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Updated 7/24/2013   

         Dr. Bernard Presser D.C.

5696 Magnolia Woods Drive

Memphis, TN 38134


If you have any questions, please contact us at 901-417-7905

 More articles coming soon.


Inflammatory bowel disease (IBD) is a general term for a group of chronic inflammatory disorders involving the gastrointestinal tract.  It is divided into two major categories: ulcerative colitis and Crohn's disease.  In the United States, there are approximately 100 cases per 100,000 population, affecting over a million people.  Colitis, enteritis, ileitis, and proctitis - depending on the location of symptoms -- are other terms used for IBD.  Victims are in misery, usually having incredible pain (often with blood and/or mucus), as well as frequent diarrhea.

Typical symptoms of ulcerative colitis are bloody diarrhea with cramps in the lower abdomen, mild abdominal tenderness, irritation around the anus, fissures, hemorrhoids, fistulas, abscesses, weight loss, and fever.  There are open sores and inflammation of the inner lining of the colon and rectum.  The small intestine is rarely affected except for the ileum or lower section.  Other health problems can include joint pain, eye inflammation, liver dysfunction, osteoporosis, skin rashes, anemia, or kidney stones. (It is not known if these are related or if there is a cause-and effect situation.)  When most of the colon is involved, there is greater risk of colon cancer.

Individuals with Crohn's disease suffer intermittent bouts of diarrhea, low-grade fever, right lower quadrant pain, loss of appetite, weight loss, flatulence, malaise, abdominal tenderness (especially in the right lower quadrant with signs of peritoneal irritation and an abdominal or pelvic mass).  Sharp, severe pain is experienced in isolated areas of the gut. Inflammation extends deeper into the layers of the intestinal tissue.  The condition is chronic and recurs at intervals during a lifetime, sometimes with long periods of remission that can last for years.  The original description of the disease in 1932 localized the disease to segments of the ileum (lower three fifths of the small intestines).  However, the same process and effects can involve the inside of the cheeks, esophagus, stomach, duodenum, jejunum and ileum.  The colon may be affected, either alone or with small intestinal involvement.

In ulcerative colitis, there is a non-specific inflammatory response primarily involving the mucous membrane lining of the colon.  The inflammation is uniform and continuous with no intervening areas of normal mucosa. In contrast,

Crohn's disease is characterized by chronic inflammation extending through all layers of the intestinal wall, involving the mesentery (fold connecting the small intestine to the abdominal wall) and lymph nodes in the region.  Whether or not the small intestine or colon is involved, the basic process is the same.  Often there are granulomas (growths).  Similarities between colitis and Crohn's include age, race, sex, geographic distribution, and many epidemiologic and etiologic features.  Both problems are associated with similar extra-intestinal manifestations, parallel causative factors, and increased risk of colon cancer.  Patients with both conditions have increased rates of fracture, lower bone mineral density, and suffer osteoporosis and osteopenia more often than others.  The disease rates differ slightly, ulcerative colitis being more common than Crohn's disease, although the rate of Crohn's is increasing.  While Crohn's and colitis are categorized as two separate diseases, there is an argument that they are two examples of the same process that affects different areas of the intestines to a different degree.

No single test is sufficient to diagnose IBD, so sufferers are often put through endless rounds of endoscopic, radiological, histologic assessments, laboratory testing and bowel studies for a definitive diagnosis.  In 10 to 15% of patients, it is "almost impossible to differentiate between the two diseases." Another difficulty is that both Crohn's and colitis mimic several other intestinal conditions and other problems such as intestinal tuberculosis, diverticulitis, endometriosis of the bowel, lymphoma, drug reactions (NSAIDs, gold salts, sulphasalazine, etc.).  The standard battery of medical tests do not reveal why the symptoms occur, or how well the individual is digesting, or how effectively nutrients are absorbed.

Intestinal permeability is "a marker of disease activity" in Crohn's and extensive colitis. Increased intestinal permeability precedes clinical relapses in Crohn's disease and is considered an indication of subclinical disease.  This means injury or damage to mucosal and epithelial tissues of the intestines, allowing inappropriate penetration of substances such as partially digested food particles into the tissue walls, causing further insult and provoking a long-lasting cycle of aggravation and injury.  IBD may occur at any age, but most often appears between the ages of 15 and 35.  Females are affected slightly more than males.  These diseases are more common in Caucasians than in blacks or Orientals, with increased incidence in Jews compared with non-Jews.  The cause of ulcerative colitis and Crohn's disease "remains unknown," although certain features of these diseases suggest several areas of importance. i


The cause(s) of IBD remains "contentious," though there are several theories.  Treatment is "supportive rather than curative and is likely to remain so until the cause(s) of the disease(s) is discovered."  Physicians often contend that an "infectious agent" is involved.  Faithful to this theory, "our failure to identify the pathogen does not diminish this likelihood."  Most researchers subscribe to the concept that Crohn's disease is a consequence of "inappropriate over-expression of immune responses" to "antigens" (particularly bacteria) normally present in the gut.  Or that there is an inadequate immune reaction, or an overload of products inside the intestines.  The concept is that the body does not properly regulate an inflammatory response in the gut wall.  According to theory, there may be multiple agents or organisms that set off the process, though evidently the bugs choose to remain anonymous.

Many studies have shown abnormalities in neutrophils (a type of white blood cell) function, including a reduction in neutrophils chemotaxis (movement of additional white blood cells to an area of inflammation).  There may be an "acquired defect in phagocyte [any type of white blood cell that engulfs foreign, damaged, or dead particles] function..."  In other words, the process of inflammation - which the body normally and constantly uses to attempt repair of damaged or injured tissues - is not functioning properly or adequately or is overwhelmed with toxic insults.  For example, smoking has been associated with impaired neutrophil function.  Defects in functions of other white blood cells such as macrophages, increased responsiveness of lymphocytes, and other immune "glitches" also occur. "Pathogenic bacteria" such as Salmonella and Mycobacterium paratuberculosis and "other pathogens" are anecdotally reported in some cases.  As bacteria are "garbage collectors" for aberrant or toxic substances, accumulation of poisonous garbage in the bacterial "garbage bags" could be a contributing factor.

Some studies seemed to indicate a "measles infection" is involved in the etiology of IBD.  Other studies did not support the theory.  The rising rates of Crohn's in children did give rise to the possibility that the measles vaccine - rather than the "measles virus" -- is responsible as the live vaccine was widely used for many years.

There is evidence for a genetic component to IBD development.  In addition to racial and ethnic prevalence, there is a familial tendency. Genetic factors are more prevalent in development of Crohn's disease than ulcerative colitis, about 20% and 6% respectively.  Yet most cases of IBD cannot be attributed to genetic susceptibility since a genetic predisposition is present in only about 10% of those who become affected and there is no consistent pattern of inheritance.

Foods have been implicated in IBD for various reasons such as: food allergies or sensitivities, toxicity of chemically processed fats (margarine, partially-hydrogenated or altered fats), chemical food additives, increased intestinal bacteria (due to refined sugars, etc.), nutritional deficiencies.  No specific diet seems to be effective for preventing or treating IBD.  One factor is individual biochemistry; each person has different needs.  However, some diets and certain foods have been linked with increased risk.  Symptoms are aggravated in some people by ingestion of milk products, alcohol, hot spices, or fiber - potential irritants.  Food intolerances have been strongly associated with IBD.  Improvement can follow elimination of common items such as wheat, corn, potatoes, chocolate, milk, oranges, tomatoes, and others. In one study, food allergy played a role in 66% of the cases ulcerative colitis.  Dairy products may contribute to IBD.  Pasteurization; homogenization; pesticide, drug, and hormone residues, enzyme destruction, lactose alteration, and altered protein residues of processed milk products may be factors that trigger symptoms in susceptible individuals.  One case of an exclusively breastfed 8-week old baby with symptoms strongly suggesting colitis was resolved when cow's milk and dairy products were eliminated from the mother's diet.  Victims of IBD must carefully rule out food sensitivities.

Some research suggests that eliminating dietary sulfur amino acids (SAAs) can be helpful. Normally SAAs are extremely beneficial (even anti-carcinogenic) as in cruciferous vegetables (cabbage, broccoli, cauliflower, brussels sprouts, etc.).  In one study, patients were taken off foods high in SAAs - cruciferous vegetables, eggs, dairy, nuts, soy, mayonnaise, mineral water, wine, cordials, - and limited in consumption of red meat (fish and chicken allowed).  The results of the 56- month-long study were impressive.  Everyone improved and no one had a relapse or attack. Intestinal bacteria convert sulfur from foods into hydrogen sulfide, the main malodorous compound in passed gas.  It can be highly toxic.  Cells lining the bowel absorb and detoxify most of this hydrogen sulfide.  But people with IBD make more hydrogen sulfide than people without the disease, and may not break it down efficiently.  SAAs are essential for cytokine production.  Cytokines are produced by white blood cells and other cells, and include interleukins, some interferons, and tumor necrosis factor.  They change the cells that produce them, alter other nearby cells and are important in controlling local and systemic inflammatory responses.

Is reduced cytokine formation in the inflamed mucous membrane a reason for the diet low in SAAs to be so successful?  Or could there be another reason?  For example, most of the items eliminated or reduced in the low-SAA diet are pasteurized at high temperatures (dairy), cooked (vegetables, eggs, nuts, red meat), contain altered fats (mayonnaise, roasted nuts), are processed and refined (soy, mayonnaise, wine, cordials), or in other ways changed from the way Nature produced them.  Thus, is it the altered SAAs or other altered by-products that irritate the intestinal walls?  The "importance of luminal content [food and toxin residues, and bacterial balance in the intestines] has been shown..."  The structural and functional integrity of the gut wall and the preservation of this integrity are also essential.  Proteins, including those containing SAAs, are crucial to this integrity.  But altered foods containing altered proteins, altered fats, altered carbohydrates, depleted nutrients, added synthetic chemicals, etc., cannot contribute to gastrointestinal health.  Rather, they can irritate, injure, and predispose for problems both by errors of commission and omission.  Overcooked meats, for example, result in sulfide generation by bacteria in the large intestine.  Bacteria gobble up the decomposing, denatured meat remnants and produce hydrogen sulfide.  Another culprit is inorganic sulfur (e.g. sulfite) which appears in processed and smoked meats, wines, and other foods subjected to human tampering.

An elimination diet and rotation program are remarkably successful in treating IBD.  The diet foods for each meal.  Common (often favorite) foods that may trigger reactions are avoided the first week.  Any food that triggers a reaction is replaced by another until the individual is free of symptoms.  After symptoms have abated, favorite foods are reintroduced to the diet one by one.  Foods that trigger a reaction twice are withdrawn for three months.  An 85 to 90% favorable response including total relief of symptoms for some is reported.  Accompanying symptoms such as atopic, respiratory, muscle, joint, kidney and emotional symptoms (anxiety, depression, fatigue, irritability) also improve in 80 to 90% of the cases. Individuality is crucial. Another key is whole, natural, unaltered food.  This eliminates "junk" foods, additives, toxic residues, or foods ground, crushed, mashed, refined, or otherwise mutilated or denatured.  Processed foods typically have over 80% of their natural nutrients removed - - nutrients needed for healing.  These non-foods (such as those containing bleached white flour, refined sugars, or hydrogenated oils) can cause food allergies that inflame the gut.  They are foreign to the body, causing irritation, depletion, and the need for detoxification.

IBD is rare in most populations (including the Third World) that have not adopted the typical "western" diet high in refined carbohydrates and altered fats, low in fiber, and low in nutrient density.  "Epidemiological data show that increasing westernization leads to a higher incidence of inflammatory bowel disease."

There is a correlation between IBD and a diet high in refined sugars.  Refined carbohydrates can create an excessively acidic lower bowel which disrupts normal bacterial flora, setting the stage for Candida or yeast overgrowth.  Refined sugars irritate or aggravate mucous membrane linings of the gastrointestinal tract and adversely affect the function of white blood cells (especially phagocytes).  Insulin secretion is enhanced.  The nutrients needed for healthy digestive tissues and their function are depleted.  Studies show that IBD patients eat more sugar and sweets than controls.  This is probably because refined foods relieve hunger due to quick absorption and do not immediately cause diarrhea.  Although there may not be immediate adverse effects, in the long-run problems abound.

"Certain" high-fat foods (particularly margarine) have been linked to increased risk of IBD . Consumption of many western foods (refined-flour breads, butter, margarine, cheese, meats - especially ham and sausage) is significantly related to increased risk of colitis.  Increased intake of animal protein and omega-6 polyunsaturated fatty acids with decreased omega-3 polyunsaturated fatty acids may contribute to development of IBD.  Animal foods are sources of the most concentrated amounts of environmental chemicals including drugs, pesticides, and hormones.  Animals are raised in unnatural ways with unnatural foods and have imbalanced fatty acids as well as other deficits and alterations.

Modern farming methods have created, among other things, disruption of the natural balance of fatty acids.  Deficits of omega-3 fatty acids prevail.  Rancid fats are commonly used to produce vegetable oils.  Fried foods are cooked in fats used repeatedly and at high temperatures. So toxic fat by-products are regularly consumed.  Fat substitutes such as Olestra are designed so they cannot be absorbed; they inhibit absorption of fat soluble vitamins such as A, D, E, and K, as well as carotenes and other fatty acids.  These nutrients are crucial for gastrointestinal health and for healing involved tissues.  Trans fatty acids like margarine and partially-hydrogenated fats directly damage cell membranes.

Biopsy samples of mucous membrane tissue from IBD patients exhibit increased oxidation (breakdown) of fats and proteins. Levels of copper/zinc superoxide dismutase are low in even non-inflamed tissue.  Iron is increased; overuse of ascorbic acid (so-called vitamin C, a synthetic fraction) can lead to excess iron absorption.  Calcium oxalate particles are common, another possible consequence of ascorbic acid ingestion.  Large peaks of calcium and phosphorus may occur.  Like the tubercles of tuberculosis, calcium phosphate can substitute for normal tissues unable to regenerate by virtue of nutrient deficits or toxicity.  Studies on colitis show a marked deficiency of a specific type of mucin, a thick mucous layer designed to protect the gastrointestinal wall from injury or "invasion" by foreign or toxic substances.  Support to the protection, repair, and function of the mucosal linings - including avoidance of items that can irritate, damage, or deplete this system - is imperative.  Because the breakdown products of a damaged digestive tract and the added insults of toxic or foreign substances overloads the liver, the gut is intoxicated or harmed even more.  Also, the liver must be strengthened.

Toxic substances have been implicated as potent contributors to IBD.  For instance, traces of aluminum, silicon, and titanium are found in Peyer's patches of the ileum in Crohn's patients.  Similar constituents are in commercial toothpaste, other dental products, food additives (e.g., titanium dioxide), and other manufactured products.  Fluoride, added to municipal water, toothpaste, some drugs, and other products, can lead to enhanced production of injurious chemicals.  Tricalcium phosphate, quartz, barium sulphate, bismuth subcarbonate, talc, magnesium trisilicate, and other chemical compounds commonly used in foods, medications, cosmetics, and other products with wide consumer exposure have been identified in animal experiments to cause penetration of and lesions to intestinal tissues.  Symptoms can be produced by any of the hundreds of food additives in common use including MSG and aspartame (NutraSweet, Equal).  For example, carageenan (a compound extracted from red seaweed, used as a stabilizing and suspending agent in foods such as dairy products), has been used to induce colitis in experimental animals and is a source of MSG (created during processing).  Toxic-metal containing white blood cells will not function normally.  Toxic metals including lead, aluminum, and nickel can disturb a variety of white blood cell functions including enzyme secretion and phagocytosis.  The success of elemental or elimination diets in IBD, "thought to be due to the elimination of dietary antigens, is consistent with the removal of inorganic particulate toxins from the diet."  Thus, toxins in foods, rather than foods themselves, may be culpable.

The increase in Crohn's disease over the past 50 years parallels the increasing use of antibiotics in medicine and in meat-animals.  "Prior antibiotic therapy also promotes the outbreak of Crohn's disease to a statistically demonstrable extent."  Crohn's disease may be caused in genetically susceptible persons whose intestinal bacteria have been altered by antibiotics, "morphologically normal flora" which becomes toxic. The capacity of non-steroidal anti-inflammatory drugs (NSAIDs - Motrin, Aleve, Advil, etc.) to injure the mucous membrane lining of the intestines is "an under recognized but common" cause of colitis. Ischemic colitis is an adverse reaction of a drug used to treat irritable bowel syndrome, alosetron (Lotronex).  There is evidence that oral contraceptive use may increase the risk of IBD.

The cause of IBD "is more complex than a single-cause and effect relation, and probably represents an interaction between genetic predisposing factors, exogenous (outside) and endogenous (inside) triggers, and modifying factors."

Over half of the immune system and about half of the body's capacity to detoxify are found in the lining of the digestive tract.  Also, it is now known that there is "a brain in the bowel."  The small intestine contains more than a hundred million spinal cord.  Adding on the nerve cells of the esophagus, stomach, and large intestine, there are more nerve cells in the digestive tract than in the spine, and more than in the entire remainder of the peripheral nervous system.  The enteric nervous system is "a vast chemical warehouse within which is represented every one of the classes of neurotransmitter [chemical messenger] found in the brain."  This system can function on its own, like a separate brain.  It works so closely with the immune system in defending the gut that "a developmental interaction between the nervous and immune system, each of which secrete chemicals that affect the other, should be anticipated."  For example, there are increased numbers of nerve cells found in segments of the intestines affected by IBD. Since nerve cells supposedly do not reproduce, how does this happen?  Obviously, body "parts" cannot be separated from each other.  A person with IBD has a systemic problem which appears in the weakest or most injured area of the body.  The clinician must look at the whole picture. ii


Conventional medical treatment of IBD involves the use of corticosteroids like prednisone, sulfa-based drugs like sulfasalazine (Azulfidine and its new cousin Asacol), immunosuppressives like azathioprine, and salicylates like aspirin and other non-steroidal anti-inflammatory drugs. These drugs may alleviate pain and other symptoms temporarily, "but they have major side-effects and they don't always control the disease." The fact is, "so far no drugs have been shown to effect an improvement that persists after withdrawal of treatment."  Drugs do not cure IBD. Of course, a medical "cure" for colitis is surgical removal of the colon.  No colon, no colitis!  Crohn's disease may "require surgery" but cannot be "cured" by an operation.  Many clinicians would not call surgery a "cure" anyway.  Patients and clinicians often opt for less drastic alternative treatments.

Most of the above medications suppress the immune response and inhibit inflammatory mechanisms.  This implies interference with repair, the goal of inflammation.  Complications of corticosteroid use include vulnerability to ‘infection' and inflammation, ulcers, intestinal perforation, adrenal dysfunction, osteoporosis, cataract, glucose intolerance, and other problems.  Immune suppressants (methotrexate, cyclosporin, 6-mercaptopurine, azathioprine, tacrolimusare) are admitted to be "far from perfect."  Adverse reactions include bone marrow suppression, numbness, tingling, heightened sensitivity to pain, lymphoma (malignant tumors of lymphoid tissues), kidney dysfunction.  There is potential for toxic neurologic symptoms such as seizures, liver toxicity (e.g. fibrosis), and increased incidence of infection or inflammation.  Side effects of sulfasalazine include lung or kidney damage so severe it can be lethal, paralysis (e.g. Guillain- Barre syndrome), vision problems, depression, low white blood cell count, hepatitis, and a decreased level of blood clotting cells (thrombocytopenia).  Sulfasalizine is "a glorified aspirin (NSAID) and sulfa drug rolled into one."  Such a "deadly duo" can make and maintain a "leaky gut" indefinitely.  The association of cancer (especially leukemia) with treatments by immunosuppressants and/or sulfasalazin "is a concern."

Antibiotic treatment (metronidazole, rifaximin, ciprofloxacin) has been used for both Crohn's and colitis.  But studies show that, if there is any positive effect on symptoms, it only lasts for two to four weeks.  Besides, it is unlikely that there is any bacterial "infection" involved in the first place.

About 51% of IBD patients use alternative or "complementary" therapies such as nutritional supplements and herbal products.  "Side effects and lack of effectiveness of standard therapies were the most commonly cited reasons for using complementary therapies."  Nutritional treatment has been shown to be as effective in treating acute attacks as anti-inflammatory corticosteroid therapy.  "Food may after all be a simpler, cheaper, and more well-established means of achieving the same effects." iii


There is a high prevalence of malnutrition in IBD.  The question is whether this is a cause or an effect - or both.  Malnutrition can arise from decreased intake of foods due to discomfort or physician-prescribed limited diets, malabsorption, electrolyte/ mineral loss in diarrhea, increased nutrient requirements, increased intestinal cell turnover, drug/nutrient interactions, susceptibility due to previous subclinical deficiencies.

Food allergy and intolerance may be a major contributing factor.  Approximately 80% of patients treated with an elemental or elimination diet achieve "clinical remission"  after about 3 to 4 weeks, "a rate superior to that produced by corticosteroids".  This treatment also results in objective (radiographic and endoscopic) evidence of remission.  Some individuals need a "Rotary Diversified Diet," made up of a highly varied selection of foods which are eaten in a definite rotation or order to control food sensitivities and prevent new ones until biochemical equilibrium is attained.  Food combining may be a concern for some sufferers, avoiding consumption of proteins and starches together, for instance.  According to Alan R. Gaby, M.D., about half of patients complete remission with dietary modification alone."  It is essential to "develop a diet specific to each patient's needs."

Refined sugars and altered fats should be eliminated.  Fiber should be gradually increased, preferably from whole, natural foods like fruits, vegetables, whole grains, and legumes. Ingestion of a germinated barley "foodstuff" created a "significant decrease in clinical activity index scores" for ulcerative colitis.  There was an increase in stool butyrate concentrations.  Butyric acid is a source of energy for cells lining  the intestines, modulating cellular proliferation and differentiation.  Thus sprouted grains or seeds and naturally fermented foods could be beneficial.  Normally butyric acid, a small-chain fatty acid, is produced in the colon by anaerobic bacteria through the degradation of food fibers and starch.  In low fiber diets (or diets high in refined carbohydrates) inadequate production of butyric acid can occur.  This leads to malabsorption of essential nutrients, "starvation" of cells in the colon, poor healing, diarrhea, and colitis.  Butyric acid enemas are used to treat IBD by stimulating some repair.  "When this is followed with a high fiber diet which contains cultured foods that support proper bacterial growth," problems like IBD can be alleviated.  It is obviously better if natural whole foods supply the materials needed for the body to produce its own compounds for tissue health, repair, and maintenance.

Nourishing the bacterial flora of the intestines is paramount to disease reversal.  Dietary fiber has a profound effect on the intestinal environment and, if the food is from unaltered sources, it can contribute to optimal intestinal flora composition.  High risk of colitis recurrence is associated with a fiber-poor diet.  A healthy, protective flora along with optimally-healthy tissues is important to prevent susceptibility to insult, injury, and inflammation.  Both probiotic (micro-organisms ingested live) and prebiotic (substrates fermented by elements of the normal flora) modulators of bowel flora are gaining interest.  Probiotics and prebiotics - healthful, natural bacteria-containing supplements or fermented foods - "may be able to remove toxic substances, stimulate the immune system, produce nutrients and defend against ‘bad bacteria.'"  Administration of probiotics resulted in remission in 75% of patients in one study.  In another only 3 of 40 patients given probiotics suffered relapses during 9 months compared with 20 of 40 in the control group.  Products containing one or more probiotic strains "have been shown in double-blind randomized studies to prevent relapses of both Crohn's disease and ulcerative colitis."  A source of lactic acid yeast, or lactobacillus and bifida bacterium would be an excellent way to reestablish normal intestinal flora.  Microorganisms including normal bacteria, yeast, and parasites, "may play a key role in modulating intestinal immunity..." Without these natural parasites and bacteria, the immune system may overreact and produce powerful inflammatory agents.  Animal and human studies using microscopic eggs (unable to reproduce) of a specific intestinal parasitic worm resulted in symptomatic improvement of subjects, the majority enjoying complete remission.  Has over-use of antibiotics in medicine and in meat animals plus a denatured diet contributed to the disruption of intestinal "inhabitants" and to IBD?

Intestinal permeability is often treated with the amino acid L-glutamine.  Biochemically, it serves as a major metabolic fuel for gastrointestinal mucosal cell integrity and gut barrier function.  Unfortunately, clinical use is pharmacological -- isolated and in large doses.  Glutamine supplementation in intravenous total parenteral nutrition has increased mucosal weight and DNA content in the bowel and decreased atrophy of the villi, at least temporarily.  But oral glutamine "by itself" has no beneficial effect on intestinal permeability or on the course of Crohn's disease.

Glutamine is naturally present in the juices of many plants, a better source.  This along with a multiplicity of other healthful substances in chlorophyll-containing plants is extremely beneficial to the mucosal and epithelial tissues, to inflammation and repair processes, and for general wellness.  Cereal grasses and any green-leafy vegetables can be used.  Since raw foods are sometimes not tolerated due to digestive difficulties or irritation of delicate surfaces of inflamed intestines, freshly-made vegetable and fruit juices would be a wonderful source of rich nourishment.  These juices may serve an invaluable role in supplying nutrients to a body "starving" for food due to chronic deficits or acute episodes of pain and diarrhea. Finely grated or pureed fresh fruits and vegetables can also be used. Rutin, flavonoids, carotenes,  vitamin K, J factors, B vitamins, magnesium, calcium, iron, potassium, other minerals and trace minerals, chlorophyll, amino acids, enzymes, and other nutritives present in green vegetable products and other raw foods are essential to the sufferer.  Many clinicians put all their IBD patients on whole raw vegetable foods with plenty of fiber.  If whole foods are not initially tolerated, the juices can be used as fiber-rich plants are gradually increased.

Nutritional deficiencies "verified" so far in patients with IBD include iron, vitamin B12, folate, vitamins B1, B2, and B6, magnesium, potassium, retinol (vitamin A), vitamin C, vitamin D, zinc, copper, vitamin K, niacinamide, vitamin E, glutathione.  These need to be supplied along with the plethora of other nutrients - known and unknown - in whole, intact, natural foods.  Magnesium helps relax muscles in the walls of the intestines and, along with calcium, supports the structural tissues and nerves.  Vitamin A complex, carotenes, and vitamin E complex are needed for healthy mucous membranes, to protect these membranes and aid in their healing.  Vitamin C complex - including flavonoids - is essential for proper immune function and healing of tissues.  Zinc deficiency is a well known complication of Crohn's disease, occurring in about 45% of patients.  Many patients do not respond to oral or even intravenous zinc supplementation.  Perhaps food sources would be a wise alternative.  Folic acid deficiency is quite common in IBD, occurrence ranging between 25% to 64%.  Usually this is due to administration of the drug sulfasalazine.  Folate deficiency promotes further malabsorption and diarrhea.  Vitamin B12 is absorbed at the portion of the intestine most commonly affected in Crohn's disease (the terminal ileum) so abnormal absorption is common, affecting 48% of patients.  Pantothenic acid may fail to be converted into Coenzyme A in colonic mucosa.

Glutathione is depleted in the intestinal mucosa and glutathione peroxidase is low in the plasma of people with IBD.  Glutathione (a tripeptide of glutamic acid, cysteine, and glycine) functions in various reactions in the destruction of peroxides and free radicals, as a cofactor for enzymes, and in the detoxification of harmful compounds.  Glutathione peroxidase, an enzyme that breaks down the detoxifying reduction of hydrogen peroxide and organic peroxides by means of glutathione oxidation, requires selenium.  A significant reduction of selenium and glutathione peroxidase in both plasma and red blood cells is found in patients who had small-bowel resection.

The role of emotional and psychological development in IBD has become increasingly relegated to the role of symptom rather than cause, though the controversy continues.  Either way, support to the nervous system - generally and for the digestive tract's "second brain" - is imperative.  Vitamin B complex, essential fatty acids, calcium, magnesium, potassium, zinc, and other nutritives all play a role.

People with chronic intestinal disorders have plasma fatty acid levels "reflective of essential fatty acid deficiencies" compared to controls." Omega-3 fatty acids, balanced with omega-6s, are particularly important.  Essential fatty acids are important in cell formation, cellular membranes, and for protection of the lining of the digestive tract.  Fish oil capsules resulted in significant improvements in test indices as well as significant weight gain, reduced physiologic components of inflammation, and improved symptoms.  Not just symptoms, but biochemical parameters of inflammation are improved.  Steroid use is often cut in half.  Relapse is reduced dramatically.  Flaxseed oil has been shown to reduce inflammation and support repair.  Unrefined flax oil is a highly effective folk remedy for gastrointestinal ulceration, inflammation, and bleeding.  Evening Primrose oil significantly improves stool consistency.  Compared with controls, patients with IBD have a reduced polyunsaturated fatty acid levels; increased monounsaturated fatty acid levels; higher ratios of mead to arachidonic acid; lower concentrations of total, saturated, monounsaturated and polyunsaturated fatty acids.  In other words, there are essential fatty acid deficiencies and imbalances.  Malabsorption may be involved, contributing to deficiencies of other fat-soluble factors such as vitamin complexes of A, D, E, and K.

Fresh figs or dried figs soaked in water is a folk remedy for intestinal inflammation.  Aloe Vera gel can often be quite supportive to the healing process.  Proteolytic enzymes are vital for proper digestion of proteins and to help control inflammatory responses.  Bromelain, a proteolytic enzyme present in pineapple, has been shown to aid in healing the mucosa, improve diarrhea, and alleviate other symptoms.  (In theory, bromelain may increase the risk of bleeding when taken with anticoagulant and antiplatelet drugs.)  Many other enzymes present in raw foods such as papain from papaya could be helpful.  Plantago seed (also called Ispaghula seed), via fermentation in the colon, yields butyrate and acetate, which may be effective for maintaining remission in persons with colitis and may help reduce risk of colon cancer.  Ispaghula husk (also known as psyllium husk) consists of the epidermis and collapsed adjacent layers removed from the seeds.  Psyllium husks lubricate, soothe inflamed mucous membranes, and absorb toxins. Human and bovine colostrum "might be useful for the treatment of a wide variety of gastrointestinal conditions," including IBD.  Enemas of wheatgrass juice are reported to relieve the pain of gaseous buildup and clean the colon of waste.  Pomegranate fruit and rind promote digestion, have stomachic properties, and are astringent and anti-inflammatory to mucous membranes.

Herbs such as slippery elm bark coat and soothe mucous membranes.  Yarrow reduces bile and inflammation in the intestinal tract and helps strengthen mucous membranes; it has some calmative, nervine action as well.  The Ayurvedic herb, Boswellia serrata, was found to be equal to sulfasalazine in the treatment of IBD.  An infusion of peppermint may help protect the gut lining from irritation and help soothe any griping; the bitters stimulate and cleanse the bowels.  Garlic assists proper inflammation and repair processes and has a healing effect on the intestines.  Alfalfa supplies chlorophyll, vitamin K, potassium and many other nutrients needed for healing.  Nettle, chamomile, dandelion, feverfew, red clover, buchu leaves, coriander (cilantro), lobelia, and turmeric have also been used effectively in IBD. iv


IBD is a complex, individualized disease.  The fact that Western foods and lifestyles have a profound effect on the development and manifestation of IBD strongly indicates that, rather than a "germ" (unless it is imperialistic), environmental factors are the culprit.  While conventional medical treatment attempts to inhibit or stop inflammation and suppress the immune system, the natural approach is to enhance the body's natural defenses, support the inflammation and repair processes, and eliminate noxious stimuli.  Aiding the individual to cope with stress in healthy ways and encouraging him/her to deal with psychospiritual issues may affect immune function, endocrine status, and nerve condition.  Body/mind techniques - such as meditation and massage - can have favorable impacts.

When the intestines are inflamed they:  1) do not secrete digestive enzymes for proper digestion of foods and absorption of nutrients,  2) are more prone to react to foods so food sensitivities develop,  3) experience damage to carrier proteins so malabsorption and nutrient deficits develop or worsen,  4) contribute to compromises of the detoxification pathways that line the gut so chemical sensitivities arise, toxins overburden the liver, and food intolerances become more likely,  5) compromise the protective lining of the gut, leading to increased susceptibility to insult or injury, and 6) lessen ability to handle total load, so "abnormal" or "bad" bacteria may arise as well as overgrowth of ordinarily helpful yeast.

Each area can be approached in a natural, effective manner with an individualized diet of nutrient-dense foods, additional food complex supplements, whole herbs, and other modalities. In severe and acute cases, medical attention may be imperative.  But only the body can cure or heal.  Natural therapists hope to facilitate the innate tendencies for healing and balance with the tools and energies provided by Nature. v

i Harrison's Principles of Internal Medicine, 13th Ed., Isselbacher, Braunwald, Wilson, Martin, Fauci, Kasper, eds.; NY: McGraw-Hill, Inc., 1994, pp.1403-1417; M. Murray, Amer J of Nat Med, Vol.4, No.6, Jul/Aug 1997, p.8; K. Miki, et al, J Pediatr, Vol.133, No.6, Dec 1998, pp.750-54; J. Wyatt, et al, Lancet, Vol.341, No.8858, 5 Jun 1993, pp.1437-39; J.R. Hilsden, et al, Gastroenter, Vol.110, 1996, pp.1395-1403; Postgrad Med J, No.112, 1995, pp.46-8 and No.54, pp.57-8; C. Bernstein, et al, Ann Intern Med, Vol.133, No.10, Nov 2000, pp.795-99.

ii H. Hodgson, Lancet, Vol.353, No.9151, 6 Feb 1999, p.425; J. Satangi, et al, Lancet, Vol.347, No.9010, 4 May 1996, pp. 1212-17; Science News, Vol.150, No.19, 9 Nov 1996, pp.302- 3; P. Rutgeerts, Lancet, Vol.341, No.8858. 5 Jun 1993, pp.1443-4; Lancet, Vol.347, No.8993, 6 Jan 1996, pp.40-44; S. Taylor-Robinson, et al, Lancet, Vol.1 for 1989, No.8647, 20 May 1989, p.1145; A. Ekbom, et al, Lancet, Vol.348, No.9026, 24 Aug 1996, pp.515-17; P. Jones, et al, Lancet, Vol.349, No.9050, 15 Feb 1997, p.473; J. McConnell, Lancet, Vol.350, No.9087, 1 Nov 1997, p.1302; Gut, Vol.30, 1989, pp.618-22; Lancet, Vol.345, 1995, pp.1071-73, 1363 & Vol.347, 1996, p.263; Gastroenterol, Vol.344, 1995, pp.48-51; Gut, Vol.37, 1995, p.63; S. Middleton, et al, Lancet, Vol.341, No.8843, 20 Feb 1993, pp.465-6; N. Boughton-Smith, Lancet, Vol.342, No.8867, 7 Aug 1993, pp.338- 40; J. Kirsner, Lancet, Vol.352, No.9136, 17 Oct 1998, pp.1303-05; H. Hodgson, J R Coll Physicians Lond, Vol.20, No.1, Jan1986, pp.45-8; S. Mishkin, Am J Clin Nutr, Vol.65, No.2, Feb1997, pp.564-7; N. Fuchs, Women's Hlth Lttr, Vol.VII, No.12, Dec 1998, p.7; W. Roediger, Lancet, Vol.352, No.9115, 23 May 1998, p.1555; G. Vantrappen, et al, Lancet, Vol.341, No.8847, 20 Mar 1993, pp.730-1; J. Klotter, Townsend Lttr D&P, Apr 1998, pp.18-19; J. Hunter, European J Gastroenter & Hepat, Vol.10, 1998, pp.235-7;E. Magee, Am J Clin Nutr, Vol.72, No.6, Dec 2000, pp. 1488-94; K. Khalsa, Herbs for Hlth, Vol.5, No.5, Nov/Dec 2000, pp.52-7; R. Shoda, et al, Am J Clin Nutr, Vol.63, No.5, May 1996, pp.741-5; G. Mingrone, et al, Am J Clin Nutr, Vol.69, No.2, Feb 1999, pp.325-30; J. Roge, et al, Lancet, Vol.337, No.8739, 23 Feb 1991, pp.502-3; L. Lih-Brody, et al, Dig Dis Sci, Vol.10, 1996, pp.2078-86; Y. Patenaude, et al, Pediatr Radiol, Vol.30, 2000, pp.379-82; Lancet, Vol.336, No.8727, 1 Dec 1990, p.1382, 1580; S. Sullivan, Lancet, Vol.336, No.8723, 3 Nov 1990, pp.1096-7; L. Delming, Hepato-Gastroenter, Vol.41, No.6, 1994, pp.549-51; M. Gleeson, et al, Lancet, Vol.344, No.8928, 8 Oct 1994, p.1028; Worst Pillts Best Pills News, Vol.6, No.12, Dec 2000, p.95; PCHRG Hlth Ltter, Vol.10, No.9, Sept 1994, p.6; F. Shanahan, Lancet, Vol.342, No.8868, 14 Aug 1993, pp.407-17; S. Rogers, No More Heartburn, NY:Kensington Pub, 2000, pp.28-46, 105-168; M. Gershon, The Second Brain, NY:HarperCollins, 1998, pp.xiii-xv, 311.

iii D. Bonn, Lancet, Vol.351, No.9117, 6 Jun 1998, p.1710; S. Bickston, Hlth News, Vol.4, No.11, 10 Sept 1998, p.4; S. Wu, et al, Lancet, Vol.337, No.8734, 19 Jan 1991, p.174-5; K. Hatake, et al, Lancet, Vol.347, No.9007, 13 Apr 1996, pp.1049-50; P. Rawsthorne, et al, Am J Gastroenter, Vol.94, No.5, May 1999, pp.1289-1302; S. Bock, Inter J Integrat Med, Vol.2, No.5, Sept/Oct 2000, p.4; S. Rogers, No More Heartburn, pp.146-7; R. Heatley, Lancet, Vol.349, No.9066, 7 Jun 1997, p.1702.

iv K. Jeejeebhoy, Am J Clin Nutr, Vol.67, No.5, May 1998,  pp.839 & B. Geerling, et al, pp. 919-26; A. Gaby, Townsend Lttr D&P, #181/2, Aug/Sept 1998, p.26; A. Riordan, et al, Lancet, Vol.342, No.8880, 6 Nov 1993, pp.1131-34; K. Mitsuyama, et al, Aliment Pharmacol Ther, Vol.12, 1998, pp.1225-30; B. Baker, Fam Pract News, 15 Oct 1999, p.8; S. Levine, Townsend Lttr D&P, #210, Jan 2001, pp.114-5; P. Peck, Fam Pract News, 1 Jun 1994, p.22; E.Hond, et al, J Parenter Enteral Nutr, Vol.23, No.1, Jan/Feb 1999, pp.7-10; N. Walker, Fresh Vegetable & Fruit Juices, Prescott::Norwalk, 1978, p.95; R. Lee, Food Integrity, Lecture April 1955, pp.26,

32; M. Murray, Am J Nat Med, Vol.4, No.6, Jul/Aug 1997, pp.8- 19; What Doctors Don't Tell You, Vol.8, No.9, Jan 1998, p.3; Nutr Rep, Feb 1996, p.13; E. Siguel, Metabol, Vol.45, No.1, 1995, pp.12-13; W. Stenson, et al, Annals Inter Med, Vol.116, No.8, 15 Apr 1992, pp.609-14; A. Belluzzi, et al, NEJM, Vol.334, No.24, 13 Jun 1996, pp.1557-60; Y. Kim, Nutr Rev, Vol.54, No.8, Aug 1996, pp.248-57; S. Greenfield, et al, Aliment Pharmacol Ther, Vol.7, No.2, Apr 1993, pp.159-66; E. Siguel, et al, Metabol, Vol.45, No.1, 1996, pp.12-23; S. Kane, et al, Ann Intern Med, Vol.132, No.8, 18 Apr 2000, p.680; Alternative Med Alert, Vol.3, No.7, Jul 2000, p.84; A. Gaby, Townsend lttr D&P, #208, Nov 2000, p.29; R. Playford, et al, Am J Clin Nutr, Vol.72, No.1, Jul 2000, pp.5-14; T. Rannem, Am J Clin Nutr, Vol.56, No.5, Nov 1992, pp.933-7; F. Kuroki, et al, Digest Dis and Sciences, Vol.38, No.9, Sept 1993, pp.1614- 18; D. Williams, Alternatives, Vol.7, No.10, Apr 1998, pp.79-80; Clinical Pearls News, Vol.10, No.7, Jul 2000, p.124; S. Bock, Internat J of Integrat Med, Vol.2, No.5, Sept/Oct 2000, pp.21-9; M. Werbach, Nutritional Influences on Illness, 2nd Ed, Tarzana: Third Line, 1993, pp.222-6 & 591-6; P & J Balch, Prescription for Nutritional Healing, 3rd Ed, NY: Avery, 2000, p.666; C. Shealy, Illustr Enzyclop of Healing Remedies, Boston:Element, 1998, p.372; G & J Kirschmann, Nutrition Almanac, 4th Ed, NY: McGraw-Hill, 1996, pp.194-5; P. Pitchford, Healing With Whole Foods, Berkeley:North Atlantic, 1993, pp.339-40; D. Frawley & V. Lad, The Yoga of Herbs, Twin Lakes:Lotus, 1988, pp.135- 152.

v S. Rogers, No More Heartburn, pp.107-9, S. Bock, Internat JIntegrat Med, p.27.

 Originally published as an issue of Nutrition News and Views, reproduced with permission  by the author, Judith A. DeCava, CNC, LNC.