Leaky Gut Syndrome

[Laura]

LEAKY GUT SYNDROMES: BREAKING THE VICIOUS CYCLE

BY LEO GALLAND, M.D.

From the perspective of function, the contents of the gut lumen lie outside the body and contain a toxic/antigenic load from which the body needs to be protected. Protection is supplied by complex mechanisms which support one another: intestinal secretions (primarily mucus and secretory IgA), the mucosal epithelium, and intramural lymphocytes [1]. This primary, intestinal barrier is supported by the liver, through which all enterically-derived substances must pass before entering the arterial circulation for transport to other tissues and organs. Kupffer cells in the hepatic sinusoids remove absorbed macromolecules by phagocytosis. Hepatic microsomal enzymes alter gut-derived chemical substrates by oxidation and by conjugation to glycine and glutathione(GSH) for excretion into bile and for circulation to the kidneys. The cost of detoxification is high; reactive intermediates and free radicals are generated and anti-oxidants like GSH are consumed [2, 3]. Any compromise of intestinal barrier function increases the production of oxygen radicals and carcinogens by the liver's cytochrome P-450 mixed-function oxidase system. The excretion of oxidation by-products into bile and the reflux of this "toxic" bile into the pancreatic ducts may be the major cause of chronic pancreatic disease.[4, 5]

Compromised intestinal barrier function can also cause disease directly, by immunological mechanisms.[6-9] Increased permeability stimulates classic hypersensitivity responses to foods and to components of the normal gut flora; bacterial endotoxins, cell wall polymers and dietary gluten may cause "non-specific" activation of inflammatory pathways mediated by complement and cytokines. [10] In experimental animals, chronic low-grade endotoxemia causes the appearance of auto-immune disorders.[11-13]

Leaky Gut Syndromes are clinical disorders associated with increased intestinal permeability. They include inflammatory and infectious bowel diseases [14-19], chronic inflammatory arthritides [9, 20-24], cryptogenic skin conditions like acne, psoriasis and dermatitis herpetiformis [25-28], many diseases triggered by food allergy or specific food intolerance, including eczema, urticaria, and irritable bowel syndrome [29-37], AIDS [38-40], chronic fatigue syndromes [Rigden, Cheney, Lapp, Galland, unpublished results], chronic hepatitis [41], chronic pancreatitis [4, 5], cystic fibrosis [42] and pancreatic carcinoma. Hyperpermeability may play a primary etiologic role in the evolution of each disease, or may be a secondary consequence of it which causes immune activation, hepatic dysfunction, and pancreatic insufficiency, creating a vicious cycle. Unless specifically investigated, the role of altered intestinal permeability in patients with Leaky Gut Syndromes often goes unrecognized. The availability of safe, non-invasive, and inexpensive methods for measuring small intestinal permeability make it possible for clinicians to look for the presence of altered intestinal permeability in their patients and to objectively assess the efficacy of treatments. Monitoring the intestinal permeability of chronically ill patients with Leaky Gut Syndromes can help improve clinical outcomes.
TRIGGERS AND MEDIATORS OF THE LEAKY GUT

Leaky Gut Syndromes are usually provoked by exposure to substances which damage the integrity of the intestinal mucosa, disrupting the desmosomes which bind epithelial cells and increasing passive, para-cellular absorption. The commonest causes of damage are infectious agents (viral, bacterial and protozoan) [43-46], ethanol [47, 48], and non-steroidal anti-inflammatory drugs [20, 49, 50]. Hypoxia of the bowel (occurring as a consequence of open-heart surgery or of shock) [51, 52], elevated levels of reactive oxygen metabolites (biliary, food-borne or produced by inflammatory cells) [53], and cytotoxic drugs [54-56] also increase para-cellular permeability.
THE FOUR VICIOUS CYCLES
CYCLE ONE: ALLERGY

The relationship between food sensitivities and the leaky gut is complex and circular. Children and adults with eczema, urticaria or asthma triggered by atopic food allergy have baseline permeability measurements that are higher than control levels [57-59]. Following exposure to allergenic foods, permeability sharply increases. Most of this increase can be averted by pre-treatment with sodium cromoglycate [32, 34, 57-59], indicating that release from mast cells of atopic mediators like histamine and serotonin is responsible for the increase in permeability. It appears that an increase in intestinal permeability is important in the pathogenesis of food allergy and is also a result of food allergy.

Claude Andre, the leading French research worker in this area, has proposed that measurement of gut permeability is a sensitive and practical screening test for the presence of food allergy and for following response to treatment [57]. In Andre's protocol, patients with suspected food allergy ingest 5 grams each of the innocuous sugars lactulose and mannitol. These sugars are not metabolized by humans and the amount absorbed is fully excreted in the urine within six hours. Mannitol, a monosaccharide, is passively transported through intestinal epithelial cells; mean absorption is 14% of the administered dose (range 5-25%). In contrast, the intestinal tract is impermeable to lactulose, a disaccharide; less than 1% of the administered dose is normally absorbed. The differential excretion of lactulose and mannitol in urine is then measured. The normal ratio of lactulose/mannitol recovered in urine is less than 0.03. A higher ratio signifies excessive lactulose absorption caused by disruption of the desmosomes which seal the intercellular tight junctions. The lactulose/mannitol challenge test is performed fasting and again after ingestion of a test meal. At the Hospital St. Vincent de Paul in Paris, permeability testing has been effectively used with allergic infants to determine which dietary modifications their mothers needed to make while breast feeding and which of the "hypoallergenic" infant formulas they needed to avoid in order to relieve their symptoms [60].
CYCLE TWO: MALNUTRITION.

Disruption of desmosomes increases absorption of macromolecules. If the epithelial cells themselves are damaged, a decrease in trans-cellular absorption may accompany the increased para-cellular absorption. Because nutrients are ordinarily absorbed by the trans-cellular route, malnutrition may occur, aggravating strucutural and functional disturbances [61]. Under normal conditions, intestinal epithelium has the fastest rate of mitosis of any tissue in the body; old cells slough and a new epithelium is generated every three to six days [62, 63]. The metabolic demands of this normally rapid cell turnover must be met if healing of damaged epithelium is to occur. When they are not met, hyperpermeability exacerbates [64, 65].

Correction of nutritional deficiency with a nutrient-dense diet and appropriate supplementation is essential for the proper care of patients with Leaky Gut Syndromes. Specific recommendations are made in the last section of this review. Because of the association between hyperpermeability and pancreatic dysfunction, pancreatic enzymes may also be required.
CYCLE THREE: BACTERIAL DYSBIOSIS

Dysbiosis is a state in which disease or dysfunction is induced by organisms of low intrinsic virulence that alter the metabolic or immunologic responses of their host. This condition has been the subject of a recent review article [66]. Immune sensitization to the normal gut flora is an important form of dysbiosis that has been implicated in the pathogenesis of Crohn's disease and ankylosing spondylitis[67-81]. Recent research findings suggest that bacterial sensitization is an early complication of altered permeability and exacerbates hyperpermeability by inducing an inflammatory enteropathy [82, 83]. This has been most studied in the response to NSAIDs. Single doses of aspirin or of indomethacin increase para-cellular permeability, in part by inhibiting the synthesis of protective prostaglandins [20, 49, 50, 84, 85]. Hyperpermeability is partially prevented by pre-treatment with the prostaglandin-E analogue, misoprosterol. Chronic exposure to NSAIDs produces a chronic state of hyper-permeability associated with inflammation, which can not be reversed by misoprosterol but which is both prevented and reversed by the administration of the antibiotic, metronidazole [83, 86]. The effectiveness of metronidazole in preventing NSAID-induced hyperpermeability probably reflects the importance of bacterial toxins in maintaining this vicious cycle. A single dose of bacterial endotoxin, administered by injection, increases the gut permeability of healthy humans [87]. Chronic arthritis can be induced in rats by injection of cell wall fragments isolated from normal enteric anaerobes[88]. Patients with rheumatoid arthritis receiving NSAIDs have increased antibody levels to Clostridium perfringens and to its alpha toxin, apparently as a secondary response to NSAID therap[89].

There is ample documentation for a therapeutic role of metronidazole and other antibiotics in Crohn's disease and rheumatoid arthritis[90-98]. The mechanism underlying the response has been in dispute. In the case of tetracyclines, one group has asserted that mycoplasma in the joints cause rheumatoid arthritis, others have countered this argument by demonstrating that minocycline is directly immunosuppressive in vitro [99]. Because all patients with arthritis have used NSAIDs, and because NSAID enteropathy is associated with bacterial senisitization, it is possible that the the antibiotic-responsiveness of some patients with inflammatory diseases is a secondary effect of NSAID-induced bacterial sensitization which then exacerbates the Leaky Gut Syndrome. Altering gut flora through the use of antibiotics, synthetic and natural, probiotics, and diet is a third strategy for breaking the vicious cycle in Leaky Gut Syndromes. With regard to diet, patients whose disease responds to vegetarian diets are those in whom the diet alters gut ecology; if vegetarian diets does not alter gut ecology, the arthritis is not improved[100].
CYCLE FOUR; HEPATIC STRESS

The liver of Leaky Gut patients works overtime to remove macromolecules and oxidize enteric toxins. Cytochrome P-450 mixed-function oxidase activity is induced and hepatic synthesis of free radicals increases. The results include damage to hepatocytes and the excretion of reactive by-products into bile, producing a toxic bile capable of damaging bile ducts and refluxing into the pancreas [4, 5]. In attempting to eliminate toxic oxidation products, the liver depletes its reserves of sulfur-containing amino acids [101]. These mechanisms have been most clearly demonstrated in ethanol-induced hepatic disease [47]. Sudduth [102] proposes that the initial insult is the ethanol-induced increase in gut permeability which creates hepatic endotoxemia. Endotoxemia can further increase permeability, alter hepatic metabolism, and stimulate hepatic synthesis of reactive species which are excreted in bile. This toxic bile, rich in free radicals, further damages the small-bowel mucosa, exacerbating hyperpermeability.


A PRACTICAL APPROACH

Suspect a pathological increase in gut permeability when evaluating any patient with the diseases listed in Table 1 or the symptoms listed in Table 2. Measure permeability directly using the lactulose/mannitol challenge test. Indirect measures of gut permeability include titres of IgG antibody directed against antigens found in common foods and normal gut bacteria.

These tests may be useful but cannot substitute for the direct permeability assay, especially when one is following the response to treatment.

IF ALL COMPONENTS OF THE LACTULOSE/MANNITOL TEST ARE NORMAL, repeat the challenge after a test meal of the patient's common foods. If the test meal produces an increase in lactulose excretion (signifying hyperpermeability) or a decrease in mannitol excretion (signifying malabsorption), specific food intolerances are likely and further testing for food allergy is warranted. Once the patient has been maintained on a stable elimination diet for four weeks, repeat the lactulose/mannitol challenge after a test meal of foods permitted on the elimination diet. A normal result assures you that all major allergens have been identified. An abnormal result indicates that more detective work is needed.

IF THE INITIAL FASTING MANNITOL ABSORPTION IS LOW, suspect malabsorption. This result has the same significance as an abnormal D-xylose absorption test. Look for evidence of celiac disease, intestinal parasites, ileitis, small bowel bacterial overgrowth and other disorders classically associated with intestinal malabsorption and treat appropriately. After eight weeks of therapy, repeat the lactulose/mannitol challenge. An improvement in mannitol excretion indicates a desirable increase in intestinal absorptive capacity. The lactulose/mannitol assay has been proposed as a sensitive screen for celiac disease and a sensitive test for dietary compliance [46, 103-106]. For gluten-sensitive patients, abnormal test results

demonstrate exposure to gluten, even when no intestinal symptoms are present. Monitoring dietary compliance to gluten avoidance by testing small bowel permeability is especially helpful in following those patients for whom gluten enteropathy does not produce diarrhea but instead causes failure to thrive, schizophrenia or inflammatory arthritis [107-115].

In the case of relatively mild celiac disease or inflammatory bowel disease, mannitol absorption may not be affected but lactulose absorption will be elevated. A recent study published in the Lancet found that the lactulose-mannitol ratio was an accurate predictor of relapse when measured in patients with Crohn's disease who were clinically in remission [116].

IF THE INITIAL FASTING LACTULOSE IS ELEVATED, OR IF THE INITIAL FASTING LACTULOSE/MANNITOL RATIO IS ELEVATED, consider the possibility of mild inflammatory bowel disease or gluten enteropathy. There are four other primary considerations:

(A) Exposures. Does the patient drink ethanol, take NSAIDs or any potentially cytotoxic drugs? If so, discontinue them and have the lactulose/mannitol challenge repeated three weeks later. If it has become normal, drug exposures were the likely cause of leaky gut. If it has not, bacterial sensitization may have occurred. This may be treated with a regimen of antimicrobials and probiotics. My preference is a combination of citrus seed extract, berberine and artemisinin (the active alkaloid in Artemisia annua), which exerts a broad spectrum of activity against Enterobacteriaceae, Bacteroides, protozoa and yeasts [117-120].

If the patient has no enterotoxic drug exposures, inquire into dietary habits. Recent fasting or crash dieting may increase permeability. Counsel the patient in consuming a nutritionally sound diet for three weeks and repeat the test.

Patients with chronic arthritis may have difficulty stopping NSAIDs. Alternative anti-inflammatory therapy should be instituted, including essential fatty acids, anti-oxidants or mucopolysaccharides[121-125]. Changing the NSAID used may also be helpful. NSAIDs like indomethacin, which undergo enteroheaptic recirculation, are more likely to damage the small intestine that NSAIDs that are not excreted in bile, like ibuprofen [126]. Nabumetone (relafen) is a pro-NSAID that is activated into a potent NSAID by colonic bacteria; the active metabolite is not excreted in bile. Nabumetone is the only presently available NSAID that does not increase small intestinal permeability.

(B) Infection. The possibilities include recent acute viral or bacterial enteritis, intestinal parasitism, HIV infection and candidosis. Stool testing is useful in identifying these. Repeat the permeability test six weeks after initiating appropriate therapy.

(C) Food allergy. Approach this probability as described in the section above on food allergy in patients with normal fasting test results. The difference lies in degree of damage; food intolerant patients with abnormal fasting permeability have more mucosal damage than patients with normal fasting permeability and will take longer to heal.

(D) Bacterial overgrowth resulting from hypochlorhydria, maldigestion, or stasis [41, 127, 128]. This is confirmed by an abnormal hydrogen breath test. Most of the damage resulting from bacterial overgrowth is caused by bacterial enzyme activity. Bacterial mucinase destroys the protective mucus coat; proteinases degrade pancreatic and brush border enzymes and attack structural proteins. Bacteria produce vitamin B12 analogues and uncouple the B12-intrinsic factor complex, reducing circulating B12 levels, even among individuals who are otherwise asymptomatic [129, 130]. In the absence of intestinal surgery, strictures or fistulae, bacterial overgrowth is most likely a sign of hypochlorhydria resulting from chronic gastritis due to Helicobacter pylori infection. Triple therapy with bismuth and antibiotics may be needed, but it is not presently known whether such treatment can reverse atrophic gastritis or whether natural, plant-derived antimicrobials can achieve the same results as metronidazole and ampicillin, the antibiotics of choice.

Bacterial overgrowth due to hypochlorhydria tends to be a chronic problem that recurs within days or weeks after antimicrobials are discontinued. Keith Eaton, a British allergist who has worked extensively with the gut fermentation syndrome, finds that administration of L-histidine, 500 mg bid, improves gastric acid production in allergic patients with hypochlorhydria, probably by increasing gastric histamine levels [personal communication]. Dietary supplementation with betaine hydrochloride is usually helpful but intermittent short courses of bismuth, citrus seed extract, artemisinin, colloidal silver and other natural antimicrobials are often needed. The first round of such treatment, while the patient is symptomatic, should last for at least twelve weeks, to allow complete healing to occur. Repeat the lactulose/mannitol assay at the end of twelve weeks, while the patient is taking the antimicrobials, to see if complete healing has been achieved. The most sensitive test for recurrence of bacterial overgrowth is not the lactulose/mannitol assay but the breath hydrogen analysis.

TROPHIC THERAPIES

Many naturally occurring substances help repair the intestinal mucosal surface or support the liver when stressed by enteric toxins. Basic vitamin and mineral supplementation should include all the B vitamins, retinol, ascorbate, tocopherol, zinc, selenium, molybdenum, manganese, and magnesium. More specialized nutritional, glandular and herbal therapies are considered below. These should not be used as primary therapies. Avoidance of enterotoxic drugs, treatment of intestinal infection or dysbiosis, and an allergy elimination diet of high nutrient density that is appropriate for the individual patient are the primary treatment strategies for the Leaky Gut Syndromes. The recommendations that follow are to be used as adjuncts:

(1) Epidermal Growth Factor (EGF) is a polypeptide that stimulates growth and repair of epithelial tissue. It is widely distributed in the body, with high concentrations detectable in salivary and prostate glands and in the duodenum. Saliva can be a rich source of EGF, especially the saliva of certain non-poisonous snakes. The use of serpents in healing rituals may reflect the value of ophidian saliva in promoting the healing of wounds. Thorough mastication of food may nourish the gut by providing it with salivary EGF. Purified EGF has been shown to heal ulceration of the small intestine [131].

(2) Saccharomyces boulardii is a non-pathogenic yeast originally isolated from the surface of lichee nuts. It has been widely used in Europe to treat diarrhea. In France it is popularly called "Yeast against yeast" and is thought to help clear the skin in addition to the gut. Clinical trials have demonstrated the effectiveness for S. boulardii in the treatment or prevention of C. difficile diarrhea, antibiotic diarrhea and traveler's diarrhea[132, 133]. Experimental data suggest that the yeast owes its effect to stimulation of SIgA secretion[134]. SIgA is a key immunological component of gut barrier function.

Passive elevation of gut immunoglobulin levels can be produced by feeding whey protein concentrates that are rich in IgA and IgG. These have been shown to be effective in preventing infantile necrotizing enterocolitis[135].

(3) Lactobacillus caseii var GG is a strain of lactobacillus isolated and purified in Finland. Like S.boulardii, Lactobacillus GG has been shown effective in the prevention of traveller's diarrhea and of antibiotic diarrhea and in the treatment of colitis caused by C. difficile. Lactobacillus GG limits diarrhea caused by rotavirus infection in children and in so doing improves the hyperpermeability associated with rotavirus infection.[136-139] The mechanism of action is unclear. The ability of other Lactobacillus preparations to improve altered permeability has not been directly tested, but is suggested by the ability of live cultures of L. acidophilus to diminish radiation-induced diarrhea, a condition directly produced by the loss of mucosal integrity.

(4) Glutamine is an important substrate for the maintenance of intestinal metabolism, structure and function. Patients and experimental animals that are fasted or fed only by a parenteral route develop intestinal villous atrophy, depletion of SIgA, and translocation of bacteria from the gut lumen to the systemic circulation. Feeding glutamine reverses all these abnormalities. Patients with intestinal mucosal injury secondary to chemotherapy or radiation benefit from glutamine supplementation with less villous atrophy, increased mucosal healing and decreased passage of endotoxin through the gut wall[140-143].

(5) Glutathione (GSH) is an important component of the anti-oxidant defense against free radical-induced tissue damage. Dietary glutathione is not well absorbed, so that considerable quantities may be found throughout the gut lumen following supplementation[144]. Hepatic GSH is a key substrate for reducing toxic oxygen metabolites and oxidized xenobiotics in the liver. Depletion of hepatic glutathione is a common occurence in Leaky Gut Syndromes contributing to liver dysfunction and liver necrosis among alcoholics and immune impairment in patients with AIDS. The most effective way to raise hepatic glutathione is to administer its dietary precursors, cysteine or methionine. Anti-oxidant supplementation for Leaky Gut Syndromes should therefore include both GSH and N-acetyl cysteine. Because protozoa are more sensitive to oxidant stress than are humans and because most anti-parasitic drugs and herbs work by oxidative mechanisms, high dose anti-oxidant supplementation should be witheld during the treatment of protozoan infection, especially during treatment with Artemisia. (6) Flavonoids are potent, phenolic anti-oxidants and enzyme inhibitors with varied effects depending on the tissues in which they act. Quercetin and related flavonoids inhibit the release of histamine and inflammatory mediators. Taken before eating, they may block allergic reactions which increase permeability. Catechins have been used in Europe to treat gastric ulcerations. The flavonoids in milk thistle (silymarin) and in dandelion root (taraxacum) protect the liver against reactive oxygen species[145].

(7) Essential fatty acids (EFAs) are the substrates for prostaglandin synthesis. Differential feeding of EFAs can profoundly affect prostanoid synthesis and the systemic response to endotoxin. In experimental animals, fish oil feeding ameliorates the intestinal mucosal injury produced by methotrexate and, additionally, blunts the systemic circulatory response to endotoxin[146]. The feeding of gamma-linolenic acid (GLA), promotes the synthesis of E-series prostaglandins, which decrease permeability. EFAs should be consumed in the most concentrated and physiologically active form to avoid exposure to large quantities of polyunsaturated fatty acids from dietary oils. Consumption of vegetable oils tends to increase the free radical content of bile and to exacerbate the effects of endotoxin[147].

(8) Fiber supplements have complex effects on gut permeability and bacterial composition. Low fibre diets increase permeability. Dietary supplementation with insoluble fibre, such as pure cellulose, decreases permeability. Dietary supplementation with highly soluble fibre sources, such as fruit pectin or guar gum, has a biphasic effect. At low levels they reverse the hyperpermeability of low residue diets, probably by a mechanical bulking effect which stimulates synthesis of mucosal growth factors. At high levels of supplementation, they produce hyperpermeability, probably by inducing synthesis of bacterial enzymes which degrade intestinal mucins[148-151]. For maximum benefit with regard to intestinal permeability, dietary fibre supplementation should therefore contain a predominance of hypoallergenic insoluble fibre.

(9) Gamma oryzanol, a complex mixture of ferulic acid esters of phytosterosl and other triterpene alcohols derived from rice bran, has been extensively researched in Japan for its healing effects in the treatment of gastric and duodenal ulceration, thought to be secondary to its potent anti-oxidant activity[152, 153].



SUMMARY

Altered intestinal permeability is a key element in the pathogenesis of many different diseases. Hyperpermeability initiates a vicious cycle in which allergic sensitization, endotoxic immune activation, hepatic dysfunction, pancreatic insufficiency and malnutrition occur; each of these increases the leakiness of the small bowel. Effective treatment of the Leaky Gut Syndromes requires several components: avoidance of enterotoxic drugs and allergic foods, elimination of infection or bacterial overgrowth with antimicrobials and probiotics, and dietary supplementation with trophic nutrients. Direct measurement of intestinal permeability allows the clinician to plan appropriate strategies and to gauge the effectiveness of treatment, using objective parameters.

TABLE 1
DISEASES ASSOCIATED WITH INCREASED
INTESTINAL PERMEABILITY
Inflammatory bowel disease

Infectious enterocolitis
Spondyloarthropathies
Acne
Eczema
Psoriasis
Urticaria
HIV infection
Cystic fibrosis
Pancreatic insufficiency
AIDS, HIV infection
Hepatic dysfunction
Irritable bowel syndrome with food intolerance
CFIDS
Chronic arthritis/pain treated with NSAIDS
Alcoholism
Neoplasia treated with cytotoxic drugs
Celiac disease
Dermatitis herpetiformis
Autism
Childhood hyperactivity
Environmental illness
Multiple food and chemical sensitivities

TABLE 2
SYMPTOMS ASSOCIATED WITH INCREASED INTESTINAL PERMEABILITY

Fatigue and malaise
Arthralgias
Myalgias
Fevers of unknown origin
Food intolerances
Abdominal pain
Abdominal distension
Diarrhea
Skin rashes
Toxic feelings
Cognitive and memory deficits
Shortness of breath
Poor exercise tolerance

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[Laura]

From Mark Hyman:

Imagine having a condition with symptoms so severe that you can't leave the house, yet your doctor calls it a "functional," or "psychosomatic," disease -- meaning that it's all in your head.

Frustrating? Absolutely.

But it's a very real problem for the 60 million people -- that's 20 percent of Americans -- who have irritable bowel syndrome (IBS). These people are plagued by uncomfortable and often disabling symptoms like bloating, cramps, diarrhea, constipation, and pain.

I have lots of patients with IBS, some of whom have suffered for decades without relief. Their previous doctors couldn't find the cause of the illness, so they were told to just get more fiber or take Metamucil, or were prescribed sedatives, anti-spasm drugs, or antidepressants.

That is NOT the answer. I've found a better way. And in today’s blog I am going to share 5 steps you can take right now to cure IBS without drugs.

But first I want to tell you about a patient of mine ...

Alexis and Her Lifelong Irritable Bowel

At age 45, Alexis had suffered from IBS for 33 years -- almost all of her life! Her major symptom was sudden, painful, cramping diarrhea. She was doing the best she could to prevent it. She didn't consume dairy, didn't drink or smoke, and took Citracel every day. Yet nothing helped.

She would go to the bathroom 4 to 5 times before she even left the house in the morning. And she couldn't go out of the house at all without knowing where all the closest bathrooms would be in case she had what she called "s--- attacks."

That wasn't Alexis' only problem ... She also felt full and bloated after every meal, which starchy foods made worse.

An upper endoscopy had shown that she had gastritis, or inflammation of the stomach, and she had taken many antibiotics over the years. She also had severe premenstrual syndrome (PMS), with irregular periods, breast tenderness, sugar cravings, headaches, and agitation.

She also had unusual symptoms like rectal itching (often a clue to yeast infections or food allergies). And she was tired all the time.

Alexis tried to eat healthy, but her diet was less than ideal. She had a bran muffin and coffee in the morning and a salad for lunch. But her "drug of choice" was sugar -- in the form of cakes, ice cream, Jell-O, diet sodas, and other junk food. Not surprisingly, she was also about 20 pounds overweight.

To help Alexis, all I really did was identify and treat the UNDERLYING CAUSES of her digestive problems! To understand how I did that, you first have to understand a little bit about how the gut works.

How Gut Imbalances Can Lead to IBS

Imagine a tennis court. That is the surface area of your small intestine, where food is absorbed. Your small intestine is also the site of about 60 percent of your immune system. And this sophisticated system gut-immune system is just one-cell layer away from a toxic sewer -- all of the bacteria in your gut.

If that lining breaks down -- from stress, too many antibiotics or anti-inflammatory drugs, intestinal infections, a low-fiber, high-sugar diet, alcohol, and more -- look out! Your immune system will suffer and you can develop all sorts of digestive problems -- including IBS.

Let's talk a little more about all that bacteria. You've got about 3 pounds of it -- 500 species -- in your gut. In fact, there is more bacterial DNA in your body than there is human DNA! Among all that gut bacteria, there are good guys, bad guys, and VERY bad guys.

If the bad guys take over -- or if they move into areas that they shouldn't (like the small intestine which is normally sterile) -- they can start fermenting the food you digest, particularly sugar or starchy foods.

This is called small bowel bacterial overgrowth -- and it's a major cause of IBS.

The major symptom it causes is bloating, or a feeling of fullness after meals. What causes this bloating? The overproduction of gas by the bacteria as they have lunch on your lunch!

Small bowel bacterial overgrowth can be diagnosed by a breath test, which measures gas production by the bacteria, or by a urine test that measures the byproducts of the bacteria after they are absorbed into your system.

Bacterial overgrowth is a real syndrome and was recently described in a review paper published in the Journal of the American Medical Association. The condition can be treated. In fact, a major paper was recently published in the Annals of Internal Medicine that showed using a non-absorbed antibiotic called rifaximin for 10 days resulted in a dramatic improvement in bloating and overall symptoms of IBS by clearing out the overgrowth of bacteria.

That's great news for many IBS patients. But, unfortunately, not all patients with the same diagnosis are created equal. There's more than one factor that leads to IBS. Another major cause of IBS is food sensitivities.

A landmark paper, was recently published in the prestigious British medical journal Gut that found eliminating foods identified through delayed food allergy testing (IgG antibodies) resulted in dramatic improvements in IBS symptoms. Another article, an editorial in the American Journal of Gastroenterology, stated clearly that we must respect and recognize the role of food allergies and inflammation in IBS.

So the research tells us that these are the two main causes of irritable bowel -- food allergies and overgrowth of bacteria in the small intestine -- but there may be others, including a lack of digestive enzymes, parasites living in the gut, zinc or magnesium deficiency, and more.

And this is precisely why it is so critically important to personalize treatment based on the unique circumstances that exist for each person who suffers from IBS -- the solution is most certainly not a one-size-fits-all one. But solutions can be found if we look carefully at the underlying causes and treat them.

Which leads me back to Alexis ...

How I Helped Alexis Heal from IBS

I prescribed Alexis a non-absorbed antibiotic, an antifungal drug for her yeast problem, and had her eliminate the foods to which she was allergic. I believe in treatment that addresses the underlying cause of the problem. If there is a bacterial or yeast infection, then medications are often the best treatments. The key is to effectively treat the cause. If medications do that, then I use them.

Then I gave her supplements of healthy bacteria to normalize her gut and zinc to help with her digestive enzymes (chronic diarrhea can result in zinc deficiency).

I also gave her extra fiber to feed the healthy bacteria, fish oil to reduce gut inflammation, a multivitamin, and herbs to balance her hormones (which are greatly affected by abnormal bacteria).

What happened then may shock some, but I wasn’t surprised. It is the same result I have seen in patient after patient when the principles of functional medicine are applied ...

Alexis came back to see me two months later, and she was a different person. Not only did she lose 20 pounds, she had not had a "s---- attack" and was having normal bowel habits for the first time in 33 years! She also had more energy, and her PMS vanished.

She looked and felt 10 years younger and was free of the suffering she had endured for over three decades.

Do you suffer like Alexis did? It doesn't have to be that way. We have the understanding and tools to deal with this chronic problem and the suffering it causes one in five people. There is no need to wait for any more studies. I have been treating IBS in my practice for over 10 years with dramatic success.

In fact, just recently, one of my patients told me that, for the first time in his life, he didn't have any more stomach pains or digestive problems. He had previously been so bad that he had to have a phone installed in his bathroom!

To take advantage of these discoveries today, simply follow these five steps.

5 Steps to Curing IBS

1. Get tested. Try to get a test for IgG food allergies (see Immunolabs for more information on this testing) and eliminate the foods that test positive for 12 weeks.

2. Test yourself. If you can't afford the test mentioned above, then just eliminate the most common food allergens for 12 weeks -- that's dairy, gluten, yeast, eggs, corn, soy, and peanuts. And then reintroduce them to see if they cause symptoms. This is an effective way to isolate the foods that may be causing you problems.

3. Get rid of the unwanted visitors in your small bowel. Ask your doctor to prescribe rifaximin (Xifaxin) and take two 200 mg tablets 3 times a day for 7 to 10 days. This is often the best way to deal with the chronic bacterial overgrowth that causes bloating and irritable bowel syndrome.

4. Repopulate your digestive tract with good bacteria. I don't usually recommend brands, but when it comes to probiotics the quality varies so much that I suggest taking two specific brands. Take one packet of VSL3 or other high potency probiotic twice a day for 1 to 2 months. This probiotic has over 450 billion organisms per packet. I also recommend a probiotic called S. boulardii take two capsules twice a day for 2 months. This is a special probiotic that helps to further normalize gut function.

5. Read more about the condition and your options. My favorite book on this subject is Digestive Wellness by Elizabeth Lipski.

By taking these steps and seeking out the underlying causes of IBS, you can dramatically improve your health and overcome your digestive disorder.

 

[Gimpy]

Thank you for this.

One of my girlfriends is really suffering with IBS, I'm sending her a copy of these in hopes it helps her out.

 

[Laura]

Notice all the other conditions where a leaky gut is implicated.

 

[Gwenllian]

Re: French muck: Is this the new penicillin?

Very interesting. I have often used french green clay in homemade skin products and find it beneficial. It is also used in soapmaking, not only for the skin benefits but also as a natural colorant. I had not thought of actually drinking it though, but I do have some on hand I could try.

I have some at home and I bought it last year in case of the vaccine would be mandatory.

Very useful to neutralize the vaccine and get it out of the body rapidly if you use the green clay just after the vaccine has been given.

This is so good to know! Thank you.

Mandatory inoculations are still on my mind. In The Netherlands the last secretary of Youth and Family developed a proposal where people would be deprived of their parental rights, if they chose not to have their children vaccinated. I am sure other countries have thought about this, too or even implemented this measure.

 

[Gwenllian]

Re: French muck: Is this the new penicillin?

The reason I like the idea of salt had to with a cd that I listened to. A dentist explained how you could re-mineralise your teeth by rinsing water that is as hot as you can possibly stand with as much salt in it as much as you can stand. However, I think that if you have amalgam fillings this could be a problem. But I prefer clay instead.

Why instead ? Salt is a medicine as old as clay I believe. Like clay it pulls nasty stuff out of body tissue, and natural salt reinforces the action of clay in the poultice (not on open wounds: it burns, like nigari). I didn’t, but many people use salt for the gums.
So I add salt in poultices when necessary but just wanted to tell you to caution with salt if used as part of toothpaste, as it contains grains that must be eliminated to avoid damaging the enamel.


Due to surgery performed by those who won’t be indicted of being a cult, my eyes have been very damaged and I completely lost sight in one eye. I found critical help in Psyche’s precious Iodine research thread (I’ll go and write about asap). But despite this and the clay, the blind eye began to shrink more and more, and it looked like much trouble ahead, again.
The fat diet came before it was too late. Within one month my eye “grew” again its size of before.

Have you ever used clay for your hair?

Yes I use clay/oils/essential oils for my hair, clay for my head too, and clay with magnesium oil but perhaps there is another thread more appropriate for the subject, so that the moderators are not obliged to do the sorting out themselves ?

You are more and more confident using clay, that sounds good Mariama !
Danse la vie

Mariama, I take your kindness with me. Other difficulties, and also other discoveries made the thing with my eyes appear almost casual, though. No more being able to read normally is the hardest.
Regarding the clay I will look for your post later, because now I probably won't be able to make posts longer than one line during the next 8 days
Danse la vie

Well, then you are going through a tough time, or so it seems to me. Just having to cope with the loss of one eye is far from easy, I would imagine.

I was thinking about that during EE last night and these past few weeks. People that have problems with their eyesight, like you, cannot connect to this forum in a way that they would perhaps like.
Since real seeing has nothing to do with the physical eyes I was wondering if it is possible for you to tune into some thoughts that are expressed here? Not that this is a good substitute, but I was wondering.
I am sorry, mods, this has nothing to do with the topic on hand (again).

Now back to clay. I have used it a couple of times now for my teeth and I am amazed at how clean they are. I found out after flossing.
I will experiment with some salt and clay as well, but I do not like the idea of my enamel being damaged by it.

I used salt foot baths for my kids when they were ill. They loved it. And it helps as you said draw out the nasty stuff.

I also tried making a compress with clay and put it on my child's throat, but I guess I put too much essential oil in the clay, because it started burning straight away. Or he was just particularly sensitive to the oil. As far as I can tell he is not sensitive to clay.
He did not want to gurgle with clay water, when his throat was really raw.

I hope you are doing okay.

 

[Persej]

There's been some interesting discoveries about clay, which approach it from a little bit different perspective than how people usually perceive it's beneficial affect on human body. In short, the right type of clay can help the probiotics form the biofilms which helps them stick to human intestines.

Scientist were basically trying to discover the way to help the probiotics to survive the passage through human stomach and then to successfully colonize human intestines, and they found out that the best way to do that is to help the probiotics to form the biofilms. And one of the ways to do that is to combine them with clay. In some other studies, they also used things called dextranomers for the same purpose, which they combined some sugars, like sucrose or maltose.

The type of clay that works really well for this purpose is smectite, which has a specific charge of it's surface, and it seems that a charge of clay is important for bacterial attachment and formation of biofilms.

Administration of probiotics to regulate the immune system is a potential anti-tumor strategy. However, oral administration of probiotics is ineffective because of the poor inhabitation of exogenous bacteria in host intestines. Here we report that smectite, a type of mineral clay and established anti-diarrhea drug, promotes expansion of probiotics (especially Lactobacillus) in the murine gut and subsequently elicits anti-tumor immune responses. The ion-exchangeable microstructure of smectite preferentially promotes lactic acid bacteria (LABs) to form biofilms on smectite in vitro and in vivo. In mouse models, smectite laden with LAB biofilms (Lactobacillus and Bifidobacterium) inhibits tumor growth (when used alone) and enhances the efficacy of chemotherapy or immunotherapy (when used in combination with either of them) by activating dendritic cells (DCs) via Toll-like receptor 2 (TLR2) signaling. Our findings suggest oral administration of smectite as a promising strategy to enrich probiotics in vivo for cancer immunotherapy.

Smectite promotes probiotic biofilm formation in the gut for cancer immunotherapy - PubMed

Administration of probiotics to regulate the immune system is a potential anti-tumor strategy. However, oral administration of probiotics is ineffective because of the poor inhabitation of exogenous bacteria in host intestines. Here we report that smectite, a type of mineral clay and established...

pubmed.ncbi.nlm.nih.gov

 

[Persej]

Session 981205:

Q: (L) What about the clay and the montmorillonite, and the connection of the clay TO the montmorillonite, and what you once said about trace minerals unlocking secrets in some way?
A: Yes.
Q: (L) Yes what? (A) How much should we drink?
A: No.
Q: (L) We shouldn't drink it?
A: Be vague, we vague.
Q: (L) Is this montmorillonite the objective of the clues about tritium? The fact that tritium pointed to this clay, and that this clay is situated in the Rhineland, among other select sites, and alfalfa possibly grows there. Is this where the clue was supposed to lead us?
A: The question is about the mind, spirit and body, and what happens hence.
Q: (L) Well, what I am trying to get to here is: is it useful for us to ingest this montmorillonite? Will it assist in this mind/body/spirit connection?
A: What is more to the point is who was assisted before, how and why.
Q: (L) I don't get it. Maybe it is because I am so tired, but I am hitting a blank on that.
A: You must be, as the obvious is quite oblivious!
Q: (A) We are not getting anything about this mineral... who was assisted before, how and why... (F) I can figure that out! (L) Well, go ahead! (F) If this clay is in Germany, and if the implication is that the mineral causes some sort of beneficial effect, perhaps, in antiquity, somebody was using it for that reason. (L) Is F**** right on this?
A: Yes, he is.

The above sounds like the C's wanted us to discover the whole story about usage of minerals in ancient world. Who, how and why?

While searching for more information about connection between clay and bacteria, I stumbled upon a group of scientists who are interested in such topic. I have yet to read their works, but they sound interesting:

Ethnopharmacological relevance: Medicinal Earths (MEs), natural aluminosilicate-based substances (largely kaolinite and montmorillonite), have been part of the European pharmacopoeia for well over two millennia; they were used generically as antidotes to 'poison'.

Conclusions: Antibacterial activity in kaolinite and smectite clays can arise either from spiking natural clays with elements like B and Al, or from an organic (fungal) load found only within some archaeological earths. It cannot be assumed, a priori, that this organic load was acquired randomly and as a result of long-term storage in museum collections. This is because, at least in the case of medicinal Lemnian Earth, there is historical evidence to suggest that the addition of a fungal component may have been deliberate.

The interweaving roles of mineral and microbiome in shaping the antibacterial activity of archaeological medicinal clays - PubMed

Antibacterial activity in kaolinite and smectite clays can arise either from spiking natural clays with elements like B and Al, or from an organic (fungal) load found only within some archaeological earths. It cannot be assumed, a priori, that this organic load was acquired randomly and as a...

pubmed.ncbi.nlm.nih.gov

This paper focuses on a select number of earth pigments deriving from the island of Melos in the SW Aegean, celebrated in antiquity for its Melian Earth, a white pigment, and asks whether they might display antibacterial activity. We demonstrate that some (but not all) yellow, green and black earth pigments do. We also show that the manner in which they were dispensed (as powders or leachates) was equally important. The results, although preliminary, are informative. Given their use since deep time, earth pigments have never lost their relevance. We suggest that the study of their ecology/mineralogy and potential bioactivity allows for a better understanding of how our perception of them, as both pigments and therapeutics, may have evolved.

The ecology and bioactivity of some Greco-Roman medicinal minerals: the case of Melos earth pigments - PubMed

Mineral compounds, as pigments and therapeutics, appeared regularly in the technical and medical texts of the Greco-Roman (G-R) world. We have referred to them as 'G-R medicinal minerals' and we suggest that despite their seeming familiarity, there are actually many unknowns regarding their...

pubmed.ncbi.nlm.nih.gov

Western biomedicine has only partially developed its own tradition of mineral medicinals (lithotherapeutics), at least compared to botanicals. This is perhaps because these minerals were site-specific, and fundamental information associated with the empirical processes of mineral extraction, beneficiation, storage, trade and preparation was not widely available. In other words, there are many and serious breaks in the multi-link chain from mine to apothecary. This long-term investigation aims to rebuild this chain, on a mineral-by-mineral basis, by pulling together the extant documentary record, material culture, mineralogy, geochemistry and microbial ecology, as well as by testing against known pathogens as an indicator of their antimicrobial activity. Critical to understanding the nature and efficacy of lithotherapeutics is the recognition that these materials need to be investigated simultaneously at two levels: the empirical (ancient sources and practices); and the biomedical (application of physical and biological sciences). Both approaches require the same starting point, namely the field (mine or quarry) and in particular the 'point of contact' (relationship) between minerals and their microbiome.

From mine to apothecary: an archaeo-biomedical approach to the study of the Greco-Roman lithotherapeutics industry - PubMed

Western biomedicine has only partially developed its own tradition of mineral medicinals (lithotherapeutics), at least compared to botanicals. This is perhaps because these minerals were site-specific, and fundamental information associated with the empirical processes of mineral extraction...

pubmed.ncbi.nlm.nih.gov

Medicinal earths are an important and yet, so far, little scientifically explored archaeological resource. They are almost always identified by their source locality. Our work over the last few years has focused on their chemical and mineralogical characterization and their testing as anti-bacterials. This paper presents the results of the mineralogical analysis and antibacterial testing of six medicinal earths, bole or Terra Sigillata (stamped earth) of unknown date and provenance in the Pharmacy Museum of the University of Basel. Only one of them, a red (Armenian?) 'bole', was found to be antibacterial against both Gram-positive and Gram-negative bacteria. A yellow powder of Terra Tripolitania was mildly antibacterial and against one pathogen only. We argue that medicinal earths are in a pivotal place to bridge the gap between currently dispersed pieces of information. This information relates to: (a) their nature, attributes, and applications as described in the texts of different periods, (b) the source of their clays and how best to locate them in the field today, and (c) the methods employed for their beneficiation, if known. We propose that work should be focused primarily onto those medicinal earths whose clay sources can be re-discovered, sampled and assessed. From then on, a parallel investigation should be initiated involving both earths and their natural clays (mineralogy at bulk and nano-sized levels, bio-geochemistry, microbiological testing). We argue that the combined study can shed light into the parameters driving antibacterial action in clays and assist in the elucidation of the mechanisms involved.

Bridging the Gaps: Bole and Terra Sigillata as Artefacts, as Simples and as Antibacterial Clays - PubMed

Medicinal earths are an important and yet, so far, little scientifically explored archaeological resource. They are almost always identified by their source locality. Our work over the last few years has focused on their chemical and mineralogical characterization and their testing as...

pubmed.ncbi.nlm.nih.gov

This paper introduces a holistic approach to the study of Greco-Roman (G-R) lithotherapeutics. These are the minerals or mineral combinations that appear in the medical and scientific literature of the G-R world. It argues that they can best be described not simply in terms of their bulk chemistry/mineralogy but also their ecological microbiology and nanofraction component. It suggests that each individual attribute may have underpinned the bioactivity of the lithotherapeutic as an antibacterial, antifungal or other. We focus on miltos, the highly prized, naturally fine, red iron oxide-based mineral used as a pigment, in boat maintenance, agriculture and medicine. Five samples (four geological (from Kea, N. Cyclades) and one archaeological (from Lemnos, NE Aegean)) of miltos were analyzed with physical and biological science techniques. We show that: a. Kean miltos and Lemnian earth/miltos must have been chemically and mineralogically different; b. Lemnian miltos must have been more effective as an antibacterial against specific pathogens (Gram + and Gram - bacteria) than its Kean counterpart; c. two samples of Kean miltos, although similar, chemically, mineralogically and eco-microbiologically (phylum/class level), nevertheless, displayed different antibacterial action. We suggest that this may constitute proof of microbial ecology playing an important role in effecting bioactivity and, interestingly, at the more specific genus/species level. From the perspective of the historian of G-R science, we suggest that it may have been on account of its bioactivity, rather than simply its 'red-staining' effect, that miltos gained prominent entry into the scientific and medical literature of the G-R world.

Greco-Roman mineral (litho)therapeutics and their relationship to their microbiome: The case of the red pigment miltos - PubMed

This paper introduces a holistic approach to the study of Greco-Roman (G-R) lithotherapeutics. These are the minerals or mineral combinations that appear in the medical and scientific literature of the G-R world. It argues that they can best be described not simply in terms of their bulk...

pubmed.ncbi.nlm.nih.gov