Collaborative CE Event with
Houston Methodist Hospital

Gut Feelings: The Microbiome's Growing Role in Mental Health Treatment

This event showcases groundbreaking research on the gut microbiome’s influence on mood, cognition, and even personality.

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  • Dietary interventions can have antidepressant effects that are 3-4 times stronger than standard psychotherapy or SSRIs.
  • Gut bacteria can reveal past trauma. A study has shown that adults who had experienced childhood physical abuse still present with distinct inflammatory bacterial signatures.
  • Reduced bacterial diversity (dysbiosis) and chronic inflammation appear consistently across psychiatric conditions including depression, anxiety, bipolar, and schizophrenia.

Dr. Amanda Fialk: My name is Dr. Amanda Falk. I use (she, her) pronouns. I am a partner and chief clinical officer at The Dorm, which is an IOP and PHP treatment community for young adults located in both New York City and Washington, D.C.

I am so thrilled to be here today with Dr. Madan to be discussing how gut health and mental health intersect, and this is an area that is gaining rapid traction in both research and in clinical practice. It’s a topic that really hits home for us at The Dorm and our treatment community with our young adults. We certainly know firsthand the benefits of having full-time registered dietitians and health and wellness professionals on our team, because the work that they do is critical to client outcomes.

We believe that every client entering treatment, regardless of their presenting diagnosis, needs to meet with a dietitian and a health and wellness provider for an assessment. And while we have found that maybe only a portion of our clients are assessed as meeting criteria for an eating disorder or disordered eating, the overwhelming majority of our clients really greatly struggle with executive function issues related to food, to meal planning, to meal prepping, and for many of them, sometimes just simply remembering to eat.

Just last week, I was speaking to one of our dietitians, and she shared with me that a client had been telling her that in doing their work together, they realized that their struggles with focus and energy were intimately tied with their inconsistent eating, and making just small and realistic adjustments to meal planning and meal prepping that help them to nourish themselves differently and regularly had an immense impact on their mood and their ability to participate in treatment, in the way that they wanted to participate in treatment.

So, all of this is to say, this is why we are really grateful here today to welcome Dr. Madan from Houston Methodist Hospital to share his extensive research into how diet and nutrition play a direct role in mental health treatment.

Dr. Madan is a clinical psychologist and vice chair of the Department of Psychiatry and behavioral health at The John S. Dunn Foundation Distinguished Centennial Chair in Behavioral Health at Houston Methodist. And he helps lead a team of world-class clinicians and researchers in cutting-edge research related to the microbiome and mental health connection across different populations.

For over two decades, his research has been targeted at improving the quality of care for individuals with both chronic medical conditions and acute mental illness, specializing in studying gut-based contributions to psychiatric illness and the development of novel brain stimulation techniques. We are thrilled to be learning from him today. And with that, I’m going to turn the presentation over.

Dr. Alok Madan: Thank you for that very kind and generous introduction, Dr. Falk. Thank you all for joining. We’ve got a whole bunch of folks, so with that, let me get started on this presentation.

I was telling Amanda here just earlier that I had an emergent root canal last night, so I am doing my best here, y’all. So yeah, today we will be talking about the interconnection between the gut microbiome and mental health. I’ll try to keep this moving along and try to keep this presentation done with enough time that we have an opportunity to actually speak at the end.

Here are some disclosures. I don’t have any financial relationships with this presentation. Here’s some folks who’ve covered my salary currently and or in the past. I think the big one I really want to talk about is that I will be presenting on some non-FDA-approved approaches to actually manipulate the gut microbiome. So, just know that whatever I say in that regard is not sanctioned by the FDA. It’s kind of my thoughts and opinions based on the state of the science.

This is kind of a big, broad overview of what we’re going to be talking about: how the gut microbiome might influence mental health, how we might look at nutrition within a mental health care setting, and kind of what the science behind some of this is, and kind of how we can shift towards more nutrition as part of our mental health care.

As Amanda said, over at The Dorm, I think there are a few of us that are moving in this direction where nutrition has become not as an adjunctive or maybe an as-needed thing to care, but rather that is part and parcel of our treatment. Here at Houston Methodist in our PHP, we have the exact same thing, and actually, we have finally got a health and behavior specialist where everyone is now meeting, and with our assessment program meets with her, and we’re talking about diet, nutrition, exercise, physical activity, all of that. And this isn’t just for folks who have glaring, disordered eating, or an obvious sedentary lifestyle, but this is just part and parcel of what we’re doing. And I’m glad to hear that there are more, more or less across the country that are doing this, and hopefully across the globe.

This is a really, really, really big, high-level picture of what’s going on. Now, this is from my daughter when she was 7. She is now 14, so she is horribly embarrassed that I still show up this slide. And really, I want you to – this is – we were doing free drawing, right? So we do this plenty, and this was a magical flying unicorn pooping out useful stuff. So this is absolutely what we’re talking about – our poop. So this is going to be a very poop-centric talk, and so this is a taboo topic, actually. We don’t like talking about our poop.

And this is where a lot of information lives. So in this particular free drawing of hers from 7 years ago, when she was a wee little 7-year-old, this is a strawberry, I think this was her iPad, and some lettuce, this is a phone. So it is useful stuff. I don’t know that this is what we’ll be talking about today in terms of the content, but we will be talking about poop.

So, poop we don’t like talking about, it makes us giggle, it makes us laugh, makes us feel uncomfortable. And there are plenty of reasons, culturally, why that might be. It’s probably associated with a lot of, kind of, bacteria and illness, but I think at this point, like, one of the questions was, is like, what do we as mental health professionals need to do? I think we need to talk about diet and bowel movements, actually, a little bit more with our patients. And not run and shy away from our own discomfort when we could get a lot of information, because our poop has a lot of information in it, and hopefully we’re pooping regularly, and if not, that’s worthy of conversation, actually. For it doesn’t matter what letters are after your name.

So what is the gut microbiome? This is all of – and the gut is kind of, you know, this is really speaking of small and large intestines, but this is kind of all the bacteria, viruses, and kind of their collective material as well as the products that they produce that live in your gut. Now, while it’s called the microbiome, saying this big umbrella of all this, the vast majority of the research has been done on the bacteria.

The total number of bacteria are, you know, there’s a vague range, up to a trillion of them or so, and it’s a few thousand species, and the numbers keep on jumping up and down, but this is where we are right now. And collectively, all the bacteria weigh about 3 pounds. And curiously, that’s how much our average brain weighs as well. And the reason we’re talking about poop is because our fecal material, our fecal samples, actually have bacteria in them. That’s about where we can get an easy view of what our gut bacteria look like.

And all of these kinds of factors contribute: diet, the medicines we take, where on the planet we live, kind of where we are in life and lifespan, how we were born. We’re actually born with no bacteria. We have no microbiome. But passing through the birth canal is our first exposure to mom’s bacteria, and then skin-to-skin, how we’re fed, and then kind of how we live our lives, and kind of what we eat along the way. This has a direct bearing on what’s going on in our gut.

Now, the brain and the gut are intimately connected. This is a bi-directional relationship, meaning what’s going on up here affects what’s going on down in our gut, what’s going on in our gut affects what’s going on upstairs. Now, this is a very complicated system. I’m not going to get into the nitty-gritty of it. That’s for a very different talk, and probably a different audience, and different time, because that’ll be, like, hours on itself. But I do want to kind of say that the two are connected, and we’ve known this forever.

I mean, our language has it. Butterflies in our stomach. We have these things, scared shitless. I mean, these are – this is the English language. This is not just limited to the English language. There are terms all across the globe that have connected our emotional health and well-being, our brain space, and our guts. So we’ve known this. It’s just probably over the past couple of decades, that the science, really, it’s really the microbiology, the genetics have advanced to the point where we have a better understanding of what’s going on, and really the analytics. The analytics are really probably the most complicated of them all at this point. And it really takes a whole team of folks to try to do this line of research, of trying to really understand this brain-gut microbiome axis and how they’re interconnected.

This is complicated and complex. So down here, this is essentially your gut. This is the lining of your intestine. So all these bacteria live in your intestine, they produce a whole bunch of stuff that gets, goes into your bodies and affects, but what’s going on in the brain also has directions. They go down. So it is a top-down, bottom-up type of communication. It’s kind of chronically moving, and our understanding right now of this complex interplay is rudimentary at best. So, it’s some of the preliminary questions that have come in are looking for a whole lot of specificity. Even with this horribly complicated slide. This is probably a gross under-appreciation of the complexity of what’s going on.

So, I wish I could give a lot more specifics. I can’t, because the science is not there, and I’m not going to over-interpret the science, and that’s one of my big concerns about a lot that’s out there right now. It’s over-interpreting small studies and making grand conclusions. So, one of the big take-homes is that what we know about the brain-gut interconnection is that the two are interconnected. They influence one another exactly how and under what conditions, and under, for what illnesses. I think that’s less understood, but it is, every day, we’re learning more about it.

So how do we know all of this, right? So, again, you’ll see there’s a lot of poop here on this slide. It’s easier. We don’t have to draw blood, we don’t have to expose anyone to radiation, like in a like with a CT scan, or – it’s literally fecal samples are able to give us an idea of what’s going on. So you’re taking people who don’t have disease compared to people who have disease. You collect fecal samples from them, you run kind of the analysis, and the two groups are somehow different based on their fecal matter and the bacteria in their waste.

This is probably the vast majority of our understanding of, maybe, of causality is based on small animal studies. So we get poop from humans – a depressed person, an anxious person, a psychotic person – and we transplant that fecal matter into mice who are germ-free, who actually don’t have a gut microbiome. And what you can see is you start seeing depressive-like behaviors in mice, you see anxious-like behaviors in mice. So, if you can get, kind of, depressed poop or anxious poop, you can make mice who don’t have a microbiome into behaving depressed or anxious.

This is the vast majority of the research. While it is informative, humans are not mice. It’s not a one-to-one translation, and it doesn’t always work that way. So, what we do sometimes is we’ll get fecal transplants, and get them from healthy and transform the sick, and sometimes you can get better. This is much smaller. There’s only one FDA-approved indication for a fecal transplant in humans. And that’s for a horrible, horrible bacterial infection called C. Diff. It’s once you’ve had all the treatments out there, and you still end up in the hospital with diarrhea that’s putting you essentially on your deathbed. You can get a fecal transplant, and it works magically.

Now, curiously, while these trials were going on, we also learned something, and this really affects the ethics and the questions of the research today. In some of these trials, we actually transplanted obesity also, accidentally. So we were treating C. Diff, we did treat the C. Diff, but we also transplanted obesity. So there’s something in the bacteria that actually transplanted into a person, and so it’s good intentions don’t always work out exactly as we’d hoped, and there can be consequences, so I’ll get back to that and my root canal in particular.

Now, there are some studies, these are smaller studies, again, that we do dietary interventions – either change up what we eat, prebiotics are the bacteria that feed the or the materials that actually feed our bacteria in the gut. Probiotics are actually the bacteria, you’re putting in the bacteria into your guts, and you see, is there improvement? So this is the way that this research is done. Mice are really easy to research. Mice you have influence over. Humans, not so much. Even asking people for a fecal samples is actually very hard to do. We don’t like sharing our poop.

Now, mind you, as a psychologist, I can get intimate details from patients of horrible trauma experiences. But if I ask for a fecal sample, I’ve gone too far. So, it really, this line of research is not easy to do.

So, again, brain-gut has been implicated in a variety of diseases, and these are all small studies. There’s nothing that we have an absolute causal relationship or idea of, you know, this bacteria, or this class of bacteria cause MS, cause depression, cause autism, cause Parkinson’s. We don’t have any of that. Figure it out. These bacteria have been implicated in the presentation with these diseases, but I don’t know that causality, we are there yet.

This is kind of our work in this field of psychiatric microbiology. Mind you, the term psychiatric microbiology is one that I made up and introduced in the literature, scientific literature about 3-4 years ago. It is the interface of psychiatry and microbiology, and we started this line of inquiry about a decade ago. At the time when we launched this study, in the scientific literature, at that particular point, there had been two published studies with actual patients. So ours was quite an endeavor, and we ended up collecting fecal samples from 100-plus psychiatric inpatients. And then we had clinical data admission and discharge, but the samples were collected only at shortly after admission, and this is the bulk of the research. This cross-sectional research that any of the research that really exists within the field right now. The vast majority of it, I can’t say any of it, the vast majority of it is really cross-sectional.

So some of the strengths of the study, though, were that it was in a hospital setting. So, we had some control over potential confounding variables, such as, kind of the medications people were taking, they’re exposed to the same environment. Same, you know, bed sheets were cleaned with the same detergent. So those factors that could influence, we were able to account for.

Essentially, this slide right here is telling us that what we found was what you looked like in terms of your clinical presentation really, at admission. Varied by your bacteria varied if you had mild, moderate, or severe depression. Don’t worry about the specifics. I’ve left these very blurry and small in particular, because I don’t want you to generalize these. But what we also found was that what’s your gut bacteria look like when you walked into the hospital actually was able to predict whether you got better or not in terms of depression after your hospitalization. But this was at a very high level. So, the degree of diversity, the heterogeneity of your bacteria. If you had a more diverse bacterial profile at admission, you were more likely to respond to treatment than if you had a less heterogeneous. Nothing specific about the bacteria, but it was just the variety of the bacteria.

Now, curiously, since I didn’t want to over-interpret this at the time, we did find one bacterial strain, one bacterial taxa. This Coprococcus that was reduced in the context of more severe depression. Again, didn’t want to over-interpret it, but I think, you know, the two studies that I told you about that existed at the time, this was a Dutch study of 100 outpatients, it was buried in a footnote there. This was the same bacteria that was reduced. And in a Chinese sample, I think out of Beijing, this was looking at a few hundred patients in the hospital, again, buried in the little footnote there was also Coprococcus was reduced.

Now, Coprococcus is actually associated with chronic inflammation. And inflammation and depression, I think that story is gaining a lot more traction these days. So that may be, in part, mediated by the gut bacteria.

What we did a few years later was looking at, again, this is not to get too caught up under the weeds. These bacteria look different from these bacteria, these bacteria look different from these bacteria, and essentially what we were able to do was, like I was saying, the analytics, I couldn’t even tell you the complexity of these analyses, because I have to outsource, kind of, and partner with really bright folks to do this. Data scientists. Essentially from about 10,000 different bacteria, we were able to reduce it down to 43 that were conferring treatment resistance to in terms of depression and anxiety, and these bacteria collectively were associated with inflammation.

Now, again, we’re not the only ones. This group out of China, a couple of years ago – actually, not even a couple of years ago, last year – were able to identify specific bacteria that were associated with response to SSRI for depression. Which is kind of cool now, right? We’re starting to get, collectively, like, what you look like early in treatment might identify you as someone who is able to respond to treatment. Maybe we haven’t figured out exactly what is defining what your illness is. But based on what your, kind of, your microbial signature looks like when you enter treatment, we might be able to identify whether you are likely to respond to kind of standard care, or you may need something a little bit different because of your bacterial signature. Again, this was out back in 24 as well.

Another group of, you know, a different set of bacteria. So I guess, collectively, you’re saying, like, we’re finding different signatures of treatment resistance or response to treatment. So this is where the state of the science is. There’s so much variety. I don’t think any of us have honed in on any one thing. But it’s when we’re collectively putting into the literature. It is, we’re starting to get a signal.

You know, we tried to look at suicidality in the gut microbiome, and we sliced and diced this every possible way, and really found no signal. Now, I put this study up to say that this is no signal, because this is very hard research to do, it’s very expensive research to do. And there is a bias in the scientific literature to only publish the kind of results that have significant findings. But non-significant findings are just as important sometimes in terms of how we did this line of inquiry. It’s expensive, it’s time-consuming, and it’s difficult to do with patients. Don’t do exactly what we did, because we didn’t find a signal. So, this is my little contribution to science. We were able to sneak in a non-significant result into a peer-reviewed publication. I think they’re probably quite a coup, actually.

What we also found in this sample was that, you know, this was just fantastic. Not fantastic, this was just fascinating. So, this is, remember, these folks were these psychiatric inpatients. Average age was about 37, 38 years old. And we got their bacteria shortly after they or their fecal samples shortly after they entered the hospital. And not only do we ask them about current symptoms, we ask them about lived experiences, especially traumatic life events. And these are events that could have happened at any point of their lifespan. What we found, though, was these adults, these 38-year-old men and women. Those who endorse childhood physical abuse. Their gut bacteria look different than those who did not. And the folks with childhood physical abuse, they actually had bacteria that are associated with inflammation. So stuff that happened two, three decades ago. Life experiences that happened 2-3 decades ago have bearing on what your gut bacteria look like in adulthood. That’s fascinating.

That this is, like, so it suggests that these life events have some kind of genetic, epigenetic influence that you carry on into adulthood, and there’s a signal in your bacteria that are associated in your gut bacteria that are associated with inflammation. This one was a fascinating finding as well, and this is really adding to the literature that there’s a social transmission of bacteria. So, it these screens are great and all, we’re able to engage with one another, but physical contact actually makes a difference.

So, this is looking at, kind of, personality traits and the gut bacteria and the gut microbiome, and we found that folks who said that they had didn’t have a whole lot of friends, other than their first-degree relatives, looked very different than people who said didn’t endorse this item. You know, people who were more socially detached. Their gut bacteria actually looks very different from people who are more socially engaged. Again, so there’s something to be said of, of, kind of, our human contact. It is actually adaptive in some regards, because these bacteria that differentiated the two groups, again, are associated with inflammation. So maybe, I mean, most of us have read and heard of this loneliness epidemic that’s affecting all of us, and is actually killing us. It may be, in part, mediated by kind of a more homogenization of bacteria and lack of exposure to specific bacteria that we get from one another, and we’re staying in a more inflamed state.

So, this one was a fantastic paper that came out a couple of years ago in 22. And like I was saying, you know, all of us are putting out our research, we’re finding a little signature here, a little signature here, a little signature here. There’s not a whole lot of overlap, but there is some overlap. And this is looking at, across studies with schizophrenia, across studies in depression, across studies in bipolar disorder. This shared area of this Venn diagram. It’s kind of this signal that we’re finding across psychiatric illness is that we have a relative increase in these bacteria and a relative decrease in this bacteria. Again, this Coprococcus that we found in this 2015 sample actually, that signal is showing up a decade later. So, I was hesitant to over-interpret, and I could have said a little bit more, but it’s perfectly fine at being cautious and interpreting.

Let’s talk about these three bacteria in particular. This Enterobacteriaceae level. Remember, it’s increased. These two are increased, and this is decreased across psychiatric illness. Stress and inflammation. This, when you have too much of this Lactobacillus. If you have inflammation and what you have is reduced biodiversity. So just the variety of bacteria go down. And this Coprococcus is reduced, but what it does is it actually ferments dietary fibers, which produce short-chain fatty acids, such as butyrate. And what does butyrate do? It is one of the building blocks of not only neurotransmitters, but it also reduces inflammation. So remember this. Coprococcus is reduced. You need more Coprococcus to actually ferment bacteria, ferment your fibers. So we’ll get back to this, and this will be relevant to kind of more of how to actually intervene.

So kind of this is the state of the science. We don’t know a whole lot, but we are in the process of actually contributing to better understanding. And one of the challenges with what we’re doing, all of us across the planet, is that they’re cross-sectional studies, so we’re not able to really get to, kind of, mechanisms and or any causal relationships.

So the big question is, it’s okay, we’ve seen that there is a signature across psychiatric illness of what the gut looks like. But is this, is this a state, or is this a trait? Does this actually change with treatment? Or is this our destiny? I don’t know. That’s a complete question.

So, we have embarked on trying to answer this question across a number of studies. So what we’re doing is we’re getting folks in one of our outpatient clinics here at Houston Methodist. As soon as they enter treatment, we’re asking them if they’d be willing to participate in this in this research. So we asked them for fecal samples when they start treatment, 1 month, 2 months, 3 months into treatment, and we’re getting their symptoms, and we’re tracking their symptoms across that. So, that study is in progress. We plan on doing the same thing with looking at, I’ve got a partner who’s got a partnership with a residential treatment facility for addiction. And we’re going to look to see if the gut actually is implicated in opioid dependence and how that might change during the course of treatment, again, serial assessment.

And colleagues here at Houston Methodist in collaboration with folks, kind of not only here at Houston Methodist, but across the street at Baylor College of Medicine. We have a big research project, kind of, in progress, hoping to get funded, and if not, we’re going to probably start it anyway in January. It’s looking at what the gut bacteria and gut microbiome look like and or change during the course of pregnancy, in addition to that and how the gut bacteria and sleep might interact during the course of pregnancy to predict postpartum depression.

Now, that’s kind of where we’re moving next. It’s more longitudinal studies with more than just one fecal sample to see if you get better with treatment. Does the gut bacteria change? Does the bacteria change before you have symptomatic improvement? Do you have symptomatic improvement? And then your gut bacteria change? These are all questions, or can we predict who’s going to get better, who’s not going to get better?

And then kind of the one of the next lines of research that is, again, harder to do and more expensive. It’s not just looking at what the gut bacteria do, and you’ve heard me say these bacteria are associated with inflammation, these bacteria do this, do that. Well, there’s a whole next phase of the research is these bacteria. They produce stuff, and those metabolites. We want to study those. Like, and that’s a whole other field called metabolomics. So hopefully, one day, we are in the world of psychobiotics. I didn’t come up with that word that’s been in the literature for a few years now. It’s, can we intervene with psychiatric illness at the gut bacterial level either with stuff that feeds the bacteria, these prebiotics. Or can we supplement the gut with beneficial bacteria, or can we use antibiotics to kill off specifically, bad bacteria. That’s, that’s, we’re not there yet. That is, that’s years away. Hopefully, in my lifetime, but I don’t know that we’ll get there. It is ambitious, and one that I’d say we were aiming for, but psychobiotics is something that may be part of our kind of psychiatric toolbox of addressing illnesses that aren’t always fully understood. Treatments that are modestly, that are modestly effective on a large scale. And can we supplement with psychobiotics, by manipulating the gut.

So let’s summarize the state of the science, small animal research, mostly animal research. Some studies with humans, but they’re small, mostly with healthy controls. Here’s one thing that really, it’s, it’s, we talk about the human gut microbiome. 70% of the research that’s been done is based out of Europe or the United States, or Canada. That doesn’t include the rest of the globe. So it’s really going to be hard to generalize on the human gut microbiome, when the science is so biased towards Western community so far. We don’t have a very good understanding of the mechanism of action. So, kind of dysbiosis, just another fancy way of saying it’s becoming more homogenized, it’s becoming more the same. More of the same bacteria, and systemic inflammation is really kind of where we are across disease states. That’s depression, anxiety, psychosis, bipolar disorder, and really, it’s a very similar signature when you’re talking about obesity, when you’re talking about heart disease, when you’re talking about diabetes, and the gut microbiome. It is, kind of generally speaking.

So, I put this up to say that this was published online this past Saturday. This is the review article out of Nature Mental Health. This is one of the premier journals. This is essentially summarizing what I just summarized in the previous 25 minutes. In those small studies, we don’t know causality, so this is the state of the science that just came out, you know, 5 days ago.

Here’s also an unfortunate fact. We don’t even know what a normal or what a healthy gut microbiome looks like, and this is coming from Ted Dinan, who’s kind of sometimes thought of as kind of the godfather of the brain-gut research area. So there are some small studies that say, okay, this is, this is a big, this got in 23, there’s a significant antidepressant effect of agents that contain probiotics. And this is a big meta-analysis, too. This is looking at all the state of the science. When you look at what the state of the science is, there may be a dozen studies with 20 people. That doesn’t mean this is national news. This is not headline news. Probiotics are not antidepressants. You can’t make that claim based on a dozen studies with 20 people in them. Yeah, but we keep on doing it.

This is in 25 with schizophrenia. Yep, we can do this. We’re going to solve all the psychosis with probiotics. And now this has been published because it’s a systematic review and meta-analysis. Let’s count the studies. 1, 2, 3, 4, 5, 6, 7, 8, 9! We’re not making grand conclusions, we’re not treating psychosis with probiotics, based on 9 studies.

So, how do we treat this? I’m going to speed this up a little bit. I know we’re going to talk about nutrition a lot, and I want to leave time for questions. Everything that our grandma told us to do that’s good for us is good for your gut, is good for your brain. An environment that’s enriching. Healthy diet, get some exercise. Hang out with people, and get some stimulation. Don’t just sit around in your room.

Now, there is science that is emerging now that what we eat has direct bearing on our mental health and well-being. Poor diet. What does a poor diet mean? A poor diet means ultra, ultra-processed foods. Ultra-processed foods are foods that are made in a factory. If it comes in a box, it’s probably not good for you. And if you eat exclusively box foods. That’s not good for you. Box foods that do not have colors that exist in nature are even worse for you. Boxed foods that have colors that don’t exist in nature that are loaded with sugar, are even worse for you. And if all those factors are meat, or a meat product, that’s really bad for you. You have almost a 50% increased odds of developing depression or anxiety if you eat these foods, versus if you don’t.

This is straight out of CDC, FDA, dietary guidelines for the Americans for 2025. All these numbers, these are different age groups. We’re not following guidelines. Well, half of us are. Half of us aren’t, right? What are we particularly not doing? 90% of us are not getting our recommended veggie intake. 97% of us are not getting our recommended whole grain intake. We do a great job with refined grains. These are all the things we should be eating. Veggies, veggies, lentils. Vegetables, fruits, we’re not doing essentially, we’re not following. Fruits and veggies. We do like potato chips, though. And we do like hot dogs.

So a high-fat diet? Inflammation. Red meat. This is not to say do not eat burgers, do not eat steak. This is don’t even give up. Yo-yo, your fast food. This is to say, you cannot live exclusively off of these things. You need fruits and veggies. You need whole grains. These things are helpful. They are anti-inflammatory. Remember, that bacteria that’s reduced in depression, Coprococcus, and across psychiatric illnesses. Coprococcus actually uses fibers. It takes fiber, it turns it into short-chain fatty acids which are essential to turning the volume down on your system.

Again, 2025 guidelines. This is the big meta message. This is, like, what can I do to improve my gut health? Should I take probiotics? Should I do this? Should I do that? Don’t do any of that, but focus on one thing. One thing and one thing exclusively for the next year. Follow and track your fiber. 90% of women, 97% of men. This is all of us. We don’t get enough fiber. We need 30 grams of fiber.

This is not to eat your Fiber One bars, this isn’t the Eat Metamucil. Don’t take it the easy way. Get an apple, eat a salad, eat some spinach. Go slowly. Your body will revolt, which means you will have diarrhea. You can’t go from 0 to 30 overnight. Start tracking it. I don’t know how many people are on the talk, I think 400 or 500 signed up. That’s about 400 or 500 people that aren’t getting enough fiber in their diet. So 90% of women, 97% of men, I don’t think we’re special at this talk unless you make a concerted effort. This is your intervention. This is your treatment. This is very small, very simple, very easy.

I’m not going to give a specific recommendation of this probiotic, that prebiotic, eat an apple. Eat, get yourself a salad mix. Get yourself some fruits and veggies, get your fiber up. Now, what happens if you actually change up your diet? This is over 3 months. Whole grains, veggies, fruits, legumes, low-fat, unsalted nuts, fish, lean meats, eggs, olive oil, this is all. Look, these are all real foods. These are all whole foods. These are on the perimeter of the grocery store. They’re not in the aisles. And this reduces your extra food. This isn’t to get rid of. So I say, kind of, recommend the 80-20 rule. 80% of this, 20% of this.

This lady, Felice Jacka, is a powerhouse. She was the first one to publish this in 2017. She consults with the World Health Organization, she was in Houston, she was consulting with NASA, I got to have dinner with her, which was very intimidating to have dinner with the person who’s done this line of research. What do you eat?

Now. This antidepressant effect. Greater than 1. For the stat nerds in this group. What are our antidepressant effects for any three-letter psychotherapy? About 0.3. What is our antidepressant effect for almost any SSRI? About 0.3. Dietary intervention over the course of 3 months is about 3 to 4 fold more effective in treating depression than our frontline treatments are. Let that settle in for a second. Four-fold more effective than frontline CBT, ACT, DBT. Zoloft, Prozac. Take your pick.

This isn’t making mainstream because there is no drug company that’s going to make money off of this. And this requires a whole lot of work. Changing up our diet is a lot of work. You need help, you can’t do it alone. Get help.

So here are my non-FDA-approved recommendations for manipulating the gut health. This is much better than this. I don’t even know where this is served. These are 3-foot-long hot dogs. One has chili and chips on it, the other has mac and cheese on it. The other one has a brisket-like material with barbecue sauce on it, with a side of fries. This is a meal, y’all. This is what we eat. We don’t need enough of this. This is likely contributing to our poor mental health, we do more of this. This is likely to make us feel better psychiatrically.

Okay, yogurts, the kombucha, the kimchi, the kefir, the apple cider vinegar, maybe. Maybe. Not without consequence. Remember I told you you got a root canal? Well, this is my second one in a 12-month period. I used to have apple cider every day for years. And I think I killed off my tooth enamel. So I’m trying to improve my gut health but not without consequence. Again, moderation. Some of these things might be helpful, they might be helpful for you. I don’t know if they’re going to be. This is definitely going to be helpful in terms of your mental health and well-being. Get the rainbow on your plate. Have it be real. And fruits, vegetables, whole grains heavy. Not that you don’t eat meat, lean meats are great, we need protein. Red meats are great, too. It’s, again, we need more of this. Remember, 90 plus percent of us don’t get enough fiber, and fiber feeds our good bacteria.

So, it went a little bit long, but I want to say thank you to a whole lot of people. This is not done alone. This is done over decades of thinking and learning and figuring out. And a lot of the learning and figuring out has been with patients and families who are willing to share their personal data. Most, most importantly, their poop. Because without their poop, I can’t do any of this research. So, really very thankful for all the patients and families who have contributed to what we’re doing, what’s going on around the globe. Let me pause and stop sharing and get questions.

Dr. Amanda Fialk: Thank you. Thank you so much, Dr. Madan. We have so many questions that came in. As I said, there’s no way we’re gonna get to all of them. We’re probably gonna have to do another presentation, and maybe the presentation is all sort of Q&A style. We can brainstorm on that. We will get to as many as we can, and then please, please don’t hesitate to reach out following the presentation to engage in dialogue. I’m gonna try to pick out some questions and consolidate them.

We did have a lot of participants asking questions about prebiotics versus probiotics. Is one more advantageous than the other, and also, like, there’s so much out there in the world about probiotics and prebiotics, like, how do you know which ones are the right ones, and how do you advise clients when there is just so much out there.

Dr. Alok Madan: All right, so what I go with is the prebiotics. Remember, just by definition, those are the foods that feed our bacteria. So back to the fiber. It really, it’s don’t go with supplements, go with real things. Eat an apple, eat some spinach. Get variety. Get variety. It’s my girls and I, we would compete to see how many fruits and veggies we were able to get on our plate at a given time. Buy those salad mixes, they have, like a dozen or so vegetables already in them chopped up. Those are very easy ways. So you get to feed your bacteria, you get high fiber, and you’re feeding your bacteria, and the variety helps.

The probiotics, there are a whole bunch out there. I don’t know the exact number. A significant portion of them are nothing. So even if you think you’re buying it, you’re not actually getting the bacteria. So, when and those probiotics are literally replacing your bacteria. Yogurt has a whole bunch of good bacteria in it. So you can actually supplement your bacteria rather than getting something out of a bottle that you may or may not know, yogurt actually has good bacteria in it. So those are your probiotics. You can get it that way.

These natural supplements aren’t FDA regulated, so that’s where I cannot say, this is the bacteria, this is the probiotic you need to take or don’t take, because we just don’t know what’s actually in that bottle. So, an apple, I know what it is. Yogurt, I know what it is. So if you want something definitive, that’s where I’d go in that direction. It’s keep it simple, it’s just not you don’t need to get a pill form to solve it all. Really, it’s, I think, changing up our diets a little bit will have a significant bearing on our health and well-being.

Dr. Amanda Fialk: Thank you. We’ve also had a handful of questions come in about ketogenic diets. I know that there’s a lot of research out there, and we get a lot of questions about it as it relates to psychosis, schizophrenia, but is there can you speak at all to a ketogenic diet, and how that is could be helpful to the microbiome, not helpful, how it’s related, not related, etc.

Dr. Alok Madan: That I don’t want to speak outside of, kind of, my line of, kind of, understanding. I know that there is a small emerging literature, especially in helping to supplement the kind of standards of care for psychosis. I don’t know that any diet, whether it’s ketogenic, Mediterranean. Or, you know, which one did we have? We’ve had to eat all these diets, their names and things, they change over time. They tend to get a whole lot of news and hype.

I really do feel like the very basic fundamentals of a balanced diet that is rich in fruits, vegetables, nuts, grains, lean meats, you know, reduce the processed sugary foods. I think that’s going to have, kind of, overall effects as opposed to, this is the diet du jour that’s getting all the attention. It’s, I think, more the basics that we all know. But less than half of us actually follow, kind of, what we’re supposed to be doing. So it’s like, if we could follow, kind of, what we know that has decades and decades and decades of research versus, kind of, this is the fad of the day, and small studies are showing some promise.

And I get it. People want to believe these diets to work, or this intervention to work. Because, the state of the science with psychiatric illnesses, it’s we don’t fully understand what causes them. Our treatments are modestly effective. We’re desperate. We want. And we’re a community. As a, you know, not just across the United States, across the globe. More of us are affected with psychiatric illness. More of us are suffering, it’s more severe. And we’re looking for answers.

So, this is, like, I think it’s, like let’s go with the ketogenic diet, and this is gonna this is gonna be the thing that’s gonna well you know, it’s like, I’ve known of people who’ve literally, with psychosis, who’ve died of, kind of died secondary to Doritos and Dr. Pepper because that’s that became their diet for so many years. So it’s I I can’t endorse one thing or another, other than these very basic diets.

Dr. Amanda Fialk: I want to try to get one more in quickly, because it’s also one that’s sort of like a repeat question that many different people have asked in different forms. When approaching work with clients who do have a diagnosed eating disorder, any thoughts, feedback around how to approach talking with them about the microbiome, about foods, especially when we look at, you know, different approaches, like an all-foods-fit model, etc.

Dr. Alok Madan: I have it as part of my intake. Just like as if you’re asking about, you know, substance use, or sleep, or trauma history, it’s like hey, what’d you eat yesterday? Just get a 24-hour food recall. And that gets you a starting point. I don’t know, versus well, you know, for breakfast, I had this. For lunch, I had this. I had a snack, and then you get a lot of information. Talk to me about your bowel movements. It’s we have to be we as the mental health professional have to be, kind of a bit more comfortable about discussing food, and really bowel movements without our own comfort, and kind of real acceptance that this is, you know. All of the feet, all of us poop. It’s part and parcel of the human condition. This is also part of, I think part of everyone’s intake. This is just I think it’s just as important, just as meaningful as anything else that we ask about.

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