Crohns Disease Causes and Treatment

Cured My Crohns

If you've ever gotten the fateful diagnosis you've got Crohns, you will know the massive upset that it can have on your way of life and how you feel about yourself and your relationship to other people. If you talk to your doctor about natural diets or some other method of curing your Crohns disease they will tell you that there is no way to fix it. However, there is often more to the story than modern medicine will tell you. New Age medicine is not a bunch of nonsense that hokey people subscribe to; New Age medicine fills in the gaps of knowledge that we have with modern medicine and helps us understand what is going on with our bodies. You will learn how to cure Crohns from someone who has cured it himself and has lived for over 10 years completely free of disease!

Cured My Crohns Summary


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No More Crohn's Disease

If you are looking for an easy, safe, and affordable way to get rid of Chron's disease, you need No More Crohn's Disease by Cathy Rubert. Cathy used to suffer from this terrible disease too, but when she discovered the techniques she shares in No More Crohn's Disease, she was able to heal herself in the safest and most natural way. Inside her book you will discover how to quickly and easily implement the 4-main all-natural steps that will immediately start combating Crohn's Disease (put the simple steps into action and Crohn's Disease will become a problem from the past!) Time to be freed from the pain and discomfort caused by Chron's disease. With the help of Cathy Rubert's No More Crohn's Disease, you can now enjoy an effective cure without the costly trips to the doctor. You will also be safe from any side effects because the entire program is natural. Read more here...

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Inflammatory Bowel Disease Ulcerative Colitis and Crohns Disease

There are two major forms of chronic inflammatory bowel disease (IBD). Ulcerative colitis is an ulcerative disorder of the mucosa of the colon, whereas Crohn's disease is characterized by transmural inflammation, most often in the small intestine. Both produce abdominal pain and diarrhea, which can be bloody. iBd tends to wax and wane, with periods of intense active disease followed by long periods of remission. Although the cause is not clear, IBD appears to be an autoimmune reaction, in which overzealous immune cells attack the tissues of the intestinal wall. for hospital care and intestinal surgery. Food sensitivities may aggravate IBD, and identification and avoidance of offending foods may increase chances of remission.14 During acute exacerbations of Crohn's disease, enteral nutrition with protein hydrolysate diets is effective and reduces need for steroid therapy.15

Crohns Disease

The incidence of Crohn's disease has been rising steadily. Crohn's disease is a chronic transmural inflammation that may involve any portion of the gastrointestinal tract but most commonly involves the ileum. Malnutrition, due to reduced dietary intake, malabsorption, enteric loss of nutrients, increased caloric needs, and drug-nutrient interactions, accompanies Crohn's disease in 25-80 of cases 1,2 . The nutritional status of patients with Crohn's disease is already affected negatively at the time of diagnosis 3 . Considering that malnutrition has a negative effect on morbidity and mortality of hospitalised patients 2, 4 , an early diagnosis is of great importance to improve the prognosis of these patients. In the following sections, malnutrition in Crohn's disease is discussed according to the deficiency of macronutrients (protein and energy) and micronutrients (vitamins, minerals and electrolytes) (Table 1).

Colon Cancer as an Example of Inflammatory Induced Cancer

In earlier studies, we demonstrated the importance of the IL-6 trans-signaling pathway for the maintenance of chronic inflammatory bowl disease (Crohn disease) (Atreya et al. 2000). Interestingly, our studies showed that in Crohn disease patients the T cells from gastric tissue are extremely resistant to apoptosis. Biochemical examinations showed that these T cells produced large amounts of IL-6 and that the intracellular JAK-STAT signal transduction pathway was activated. Surprisingly, treatment of these cells with a neutralizing monoclonal antibody to IL-6R induced apoptosis, although the cells lacked a membrane form of the IL-6R. As the treatment of the cells with sgp130 also induced apoptosis, this effect must have been mediated via the IL-6 trans-signaling pathway (Fig. 2). This finding showed that IL-6 trans-signaling is responsible for the surveillance of activated T cells within gastric tissue from Crohn disease patients by inhibiting apoptotic processes. The sIL-6R needed for...

The Intestinal Stem Cell Niche Studied Through Conditional Transgenesis

Despite a wealth of experimental data, the precise mechanisms governing the maintenance and regeneration of the intestine remain relatively poorly elucidated. After physical or genetic injury, stem cells from the intestinal crypt are killed and the subsequent repopulation process recruits new stem cells from sources currently unknown. Understanding the genetic elements that determine stem cell fate and the basis by which repopulation occurs will greatly aid our understanding of both stem cell plasticity and the contribution made by the stem cell compartment to malignant disease. It would also provide a better platform to develop therapies to regenerate damaged intestinal epithelia as seen after radiation injuries or inflammatory bowel disease such as Crohn's disease. In this review we discuss some of the basic mechanisms that regulate intestinal stem cell viability and maintenance, and also summarise recent data from our laboratory on the requirement for the Wnt pathway in...

Calcium and Vitamin D

Osteoporosis is increasingly being recognised as a leading extra-intestinal complication of inflammatory bowel disease. Calcium is absorbed in the proximal small intestine by a vitamin D-depend-ent Ca2+-binding protein, and vitamin D is absorbed in the duodenum and jejunum. Therefore, in Crohn's disease patients with extended inflammation or resection of the small intestine, osteoporosis results from impaired absorption of calcium and vitamin D. However, there are also some conflicting data suggesting that many factors, other than calcium or vitamin D deficiency, contribute to the pathogenesis of osteoporosis in Crohn's disease 23, 24 . These factors include cytokines, such as TNF-a, that disproportionately stimulate osteoclast activity, or corticosteroid usage 25, 26 . Overt vitamin D deficiency disease may occur in Crohn's disease patients and patients often present with bone pain and mild myopathy. Other symptoms at presentation include bone pain and mild myopathy.

Inflammatory Bowel Diseases

The inflammatory bowel diseases (IBD), which include Crohn's disease (CD) and ulcerative colitis (UC), are chronic inflammatory disorders effecting 0.3 of the Western population (Podolsky 2002). CD can affect any part of the gastrointestinal tract, from the oral cavity to the anus, whereas UC is limited to the colon and rectum. The etiology of CD and UC remains unknown, but it probably involves a combination of genetic predisposition, environmental conditions, and abnormalities in immune regulation (Chutkan 2001 Farrell et al. 2001 Podolsky 2002). In particular, the intestinal mucosal immune system

Stages Of Diverticulitis

Patients usually present with visceral pain that localizes later to the left lower quadrant and that is associated with fever, nausea, vomiting, or constipation. A right lower quadrant presentation would not exclude this diagnosis because ascending colon or cecal diverticulitis can occur. If a colovesical fistula is present, the patient may present with pneumaturia or fecaluria (a virtually pathognomic finding). On examination, the patient may have localized left lower quadrant tenderness or more diffuse abdominal tenderness with peritoneal irritation signs, such as guarding or rebound tenderness. The differential diagnosis includes painful diverticular disease without diverticulitis, acute appendicitis, Crohn disease, colon carcinoma, ischemic colitis, irritable bowel syndrome, and gynecologic disorders such as ruptured ovarian cyst, endometriosis, ectopic pregnancy, and pelvic inflammatory disease.

Test Methodology 104 Fecal Fat Analysis

A D-xylose absorption test is an indirect but specific method for assessing mucosal absorption of the small intestine. D-Xylose is not normally present in blood or urine and digestive enzymes are not necessary for its metabolism. Normally, approximately 60 of D-xylose taken in an oral dose will pass through the intestinal mucosa and, over time, into the circulatory system, eventually to be excreted into urine. Low absorption of xylose will occur in disorders of the small intestine, such as intestinal malabsorption, Crohn's disease, celiac disease, AIDS, pellagra, and ascariasis.

Inflammatory Bowel Disease

Thirty-five patients (17 women and 18 men) with inflammatory bowel disease (IBD) were followed prospectively for 19 months with BMD measurements at the PA lumbar spine and proximal femur with DXA (Hologic QDR-1000) (58). Fourteen patients had Crohn's disease and 21 had ulcerative colitis. They ranged in age from 17 to 60 years with a mean age of 36 years. Crohn's disease patients lost 3.08 4.91 per year in the lumbar spine and 6.91 6.57 per year in the femoral neck. Ulcerative colitis patients without ileoanal anastomosis lost 6.42 7.5 per year in the lumbar spine and 5.59 11.12 per year in the femoral neck. No ulcerative colitis patient with ileoanal anastomosis had a significant bone loss from either site. Patients on steroids had mean bone loss of 6.23 7.04 per year in the spine and 8.97 9.57 per year in the femoral neck. Patients not on steroids had gains of 0.87 0.002 per year in the spine and 0.20 5.78 per year in the femoral neck. In another study of 79 patients with IBD (34...

Absorption And Transport

In stagnant loop syndrome (bacterial overgrowth which competes for the available cobalamin and can be remedied by a broad-spectrum antimicrobial), ileal resection, Crohn's disease and chronic tropical sprue affecting the terminal ileum, vitamin B12 deficiency is common although megaloblastic anaemia occurs only relatively late. The fish tape worm Diphyllobothrum latum which can infest humans who eat raw or partially cooked freshwater fish roe can grow up to 10 meters in the gut and competes for ingested cobalamin.

What is Mycobacterium avium subsp paratuberculosis and how is it controlled

Mycobacterium avium subsp. paratuberculosis (MAP) causes paratuberculosis, or Johne's disease, an inflammatory bowel disease affecting ruminants. This disease is chronic and contagious and eventually results in death of affected animals. In the US, approximately 22 of the dairy herds are affected with Johne's disease. Infected dairy cattle are able to shed MAP in milk. This pathogen has been epidemiologically implicated in association with Crohn's disease in humans. While pasteurisation is thought to provide public health protection from this organism, several studies have revealed the presence of MAP in retail fluid pasteurised milk.

Gastrointestinal and Respiratory Epithelium

Avidine Biotine Peroxydase

Stomach and the intestines have a non-stratified epithelium rapidly renewed from the bottom of the intestinal crypts or glands. Like many other simple epithelia, these epithelial cells do not show hyaluronan except for a little in the basolateral surfaces of some cells at the bottom of the crypts (Fig. 3d) (34). However, the enterocytes become positive for hyaluronan and CD44 in the immunological injury caused by Crohn's disease and celiac disease (Kemppainen et al., unpublished data). Introduction of allergens increases hyaluronan in the gut lumen (35). Likewise, transformation of the colon epithelial cells is frequently accompanied by the expression of hyaluronan, while normal colon epithelium is virtually hyaluronan free (Fig. 3g and h) (23). In colon cancer cells, the level of hyaluronan is a strong, unfavorable prognostic indicator of the patient survival (36). The emergence of hyaluronan expression on gastric cancer cells (Fig. 3e) shows a similar negative correlation with the...

951 IL6 Knockout and Transgenic Mice

When sections of the liver were cut away, the mice would deteriorate and die. However, when the mice were pretreated with IL-6, hepatocyte proliferation returned to normal and liver damage was prevented. Thus, IL-6 therapy may be of benefit in patients undergoing liver transplant, or in those suffering from cirrhosis or chronic hepatitis, which are characterized by liver degeneration. The possible role of IL-6 in autoimmune disease is made apparent with trans-genic mice that overexpress the cytokine and show an increase in agalactosyl IgG (499). This immunoglobulin is increased in a variety of autoimmune diseases such as RA, Crohn's disease, type I diabetes, and pulmonary TB (500-502). Transgenic overexpression of IL-6 in the CNS can lead to significant neurodegeneration and subsequent motor uncoordina-tion, ataxia, and tremor (503).

Alphaglucosidase inhibitor blocks hydrolysis of an

Credentialing - the processes involved in identifying those institutions and individuals meeting acceptable standards in areas of accreditation, certification, or licensure cretinism - growth deficiency and mental retardation Crohn's disease - inflammatory disease of the gastrointestinal tract that can lead to intestinal obstruction

Nonsnp Technology The Protein Chip Microfluidics And Assorted Engineering Marvels

Glycominds Ltd. (Lod, Israel,, Figure 19.2C) has developed several protocols for detecting carbohydrate moieties from a variety of substrates, including intact cells 15 . The concept of a glycomics profile is becoming widely accepted, as many debilitating diseases (such as Crohn's disease) are characterized by variant carbohydrate levels in the blood. Protein arrays face numerous challenges narrowing the field of protein detection down to a clinically relevant

Resuscitation Promoting Factors

J. (2003) Is Crohn's disease caused by a mycobacterium Comparisons with leprosy, tuberculosis, and Johne's disease. Lancet Infect. Dis. 3, 507-514. 75. Hermon-Taylor, J. and Bull, T. (2002) Crohn's disease caused by Mycobacterium avium subspecies paratuberculosis a public health tragedy whose resolution is long overdue. J. Med. Microbiol. 51, 3-6.

Vitamins Minerals and Electrolytes

A wide array of vitamin, mineral, and electrolyte deficiencies frequently occurs in Crohn's disease patients and with variable clinical significance. These deficiencies may result from extensive inflammation, surgical resection of small bowel, or both, and require haematological and biochemical examination. The prevalence of decreased nutrient levels among patients with Crohn's disease is summarised in Table 2. Of particular clinical relevance is the deficiency in iron, vitamin B12, folate, calcium, vitamin D, and zinc. Table 2. Prevalence of nutritional deficiencies among patients with Crohn's disease. (Data from 20 )

Clinical Presentation

Anemia with an elevated MCV. macrocytic anemia, is most often a manifestation of folate or vitamin B,, deficiency. The presence of macrocytic anemia. with or without the symptoms previously mentioned, should lead to further testing to determine Bp and folate levels. An elevated methylmalonic acid (MMA) level can be used to confirm a vitamin B,2 deficiency. Folate deficiency anemia is usually seen in alcoholics, whereas B 2-deficiency anemia mostly occurs in people with pernicious anemia, a history of gastrectomy, diseases associated with malabsorption (e.g bacterial infection, Crohn disease, celiac disease), and strict vegans (rare).

Conclusion and Clinical Perspectives

Interestingly, recent investigation of Nod family proteins, which may function as intracellular pattern-recognition sensors, has yielded information relevant to clinical diseases. In particular, mutation of Nod2 is thought to be associated with Crohn's disease (114,115), which, along with ulcerative colitis, are the prominent inflammatory bowel disorders. Nod2 acts as a signal modulator alongside TLR signals, and Nod2 mutation found in Crohn's disease results in enhanced NF-kB and cytokine signals (116-118). Further studies of Nod proteins will provide useful information that complements the investigation of TLR signal regulation outlined in this chapter. 114. Hugot, J. P., Chamaillard, M., Zouali, H., et al. (2001) Association of NOD2 leucine-rich repeat variants with susceptibility to Crohn's disease. Nature 411, 599-603. 115. Ogura, Y., Bonen, D. K., Inohara, N., et al. (2001) A frameshift mutation in NOD2 associated with susceptibility to Crohn's disease. Nature 411, 603-606. 117....

Is Hyperalgesia Limited to the Gut in Irritable Bowel Syndrome

The first studies to investigate visceral sensitivity in IBS concluded that enhanced sensitivity in IBS was limited to the gut (43-46). Interestingly, two prior studies have examined cutaneous pain in IBS patients using electrocutaneous stimulation (43,44). In one study, 13 patients with Crohn's disease, 13 control subjects, and 12 patients with IBS had electrodes positioned on the skin of their hands (44). Touch threshold, defined as the current just detectable by the subject, and pain threshold, defined as the current at which the subject first described the stimulus as painful, were significantly higher in both IBS and Crohn's disease, compared to normal subjects. A later study compared somatic transcutaneous electrical nerve stimulation in 17 patients with IBS and 15 healthy controls (43). The perception threshold and threshold for discomfort were both higher in the IBS subjects than controls. A possible limitation common to both studies is that the thresholds for perception and...

The Cancerogenicity Of Cya Experience From Other Immunemediated Diseases

CyA has been proposed as a rapid acting alternative or adjunct to other drugs for refractory inflammatory bowel diseases (IBD). Only a high, and potentially more toxic, dosage seems to be effective for severe ulcerative colitis (UC) and fistulous Crohn's disease, therefore CyA may be used as a rescue therapy for short intervals 3 . It is well known that UC bears an intrinsic risk of colonic cancer which would makes the use of an immunosuppressant like CyA for long periods rather worrisome, but as far as we know, no malignancy due to CyA has been reported in patients with IBD, in particular no colonic cancer has been observed either during or after treatment 89, 90 ,

The Mycobacterium avium Complex

MAC includes a variety of genetically related species with diverse pathogenic potential (10). M. avium subsp. avium (Maa) is common in the environment. It causes avian tuberculosis and sporadic infections of wild mammals (e.g., deer), as well as opportunistic infections in immunocompromised humans. M. avium subsp. silvaticum (Mas), the so-called wood pigeon bacillus, is primarily a bird pathogen. M. avium subsp.paratuberculosis (Map) causes Johne's disease and, although the hypothesis remains controversial, has been implicated as a cause of Crohn's Disease, a chronic inflammatory bowel disease in humans (73-75). MAC organisms exhibit greater heterogeneity than members of the M. tuberculosis complex. Multiple sequevars have been revealed by rDNA analysis and unidirectional deletion events cannot account for relationships between all isolates (9,76). Different branches appear to have acquired new genetic material via horizontal transfer (77). Genome comparison of Maa strain 104 (a human...

Test Methodology 101 Vitamin Testing In The Clinical

Vitamin B12 deficiency may result from infestation of intestinal parasites such as Diphyllobothrium latum that compete for the vitamin, stomach removal surgery or ileal resection, celiac sprue, Crohn's disease, or drugs such as alcohol, neomycin, or para-acetylsalicylic acid. Crohn's disease - inflammatory disease of the gastrointestinal tract that can lead to intestinal obstruction

Potential Risks of AntiTNFa Therapy

Inhibition Tnf

Infliximab is a chimeric (human-murine) IgGlK monoclonal antibody with an approximate molecular weight of 149100 daltons, in the pharmacological class of selective immunosuppressive agents. It is composed of human-constant and murine-vari-able regions and binds specifically to human TNF-a with an association constant of 10-10 M (Fig. 1). Infliximab has a well-documented safety profile throughout clinical development and in post-marketing safety surveillance for the approved indications of Crohn's disease and RA 62-65 . The FDA reported on the risks of histoplasmo-sis 71 , lymphoma 72 , and or listeriosis 73 . The Mayo clinic reviewed the safety of infliximab in 500 Crohn's patients treated with infliximab

Protein Energy Malnutrition

The main cause of protein-energy malnutrition in Crohn's disease patients is anorexia, probably resulting from postprandial abdominal pain, diarrhoea, dietary restriction, and the side effects of medications 5,6 . In addition, animal studies have shown that anorexia can result from increased levels of tumour necrosis factor (TNF)-a, interleukin (IL)-1, and other cytokines 7, 8 . These weight-loss-inducing cytokines increase the expression of leptin mRNA in adipose tissue as well as plasma Table 1. Nutritional problems of patients with Crohn's disease. (Data from 9 ) levels of leptin, despite the decrease in food intake that normally suppresses leptin expression 1011 . Thus, leptin may also be involved in anorexia accompanying Crohn's disease. In contrast, Lanfranchi and Geerling showed that energy intake was not decreased, but tended to increase in patients with Crohn's disease in the stage of remission or low activity 13, 14 . These results suggest that the amount of dietary intake...


The precise mechanism involved in the development of Crohn's disease is unknown however, the effects of oxidative stress on the bowels of patients with active Crohn's disease are thought to play a role 29,30 . Unlike normal conditions in the intestine, an imbalance between endogenous anti-oxidant defences and free-radical production is seen in Crohn's disease 31 . Circulating nutritional antioxidants, such as p-carotene, vitamin C, vitamin E, selenium, and zinc, are important factors in the prevention of free-radical-mediated tissue injury however, serum concentrations of these anti-oxi-dants were reported to be low in patients with Crohn's disease 32 , whereas no clinical signs of deficiency were seen.

Nutritional Support

The indications for nutritional support of patients with Crohn's disease are largely based on clinical experience, although the role of enteral diets for inducing remission continues to be debated. Three meta-analyses on enteral nutrition as primary therapy in Crohn's disease have been published 33-35 . These reports similarly demonstrate that clinical remission is more often successfully induced with corticosteroids than enteral diets, although enteral nutrition remains an important therapeutic tool. The precise mechanism by which an enteral diet induces remission in Crohn's disease is not understood, although several mechanisms of action have been proposed, including reduction of immune stimuli in the gut 36 , nutritional improvement 37 , bowel rest, a trophic effect of glutamine 38 , and reduction of intestinal permeability 39 . In any event, more randomised, controlled trial data subjected to meta-analyses are required to confirm the clinical effect of enteral nutrition in the...

Bradykinin Receptors

In 66 of serosal afferents (84), an effect that was mediated via B2 receptors, and responses to probing were potentiated after bradykinin. In this study, another group of bradykinin-responsive LSN afferents were mechanically insensitive. Fewer (11 ) mouse pelvic nerve serosal afferents responded to bradykinin, and no mechanically insensitive pelvic nerve afferents were recruited by bradykinin. This suggests differences in the way each pathway signals bradykinin activation and reveals a chemospecific population of afferents. Interestingly, Bx but not B2 receptor protein is significantly increased in the intestines of both active ulcerative colitis and Crohn's disease patients compared with controls (116), but the relationship of this to symptoms is not known.

Secretory Diarrhoeas

The main drugs used in the treatment of ulcerative colitis and Crohn's disease are the aminosalicylates and corticosteroids. Their mode of action is obscure. Other immunosuppressives also have a role and recent studies into the mechanisms of inflammation are leading to the introduction of novel therapies to inhibit the inflammatory process.

Vitamin B12

Since Crohn's disease frequently involves the terminal ileum, where the vitamin B12-intrinsic factor complex is absorbed, serious impairment of the enterohepatic circulation of vitamin B12 is commonly observed in Crohn's disease patients. Moreover, because vitamin B12 stores in the liver must decrease before serum concentrations become low, the incidence of decreased vitamin B12 stores is probably quite high 21 . Megaloblastic anaemia is commonly seen with vitamin B12 deficiency however, the patient seldom manifests symptoms of deficiency, such as paresthaesia, numbness, gait

Approach To Colitis

The differential diagnosis for colitis includes ischemic colitis, infectious colitis (C. difficile. E. coli, Salmonella, Shigella, Campylobacter), radiation colitis, and IBD (Crohn disease versus ulcerative colitis). Mesenteric ischemia usually is encountered in people older than 50 years with known atherosclerotic vascular disease or other cause of hypoperfusion. The pain usually is IBD is most commonly diagnosed in young patients between the ages of 15 and 25 years. There is a second peak in the incidence of IBD (usually Crohn disease) between the ages of 60 and 70 years. IBD may present with a low-grade fever. The chronic nature of the patient's disease (several months) is typical for IBD. The hemoglobin level of 10.3 g dL suggests that the patient likely has been slowly losing blood in his stool for at least a few weeks to months. Patients with IBD often present with fatigue and weight loss. Ulcerative colitis usually presents with grossly bloody stool, whereas symptoms of Crohn...

Inflammation Marker

In addition to reactive oxygen species, inflammatory cells and cytokines are also found in tumors, which mediate the inflammatory pathway (e.g., NF-kB and COX-2) and are likely to contribute to tumor growth and progression. They increase cell cycling, cause the loss of tumor suppressor function, and stimulate oncogene expression, all of which may lead to malignancy. For example, both hereditary and sporadic forms of chronic pancreatitis are associated with an increased risk of developing pancreatic cancer. The combined increase in genomic damage and cellular proliferation, both of which are seen with inflammation, strongly favors the malignant transformation of pancreatic cells (4,5). Ulcerative colitis and colonic Crohn's disease (known collectively as inflammatory bowel disease IBD ) are both associated with increased risk for colorectal cancer (6). The genetic alterations found in ulcerative colitis associated colorectal cancer involve many of the same targets found in sporadic...