Is SIBO Delaying Improvements in Autoimmune Diseases?

I believe that after I developed SIBO (small intestine bacterial overgrowth), there have been delays in improving my autoimmune disease symptoms. The SIBO syndrome means that the bacteria throughout the small bowel have increased in number and they produce increased fermentation of carbohydrates from any starchy foods, many fruits, and some vegetables. This leads to increased intestinal gas producing abdominal pain and bloating, and changes in bowel movements. The same fermentation process results in formation of other substances responsible for symptoms usually present in other diseases such as, fibromyalgia (widespread muscular pain), restless-leg syndrome (the urge to move the legs), interstitial cystitis (painful bladder syndrome), or rosacea (redness and acne-like pimples on cheeks and nose); these can also be seen in patients with SIBO.

This syndrome is often overlooked at diagnosis and many symptoms that can be related to it are often ascribed to something else. Although it has been a factor delaying improvements of my autoimmune disease symptoms, it took me quite long to figure out that I had developed SIBO. Researching more about it, I was able to explain why along with the abdominal symptoms I also felt more achiness: it’s part of the SIBO-associated symptoms mentioned above.

Having noticed my joints felt worse after I developed SIBO, I tried to help it with limiting dietary carbohydrates along with a few rounds of herbal antibiotics and prescription ones. Nothing seemed to help for a longer duration and I couldn’t tolerate even the permitted, small amounts of fruits; not being able to eat fruits has been for me a major inconvenience. During my most recent strict diet attempt to tackle SIBO again, I decided for one month to limit even more the amounts of permitted types of fruits. Since this diet is very close to autoimmune elimination diet, I followed the additional restrictions during the same 4 weeks interval. The results have been disappointing because I didn’t feel any improvement in my autoimmune disease, let aside to be able to decrease the prednisone. Besides, it gave me a 10-pound weight loss and I felt weaker, more tired, headachy—probably as a result of hypoglycemia.

The weight loss didn’t quite surprise me because that’s an established fact for me when I go on low-carbs diets. The lack of any improvement in my autoimmune disease (arthritis) symptoms was something I didn’t expect since the elimination diet is being regarded by functional medicine as the most important step. Many authors promoting the autoimmune diets also reinforce numerous supplements, sometimes building up to more than 20 (expensive!) capsules every day, supposedly with multiple types of benefits. I didn’t take them because, looking at the inactive ingredients, many of them had some of the derivatives I avoided for years. And it was this avoidance and replacement of the routinely used products containing these allegedly “inert” ingredients that allowed me to see some steady improvements in my autoimmune disease symptoms. My thought process was that if I see some benefits from the diet alone, I’ll try to figure how to work it out with some supplements, but that was not the case for me.

Orencia (abatacept) treatment made me extremely prone to infections and this is ongoing for over 9 months after the last intravenous infusion. The infections were mostly upper respiratory, sinuses, or urinary tract, but occasionally in other locations. These numerous episodes produced worsening of my autoimmune disease making my joints feel worse. Trying to understand why the infections were persistent for so long, I learned about the biofilm formation as a possible explanation, at least for some of them. I often wondered if SIBO can be blamed for the intestinal bacteria (increased in number) spreading to other sites. Can they cross the intestinal wall? It wasn’t until very recently that I found this can happen.

In medical terminology this process is known as translocation of the intestinal bacteria across the wall, reaching first the lymph nodes closer to the gut (mesenteric lymph nodes), and other distant (extra-intestinal) sites thereafter. Although it was well described in many animal studies, in humans it was first noted in patients with severe liver disease (cirrhosis) and was explained by the impaired immune defenses known to occur in this condition. The exact ways for crossing are through intestinal cells (process called pinocytosis), or in between the cells because this space is widened in cirrhosis. In addition, bacterial overgrowth due to decreased intestinal motility, present in cirrhosis as well, is also playing a role in bacterial migration across the intestinal wall. Lately, small intestine bacterial overgrowth alone—without liver disease—was found to trigger the same translocation process in conditions of slow intestinal transit and associated decreased immunity.

Normally, the number of bacteria in the small bowel is much lower compared to the colon and the composition is different as well. It mostly consists of E. coli, Klebsiella, Proteus, enterococci, and streptococci species and you likely heard some of these names before. In normal individuals (with healthy gut structure and function), if some of these bacteria do “travel” across the intestinal wall, they are captured by the scavenger cells and engulfed (phagocytosed) before reaching the nearby lymph nodes or the lymphatic vessels. Intestinal bacteria multiply if the individual has slower intestinal transit, and if there is also decreased immunity it’s more likely for these bacteria to reach distant sites once they translocate. Impaired immunity can occur due to other co-existing diseases; in patients needing urgent surgery; cancers—such as leukemia, or chemotherapy. Other reasons are medications that act as immunosuppressants, as most of the medications used to obtain improvements in autoimmune disorders are.

Of course, most of the above facts were documented first in many animal studies (mice), and afterwards in a few human studies. As I said it before in the book, Of Mice and Men title of Steinbeck’s famous novel keeps coming back to my mind, but more as Of Mice and Me, because so many things that apply to mice apply to me as well! If I would believe in reincarnation, I can definitely think I was a mouse in a previous life. Joking aside, human studies were performed in patients undergoing surgery, and revealed that this translocation process occurs for a significant 15 percent of them! Surgical procedures, especially the urgent ones, are a major stress for our body, as are critical illnesses. In these circumstances, additional factors (decreased biliary or pancreatic secretion, decreased intestinal transit, certain medications— including antibiotics and stomach acid suppressing drugs) contribute to the increased number of bacteria in the small intestine and their migration across the wall.

Therefore, in addition to a degree of my impaired immunity related to immunosuppressive medicines, SIBO has been probably partly responsible for some of my ongoing infections that I experienced with and after Orencia. This may perhaps explain why many of my urinary infections started with flank (kidney) pain, since the bacteria most frequently migrating are E. Coli, the same type that causes most of the upper or lower urinary tract infections. In turn, the ongoing infections are additionally contributing to my lack of progress in my autoimmune disease recovery.

Another interesting association with the phenomenon of bacteria migrating across the gut wall is the local release from the scavenger cells (macrophages) of pro-inflammatory substances called cytokines. One of them is called TNF-alpha and if you suffer of an autoimmune syndrome, you may have well heard or even been given one of the medications in the class called TNF—alpha inhibitors. These are commonly used to achieve improvement of autoimmune disease symptoms. I presume these locally released pro-inflammatory cytokines can spread throughout the body, and may be responsible for the increased achiness I felt since I developed SIBO.

My plan to improve SIBO is to try to walk more (hard to do with swollen knees and painful hips) and make sure I use, as some articles say, “gut-specific nutrients.” These were studied mostly in animal experiments and some findings apply to humans, while others don’t. As I already “established” that many things that apply to mice, also apply to me, I’ll make some adjustments. My diet is already very rich in proteins and vegetables foods containing glutamine—needed for good nutrition of the intestinal cells. Glutamine along with other amino-acids present in about the same foods, are used by liver to produce the antioxidant glutathione—which maintains healthy intestinal cells.

Zinc and vitamin A maintain the intestinal cells integrity and can improve the immune function. Moreover, zinc is an antioxidant. I’m quite sure that my diet contains enough vitamin A and beta-carotene, therefore I will only use some zinc supplements 2-3 days a week, for a few weeks. More important, I will include fermented foods and probiotics, but I need to research a bit more about which ones would be best to use. After I’ll see the intestinal motility improved, I will try again Manuka honey as intestinal biofilm disruptor, and hope the infections will not be as bothersome as they were a few weeks ago. All these will hopefully allow me to decrease the need for antibiotics, eventually allow me to further decrease the prednisone dosage, and finally see some more improvements in my autoimmune disease symptoms.

Resources:

Is SIBO Delaying Improvements in Autoimmune Diseases?

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