Category Archives: Bowel Disease

Update: Attacking Ankylosing Spondylitis with PHD

Posted by on November 18, 2014 52 comments

UPDATE: Steven has created his own website with more information, www.recoveryfromas.com. Check it out!

In January I wrote about Steven Morgan’s recovery from Ankylosing Spondylitis on a modified version of PHD. Steve generously shared his email address and has been trading ideas with other Ankylosing Spondylitis (AS) sufferers.

Steve had a flare of his AS recently after drinking some dirty water on a camping trip, so he has had to re-recover from AS. He recounts his recent experiences here:

Commentary

AS sufferers often see symptoms flare when consuming starch. This may be, as Alan Ebringer has argued for the last 20 years, because the disease is caused by a Klebsiella infection in and around the gut. Infiltration of Klebsiella into lymph nodes around the gut can lead to formation of antibodies that cross-react between Klebsiella lipopolysaccharides and our native HLA-B27 and collagen. These autoantibodies can generate autoimmune attacks on collagen, a characteristic of all the spondyloarthropathic diseases. [1] [2] [3] [4] [5] [6] [7]

Klebsiella is a carbohydrate-metabolizing bacterium; in cell cultures, any carbohydrate – glucose, fructose, galactose, and compound sugars such as sucrose, lactose, and starch – will facilitate Klebsiella growth. This has led Ebringer to advocate a diet low in carbohydrate for AS patients. Since resistant starch is the largest source of carbohydrate fiber in modern diets, that means a low-starch, low-carb, high-protein diet.

The general tendency of PHD is the opposite: we recommend getting about 30% of calories as carbs, and 5/6 of all carb calories from glucose. On a natural whole foods diet, this means that starches are a significant part of the diet.

PHD is generally a gut-friendly, fiber-rich diet. A diverse gut flora is associated with good health, and achieving a diverse gut flora requires a diet rich in carbohydrate fiber including resistant starch from cooked-then-cooled starchy foods.

This raises a tension in many gut diseases:

  • Symptoms flare whenever starches and other foods rich in carbohydrate fiber, such as the FODMAP bearing fruits and vegetables, are eaten.
  • However, there cannot be a full recovery until a complete gut flora has been restored, which requires feeding probiotic bacteria with starches, fruits, and vegetables.

Ebringer’s recommendation of a low-carbohydrate diet is palliative but not necessarily curative. It reduces symptoms, but it doesn’t by itself roll back the infection or bring about growth of a beneficial gut microbiome.

As a temporary therapeutic measure to facilitate a full recovery, I often suggest using dextrose in place of starches as a source of carbs, along with steps to support immunity and development of a probiotic gut flora.

Dextrose is pure glucose. It is rapidly absorbed in the small intestine and therefore is unavailable to gut bacteria. Dextrose can therefore provide enough carbs to support immune function, mucus production, collagen repair, and general good health, without providing any fiber to gut bacteria.

Steps like consumption of liver, sun exposure, intermittent fasting, and circadian rhythm entrainment will further support immune function and aid suppression of the infection that caused the disease.

During this period of low-fiber dieting, eating fermented vegetable juice and other sources of probiotic bacteria can help displace bad bacteria from the gut. As probiotic microbes become more dominant in the gut, normal whole foods can gradually be restored, allowing a probiotic bacterial population to grow in place of the pathogenic bacteria.

Steven has largely followed this plan of attack, with success. It should work for all the spondyloarthropathic diseases including rheumatoid arthritis. I’d love to hear from others who try it.

References

[1] Fielder M et al. Molecular mimicry and ankylosing spondylitis: possible role of a novel sequence in pullulanase of Klebsiella pneumoniae. FEBS Lett. 1995 Aug 7;369(2-3):243-8. http://pmid.us/7649265.

[2] Ebringer A et al. Molecular mimicry: the geographical distribution of immune responses to Klebsiella in ankylosing spondylitis and its relevance to therapy. Clin Rheumatol. 1996 Jan;15 Suppl 1:57-61. http://pmid.us/8835505.

[3] Tani Y et al. Antibodies to Klebsiella, Proteus, and HLA-B27 peptides in Japanese patients with ankylosing spondylitis and rheumatoid arthritis. J Rheumatol. 1997 Jan;24(1):109-14. http://pmid.us/9002020.

[4] Rashid T et al. The potential use of antibacterial peptide antibody indices in the diagnosis of rheumatoid arthritis and ankylosing spondylitis. J Clin Rheumatol. 2006 Feb;12(1):11-6. http://pmid.us/16484874.

[5] Ebringer A et al. A possible link between Crohn’s disease and ankylosing spondylitis via Klebsiella infections. Clin Rheumatol. 2007 Mar;26(3):289-97. http://pmid.us/16941202.

[6] Rashid T, Ebringer A. Ankylosing spondylitis is linked to Klebsiella–the evidence. Clin Rheumatol. 2007 Jun;26(6):858-64. http://pmid.us/17186116.

[7] Rashid T et al. The link between ankylosing spondylitis, Crohn’s disease, Klebsiella, and starch consumption. Clin Dev Immunol. 2013; 2013:872632. http://pmid.us/23781254.

More on Fecal Transplants

Posted by on November 3, 2010 43 comments

We’ve had ongoing interest in the topic of fecal transplants from readers of our bowel disease series, and we’ve recently had comments from two biomedical professionals reminding us that it is desirable to have fecal transplants performed by doctors after screening of the stool for pathogens.

Coincidentally, The Scientist ran a nice story today on fecal transplants. [1]

Fecal transplants are effective against C. difficile, ulcerative colitis, and probably other inflammatory bowel disorders:

By producing sturdy spores that can linger in the intestinal tract even after repeated antibiotic treatment, C. difficile can continually give rise to new toxin-producing colonies that wreak havoc on the colon. But these colonies prove no match for fecal transplants, which boast a cure rate of up to 95 percent….

Borody did his first fecal transplant back in the mid 1980s, when he was confronted with one of the most difficult cases he had seen at the time: a woman who had vacationed at Fiji and had developed an incurable colitis through an unknown pathogen.

While searching the literature for alternative treatments, he stumbled upon a paper published in 1958 in the journal Surgery that described four cases in which a similar condition was cured by infusing the inflamed guts of the patients with fecal samples from healthy donors. “So I looked at the method and I kind of made up the rest of it,” Borody said.…

The stool, now turned into slush, was administered to the patient — who had her gastrointestinal tract previously flushed — via two enemas over the course of two days.

The results were nothing short of surprising, Borody said. Within days her colitis was gone, never to return.

It’s a well-proven procedure in animals. Veterinarians don’t bother to screen rumen fluid for pathogens, and yet the procedure is almost always healthful for the recipient:

The procedure, which has deep roots in veterinary science, has been tried and tested in animals for centuries. Farmers handling livestock have long realized, for example, that indigestion following a change in diet in grazing animals, such as cows, can be treated by feeding the sick cow rumen fluid that has been sucked out of a healthy cow’s stomach.

Yet it’s hard to find doctors who will perform the procedure for any ailment except C. difficile infections:

Currently, while most fecal transplants in the U.S. are performed exclusively to treat C. difficile, a growing list of doctors, such as Lawrence Brandt, chief of Gastroenterology at Montefiore Medical Center in New York, are beginning to expand to other gut disorders such as inflammatory bowel diseases….

“It is currently considered a last resort,” he said. But he hopes that will soon change. “It’s relatively simple, relatively inexpensive, and it’s very rapid in its actions.”

Conclusion

In chronic infections of the colon, fecal transplants should be among the first treatments resorted to, not the last resort.

This is one treatment where experience with animals and human patients, demonstrating that fecal transplants are fairly safe and often highly effective in colonic disorders, should trump the normal regulatory barriers to new procedures.

However, given the cautious nature of regulators and most doctors, it seems unlikely that the therapy will be widely available any time soon.

It’s good to hear that there is a “growing list” of doctors who will perform a fecal transplant. Anyone with a seemingly incurable colonic disease should seek one of them out.

References

[1] Cristina Luiggi, “Same Poop, Different Gut,” The Scientist, Nov 3, 2010, http://www.the-scientist.com/news/display/57795/.

Wheat Is A Cause of Many Diseases, I: Leaky Gut

Posted by on October 26, 2010 81 comments

I realized last week that I often call wheat the most toxic food, but I haven’t really explained why on the blog. The book has a detailed explanation, which focuses on toxicity effects and on autoimmune processes attacking the gut and thyroid. Here I would like to add to the book’s argument by showing how wheat causes other autoimmune diseases.

There are about 50 diseases which are thought to have an autoimmune basis. Autoimmune diseases are caused by three processes:

  1. Leaky gut and inflammation. A leaky gut lets bacteria and food toxins enter the body. In the body, these precipitate an immune response which creates inflammation and a chance for antibodies to form.
  2.  “Molecular mimicry.” A bacterial protein or food toxin resembles a human protein sufficiently closely that an antibody to the foreign protein may also recognize human proteins, potentially precipitating attacks on self tissue.
  3. Adjuvant activity. Vaccines are produced by bonding an antigen (the target of the hoped-for antibody) to an adjuvant (a molecule that greatly increases the likelihood antibodies will be made – a sort of catalyst). If a “molecular mimic” can bind to an adjuvant, then autoimmune disease becomes much more likely.

Wheat causes many autoimmune diseases because it promotes all three aspects. I’ll look at each aspect in a separate post this week.

Leaky Gut

In a recent comment – it’s nice to have smart readers! – Rich brought up the links between wheat and leaky gut.

Leaky gut is the first step toward autoimmune disease. As a recent review states:

Susceptibility to at least 50 diseases, including celiac disease (CD) and type 1 diabetes (T1D), has been associated with specific HLA class I or class II alleles. A common denominator of these diseases is the presence of several preexisting conditions that lead to an autoimmune process…. In all cases, increased permeability precedes disease and causes an abnormality in antigen delivery that triggers immune events, eventually leading to a multiorgan process and autoimmunity. [1]

Gluten is a complex of proteins found in wheat, rye, oats (PAJ: see comments), barley, and other grains. One part of gluten is a type of protein called prolamins, which are chiefly responsible for gut damage:

It is the gliadin fraction of wheat gluten and similar alcohol-soluble proteins in other grains (collectively known as prolamins) that are associated with the development of intestinal damage. A common feature of the prolamins of wheat, rye, and barley is a high content of glutamine (>30%) and proline (>15%), whereas the nontoxic prolamins of rice and corn have lower glutamine and proline content. [1]

I’m quoting this because it speaks to the differences among grains. Rice and corn do not contain gluten. Corn contains other dangerous toxins, but is not a primary cause of autoimmune disease. Rice is the only grain we consider safe to eat.

From Cholera to the Cause of Leaky Gut

The mechanisms by which wheat causes leaky gut have been intensively studied by Dr. Alessio Fasano’s group. In 1995 Dr. Fasano and colleagues discovered that a toxin released by Vibrio cholerae, the bacterium that causes cholera http://en.wikipedia.org/wiki/Cholera, causes tight junctions to open for a time. [2] This makes the small intestine leaky.

Dr. Fasano and colleagues suspected that the bacterial protein’s action must mimic some natural human protein which controls intestinal permeability. In 2000, they discovered this human protein and named it “zonulin.” [3]

Wheat and Crohn’s Disease

They subsequently showed that gliadin stimulates zonulin release. Gliadin binds to a receptor called CXCR3, and activation of this receptor triggers zonulin release and increased intestinal permeability.

Interestingly, zonulin release was much higher and longer-lasting in Crohn’s disease patients than in healthy patients. [1] Restriction of gluten restores intestinal integrity in Crohn’s disease patients.

So Crohn’s disease patients should absolutely not eat wheat!

Leaky Gut and Type I Diabetes

A leaky small intestine is a feature of many autoimmune diseases, but Crohn’s disease and Type I diabetes are notable for highly permeable small intestines. Patients with both diseases have high serum levels of zonulin. [1]

In a rat model of Type I diabetes, the BioBreeding diabetes prone or “BBDP” line of rats often develops a leaky gut at age 50 to 75 days when eating a (toxic) diet of rat chow. Zonulin levels increase up to 35-fold at this time, but were reduced if the rats were fed a gluten-free diet. Rats with the highest zonulin levels developed Type I diabetes develops 15 to 25 days later. If a compound that blocks the action of zonulin is given to the rats, Type I diabetes incidence is reduced 70%. [1, 4]

This shows how crucial a leaky gut is to onset of autoimmune diseases like Type I diabetes, and also how quickly diseases can develop once the gut is compromised. The longer the gut is leaky, the greater the likelihood that some autoimmune disease will develop.

In humans, the relationships between these diseases are much the same as in rats. Crohn’s disease and Type I diabetes are co-morbid: the prevalence of Crohn’s among Type I diabetics is 6- to 9-fold higher than in the general population. Meanwhile, newborn children exposed to wheat at 3 months of age or earlier, when the gut is immature, are 4- to 5-fold more likely to develop Type I diabetes. [4]

Conclusion

Leaky gut is a prerequisite for development of autoimmune disease. Wheat seems to create a transient, mild leaky gut in nearly everyone, but in Crohn’s disease the gut becomes chronically and severely leaky in response to wheat consumption.

In rats, this leaky gut can lead to development of autoimmune diseases like Type I diabetes in as little as a few weeks.

If you eat wheat, it’s probably only a matter of time before you develop some disease or other. All of the autoimmune diseases, from rheumatoid arthritis to Hashimoto’s to lupus, are made more likely by wheat consumption. Why not switch to rice or other “safe starches” and save yourself some trouble?

Related Posts

Other posts in this series:

  1. Why Wheat Is A Concealed Cause of Many Diseases, II: Auto-Antibody Generation. Oct 28, 2010.
  2. Why Wheat Is A Concealed Cause of Many Diseases, III: Adjuvant Activity Nov 1, 2010.

References

[1] Visser J et al. Tight junctions, intestinal permeability, and autoimmunity: celiac disease and type 1 diabetes paradigms. Ann N Y Acad Sci. 2009 May;1165:195-205. http://pmid.us/19538307.

[2] Fasano A et al. Zonula occludens toxin modulates tight junctions through protein kinase C-dependent actin reorganization, in vitro. J Clin Invest. 1995 Aug;96(2):710-20. http://pmid.us/7635964.

[3] Wang W et al. Human zonulin, a potential modulator of intestinal tight junctions. J Cell Sci. 2000 Dec;113 Pt 24:4435-40. http://pmid.us/11082037.

[4] Watts T et al. Role of the intestinal tight junction modulator zonulin in the pathogenesis of type I diabetes in BB diabetic-prone rats. Proc Natl Acad Sci U S A. 2005 Feb 22;102(8):2916-21. http://pmid.us/15710870.

Bowel Disease, Part IV: Restoring Healthful Gut Flora

Posted by on July 27, 2010 384 comments

A healthy gut is a multi-species society: it is the cooperative product of the human body with trillions of bacterial cells from a thousand or more species.

An unhealthy gut is, more often than not, the product of a breakdown in this collaboration. Often, it is triggered by displacement of cooperative, commensal species of bacteria by pathogenic bacteria, fungi, viruses, and protozoa. This is why a long course of antibiotics, killing commensal bacteria, is often the prelude to bowel ailments.

It is difficult for the immune system to defeat gut infections without the help of commensal bacteria. Think about what the immune system has to deal with. The ulcers in ulcerative colitis are essentially the equivalent of infected skin abscesses, but in the colon. Here is a description of a bowel lesion in Crohn’s disease:

Ileal lesions in Crohn’s disease (CD) patients are colonized by pathogenic adherent-invasive Escherichia coli (AIEC) able to invade and to replicate within intestinal epithelial cells. [1]

Now imagine an infected skin abscess, but with feces spread over it three times a day, or stomach acid and digestive enzymes.  How quickly would you expect it to heal?

Commensal “probiotic” bacteria are like a mercenary army fighting on behalf of the digestive tract.  By occupying the interior lining of the digestive tract, they deprive pathogens of a “home base” that is sheltered from immune attack. If commensal bacteria dominate the gut, the immune system can usually quickly defeat infections.

This suggests that introduction of probiotic bacteria to the gut should be therapeutic for bowel disease.

Probiotic Supplements Are Inadequate

Most supermarket probiotics contain Lactobacillus or Bifidobacterium species. These species are specialized for digesting milk; they populate the guts of infants as they start breastfeeding, and are used by the dairy industry to ferment cheeses and yogurt.

These supplements are very effective at fighting acute diarrhea from most food-borne infections.  A fistful of probiotic capsules taken every hour will usually quickly supplant the pathogens and end diarrhea.

However, against more severe bowel diseases caused by chronic infections and featuring damaged intestinal mucosa, these species are usually not helpful.  One issue is that they provide only a tiny part of a healthful adult microbiome.  A recent study surveyed the bacterial species in the human gut, and found these species to be most abundant [2]:

Figure: Abundant gut bacterial species

As this figure shows, Bacteroides spp. are the most common commensal bacteria, with Bacteroides uniformis alone providing almost 10% of all bacterial genes in the gut. Lactobacillus and Bifidobacterium do not appear among the 57 most abundant species.

This study showed, by the way, that patients with irritable bowel syndrome have 25% fewer types of bacterial gene in their gut than healthy people, and that the composition of bacterial genes in feces clearly distinguishes ulcerative colitis, Crohn’s disease, and healthy patients.  In other words, in the bowel diseases a few pathogenic species have colonized the gut and entirely denuded it of about 25% of the commensal species that normally populate the gut. This finding supports the idea that restoring those missing species might be therapeutic for IBS.

Bacterial Replacement Therapies Work

So if IBS patients are missing 25% of the thousand or so species that should populate the gut, or 250 species, and if common probiotics provide only 8 or so species and not the ones that are missing, how are the missing species to be restored?

The answer is simple but icky. Recall that half the dry weight of stool consists of bacteria. A healthy person daily provides a sample of billions of bacteria from every one of the thousand species in his gut. They are in his stool.

So a “fecal transplant” of a healthy person’s stool into the gut of another person will replenish the missing species.

Scientists have known for a long time that this was likely to be an effective therapy, but it is only now entering clinical practice. The New York Times recently made a stir by telling this story:

In 2008, Dr. Khoruts, a gastroenterologist at the University of Minnesota, took on a patient suffering from a vicious gut infection of Clostridium difficile. She was crippled by constant diarrhea, which had left her in a wheelchair wearing diapers. Dr. Khoruts treated her with an assortment of antibiotics, but nothing could stop the bacteria. His patient was wasting away, losing 60 pounds over the course of eight months. “She was just dwindling down the drain, and she probably would have died,” Dr. Khoruts said.

Dr. Khoruts decided his patient needed a transplant. But he didn’t give her a piece of someone else’s intestines, or a stomach, or any other organ. Instead, he gave her some of her husband’s bacteria.

Dr. Khoruts mixed a small sample of her husband’s stool with saline solution and delivered it into her colon. Writing in the Journal of Clinical Gastroenterology last month, Dr. Khoruts and his colleagues reported that her diarrhea vanished in a day. Her Clostridium difficile infection disappeared as well and has not returned since.

The procedure — known as bacteriotherapy or fecal transplantation — had been carried out a few times over the past few decades. But Dr. Khoruts and his colleagues were able to do something previous doctors could not: they took a genetic survey of the bacteria in her intestines before and after the transplant.

Before the transplant, they found, her gut flora was in a desperate state. “The normal bacteria just didn’t exist in her,” said Dr. Khoruts. “She was colonized by all sorts of misfits.”

Two weeks after the transplant, the scientists analyzed the microbes again. Her husband’s microbes had taken over. “That community was able to function and cure her disease in a matter of days,” said Janet Jansson, a microbial ecologist at Lawrence Berkeley National Laboratory and a co-author of the paper. “I didn’t expect it to work. The project blew me away.” [3]

Fecal transplants can be done without a doctor’s help:  someone else’s stool can be swallowed or inserted in the rectum. If taking feces orally, swallow a great deal of water afterward to help wash the bacteria through the stomach and its acid barrier.

Dogs and young children sometimes swallow feces.  It is unpleasant to consider, but desperate diseases call for desperate measures. Perhaps one day, healthy stools will be available in pleasant-tasting capsules, and sold on supermarket shelves.  Not yet.

Attacking Pathogenic Biofilms

Most bacterial species will build fortresses for themselves, called biofilms.  These are polysaccharide and protein meshworks that, like bone, become mineralized with calcium and other minerals. These mineralized meshworks are built on bodily surfaces, like the gut lining, and protect bacteria from the immune system, antibiotics, and other bacterial species. 

Pathogenic species known to generate biofilms include Legionella pneumophila, S. aureus, Listeria monocytogenes, Campylobacter spp., E. coli O157:H7, Salmonella typhimurium, Vibrio cholerae, and Helicobacter pylori. [4]

Biofilms favor the species that constructed them. So, once pathogens have constructed biofilms, it is hard for commensal species to displace them.

Therapies that dissolve pathogenic biofilms can improve the likelihood of success of probiotic and fecal transplant therapies. Strategies include enzyme supplements, chelation therapies, and avoidance of biofilm-promoting minerals like calcium.  Specifically:

  • Polysaccharide and protease digesting enzymes. Human digestive enzymes generally do not digest biofilm polysaccharides, but bacterial enzymes that can are available as supplements. Potentially helpful enzymes include hemicellulase, cellulase, glucoamylase, chitosanase, and beta-glucanase. Non-human protease enzymes, such as nattokinase and papain, might also help. [5]
  • Chelation therapy.  Since biofilms collect metals, compounds that “chelate” or bind metals will tend to gather in biofilms. Some chelators – notably EDTA – are toxic to bacteria.  So EDTA supplementation tends to poison the biofilm, driving bacteria out of their fortress-shelter. This prevents them from maintaining it and makes the biofilm more vulnerable to digestion by enzymes and commensal bacteria. It also tends to reduce the population of pathogenic bacteria.
  • Mineral avoidance. The supply of minerals, especially calcium, iron, and magnesium, can be a rate-limiting factor in biofilm formation. Removal of calcium can cause destruction of biofilms. [6] We recommend limiting calcium intake while bowel disease is being fought, since the body can meet its own calcium needs for an extended period by pulling from the reservoir in bone. Upon recovery, bone calcium can be replenished with supplements. Iron is another mineral which promotes biofilms and might be beneficially restricted. We do not recommend restricting magnesium.

Some commercial products are available which can help implement these strategies. For instance, Klaire Labs’ InterFase (http://www.klaire.com/images/InterFase_Update_Article.pdf) is a popular enzyme supplement which helps digest biofilms, and a version containing EDTA is available (InterFase Plus).

Attacking Biofilms With Berries, Herbs, Spices, Vinegar, and Whey

Plants manufacture a rich array of anti-microbial compounds for defense against bacteria.

There is reason to believe that traditional herbs and spices, which entered the human diet during the Paleolithic and have been passed down through the generations for tens of thousands of years, were selected by our hunter-gatherer ancestors as much for their ability to promote gut health as for their taste. Dr. Art Ayers notes that:

Plants are adept at producing a wide array of chemicals with refined abilities to block bacterial functions. So when researchers sought chemicals to solve the problem of pathogens forming biofilms, it was natural to test plant extracts for inhibiting compounds. In a recent article [7], D.A. Vattem et al. added extracts from dietary berries, herbs and spices to bacterial pathogens, including the toxin producing Escherichia coli (EC) O157:H7, and checked for the ability to produce a chemical that signals the formation of a biofilm. The effective phytochemicals inhibited the bacteria from recognizing a critical density of bacteria, i.e. quorum sensing, and responding with the production of the biofilm-triggering chemical.

Blueberry, raspberry, cranberry, blackberry and strawberry extracts were effective as quorum sensing inhibitors (QSIs). Common herbs such as oregano, basil, rosemary and thyme were also effective. Turmeric, ginger and kale were also tested and found to contain QSIs. [8]

A few other remedies can weaken biofilms:

  • Acetic acid in vinegar can solubilize the calcium, iron, and magnesium in biofilms, removing these minerals and weakening the biofilm; citric acid binds calcium and can disrupt biofilms. [9]
  • Lactoferrin, a molecule in milk whey, binds iron and inhibits biofilm formation and growth. [10]
  • N-acetylcysteine can destroy or inhibit biofilms. [11]

Conclusion

Fecal transplants are the best probiotic. Tactics to disrupt pathogenic biofilms can assist probiotics in bringing about re-colonization of the digestive tract by commensal bacteria.

Along with a non-toxic diet (discussed in Part II) and nutritional support for the immune system and gut (discussed in Part III), these steps to improve gut flora make up a natural program for recovery from bowel disease.

UPDATE: Please read the cautions by two health professionals, annie and Jesse, about potential dangers of self-treatment with fecal transplants and EDTA. It is always better to pursue these therapies with a doctor’s assistance and monitoring.

Related Posts

Other posts in this series:

  1. Bowel Disorders, Part I: About Gut Disease July 14, 2010
  2. Bowel Disease, Part II: Healing the Gut By Eliminating Food Toxins m July 19, 2010
  3. Bowel Disease, Part III: Healing Through Nutrition July 22, 2010

References

[1] Lapaquette P, Darfeuille-Michaud A. Abnormalities in the Handling of Intracellular Bacteria in Crohn’s Disease. J Clin Gastroenterol. 2010 Jul 7. [Epub ahead of print]. http://pmid.us/20616747.

[2] Qin J et al. A human gut microbial gene catalogue established by metagenomic sequencing. Nature. 2010 Mar 4;464(7285):59-65. http://pmid.us/20203603.

[3] Carl Zimmer, “How Microbes Defend and Define Us,” New York Times, July 12, 2010,  http://www.nytimes.com/2010/07/13/science/13micro.html.

[4] Donlan RM. Biofilms: microbial life on surfaces. Emerg Infect Dis. 2002 Sep;8(9):881-90. http://pmid.us/12194761.

[5] Tets VV et al. [Impact of exogenic proteolytic enzymes on bacteria]. Antibiot Khimioter. 2004;49(12):9-13. http://pmid.us/16050494.

[6] Kierek K, Watnick PI. The Vibrio cholerae O139 O-antigen polysaccharide is essential for Ca2+-dependent biofilm development in sea water. Proc Natl Acad Sci U S A. 2003 Nov 25;100(24):14357-62. http://pmid.us/14614140.  Geesey GG et al. Influence of calcium and other cations on surface adhesion of bacteria and diatoms: a review. Biofouling 2000; 15:195–205.

[7] Vattem DA et al. Dietary phytochemicals as quorum sensing inhibitors. Fitoterapia. 2007 Jun;78(4):302-10. http://pmid.us/17499938.

[8] Art Ayers, “Spices are Antimicrobial and Inhibit Biofilms,” Dec. 7, 2008, http://herbal-properties.suite101.com/article.cfm/spices_are_antimicrobial_and_inhibit_biofilms.

[9] Art Ayers, “Cure for Inflammatory Diseases,” Sept. 2, 2009, http://coolinginflammation.blogspot.com/2009/09/cure-for-inflammatory-diseases.html. Desrosiers M et al. Methods for removing bacterial biofilms: in vitro study using clinical chronic rhinosinusitis specimens. Am J Rhinol. 2007 Sep-Oct;21(5):527-32. http://pmid.us/17883887.

[10] O’May CY et al. Iron-binding compounds impair Pseudomonas aeruginosa biofilm formation, especially under anaerobic conditions. J Med Microbiol. 2009 Jun;58(Pt 6):765-73. http://pmid.us/19429753.

[11] Cammarota G et al. Biofilm demolition and antibiotic treatment to eradicate resistant Helicobacter pylori: A clinical trial. Clin Gastroenterol Hepatol. 2010 May 14. [Epub ahead of print] http://pmid.us/20478402. Zhao T, Liu Y. N-acetylcysteine inhibit biofilms produced by Pseudomonas aeruginosa. BMC Microbiol. 2010 May 12;10:140. http://pmid.us/20462423.