Patient Information

The IC diet is a symptom management tool. Since there are lots of mast cells in the IC bladder wall, limiting foods that are fermented can reduce symptoms. Other foods that can be irritating to a bladder wall include those with alcohol, caffeine, and are highly spicy. There is nothing magic about the diet. Common sense says if a food makes your bladder symptoms worse, avoiding it can make life more comfortable. The list is extensive and not everything on it bothers everyone. Some can can eat foods on the list without difficulty and foods not on the list can be a problem for others. Using it at a starting point to determine what is and isn't a symptom trigger can be helpful but it will likely need to be individualized. Having some measure of control over symptoms while working on the underlying cause (infection) definitely improves quality of life for many IC patients but avoiding certain foods isn't going to treat or repair an infected bladder.

Biofilms don't become resistant to disrupters since they can't develop resistance genes like bacteria which are alive. However disrupter choice isn't just an issue of what biofilm the pathogen makes (eDNA or amyloid fiber - some make both), but your genetics. Twenty percent of the general population world wide have one of four genetic mutations/deletions that result in either too much fibrin being produced (Factor II or V mutations) or difficulty activating plasminogen to make plasmin which breaks down fibrin (PAI-1 4G deletion or elevated lipoprotein(a)). Seventy percent of my chronic UTI/IC patients had at least one of these and some even multiple ones. Due to the extra fibrin, patients with these genetics have extensive biofilms making antibiotics 10 to 1,000 times less effective and often results in multi-drug resistance with the survival of exposed but not eradicated bacteria. The accumulation of fibrin due to genetics has to be addressed as well identifying what contribution various pathogens make to biofilm production. LabCorp has put together a custom panel #505443 (not on website but can be ordered through the Link system) to test for all of these genetics as well as measuring how much fibrin you may be producing due to other causes (tick-borne, mold toxins, auto-immunity, high homocysteine, etc.). Knowing that information also helps determine what your body needs to stop biofilm production. Wish there was a one size fits all but the disrupters needed will change based on pathogens found. The ones for your genetics will stay the same to "normalize" the fibrin/fibrinolysis balance and prevent future infections from becoming chronic.

An increase in D-dimer (a degradation product of fibrin) will indicate that a fibrinolytic like lumbrokinase is working on the biofilms. Additional pathogens will also surface out of the biofilm in greater quantities so the MicroGenDX test can find them and antibiotics can reach them. This testing is needed since many pathogens that have been embedded don't grow well on standard urine culture plates (anaerobes, slow growing ones, and cell wall deficient bacteria). Cultures also report as contaminated if they find healthy lactobacilli (they show up to acidify the urine and discourage the growth of higher pH loving pathogens) or any fungal growth (can also be released from biofilms). Many pathogens also make their own biofilms and once we identify what those pathogens are, will add in specific disrupters for those types. Selection of antibiotics is aimed at the major pathogens. Exposing low percentage ones to an antibiotic only creates more drug resistance since only a sub-therapeutic will have reached the bacteria still embedded. This isn't a one and done. It can take multiple rounds of testing and treatment to get to the bottom of infections that have been multiplying inside of biofilms for months or years. That being said, we are seeing many patients who have struggled for decades become and stay infection free once the biofilms are addressed properly based on your genetics for fibrin production, keeping your vitamin D above 50, and clearing excess ammonia which damages the bladder wall, stabilizes biofilms, and raises the pH. I am happy to discuss the various pieces needed with your provider: https://ruthkriz.intakeq.com/booking This does work but there is more involved than just addressing biofilms.

Since only a small percentage of pathogens are free floating when infections are embedded in biofilms, it is difficult to identify what pathogens are causing symptoms. Taking the correct biofilm disrupter prior to collecting a specimen allows many of the pathogens to become free floating so they can be collected and identified. This is called a provocation test and this process is used for many laboratory tests to improve diagnostics. "Biofilm disruption is a critical strategy for improving the detection and treatment of pathogens, particularly because up to 80% of human bacterial infections are associated with these structured protective communities." Mendhe, Sakshi, Ankit Badge, Sarita Ugemuge, and Dhurba Chandi. “Impact of Biofilms on Chronic Infections and Medical Challenges.” Cureus 15, no. 11 (n.d.): e48204. https://doi.org/10.7759/cureus.48204.

Dr. Bill Costerton was a microbiologist who published articles in the 1990's which demonstrated the importance of disrupting biofilms to improve the ability of antibiotics to reach embedded infections. Biofilms are known to limit penetration of the antibiotic, inactivate antibiotics by the pH inside the biofilm, and promote the development of drug resistance when only a low dose of antibiotics reaches the bacteria. They also can pump antibiotics out of the biofilm structure and harbor persister cells that can't be killed by antibiotics until they are released from the biofilms. Without biofilm disruption, bacteria in biofilms are 10 to 1,000 times more resistant to antibiotics. Drug resistance forms when the bacteria are exposed to a sub-therapeutic dose. Costerton, J. W., P. S. Stewart, and E. P. Greenberg. “Bacterial Biofilms: A Common Cause of Persistent Infections.” Science (New York, N.Y.) 284, no. 5418 (1999): 1318–22. https://doi.org/10.1126/science.284.5418.1318. Mah, T. F., and G. A. O’Toole. “Mechanisms of Biofilm Resistance to Antimicrobial Agents.” Trends in Microbiology 9, no. 1 (2001): 34–39. https://doi.org/10.1016/s0966-842x(00)01913-2.

Without biofilm disruption, bacteria in biofilms are 10 to 1,000 times more resistant to antibiotics. Drug resistance forms when the bacteria are exposed to a sub-therapeutic dose. Costerton, J. W., P. S. Stewart, and E. P. Greenberg. “Bacterial Biofilms: A Common Cause of Persistent Infections.” Science (New York, N.Y.) 284, no. 5418 (1999): 1318–22. https://doi.org/10.1126/science.284.5418.1318. Mah, T. F., and G. A. O’Toole. “Mechanisms of Biofilm Resistance to Antimicrobial Agents.” Trends in Microbiology 9, no. 1 (2001): 34–39. https://doi.org/10.1016/s0966-842x(00)01913-2. "Biofilm disruption is a critical strategy for improving the detection and treatment of pathogens, particularly because up to 80% of human bacterial infections are associated with these structured protective communities." Mendhe, Sakshi, Ankit Badge, Sarita Ugemuge, and Dhurba Chandi. “Impact of Biofilms on Chronic Infections and Medical Challenges.” Cureus 15, no. 11 (n.d.): e48204. https://doi.org/10.7759/cureus.48204.