conjunction with rebalancing her life so as not to put her in a chronic stress response.
SM: Because the SIBO will just come back. You can treat the SIBO, but if you don’t fix everything else, you still have all the negative impact of the gut.
DR: Exactly. And the adrenal fatigue will come back.
DR: She can certainly use adrenal supplements to help support this process and to help support her system back to a little more vitality, but a really common mistake I see people making is thinking that the problem is the adrenals, and the problem is never the adrenals unless you have adrenal disease, like Addison’s or Cushing’s. So, for me, we support the adrenals, but we don’t get sidetracked in diagnosing an adrenal problem because it’s not the cause of the problem. Right?
SM: Right, exactly. For me, I’ve been diagnosed with adrenal fatigue or HPA axis dysfunction, and the things that helped me the most weren’t the supplements. The things that helped me the most were adding meditation in, making sure my sleep was good, walking every day. Those were the things where I saw the most dramatic improvement.
DR: Exactly, which really reaffirms what I’ve been finding in the clinic over the past couple of years. I haven’t done an adrenal test on a patient in over a year and a half now, and the results I’ve gotten are probably better than they were a year and a half ago because we’re focusing more on the underlying cause of the problem, and that really takes all the pressure off the adrenals.
Microbiota stress piece
DR: Let’s come back to the microbiota stress piece because now we’ve laid out some of the mechanisms, we’ve laid out how this might look in the real world, but I want to give a little more context and kind of sharpen the picture of stress and the microbiota.
Stress has been documented to worsen the symptoms in both IBS and inflammatory bowel disease (1) (1). We certainly see from a very practical standpoint, all this mechanistic stuff aside, that when people are under stress, it makes the SIBO worse and it makes the IBD worse, and that goes back to the point you just brought up, Susan, which is if you don’t treat the underlying lifestyle imbalance, then these things are going to come back.
SM: Right. And I have IBD, so I will second you on that one. If I let my stress get out of control, my digestion and everything, my gut is a mess. I have to be really careful or I’ll flare.
DR: Right. So what might be happening underneath the surface that contributes to some of this on a more microbiotal level? Well, we don’t have a lot of human data here, but we do have a couple of human studies and then some fascinating animal data.
We have observed that college students have decreased levels of lactobacillus species during periods of exam stress when compared to their non-stressed peers. One of the things that we see—at least according to this study, and it’s a human observational study, of course—but we see that stress decreases lactobacillus, and this has been found in two research studies (1) (2), and I’ll put the links in the transcript. Now, when we look at that in the context of how some of the most successful probiotic supplement trials or interventional trials have been with multistrain probiotics, oftentimes that have many strains of lactobacillus in them, we see, OK, people that have stress have decreased lactobacillus, and when we take people that have IBS or IBD or other gut problems or symptoms or conditions and we supplement them with a probiotic that has lactobacillus, they show a favorable response. So that really paints a nice picture for the stress-microbiotal kind of connection, right, Susan?
SM: Totally, yes.
DR: OK. Now, what might be happening? Is there other stuff that we know from the literature in terms of what happens? And this is where some of the animal data comes in because what we can do with animals is… we can be kind of cruel to animals, I guess, that’s how to put it.
SM: Yeah, unfortunately, in the name of science.
DR: Right. And not all these studies are cruel. Sometimes mice are put in water, and mice can swim, but they’re put in a situation where they have to float and swim and evade drowning, which is stressful.
DR: Or there are conditions where they call it “social stress,” where they put mice or rats in cramped, kind of uncomfortable living environments for a mouse or for a rat, and this is what they would term “social stress.” So we have noticed that just two hours of social stress in a mouse model can induce also a reduction in lactobacillus in the mouse gut (1). And other researchers have found that the stress hormones, specifically, may be somewhat pronounced in this effect, where they have injected stress hormones into either mice or rats, and they’ve seen potentially dangerous strains of bacteria start to grow in the gut after doing that (1) (2). So we certainly see that there is a stress and a stress hormone connection to the microbiota.
Here’s where things get really interesting. In another mouse model of social stress, the researchers, while tracking the microbiotas, noticed that after social stress, the mouse gut microbiota shifted in such a way that made it more proinflammatory. So the stress induced a proinflammatory or inflammatory microbiota, if you will. Now, they gave the mice a little time to unwind or de-stress, if you will, and then they exposed them to the stressor again, and they noticed again a shift in the microbiota, an inflammatory release. However, if they treated the mice with antibiotics before that second round of stress, they did not see that same inflammatory response (1).
SM: What type of antibiotics? Did the study state? Like, was it a broad spectrum?
DR: That’s a great question. I didn’t dig that deeply into the specific antibiotic used.
DR: I don’t know how translatable the antibiotic from the mouse to a human would be, but more so what I’m after here is—and what I found more novel here—was that this validates a concept that many of us in functional medicine have seen for a while, which is that interventions that—to use a term that I picked up from Robb Wolf which I like—“prune” the microbiota may really help those with gut imbalances. This may include low carb, low FODMAP. It may include herbal antimicrobials, or in select cases, targeted antibiotics, like for SIBO, rifaximin or potentially rifaximin and neomycin.
So you’re starting to see some validation of a concept that we’re already noticing works very well in humans. That’s why I think this is so important, because we see a potential mechanism for why doing these things in humans might work so well. (1)
SM: Right, and it’s not like we’re saying all antibiotics are great and everybody should go out and take antibiotics, but it’s just in this specific model showing that by pruning the microbiota, the next time the stressor is induced, they’re not there to overgrow, and the inflammatory ones don’t take over.
DR: Right, and certainly, if all we had was that mouse model study, I would not be making a clinical recommendation based upon that, but when we look at that relative to the fact that many people in the SIBO community or many functional medicine providers that are fairly savvy with gut health are going to be diagnosing overgrowths or infections or dysbiosis and treating that and we see really favorable patient responses to that, now we can really firm up that recommendation and make it responsibly, absolutely.
But this does beg the question, do we want no bacteria in our gut? Right? Because I always try to cater to the person that is going to have the little-is-good, more-is-best sort of mentality. So what if you’re saying, “Well, would no bacteria be preferential?” And we do have animal data that looks at this. We can breed mice in what’s known as “germ-free conditions,” where we can essentially breed a mouse that had a sterile or a bacteria-free intestine.
SM: Right. We talked about that in the sleep podcast.
DR: Right, exactly. Now, when we do this, we notice that mice with no intestinal bacteria respond much more negatively to stress through their HPA axis than normal mice (1). So it seems that somehow the bacteria in the gut—at least according to this mouse model—helps prevent excessive HPA axis response to stress, and I want to tie that back in with some human interventional trials because it’s important that we don’t just speculate and overreach from animal data, but we have some human data to kind of help us fill in these gaps and make a clinical recommendation in a little bit more confidence.
We do have a handful of randomized controlled trials that have found that probiotics can alleviate depression, anger, hostility, and anxiety while also decreasing stress hormone levels (1) (2) (3). We see an interesting mechanism in the animal models, and then we see human randomized controlled trials supplementing with probiotics, and we see these things have a positive impact on stress hormone levels and a positive impact on things like depression, anger, hostility, and anxiety.
SM: And that makes sense when you’re talking about neurotransmitter production in the gut, especially serotonin, and the health of your gut.
DR: Exactly. Absolutely. I guess it just comes back to this concept of balance, where we don’t want to have no bacteria, but we also don’t want to have bacterial overgrowth.
SM: It’s like Goldilocks and the Three Bears.
DR: Exactly. We have to find that just-right!
Probiotics and SIBO
DR: Now, there’s one more point I wanted to mention, and this, I think, may help some people who are looking at or concerned about SIBO and still not sure what to do with the conflicting data as to whether to use a probiotic with SIBO or to not use a probiotic with SIBO.
I was actually on the phone with Dr. Allison Siebecker the other day. We were just kind of catching up on some things, and this is an issue that we discussed in trying to kind of reconcile what we think about probiotics and SIBO. And we were both actually in agreement that in our SIBO patients that we use probiotics, we both see roughly a 30 percent improvement from the probiotics. And there have been a number of studies showing that probiotics as a stand-alone treatment help with the eradication of SIBO. So we have published literature to firm up this recommendation, and then we also have our clinical reflections with patients, and we’ve estimated about 30 percent, so I don’t think a probiotic is going to fix the whole SIBO problem, but it’s going to be one of a couple of different therapies that we can use in combination to really have a successful outcome.
SM: Now, is there as specific probiotic that you guys were talking about? A specific strain or a combination of strains?
DR: There have been lactobacillus species used, there have been bifidobacterium species used, and there have even been bacillus or spore-forming or soil-based, as they’re also known, probiotics used, so there have been different bacterial classes used. They have all shown success.
The best success has been with the more classical lactobacillus and bifidobacterium strains, so your lactic acid-forming bacteria. And I know a lot of people have shied away from those after there’s been some of this question of high lactic acid levels and people in SIBO having high lactic acid, and I do not agree with that at all. This is after I spent several weeks reviewing all the literature on what’s called D-lactic acidosis, where we see high D-lactate levels. And while it is true that lactic acid bacteria, like lactobacillus and bifidobacterium, can produce lactic acid, adults have a very robust ability to clear D-lactate from the system. Infants and young children do not, and I’m actually in the process of drawing up a case series with an autistic infant in my clinic whose mother was a GAPS-trained practitioner and had the child on a very high amount of fermented foods and a very high amount of probiotics, and this child came back with elevated D-lactate and also had SIBO. So it made a very large difference in this child’s case because children have an impaired ability to clear D-lactate. However, adults don’t seem to have this problem, and even when I’ve seen high D-lactate on lab values, I haven’t seen patients respond favorably from taking out the lactic acid-forming probiotics. I question a certain lab’s D-lactate levels. I’m going to look into some of their methods, and I’m cross-checking the D-lactate with LabCorp and Quest to kind of firm up the legitimacy of that, but without getting too far afield, the lactic acid bacteria have shown the best results clinically, in the clinical studies, in treatment of SIBO, and I do not think D-lactic acidosis, or high D-lactate, is something that adult populations have to worry about because it’s been very well documented that they have a robust ability to clear D-lactate from the system. I’m open to a one-in-a-million exception to that rule, but—
SM: There’s always one of those!
DR: Yeah. But I think as a general rule, they’re going to be fine for people, and we see some good clinical evidence showing that they can be very helpful for people with SIBO.
Now, there’s one other thing I want to mention, though. I believe we’ve talked about the concept of probiotics potentially kind of crowding out SIBO, right? So you have bacteria fighting with bacteria, and there may not be enough resources for the SIBO because the probiotics are competing for resources with the SIBO. That’s one mechanism. It’s a theorized mechanism. I haven’t seen a tremendous amount of definitive data firming that up, but we do have from an animal study some other data that shows another mechanism through which probiotics may help in the treatment of SIBO.
There’s one or two things you have to link together for this. First of all, when we look at germ-free mice again—again, mice with no bacteria in their intestines—they have very impaired motility. Their migratory motor complex, or their intestinal motility, is very poor. When we reinoculate these mice with bacteria, their motility improves (1), and we’ll put the reference for that in the transcript.
Now, as researchers have looked at this further, they have found what may happen is the LPS—lipopolysaccharide; it’s a fraction of bacteria cell walls or cell membranes—these bind to certain receptors in the gut known as toll-like receptors, specifically toll-like receptors 4, and this actually stimulates the nervous system in the gut, or the enteric nervous system, to keep things moving or stimulates the migratory motor complex (1), so it’s almost like bacteria or bacterial fragments can help flip the switch in your gut to help keep things moving (1). So to summate that, bacteria, probiotics have a positive effect on the migratory motor complex.
SM: Right, and it makes sense that we’ve evolved for millennia with bacteria in our guts, that not having any bacteria at all—like you said, having the clean mice—that doesn’t make evolutionary sense.
DR: Right, it doesn’t. And also, if you think about it, we know that the gut wants to keep itself clean to some extent, right? The gut has the migratory motor complex as a method of performing housekeeping or sweeping, if you will, and if one of the things that’s being swept is bacteria, then it would make sense that high bacteria load would stimulate that sweeping, right?
DR: It’s almost like you have your trash can in your house. If the trash can gets full, that sends the signal to take out the trash. I think that’s very interesting that we’re seeing a highly specific mechanism. It’s also interesting to speculate or just to reframe LPS because I know lipopolysaccharide has been villainized in some circles, but remember that all these things have a time and a place in terms of what they do and how they signal and how they kind of help with overall health. LPS, even though it may be villainized in certain aspects, seems to really have some positive effects on the gut, specifically gut motility.
Are you with me on that, Susan?
DR: All right. I was afraid I maybe put you to sleep.
Diet and lifestyle solutions
SM: No! I was circling back to Sue because, you know, we talked about Sue’s life. So what are some real-world tips that we can give people? Now everybody’s on board. They know that stress is bad for their microbiota, their gut, their overall health, mental health. We’ve given them example after example, but what do you do?
DR: Well, we certainly want to start with the diet and lifestyle, and I share Robb Wolf’s frustration where you feel like we’re always just saying the same thing over and over again.
SM: Oh, I always am!
DR: We want to go back to starting with the diet, and we’ve done a couple of podcasts about how to navigate the diet. There’s paleo. There’s potentially autoimmune paleo to take it a step or a level further. You could try low FODMAP or even low FODMAP with SCD restriction. And of course, mind your sleep, mind your stress, and don’t over-exercise. We’ve done podcasts about how to tell if you’re over-exercising, and we even talked about the HRV, which might be a novel tool for tracking that.
Before we go into the next step, which would be addressing the SIBO, another thing I think is important just conceptually from a lifestyle and stress perspective is the law of diminishing returns. I was talking with Melissa Hartwig about this concept, and she really did a great job of encapsulating, if people are putting time and effort into getting healthier, so they’re on the computer, they’re reading, and they’re researching, and they’re doing all this stuff, you almost have this inverted U of your yield on that or your return on that, right? It follows the law of diminishing returns, and what this means is at first, you have a high payout for your time and effort invested, but as you continue investing more time and effort, you can have a law of diminishing returns, and if you keep investing more time and effort, you can even have a law of diminishing returns or negative returns. All this means is that if you are putting so much time into researching your own health—which I absolutely think you should. Do not get me wrong at all. You absolutely should do that. But if you’re doing that to a point where now you’re starting to sacrifice your hobbies, your friends, your time outside, your relationships, you are now cutting into therapies or activities that have proven health benefit, and you’re now truly voyaging into the realm of negative return (1).
DR: Because now you’re depriving yourself of healthy stimulus in order to try to make yourself healthy, which, of course, is absolutely flawed sort of logic.
SM: When health is your only hobby, there’s a problem.
DR: Right. And I know we’ve talked about that before. I don’t want to harp on that too much, but I thought the law of diminishing returns was kind of a unique way for people to encapsulate that.
What to do when diet and lifestyle changes do not work
DR: So if people have taken some time to play with their diet, they’ve tried a probiotic, they’ve tried potentially a digestive enzyme formula, and then they’ve worked on their lifestyle, meaning they’re getting sleep, they’re getting some activity—maybe even preferably outside with a friend, like we’ve talked about, so they’re getting social time, they’re getting the time in nature, and they’re getting the activity time—and then maybe meditating or picking up a hobby that has kind of fallen by the wayside, if they’ve done all those things and they still feel like something’s not right, then the answer is probably not a dietary answer, right?
This is something I think is important for me to reiterate because I have some patients that come in that are so obsessed with their diet and they’re trying to force a dietary solution to a non-dietary problem. For those people, the real next step is a thorough, comprehensive gut workup to try to figure out what’s the matter. Could it be SIBO? Could it be a fungal infection? Could it be a toxoplasmosis infection? Could it be low-level IBD? Could it be a motility impairment? That’s really the next step, and that’s where it’s a better investment to hand this over to a clinician, I think, rather than figuring it out yourself because it’s challenging. I mean, it’s challenging for clinicians that spent their whole life training in this and doing this, nevermind if you already have a full-time job and you’re trying to tack this on on the side. That’s where I think a good investment would be to turn this over to a competent functional medicine clinician, get a solid GI workup, and then go from there.
SM: And you are still taking patients, am I right?
DR: We are. We are still taking patients. I don’t know how much longer because I kind of want to scale back my patient load a little bit, but fortunately I’ve been given really good adrenals and a good life.
SM: Don’t burn them out!
DR: Yeah, I tend to be able to do a lot because I have a rich life waiting for me on the other side of work and health, and so that really helps keep me balanced out.
Susan’s IBD/parasite story
SM: Well, that’s good. Yeah, I second it because every once in a while I go in for a gut check-up. You know, I have IBD and I just did that this week, and I found out I have a parasite!
SM: I had my check-up last year and everything was clear, and so between May of last year and October of this year, a parasite decided to join me. I wasn’t feeling right, and I knew something was a little off, and I just didn’t know what it was, and so it’s a parasite!
DR: Yeah, well, I think what you’re doing makes a ton of sense, just having that yearly check-up on your gut. Do you track lactoferrin or calprotectin as ways to preempt any sort of IBD flare?
SM: I don’t track them. I mean, I had them tested, and they were both very low or nonexistent.
SM: I don’t know the second one. I know the lactoferrin was either nonexistent or really, really low.
DR: OK. Well, if you’ve been in remission for a while, then you may not need to do that, but those markers have both been shown to be able to predict relapse, so they’re important markers for people to be aware of and to be tracking either themselves or with their doctors because they may tip you off to a coming relapse in the future.
SM: Right. It’s kind of funny because we talked a couple of months ago about how I got glutened, and now I’m wondering if that’s when I got the parasite instead and it wasn’t gluten because the symptoms of both are very similar, so now that’s the only time that I had such GI distress. I’m rethinking my gluten exposure!
DR: Now, did the gastrointestinal symptoms come back to your baseline? Did your gut symptoms recover completely, or did you have a little bit of lingering stuff that never went away?
SM: I still have a little bit of lingering stuff that never went away.
DR: Mm-hmm, so that definitely fits the presentation.
SM: And that’s why I went in.
SM: Yeah, it was acute, and I’m not going to go into all the symptoms—it’s TMI!—but acute for, like, two days, and then I couldn’t do the podcast one day. We had to reschedule. And then it got better, but it just never got all the way better, and that’s just typical parasite.
DR: Right, and I think it’s really important for people to hear that, especially because I could see someone having that happen and thinking that they need to ratchet the gluten-free diet harder and harder and harder and really beating themselves up because they’re trying to force a gluten-free solution onto what may not be a gluten-free problem.
SM: Right. And the exhaustion that came afterwards was much more than any exhaustion I had ever had with a gluten exposure in the past.
DR: Good. Well, I mean, not good!
DR: Glad that we’re sharing this dialogue.
SM: I was knocked out for a good couple of weeks, and usually with gluten… I don’t have celiac; I have IBD, so it’s different. It doesn’t really knock me down and take me a while to get back. Usually it’s a day or two and I’m OK. But this really kind of knocked my socks off for a little bit.
DR: Well, do you mind sharing what the organism was?
DR: Do you not remember?
SM: It starts with a C. It’s really long.
SM: Yep. That’s it.
DR: OK. Yeah.
SM: Yeah, and I did all the research, and I thought, “Yeah, I want to get rid of that. I don’t want that inside me anymore!”
DR: Well, I’ll give you some tips when we hang up the call about some things you can do clinically. I’d share these on the air, but I’m afraid people are going to go do this on their own.
DR: There are a couple of things you can do specifically that are good for protozoa like that, so yeah, a few tips to follow on that.
SM: Yeah, that’s why you always need to get a stool test to get these things diagnosed. Don’t ever assume that you have something that you might not because it’s just never a good outcome.
DR: Mm-hmm. And then also working with a clinician that’s skilled in knowing how to use herbal medicines because there are certainly lots of herbs that are antimicrobial or antibiotic in nature, but some are more antiparasitic or some are more antiprotozoal or some are more antibacterial or some are more antifungal, and they can be combined synergistically with certain probiotics or biofilm agents if the presentation fits that, to really enhance results. Those nuances are sometimes what can make the difference between someone having had treated, let’s say, Blastocystis hominis three times and not clearing it or them treating it one time and clearing it. And I’m sure this at some point—you know, knock on wood—this will no longer be the case, but I’ve not had one case of Blasto yet that we haven’t eradicated after one round of treatment, and I think it’s because we’re just using a more specific approach. We’re treating this rather than just throwing broad-spectrum herbals at it.
SM: And you made a really good point: Always retest. Just because your symptoms go away or the majority of your symptoms go away, it doesn’t mean that you’ve cleared completely.
DR: Right. And that’s what I learned the hard way.
SM: I did, too.
DR: I spent a good year of my life suffering because I was too dumb to retest
SM: Yes, I did, too. A lot of supplements. I spent a lot of money on supplements and misery when it would have been easy just to retest.
DR: I would have saved more than the $300 from the test. Yeah, exactly. Oh, well.
SM: Yeah. In fact, my doctor already ordered my second test, so I already have it ready to go after the treatment and wait the two weeks and then retest. I said, “Let me go ahead and pay for it right now so I’m not tempted to say, ‘Oh, I feel fine!’”
DR: Right. Good! Good job.
SM: OK, any last parting words of wisdom for everybody at home?
DR: That’s it. Hopefully people got some good stuff out of this and this will reaffirm people’s commitment to the lifestyle piece or the anti-stress piece.
SM: Yeah, stress is huge. If I could leave anybody with anything, it’s that you really have to look at things and prioritize what’s important in your life. If you’re sick, is that three-hour commute important? What can you do? What changes can you make? Sometimes people feel stuck, but if you take a 360-degree view, there might be things that you can change to alleviate whatever predicament you’re in, or there’s stress management tools, like meditation, that can help you react to that stress better.
DR: Absolutely. I agree 100 percent.
SM: OK! Well, we’ll talk to you guys next time!
DR: All right. Thanks, guys.
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