This is the sixth post in my series on small intestinal bacterial overgrowth (SIBO). Today I want to talk about those dietary factors that cause impaired intestinal motility and inflammation. I was hoping to include my thoughts on plant lectins in this post, but once I realized I was closer to writing a small book and not a blog post, I decided to cover that topic in the next post instead.
As we learned in part four, anything that impairs the “housekeeping function” or peristalsis of your small intestine will predispose you to getting SIBO. Recall that proper small intestinal motility helps keep any pathogens that enter via the stomach from attaching themselves to the gut wall. And this same peristaltic movement, not the ileocecal valve, is what likely stops gram-negative bacterial invasion from the colon.
I must also add that anything that negatively impacts your community of beneficial gut flora will make you susceptible to coming down with a case of SIBO. Although the small intestine has far fewer friendly bacteria than the colon, it isn’t entirely sterile. In this part of the GI tract, commensal gut flora ranges from between 101 to 103 cells per gram of contents of the intestinal lumen and they occupy both the lumen and outer mucus layer of your small intestine.
A very important function of gut flora is proper regulation of our immune system. Disturb these beneficial bacteria and you open yourself up to infections of all types, including infections of the small intestine.
Another vital function of friendly gut flora is to prevent colonization of the gut wall by pathogens. They do this by producing lactic acid that makes the pH of the gut wall uninviting to bad bacteria as well as outcompete them for attachment sites and food.
So once this ecosystem is disturbed for whatever reason, you risk an overgrowth of nasty intestinal critters, gut wall inflammation, impaired peristalsis and leaky gut.
Both mucus and Lactobacillus bacteria form a barrier between the contents of the small intestine and the cells or enterocytes that make up the gut wall.
Proper peristalsis is dependent on an intact and healthy mucosa-gut flora barrier. Any dietary substance or mode of eating that causes alterations in beneficial gut flora populations and injury to the mucosa will cause impairment of peristalsis via inflammatory and toxic effects upon the nerves responsible for these wave-like involuntary movements. Compromised small intestinal motility goes hand in hand with compromised barrier function. The one rarely exists without the other, at least not in the long run.
This injury to barrier function is cumulative and age dependent.
The insults to barrier function because of binge drinking, for example, can be compounded by repeated gluten exposure. Or overindulging in irritating nightshades may be exacerbated by a small intestine clogged full of insoluble fiber that increases the time these potentially irritating foods are in contact with the gut wall.
By the fourth or fifth decade of life, cumulative insults to gut barrier function via multiple courses of antibiotics, environmental toxins, chronic stress, NSAID use, diet, bacterial or viral infections, yeast overgrowth, etc. begins catching up to many people predisposing them to SIBO and increased intestinal permeability.
And aging means that what we could get away with when we were younger no longer holds true. Many of us know this from personal experience. How many older people can binge drink like they used to or swallow mouthfuls of hot peppers with very little ill effect the next morning? And since aging slows the healing process, including along the gut wall, recovery takes longer.
Ain’t growing old a hoot?
OK, let’s now review some diet-related factors that can negatively impact gut barrier defenses and movement.
What follows is more applicable to binge drinking than light to moderate drinking.
First the good news…..well, kinda good news. You’ll be happy to know that alcohol can really move things right along in the old plumbing department. It’s not unusual for alcoholics and binge drinkers to have diarrhea so motility isn’t an issue, quite the opposite. However, the reason this is true is because alcohol reduces the muscle movements that keep food in the small intestine during digestion. Like s**t through a goose, so too your food leading to the chronic diarrhea and nutritional deficiencies often seen in these groups.
SIBO is prevalent in binge drinkers, not because of compromised peristalsis per se, but because of compromised gastric barrier function and small intestinal inflammation caused by damage to the mucosa and cells of the small intestinal brush border. This damage is due to acetaldehyde, the major toxic byproduct of alcohol metabolism. Acetaldehyde is not only very hard on the liver, but on your intestines and gut flora. This damage occurs even after a single bout of binge drinking. The more you drink, the more the damage. Weekend warriors take note!
If you already have an overgrowth of gram-negative pathogens in the small intestine, these bacteria will also metabolize alcohol into more acetaldehyde leading to even more injuries to the gut wall apart from the damage already caused by the bacteria themselves. All of this inflammation and damage negatively impacts your beneficial gut flora populations further adding fire to your gut wall and predisposing to SIBO.
There is some potentially good news though. In animal studies, feeding mice probiotics containing both Lactobacillus and Bifidobacterium protects them against proliferation of gram-negative bacteria and liver injury even when fed high doses of alcohol. I’ve never seen a drunk mouse in person but how cool would it be to see them staggering about in their cages wearing miniature lampshades on their heads? Way cool if you ask me!
Anyway, whether this is true for humans requires further study, but I wouldn’t wear a lampshade on my head without supplementing with both probiotics and prebiotics.
If this does turn out to be true for humans, would this mean you could drink without ill effects? By no means. Probiotics and prebiotics can’t prevent the negative impact caused by binge drinking on gastric barrier function I wrote about in the previous post. Besides, there are plenty of other negatives to overindulging in alcohol like accidental falls, strained interpersonal relationships, higher risk of mouth, throat, esophageal, stomach, breast and colon cancer, increased propensity to violence or depression, elevated risk of waking up next to one seriously ugly one-night stand plus the increased propensity of becoming a loud, obnoxious asshole.
While insoluble fiber has been known to speed up movement through the colon (at least in the young whose colons haven’t been fully stretched like balloons from years of copious gas production caused by fermenting high-fiber foods), it has the opposite effect in the small intestine. Here, all that sticky, gooey, expanded and scratchy muck clogs up the plumbing as it slowly scrapes its way along the many twists and turns of this very convoluted part of the digestive tract. Imagine swallowing a sticky Brillo Pad® and you get the ideal. This inevitably leads to physical injuries to the mucosa.
Lucky for us the cells that produce mucus along the digestive tract are quite efficient at repairing the damage. However, the possible presence of appreciable amounts of lectins in these same high-fiber foods inhibits this repair function. I’ll talk more about that in the next post. For a fuller explanation of the physical wear and tear on your intestines caused by too much insoluble fiber, I again refer you to the book Fiber Menace.
The adenosine and opioid peptides discussed in the last post both exert a directly nerve depressing effect on small intestinal peristalsis. How much so will obviously depend on the quantities and frequency of gluten consumption along with individual susceptibility. I would imagine the poor soul sitting on the toilet above really “enjoys” eating a wheat-heavy diet. Perhaps binge drinking might help!
Gluten is also directly inflammatory to the cells lining our small intestines. It has been shown to elicit an interleukin 15 cytokine response when intestinal biopsies are exposed to it regardless of genetic predisposition to celiac disease. Cytokines are signaling molecules that regulate inflammatory immune responses. As all gut inflammation predisposes to SIBO, this is yet another strike against it.
Finally, gluten increases zonulin production in the small intestine, a protein that directly regulates intestinal permeability. The quick and the short of it is that the more zonulin produced, the more leaky your gut and the more apt you are to suffer from low-grade gut wall inflammation and increased risk of developing SIBO. In celiacs this increase in zonulin production lasts ,far longer than in non-celiacs who only experience a transitory increase.
For a more comprehensive discussion on zonulin, I recommend listening to this webcast featuring the world authority on celiac disease and gluten sensitivity, Dr. Alessio Fasano.
Just as gluten opioids slow digestive function, so too A1 beta casein. However, whole pastured dairy is chock full of fat-soluble vitamins, minerals, conjugated linoleic acid, anti-microbial agents and whey protein, all of which have beneficial effects on human health.
Many observational studies that show an association between dairy consumption and poor health outcomes fail to account for gluten consumption. Dairy and wheat often go together: cereal and milk, milk and cookies, ice cream and cake, butter and toast, cheese and crackers, etc. So is it the dairy or the wheat? My bet is on the wheat, but we don’t really know as there are no clinically controlled trials that have studied this.
If consuming A1 casein dairy slows things down for you and you’re battling SIBO or trying to heal your leaky gut, you may want to cut it out of your diet or try switching to A2 casein dairy sources until you get things under control. Many feel better cutting dairy completely out of their diets for good while others feel better when they eat it. I certainly credit whole-pastured, A2 casein Jersey milk for part of my recovery from a damaged gut wall caused by SIBO. But that’s my experience not yours. Only you can decide what’s right for you.
Nightshades can be very irritating with sensitivity to them probably increasing with age. I know I can’t handle the same amounts of spicy food like I used to. It, along with large quantities of uncooked tomatoes with skin, sends me running to the little boy’s room without fail. Because it decreases intestinal transit time, slowed peristalsis is not really an issue.
However, I can see a problem due to chronic inflammation caused by eating these irritating foods in large quantities especially if you are genetically susceptible. And if they are in contact with the mucosa for an extended period because of a small intestine clogged by loads of indigestible fiber or partly paralysed by gluten derived adenosine or opioids from any source, then I can easily see how they might promote SIBO and leaky gut.
Many people have experienced weight loss and improved health outcomes on low-carb diets. I too have experimented with these diets with positive results. I see no issue with moderate low-carb diets and there is no evidence that they are injurious to long-term health.
What I want to warn against, however, are extremely low-carb or ketogenic diets. These types of diets are used to treat epilepsy in children under medical supervision. Many, however, tout this type of high-fat, near-zero carb diet as the answer to obesity and all manner of disease. My major issue with long-term ketogenic diets is the increased risk of developing a glucose deficiency. Paul Jaminet over at the Perfect Health Diet blog first alerted me to the dangers of glucose deficiency in a series of posts you can read here.
Glucose deficiency impairs mucosa barrier function everywhere in the body. The mucus layer that lines the insides of our nose, mouth, lungs, throat and stomach prevents pathogen attachment and entry due to the physical barrier it presents to the outside world and because this is where populations of healthy commensal bacteria live.
Inadequate mucus and disturbed friendly bacteria can lead to pathogens proliferating in your respiratory tract, mouth, throat, esophagus and stomach. Couple this with impaired stomach barrier function and you increase the chances of colonizing your small intestine with some seriously nasty dudes that you swallowed with your food or drink. And obviously any mucus deficiency along the small intestine will clearly pose a risk for developing SIBO and a leaky gut.
Finally, in the presence of SIBO, large quantities of fat can increase the translocation of these harmful bacteria from the lumen into systemic circulation by the same mechanism that allows fat-soluble vitamins and minerals to cross through the gut wall.
Bacteria from the gut always hitches a ride with fat across the intestinal wall. However, potentially dangerous organisms are normally bound by cholesterol in the liver, inactivated and safely excreted through the bile duct and feces. This is all dependent on having a healthy liver, however. If you’re eating ridiculous quantities of fat, especially cholesterol-lowering omega 6 fats in the presence of both a liver that isn’t functioning properly and SIBO, you run the very real risk of exceeding the limits of this bacterial-clearance system.
If you are on a low-carb diet and suffer from chronically dry eyes, nose or mouth, you need to increase your consumption of glucose, preferably from whole-foods like starchy tubers and other safe starches as recommended in the Paul Jaminet’s book, the Perfect Health Diet.
Excess Dietary Fructose
Fructose makes up half of the sucrose or sugar molecule. Also found naturally in fruit and maple syrup, it’s what is responsible for the sweet taste imparted to various foods. Fructose is quickly transported to the liver because it is quite damaging to protein structures in the body, readily forming advanced glycation end products or AGEs.
Fructose has the unique property of rapidly breaking down adenosine triphosphate or ATP in cells that use oxygen, including those cells capable of absorbing fructose in the digestive tract. By doing so it also rapidly elevates reactive oxygen species or free radicals to a point that overwhelms the cell’s built-in defenses to neutralize them.
Getting your fructose from fruit is normally not an issue because it comes packaged with fiber, antioxidants and vitamins that help counteract its oxidizing effects on cells while limiting the amount you can realistically eat. While eating two whole oranges at one sitting can be quite satiating, removing its fiber and making juice from it can allow you to easily drink the fructose equivalent of four or more oranges at one go.
Getting your fructose from refined sources like sugar and high-fructose corn syrup is even worse as not only is it devoid of fiber that might limit its ingestion, it is also lacking any of the natural antioxidants that might counter its ill effects on intestinal cells. As it increases oxidation and inflammation in the small intestine, it will promote the growth of pathogens by reducing beneficial Lactobacillus bacteria. Fructose will also impact colonies of bifidobacteria in the colon. Refined sugars should therefore be kept to a minimum to avoid the chances of developing SIBO.
Omega 6 Vegetable Oils
Vegetable oils are an exceedingly rich source of omega 6 fats. While omega 6 is an essential fatty acid, meaning it must be obtained from the diet, in excess quantities it is quite inflammatory. Both non-inflammatory omega 3 and omega 6 compete for the same biological pathways in the body meaning that an excess of one can crowd out the other. The typical Western diet is imbalanced in favor of omega 6.
In the gut, excess omega 6 fatty acids will increase oxidative stress thus promoting the growth of pathogens both in the small intestine and colon. Polyunsaturated oils are extremely prone to forming free radicals when exposed to heat and high pressure. As most industrial seed oils are produced using both, they are already full of free radicals when you buy them. If used for cooking, the damage is compounded further. Eating foods cooked in these types of oils is to be avoided if maintaining gut health is your goal. By their very chemical structure, saturated fats are the most resistant to heat and oxidation, followed by monounsaturated fats like olive oil.
In the next post, I’ll tackle the subject of dietary plant lectins and their role in promoting SIBO…
Bishop, H., Frazier A. C., Robinson G. B., Schneider R. (1963). The Nature of the Antiperistaltic Factor From Wheat Gluten. British Journal of Pharmacology, 21: 238-243.
Bujanda, L. M.D. (2000). The Effects of Alcohol Consumption Upon the Gastrointestinal Tract. The American Journal of Gastroenterology, 95(12): 3374-3382.
Clemente-Postigo M., Queipo-Ortuño M.I., Murri M., Boto-Ordoñez M., Perez-Martinez P., Andres-Lacueva C., Cardona F., Tinahones FJ. (2012) Endotoxin increase after fat overload is related to postprandial hypertriglyceridemia in morbidly obese patients. Journal of Lipid Research, 53(5):973-78.
Elliott S.S., Keim N.L., Stern J.S., Teff K., Havel P.J. (2002). Fructose, weight gain, and the insulin resistance syndrome. American Journal of Clinical Nutrition, 76:911–922.
Fukudome S., Jinsman Y., Matsukawa T., Sasaki R., Yoshikawa M. (1997). Release of opioid peptides, gluten exorphins by the action of pancreatic elactase, Federation of European Biochemical Societies Letters, 412: 475-479.
Fukudome S. and Yoshikawa M. (1991). Opioid peptides derived from wheat gluten: their isolation and characterization. Federation of European Biochemical Societies, 296: 107-111.
Fukudome S. and Yoshikawa M. (1992). A novel opioid peptide derived from wheat gluten. Federation of European Biochemical Societies, 316 (1): 17-19.
Gropper, S. R., Smith J. L., Groff J. L. (2009). Advanced Nutrition and Human Metabolism, Fifth Edition. Belmont, CA: Wadsworth Cengage Learning.
Huebner F. R., Lieberman K. W., Rubino R. P., Wall J. S., (1984). Demonstration of High Opioid-Like Activity in Isolated Peptides From Wheat Gluten Hydrolysates. Peptides, 5: 1139-1147.
Kirpich I. A., et al. (2012) The Type of Dietary Fat Modulates Intestinal Tight Junction Integrity, Gut Permeability, and Hepatic Toll-Like Receptor Expression in a Mouse Model of Alcoholic Liver Disease. Alcoholism: Clinical and Experimental Research, 36(5): 835-846.
Lammers K. M., Lu R., Brownley J., et al. (2008). Gliadin Induces an Increase in Intestinal Permeability and Zonulin Release by Binding to the Chemokine Receptor CXCR3. Gastroenterology, 135:194–204
Monastyrsky, K. (2005). Fiber Menace: The Truth About Fiber’s Role in Diet Failure, Constipation, Hemorrhoids, Irritable Bowel Syndrome, Ulcerative Colitis, Crohn’s Disease, and Colon Cancer. USA: Ageless Press.
Robinson G. B., Schneider R., Frazer A. C. (1964) A Substance From Wheat Gluten, Which Inhibits the Intestinal Peristaltic Reflex. Biochimica Et Biophysica Acta, 93: 143-149.
Szabo G. and Bala S. (2010). Alcoholic liver disease and the gut-liver axis. World Journal of Gastroenterology, 16(11): 1321-1329.
Woodford, K. B. (2007). Devil in the milk: illness, health and politics: A1 and A2 milk. Vermont: Chelsea Green Publishing.
Zuhl M., Schneider S., Lanphere K., Conn C., Dokladny K., Moseley P. (2012). Exercise regulation of intestinal tight junction proteins. British Journal of Sports Medicine, 0: 1-9.