As a gut health coach coming from a functional medicine perspective, I believe in treating the root cause of disease rather than just masking symptoms. And when it comes to gut health, fiber is one of the most important factors to consider.
First of all, fiber plays a critical role in maintaining regular bowel movements. With a standard American diet full of sugar and processed foods, you definitely don’t get enough fiber. And without enough fiber in your diet, you may get constipated or at minimum have a less healthy gut microbiome, which may be one of the reasons that people who are constipated have an increased risk of gastrointestinal cancers, as well as breast, ovarian and other cancers, in particular in the year following constipation, although the direction of causality is not definitive in the studies, and undiagnosed cancer could be causing constipation as well. But the theory is that stool sitting around has toxins that get reabsorbed into the body.
So fiber is good for you because it serves as food for the trillions of bacteria that reside in our gut microbiome, which plays a critical role in our immune system, our metabolism, and our mood, as well as our gut health. Research has shown that a diet high in fiber can reduce inflammation, improve cholesterol levels, and even lower the risk of chronic diseases such as heart disease, diabetes, and certain types of cancer. So I recommend that most of my clients prioritize their fiber intake, except when it’s contradindicated, which I’ll discuss later. Normally I suggest this in the context of diet, but for those who may struggle to get enough fiber from their diet alone, fiber supplements can also be a useful tool to consider.
What are the different types of fiber?
So you’ve probably heart that there are two main types of dietary fiber: soluble and insoluble, and a healthy diet will give you some of both types. Soluble fiber dissolves in water and forms a gel-like substance in the digestive tract, which can help slow down the digestive process, which is beneficial in particular for those with blood sugar concerns or while you’re eating anything sugary. Soluble fiber is also known for its prebiotic effects, which means that it feeds the beneficial bacteria in the gut. This will support a healthy gut microbiome and reduce inflammation in the body. Good sources of soluble fiber include oatmeal, beans, peas, lentils, and fruits like apples and citrus.
On the other hand, insoluble fiber does not dissolve in water and passes through the digestive system mostly intact. This type of fiber promotes regular bowel movements, prevents constipation and supports healthy digestion and nutrient absorption by adding bulk to stool and preventing it from becoming too loose. Good sources of insoluble fiber include whole grains, vegetables like broccoli and carrots, and fruits like berries and kiwi, although most foods have a combination of both types of fiber.
Resistant starch is another type of dietary fiber that resists digestion in the small intestine and reaches the large intestine intact. In the large intestine, it acts as a prebiotic and feeds the beneficial gut bacteria, promoting a healthy gut microbiome and in particular higher butyrate production, which is important for feeding the cells lining the large intestine or colonocytes. Resistant starch has been linked to improved digestion, reduced inflammation, improved insulin sensitivity and lower blood sugar levels. It may also promote feelings of fullness, leading to a reduced calorie intake and potential weight loss. Sources of resistant starch include foods such as green bananas, legumes (beans, lentils, chickpeas), oats, some whole grains and cooked and cooled potatoes or rice. When cooked and cooled, potatoes and rice undergo a process called retrogradation, which changes the structure of the starch, making it more resistant to digestion. My favorite way of getting resistant starch is just making a large batch of jasmine rice and putting it in the fridge to eat with leftovers. If you eat it cold or don’t reheat it too much, you retain much of the resistant starch.
Which fiber supplements are best for gut health?
I often recommend that my clients incorporate fiber into their diets to support recovery of a healthy gut microbiome, because for some reason, pathogenic bacteria tend to like things like sugar and white flour and commensals or beneficial bacteria, like fiber. I think about this particularly during treatment for H pylori, which typically causes reflux and constipation, but not so much bloating, either through diet or through supplements, and after SIBO treatment, especially for diarrhea or soft stool, to help restore butyrate producers in the colon.
Here are some types of fiber supplements you may want to consider.
Psyllium husk is a type of soluble fiber that comes from the husks of plant seeds and is one of my favorite to recommend. Research has shown that psyllium can help to reduce constipation and firm up stool for those with softer stool. What’s more, psyllium has been shown to help reduce LDL cholesterol levels, making it a potential adjunct therapy for those with high cholesterol. My husband swears by his daily psyllium husk. You can build up slowly to a tablespoon of psyllium husk powder in 8 oz. of liquid, but drink it fast because it gums up quickly. Or put it in less liquid but follow it up with the rest of 8 ounces of liquid. It’s best to do this away from any supplements you take as it may impede absorption of the supplements. You can also take it in capsule format, but it takes 6 to get to a tablespoon, so it’s a bit impractical. By the way, Metamucil is primarily psyllium husk, but it’s got other non-beneficial chemicals, so I’d avoid it and get a pure psyllium husk product.
Inulin* is a type of soluble fiber that is found in many plants, including chicory root, Jerusalem artichokes, asparagus, garlic, onions and leeks and can also be purchased as a supplement. Studies have shown that inulin can help to improve gut microbiota composition and reduce inflammation in the gut. Inulin may also have potential benefits for those with diabetes, as it has been shown to help regulate blood sugar levels.
Guar gum* is another type of soluble fiber that is derived from the seeds of the guar plant and is used as a thickening agent in many gluten-free foods. Research has shown that guar gum can help to improve stool frequency and consistency in individuals with chronic constipation. Additionally, guar gum has been shown to have potential benefits for those with high cholesterol, as it can help to reduce LDL cholesterol levels. Partially hydrogenated guar gum (PHGG) or Sunfiber (which you can find in my Fullscript Dispensary*), however, is particularly used in IMO (Intestinal Methanogen Overgrowth) as a beneficial fiber to help with constipation. It’s a type of guar gum that has been partially broken down enzymatically, making it easier to digest and less likely to ferment in the gut. PHGG has been shown to have similar benefits to regular guar gum, such as improving stool frequency and consistency, without the risk of worsening symptoms in individuals with SIBO or IMO.
Acacia fiber*, also known as gum arabic, is a type of fiber derived from the sap of the Acacia Senegal tree. It is commonly used as a food additive to provide texture and stability, but it can also be taken as a dietary supplement. Acacia fiber is a highly soluble fiber that is fermented slowly by gut bacteria, producing short chain fatty acids that can support gut health. Research has shown that acacia fiber can have a range of health benefits, including improving gut barrier function, reducing inflammation, and supporting healthy immune system function. Acacia fiber is a better choice in SIBO as it’s less likely to cause bloating.
Pectin* is another type of soluble fiber that is commonly found in fruits and vegetables, particularly apples and citrus fruits. It is also used as a food additive to thicken and stabilize products like jams and jellies. Pectin is fermented quickly by gut bacteria, producing high levels of SCFAs that can support gut health. Studies have shown that pectin can have a range of health benefits, including reducing inflammation, promoting healthy gut barrier function, and improving lipid metabolism. Modified citrus pectin* is also used in particular to help with chelation of heavy metals.
Glucomannan* is a type of soluble fiber derived from the root of the konjac plant. It is commonly used as a dietary supplement to aid in weight loss, as it has been shown to promote feelings of fullness and reduce appetite. Glucomannan is fermented slowly by gut bacteria, producing SCFAs that can support gut health. Research has shown that glucomannan can have a range of health benefits, including improving glycemic control and reducing constipation.
If you’re not dealing with bloating, you may want to try a combination fiber product like Thorne FiberMend or Pure Encapsulations PureLean Fiber, which you can find in my Fullscript Dispensary*. When starting any new fiber product or adding fiber to the diet through sources like beans and legumes, be sure to start slowly and build up so that your microbiome has time to adjust to avoid gas, bloating or constipation. Aim to increase fiber intake from food or supplements by 5 grams per day until you reach the recommended daily intake of 25-30 grams per day. I like the tool Cronometer, which is an online nutrient, calorie and macro checker, to see how you’re doing with your current levels of not just fiber but all nutrients. You can even enter your supplements in there to see if you’re getting the recommended daily allowances.
How can I get enough fiber from my diet?
If you want to avoid fiber supplements, my best advice for a diet high in fiber is to eat beans and legumes. I know they’ve gotten a bad rap because of lectins, saponins and phytic acid but I don’t find that most people are sensitive to lectins, and you can do things like soak them and cook them slowly to get rid of most of those problematic substances. And I’ll provide a link on how to do that. Unfortunately, most canned beans do not undergo pre-soaking so it’s best to make them yourself from dried beans.
While fiber is found in a variety of foods, including fruits, vegetables, whole grains, nuts, and seeds, beans and legumes really stand out for their high fiber content, and in my opinion, it’s very hard to hit the RDA for fiber (25-30 grams of fiber per day, based on your calorie intake) without eating them. Overall, beans contain more fiber per serving than any other type of food.
For example, here’s a comparison of ½ cup of the highest fiber beans with many other fruits and vegetables:
• Black beans: 7.1 grams of fiber
• Kidney beans: 7.3 grams of fiber
• Pinto Beans: 6.9 grams of fiber
• Lima Beans: 6.6 grams of fiber
• Chickpeas: 5.3 grams of fiber
Compare that to:
• Raspberries: 4.2 grams of fiber (but think about how expensive raspberries are and realistically, who ever eats an entire ½ cup of raspberries at a sitting? That’s like the entire container)
• Artichoke: 4 grams of fiber
• Broccoli: 2.3 grams of fiber
• Blueberries: 2 grams of fiber
• Carrots: 2 grams of fiber
• Green beans: 2 grams of fiber
• Cauliflower: 1.5 grams of fiber
• Cooked cabbage: 1 grams of fiber
• Raw Spinach: 0.8 grams of fiber
• Romaine lettuce: 0.5 grams of fiber
One way I recommend getting more beans and legumes into your diet is adding them to breakfast. Just make a batch and use them as your breakfast carb. Start with a tablespoon and work your way up. Or do a combo of rice and beans. That was a common breakfast that went great with an egg with a soft yolk over it when I lived in Costa Rica. They called it gallo pinto there, but there are many varieties of this from different Latin American countries. I’ll include that recipe in the show notes. I suggest breakfast because most people don’t vary their breakfasts a lot, so it makes it easier to make it a habit.
Nuts are also another good source of fiber but for a ¼ cup serving, it’s still only 2-4 grams of fiber. And of course it’s important to note that fruits and vegetables also provide a wide range of other important nutrients, such as vitamins, minerals, and antioxidants, that are important for overall health, so it’s best to get some of your fiber from other fruits and veggies, and balanced diet will include a variety of fiber-rich foods, including fruits, vegetables, nut and legumes.
Should I take fiber with IBS or IBD?
So as I mentioned earlier, there are some contraindications for taking fiber or getting much fiber in your diet in certain gut health conditions.
If you are in an active flare of inflammatory bowel disease, meaning Crohn’s Disease or colitis, studies a show that a high fiber diet will cause increased inflammation and disease activity. Therefore, low-fiber diets like the Specific Carbohydrate Diet, low FODMAPs or IBD-AID are recommended during times of active cramping or diarrhea. However, slowly introducing fiber once your symptoms have settled and could be described as mild or not present, one food at a time, is recommended to help keep your condition in remission. In human studies, psyllium husk, inulin and germinated barley foodstuff all showed positive results for decreasing remission rates, while wheat bran showed no benefit.
If you’re suffering with IBS-like symptoms, in particular bloating and gas after eating, or have diagnosed SIBO (small intestine bacterial overgrowth), it’s also recommended that you decrease your fiber, and avoid prebiotics like inulin, fructans and GOS (galacto-oligosaccharides), because they are high in FODMAPs, aka Fermentable Oligosaccharides, Disaccharides, Monosaccharides, and Polyols, which feed the bacteria and archaea that are typically overgrown in SIBO. So for people with active SIBO, I usually recommend either a low FODMAPs diet, Nirala Jacobi’s Biphasic Diet or Marc Pimentel’s low fermentation diet. If you do want to continue fiber supplementation to help with bowel movements by either bulking up the stool and decreasing diarrhea or to help promote more frequent bowel movements during a low fiber diet, acacia fiber* is a SIBO safe fiber, and partially hydrogenated guar gum or PHGG, aka Sunfiber (find in my Fullscript Dispensary*) is helpful in IMO or methane SIBO.
Because fiber can be irritating in certain conditions, one way I help people get the microbiome benefit of fiber without the irritation of it, while healing from gut health conditions, is to recommend supplemental butyrate or tributyrin, the preferred form of butyrate, while healing. This is something I tend to recommend only to people with soft stool or diarrhea, as it can be constipating. It’s one of the short-chain fatty acids that people tend to most lack when they have conditions like SIBO-D and IBD, which tend to go along with overgrowths of proteobacteria, which do not produce butyrate. And I’m sure you’re heard that I have my own tributyrin supplement called Tributrin-Max, which you can get for 15% off your first order with the code INTRO15 or super exciting, I now finally have it for sale on Amazon, and discount code TMINTRO15 will get you 15% off your first order there.
You may be asking yourself about prebiotic fibers too beyond traditional fiber supplements, and I have done another podcast on that, which may have some overlapping material, episode 28 Prebiotics and Fiber.
And of course if you’re struggling with some type of chronic disease, chronic inflammation, bloating, constipation, diarrhea, soft stool, acid reflux, etc. and want to get to the bottom of it, that’s what I help my clients with. You’re welcome to set up a free, 30-minute breakthrough session with me (Lindsey). We’ll talk about what you’ve been going through and I’ll tell you about my 3- and 5- appointment health coaching programs in which I recommend lab tests, educate you on what the results mean and the protocols used by doctors to fix the problems revealed. Or if you’re ready to jump in right away or can just afford one appointment at a time, you can set up an 1-hour consultation with me.
*Links are for affiliate web sites, thanks for your support of the podcast and blog by using them.
Lindsey: So today we discussed that we would talk about bile. I don’t think we’ve really had anybody on the podcast to talk about that topic. Let’s start out with what is bile and why do we need it.
Dr. Laura Brown: Really good question. I did a little bit of recent research. It’s been a while since I had dipped into this topic myself. We always take bile for granted. Bile is something that our liver makes, our gallbladder stores. And then upon a trigger, which comes from an enzyme in the small intestine, the gallbladder releases bile to help us digest fats. But there’s so much more to it, as we’re going to talk about today. Even if somebody has their gallbladder removed, the liver still makes bile, and it releases it as needed. It doesn’t have the chance to store it and concentrate it in the gallbladder. So the body has backup plans, like Plan B, to help us digest our food, especially fats, which we use bile for. But we’re finding out so much more about bile acids, which we’ll also talk about today.
Lindsey: Great. So isn’t the base of bile dead red blood cells?
Dr. Laura Brown: Yes, there are red blood cells in there as well. There’s also cholesterol, and other components. We’re learning more and more about what’s in there and what it’s used for. Our interest today is more on the gastrointestinal tract and what these things are doing. Bile acids are a big component of this, and when we first touched base together, you mentioned TUDCA, which is a secondary bile acid created through processing with the gut microbiome and the recirculation of bile. Bile is released, but it’s also brought back into circulation. We only excrete about 5% of it through our stool, and then 95% of it comes back up to be reused. As it’s going through these processes, it goes through a number of different chemical reactions. There are about four different kinds of primary bile acids, which are initially released from the liver, and then they get turned into secondary bile acids by the gut microbiome when they reach the large intestine. Those get changed and recirculate, and they have different purposes. TUDCA is one of them, and there are a lot of studies on mice right now, and they’re starting to do more in humans. They’re looking at a lot of the neurodegenerative diseases like Alzheimer’s, ALS, Huntington’s, Parkinson’s, and they’re seeing some positive results or influences with TUDCA* (access products using my patient direct code: I0rdLMOm) acting as an antioxidant or preventing that misguided protein folding that we see so often in Alzheimer’s. It’s really early in this type of research, so there are lots of mice studies and starting human trials. So I think before we stop the presses on some of the other drugs that they’re doing, but to continue the research on the synthetic TUDCA and TUDCA stands for Tauroursodeoxycholic acid. It’s a bit of a mouthful, so they call it TUDCyondA.
Lindsey: Yeah, exactly. So what are some of the things that can go wrong with the bile and the organs that produce and store it?
Dr. Laura Brown: Well, there are lots of things that can go wrong. For instance, if you have issues with your liver and it’s not making proper bile, then we have an issue. So we have to address liver health in that case. The liver makes the bile in one area and receives the recirculated bile acids in another area of the liver. There can also be issues with the gallbladder in the storage of bile, which I often see in clinic with patients coming in. It’s always sad when somebody says, “Oh, I had to have my gallbladder removed.” I wonder if they really had to because we see a lot in celiac and non-celiac wheat-sensitive patients. And I’m like, what’s going on?
What’s going on is that wheat is affecting us. None of us have the digestive enzymes to break down wheat. It’s a fiber that goes through our digestive processes and gets fermented in our large intestine. And that’s why they’ve always promoted whole grain products to help feed the microbiome and promote bowel regularity. However, for some people, for most people, they will have damage in the small intestine from eating wheat or gluten. Wheat has over 100 different proteins, gluten being one of them. The wheat damage happens in everybody and is usually healed up within 20 minutes. But for those who are celiac or non-celiac wheat-sensitive, the damage can last for up to five hours. And then typically, it’s time for the next meal. And usually there’s gluten in it again, right? Like if they’re not knowing, right, undiagnosed.
This repeated damage prevents the enzyme called cholecystokinin or CCK from releasing. When that doesn’t release, the bile isn’t triggered to be released. And if the bile sits around because the liver makes the bile, sends it to the gallbladder, and the gallbladder condenses it, then it can get sludgy and form gallstones. These gallstones are like prickly little things and can be centimeters in size. I had somebody walk in yesterday, two centimeters, can you imagine this two centimeter stone sitting in this tiny little organ, they can be bumping up against the sides of the walls and as they roll around, they can create scar tissue, which can cause inflammation in the gallbladder. So now we have cholangitis right, so we have the inflammation of the gallbladder, or inflammation of the ducts.
So you’ve got these little stones or the sludge sitting around too long, or bumping against the walls and causing damage. And now we have those nice little ducts getting damaged. And we also see a kind of blocking up of the ducts, it gets sludgy and it blocks it up. And then that can backflow and block up the duct that comes down kind of in the same neck, the same wire, kind of an intersecting highway, where the pancreas sends down its enzymes Okay, so then we get back up of the enzymes from the pancreas with all this, this blocked duct stuff going on, and this is all because bile isn’t moving freely, right? It’s not flowing. And this can cause issues with the gallbladder, inflammation with the gallbladder, gallstones, the duct blockage, and this all can happen from a trigger. And it’s not the only trigger, the wheat, right? It’s not the only thing that can cause all this. But that’s one thing that I often think about. And when we do a wheat-free, sugar-free, an anti-inflammatory diet, essentially, you know, no alcohol, no wheat, no sugar, low dairy, and then just lots of vegetables, that seems to help the cause. Of course, everybody’s individual and we’re not giving medical advice today. We’re just kind of talking and educating about what can happen here.
Lindsey: That’s interesting. I didn’t know that there was any relationship between wheat and gallbladder issues. So that’s great to know. If you do have thick bile, what kind of foods can help you thin it and get rid of that sludge?
Dr. Laura Brown: Yeah, so we want bitter foods to help trigger bile release, right? All of our bitter foods will stimulate all of our digestive juices. And it’s not just bile that starts, so I want you to picture a nice bright juicy lemon, okay? And then I want you to picture taking a knife, cutting that lemon in half, and now taking that half a lemon and then just squeezing it into your mouth. And I bet that you’ve already got digestive juices flowing in your mouth.
Lindsey: I do.
Dr. Laura Brown: Even the thought or the imagery of a bitter food gets that going and flowing in your mouth. But not just getting the salivary juices flowing, you’re now stimulating the whole digestive tract including the bile release to get things moving and get things ready for digestion. So having a hot cup of lemon water in the morning, I think most people have kind of heard like, oh, what did we do that for? So that can help stimulate or a nice bitter green salad: the endives, radicchio, that kind of thing.
Lindsey: Arugula…
Dr. Laura Brown: Arugula. That can, yep, dandelion. Those bitter teas. And then sometimes in naturopathic medicine, we use tinctures of gentian* or bupleurum*, or things like that are really bitter, that helps stimulate the digestive tract. Even a cup of chamomile tea or dandelion root tea are nice and bitter. They can stimulate as well.
Lindsey: That’s what bitter aperitifs are for, right?
Dr. Laura Brown: Right. You got it. You got it. Yeah. So these things can help stimulate the bile to keep it flowing and the digestive juices to keep them flowing. Because anything that becomes stagnant, obviously doesn’t flow so well, right?
Lindsey: And so what are the symptoms of gallstones?
Dr. Laura Brown: So lots of sharp, intense pain, usually it can be under the right breast, you can feel it there. Your liver, if you’re to take the palm of your hand and kind of nestle it up under your right breast, that’s kind of where your liver sits, is kind of there. And then your gallbladder, the ducts and stuff come off of where your index finger would be kind of in that area. So sometimes you get pain right there. But unusually, you can get pain in your right shoulder and have pain in the right shoulder. So that can be part of it as well. Nausea, vomiting, those can be issues. If it’s extreme, and you have blockage, you can end up with jaundice, that will show in the whites of the eyes, yellowish skin, sometimes you can end up with diarrhea. Okay, so some issues there. So those are some of the some of the symptoms: nausea, not feeling well, pain, diarrhea, that you can think, oh, what’s going on here? Oh, that might be a gallstone kind of kicking around.
Lindsey: So are there some early signs on any of the functional medicine tests that you do with patients that tell you that there may be a bile issue?
Dr. Laura Brown: That’s a good question. Some people suggest looking at small intestinal bacterial overgrowth to see if something’s going on there. We see different things in stool tests. Those with inflammatory bowel diseases have imbalances of Firmicutes and Proteobacteria, which affects how we shift bile acids and that affects the recirculation. So that’s something to watch for. You can also look at liver enzymes and things like that. But, you know, often you have to have severe inflammation or something really strong going on before the liver enzymes rear their head. Often it’s caught inconsequently, maybe on an ultrasound image, if somebody’s having it done for something else. It could be that indigestion, sometimes people will complain of indigestion or that little bit of pain, sort of watching for those kinds of complaints, family medical history of what’s going on, food sensitivities, understanding what’s happening there. So just picking up on different things, as far as screening tests and trying to look at bilirubin and things like that. But again, it you’d have to be pretty far down the road before those things would be red flagging.
Lindsey: And where would you find the bilirubin test, that’s part of a CMP (Comprehensive Metabolic Panel)?
Dr. Laura Brown: You can do that through blood. You can do that through looking at the urine; the urine is more measuring how the kidneys are functioning. So kind of looking at the blood tests.
Lindsey: What about markers for fat in stool? Are those indicative of bile sufficiency?
Dr. Laura Brown: Sometimes. Like a floating stool might indicate that we’re not releasing enough bile to digest fats. I don’t think I’m talking about on the test though.
Lindsey: Like steatocrit the GI map, for example.
Dr. Laura Brown: Yeah, you can use that as a clue. I don’t think it can be diagnosed from that. I would put together other symptoms and other things going on. That’s just one way the body’s talking to us when you’re looking at it that way. It’s like, okay, you know, let’s look at the bile. What’s going on there? Yeah.
Lindsey: So what does total bilirubin on a blood test mean?
Dr. Laura Brown: Bilirubin is your breakdown product of your red blood cell. And it is a part of bile. So you’d be looking at how much is there? And do you have enough? Is it too much or not enough sitting there? Usually you’re more concerned if it’s not releasing, right? If there’s blockage, depends on what’s going on, right? If there’s blockage, your stool might even look whitish or grayish, right? If your bile ducts are blocked, because you’re not getting any, you’re not getting into that red blood cell breakdown product or bilirubin into the stool, which is typically what makes it look kind of brown. So if you have a clay colored stool, and floats. Yeah, let’s think about that. Right? Let’s see, is the bile being blocked? And then why is it being blocked? Is it because the liver is not making enough? Or is it because something’s clogged there? Or are we trying to pass a stone? So there’s different things that could be going on. So you are always taking things as clues. Right?
Lindsey: Right. So what are the different supplements that one uses to deal with bile issues and what types of situations might warrant their use?
Dr. Laura Brown: So the different types of supplements that I look at: vitamin C seems to be helpful vitamin D seems to be helpful. Then I look at Malic Acid*. I found this that was very interesting. So malic acid, which is in crab apples, there’s a great gemmotherapy, and gemmotherapy is where you take the twig in the springtime of the plant that has the new fresh buds on it. And then you crush the buds of the leaves, which would have all the genetic material to help it grow and do its thing, and you would crush that down and soak it in alcohol, glycerol and water. And then that’s extracting the components that would be dissolvable in alcohol and water and glycerol. And then so you make a tincture or syrup out of that. And when you do that with the crab apple or the May apple, you’re able to create a medicine that helps dissolve the gallstones. So that can be helpful.
Lindsey: That’s called malic acid?
Dr. Laura Brown: Malic acid. Also berberine, which is found in Oregon grapefruit, hydrastis canadensis. Berberine is really great for the health of the liver. It’s good for blood sugar control, good for the gut. It’s anti-microbial in its physical form, or in a homeopathic form I’ve used for addressing gallstones and bile. If you want to just stimulate bile itself, as we mentioned, bitter tasting foods and tinctures can stimulate what’s going on there. If you’re trying to look at the health of the liver, Mary’s thistle, or milk thistle is always great to help the health of the liver. So that would maybe indirectly help the production of bile. And then if we want to stimulate new bile, we take bile acid sequesterants, which would be fiber essentially, maybe some psyllium or something to help pull that out of the system so that we have less recirculating, so it forces us to make more fresh bile. So that’s sometimes helpful to help reset the system a little bit there. So there’s lots of different things that I think about. It’s kind of like where we are at, what seems to be the issue because we want to balance; we don’t want to overproduce this stuff.
We know when we eat too many fatty foods, then we end up with too much bile acid being released. And this can be an issue as well. It’s acid. And when it’s a primary bile acid or when that’s initially released, it’s an acid so it can actually cause damage. And that’s why the body quickly throws you know hydroxylase to add some kind of chemical to buffer it a little bit. So it’s not so damaging. And that’s what’s a secondary bile acid is. But if we end up with too many secondary bile acids, this can be damaging as well. So we want to balance right and the balance is key. So it’s not just more is better or less is better. It’s the balance between the primary and the secondary. And that means having a good balance of the right gut microbes, so having a good balance of the Firmicutes and Proteobacteria, so that we’re actually changing the primary bile acids into the secondary bile acids. Those with inflammatory bowel disease have this issue, they have low levels of Firmicutes and Proteobacteria. So they’re not transforming as much of the primary bile acids into the secondary bile acids. So then this is causing inflammation, or this is contributing to the inflammatory picture; it wouldn’t necessarily be the only cause.
Lindsey: That’s interesting. I had never heard that about IBD. And so do they tend to have high bacteroides, then?
Dr. Laura Brown: That would be separate, right? And you would look at the different families within that. So because you break down all of the different components of the Firmicutes, it’s just the family, right?
Lindsey: Phylum. Yeah, those are the phyla.
Dr. Laura Brown: So you’re looking at what’s in there. So sometimes, that’s where you see when you get your results back from the GI map or the GI 360 test, you’re getting that breakdown of the six or seven families that are common, you can get the breakdown within them, and you could see what’s high, what’s low, we’re looking at those greater families. And you could have less or more of different phyla within the families.
Lindsey: Yeah, no, I wish the GI map would list Proteobacteria, but it doesn’t list Proteobacteria. So you kind of have to extrapolate from the overgrowth of individual bacteria, whether that’s an issue,
Dr. Laura Brown: Look up the GI360 and see if that solves what you’re looking for. Yeah, might be something of interest.
Lindsey: I like the GI Map, because it has H. pylori on it. And it’s an issue for a lot of people.
Dr. Laura Brown: Yes, you can add that to the GI 360. In Canada, at least in Ontario, we’re not allowed to add that in. But I think it is an option. We may be able to.
These harmful effects of the primary bile acids, as I mentioned, can be seen in inflammatory bowel disease, other gastrointestinal diseases, obesity, type 2 diabetes, liver diseases, cardiovascular diseases, and neurological diseases. So this gets down to some pretty nitty-gritty details of what’s going on, especially when you have four different ways that a primary bile acid could be modified, chemically modified. And then how the secondary bile acids work, and how they go into the system. So it branches out and then branches out. It’s like they told two friends and then they told two friends. It’s a lot of branching out of what can happen. A big domino effect comes back to often diet and often our standard American diet, which is high in processed foods, high in processed sugar, and processed wheat.
Lindsey: I don’t eat gluten or dairy. And sometimes, if you’re in the situation where you have to eat a meal in public, like an airplane meal or a cocktail party, it’s just shocking how dominant gluten and dairy is.
Dr. Laura Brown: Incredibly, and you know, it’s something you’ve probably had to learn to navigate. To navigate all of that, because it can be challenging and you want to boil it down. I would just focus on the people, eat something before you go, or just smile and say, no thanks.
Lindsey: Or just go and eat more carrot sticks and hummus.
Dr. Laura Brown: Yeah, and hope for the best.
Lindsey: Exactly. Okay. So when is actual supplementation with bile acids like ox bile recommended or not? Because I know there’s some types of SIBO for which it’s contraindicated.
Dr. Laura Brown: Yeah, tell me what you know about that. The SIBO and the contraindications with the ox bile. What is it? Where is your thinking on that?
Lindsey: I’m not sure. Let me let me dig up this piece of information. Okay, so ox bile is good for methane SIBO not good for hydrogen sulfide SIBO.
Dr. Laura Brown: Okay, right, that’s what you’re saying.
Lindsey: Yeah, that’s what I heard.
Dr. Laura Brown: Did they say why?
Lindsey: I’m not sure.
Dr. Laura Brown: Okay. It’s not something I have at the tip of my tongue. To be honest, I’d have to look that up. I use digestive enzymes sparingly. I use them with gallstones and to help with digestion. I’ll often start with bitters or 2 tablespoons of apple cider vinegar with a bigger meal to help the stomach make that hydrochloric acid so they can be more acidic, so they can stimulate what’s going on. So that we can suggest to help the body because, as you know, when you’re introducing, I’d like to find ways to remove the obstacles and then to support the body in what it naturally does. So when we’re putting the ox bile down there, yes, it could be helpful in some situations. But I like to see the body do what it does naturally, because it does it better than we can, right? And so supplements short term, when someone doesn’t have a gallbladder. If they don’t have a gallbladder and you’re having a higher fat meal, yes, you use it, use your digestive enzymes with the ox bile* in it, but also teach them how to have small meals or meals that are less fatty. So they’re not always taking an enzyme every time they eat.
Okay, the liver is still producing bile, so it can handle amounts of it. And you’ll see this, you may see the issue with people with short bowel syndrome, I see that as well. So if somebody has issues with short bowel syndrome, they’re not reabsorbing their secondary bile acids as much. And they’re probably having issues absorbing in what small intestine they do have. So it’s helping them out with that. So yes, so there are some situations where you would supplement and then we’re looking at what we talked about before the TUDCA, or the secondary bile acid that is being used in some of the research to help with the barrier function to help with cognitive regeneration. That’s something that I’m going to follow that research and see where that leads, it’s not something that I’m going to pull out of my pocket right now and say, to my patient, that I would trust in this not giving you Alzheimer’s. No, but it’s something I’m going to follow up because it’s very interesting.
We’ve been using bile supplementation for 1000s of years, the Chinese medicine reparatory uses it. In many different uses, 1000s of years they used the bile from bears in order to help with digestive disorders. So it’s not new. It’s just picking in and knowing some of these more detailed research studies that are coming out, to be able to understand what we might use it for, other than just, okay, we don’t have a gallbladder, we’re eating a fatty meal, we’re giving it, we’ve got a gallstone. We know that ox bile* can help dissolve cholesterol-based gallstones. We’re having issues digesting. So maybe we take a little bit, maybe we try that apple cider vinegar first. Get the diet under control and reduce the wheat, the dairy, the sugar, the alcohol, right, those types of things. Get the obstacles out of the way instead of throwing band aids and stuff.
Lindsey:
Yeah. So I’m wondering since bile is so important in digesting fat, how much fat is too much in the diet? Like I know people, and I think it kind of happened to me that when they tried to ketogenic diet, they started having sharp abdominal pains and I’m thinking maybe they were gallbladder pains.
Dr. Laura Brown:
Yeah, likely they were because some people can’t handle it, especially those with their gallbladders. removed. Right? They can’t handle that bullet.
Lindsey:
Oh, yeah. For sure if they’d had it removed. Yeah.
Dr. Laura Brown:
Right. So it’s spreading that out throughout the day. Sorry, the question again . . .
Lindsey:
. . . was how much fat is too much in the diet? Because like a ketogenic diet is supposed to be 70% fat?
Dr. Laura Brown:
Yeah, I mean, it’s individual, right? I mean, there’s no one right diet for anyone and no one diet for any of us for life. So it’s finding out what works and what doesn’t work. And you might find the keto diet is not for you. So maybe you just modify it a little bit. And then you’re okay. But just be watchful for those symptoms, like the sharp pains, or the nausea, or the gray and floating stools, or the pain in the shoulder, maybe it’s the right shoulder that you’re getting that pain in. Or you’re just not feeling well when you’re eating that level of fat. It’s not for everyone.
Lindsey:
Yeah, no, I discovered it. It definitely wasn’t for me, because I love carbs too much. But it also wasn’t for me because of the pain. So how do constipation or diarrhea relate to bile? Is there one more than the other that might point to an issue related to bile if other causes are ruled out?
Dr. Laura Brown:
I mean, there’s bile acid diarrhea, right? That’s something that we know is part of IBS-D, it could be bile acid diarrhea. And that is, essentially you don’t have the bile to break down the fat. So you’re getting that immediate kick. And it sometimes happens with people with undiagnosed celiac disease, the problem is that they’re not digesting the fats. And it’s just like quickly getting exited because the body is going and we can’t digest this here. Right. So it’s a fast exit. So that could be part of what’s going on.
Lindsey:
So in that case, it probably be likely there would be fat in the stool, and there’d be diarrhea.
Dr. Laura Brown:
And you got it. Yeah, yeah.
Lindsey:
Okay. And what does the research say about the impact of saturated fat on the microbiome?
Dr. Laura Brown:
Well, different people handle saturated fats in different ways. We know too much fat is inflammatory, and there’s some saturated fat that we can handle little bits of, other people not so much. We know saturated fat in some people, especially with the familial hypercholesterolemia. So high cholesterol runs in the family, these people tend to absorb more saturated fats from their diet easier, and then they end up driving up their cholesterol and it affects them. For others, the saturated fats don’t affect the cholesterol so badly. So in moderation, they’re okay. But we know too many fats of any kind, especially the saturated, or the hydrogenated or the industrial seed oils are inflammatory, they promote the arachidonic acid cycle, which is inflammatory. So this is affecting the gut barrier, and sorry, my brain just kind of going into different things, because the bile acids hit vitamin D receptors, and there’s a lot more there to unpack, that I’m just getting into now. So there’s different ways that that high fats, affecting more primary bile acids being released, if we have more primary bile acids being released, so we end up with more secondary bile acids, some secondary bile acids are helpful, too much are now inflammatory and not helpful. So that can cause issues as well. So it’s a lot about balance, right, starting with what we put on our plate, and what we put in our mouth.
Lindsey:
I guess the best thing a person can do is experiment with what feels good, right? Like I know personally, that if I eat a pork belly, that I’m not going to feel good. That’s a guarantee. I better take some digestive enzymes, I better do something because it’s just going to be too much.
Dr. Laura Brown:
Right? So you’ve learned.
Lindsey:
I’ve learned yeah, but I can handle a couple slices of bacon, it’s not going to make me feel bad. So I think our bodies give us clues as to what works.
Dr. Laura Brown:
I always say the body sends us lots of messages, like 1000s of messages. And if we’re quiet enough, we can hear the whispers. Sometimes it even screams, right? Sometimes the body just screams at us. And we just have to know what the body’s telling us and or at least relay what the body is telling us. So people come in my office and they’re trying to find words for what’s going on. I’m like, just give me the motions just just like because the body doesn’t speak in words, the body speaks in messages, right? Or hand gestures, things like that. So I just try to get people to explain, it doesn’t have to be a real word. Because this is often how the body speaks is in gibberish, because it just can’t get it out. And then that is such a great clue to what’s happening and what’s going on. And then we keep pulling on the loose strings to figure out the puzzle.
Lindsey:
So are there dangers of following a super low fat diet following a gallbladder removal?
Dr. Laura Brown:
That’s a good question. I think you have to introduce the fat slowly to help train the liver, right. So I wouldn’t go out and eat a bacon and avocado sandwich with cheese, right? Or a really high fat meal immediately after having gallbladder removed; you would slowly reintroduce the amount of fat so that your body would acclimatize to its new reality.
Lindsey:
I just know that I hear I hear people who’ve said “I had my gallbladder removed, so I just can’t eat fat anymore.” And so they literally are avoiding it. Very purposefully, no added fat to cooking. And I imagine that you could end up deficient in some of your fat soluble vitamins if you went super low.
Dr. Laura Brown:
Well, exactly and you want to trigger some of that bile to come out because you need it in order to help dissolve the fat soluble vitamins or as you said, you’re not going to absorb them. And if you’re missing out on even your essential fatty acids, what’s your body going to be making your cells out of? Every cell in the body has a phospholipid bilayer, which means it’s made of fats. And if it doesn’t have healthy essential fats, like omega 3s from fish or walnuts or flax seeds or things like that, then it’s going to make it out of whatever it can. And when it’s not making it out of the more fluid fats, it’s going to make it out of other stuff. And typically, that membrane ends up being a little more rigid. And if it’s more rigid, it’s not going to let the toxins out or the nutrients in as easily as if it were more fluid. So you still need some fat, it’s not a no fat diet, it’s a low fat or kind of a trickle fat. But you know, it’s adjusting, and acclimatizing and just retraining the liver to deliver it just in time, right? You want that bile to be delivered just in time.
Yeah, you’re right, your vitamins A, D, E, and K are all your fat soluble vitamins. And you need to have them with some fat and you need the bile to be able to go in and emulsify or break it apart, just like the dish detergent does in the sink – takes those bigger fat droplets and breaks them all into little smaller ones so that it can be absorbed in the small intestine. And then if we’re not absorbing those things, you’re not getting the fat or getting the bile to help digest that, we’re going to miss out on those key nutrients, which is important. But you have to think, lots of foods that we might not think have a lot of fat. Sometimes just a little bit of fat can be enough for somebody. So nuts and seeds, for example. Sometimes people don’t think of them having a lot of fat, but they are they’re pretty high in fat, right? It’s sometimes thinking that, oh, I didn’t realize that had fat in it. They’re just thinking the overt pouring oil on.
Lindsey:
Right, right. And meat and fish, those have fat too.
Dr. Laura Brown:
Yeah, absolutely. Like salmon, right? Or fatty fishes with your essential fatty acids. Those are key. Yeah. So you’ll be getting some of that. So the body learns; it’s very resourceful.
Lindsey:
Right, very resourceful. I know. You can take out any number of pieces of our body and it still manages to function, perhaps not optimally, but it functions.
Dr. Laura Brown:
Exactly. Yeah, exactly.
Lindsey:
So we’ve been focusing very much on bile, but what else is involved in fat digestion?
Dr. Laura Brown:
So we’re looking at those enzymes, we’re looking at that fat coming in. I’m not sure what you’re getting at, because we’ve talked about those things, as well. What do you think, what are you thinking?
Lindsey:
Oh, I was just thinking, you know, the other digestive enzymes like lipase and such that are involved in that digestion and that process.
Dr. Laura Brown:
Right, and the lipase coming from the pancreatic area. And those types of things are often included in a digestive enzyme as well. It’s not just ox bile, that type of thing. So if we’re having issues digesting, those would come with it. Yeah, so the digestive enzymes are coming from yes. . . for starches it starts in the mouth. And then stomach is meant to kind of break things down chemically. And also with the acid, but then we’re needing the bile, and then the digestive enzymes from the pancreas to do that first breakdown. And then obviously the microbiome, as we talked about before, changes those primary bile acids into the secondary bile acids. So that’s part of our digestion for fats too, in order to help do things that way. Most of the fats are ideally absorbed in the small intestine, the first part of the digestive tract. Okay.
Lindsey: And so earlier you mentioned you use digestive enzymes sparingly. So I’m wondering why so sparingly and whether what kind of situations you use them in?
Dr. Laura Brown: Well, I say sparingly, because I don’t like to use anything unnecessarily. And I believe everything has a time and a place for it. There’s some people that have issues with their pancreas, sometimes, advanced celiac disease, patients need a digestive enzyme with every meal. We know that there’s different types of digestive enzymes, not just ox bile, there’s papain, there’s bromelaine, there’s other types of ones that help break things down. There’s ones that cystic fibrosis patients might use to break down mucous. And the types of things that you would use those in those cases, if you’re using something, to act systemically not to digest food, you would take it away from food, right.
So that might be a different use of a digestive enzyme, or you might call it more of an enzyme, not just digestive. Because an enzyme is really something that helps a chemical reaction occur without consuming itself. So that is what an enzyme is. So it helps a chemical reaction occur. And we have lots of different chemical reactions happening in our body all the time. So the digestive enzymes taken away from food can help break down mucus, can help bring down inflammation, can help with inflammation in joints, arthritic conditions, gout conditions. So that’s one area to use digestive enzymes between meals or away from food on an ongoing basis to help with that type of thing.
If you’re using it to help digest food, or is there some kind of physical roadblock to our own digestive enzymes? Is the pancreas damaged? Is the gallbladder removed? Is the liver damaged? Can we heal the liver? You know if the gallbladder is just sludgy, can we clean it out first, right, or while we’re cleaning it out, take the enzymes, but then when we’re done, we don’t need them anymore. There was some thought with the secondary bile acids, some of them might help heal some of the pancreatic cells. So there were some ideas there that I saw in some of the research, you might use them to help the healing. But then when you get the healing done, or when you using them in the meantime, while you’re doing healing with other things, then when you’re done, you’re done. Right? So as I said, using it sparingly. There’s a dose at a time and there’s a duration. It’s not in all circumstances that once you start it, you have to be on them forever.
Lindsey:
Do you think they’re useful in SIBO? Because I have I have post infectious IBS. So I’m always getting bloated after a time. I mean, I can take antimicrobials and then it starts over again. So my thinking was I take a digestive enzyme with each meal just because I want to make sure everything’s getting digested and everything’s not hovering for the bacteria to grow.
Dr. Laura Brown:
So then I’d look at what’s the mechanism of the recurrent SIBO? And what’s going on there. And what can we do to prevent that? And is there something that we can do to halt the presses on that? Often I see food sensitivities that impact the ileocecal valve, which is the valve between the large intestine and the small intestine. And it gets a little grumpy when it gets constantly irritated by foods it doesn’t like, so then it gets lazy, and lets the bacteria that’s supposed to stay in the large intestine up into the small intestine. This is small intestinal bacterial overgrowth. And our large intestines are designed to ferment foods. And if it’s sitting up in the small intestine, it starts to ferment and it goes crazy because it’s where you get more of the sugars and things like that. So it starts to ferment and that’s the bloating, the gas, an uncomfortableness, but it was looking at food sensitivities and what’s going on there. We also know there’s things like, Levothyroxine can promote small intestinal bacterial overgrowth. So if it’s something that you need to be on because you have hypothyroidism, then maybe every once in a while we’re doing that maybe once a year, we’re doing a gut cleanup and, and doing some antimicrobials. Just to help prevent that from happening.
There’s a nice little move that I do in the clinic to help shut the ileocecal valve. And that can happen. So I’ll do that for some people. I had a lady walk in one time, just off the street. I’ve had this pain for two years, can you do something about it? I’m like, okay, you’re just telling me about it. Okay, lay on the table. And then I’m just poking around, you know, just to the right of the bellybutton and over a couple inches, depends on the person. So I’m feeling around that you could tell that there was some irritation there. So I just do the move that helps close the ileocecal valve. And, her appointment was over, and I said “let me know how you feel”, and I never hear from her. So, some time goes by, and I reached out to her and I thought maybe I offended her. She didn’t like that or it felt weird or hurt or whatever. And I said, “Oh, was everything okay after your last appointment?” And she goes, “yeah, I walked out of there with no pain.” She was in pain for two years. It’s gone. And it’s never come back. Yeah, I mean, that doesn’t happen every day in practice, but I mean, it’s like, hey, this is great. It’s not bad for business, but great for the patient.
So so many things like that can be helpful to watch out for. But then it’s looking at the diet, looking at the food sensitivities, looking at why do we have this recurrent SIBO going on. And that’s individual for the patient to dig into that. So that we can get moving forward, and sometimes it is food restriction. Sometimes it is antimicrobials on a rotating basis. Sometimes it’s fasting just to give that whole digestive engine a break, right, just a rest. Sometimes that’s as good as anything, and it’s finding what works for you, as an individual, what works for you to help reset. You know, I kind of find my little arsenal of stuff and, and know what works like I love bitters*. I know things get slow for me, I’ve got a lovely bitter formula that I put together. And it’s Chinese bitters. And I mean I’m lucky that I don’t have a strong bitter receptor. Some people do. So I can get it past my mouth. And it’s not an issue. But I find that it can be really helpful for me and it doubles as an antimicrobial. But if I think fine, things are just kind of slow to digest. I feel like foods kind of sitting there too long, because you get that sensation, right? It just feels like the things aren’t moving through, it’s sluggish. So I find for me, bitters are a really awesome way to get things flowing and going.
Lindsey:
In my case, I have elevated vinculin antibodies. So I know I’m going to be getting SIBO over and over again. So it’s just a matter of continuing to, to chip away at it. So prokinetics and trying not to eat constantly. I’m not a big fan of fasting, though.
Dr. Laura Brown:
And it’s fine. And there’s no one right way to fast. You could just extend to, maybe it’s a 12 hour fast.
Lindsey:
I shoot for 12 hours at night. Shoot. I’m not sure I always hit it, but I shoot for it.
Dr. Laura Brown:
And then maybe every once in a while you make a bunch of bone broth, or you just have something that’s a little more simple to digest. Or you have like I’m going to eat vegetables all day today. Right? That kind of thing. Just to give the body a break from heavier stuff. Digesting heavier things. So you give it a break from the fat and the protein and the heavy carbs. You just eat vegetables all day. Nothing wrong with that. Right? You can do it for a day or a morning, right? Maybe you don’t want to do it all today. So yeah, just to give a little digestive break. I can tell my brain that I’m doing a digestive break. But if I say I’m not going to eat the first thing I want to do is eat. So but a digestive break, that’s fine, because it’s a whole engine. Right? We talked about how things start when we think about it. We thought about that lemon, and boom, what happened? We didn’t even eat a lemon and we were just thinking about it and everything started to flow.
Lindsey:
Yeah, right. So it’s amazing the power of the mind.
Dr. Laura Brown:
Our experience with food starts when we think about it. It’s intensified when we see it and smell it and that is the beginning of our digestive process. Then we eat it, then it starts to go down through that whole process. So sometimes we do need to give it all a bit of a break.
Lindsey:
Okay, so we’ve sort of covered this in a roundabout way. But just concretely, if somebody is staring at a suggested gallbladder removal, what would you tell them to do, to try and avoid?
Dr. Laura Brown:
Depends on how far along we are, how much damage has been done? Is the gallbladder intensely inflamed? Are we in a lot of pain? Are we able to eat? So we kind of take those things into consideration, if I have somebody that has some gallstones, and the doctor said, well, let’s just remove it. It’s bothered them. Now, they’ve been to emergency a couple of times, but we’ve kind of figured out that’s when they eat pizza, and a lot of biscuits or something. It’s like, okay, hey, let’s change up the diet. Right, let’s get the gluten and the processed foods out of there, and the sugar. Let’s get that out of there. Let’s hold up the alcohol. And these sometimes are stepping stones or can be roadblocks for some people. So it’s helping them understand how to do that. And then getting more vegetables, lots of cabbage-based family vegetables, getting some bitters in there, getting some of maybe that hot lemon water, or the chamomile tea or the dandelion root tea, just getting some of these things into the diet. And then seeing maybe using some of that malic acid tincture that I talked about, or some of the homeopathics. Or maybe we’re using some ox bile or some combinations of these things. And then we’re giving it a month or so to see how we’re feeling. Are we feeling better? Do we have less pain, and are we not doubling over anymore? We’re able to eat and feel fine. And then usually they’ll go back for an ultrasound or something to see if there’s further inflammation or whether gallstones are out. So we can see oh, do we have this under control? Okay, sounds like a good plan.
Lindsey:
Well, that was all the questions I had about bile, anything you would care to add.
Dr. Laura Brown:
Just that there is ongoing research on what the secondary bile acids do for us, the secondary bile acids are a byproduct of the gut microbiome in the large intestine. So it makes three different things, it makes things made from the short chain fatty acids, and it makes the secondary bile acids. And then there was one other thing, I think it was a taurine-based byproduct that it also makes. And it’s taking a look at what these things are responsible for in the gut and just understanding and appreciating the complex interaction of the gut microbiome, its byproducts, and our human immune system, our gut lining, and not only the gut lining, but the blood brain barrier, and just how those things go together. And just appreciating the health of the gut and how it affects the rest of the body. I mean, this is why I wrote a book on it, that book I wrote is called Beyond Digestion*. And it’s just I found so many things started in the gut, and just appreciating that if we take care of our gut, it’s going to take care of us, our microbiome is is huge 99% of the genes that we carry around with us on tests that our microbiome, and if we take care of it, we’re going to be much healthier, and we’re learning this more and more and more. And it comes first and foremost with diet, what we’re putting on our plate and then how we’re treating ourselves. Stress is huge, finding ways to manage that. There’s many different things that affect the health of the gut. It’s been great talking about bile and it was interesting doing a deep dive on some of the more recent research, so I appreciate that stimulation Lindsey to bring that to light and just know that some of these things like the TUDCA is of great interest for the neurodegenerative diseases. And just to keep following up on that if you have family members with Alzheimer’s or Parkinson’s or Huntington’s or ALS. This might be something that would be really helpful in the future where we have little to offer otherwise, but everything comes back to the data and food is medicine.
Lindsey:
Yeah. Okay, awesome. Well, thank you so much for doing that deep dive on bile.
If you’re struggling with bloating, constipation, diarrhea, soft stool, acid reflux, IBS, IBD or any type of chronic disease, etc. and want to get to the bottom of it, that’s what I help my clients with. You’re welcome to set up a free, 30-minute breakthrough session with me (Lindsey). We’ll talk about what you’ve been going through and I’ll tell you about my 3- and 5- appointment health coaching programs in which I recommend lab tests, educate you on what the results mean and the protocols used by doctors to fix the problems revealed. Or if you’re ready to jump in right away or can just afford one appointment at a time, you can set up an 1-hour consultation with me.
Rich Maurer: Yes, thank you, Lindsey. I really appreciate you having me on your podcast. I have to say I really enjoy your podcast, been listening for probably over a year. Then there’s one thing I did not see, though until recently, that you’re actually sitting on a little stool. So I assume you intended that as a play on words. Well done there.
Lindsey: Thank you. That’s funny you say that because I thought of that right at the very beginning and not much since then. No one’s ever mentioned it. But that was part of the design of the cover photo.
Rich Maurer: Sure. Now everybody knows.
Lindsey: Indeed, now they do. Secret’s out. So you reached out to me because I had interviewed Bo Berman from Layer Origin about their human milk oligosaccharides or HMO prebiotic. And you’d had some interesting results that you’re tracking using stool tests following your use of that prebiotic, and we’ll get into your results in a minute. But can we start with what your starting conditions were that made you want to try it?
Rich Maurer: Right, you know, I listened to your podcast and others, and I hear so many people that are really struggling with all sorts of health problems. And I always considered myself a fairly healthy person, even though lifelong migraines, lifelong IBS-D, decades of asthma, lots of family history of various things. But I said to myself, I’m pretty fit, I exercise. I don’t have heart disease, diabetes, cancer, you know, I’m on some prescriptions, but whatever, you know, I’m pretty healthy. But I realized I was fairly fit but not actually that healthy. Then COVID happened actually, that was a big point, January of 2021. Got COVID, for the first time, really bad case of it. Wasn’t hospitalized, so wasn’t life-threatening or anything but really, really sick for a couple of weeks and had some serious gut symptoms from that. A couple of episodes of excruciating gut pain, and my wife was so kind, she started looking for some foods and diets that could help during that time. So I look back on that time, and I say, I thank God for COVID. And I say that carefully not to say that I’m glad that COVID exists, that people would be harmed or killed from it. But the impact of COVID in my life was really beneficial, was a turnaround, helped us to look at our diet or overall health. So we started on that time, a FODMAP diet, which I’d never heard of before. Not sure if it helped, but I think just eating good food and getting rid of other things. And then the first thing I noticed was migraines went away. I had a migraine 24 hours for two weeks. Shortly after that, they were going away. And I think that was mostly elimination of sugar is what that was. And then through nutrition, continued exercise, and then the prebiotics – HMO is one prebiotic we’ll talk about – I was able to eliminate migraines, IBS-D, asthma. And a more recent discovery, which I didn’t start with, was that my HbA1C, you know, it’s an average of your glucose in your blood, went down by 14% from a pre-diabetic level to an optimal level, and then also lowered my cholesterol, triglycerides, and LDL by 15%. And then went off all prescription meds, and I feel like at age 59, I’m healthier than I’ve been in decades.
Lindsey: That’s awesome. And so I’m sure people are interested in particular in the IBS-D. Do you feel that the HMOs had an impact on that? Or did something else prior to you trying HMOs have an impact on that?
Rich Maurer: That’s a great question. And I’m not absolutely certain. But getting off of dairy products seemed to have the biggest impact. I think it’s multifactorial, but for me, I think it was the dairy products. And I’ve gone my whole life and I don’t understand that, you know,
Lindsey: I am lactose intolerant. And I knew that and I took pills for that, you know, lactose digestant tablets for years. But it wasn’t until I read this book, that ironically was sitting in the bathroom at a place I was working at. And it was all about poop. Every single page was a different kind of poop. And then there was one that was called the lactose poop. And it was like loose, painful. And I was like, that’s exactly what it is when I don’t take enough enzymes, or when I’m not careful, or I eat too much. And then just try and throw some ice cream on top. That was exactly what it was like. It took me reading that book to realize that this. That was long before I was a gut health coach.
Rich Maurer: Sure, yeah. Interesting. Just curious. I’ve just started experimenting with lactase. I’ve only done it a couple of times. I’ve been so quote unquote afraid of dairy products. Although yogurt, some fermented dairy doesn’t seem to bother me at all. Does Lactaid help in the short term and occasional?
Lindsey: When I eat dairy now, I will take a lactase enzyme. Yeah. And Lactaid is one of the brands of those. Yes, it definitely helps. But I found that it was never foolproof, right? Like if I ate too much, and then I just tried to try to stick a dessert on top that had lactose in it or, or if I just didn’t time it right, you know, maybe I didn’t take enough with my meal, or my dose wasn’t big enough, or just there’s too much food in there. It just didn’t mix up right and take care of the lactose. It was really bad coming out the other end.
Rich Maurer: Gotcha, gotcha. No, thanks for that. Yeah, I stay away from dairy. Most of the time, it’s an occasional treat.
Lindsey: So can you just explain a little bit about what HMOs are, since it’s been a while since I’ve had that podcast on them?
Rich Maurer: Sure. HMOs stand for human milk oligosaccharides. And oligosaccharide is a medium chain sugar, it’s non digestible by humans. So HMOs would fit into the larger category of a prebiotic fiber. And again, they are soluble fiber, indigestible to humans, but they directly feed the good gut bacteria. One of the things that really fascinates me about HMOs is the fact that it’s the third leading ingredient in human breast milk and mother’s breast milk. And I used to work in hospital labs, I got a Bachelor’s of Science degree, but most of my life, I’ve been a pastor. So I definitely look at life through what we call a Biblical worldview. And I see this as the creator, the divine designer, just putting this into his creation, the fact that a large part of mom’s breast milk contains these HMOs, which again, since they’re not digestible by the baby, or adult and any human, it doesn’t help the baby directly. It only feeds the baby’s beneficial bacteria. So that was all designed and put into HMOs. But obviously, HMOs are not human breast milk. It’s a derived thing in the laboratory that contains only the HMO and not the other aspects of the breast milk derived from cow milk. I think that’s correct, right?
Lindsey: Yeah. That’s what I recall from my conversation with Bo Berman. Yeah. And that’s a beautiful perspective. The other perspective I heard on a podcast yesterday was, it may be that we’re just the host for the bacteria, that they’re actually the ones in charge, and we’re just carriers for the bacteria. There’s more of their cells than there are of us.
Rich Maurer: That’s a very pessimistic viewpoint. But yeah, okay.
Lindsey: Just a floating viewpoint. Anyway, what kinds of changes did you see in your stool test results and other test results after being on the Layer Origin HMOs? And what dose were you taking of them?
Rich Maurer: Right, so let me back up and say, before I discovered HMO, I was taking some other prebiotic fibers, about five different ones for a while. Now I’m down to two or three. So I did a stool test while on five prebiotic fibers, did a second stool test, then started on an HMO, and then the third stool test. I’ve got a couple of videos out that monitor the progress. But I saw, by far, the most dramatic changes just with the HMO. And there are three keys that I saw, which I think are really absolutely crucial for a healthy gut or elimination of what would be a leaky gut. The opposite of that would be an increase in butyrate. I’m just going to list these, and we can talk about them: an increase in butyrate, an increase in gram-positive bacteria, which are the “healthy” bacteria in the gut, and an increase in a certain type of gram-positive bacteria, specifically Bifidobacteria. I can talk through those a little bit.
Butyrate is a short-chain fatty acid that is actually what’s called a postbiotic. So the gram-positive bacteria in your gut produce that as a byproduct of their own metabolism, which is again, another one of these symbiotic relationships that benefits all of us. All the species in our body need butyrate. In fact, in the colon, there’s a single layer of epithelial cells called colonocytes. The only thing separating all the fecal material, all the bacteria, all the toxins is a single layer of these colonocytes that separate all of that from your bloodstream. So when we talk about a leaky gut, we’re talking about fecal material, especially the toxins that get through that single layer of colonocytes. Something called tight junctions will open up and allow these things to get through. But the colonocytes, that’s their food. They consume butyrate. So that will heal them and give them the energy that they need to repair or maintain a healthy gut. So that’s butyrate, a short-chain fatty acid.
Secondly, an increase in gram-positive bacteria. And why that is so important is because the gram-negative bacteria produce a toxin called LPS (lipopolysaccharide) that exists on the cell wall of the gram-negative bacteria. If it gets into your bloodstream, it’s a toxin. If it gets in your bloodstream, it can travel anywhere in your body and cause systemic inflammation, leading to all manner of metabolic disorders and diseases. So it’s extremely important to reduce that, and one of the ways you reduce LPS is by reducing the numbers of gram-negative bacteria. And you do that by also increasing the gram-positive bacteria. I’ll give you my butyrate results. I went from 52% butyrate. And now let me say these numbers are from a website called Biomesight. So what you do is you take your gut test, and any gut test that has fast Q data, you can upload it to Biomesight. And I love it because they track the changes. So I’ve got three stool tests that are uploaded to Biomesight. So I can literally chart it, it’s actually charted for you, the increase is specifically in regard to butyrate. They’re not measuring directly the amount of butyrate in your gut, they’re measuring the bacteria that produce butyrate. So when I talk about percentages, I’m talking about the percentages of butyrate-producing bacteria. And mine went from 52% to 65%, which, at that time, several months ago, put me at the 100th percentile of everyone that had the data on Biomesight. So that was a massive increase. Since then, my daughter, actually, she’s second place, as far as I know, she went from 41% to 67%. And now she’s at 99%. I just talked to a friend yesterday, he went from 49% to 74%. So that’s a tremendous amount of butyrate, right? You look at his distribution chart, and it’s literally off the chart. It’s so high, and my daughter and this friend only utilized HMO as a prebiotic, whereas I had the other prebiotic fibers prior to that.
Lindsey: Which stool tests are you using that you can afford to be doing this frequent tests on everybody?
Rich Maurer: Right? Well, of course, I’m not paying for their tests. Yeah. But paying for my wife’s and mine. I used what used to be Thryve Inside (now Ombre) through discount codes. I don’t pay more than $60. It’s not cheap. But compared to some others, a couple $100 each, it becomes more tenable.
Lindsey: And is that 16S? Or is that metagenomic?
Rich Maurer: That’s 16S.
Lindsey: Okay.
Rich Maurer: Yeah, I believe. So butyrate results have been fantastic. And then talking about an increase in gram-positive bacteria. It’s my daughter’s who holds that record. My friend increased his greatly, his went from 50% (so these are also percentages). So he had an even amount of gram-negative and gram-positive bacteria to 87% gram-positive bacteria, where my daughter went from 62 to 89% gram-positive bacteria. So the vast majority of their colon is filled with healthy, gram-positive bacteria, which again is going to reduce the LPS and the toxins, etc. In regard to LPS, just for a moment here, this is just an analogy that helps me think about the damaging effects of toxins. E. coli is a gram-negative bacteria. And most people are familiar with E. coli outbreaks and they cause hospitalization, and unfortunately, sometimes death. That’s a different toxin that’s called a Shiga toxin. And that toxin, of course, it’s similar, right? It gets in your bloodstream, it travels throughout, shuts down organs, especially kidneys. So I say that toxin from a gram-negative bacteria can kill you fast, whereas LPS from gram-negative bacteria can kill you slowly. That’s ultimately what it’s doing. But it’s still a toxin. And it’s this slow killer, really is the way I look at it.
And then thirdly, an increase in a certain type of gram-positive bacteria, specifically Bifidobacterium, and this is where I did a lot of research just looking for reputable research papers, meta-analysis, etc. And again, what I’m seeing is when you have type 2 diabetes, you consistently show a decrease in Bifidobacteria. And what’s happening is that is decreasing insulin sensitivity or increasing insulin resistance, I can talk about that for a moment. Insulin is what drives glucose into the cells. So if you picture your cell is waiting there, it needs glucose, right, to produce ATP and energy and feed itself. And if the receptors for the insulin are blocked, it can’t get the glucose. That’s insulin resistance. And if that happens, and it continues to happen, of course, your bloodstream increases the amount of glucose, and that then is a measurement of HbA1C, which is a three-month average of glucose in your bloodstream. And that leads to the beginning of type 2 diabetes. But when you increase the Bifidobacteria, it increases the insulin sensitivity, which allows that channel of glucose to regularly enter into your cells. So what I saw is a pretty dramatic decrease. I was at 5.7, my A1C, which was just inside prediabetic, and barely. If I tested the next day, it might have been 5.6. But over about four or five months, it went down to 4.0, which is an optimal level. And as far as I can tell, the only thing I did different was HMO. And of course, during that time, my Bifidobacteria went from almost undetectable. It went up some on prebiotic fibers and then just skyrocketed on the HMO. And specifically, again, in a symbiotic relationship, one particular species of bacteria that skyrocketed only on HMO is Bifidobacterium adolescentis. And it produces a different type of short-chain fatty acid, propionate. And a key butyrate producer, Faecalibacterium prausnitzii, consumes the propionate produced by the Bifidobacterium adolescentis, and then in turn produces butyrate. So, again, just that symbiotic relationship working together. Those are my changes, both on the gut tests, blood tests, and symptoms.
Lindsey: Yeah, and I have certainly seen studies showing that Bifidobacterium decreases. I think Bifidobacterium infantis is the primary bacteria that starts in the gut of a child who’s born vaginally, at least. Then all Bifidobacteria in general decrease as you age, and I think those decreases are associated with some of the problems of aging or the normal consequences of aging. So yeah, an increase in Bifidobacteria seems like it would be a net positive for sure.
Rich Maurer: Yeah, for sure. Interestingly, I’m helping some family members and friends through this process. We’ve done before and after tests on an HMO, and so far, all of the adults have almost undetectable Bifidobacteria. That’s a small sampling, but it makes you wonder if the average adult has almost zero Bifidobacteria, which is the very thing we need to have lots of. It’s fascinating. Also, in my own experience, I have found that probiotics, which people talk a lot about, hopefully help some people. I was on probiotics for years, and I didn’t see any changes in symptoms. Obviously, it had no impact on my gut test actual bacteria. I’m still not on probiotics, but I do believe that if you’re feeding the bacteria with the prebiotics, then you can seed the gut with probiotics. I think that can be really beneficial. For example, I talked to my friend yesterday, who has skyrocketing gram-positive bacteria and fantastic butyrate levels. His Bifidobacteria was still quite low. It wasn’t nonexistent; it was quite low. So we talked about getting him on a quality probiotic that has mostly Bifidobacteria, and he thought it’s a great idea. We’re going to retest, and I’m really excited to see how that might turn out.
Lindsey: Yeah, that was something interesting to me when I had the folks from Layer Origin. They have a probiotic prebiotic combo formula, the Pure HMO Synbiotic, and I was just looking up the strains in it. So it’s Bifidobacterium bifidum plus the strain number, Bifidobacterium lactis, Bifidobacterium longum. They’ve got three of them in there so that you can help feed it and seed it as you’re going. It’s very reasonably priced at that. I’m on Amazon right now, and I can provide a link for people. It’s $29.69 for 40 billion CFU. Plus, it’s got the 1000 milligrams of HMOs in it. So I thought that was a good deal.
Rich Maurer: Yeah, yes. Thank you for that. Honestly. Can you see how many days supply it is?
Lindsey: I assume that that’s a one-month supply.
Rich Maurer: Let me see. It’s two capsules, 30 servings, okay. By comparison, just the HMO powder is 1000 milligrams. So only HMO, but it’s a 45-day supply.
Lindsey: Right? So you’re going to spend a little bit more to get the probiotics. But if you need to seed that as well, like if you’ve got no Bifidobacteria at all.
Rich Maurer: Exactly. And probiotics get crazy expensive. So that is a good deal. Thank you for reminding me of that one.
Lindsey: Yeah, I think that’s what I had originally tried to take. I just went out after our last recording – confession: this is the second recording for Rich because I forgot to press record on the first recording. And after our last recording, I’m like, “You know what, I need to try those HMOs again.” So I went out and got some, and I’ve been taking them I’ve been tossing them in my yogurt each day along with any number of other things that I try. I’m not as scientific as you or I should say, I don’t have the patience that you do, to try one thing at a time and have not done the pre and post testing, but just seeing how it impacts me.
Rich Maurer: You’re taking the one with probiotics or no?
Lindsey: I’m just taking the straight HMO powder. I do have another Bifido. I just keep getting free stuff. So sometimes I take a lot of stuff just because someone gave it to me. So yeah, I was on a different probiotic. And now I’m on to another one that I had leftover in my closet.
Rich Maurer: Oh, I’m sure you’ve got a lot. But if you don’t retested, how are you going to know if it’s helped you?
Lindsey: Believe me, I have all sorts of signs. But I’m do have post-infectious IBS. So I just keep getting it over and over again. So my body will tend to overgrow Proteobacteria, which are those gram-negative, and that will just keep reoccurring. So I know that I always need to be fighting that battle.
Rich Maurer: Well, interesting. Yeah, I could see that. Interesting, though. My wife, HMO increased her Akkermansia too much. Akkermansia is a very good, beneficial bacteria. But what happened is she went so high, 20%. Normally, like 1% is pretty good. Most people I found can’t really grow any. She went to 20%. What it did is that reduced butyrate and her gram-positive bacteria, the very good things we’re talking about. So I just said, “Stop taking HMO.” I mean, it’s just one thing. Some people call it the Goldilocks. Yeah, it doesn’t work the same for everybody. So that should be said.
Lindsey: Yeah, there’s an interesting thing that I’ve noticed on stool tests, which is that often people who have H Pylori in their gut have elevated levels of Akkermansia. I don’t know if the test you’re taking shows that one. But I assume that because it causes constipation and some amount of delay in emptying, there’s more time for those Akkermansia to be feeding on the mucus layer. They feed on that mucus layer, so there’s more fuel for them, and then they increase. That’s my theory anyway.
Rich Maurer: Thank you for that. I’ll check to see if Ombre has H. Pylori. Yeah, that’s a really good clue.
Lindsey: Yeah. People who tend towards the Proteobacteria increase . . . Well, I actually just listened to a really good . . . Marc Pimentel, who invented the IBSsmart test and the trio-smart and has done a lot of research on SIBO. He’s a doctor at Cedars Sinai. In SIBO, it’s typically certain gram-negative bacteria that increase. They’re all in the family Proteobacteria. E coli and Klebsiella are two of them. Those are the ones that tend to be increasing in the small intestine in people with SIBO. If you are positive for post-infectious IBS and have positive vinculin antibodies, you typically have a diarrhea type of SIBO, not a constipation type. Although I have seen clients who have positive IBSSmart tests and have constipation type. So obviously things can mix up, like you can have an overgrowth of hydrogen-producing bacteria plus an overgrowth of methanogens, and somehow it all nets out to constipation.
Rich Maurer: Have you seen anyone who could still have H Pylori even though they’re asymptomatic? For example, my wife doesn’t have dysbiosis symptoms.
Lindsey: Oh, people have it all the time. I mean, plenty of healthy people have it. It may just not be overgrown. There’s an entire book written about how it has healthy impacts on us as well. That’s a classic in the world of gut stuff by Martin Blaser, Missing Microbes. The entire book is about H. Pylori.
Rich Maurer: Okay. Yeah, the fact is, it’s expanding our knowledge exponentially, and nobody knows for sure yet. So it is exciting to watch it develop. But certain things you do know with a fair degree of certainty.
Lindsey: Yeah. And your wife’s A1C level went down as well, right?
Rich Maurer: On HMO? It did, it did. But then, because of the results and I mentioned reducing butyrate and gram positive, I took her off of HMO.
Lindsey: Right. But what was the reduction for her?
Rich Maurer: So she was only on it for like four or five weeks, and she went from 6.0 to 5.4 or 5.
Lindsey: So in the pre-diabetic range.
Rich Maurer: Yeah, yes. Yeah. She went from prediabetic to normal.
Lindsey: Yeah. Okay. Again, with all of you, how can you be sure the changes can be attributed to the HMOs and not something else? Like any other diet changes or any other supplements?
Lindsey: Right, good question. In fact, when I did a video about insulin resistance and HMOs, my wife afterwards said, “Well, you know, about the same time you started HMOs, you started on cinnamon, and that is proven in good doses to also lower A1C.” And I was like, “Oh, you’re right.” So what I did is I took myself off of all that cinnamon for three or four months, I think at least four months, and then retested my A1C, and it went down a little lower yet. So I eliminated that variable. And as far as I know, I hadn’t made any other changes.
Lindsey: So if it went down from the 5.9 or it went down from the-
Rich Maurer: It went from 5.7 to 5.0, and then it went down from 5.0 to 4.9, which again is statistically insignificant, but the point is, it didn’t go up after going off the cinnamon.
Lindsey: Okay, right. At the very least, if you’ve got an A1C issue, you could take the cinnamon and HMOs. And you’d be in good shape.
Rich Maurer: There you go.
Lindsey: Yeah. And cinnamon is yummy, too. So I assume you’re taking pills, though, not just sprinkling it on your food?
Rich Maurer: Yeah, you know, to get three to six grams.
Lindsey: Oh, that’s a lot.
Rich Maurer: Yeah, that’s the recommended amount for reducing A1C.
Lindsey: Yeah. And I’m curious as you were reducing your A1C, and your wife, too, did you notice any changes in your energy or anything else?
Rich Maurer: Oh, good question. We both exercise and we’ve made those nutritional dietary changes. So I don’t think either of us noticed it, that I can tell.
Lindsey: Yeah. Okay. So I understand that your daughter, too, was taking the HMOs and that she had some other positive health changes?
Rich Maurer: Yeah, right. Sort of accidentally, you might say, within a couple of weeks of taking the HMOs, she noticed that her acne was improved. She would have had what would be called mild acne, I think in the spectrum of things. But she thought it significantly improved. And in one of my videos, she was kind enough to provide before and after photos. So that intrigued me, of course, so I found plenty of research papers that showed Bifidobacteria and the results that she demonstrated in her gut tests, indeed, can reduce acne.
Lindsey: I’m sure that’s very appealing to the teenagers out there.
Rich Maurer: Yeah, for sure. Or adults that have had acne. Exactly.
Lindsey: Yeah. And so you mentioned at the very beginning about having had COVID and some problems that developed subsequently. And I don’t know if you’ve probably listened to the episodes. Actually, I’m not even sure if I’ve published them yet because I’ve now got like five episodes sitting in my queue to publish. But there was at least one episode where someone was talking about having gotten an ulcer from COVID. And that’s a very rare side effect, which you were talking about excruciating stomach pain. I assume you wouldn’t know if that’s what happened to you.
Rich Maurer: Yeah, I don’t think so. So that was my first bout of COVID in January 2021. This past January 2022, I had COVID again, which I discovered over lots of testing over the summer. And then had a dramatic increase in symptoms. I first noticed some symptoms a couple of weeks after I had COVID in January 2022. But then, a dramatic increase in symptoms over the summer. So, lots of testing done and landed on COVID-induced autonomic dysfunction, which is just another type of long COVID symptoms and a wide variety of symptoms there.
Lindsey: Such as?
Rich Maurer: It would sort of take over and sneak up on me. And it’s never the same thing. And not always all the symptoms at once. But extreme exhaustion, diarrhea, and nausea, feeling flush, rapid increase in both tachycardia and bradycardia. So, an increase in heart rate, decrease in heart rate, increase in blood pressure. I never had a blood pressure problem in my life, and I’m shooting up to 160. Thankfully, in my case, (this can be very debilitating for some people), the symptoms pass quickly. You know, my wife says, “You’re the epitome of the phrase, ‘this too shall pass.'” Literally, Sunday afternoon, I just felt rotten for two hours. But while I’m sitting there, I’m thinking to myself, you know what, in about two hours, I’m going to feel good. And I did, so I’m very thankful for that. But, wide variety of symptoms. So, yeah, that might be something your listeners might key in on because I had a difficult time, first of all, understanding myself but also trying to walk through with my practitioner what this might be, and it seems my experience and things I’ve read that doctors just still even two years right into this COVID, post-COVID, aren’t understanding long COVID, aren’t able to see autonomic dysfunction symptoms, and then connect the dots.
Lindsey: Yeah, no, I have watched many webinars on long COVID and how to treat it and some of the tests that you can use to see what’s going on on the nutritional level. Because there’s a lot of oxidative damage to cells, and you know, you need your antioxidants, and heavy doses post-COVID. There is sometimes damage to blood vessels, and you need to keep those open. So I think L-Arginine. It is known for helping produce nitric oxide, which keeps your blood vessels open. So there are a number of tools that are out there, if you are dealing with that sort of thing.
Rich Maurer: I’d love to get the links to some of those podcasts because I have found so precious little, honestly, it’s just the standard, you know, plenty of hydration and electrolytes and exercise, you know, all things I’m already doing. So, yeah, that’d be great.
Lindsey: Yeah, no problem. So I will put all these links, by the way, in the show notes for the Biomesite where you can upload your results from Ombre and to your videos (here and here) that show the before and after photos and all the stuff, because they’re great videos. I mean, it’s really interesting stuff and you get to see the charts that you’ve made and of how things have gone up and down. Anything else that you want to talk about, though, before we get off?
Rich Maurer: I don’t think so. I think that about covers it, Lindsey.
Lindsey: Okay, awesome. Well, I think that this is actually a much better conversation than our last one. So we’ve done well.
If you’re struggling with bloating, constipation, diarrhea, soft stool, acid reflux, IBS, IBD or any type of chronic disease, etc. and want to get to the bottom of it, that’s what I help my clients with. You’re welcome to set up a free, 30-minute breakthrough session with me (Lindsey). We’ll talk about what you’ve been going through and I’ll tell you about my 3- and 5- appointment health coaching programs in which I recommend lab tests, educate you on what the results mean and the protocols used by doctors to fix the problems revealed. Or if you’re ready to jump in right away or can just afford one appointment at a time, you can set up an 1-hour consultation with me.
Today I’m going to be talking about a topic that may be unfamiliar but deeply connected with a lot of gut issues, which causes chronic inflammation and contributes to numerous other chronic health conditions common in the developed world and that’s metabolic endotoxemia.
What is metabolic endotoxemia?
So, you may have heard that bacteria are divided into two groups, gram-positive and gram-negative. Gram-negative bacteria are surrounded by an outer membrane containing something called lipopolysaccharide or LPS. Gram-positive bacteria lack an outer membrane. And when you stain them when looking under a microscope, they look different than gram-negative ones. So you may know that the two primary phyla of bacteria in the human gut are Firmicutes, which are gram positive, and Bacteroidetes, which are gram negative. Then the next two largest phyla are proteobacteria, which are gram-negative and actinobacteria, which are gram positive. Most of the major bacterial gut pathogens that you’ve heard of are gram negative proteobacteria, like salmonella, E coli (although most types of E coli are not pathogenic) and camphylobacter. Probably logically because they are facultative anaerobes, so they can live in the presence of oxygen, hence are easy to pass between people and make you sick.
So endotoxins are toxins in the bacterial cell wall of gram negative bacteria, which are released when the cell disintegrates upon death and also released in much smaller amounts when they’re alive. And this endotoxin is composed mainly of LPS, which activates the inflammatory response. So even small amounts of LPS in the blood from a bacterial infection can elicit an inflammatory response and trigger the release of inflammatory cytokines or chemical messengers, which leads to low-grade chronic inflammation.
So to put it all together, metabolic endotoxemia is a diet-induced 2-3 fold increase in plasma LPS levels. And if it happens after eating, it’s called post-prandial metabolic endotoxemia. So in other words, you eat a meal, and mostly dead bacterial body parts start escaping out of your gut and sparking off inflammation.
So as you may be guessing, something that goes hand and hand with metabolic endotoxemia is intestinal permeability, aka leaky gut. I did an entire episode on leaky gut, which is episode 24, from March of 2020, so you can listen to that to get the lowdown, but to summarize briefly, leaky gut can come from an overgrowth of the very proteobacteria that you don’t want escaping out of your gut, as in SIBO (small intestine bacterial overgrowth), from certain foods that contain lectins, added sugar, alcohol, nutrient deficiencies, chronic stress, smoking, toxin overload and dysbiosis. So there’s lots of ways you can end up with a leaky gut.
What conditions are associated with metabolic endotoxemia?
The consequences of metabolic endotoxemia are many. Symptoms and diseases associated with it include insulin resistance, obesity, type 2 diabetes, non-alcoholic fatty liver disease, chronic kidney disease, atherosclerosis, chronic constipation, low testosterone, chronic pain, cognitive decline, memory loss, appetite disorders, depression and anxiety. It can also promote autoimmunity and suppress the activity of your thyroid and cause autoimmune thyroid disease, which is Hashimoto’s thyroiditis, if you’re hypothyroid and Grave’s disease if you’re hyperthyroid. Endotoxemia also plays a role in Chronic Fatigue Syndrome and is associated with markers seen in early Parkinson’s disease patients.
So there are a number of causes beyond just a leaky gut for metabolic endotoxemia, and many of these causes also cause the gut to be leaky, so it’s all intermingled as you will see. The first is a high fat diet, but in studies but these were typically high junk food diets as well, so I don’t think we can assume that this applies to a carefully constructed ketogenic diet, for example. Fructose consumption is another cause, but this is referring to high fructose corn syrup and other fructose added to foods, and consumed in high quantities in the absence of fiber and nutrients found in fruit.
SIBO is another cause of metabolic endotoxemia. It turns out that the primary bacteria in people with a positive hydrogen breath test, which is a diagnostic tool for SIBO, are Enterobacteriaceae, which are gram negative. The most common specific overgrown bacteria found in SIBO include Escherichia coli (gram negative), Enterococcus spp. (gram positive), Klebsiella pneumoniae (gram negative) and Proteus mirabilis (gram-negative). So the majority are gram negative and produce LPS, and just having an overabundance of those gram negative proteobacteria will itself cause leaky gut and then these are the bacteria with LPS.
Chronic alcohol consumption can also be a cause. This happens because alcohol can increase pathogenic bacteria and decrease beneficial bacteria. Also, the metabolism of alcohol generates reactive oxygen species (also known as oxidative stress), which can damage gut cells and impair gut barrier function, allowing for the translocation of LPS into the bloodstream.
Periodontal disease is another possible cause, because in periodontal disease you have an overgrowth of harmful bacteria in the oral microbiome, which of course leads into the gut microbiome, and can cause dysbiosis and intestinal permeability and the leakage of LPS. And the primary pathogens in periodontal disease are also gram negative.
This one doesn’t seem fair, but aging itself can lead to metabolic endotoxemia, because it’s known that as we age our gut diversity decreases, which can then contribute to an imbalance in the gut microbiota and promote the growth of pathogenic bacteria that produce endotoxins. Aging is also associated with an increase in intestinal permeability, which may be due in part to age-related changes in gut physiology, such as decreased gut motility. In addition, aging is associated with a decline in organ function, including the liver and kidneys, which are important for detoxification and elimination of bacterial toxins. Impaired liver and kidney function can lead to an accumulation of bacterial toxins, contributing to metabolic endotoxemia.
And finally, smoking causes metabolic endotoxemia in the same way that alcohol use does, by creating dysbiosis and oxidative stress, which damage the gut barrier and create intestinal permeability, and by impairing liver function, which can lead to a decrease in the clearance of LPS from the bloodstream, contributing to metabolic endotoxemia.
How do I stop metabolic endotoxemia?
If you’re having lots of bloating, gas or acid reflux, the primary symptoms of SIBO, that’s the first thing to address. If you have recurrent SIBO, finding and addressing the root cause is important, and if it’s autoimmune in nature, using prokinetic supplements, and no matter what the root cause, spacing out your meals and periodically using antimicrobials and some type of SIBO diet like low FODMAPs or the Biphasic diet, is usually necessary. I did an entire episode on recurrent SIBO, episode 83, from October of 2022, so check that out for more information.
Then there are basic lifestyle interventions that can help if you suspect this is going on for you and you don’t have obvious SIBO symptoms. Reducing saturated fats, eating a Mediterranean diet rich in fruits, veggies, nuts and legumes, reducing Omega 6 fatty acids found in oils like soybean, corn, cottonseed, sunflower and peanut oils and processed foods that are high in them. Then increasing cod liver and fish oils will help. And unless you eat fatty fishes very regularly, you may want to think about incorporating a regular fish oil supplement in your regime. But look closely to make sure you’re getting plenty of EPA and DHA in your fish oil, because sometimes it’s 1000 mg of fish oil with only 300 mg of EPA and DHA, whereas the highest quality fish oil supplements, like the ProOmega 2000 you can find in my Fullscript Dispensary* has 1000 of EPA and DHA in one capsule. Then eating lots of probiotic foods or taking probiotics can be helpful. And incorporating prebiotic rich foods in your diet or supplementing with prebiotics like inulin and FOS (which is fructooligosaccrides, which won’t be great if you have recurrent SIBO). Inulin and FOS are found in chicory root, Jerusalem artichoke, onions, garlic, asparagus, jicama and bananas, among other things. Those two prebiotics help feed beneficial lactobacilli and bifidobacteria, which can crowd out the pathogenic bacteria.
Then avoiding sugar, excessive salt and surfactants found in processed foods, like polysorbate 80, mono and diglycerides, soy lecithin and carrageenan is also helpful. And then if you suspect your gut immune system isn’t working well, like you keep getting bouts of different gut pathogens, or you know based on your GI Map or other stool test results that your secretory IgA is low, you can use colostrum, or it’s more purified derivative without any dairy, serum bovine immunoglobulin powder (examples of this are MegaIgG 2000 by Microbiome Labs and Immuno gG SBI powder by Biotics Research, and IgGI Shield by Designs for Health, all available in my Fullscript Dispensary*) to protect yourself against pathogenic bacteria. And then nutrients to support secretory IgA production include omega 3 fatty acids, glutathione, glycine, glutamine, phosphatidylcholine, vitamin C and zinc. And then it’s also known that S boulardii probiotics bring up secretory IgA.
You can also support your mucin production, because the mucin layer is what protects the gut barrier, with amino acids like l-threonine, l-proline, l-cysteine and l-serine. Those are all found in Microbiome Labs Mega Mucosa, which is designed to support that mucin layer.
And then the most studied tool for helping with endoxemia are the spore-based probiotics. Microbiome Labs did a 30-day study with their spore-based probiotic, Megasporebiotic, which was published in the World Journal of Gastrointestinal Pathophysiology that showed that it reduced post-prandial (meaning after a meal) dietary endotoxemia by 42% and triglycerides by 24% (where as in the placebo group, there was a 36% rise in endotoxin and 5% decrease in triglycerides).
So I hope that was a helpful introduction to one of the likely drivers of chronic disease that has origins in your gut microbiome. And if you’re struggling with some type of chronic disease, chronic inflammation, bloating, constipation, diarrhea, soft stool, acid reflux, etc. and want to get to the bottom of it, that’s what I help my clients with. You’re welcome to set up a free, 30-minute breakthrough session with me (Lindsey). We’ll talk about what you’ve been going through and I’ll tell you about my 3- and 5- appointment health coaching programs in which I recommend lab tests, educate you on what the results mean and the protocols used by doctors to fix the problems revealed. Or if you’re ready to jump in right away or can just afford one appointment at a time, you can set up an 1-hour consultation with me.
Why don’t we start with how and when your health started going downhill?
Nita Jain:
Yeah, so I struggled with health issues for a good portion of my life. I started developing things like Ehlers-Danlos type symptoms, which is a connective tissue disorder, that means that the vasculature ends up being a little bit weak because of insufficient collagen production. And so this is something that I started dealing with at a pretty young age in grade school. And then I also started developing symptoms of acid reflux disease, or GERD, and that was in high school and college. And I had also started dealing with something called chronic fatigue syndrome, which is now renamed myalgic encephalomyelitis after having swine flu as a teenager in high school as well. But apart from those things, I was managing and I wasn’t in the best of health, but I was getting by, but then everything changed for me after a course of fluoroquinolone antibiotics in 2015. This was during my last semester at university. I had to drop out because I developed seizures as well as peripheral neuropathy, fainting spells and all of these really disabling neurological symptoms. That meant that I didn’t have much bodily autonomy anymore. I didn’t have a lot of motor control. I was wheelchair bound or stuck in bed, and I just didn’t have any autonomy. I couldn’t drive a car anymore. I couldn’t cook for myself. It was hard to be upright. Around this time, the dysautonomia started to get really bad again. It was in remission for a while after the swine flu initial months, but then all of these old problems resurfaced, but they were much more severe than before.
Lindsey:
Can you explain the dysautonomia a little bit?
Nita Jain:
Absolutely. So dysautonomia is an umbrella term for a number of different conditions, like POTS is a subset of dysautonomia, postural Postural Orthostatic Tachycardia Syndrome. But basically, dysautonomia refers to conditions that result in vital instability. So you might deal with high or low blood pressure, a slow heartbeat like bradycardia, fast heartbeat like tachycardia, there’s often just an issue maintaining stable vital signs, and it seems that the sympathetic nervous system is not able to regulate the way it normally would be. And that can lead to a lot of secondary effects as well. It’s not just things like the vital signs being affected, but then you would often, of course, have secondary fatigue, you might have cardiac issues as a result; it can just lead to a cascade of downstream effects. But dysautonomia, depending on the subset, the root causes can be different. And for some patients like myself, the first line therapies are things like increasing salt intake. That’s usually something that doctors will say is like a first go to address this issue, but if that doesn’t work, they might move to medications like alpha blockers, for instance; it just depends on the patient.
Lindsey:
And what what were your symptoms?
Nita Jain:
For me it was that vital instability, as well as just crushing fatigue. I feel like I should differentiate between like being tired and being fatigued. Because being tired is something that you can recover from, I think it’s like what normal people feel at the end of a long workday, but you go to bed, you rest up, you’re better in the morning. Fatigue is a whole other level of tired. It’s the tired where your body does not have the energy to carry out the functions that it needs to. And it’s much more severe than simply like, oh, you’re just tired all the time. Because I think sometimes when chronically ill people try to talk about chronic fatigue. It sounds like it’s this very mild condition, when it’s much more severe than what it might seem at the surface.
Lindsey:
Right. There was a documentary on chronic fatigue that someone sent me to watch. And some people are in bed, basically, all day long. They can drag themselves out of bed to do just only the very basics.
Nita Jain:
Absolutely. Yeah, I think I know that documentary you’re referring to. I think it was called The Forgotten Plague with Ryan Pryor. And he actually recently released a book called The Long Haul, which is about long COVID. And there’s a lot of parallels between chronic fatigue syndrome and long COVID. And a lot of these other post-viral syndromes, like in the aftermath of the SARS and MERS epidemics, we also saw a lot of post-viral fatigue syndrome. So I think there are a lot of related conditions out there that produce these widespread constellations of symptoms. And I think energy metabolism is probably an underlying cause of many of them. So I think any insight that we can get into one of these conditions, it’ll probably also help elucidate the causes of the others.
Lindsey:
Yeah. Did you have a somewhat of a medical background?
Nita Jain:
Yes. So in in college as an undergrad, I was a pre-medical student and I had applied to medical school and everything, but then just having had that disabling adverse drug reaction during my last semester, I wasn’t able to go to medical school and I was just in a vegetative state for about six years or so. But medical school was what I was aiming for at the time. So I studied biochemistry, I worked in a cancer laboratory as an undergraduate research assistant. And that’s a little bit of my life sciences background.
Lindsey:
Ah, okay. So back to back to your health story. . .
Nita Jain:
Right. Yes. So in the aftermath of all those symptoms that I was experiencing post Cipro, which is the antibiotic class I was given, this is the same class of antibiotics as Levaquin and Avelox, in case people have heard those words as well. But what had happened was, I was under the impression that maybe because these antibiotics are so broad spectrum, maybe the fact that my gut microbiome has been wiped out, maybe that’s why I’m having all these really systemic side effects. And that’s what got me on the path towards pursuing FMT. And in the United States, FMT use is restricted to recurrent C. difficile colitis, that hasn’t responded to at least two courses of antibiotic treatment. So if I wanted to receive FMT, the only routes were through a clinical trial with like an IND license that the researcher would have to apply for, or through a private clinic. And I had applied to some of the clinical trials, but I wasn’t accepted into any of them. So then I started pursuing private clinics. And, of course, safety was something that was of top concern. So I wanted to make sure that the donors were thoroughly vetted, in terms of doing the necessary blood and stool testing, just to make sure that everything’s safe, and the chances of an adverse reaction are low. And so I did end up going to a satellite clinic, traveling abroad to receive this procedure.
Lindsey:
Which one was that?
Nita Jain:
So I went to a clinic that was the satellite branch of Taymount. So their main branch was in the UK, but they had a satellite branch in the Bahamas. So I was living in Georgia, it was just a couple hours flight to the Bahamas. And I received several different donors while I was there, but I noticed that I only responded positively to one of them. And so when I got back home, they had sent me home with some samples as well. And I had noticed that I that there were certain patterns as to the donor that I would respond positively to like, that particular donor was enriched in butyratep-roducing bacteria. They had a lot of the Clostridial clusters 14 and 16, which, again, a lot of butyrate producers. They were more enriched in things like the Faecalibacteria, Akkermansia, Blautia, Roseburia. And these are just some of the bacteria that are associated with robust metabolic health, good GI health, things like that. And I noticed that the donors that I didn’t respond to were not as enriched in these particular organisms. So unfortunately, I did have a reaction to one of the donors and I was in the hospital when I was back in the United States.
Lindsey:
What was that reaction?
Nita Jain:
So basically, after one of the donors that I received, I had really pronounced neurological symptoms. And it was just like my brain was on fire constantly. Now, I had a little bit of this before because of the peripheral neuropathy. But it was just jacked up to 100. And it was so severe that I wouldn’t sleep at all. And it turned out that I had something called Hyperammonemia, which is when your blood levels of ammonia are very high. And that was causing all sorts of different symptoms. It felt like I was being electrocuted, like my brain was just burning. I was severely depressed. And basically, I started taking l-ornithine orally in order to counteract this because it helps with the urea cycle and the elimination of of ammonia through the urine. But it was a really scary time because no one could really tell me what was going on. And it’s just like hell in your brain. And after that, I was a little bit more weary of FMT, I mean, I still thought that it had a lot of therapeutic potential, but I felt like I really need to avoid this ammonia problem happening again. And I continued to sequence of donors privately that I received from any clinic.
Lindsey:
Okay, let me stop you for a sec. I want to back up a little bit because you didn’t discuss your inflammatory bowel disease at all. When did that come up?
Nita Jain:
That came up about a year later. But that was all.
Lindsey:
Okay, so this is after taking your first FMT?
Nita Jain:
Yes. So at this, at this point, I do have pretty bad GI issues, but I’m not dealing with GI bleeding the way I did when I had IBD.
Lindsey:
So what GI issues were you having prior to FMT?
Nita Jain:
Just a lot of diarrhea; it was pretty frequent. And that was pretty consistent, but then I would have periods of time where I would go maybe 14 days without a bowel movement, which was very unhealthy as well. So it was kind of alternating, but I think it was mostly diarrhea predominant at that point in time. Then I also ended up getting FMT from other institutes in Europe. I had it shipped over on dry ice and had to go through customs and everything. Unfortunately, it was after that sample that I developed IBD, I started having GI bleeds. And it’s really hard to know why these things happen just because, well, actually, when I had sequenced that particular donor, they had a pretty high proportion of Clostridioides difficile, which was really surprising because it came from a research institute that’s really reputable. So I don’t know, I think maybe after the C diff, maybe that triggered IBD. In a way, just having carried it, I’m not particularly sure because even after C difficile got down to normal levels, I would still have these flares where I would bleed. And the only thing that would fix it is FMT from a healthy donor, like one I responded positively to, because, again, there’s so much variability. So it feels like to me, at least, when we’re sequencing these donors, or testing donors to figure out who is a viable candidate to donate material, I think that the current qualifications that we’re using are not really sufficient. Just just because even if you’re ruling out things like C difficile, things like Salmonella, Shigella, Campylobacter, some of the more common GI pathogens, and even if the bloodwork is clean, that doesn’t necessarily mean that the person has the protective bacteria to give to somebody who’s sick. So I feel like testing for that is equally important, not just the absence of pathogens, but also the presence of protective bacteria. And so yeah, I think that might make the process a little bit safer for people who are seeking out this therapy. And I mean, I think it’s kind of unfortunate, because I do think that it has a lot of potential as a therapy. But I just think that it’s not practiced the way it needs to be to be safe for the maximum number of patients.
Lindsey:
Yeah, so again, backing up, how did you have time to sequence these microbiomes before taking the samples? Did you just like get a frozen sample, run the sequencing, and then hold onto it until you were ready to take it?
Nita Jain:
Yeah, basically, after I started reacting negatively to some of the Taymount donors, that’s when I started deciding that, yeah, I’m going to sequence them before taking the sample, just in case there’s anything alarming in them. And at the time, Ubiome was still was still running (since, they had to declare bankruptcy because of some billing issues with one of their Smart Gut tests). But at the time, I was just getting everything sequenced through 16S ribosomal RNA sequencing just to have some idea as to what’s in the sample. So I’m not like totally shooting in the dark. But after that, after those initial adverse reactions, I decided that I should probably sequence them before taking them and wait for those results to come back.
Lindsey:
I see. Okay. And when you saw a donor that had high levels of C. difficile, why would you go forward with that sample?
Nita Jain:
Yeah, absolutely. I was not aware of that at the time. And at the at the time, my condition was pretty severe. So I felt like okay, let me go ahead and take the sample while I’m waiting for the results to come back. Definitely being in a vegetative state will make you pretty desperate. So you know, I know in hindsight, it’s not intelligent to do that at all. But I also empathize with people who are open to experimenting with potentially dangerous things because of the desperation, because your quality of life is so bad, it is just like, well, I can’t get that much worse might as well try it. And of course, this is not something that should be done at all. But I think that’s just the psyche of people who are very chronically ill.
Lindsey:
Of course. Yeah. So when you said you responded well, to certain donors, when you did respond, well, what kind of positive changes did you see?
Nita Jain:
So I saw a lot of systemic benefits when I responded, Well, it was like the brain fog would be lifted. The GI stuff would calm down, I could breathe easier in a lot of ways. It was just like things were just lighter. I felt more like a regular person would. I started having more mobility, more autonomy, more motor control, just able to do regular things, again, able to engage in chores and cooking and slowly but surely pick up driving again. But it’s also very strange acclimating, like re-acclimating to civilian life, after just having been in hospitals for six years, because you don’t see anyone or at least I didn’t, in my condition. I didn’t see anyone outside of the hospital and my immediate family for that stretch of time. And so this was before the pandemic even started. So I was just already accustomed to this degree of social isolation before COVID even came around. And it’s really difficult to re-acclimate. And it wasn’t as though I wasn’t still having symptoms. Because the thing is, it wasn’t just FMT that made me better because even when I received FMT from a from a donor that I responded well to, I would relapse. And I noticed that the one thing that made it stick for me in the long term was to also adopt an autoimmune protocol diet, and FMT, in conjunction. So if I did those at the same time, then I was more likely to see that long-term remission.
Lindsey:
This is like an autoimmune paleo?
Nita Jain:
Yes, exactly. And the other thing that helped me was time-restricted feeding and not eating after dark, especially just because of the hyperpermeability that can happen if we eat after dark. Yeah, one of the mechanisms by which that happens is the fact that melatonin blunts insulin secretion a little bit. So glucose transport, after sundown, is more likely to lead to leaky gut symptoms, because of, you know, the LG the way that it’s transported after dark. So basically, for me, it was the combination of FMT, an anti-inflammatory autoimmune protocol diet, and then using this time-restricted feeding to really drive down inflammation; those three in conjunction really started moving the needle for me.
Lindsey:
Okay. And so then I understand you’ve gotten FTM samples from other places as well?
Nita Jain:
Yes, I also received samples from a local clinic called RDS infusions. That was in Florida, I believe, at the time, I think when I pursued it in 2017 or so they had three donors. I’m not sure what the case is now. But then I also received FMT from a place called Microbiomes LLC in Portland, Oregon, I believe.
Lindsey:
And were these just individuals selling their stool? Because my impression was RDS was sort of like that. But I guess you said they had other donors too?
Nita Jain:
RDS was run by a gastroenterologist at the time, but I do believe that one of their donors ended up selling his samples of his own accord, but I had received it from the gastroenterologist when he was a donor at that clinic. And for Microbiomes LLC, I had gone through Purety Clinic in California for that. And the samples came from Microbiomes LLC in Oregon, and they shipped it on dry ice as well. But those are all the different places that I pursued. And I even, at one point, tried to sequence my cousin’s sister, to see if she was a viable candidate, but, I’ve received lots and lots of donors. And yeah, there have been definite patterns as to who I will respond better to, but I think the more stringent we can make the screening process, the better, as far as safety and efficacy goes.
Lindsey:
Yeah, I understand that you you reached out to a lot of people that you knew to try and find donors. Can you tell me a little bit about that process?
Nita Jain:
Yeah, that’s true. So after I responded negatively to FMT, I was really desperate to get a sample to counteract those effects, and was just like, I just need to get a better donor, and then I can reset, it’ll be fine. And so I reached out to maybe 500 people or so among my contacts, family, friends, school colleagues, former classmates, anyone who I’d come into contact with who might be able to help me saying like, “Hey, would you mind filling out this donor questionnaire? Because I’m really sick and having a healthy stool sample from somebody could really help.” But it’s a very bizarre question to ask because I think there is more disgust around the idea of stool versus being a blood donor or something like that. I think people are a little frightened by it, to some extent. I think a lot of people think that you’re maybe just like mentally sick or something to be asking this. Because if you don’t have knowledge about the microbiome, it might seem like a very odd request. It’s like, oh, she’s just like gone off the deep end or something like that. But I did reach out to a lot of people. And so unfortunately, almost everyone I knew had some sort of, even among people who were willing to do it, most everyone had some sort of pre existing condition that would disqualify them, or they were on some sort of prescription medication that wouldn’t make it perfectly safe. So it is very much a needle in a haystack endeavor in a lot of ways. So I think there is a way to make an artificial substitute that would go a long ways towards helping patients as well.
Lindsey:
Yeah, I actually am taking one of the, well, there’s a few products that have anaerobic bacteria now from Pendulum*: Glucose Control, and their Akkermansia, and now GI Repair, which is Clodridim butyricum (since renamed “Butyricum”) (also available in my Fullscript Dispensary*), which I started taking, and I’m actually really impressed with the results.
Nita Jain:
Yeah, definitely. Because it is so hard to culture so many of these anaerobes, since they’re dying in the presence of oxygen, essentially. But yeah, I think that was one of the reasons that having that Akkermansia probiotic over the counter was such a big milestone, because it just shows us that it is possible to culture anaerobes and administer them in an oral form, which I think is huge.
Lindsey:
Have you tried any of those?
Nita Jain:
Yeah, yeah, I’ve tried pretty much everything that’s on the market. In addition to the two that you mentioned, I’ve also tried some of the bacillus types of soil-based. . .
Lindsey:
Spore-based. . .
Nita Jain:
Yeah, exactly. The spore-forming soil based organisms, a lot of those as well. Yeah, those are really good at colonizing in the long term I’ve seen because you take it once, and you can still see it in stool samples months later down the line. And I think nowadays, they’re even there. They’re also doing Bifidobacterium infantis for children or newborns who are lacking that bacteria, because a lot of moms don’t carry it. So you can’t pass it on to your children. But that also seems to colonize pretty well, surprisingly.
Lindsey:
Yeah, that’s the one I give to all my pregnant friends.
Nita Jain:
Awesome. Very cool.
Lindsey:
Yeah. So did any of those probiotics have a positive impact on you?
Nita Jain:
They didn’t move the needle for me specifically. But I do think that if people maybe have a very specific condition, it has the potential to help. I think, just for me, my condition was just to the point where so many of the species were just extinct, and they just needed to be replaced, that I wasn’t seeing much benefit from just introducing a few microorganisms here or there. I think I just needed a more comprehensive restoration protocol. But I do think that they can help in some instances, yeah, sure.
Lindsey:
How long was your course of antibiotics?
Nita Jain:
It was only a week. And it was just basically twice a day, I think it was maybe 800 milligrams twice a day for a week. And unfortunately for me, I didn’t actually have a bacterial infection. So it was all collateral damage. They had given it to me just in case of infection. And the reason it happened was because at the time, when I was in college, I dealt with recurrent iron deficiency anemia. And after receiving one of the iron infusions, which is through an intraveous line, I developed a really high 106 degree fever. And so I called my hematologist, they were just like, I don’t think it’s related. Just follow up with your PCP about it. So then I went to see primary care and primary care was like, okay, we’ll give you these antibiotics, just in case there’s an infection going on. So I took the antibiotics, when my test results came back, turned out no infection, but they were just like, just finish the course of antibiotics. And I was like, okay, I’ll do that. But, yeah, I think I think we maybe need to be more judicious about our antibiotic usage. Because if there isn’t a clear sign of infection, it really does have the potential to do more harm than good. And I think that’s something that really needs to be evaluated carefully on a case by case basis with the clinician, with the patient, like, what are the risk factors and are there any safer alternatives, especially when it comes to the fluoroquinolones class of antibiotics. Because it is a class of antibiotics that has so many black box labels for really disabling side effects like aortic aneurysm, tendon rupture, it even has a blackbox warning for psychosis, suicidal ideation and even completed suicide. And they added that warning in 2016, which is after I was prescribed them a year earlier. And you know, even Nature, the world’s premier scientific journal, had done a feature on Fluoroquinolone antibiotics and their disabling side effects in 2016. But I think the prevailing consensus in the medical community hasn’t changed much, they still very much say things like we prescribe like water, we prescribe it like candy. It’s perfectly safe. And there are thousands of patients whose lives have been forever altered by this class of antibiotics.
Lindsey:
So yeah, I think that one year, I had two 10-day courses of Cipro for urinary tract infections, and three days is actually the standard of care. I don’t know why the doctor prescribed it for so long for me.
Nita Jain:
Yes, yeah. Especially especially when it comes to like uncomplicated urinary tract infection, uncomplicated bronchitis, I think we can safely go with safer options.
Lindsey:
Yeah, well, I’m allergic to sulfa. So I think the first time Bactrim maybe is the one they usually give, but I was allergic to that. So that may be why they went to Cipro for me. Yeah. So backing up again, what made you think of FMT as a possible treatment? Like where had you even heard of it?
Nita Jain:
So I had a tangential awareness of FMT, just being a biochemistry student, I think in 2012, that’s when it first got on my radar. And when I first heard the term, I was like, What is this? It sounded very weird, fecal transplant. Like, what does this mean? So I started reading up about it, how it helped people with C. difficile infection. But it’s weird. Even though I had GI issues at the time, I didn’t make the connection that maybe this is something that I could pursue, because at the time, most of the literature around it was just in relation to C. diff. So I thought, okay, that’s just something that helps that isolated case. But then I did start following the microbiome research. And in 2013-2014, I was seeing more and more evidence about things like the hygiene hypothesis; how being too clean can maybe negatively impact our health, because we’re losing these old friends that help train our immune system and help us develop immune tolerance, help us differentiate between self and non self. And so I think as the years went on, I was getting progressively more convinced that this is really important. And I myself was a C section, baby. So I was also thinking that, well, maybe some of the things that I’m experiencing are due to the fact that I wasn’t a vaginal birth and didn’t obtain my mom’s microbes by passing through the vaginal canal. Maybe that was something and also the fact that I didn’t breastfeed for very long at all, just a few months. And that’s also something that helps to facilitate good gut health because mom’s breast milk contains HMOs, which are human milk oligosaccharides, these small sugars that feed the bifidobacteria in the infant gut, and that really helps to train the immune system. So I was thinking that maybe this combination of things like antibiotic exposure, the C, Section delivery and lack of breastfeeding was maybe contributing to my health issues, even before the Cipro fiasco happened a little bit later. When I did receive Cipro, I had read in the New York Times about this system restore, and it was about FMT. But they basically talked about FMT as system restore and like, we all know that if your computer gets a virus or a bug, you can essentially use System Restore to return to a previous point in time, and that can counteract any sort of malware that you’re experiencing on your machine. And FMT was likened to that. It was basically saying, like, we bank our stool when we’re healthy. So that if we ever get sick, we can administer that sample to ourselves – autologous FMT – use our own sample. And that will be like restoring our health to that time point. And having read that, I was just like, I think this is going to be the solution. For me, this is the thing for me to pursue, because I was just getting shuffled from specialist to specialist with no real resolution, I was very convinced that the gut microbiome was going to be the thing to get me back on track. And I was kind of upset that I hadn’t saved my stool beforehand. Like before the antibiotics I was just like, if only I had considered this earlier, then I could have just done autologous FMT with my own sample when I was healthier, because it’s so hard to find a good donor, a donor that you respond to, it is very much a needle in a haystack endeavor for a lot of patients. So I think, yeah, that’s another thing that might be beneficial, to have stool banking options for patients if they are going to need to take antibiotics. But again, it’s also a question of education. A lot of us don’t know about this until we get ill. And then it’s too late.
Lindsey:
Right, you need the stool put away before you have the thing that requires the antibiotics.
Nita Jain:
Exactly.
Lindsey:
Yeah. That’s the dilemma. And so what period of time did you go from being totally bed bound to being up and around and again, again, maybe not in perfect health, but just, you know, functional?
Nita Jain:
Yeah, so 2019 was the first year that I started seeing a little bit of that return to health after finally finding a donor that I did respond well to. It wasn’t perfect, but it was good enough to get me back 70% of my functions. I still had chronic cystitis pain. And this is something that I developed after hospitalization after a Taymount sample. So that’s something that I have still been dealing with since 2015. But basically everything else has gone into remission as a result of the strides that I’ve taken.
Can you explain what the cystitis is?
Yeah, absolutely. So basically, chronic cystitis, there is a lot of overlap with chronic UTIs. And I think the unfortunate thing is, most of the time, doctors only consider a UTI as being either acute or recurrent. There is not a lot of medical education around chronic UTI yet, but a lot of patients do experience that and I am one of them. Basically, when you do urine culture, it’s really biased for E coli detection. And that’s pretty typical because the vast majority of UTIs in females are caused by E. Coli. But there are also a lot of other organisms that can do it, like Klebsiella pseudomonas, Enterococcus at times can cause UTIs. And the thing is, because the culture process is biased to E. coli, sometimes even if a patient does have an infection, the culture can still come back negative. And you might need something like urine PCR to find those microorganisms. And urine itself, the bladder itself does have a microbiome. It’s not as though urine is completely sterile. But you do want to beware if there’s zero pathogens there. So unfortunately, urine PCR is not widely adopted right now. So sometimes you kind of have to find a urologist or somebody who’s willing to do that more in-depth testing. But for me, it seems that sometimes when UTIs have been going on for long enough, there might be something called biofilm formation, where it’s just these, these communities of microorganisms that form this extracellular matrix that protects them from antibiotics. So one of the problems is that bacteria that are forming a biofilm, it’s very hard for antibiotics to penetrate that a lot of the time. So sometimes, you might have to be on antibiotics long term or sometimes patients have to receive intravesicle antibiotics. So antibiotics directly into the bladder, because the oral stuff, it’s just not concentrated enough by the time it reaches the bladder to have enough of an effect to break up the biofilm and clear the infection. But yeah, this is just something that there’s just not a lot of good information on right now. And I think patients who are dealing with it, they’re kind of left to fend for themselves finding a specialist or finding a doctor who is well versed in the condition and the possible treatment methods. And that’s still a journey that I’m on to fix that condition. But at least for me, the dysautonomia, the IBD, the neuropathy, all the neurological stuff improved incredibly to the point where I don’t really deal with that on a day to day basis anymore. Thanks to FMT and the anti inflammatory diet and time restricted feeding.
Lindsey:
And what about your psoriasis?
Nita Jain:
Yeah, so I developed some eczema and psoriasis in the aftermath of Cipro as well. And the gut-skin axis is something that’s being more widely elucidated now, and there’s even something called topical skin microbiota transplants that some researchers are using to see if it can help with things like psoriasis and eczema, or atopic dermatitis, as it’s sometimes called. But yeah, for me, now, the skin conditions, they get bad in the winter months, but otherwise, the rest of the year, I’m in remission. But sometimes I will still have that dryness, that peeling, and just that tearing of the skin, the epidermis layer in the winter months, but the rest of the year, it’s in remission. So that is something that still crops up around that time of year. But otherwise, that’s been okay as well.
Lindsey:
I know there were some products on the market a couple of years ago, I’m not sure if they still are that were like lotions and soaps that had microbes in them. Have you tried any of those?
Nita Jain:
I have tried a few of them. Yeah, I think I tried things like Mother Dirt and AObiome. And then I think, there are some, some skin products that use terpenes, and other sorts of other sorts of compounds that are supposed to help fortify the skin barrier. And I’ve definitely tried and experimented with a lot. I haven’t found a way to prevent the recurrence in the winter yet. But there are things that have helped me, like I started using Weleda Skin Food; that helps me a little bit. And then I think a lot of it’s also just internal nourishment, like keeping my omega intake high and just making sure that my vitamin D intake stays high. There’s a lot of inverse correlations between skin, autoimmune conditions and your vitamin D levels. So those do make somewhat of a difference in terms of severity. But it does crop up a little bit in the winter nonetheless.
Sure. So in 2019, that was the first year that I was doing better. In December of that year, I was part of a research organization, it was called Open Humans. And basically this is a community of researchers as well as citizen scientists who get together and share and have n of 1 experimentation results. And the benefit of n of 1 is that while you don’t have the rigor and the generalizability of a randomized controlled trial, you do get to illustrate that certain variation exists in the human population. So it’s beneficial from that regard, just to show that this variation is possible to observe, just because all of us are a little bit unique. But long story short, one of the people who was part of the organization, Eric Daza, was creating this special issue in Frontiers that was about patient-led research and using data and so he asked if I wanted to submit I said, “Okay.” And so I wrote this short mini review on personalized approaches to microbiome research. And it was all about how the more precise we are with our approach, and really like tapping into precision medicine, personalized medicine, the better off microbiome science will be. And I had submitted the manuscript in January of 2020. And I got feedback from a couple of couple of reviewers in the fields. And I just went through that peer review process, they had just minimal notes for me. I made some small edits, sent it back. And it was published in April of 2020. And it’s ironic by the time that happened, I had already contracted COVID. And then the whole of 2020, I was unfortunately dealing with hospitalizations because of lung scarring, trouble breathing, really severe tachycardia that felt like heart attacks whenever it happened. And then I also developed a kidney infection after hospitalization. And then I also had GI surgery that year. So it was, it was a pretty awful year. But it got off to a good start with the publication. But it was pretty much downhill after that.
And what was the GI surgery for?
So they had diagnosed me with something called superior mesenteric artery syndrome (SMAS), which basically means that you have a blockage that’s preventing the normal passage of food from your stomach down into your small intestine. And they say that the blockage is at the level of the duodenum, where the superior mesenteric artery is sitting on top of it and cutting off circulation. However, all of my functional imaging tests were normal. So when I did like the barium X ray series, the barium was passing through my system as normal. I also did gastric emptying tests, where you consume the radioactive eggs, and they they track the isotope as it moves through your body. That was also normal. So even though they were seeing suggestions of a structural abnormality on an MRI, just in terms of the dilation of the stomach, and just the fact that there’s narrowing of the artery in the space, that does not mean that I’m having functional consequences as a result of it. But unfortunately, because of confirmation biases, and other psychological factors at play, my doctors stuck to that diagnosis, and they were like, we’re going to have to do surgery or you’re going to die. And they gave me two options, either one, get a feeding tube, or two, get this much more invasive surgery where they would remove my gallbladder and just connect my stomach to my small intestine, bypass my duodenum completely. I opted for the less severe option, because I again was very skeptical that this is what’s wrong with me because of my normal functioning tests. And, you know, anytime I would press my doctors for this, I would say things like, I really think this is IBD; I have blood in my stool. I don’t think this is the right diagnosis. Because, you know, with with SMAS you have pressure, you have uncomfortability, but I was just getting the searing burning pain, where it’s just like, I’m very inflamed. And I was losing weight like crazy, which is, again, something you can see with SMAS. But I just felt like it wasn’t in line with everything else that was going on, like the blood in the stool, the elevated calprotectin that’s highly diagnostic of IBD, not SMAS, right. So but again, my doctors brushed me off when I addressed these, when I voiced these concerns.
Lindsey:
And was your burning near your duodenum?
Nita Jain:
It was not! That was another thing; the location was completely off. I was just like, the burning sensation that I’m having is south of where it should be. If it was SMAS – because it’s not at all in the area where you’re saying that I have a problem. But nonetheless, I got hospitalized just because I was barely able to eat. I was in so much pain. And unfortunately, they had me on an all liquid diet for 17 days in a row. After the surgery, I wasn’t allowed to eat for a while I think maybe there was something. . .
Lindsey:
So I’m sorry, you opted for which version of the surgery, what did they do in the surgery?
Nita Jain:
So I opted for the less invasive procedure, which is a gastrojejunostomy. And basically what they do is they clean out they basically go in into your stomach, feed a tube down through your duodenum all the way down into your jejunum which is the first part of your small intestine. And that is supposed to bypass the area of obstruction so that I can be fed. So I had this feeding tube. It didn’t help me at all. My pain actually got worse because the area where the surgery is, that tissue is getting very inflamed. And the other thing is, it would sometimes get infected because it is essentially an open orifice when you have this feeding tube; it’s exposed to the outside elements and everything. So despite the fact that I would sanitize it often, the chance of infection is pretty high with these sorts of things. And you do have to be really careful about it. But I was not really gaining a lot of weight doing this, which is what they had wanted to see. I was more inflamed than before, with the cardiac issues that I was already having, with the cystitis that I was already having. It was really hard to use the bathroom, just with a tube and managing the feedings around the clock was nuts. The other thing, when you have a feeding tube, they expect you to feed around the clock. And that’s not really good from a circadian standpoint to always have food in your intestine, because then you’re not having the autophagy that normally would have happened at night; the cellular repair isn’t happening. So there’s just a lot of things that you don’t know upfront about having a feeding tube.
Lindsey:
Are you eating regular food? Or are you just using like solutions of, you know . . .
Nita Jain:
Yeah, so they basically had me feed exclusively through the tube. And I really wanted to have pureed food by mouth because, in my mind, I’m like, I can eat by mouth. I should be eating by mouth if I can.
Lindsey:
So wait, where is the tube? Exactly? Where does it start?
Nita Jain:
Yeah. So the tube, it’s going through the stomach, and it’s just passed down into the small intestine.
Lindsey:
Oh, okay. I was picturing it coming through your mouth. Okay, so it’s entering your body midway?
Nita Jain:
Yeah, exactly. Basically the entry point was right below my left rib and I still have a lot of pain from the surgery scars and the incision place because it doesn’t fully go back to normal post surgery. And sometimes, it is one of those things that’ll flare up in terms of pain when it’s really humid outside, stuff like that. But the other thing was, it was so hard to breathe for a long time, because of the fact that it’s so close to my lungs, the incision site, and just I just had so much inflammation there as well, which was not pleasant. But long story short, after about three months, I was begging my GI doctor, please let me remove this tube, nothing good is happening, I’m just in pain. And I’m just suffering and I’m not gaining any weight from it, I think I just want to go back to eating pureed food, because at least then I don’t have to deal with this anymore. Because like the tube’s getting infected, I can’t sleep at all because of how much pain it causes me. I’m just completely miserable, and it’s just debilitating. Unfortunately around the holidays and stuff, it was that time where it would be hard to get me in to have the tube removed. So I asked if I can safely remove it at home. He said, okay, it’s probably stabilized having been 8 to 12 weeks, because you don’t want to remove it before that time period, or it can be a little bit dangerous. So I did end up removing it at home by myself and just not eating anything for I think it was like six hours afterwards just to be on the safe side. So kind of letting that initial peeling process start. And then slowly reintroducing liquids and then purified food and then working my way back up to solid food. But again, it was FMT that I pursued to get that inflammation under control, because the surgery didn’t do anything for me. It worsened my inflammation. And I think the IBD was the more likely culprit, otherwise FMT would not have helped me. It was something functional, it was not something structural, otherwise, I would have not responded to FMT treatment.
Lindsey:
And how thick was this feeding tube that you could just pull this out of your body and leave a hole behind?
Nita Jain:
Yeah, so I think the catheter that they insert the tube is maybe 18 FR, or so. Maybe 20?
Lindsey:
What’s that roughly in inches?
Nita Jain:
Yeah, so it’s less than an inch, it’s definitely less than an inch in diameter, maybe half an inch in diameter.
Lindsey:
And you just pulled this out of your stomach yourself, or your intestines yourself and just left the hole there?
Nita Jain:
No, it’s not like that. Basically, what happens is, it’s held in place by a balloon. And so the balloon is filled with water. So basically, what you do is you take the syringe, and you try to drain as much of that water out as possible from the balloon because that’s what’s holding it against the abdominal wall. And once you do that, then you can start to pull, but it did kind of get stuck near the end. And I was sort of panicking for a while because I’m just like, oh no, I’m gonna have to go to the hospital if I can’t do this myself. But yeah, it just required a little bit of persuasion. Just because the balloon, even when it’s deflated, it does have a certain thickness to it. So you just have to alter your breathing pattern while pulling to get it out but then yeah, I basically put the gauze over it and cleaned the area first of course thoroughly and just waited for my body to start patching itself up.
Lindsey:
Wow. Interesting. I’ve can’t even begin to picture this. Okay, so how are you doing now? I mean, like what percentage are you back to health? You look like you’re in good health to me but I know looks can be deceiving.
Nita Jain:
Yeah, my main concern these days is the chronic cystitis pain. So that’s the most disabling part of my life these days. It’s just because I still have that burning and urgency 24/7 since it first began back in 2015. And I still just have to use the bathroom multiple times a day. It does interfere with sleep because of the pain. There are some things that help in terms of avoiding anything that’s very irritating to the bladder. But that only gets me so far, because I still have that pain regardless. So that is something I’m still trying to troubleshoot as far as dealing with all the biofilms in the bladder that I have, and hoping that I can have remission and some sense of normalcy, hopefully.
Lindsey:
Do biofilm busting herbals help at all, or is that pretty much only hitting the digestive system?
Nita Jain:
Yeah, most of them don’t make it all the way to the bladder to really have an effect. A lot of the time, the stomach acid will degrade those enzymes before they can really have much of an effect. But I have tried pretty much everything under the sun in terms of herbal antimicrobials, in terms of biofilm busters, like Interfase, stuff like that. But yeah, I haven’t been able to appreciably move the needle. That being said, it is a lot more under control than it was when it first began. When it first began, the pain was so severe that I would go six or seven nights in a row without sleeping.
Lindsey:
That’s horrible. I wouldn’t wish it on anyone.
Nita Jain:
It was just horrible. It was one of those things where I had white blood cells in my urine, but the cultures were coming back negative. So they were just like, yeah, sorry, we can’t treat you sort of thing.
Lindsey:
Yeah, yeah. No, I know someone who’s got the same problem. And what about oxalates? Did you go down that path at all?
Nita Jain:
Yeah, I did try a low oxalate diet to see if that was something that was irritating my bladder, just removing leafy greens like kale and things like that. But I didn’t see any benefit from doing that. So I was like, let me just put them back into my diet because it does provide good fiber and good nutrients.
Lindsey:
Yeah. So did you remove other things like berries and nuts and all the oxalate foods?
Nita Jain:
Yeah, definitely. For sure.
Lindsey:
Okay. Yeah. Just curious. Well, I hope you get to the bottom of that. So but your IBD symptoms are resolved? And the digestive system is working well now?
Nita Jain:
Yes, I believe so. So I’m thankful for that, at least. And I’m just hoping with this last piece of the puzzle resolved, I can finally feel a little bit more whole.
Lindsey:
Yeah, I’m sure. And one more question related to the FMT’s that I’m curious about. You mentioned, I responded to a certain donor, or I didn’t respond to another donor. So when you’re getting these samples, are you’re getting like, okay, here are 15 frozen samples of donor x and 15 of donor y, and you get like 45 total? With what frequency were you taking them? How did that all work? And could you request a certain donor like, oh, I’d like more of this guy?
Nita Jain:
Yeah, actually, after I responded to one donor at Taymount, I really did want to request that donor again, but they said that they don’t operate that way. So I think a lot of it’s dependent on the clinic itself. And there are also some clinics that prefer this multi donor approach. They say that, if any one donor doesn’t work out, then you can overwrite it with other donors. But I sort of advocate for a more precision approach versus this, I don’t know, Motley Crue approach where you’re just throwing random samples at the person because they have this idea that whatever is good is going to stick. But that’s not how it works. I mean, pathogens can easily colonize the GI tract. And I think it’s better to just be very intentional with what we’re administering in terms of making sure that these donors are safe, and that they’re enriched and productive bacteria; that they’re devoid of any pathogenic bacteria. I think we just need to be more deliberate in the process in how we go about it. But when it comes to frequency, a lot of this depends on the condition that you’re trying to address as well. At least for me, once I started doing it in conjunction with an autoimmune protocol, the benefits would last until I did something that would really skew the balance, like take antibiotics for the cystitis or something like that.
Lindsey:
The benefits from one donor?
Nita Jain:
Yes. But sometimes, with certain conditions, you might have to do it weekly for a number of months. Like I’ve definitely seen that addressing ulcerative colitis sometimes benefits from a more long term approach versus things like IBS, for instance.
Lindsey:
Are you doing it weekly?
Nita Jain:
Yeah, so I currently just do it if anything happens that throws me off, that throws me into a flare, and then I’ll administer it, and I’m good until I’m not basically.
Lindsey:
Autologous or are you getting samples still from somewhere?
Nita Jain:
I’m still getting samples. Actually, what I do is I try to make the samples last as long as possible, like a lot of the time, they’ll give you 60 CC’s. But I mean, the fact that the stool is just so densely concentrated with the bacteria, especially because most of these clinics, they filter out the food or any of the other debris that might be in the sample. So it’s basically just like microbes suspended in a saline solution of sorts, maybe some cryoprotectant, a little bit of glycerin to preserve it so that when you freeze it, they’re not damaged (the bacterial cells). But yeah, at least for me, I just make a little go a really long way. So a 60 cc sample, I can easily take it 10 or 20 times just because it doesn’t take a lot, I feel.
Lindsey:
And are you doing it in capsule format or enema format?
Nita Jain:
I’ve been doing it with enema format, and I basically use a bit of a longer rectal catheter. I know that some doctors have this idea that unless you’re doing it by a colonoscopy, where it’s being delivered, at least to the sigmoid colon that it’s not going to make a difference. But I haven’t personally noticed anything like that. I noticed that even with a rectal catheter, even with an animal bottle, I still receive the benefit from FMT, even though I’m not being sedated, it’s not getting as far up as it needs to. But nonetheless, I mean, it’s a live product. So the bacteria they know how to colonize.
Lindsey:
Yeah. So how long and wide is the rectal catheter?
Nita Jain:
So I use an 18 FR rectal catheter, and it has two eyes. So basically, it has a rounded tip. So that makes for pretty easy, painless insertion, and then it has two eyes on either side. And that’s how the material is delivered into the colon when you push the syringe through.
Lindsey:
Okay, so with with the cystitis, I imagine you must have to take antibiotics frequently.
Nita Jain:
At this point, no, I’m currently not on antibiotics right now, just because I have not really seen much benefit from it in the long term yet. I’m still in the process of doing more targeted testing. Because I think for for me, I’ve been on almost every antibiotic class to address this cystitis. But I think with biofilms it’s just one of those things where there’s a lot of layers, there’s a lot of bacteria. And sometimes, once you treat one round, you’ll notice that there’s different uropathogens than the previous time, then you’re targeting those. And sometimes it feels like a whack a mole type of situation, but I’m trying to be very targeted about it rather than taking antibiotics.
Lindsey:
So you’re not constantly having to do it. So you’ve still got remaining. And the most recent samples that you feel are good for you came from where?
Nita Jain:
So the donors that I’m using right now came from Microbiomes LLC. And I’ve had mixed results with their donors as well. But I’m just using the one that I responded well to. And the only problem is, I’m not sure if I can get this donor again. So I’ve kind of been wanting . . .
Lindsey:
But you have an idea on the donor that you could say I’d like this donor, if possible.
Nita Jain:
Yeah, if possible. But then, when you’re dealing with human material, it’s always a question of availability. Even if you get it once, can you get it again? And right, it would just be great if we could make something synthetic.
Lindsey:
Yeah. And so if somebody were were wanting to try and pursue FMT, they can reach out to this Purety Clinic to do it, or Microbiomes LLC directly?
Nita Jain:
I was not able to get in touch with Microbiomes LLC directly. So I went through Purety Clinic personally, but things are changing all the time.
Lindsey:
And is that near you? Or did you go in person?
Nita Jain:
I did not go in person. I’m in Georgia and Purety Clinic was in California. But I remember during the pandemic, a lot of clinics had ceased operations, just for concerns about transmission risks through stool even. So, we were waiting quite some time before operations could resume, before I could get samples again, just so much is dependent on the circumstances. Well, it would be great if it wasn’t something that relied on humans to provide the material for.
Lindsey:
Yeah. Okay, well, we’ve gotten a little bit over time, but there were a lot of interesting nuances to your story. Any final parting words for anybody who’s dealing with chronic health issues and is considering FMT?
Nita Jain:
I think just prioritize health and safety, safety and efficacy as much as possible. And regardless of who you’re going with in terms of a clinic or your doctor’s office, a hospital, ask if you can have the the testing results for the donor. Even if they don’t give you the exact results of the donor specifically, ask them what they’re checking for, in terms of what, like make sure that they’re at least doing the bare minimum in terms of checking for the patient’s metabolic health, CBC, CMP, making sure that they don’t have Hep A, Hep B, Hep C, just making sure that you’re covering as many bases as possible. Most of them will also be doing culture, like stool ova and parasites, things like that. But if possible, ask them if they’re also checking to see if their donors have protective bacteria in addition to not having the pathogens. And do your research as much as you can, then feel free to reach out to other people. But I think diligence is really the top most concern and, do take your time if you can. I know it’s really hard, especially when you’re suffering a lot, you can be in a place of desperation, but please do prioritize the safety as much as humanly possible.
If you’re struggling with dysbiosis, diarrhea, constipation, leaky gut, candida, IBS, IBD, orother gut health or all over body problems, you’re welcome to set up a free, 30-minute breakthrough session with me (Lindsey). We’ll talk about what you’ve been going through and I’ll tell you about my 3- and 5- appointment health coaching programs in which I recommend lab tests, educate you on what the results mean and the protocols used by doctors to fix the problems revealed. Or if you’re ready to jump in right away or can just afford one appointment at a time, you can set up an 1-hour consultation with me.
So let’s start by just the basics about what IBS is and what causes it.
Onikepe Adegbola, MD:
Sure, IBS is a functional gut disorder. The cause of IBS is not exactly known, but it’s thought to be a function of the disturbance in the sensation of intestine for the patients. Some people get IBS after infections. But for most people, the cause of IBS is unknown. There are a few criteria for diagnosing IBS called the Rome Criteria, and doctors follow that criteria. There’s a lot of items in the criteria, such as abdominal pain and other GI symptoms over a certain period of time. And of course, if the patient has what we call alarm symptoms, like blood in the stool, and things like that, though, a lot of things have to be excluded as well.
Lindsey:
Like inflammatory bowel disease
Onikepe Adegbola, MD:
Exactly. Colon cancer, things like that.
Lindsey:
Yeah. And do you want to mention SIBO at all, and the distinction between IBS and SIBO?
Onikepe Adegbola, MD:
Yeah, so it’s mentioned that a lot of people with SIBO have IBS-like symptoms as well. SIBO is overgrowth of bacteria in the small intestine that can recall in certain conditions or following surgery in some people, and and so once a while, you can use the low FODMAP diet for both conditions; the therapy is not exactly the same. So there’s a difference between the two. People with SIBO often have IBS like symptoms as well.
Lindsey:
Okay, and so tell me about the low FODMAP diet and how it manages IBS symptoms.
Onikepe Adegbola, MD:
Yeah, so the low FODMAP diet is a diet, whereby you decrease the amount of fermentable carbohydrates diet, sort of a mouthful of an acronym, right? It stands for fermentable oligosaccharides, disaccharides, monosaccharides, and polyols. So it’s a little bit of a mouthful, but quite simply, they’re all fermentable carbohydrates, that some people don’t digest properly in the intestine, and it gets broken down by bacteria, which results in gas. You know, think about fermentation, like when you’re making beer or, or bread, for example. So you’re going to get a whole bunch of gas. And that’s going to cause, because of symptoms like abdominal pain, constipation, diarrhea, and bloating, when it draws water into the intestine as well. So people with IBS generally have a problem with those type of carbohydrates. So using the low FODMAP diet, you can decrease the amount of those carbohydrates in your diet, and thereby prevent flare ups, reduce the the amount of IBS symptoms. A lot of studies have shown that about 70 to 75% of people with IBS get symptom relief from the low FODMAP diet.
Lindsey:
And what kinds of foods are FODMAPs?
Onikepe Adegbola, MD:
Yeah, that’s an interesting question. And that’s what makes the diet sometimes difficult for people to follow, because first you have a whole bunch of carbohydrates, right? And secondly, it’s not like gluten, where you just remove maybe things that have gluten like wheat, for example, you know, that’s straightforward. Or even somebody that is lactose-free, right? You just remove milk and dairy products. So there’s a wide range of foods that are FODMAPs. And I would urge anybody who is trying this diet to not wing it for sure. And there’s the Monash App to go through to find the levels of FODMAPs in various foods. So Monash and FODMAP Friendly are the two organizations that tests for the amount of FODMAPs in food and tell you what servings is okay on the low FODMAP diet, because for a lot of foods even though they may be low FODMAP in low quantities, they could easily get high FODMAP in high quantities. And so so you have to watch the amount of of each food that you take in even if you quote unquote follow FODMAP or moderate FODMAP food. But basically if you want to do a simplified diet in a very simplified manner, you would say that things like dairy for example, lactose, things that have lactose or high FODMAP foods that have onion and garlic. Garlic is high FODMAP because even a a little bit of that, it’s a problem for people who react to FODMAPs Inulin is high FODMAP; you see it in a lot of foods and even in small quantities. That can be a problem. I mean for inulin for example, I don’t even have IBS, but I react to inulin, so that’s something that a lot of people with IBS react to. Sweeteners ending in -ol . . . . . . all the sugar alcohols . . . exactly, sugar alcohols. They are high FODMAP. Even the simplest sugar alcohol, which is erythritol, can be low FODMAP. But it still causes, it’s still mentioned because it causes symptoms all on its own. So I would definitely avoid it as well. And then you also have beans, which I guess we won’t be surprised about, high-FODMAP fruits like apples, which have high fructose content, are high FODMAP. There’s a long list of foods that are high FODMAP. But I think some of the more common culprits, except for maybe onion and garlic, are not a surprise. A lot of people they eat foods, they have problems, a lot of foods, you know, dairy, sometimes I think people, some people would know that as well.
Lindsey:
Yeah, onion and garlic are definitely the hardest ones to eliminate. Because they’re kind of in everything. And then the powders as well, which are in salad dressing. When I was doing the low FODMAP diet and I went out, I would take my own salad dressing with me to restaurants because otherwise, it was just oil and vinegar, which is kind of boring.
Onikepe Adegbola, MD:
Yeah, exactly. Because it’s everywhere. Even when you’re not told that onion and garlic is there, it could be there.
Lindsey:
Right! It’s the base of every recipe practically.
Onikepe Adegbola, MD:
Exactly. Right. And that’s actually why one of the reasons why we started off with the low FODMAP seasonings, because our seasonings don’t have onion or garlic. So for people on the low FODMAP diet, that’s very, very useful. But you know, we have people who are like “Why would you have a seasoning that has no onion? No, garlic. That’s strange, right?”
Lindsey:
So you sell those seasonings?
Onikepe Adegbola, MD:
Yeah, we do. Low FODMAP certified.
Lindsey:
Okay. And so can you walk us through the process of starting a low FODMAP diet?
Onikepe Adegbola, MD:
Yeah, sure. So the process, it generally takes about six to eight weeks to go through the low FODMAP diet. And there are three stages. So in the first stage, you would eliminate FODMAPs from your diet. So that’s where the apps like the Monash app, and the FODMAP friendly app, can be very useful, because they help to tell you what serving size is normal. And I think that that’s a low FODMAP normal in that situation. But I think that for a lot of people, that’s probably the toughest part of the diet, just eliminating all those foods. And it can be very confusing for people. It can be easy to make a mistake. And even if you make a mistake, or something goes wrong during that time, you can always start again, you shouldn’t be down on yourself. So you start off with that, that part of the diet usually takes six to eight weeks. And then hopefully by that time, your symptoms will subside, and you’ll get some relief. And now then you get to the second part where you’re trying to figure out, okay, well, so I’ve taken all this stuff, all these fermentable carbohydrates out of my diet, which one is causing my problem? So let’s use a sort of reverse elimination process to figure it out. So you test each FODMAP group, one by one over a couple of weeks or so. There’s a lot of resources, we have some free resources to help you with that part of the diet, which is called reintroduction and which can be tricky for some people, and Monash also has some resources on the app to help you go through that. And then once you figure out, okay, well, this is what I’m reacting to in the diet, whether it’s fructose or oligosaccharides, disaccharides, or polyols, then going forward, you can go into the third phase of the diet, which is the maintenance phase, where you just you have a diet that eliminates what you react to. And hopefully a diet which you can follow everyday and get rid of IBS symptoms. So that’s pretty much it. And the whole process, you know, probably takes a couple of months. And if you have a dietitian helping you, that’s very helpful because it can be confusing for some people. And if you don’t do it properly, then you might not get the relief. Or you might think it doesn’t work. Well, while it might not work for 25% of people, you want to make sure that it’s not working for you because it’s actually not working for you not because you’re not doing it properly.
Lindsey:
And so I imagine that if you stay on a diet like low FODMAPs for an extended period of time that there could be some risks or downsides. What might those be?
Onikepe Adegbola, MD:
Yeah, absolutely. And that’s why it’s it’s meant to be a short term diet, even though unfortunately, some people claim that they can’t really ever go back to eating stuff, and they sort of have to keep being on a completely low FODMAP diet for a while, but it’s been shown to change the microbiome. Studies have shown that taking probiotics can help with that, relating to the levels of Bifidobacterium from the low FODMAP diet, but then the other changes with the microbiome have been shown with the low FODMAP diet. And you could, by restricting some foods in your diet, such as dairy and other foods, you could end up with some nutritional deficiencies over the long term. So that’s why it’s not supposed to be a forever diet. It’s ideally a diet which is short-term and targeted. And once you figure out what the problem is, you can move on to a more normal diet.
Lindsey:
And do you advise people like maybe to use it just when they’re flaring or once they figure out their sensitivities just to stick with that as their base diet?
Onikepe Adegbola, MD:
Yeah, once you figure out your sensitivities, I would advise people to just figure that out. That’s the best idea.
Lindsey:
Okay, and can you discuss the other treatment options for IBS? Besides the low FODMAP diet? I assume you use some adjuncts to that?
Onikepe Adegbola, MD:
Yeah, so there’s definitely medications, good adjunct to the low FODMAP diet for people who want to them. So you’re talking about medications like Linzess, Immodium, antidepressants, all depending on what the symptoms are. So for example, antidepressants, even though people hear antidepressants and they think, oh, well I’m not depressed and so this is not really useful for me, but they’re actually working on the garden. Now, this has nothing to do with depression; so they can be useful in for people with IBS. And also things like yoga, exercise, mind-body meditation. And so even some people have noticed, hypnosis can be helpful. Cognitive behavioral therapy can also be helpful. And so what is very useful is for you to find the combination of things that work for you personalized. You could call that personalized medicine, because everybody’s different with ideas, as I guess a lot of people with IBS know. Because if you are ever in an IBS forum, and people are talking about their triggers, there’s such a wide range of triggers. You talk to 10 people, you get 20 different triggers. So there’s definitely a wide variety of triggers. And what works for everybody is different. So yeah, it’s important to work with somebody if the low FODMAP diet is not helping you. Or maybe if you want to supplement it with something, it’s helpful if you work with somebody who can personalize the diet, personalize your interventions and come up with a plan, a personalized plan that can help you to get your symptoms under control.
Lindsey:
And so is the mechanism of action with the antidepressants is that these are SSRIs that are increasing your serotonin, such that you have more motility in the gut, like for more constipation SIBO? Or is this also for more diarrhea type SIBO? Or IBS I should say.
Onikepe Adegbola, MD:
So yeah, so it’s more use it in different forms of IBS. And so it acts on the gut, it helps with pain, for example, people have abdominal pain and IBS.
Lindsey:
Okay. And do you use Rifaximin at all with your patients?
Onikepe Adegbola, MD:
For patients with SIBO, Rifaximin is definitely helpful. It’s so expensive in the US and not always covered with insurance. But helpful sometimes you can use it. Also metronidazole, Flagyl, which is metronidazole can also be used because and is cheaper than Rifaximin. So that can also be used for patients who can’t get or find the cost of Rifaximin too expensive or who can’t get it from Canada. So if you get it from Canada where it is cheaper, it can definitely be used, it’s possible. And then also, placebo. People have also looked at antibiotics, herbal antibiotics like oregano on and whatnot can be effective as well.
Lindsey:
So what kind of testing do you do to determine what patients have?
Onikepe Adegbola, MD:
It’s mostly a diagnosis that you can make from symptoms and mostly from symptoms. But if the patient is having what we call alarm symptoms, like blood in the stool, change in bowel habits and things of that nature, you might want to do tests to rule out something that could be sinister. So you want to rule out colon cancer, for example. And IBD is also differential, a possible diagnosis. So you want to rule that out as well. So while IBS is a diagnosis you can make through history, if a patient has alarm symptoms, and in certain situations with age or whatnot, you might have to do some testing just to rule out celiac disease, rule out IBD, rule out colon cancer.
Lindsey:
So would you send people to their local gastroenterologist in that case for a colonoscopy?
Onikepe Adegbola, MD:
Yes, in that case, yes, we will. Although we do prefer patients who have seen their gastroenterologist already because we’re not aiming to be their primary care, or their primary gastroenterologist, we’re more an extension, a help, because people with IBS often have, you have all those symptoms and it takes time and trial and error to resolve them. And so the time that they spend, the doctors have 15 minutes or 20 minutes in a typical appointment, which is just not enough, and is often rushed for them. And also they have to make appointments to see the doctor, which could be weeks, days or whatever, in the future when they’re having symptoms like right now. And you know, they can’t get anybody to talk to them. We’re that stop gap where you have somebody you can always talk to. We have the time, we have long appointments, and we focus solely on IBS. So it’s not a situation where you know, you go to your doctor and they say, okay, well try the low FODMAP diet. And you’re like, Well, how do I do it? And oh, well Google it, they give you a short handout with two sentences. And we so we go in depth and really help you to get a hold of your IBS symptoms and take control of your symptoms with personalized plans.
Lindsey:
Okay, and so can you tell me a little bit more about your virtual IBS clinic and how you help people manage their symptoms?
Onikepe Adegbola, MD:
Yeah, sure. So we actually started off as a low FODMAP brand. So for the last few years, we’ve been selling low FODMAP products, foods like the seasonings, like I talked about salad dressings, protein powders, as well as gut health supplements, which are low FODMAP certified, so that people on the low FODMAP diet or with some food intolerances have the confidence that what they’re eating is not going to give them problems later on.
Lindsey:
Is that under the name Casa de Sante?
Onikepe Adegbola, MD:
Yeah, that is correct. Yeah. So that is under the name Casa de Sante. And in the process of doing that, we’re very in tune with clients and customers. And we would get a lot of inquiries while we tried to help them, even though we always had the disclaimer that this is not medical advice. So we saw the need interacting in groups talking to our customers for this type of service, because a lot of people are just going to Facebook groups at this point and asking questions of people. It’s always good to get information from your peers and learn from people’s experiences, I think that is very useful, but it’s also helpful to get it right also sometimes more helpful to get help that could help you in the long term rather than just ad hoc recommendations as you have problems. So we started this service as a virtual personalized service. That is integrative care. So you have not just a doctor or a GI clinician, you have a GI clinician that is specialized in IBS, as well as a dietitian who is specialized in IBS, as well as a health coach to help you resolve your your IBS problem. So we have a holistic and personalized approach. And we have you set up appointments, providers, and you have long appointments, you have access to resources, you have a community, you have meal plans that can help you, you have testing; we do advanced testing. So if you have to do food sensitivity tests, we can help you. And based on all the data we get from the testing, as well as from your symptoms, we can come up with a personalized plan for you. And if you have questions, you have an app where you can log your symptoms and then reach out to us if you have questions or if you have any issues with IBS. So we have a whole approach, which is both the consultation and the the visits with the clinicians, and also the low FODMAP products if someone needs it. Okay, so how do you work with your patients to tailor the low FODMAP diet to their individual needs and preferences? Yeah, so a lot of people who have difficulty following the low FODMAP diet, just because it can be very restrictive. Actually, it is restrictive. So it can be difficult to understand and it’s not a lot of people that go about the whole place carrying a scale to weigh their food and to be exact, right? So it can be challenging from that perspective. And so for people who can’t, or are having difficulty following the low FODMAP diet, we can do a simple or gentle low FODMAP approach, whereby we eliminate the most common common offenders such as milk, onion and garlic wheat, wheat containing products. And I just want to mention that wheat is a FODMAP so it gives people problems, not because it contains gluten but it contains fructans. So some people who think they’re reacting to gluten might actually be reacting to the fructans in wheat and those types of gluten-containing grains. And so you could you do a gentle approach and start off with eliminating those and see if it helps the patient. And if not, then you can go into the full bore low FODMAP diet. And so we tailor it to our patients based on what they can do and what we understand from their previous experience. And some people already know what they react to, to some extent, and some people don’t. So everything’s personalized. And for some people, it just doesn’t work for them. They’ve tried it before, and it doesn’t work. And so that’s not necessarily the answer. And we know that 25% of people do not get any benefit from the low FODMAP diet, even with IBS.
Lindsey:
So if the low FODMAP diet doesn’t help at all, what are the likely causes if say bloating and gas is one of the big symptoms?
Onikepe Adegbola, MD:
Yes, trying an elimination diet can be helpful, because even if you don’t react to FODMAPs, you could react to other foods. So definitely having a diary and doing an elimination diet will be a good first step. And then for bloating, bloating is a whole interesting, subject by itself. But you want to start off by saying, okay, well, when is the patient blaated? When is the client bloating? Or how soon after eating does the client bloat? And then you can divide up the possible causes. And there’s a wide range of causes depending on when the bloating occurs, how soon after eating, and, and also understanding people have a very different description of what bloating is. For some people, bloating could be distension of the abdomen, of the stomach. Also for some people it’s the sensation of fullness. So you also have to understand what the client means by bloating. So that’s where understanding what the symptoms are, when they occur and taking a good history from the patient and understanding what is really happening helps. And then based on that we can do further tests to figure out what is going on. And we recommend some general approaches that would help anybody that has boating such as, don’t drink heavily caffeinated drinks fast, things like that are just helpful for people in general that have bloating, while you figure out what exactly is causing the bloating.
Lindsey:
Are you using the functional medicine stool tests?
Onikepe Adegbola, MD:
Well, yeah, we use different various tests, depending on what the patient’s symptoms and history are.
Lindsey:
So which tests do you like?
Onikepe Adegbola, MD:
I wouldn’t say we like a particular test. Again we go through this very personalized approach. It really depends on what the patient’s history is. And various practitioners do have their favorite tests. We have a few different practitioners in our practice and they do have their favorite tests. We try to individualize it for each patient.
Lindsey:
Yeah, there’s a little different offering on each test of what’s included. So this is true. Okay, so can you talk a little bit about the research on the effectiveness of the low FODMAP diet for IBS?
Onikepe Adegbola, MD:
Yeah, so research has shown that it is effective in about 70 to 75% of patients with IBS general, generally. The FODMAP gentle approach has also been found to have high effectiveness. Even if you don’t go through the whole low FODMAP approach, it can be helpful. And even having eliminated some of the common triggers that we know about has also been, which is also more simple than the low FODMAP diet. It has also been shown to be helpful. So just eliminating wheat and milk and and high fructose foods, high fructose corn syrup, and that sort of stuff can also be helpful. So yeah, so the low FODMAP diet is clearly effective for many people with IBS, but not all.
Lindsey:
And so we talked a little bit about the low FODMAP diet and the impact on the gut microbiome, but what can you, and if you want to elaborate any more on what else it does to the gut microbiome, but what steps can you take to ensure that you still have a healthy microbiome?
Onikepe Adegbola, MD:
So it’s been shown that taking probiotics can be helpful with that.
Lindsey:
Like lacto-bifido type probiotics?
Onikepe Adegbola, MD:
Yeah, bifidobacterium varieties as well as lactobacilli, yeah, that’s also helpful. And that’s why we have a low FODMAP certified probiotic that has a number of probiotic strains that are helpful bacterial strains that are helpful for IBS. It’s low FODMAP certified.
Lindsey:
Are there are strains you should avoid when you have IBS?
Onikepe Adegbola, MD:
I can’t think of any particular strains that you should avoid. The thing is that so many different stories on probiotics that have different varying results. So the data on probiotics is not always very clear, as oftentimes, you need more stories. And so that’s why the type of probiotic and the the administration of the probiotics is just very individual to people. And so we recommend that. Okay, when you try a strain, you try it for a short period of time. See if it’s working for you, make sure it’s not making your symptoms worse. And if it’s not working, or is making your symptoms worse, then you stop it. But probiotics are also very individual as well.
Lindsey:
Yeah, I have heard the suggestion that people with SIBO, the probiotics can be overgrown themselves, that you can be essentially implanting strains that will overgrow.
Onikepe Adegbola, MD:
Yeah, I have I heard that too. And then there are also studies that show that probiotics can be helpful.
Lindsey:
I know. It’s always tricky to decide whether or not to recommend them.
Onikepe Adegbola, MD:
Yeah, exactly. The data is definitely conflicting with probiotics. And so if you could get it, you’ll try it. I just recommend that if people want to try, they try a short trial and see if it works for them or not.
Lindsey:
And so how do you recommend including low FODMAPs food and supplements into an overall healthy diet?
Onikepe Adegbola, MD:
So I think if you’re on the low FODMAP diet, and while you’re in the elimination phase, the first phase, you want to avoid high FODMAP foods and supplements. And so there was a study that came out recently, maybe a year or so ago now, that showed that a lot of people just did not realize that a lot of medications and supplements have things that are gluten, they have lactose, and they could actually be a cause of problems for people who have food intolerances or allergies. In general, there’s probably just a little bit in those in of the FODMAPs, in those supplements and medications. But some people could react to that. So you probably just want to make sure that if you’re still having symptoms, check your medications, check supplements, they could possibly have FODMAPs in them, and they could be the source of your symptoms. I think I remember someone having inulin, for example, that could be in a lot of medications. And that’s a huge, even for me in small amounts, that’s a huge trigger for bloating and gas.
Lindsey:
And it’s also a big additive to those [granola] bars.
Onikepe Adegbola, MD:
Exactly.
Lindsey:
The commercial ones because it’s a lot of added fiber. Low cost, I guess.
Onikepe Adegbola, MD:
Yeah, exactly. Exactly. So I would I use a low FODMAP certified product, low FODMAP brand is probably the way to go while you’re doing the elimination phase of the low FODMAP diet.
Lindsey:
You know, I sometimes see now the brand in stores called Fody.
Onikepe Adegbola, MD:
Yeah, they have a number of low FODMAP products as well.
Well, I just want to thank you for having me here. Always happy to answer any questions anyone has about gut health, IBS or the low FODMAP diet and you know, here’s to your health and healthy poops!
If you’re struggling with dysbiosis, diarrhea, constipation, leaky gut, candida, IBS, IBD, orother gut health or all over body problems, you’re welcome to set up a free, 30-minute breakthrough session with me (Lindsey). We’ll talk about what you’ve been going through and I’ll tell you about my 3- and 5- appointment health coaching programs in which I recommend lab tests, educate you on what the results mean and the protocols used by doctors to fix the problems revealed. Or if you’re ready to jump in right away or can just afford one appointment at a time, you can set up an 1-hour consultation with me.
Today’s post is all about butyrate and tributyrin, which is the best absorbed form of butyrate. This is a supplement I recommend frequently to my clients and which some of my favorite gut health mentors like Dr. Daniel Kalish and Grace Liu, PharmD also recommend for certain gut issues. It’s particularly indicated for people with diarrhea, loose stool, IBS-D, hydrogen or hydrogen sulfide SIBO because it slows motility and leads to firmer stool. But before I launch in, I was to make a disclaimer that this should not be construed as medical advice and that you should see you own health care practitioner to make decisions about your own care.
Some of butyrate’s known health benefits are providing the primary energy source for the cells that line the colon, or colonocytes, improving the integrity of the gut barrier, aka reducing leaky gut or a leaky colon in particular and therefore, reducing inflammation and preventing the leakage of toxins into the bloodstream.
It has also been shown to enhance insulin sensitivity, which can reduce the risk of type 2 diabetes. It also has all-over body anti-inflammatory properties. And if that wasn’t enough, if you’re short on butyrate-producing microbes, which is associated with an increase in metabolic disease, type 2 diabetes, and obesity, butyrate may also be helpful. Supplemental butyrate has been shown to lower hemoglobin A1C and reduce blood-glucose spikes in type 2 diabetics, reduce insulin resistance, and reduce obesity-associated inflammation.
In addition, in animal models, when they purposely fed the mice high fat diets, which aren’t great for mice, butyrate prevented them from becoming obese and having the accompanying metabolic issues that accompany obesity. It was also shown to bring about weight loss in a randomized clinical trial of obesity in children. But in one study it did increase the weight of rats born to mothers fed butyrate, so I generally don’t recommend it for pregnant women, although Lucy Mailing, gut health expert and my guest from episode 25 of the podcast, made a good argument for using it even in during pregnancy in one of her office hour calls, and took it herself while pregnant. (See Episode 90 Show Notes for links to those studies).
Then tributyrin, which is formed of three molecules of butyric acid combined with one molecule of glycerol is a form of butyrate that is found in newer supplements, as opposed to sodium butyrate, potassium butyrate, magnesium butyrate or calcium butyrate forms, and has been found to be preferable to other forms of butyrate because it has a low odor and chemical stability, meaning it’s resistant to breakdown by gastric and pancreatic enzymes. This means that it can reach the large intestine intact. Tributyrin is also superior to other forms of butyrate for its ability to diffuse through biological membranes, releasing butyrate over time directly into cells as opposed to other forms of butyrate, which are metabolized rapidly as soon as they enter the cells lining the colon. Tributyrin has also been found to be more effective than other forms of butyrate in uses with animals, such as improving gut health in livestock and modulating immune function.
So now I’m going to focus in on the gut health benefits I’ve seen in myself and others of supplemental tributyrin, which are supported by the research.
So when you take antibiotics, your body’s ability to produce butyrate likely drops significantly. In animal models, the use of 3 days of oral antibiotics decimated the gut’s ability to produce butyrate from fiber and increased oxygen levels in the colon. Now the colon is supposed to be oxygen-free, also known as hypoxic. And a healthy, hypoxic colon supports both anaerobic bacteria, which can’t live in the prescence of oxygen, and facultative anaerobes, which can live with or without oxygen. But importantly, the anaerobes are the ones who produce butyrate to feed the colonocytes. Most butyrate producers belong to the Clostridium cluster of the phylum Firmicutes, such as Faecalibacterium, Roseburia, Eubacterium, Anaerostipes and Coprococcus, among others. So post antibiotics, when your gut becomes unable to produce butyrate, it will pull in oxygen as an alternate fuel source. This promotes the growth of facultative anaerobic bacteria, typically proteobacteria. In my experience, this leads to messy, loose stool, a poor mucus lining, and an inflamed and leaky colon. So supplementing with butyrate during and after antibiotics can reverse this cycle and help restore the healthy balance between anaerobic and facultative anaerobic bacteria. Lucy Mailing described this process in a great blog called “The oxygen-gut dysbiosis connection” and also spoke about it when she was on my podcast.
In my personal experience, because I have post-infectious IBS leading to frequent hydrogen-dominant SIBO (or small intestine bacterial overgrowth), I often have periods of bloating and accompanying loose stool and sometimes diarrhea. Tributyrin has been my savior in these periods so that while I’m working on reducing the quantity of bacteria in my small intestine, I can still have firm stool and maintain a healthy mucus lining. I don’t know about you, but if you’re dealt with loose stool, when you have a good one, it just puts you in a great mood. The trick with using tributyrin in my experience is getting the dosing right, and that happens most easily by increasing the dose until you get firm stool, and then when it gets too firm, like rabbit pellets, decreasing the dose until it’s just right. Personally, I have found that I’d typically need something in the range of 900-1500 mg and at times even as much at 2000 mg/day to or more to start to achieve firm stool, but then I can decrease my dose after that. The nice thing about butyrate is it has very few known side effects, with even higher doses up to 2,000 mg/day, no short-term adverse reactions have been observed in studies. Of course I don’t recommend it to my clients with constipation because it does slow motility and constipation does increase your short-term risk of GI and other cancers.
And since I found that I needed such high doses to achieve the desired result, and because the available supplements in capsule or gel cap format were typically 300 to 500 mg each, I always felt bad telling clients about it and then telling them that in addition to the other 10 things they were taking they might likely need 3-4 additional pills of tributyrin once or twice a day to get the desired effect. So this is probably a good moment to mention that because I saw this obvious hole in the marketplace, I set out to solve the problem by making a higher dose tributyrin supplement. So this is actually the first time I’m announcing publicly that I have this new supplement available for sale called Tributyrin-Max, a 750 mg/capsule tributyrin supplement in a hydroxypropyl methyl cellulose capsule, which is an enteric coated capsule so that it makes it through the stomach acid and to the intestines. It is available on tributyrinmax.com (free shipping for 1-3 bottles and low cost after that) and on Amazon.
This is pretty exciting for me but I also do it with a little bit of trepidation. Up until now I have been very agnostic about supplements, meaning I don’t have loyalty to any particular brand and choose what I think is best for my clients. And because I’m a pretty skeptical person myself when I see health celebrities promoting their own products. I have to admit that it has made me question their integrity. The dilemma is that it’s really hard to make a living seeing clients the way I do, because I give them like 1-3 additional hours of prep and follow-up time for every hour they spend with me. So that only allows me to see 3 gut health clients per week in addition to all my other duties with the podcast and newsletter and answering client emails. But I spent a really long time thinking about what if anything I might sell as a supplement, and I only wanted to sell something I felt I could unequivocally recommend, that didn’t have really contradictory evidence, like probiotics, for instance, and for which there actually was a legitimate need in the marketplace.
So rest assured I wrestle with the ethical dimensions of selling my own supplements, I won’t unequivocally recommend them to anyone. Like even on the bottle I put that people with constipation or with a history of polyps in the colon shouldn’t take it, which no one else selling it warns against, because there is a little bit of evidence that because butyrate is a food for the colonocytes, it could be cancer-promoting for those with a history of polyps, although there is a much greater body of literature showing it’s preventative for colon cancer, prostate cancer, tongue cancer, breast cancer, lung cancer and neuroblastoma. I’ll link to the Lucy Mailing article called “SCFAs Part 2: The benefits of butyrate” that cites all that literature as well as the studies that show its potentially negative impact on colon cancer. In her article, she also cites additional benefits to the brain of butyrate, including increased neurogenesis, reduced oxidative stress, and improved recovery following ischemic brain injury as well as potential benefits for skin and bone health. And then in a following blog “SCFAs Part 3: Decrypting the butyrate paradox: can excess butyrate be toxic?” she talks about potential drawbacks, especially in the case of active and flaring ulcerative colitis, and about the importance of only taking physiologic doses, which she describes as 600-1200 mg/day of tributyrin.
Also, because of the capsule ingredients, because emulsifiers and other food additives have been shown to be harmful for people with inflammatory bowel disease, I might advise caution on that front as well. The studies I’ve seen are only on mice and concern something called carboxymethyl cellulose as a food additive, not hydroxypropyl methyl cellulose, which is actually used as a coating for capsules of IBD-targeted pharmaceuticals, but if you want to exercise an abundance of caution, there is one powdered tributyrin supplement called AuRx* that’s available in my Fullscript Dispensary instead, that has a delivery mechanism that makes it not gross to eat as a powder. It was actually designed for kids with autism in mind, because butyrate has been shown to be beneficial in autism. But reading through one of Lucy Mailing’s other blogs on butyrate, which is linked in the show notes, I think that butyrate may not be advisable in higher dose format for people with active and flaring Ulcerative Colitis, although I do have one client who has definitely benefitted from it.
But if that’s not your concern, the capsule is a plant-based capsule and okay for vegans or vegetarians. I would actually have used a gelatin capsule but the manufacturer told me there was a 1-year wait for those.
So to sum up, if you have loose stool, diarrhea, etc. and it’s from SIBO or dysbiosis that involves a likely dominance of proteobacteria, which is often the case in post-infectious IBS that causes SIBO and following heavy antibiotic usage, tributyrin is a good supplement for helping slow motility and firm up stool and reverse the cycle of an oxygenated gut. And of course, trying to bring more fiber into your regular diet so that the bacteria can ferment the fiber and produce butyrate naturally. So I’m talking about beans and lentils and psyllium husk fiber. Those things are all great for producing butyrate naturally. And if you have SIBO or other dysbiosis, you need to see an appropriate health care practitioner to deal with that and determine the reasons for it and address it as well. Which as you know is something I do with my clients, and you’re welcome to set up a free, 30 minute conversation with me to find out if I can help you.
And if you’re interested in trying my new butyrate supplement, Tributyrin-Max, I’m offering a 15% off discount code for your first order, which is INTRO15.
So, I heard you speaking on the Chris Kresser podcast, and I immediately went out and got some tocotrienols to try. And so I was really excited when you were able to come on the podcast. Why don’t we just start with talking about what tocotrienols are and how they differ from tocopherols, which are the typical form of vitamin E contained in most multivitamin formulas.
Barrie Tan, PhD:
Yes. Vitamin A has two groups of compounds called tocopherols and tocotrienols. The tocopherols are more known, and you can see them on your cereal box, and tocotrienols are less known. The plant makes these two compounds, when the protection in the plant is more serious, then the plant likes to make tocorienols. So you intuitively know that it’s probably more potent, and otherwise, if it’s normal ones that use tocopherol. So, in the US diet, most of our vitamin E are tocopherols with a few exceptions than the tocotrienols, so the last 30 years of my life has been spent looking for the active form of vitamin E.
Lindsey:
Okay, so the tocotrienols are the active form, whereas, the tocopherols are inactive? Is that-
Barrie Tan, PhD:
Not inactive – less active, the tocopherols and the tocotrienols are active enough that about this book, you can see from the title of the book, “Tocotrienols: Vitamin E Beyond Tocopherols.” Tocopherol is the only E people know and tocotrienols people know less. You see, I was one of the authors so it’s more an academic book, so I don’t tell people much about it. This is a more consumer book, I wrote it as a labor of love and people can download on your website free of charge: “The Truth about Vitamin E,” is the book and they can download it from here.
So I started my career as a University of Massachusetts professor in 1982. And then I started to study vegetable oil. So intuitively, if vegetable oil is where you find vitamin E, the plant makes vitamin E to protect the oil from going rancid. So that is like that. So I know we are all to some extent very self-centered, somehow the plant makes things for us. The plant never makes things for humans. We ought to be grateful that they make things that are helpful to human health like that. They make it to protect themselves and for their own survival. Plants typically don’t make a lot of fat, but when they do have a lot of fat like corn oil, soy oil – actually corn and soy is not a huge huge amount of fat, but when they take the meal out and feed the animal or make tofu, left behind would be the vegetable oil and then the vitamin E goes there to protect it. When you think of a human being we typically have anywhere from a 20%, which would be exceedingly lean, to 40% is on the obese side. If you average a person of 30% fat, so in general, a human person has more fat than the plant ever would have. From there you can tell if we carry on average of 30% fat, then this fat needs to be protected. So that’s where I study Vitamin E to find out how it can protect us from oxidative damage.
Lindsey:
Okay. So, I understand that the tocotrienols that you work with are sourced from the annatto plant, so tell me how you came across this source of tocotrienols.
Barrie Tan, PhD:
Yeah, I discovered the three major sources of tocotrienols from plants which I had said earlier are difficult to find compared to tocopherols. The first one I found was in palm – palm oil. And people have questioned about taking palm oil, saturated fat and all that, but palm oil has a fair bit of tocotrienols. And then rice bran – the brown part of the rice bran, also has tocotrienols. It’s kind of like an open secret. When you eat Japanese tempura, they deep fry it with rice bran oil and rice bran oil is stable because of the tocotrienols in it, otherwise the oil will go rancid even faster; however, rice and palm contain about 25 to 50% tocopherols. Now, I’ll come back to that later.
So I was looking for a source that is very rich in tocotrienols, then the year was 1994. There was a professor at Harvard. Her name was Joanna Seddon and she discovered that on the back of the retina of the eye, they’re laden with zeaxanthin lenses to filter out the blue light. If you fast forward to today, everybody knows that if you take lutein and zeaxanthin, it’s good to prevent macular degeneration, but this was back in 1994. It wasn’t long ago. So now I know that in South America, in Peru, there would be a huge, giant marigold plant. I went there to look for marigold petals to extract lutein from the petal that it will be good for the eye. But then, by this time I was already studying tocotrienols. Then fate has it literally 20 feet away from me, I saw the annatto plant. You will have heard of the annatto plant because we use the color for coloring cheeses, Dorito chips and macaroni and cheese. If you touch it like I pretend to do here, it will stain (the plant). I intuitively knew something was unusual. By the way, the color is also a carotene, like lutein and zeaxanthin. Except it’s very unusual. If you look at this fruit, it doesn’t have a fleshy part, like fruit has. If you think of any fruit you eat, it has the fleshy part, but this just has the seed and then this stamen. Because I was a carotenoid chemist, I thought of something. If you think of a carrot, you have to cook the carrot to get the beta carotene out. You’ve got to cook a tomato for a long time in oil to get it out if you do Italian sauce. I knew that carotenes are so unstable; they are protected inside the cell of the cytoplasm. And even in lobster and crustaceans you have to cook them and then they deprotonate. And suddenly the yucky green or blue color becomes an orange or red color. Like you come to New England to eat a lobster.
Now when I explain it, it sounds so trivial like that, but it’s in my DNA, I kind of know this thing. But when you touch this guy here, it is not bound to anything. Notice that? You just stained your finger. So, I intuitively thought, “It must be a powerful antioxidant to protect the carotene from oxidative damage.” It was only a figment of my guess. I thought that it would be a polyphenol, which will happen a lot in nature. Surprisingly, it wasn’t. And more surprisingly, it is a vitamin E molecule. And most surprisingly, it is a vitamin E molecule that only contains tocotrienol and not tocopherols. So that would be my third attempt. Palm and rice contain 25 to 50% tocopherols. Annatto tocotrienols are completely free of tocopherols. By this time, I had already been studying tocotrienols for some 2025 years. I immediately called my professor friend. At the time he was at University of Wisconsin, Madison, and asked him, “What do you think?” I remember he told me, “Barry, if tocotrienols were to mitigate human chronic conditions, this tocotrienol better be, otherwise, you and I are completely a lost cause for our desire to bring this to bear.” So the last 25 years, I’ve been committed to do a chronic condition with this sort of vitamin E. And happily, they work on many chronic conditions that we study.
Lindsey:
Interesting, and we will talk about that. But I did just want to mention I lived in Costa Rica for a year and a half. And I learned how to make a few dishes there and one of them, Arroz con Pollo, uses annatto as a spice and they come in tubs in the grocery store. They’re just bright red, orange sort of tubs that you can take a chunk out of and it was like a refrigerated margarine, about that consistency.
Barrie Tan, PhD:
Wow.
Lindsey:
Not like the pebbly stuff that you find here in the spice aisles. And of course it tastes terrible if you eat it straight but it adds a subtle flavor and of course an obvious color to the whole dish when you add like a teaspoon or two. I bought a couple of tubs years ago and I still keep it in the fridge and of course it doesn’t seem to go bad at all which is because of obviously the protection that it has.
Barrie Tan, PhD:
Yes and if you could sometime, you have my email, send me that you said the Spanish word. I will try to look for dishes. I know they’re not classically American dishes. South Americans use it for a lot of their food. I was able to track, even the Inca Indians use it for their food in Peru and other places. Here it’s a very sterilized use, like we put it in cheese, but besides that it’s not used in any food dimension that I’m aware of. And curiously, I thought of this one time. It is not known to the Asian context. I’m Asian. With the exception of Filipino, and then I was able to track it because the Spanish that went to South America also were in the Philippines for 400 years. Sometimes when I tell my American colleagues, it’s hard for them to put their heads together. The Spaniards were in the Philippines for 400 years, as long as they were in South America. So not surprisingly, many of my Filipino friends, they have Hispanic names, and they look like me. They’ve been there for a long time. A lot of Filipino foods also use annato. Isn’t that interesting? So they brought the flavor and the seeds and they grow it in the Philippines. So a lot of Filipino empanadas – and that’s a Spanish word, but if you ask any Filipino, they know empanadas. And then they make this little reddish looking and then they put this annatto in. But otherwise the other part of Asia or Southeast Asia it’s an unknown spice; they don’t use it at all.
Lindsey:
Yeah, well, I’ve got two recipes, I think, that call for it: the Arroz con Pollo which is chicken and rice, and then one another is a chicken dish. I will send you both those recipes and I’ll post them in the show notes. So I’m wondering, are tocopherols harmful to take as a supplement?
Barrie Tan, PhD:
Not harmful unless you take them in high amounts. If you remember, the late 90s into the 2000s, all the published work on Vitamin E was negative, even women who take it, Harvard Women’s Health Study, and some of the women have higher incidence of breast cancer and men who took it had prostate cancer. I think that the reason is because of all the eight Vitamin Es (four tocopherols and four tocotrienols), alpha tocopherol is the only one that has a transport protein. That means that when they cross the cell membrane, they have a right of passage. They have a protein that takes them in. Only alpha tocopherol has it, the other ones just go in by diffusion. Diffusion simply is an engineering phrase: “low concentration, high concentration.” You will move from the high concentration to the low concentration. Just like if you put sugar in a glass of water, and the sugar first sinks to the bottom. Over time, you see some wiggly thing, it will move from the high concentration as the sugar dissolves into the low concentration. That is a process of diffusion. And that’s how Vitamin E would work with the exception of alpha tocopherol. Because they have a transport protein that helps. So in those studies, when they use alpha tocopherol, they use 400 ones and 1000 milligrams. So a lot of this vitamin E goes in, it had no place to go. And I think that they are not good for you. However, if we were to eat a normal diet containing 10 to 15 milligrams (15 milligrams is 100% of the recommended daily allowance), that would be fine. However supplemented, people will have 10-20, even 30 times higher concentration of alpha tocopherols. That’s a problem. But we did not find that to be a problem with tocotrienols.
Lindsey:
And so what conditions has the research shown that tocotrienols can benefit?
Barrie Tan, PhD:
Okay, how about I tell you some of the conditions we’ve studied, and then we can fractionate them? We did a lot of studies in the last 20 years on chronic conditions. And I think that for the audience to appreciate this, right, we’re not talking about a drug. We’re talking about supplements. and this is almost my entire lifetime studying this. So this is, if I weren’t here, I doubt a very large company would put this kind of money and time and effort and energy to do it. So we did probably about 15 to 20 clinical trials. And the kinds of studies we were involved in, chronic conditions we initially studied were dyslipidemia: high cholesterol, high triglycerides; insulin resistance; people who are prediabetic (but not yet diabetic) and finally we studied a group of people who are diabetic. And now we have committed to have a huge amount of resources to study fatty liver disease.
Now if the audience is having any of these conditions, you would understand. For the audience members that do not have these conditions, you’re blessed, but just to give you some numbers. People who are prediabetic are about 90 million Americans. People who are diabetic, 35. And about another 100 million people who have fatty liver disease. Of course, some of these things overlap. So therefore, huge numbers of the American population has this kind of problem. Most recently, we are studying people beyond overweight. They are obese – men and women in Texas. So in the studies that we are doing, people with prediabetes and dyslipidemia, our study calls for anywhere from 100 to 250 mg. Say you round it up 100 to 200 mg. For people who are diabetic, the studies were about 250 to 350 mg. For fatty liver disease, (remember, the liver is a larger solid organ), we actually did three studies on this, Lindsey. We did a three-month study, a six-month study and a 12-month study. We already were convinced 600 mg was needed for this. We didn’t change the amount, we just did the time, because I wasn’t sure that after three months, if we were to be successful, that it would continue to be so in six months. So therefore, it’s not a dose-dependent study, but instead a time-dependent study. So we stayed with the same dose. We studied different things at three months. We studied stress enzymes and the stress enzymes come down and drop.
And the second study, we studied steatosis, which is fat in the liver. We used our ultrasound to map it like you use ultrasound to look for a baby in a mother. We were able to see the fat egress from it in a six-month study. In the 12 month study, we decided to go for gold. We decided that I have to go beyond getting consumers to be interested, or a primary physician to be interested. I have to convince the specialist to be interested, which means that these are liver specialists. So we decided to do CAT scans. And we saw that the fibrosis score is reduced the steatosis also is reduced. When the fat stays in the liver for too long, it forms a scar. So the doctors call it fibrosis. And that’s kind of like considered not reversible. So now we can clearly confirm that fat is reduced. Inflammation is reduced, liver enzyme is reduced, steatosis and fibrosis.
But there is something I will keep last to tell because I’m initially very skittish to talk about this. We noticed this in the three months. I was not very convinced. So in the six months, we saw it again. And my science director, says, Barry did you notice this?” I saw this, but I’m hesitant to make a comment on this. How about we do a 12-month study? And we repeated it. The shorthand is, the people who have fatty liver are already generally overweight; they lost weight. And in our clinical trials, we did not have that as a primary outcome. See, when you design a trial, you have to make a hypothesis. What are you looking for? We did not look for weight loss, but then they lost about 10 to 15 pounds consistently in three months, six months and 12 months. So I asked, “How are we going to report this? Factually it is true.” Can you imagine that? Most people will do the opposite. They just say weight loss and then they go sell a heck of a lot of product. I’m doing the opposite. You know why I was worried Lindsey? When when you say the word weight loss, people expect a weight loss in two to four weeks. Well, I never had data at one month. My shortest data was three months, even so you saw weight loss at three, six and 12 months and just say that. If people say, “Would I see weight loss in one month?” No, we don’t have data on that, but you can say that we saw the weight loss. So now we can consistently see sustainable weight loss on the largest organ in the body that at three, six and 12 months. I think tocotrienol is not intrinsically a weight loss product. Instead, it helps people’s metabolism out of kilter to come back to balance and the inflammation drops, the stress to the liver drops, and as a consequence of that, their weight also comes back to normality.
Lindsey:
Interesting. So does it matter whether the fatty liver is non alcoholic or could it be alcoholic fatty liver too that this would impact?
Barrie Tan, PhD:
This is a brilliant question. We only studies non alcoholic fatty liver. But the reason this disease was called non alcoholic fatty liver disease – It was discovered by the Mayo Clinic in 1984. Not so long ago. I don’t know if you know this story. This is a cute story. Well, it wasn’t cute when it happened. There was this guy. He went to see the doctor. And the doctor looked at the numbers came back and said (I just made up his name), “Mr. Jones. Do you drink alcohol?” Mr. Jones says, “No, I don’t drink alcohol.” So the doctor went back to the lab and came back again. And now a little bit more accusatory tone. He spoke with Mr. Jones and said, “Are you sure you don’t drink alcohol?” See, with that kind of intonation, Mr. Jones is upset. He says, “I told you I don’t drink alcohol!” So that was the reason because Mr. Jones’ liver looked like a cirrhotic liver from somebody who drinks alcohol. It wasn’t. So all this to say that when we take in a lot of carbohydrates and fat, we can make the liver almost look like someone who drinks alcohol. So a short way to answer your question is we believe that people who have a cirrhotic liver caused by alcohol also would benefit from tocotrienols because their liver looks the same, which is why awkwardly this disease is NAFLD. After NAFLD, they become NASH – non alcoholic steatohepatitis. So the liver looks like a person with hepatitis A, B and C. Hep A, B and C are different because they are caused by a virus. And by the way, this tocotrienol worked positively for people with hep C virus, totally different mechanism.
And that was done, sorry I to have to tell so many stories, but when we designed this study, Lindsey, the investigator and I decided that if you have people with Hep C, you have to recruit people. He said we have to exclude people with Hep C, if they have alcoholic liver, we have to exclude them, otherwise, we have all the “monkey on my back.” I cannot interpret my data. That’s how you randomize a study. He was fine with that. When he was recruiting the 100 older patients, about 12 to 15 of them had hepatitis C. So he had to exclude them. But what he didn’t tell me was curious. He separately gave them a tocotrienol. It was not in the study, it was excluded. He didn’t tell me. A few years later, I found an answer “Barrie, did you see this? Our tocotrienol is used on people with Hep C. It actually worked to reduce the viral titre in the people.” Then it tracked back to the author, and the author is the same one that did the NAFLD. So he excluded it. It also helped people with that. So we did not continue that study because Hepatitis C is a different direction; it is caused by a virus but it probably, I think, any damage to the liver, whatever the reason might be, at minimum, tocotrienols would help the liver.
In animal studies. we also studied hepatoma, animals with liver cancer. It also has support to reduce the severity of the cancer in the liver. So you can generalize the phrase that tocotrienol is hepatotonic, a liver tonic. But well, of course, if you say it like thatm it’s too general and people don’t know what it’s for. So I have to tell people about the clinical studies. The best we have done so far is this huge group of people with fatty liver due to dietary mismanagement and that works on them.
Lindsey:
Was the dosage for those people 600 mg a day?
Barrie Tan, PhD:
Yeah, for the fatty liver 600 mg. For the type two diabetes anywhere from three to 400 mg in those studies. And for the prediabetic and people with dyslipidemia, it’s about 125 to 250 milligrams. So those are the range I know. We didn’t discuss this. We have about six or so clinical trials in Denmark, of people with cancer and the cancer we studied, two of them are specifically for women. Ovarian cancer, breast cancer, lung and colon cancer. And my colleague in Florida is studying pancreatic cancer. And in that case, we are studying stage four cancer. So as you know, stage four, there are no options available, it is the end stage. So we use the highest dose, which is 900 mg, people take 300 mg for breakfast, lunch and dinner. And in that series of trials, we have the ovarian cancer result back. The audience should remember, this is stage four cancer, which means that there are no more options available. So they were taking Avastin, which means that this is anti-angiogenic. It prevents the tumor from sucking food from the nearby artery. Angiogenesis is the growth of arteries, anti-angiogenesis is you cut the artery off, essentially, you starve the tumor to death. They take chemo for that. And in another group that does the same, they take chemo because it’s the standard of care, plus tocotrienols. That’s it, no other differences. Inoperable, not radiatable like that. And they have in the registry in Denmark already, after six months, then in the group that had Avastin, they are not around anymore. In the group that took the tocotrienols as well, 60% of them survived. In Denmark, this is a woman’s disease, so the nurses are predominantly women, and they really want the study to continue. The principal investigators said, “If we continue to study, what do we compare it with?” The group that they compared with were no longer there. Anyway, for good reason they persisted and they were able to, and I’m glad they did. They persisted the study for four times longer into 24 months, two years. And even after two years, 25% are living. So that’s a remarkable thing I consider.
We are still hopeful that the tocotrienol would work on cancer, but I don’t think I’ll have a prayer to ask the FDA for any claim. Maybe under the Compassionate Care Act of United States passed by Congress. When there are no options available, then the FDA may allow its usage. I don’t know if we have the wherewithal and financial muscle power at FDA, but we’re willing and have the will to complete the study. And then let people read the study. So hopefully, in another year or two, if you still remember me, you can call me, “Dr. Tan, have you completed the study, I’d like to find out more on that.” At the end of the day, I am as fascinated and as touched by this as an audience listening to this would be. I believe that it is this powerful because it is uniquely tocotrienols and it’s the most potent Vitamin E I have ever put my hands on.
In the end, and as I told you in the story earlier, I didn’t even go to South America to look for this. I was looking for something else. And I consider this spiritual to me. If you look at me, I’m Asian, I’m supposed to go to Asia and look for this thing. And then I cannot speak a word of Spanish. And then everything is an oddity, but then this meant to me when I get to this part of the Amazonia, other people could have discovered it, but they didn’t. They weren’t curious enough to look. I was curious enough to look. And I’m not supposed to be there. I’m supposed to be in all these other wonderful places in Asia. But that was not where I found it. I showed you the picture. I was in Peru. And I cannot speak – I’m sure you speak a lot more Spanish than I do. I do speak it, yes. That’s amazing.
Lindsey:
So you mentioned dyslipidemia, and I’m curious, do tocotrienols have any impact on Apolipoprotein A?
Barrie Tan, PhD:
We only did a study early on. It did drop the Lp(a) a little bit, but it’s not dramatic. On the whole cardiovascular emphasis, I should bear out so that you will know where it works better than others. It consistently dropped triglycerides. That’s a good thing. I’m going to give you a teaching moment here. Before people become diabetic when they’re prediabetic, their triglycerides are high, but the sugar is normal high, but still normal. The person who discovered metabolic syndrome, he call it syndrome X before, and that was a professor Gerald Reaven, you can Google, he gave talks. He is a retired Stanford endocrinologist and passed away now. I remember one time, I caught him when he finished his talk on the run to catch his flight. So he was a little bit irritated that I stopped him as he was walking out. I said, “Just tell me how to put my hand around this metabolic syndrome thing.” He said one sentence, and then he left like that. He said, “Dr. Tan, 10 hypertriglyceridemia always precedes hyperglycemia.” I never forgot it. So, in other words, before people have high sugar, they have high triglycerides. So therefore, if the triglycerides dropped, that’s a very good sign, and then the LDL drops. Most of the LDL that dropped are the dense LDL, not the buoyant LDL, but in LP(a), we didn’t study that in serious depth. We also studied oxidized LDL, because oxidized LDL is atherogenic. And then tocotrienols is a very powerful antioxidant. So not surprisingly, the LDL stays LDL and does not get oxidized. So we were thrilled to see that as well. So pretty much that is the group. Oh, the HDL did increase, not by a lot. It’s very difficult to increased HDL except when you exercise and the HDL increased typically about 5% better than the other direction. When people take a lot of carbohydrates, the HDL drops. And when you exercise the HDL increases, we noticed that tocotrienols, the HDL increases, not dramatic, by 5%, consistently, we see this.
Lindsey:
Okay, so I know that soluble vitamins do build up in the body. So I’m wondering if you can reach harmful or excessive levels of tocotrienols?
Barrie Tan, PhD:
To the best of our knowledge? No, because of the 15 to 20 clinical trials we study, the short one is about two to three months. And the long one is about a year, we didn’t see that. Like this fat delivery study, we asked the physician please to report any unbecoming side effects. They reported and they did not see any liver enzymes go up, no kidney function was compromised, nothing like that, that they saw. We didn’t see that at all. By the way, right now, the study in Texas is of men and women who are obese. So we were able to get an IRB, Institutional Review Board to approve. We found this in animals all the time. There when you take tocotrienol because they’re lipid soluble, they are deposited into fatty tissues like vitamin D or K. So we knew that in the animal. So this is a first study, where we have biopsies of the adipose tissue. And then so we will be able to measure how much storage of the tocotrienol is in the adipose tissue in this obesity study. So the obesity study will also be complete by the end of next year.
Lindsey:
Okay, and is it important to divide up the dosage that you take each day? Or can you take it all at once?
Barrie Tan, PhD:
It’s important if you can take tocotrienol up to about 300 milligram and after that, if you need to take more than that, you divide it, which is the classic example in the Kansas study. They take 900 mg at 300 mg soft gel for breakfast, lunch and dinner to get the 900 mg. And indeed, in the fatty liver study they take two 300 mg with lunch and dinner. And notice I always say with a meal, they’re lipid soluble so you shouldn’t take it with on an empty stomach like that. And then for studies that only require 100 to 200mg, they can take all of it at one time. Do not take more than 300 mg.
Lindsey:
Okay, so I use some of the typical functional medicine lab tests with my clients like the Genova NutrEval or the Metabolomix. And they only show tocopherol levels on those tests. So can you infer anything about tocotrienol status from tocopherol levels?
Barrie Tan, PhD:
No, you cannot. On tocopherols, they readily do that. And I know that had made the tocopherol story last as long as it did, because of the alpha tocopherol transport protein. Frequently when people take bloodwork because they’re looking for lipid profile for cholesterol in a fasting stage. And then it’s about 12 hours overnight fast. Then they look for vitamin E. If you asked for a blood work for vitamin E, besides alpha tocopheral like tocotrienol, in 12 hours, you’re not going to see any tocotrienol, even if they take it with the dinner about 10-12 hours last night before. On that one, it also has a story too. We did that 20 years ago and we found out that there were no tocotrienols in the fasting blood 12 hours after and, the research professor said, “See, the tocotrienol is not absorbed, it’s useless.” It nearly got thrown away, the baby with the bathwater. So then I said, “Wait a minute, you cannot say that, because the blood is only a snapshot on that day. Not that in the blood is no good based on a snapshot.”
So I have to go back to animal study. And in the animal study, this is it. In the cholesterol thing, because of the alpha tocopherol, let’s say if you think of it 2, 3, 4- 10 hours like that, the alpha tocopherol will go up like this. But with the tocotrienol let’s say this is five hours. It goes up for five hours, and then it quickly goes down six, eight hours. So if you have an overnight fast, it’s almost zero. First we showed this an animal and we showed this in humans. For me, it is as painful as it is heartwarming, we actually did the study just to show the pharmacokinetic at five hours, and then it dropped back like that. So why did it drop? It doesn’t have a transport protein, and when it dropped back, it was not picked up. It has already delivered to the organ. But the alpha tocopherols kept being in the blood. So therefore, as a clinician, if you say that it is in the blood, therefore it is absorbed, believe that but only to a certain extent.
Many things are not shown in the blood. It’s already been deposited into the organ, or if it’s deposited in the organ, it is not going to spool and continue to be in the blood. We found that we have consistently found that in all the different organs like I expressed in the liver, and when in animals, you can excise all the tissue, we see them all over in the brain, in the eye and in the other organs. Each person with 130 to 160 pound weight, has 38 trillion cells about 5000 times the population of the Earth. Each one of them is like a cell, say like a bean shape and has a cell wall. And most of the fat in the body is in the cell membrane. And the tocotrienol goes to the cell membrane and the fattier the organ is the more tocotrienol would be there. So you would expect that the tocotrienol would be found in your brain, in your liver, in your lung and in all fatty tissues, of course in your adipose tissue. Of course in people who said well, “How do you know that?” We know this because they work to kill the cancer in those tissues, but we cannot poke and get a biopsy because humans are not animals. In the fatty liver study, we were not allow to do biopsies. It’s a luxury we cannot have, however; if the person has cirrhosis, has liver cancer or Hep C, well that’s different, so they’ll do a biopsy.
The closest and the first ever we have this is with the obesity study. And for that we are only allowed to have biopsies of the adipose tissue where the love handle is. It is minimally invasive, but otherwise we are not allowed to do that. So therefore, in that case, it is legitimate to study it from the animal. We did have one study, it is a cadaver study and it was from that that we found out the liver thing. A lot of these are story findings. This professor at Ohio State got a US government grant to study tocotrienols in the brain. He was going to get a $5 million grant, but NIH told him, you have to show us before we give you the 5 million bucks to do your study that the tocotrienol is in all the different tissues and he said he was drawing a blank. How am I going to show him that the tocotrienol is in all the tissues? The reason NIH asked that was because they did not see it in the blood. That was the reason. so he had a problem. He didn’t know how to deliver to the government. And then the university was so creative. He said, “We have end stage liver failure patients and if they are on a liver transplant list and waiting, they may wait in vain and they may not get the transplant and then they die.” So if they give consent to take the tocotrienols and if and when they die, and they allowed their organs for human research, then you are good. So he did, he gave it to give it to the 20 or so patients, half of them passed away. That’s when he showed that the tocotrienols were found in the brain, in the eye, in the heart, in the lung, everywhere. So he’s got his money. A side note was half of the patients improved. Remember, he was doing this to show what he needed to get the grant for the brain study.
It was because of that that we decided to do a study on fatty liver. The study was, just show me that the tocotrienols go to different organs. He did! He got his money. But he published a study in the Journal of Nutrition, then he did, and we did. And so now, because he was asked by the US government to show that is found in different organs, now we’re able to find that, indeed, it even helped people with fatty liver. So sometime, findings are not a straight path. But it did lead to a good path. So that’s a blessing. So it did not come from me, Lindsey, so I cannot make the claim. I’m thankful that that professor did it. So we took the the cue from that and decided to engage in clinical studies.
Lindsey:
That’s awesome. So we’re kind of running out of time, but I want to get to GG or geranylgeraniol? So I know you’ve done research on that, and that it might have some relationship to gut health. So can you tell me about that?
Barrie Tan, PhD:
GG is an endogenous nutrient, which means your body makes it. I know that the body makes GG for at least three reasons, probably more. The body makes GG to make the first two easier. Behind me, that’s a molecule of GG here, and the other molecule is Coenzyme Q10. So GG is used in the human body for the synthesis of CoQ10. So everything you know about CoQ10, which I don’t have time to explain, you need GG, otherwise, you cannot make CoQ10 in the body. So second, GG is required in the body for making MK4. Everybody in our industry knows the gut fermentation makes MK7 so you can read everything about MK7, and other menaquinones using vitamin K. But I wanted to change the audience and your understanding. In the colon our body makes MK7 and other MKs. That is to make the good bugs go up and the bad bugs go down so that your gut is in a good place. But when people push the idea of making menaquinones remember, when menaquinone 7 is made in the gut, they are not absorbed. Absorption of nutrients is in the small intestine. So when you make it in the colon, it’s in the process of making poop. It’s excretory material through the rectum. So only water is absorbed back and forth like that. I’m saying that GG helps the good bugs to grow because they’re feeding material for the bugs to grow into. So they are growing more like a prebiotic.
By the way, another time, if you send me an email, we can send you the study: tocotrienols work in people with Crohn’s disease and inflammatory bowel syndrome. Maybe you should have me for another interview where I just talk about the colon. This one is more a general health. But for the GG PPs, the GG goes in the body and makes MK4. And the last part is, about 30 to 40% of our body weight is skeletal muscle. Skeletal muscle cannot be synthesized without GG. We need GG for making skeletal muscle. Not surprisingly, as we age we have sarcopenia and loss of muscle mass. And in the very specific instance, and I’m sure your audience will know this, many people take statin drugs to lower cholesterol. The same pathway to lower cholesterol, just right below it is GG. So therefore when you inhibit cholesterol, it’s obligatory, you will inhibit GG and the inhibition of GG is the reason why when people take statins they have low CoQ10. Now, did I connect the dots? Because you inhibit cholesterol synthesis, GG drops, and when GG drops, CoQ10 drops. So CoQ10 did not drop just because they took statins. CoQ10 drops when people take statins, it’s because there isn’t enough GG that statins inhibit and therefore CoQ10 drops. So in other words, if your patient takes statins, if you measure CoQ10 and the CoQ10 drops, it is very likely that the GG has dropped because GG is required for the synthesis of CoQ10.
And of course also MK4 and MK4’s story is very simple. It will affect the bone health process, the porosity, it would also litter the calcium in places you don’t want it to be like calcified arteries, kidney stones and gallstones. So that’s a very short story about the GG piece, it’s a very powerful biochemical. And I’m only talking about it today because humbly, on the same plant that I extract tocotrienols from, after I removed the tocotrienols and color, I still had some some chemical there. It looks yellowish like corn oil when extracted and studied it. And would you believe it? It is GG. So I’m blessed, you know? So this particular plant is an ancient plant in South America. It yielded the secret of tocotrienol, which I explained to you and now further yielded the GG, which the plant makes for making all kinds of things. For the human, it makes the three things I mentioned to you.
Lindsey:
Would GG then be something that’s helpful for people who have already calcified arteries?
Barrie Tan, PhD:
Yes, we are hoping to do a study now. Currently, our two studies we are doing: the main one we are doing is people who are on statins, who are under a cardiologist’s care and have myopathy. And if they take a GG, it it would mitigate the myopahty on those on statins. And so it’s a muscle type question at this point. And then we’re hoping to do some exercise sign on the muscle thing. And someday we also will get to the sarcopenia on the elderly population, we hope to get into those areas. And we hope also to study MK4; we believe the calcification is the MK4 piece. When the body does not have enough MK4, the calcium is not shuttled to the bone. You need MK4 for the shuttle to the bone and not leave it in the artery nor the gallbladder nor the kidney. So we are now working to see how we can conduct a study to do that. It is so exciting. I’m supposed to retire after the tocotrienols. And then I fumble on this GG. And GG is very exciting.
I know that the time is up, I want to tell you one thing. Please allow me, it will only take less than a minute. GG is found in the plant. It is the last common step that the plant and the animal share. The plant and animal are vastly different. They need green chlorophyll to photosynthesize. We need heme red to make oxygen, one needs carbon dioxide the other one needs oxygen. Like do you know that tonight when you go home and then you eat your food, your vegetables, you see green, you think GG. Without GG there’s no chlorophyll. And then when you see your color, your beta carotene, your lycopene, your astaxanthin, your lutein, everything, all this beautiful color, you have to think GG. Without GG, there will be no cartenoids. So now I feel very spiritual that I had this finding. GG is the last common step between these two. In the plant, it is essential. The plant cannot survive without GG. In the human, I just told you the three things that are essential. So I’m just thinking, wow, this GG is really cool. It is really an endogenous nutrient. And even if you take the statin thing away, when we grow old, why do we have low energy, and then we don’t make enough CoQ10. But nobody told me we don’t make enough CoQ10 because we don’t make enough GG SBH. Oh that’s an important thing. And we have a calcified artery because we don’t make enough GG and it’s unable to make MK4. And then don’t quickly jump onto MK7. They are several menaquinones, but the only menaquinone that is made in the human body is MK4 using GG, not the other menaquinones. The other menaquinones are made in the gut however, but they’re not absorbed.
Lindsey:
So would you be an advocate of the MK4 form of vitamin K, as opposed to the MK7?
Barrie Tan, PhD:
That is correct. I am a pro that; not for pushing any people to buy my GG. I’m saying that in true honesty. If our body makes MK4 to the exclusion of all the other MKs, don’t you think we should take notice? You can Google, do that. If not, you send me an email, I will send you all things. I hope the Japanese scientists and the scientists in the world who figured this out, I hope that they are nominated for the Nobel Prize. This is actually a classic vitamin thing. They deserve a Nobel Prize. I don’t deserve. I’m lucky that they told me this. And then I’m bearing these things out to people. If you Google menaquinone 4, it’s the only menaquinone made in 25 to 30 organs. You will never find an organ in the human body that makes MK7 or 9 or 11 or 13. Those menaquinones are made by the bacteria in the colon. Now in the colon however, you want them to be made, so the good bugs go up and the bad bugs are controled. That you want. So I don’t want to confuse that. That’s a good place, but when they make them, they’re not reabsorbed therere, only water is absorbed so that you either have diarrhea or constipation, you know, at that stage. But MK4 depends on vitamin K1 being absorbed and then the tail is cut off. The ring, which is on your dark green vegetables, go in and look for 25 to 30 organs, look for GG endogenous, stitch it on and when they do, that’s your MK4. I’m giving you it as simple as I possibly can. And then if you Google it, you’ll find a Japanese scientist studying this.
Lindsey:
Okay, well now I know I should be recommending the vitamin D/K MK4 supplements not the MK7.
Barrie Tan, PhD:
Yes. And then if you want to know of a company to do that, Designs for Health, they are a very good company. I think their product is called Tri-K. So they have three: vitamin D/GG, they have GG in it, and then vitamin MK4, I forgot. So if you just go to Designs for Health Tri-K.
Lindsey:
Yeah, I have a dispensary. I’ll put a link to it and people can go in there and I’ll put in my discount code (HDH15OFF) for the dispensary in the show notes.
Barrie Tan, PhD:
Wow, thank you Lindsey! Bless you and bless your all your listeners! Hopefully in another year from now when more of my clinical studies come out, you can have another interview of me particularly more specific on the colon health thing. And also on the other general overall health of the people. By then I will have more clinical trials completed.
Lindsey:
I’d love to. So briefly, can you just tell me about the supplements that you have that has the tocotrienols and the GG?
Barrie Tan, PhD:
Okay, you mean who sells them? Designs for Health as I mentioned, AC Grace, Allergy Research Group and then there are many people sell them on the internet. If you go to my website, American River Nutrition, and you say buying tocotrienols; usually people say you can buy from me. We don’t sell the finished product, so we’ll list all the companies that use ours. If you want to be sure that they come from us and not from other people, if it’s referring to GG, it’s called GG Gold, and if it’s annatto tocotrienols, it will be Delta Gold, because the main component is delta tocotrienol. We call it Delta Gold. We also make a product which is CoQ10 and GG. We call it DuoQuinol, it’s a play on the word. And then some companies out there sell it. So make sure that at the back of the bottle it will say DuoQuinol, GG Gold or Delta Gold, you will know it is from us. And we make this product in the United States of America, right here in Massachusetts.
Lindsey:
So the supplements sold through Designs for Health are sourced through your stuff.
Barrie Tan, PhD:
Yes, they are. They validated us to the nth degree and then we worked with them and we are pleased that they did a thorough job. They came, they looked, they did definitely, and then we’re also FDA approved, GRAS, kosher, halal and the whole works.
Lindsey:
Awesome. And then listeners can find you at BarrieTan.com?
Barrie Tan, PhD:
And if you want the book, BarrieTan.com/book, otherwise, if you lost that track, just simply type American River Nutrition, it will lead you there.
Lindsey:
And I’ll have these links in the show notes so they should be able to find them quite easily. Well, thank you so much. This was awesome. I love your stories and I’ll definitely have you back on and we’d love to hear more about Crohn’s and colitis and the outcomes of your studies.
Barrie Tan, PhD:
Thank you so much.
If you’re struggling with dysbiosis, diarrhea, constipation, leaky gut, candida, IBS, IBD, or other gut health or all over body problems, you’re welcome to set up a free, 30-minute breakthrough session with me (Lindsey). We’ll talk about what you’ve been going through and I’ll tell you about my 3- and 5- appointment health coaching programs in which I recommend lab tests, educate you on what the results mean and the protocols used by doctors to fix the problems revealed. Or if you’re ready to jump in right away or can just afford one appointment at a time, you can set up an 1-hour consultation with me.
I got this recipe orally from Doña Carmen, my landlady when I lived in Costa Rica. Hence no specific amounts of things.
Ingredients for Broth onion red bell pepper garlic butter celery thyme oregano tomato sauce – roughly 4 oz. a bay leaf salt white wine 1 or 2 chicken breasts
Cut up a small quantity of the above ingredients and put in 3-4 cups of water and cook with chicken. Take out chicken when cooked, and then strain the broth, throwing out all the spices, etc. Shred chicken.
Ingredients 1 tbsp. olive or avocado oil 1 tsp. butter 2 cups chicken broth (above) 1 cup frozen peas 2 cups cooked rice (cooked hard, with little water) 1/2 red pepper, cut in strips and then thirds 1-2 tsp. achiote paste (annatto seed paste – find in Latin American food stores)
Heat oil and butter on medium. Add broth for 4 minutes. Turn to medium low then add achiote, mix, then rice, and mix. Add chicken and red pepper, cook until broth is absorbed, turning frequently so the bottom doesn’t burn. Add peas at the end and cook until warm, turning frequently.
Ingredients A big package of chicken-whichever kind you like (with bones) 3 cloves of garlic, crushed 1 tsp. salt 4 oz. tomato sauce 1/2 tsp. chili powder 1/2 tsp. achiote (annatto seed paste, find in Latin American food stores)
Skin the chicken. Put it in a pot with about a cup of water, the garlic, the salt, the achiote and the chili powder. Cook it on a low flame for an hour, or until chicken is done. Take out the chicken and then strain the juice in the pan (save it!) to remove the garlic. Throw out the garlic. Combine the juice from the pan with the tomato sauce and add the chicken to the sauce. Heat up the chicken and sauce for 5 minutes and serve over rice.
