How I Healed my Crohns Disease

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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My Cured My Crohns Review

Highly Recommended

I started using this book straight away after buying it. This is a guide like no other; it is friendly, direct and full of proven practical tips to develop your skills.

This ebook does what it says, and you can read all the claims at his official website. I highly recommend getting this book.

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No More Crohn's Disease

No More Crohn's Disease is a product of Cathy Rubert's personal research and many years of trial and error. This book reveals Cathys powerful 4-step plan against Chron's disease. You will learn about these 4 main natural steps that will immediately get rid of the pain in your lower abdomen. You will learn the single cheap ingredient that will bring your body's digestive system back in balance. This ingredient has the power to eliminate your pain in just days, no matter how bad your condition is. You too can start living a life free from Chrons disease with the help of her book. Read more here...

No More Crohns Disease Summary

Contents: EBook
Author: Cathy Rubert
Official Website: livecrohnsfree.com
Price: $29.95

The Crohns And Ulcerative Colitis Bible

The Isaac protocol is backed with over 50.000 hours of nutritional expertise and most importantly centered on a groundbreaking research about underlying causes of the autoimmune reaction in Crohn\'s disease and ulcerative colitis (and I am not talking about eating wrong). It is also proven by over 250 case recovery studies officially submitted and approved as legit!

The Crohns And Ulcerative Colitis Bible Summary

Official Website: crohns-colitis-bible.com

Crohns Disease

Crohn's disease is a systemic inflammatory disorder affecting the entire GI tract. Although Crohn's disease most commonly affects the distal alimentary tract, esophageal involvement does occur. One study of patients without esophageal symptoms showed evidence of esophageal involvement in 5 by upper endoscopy (21). The typical findings are small, punctuate ulcerations in the esophageal mucosa. Rarely, fissures may form leading to fistula formation with adjacent organs. When patients are symptomatic, the typical symptoms are dysphagia, odynophagia, and epigastric discomfort. See Chapter 20 for further discussion of Crohn's disease.

Full Thickness Biopsy

Full thickness biopsy is a peroperative or laparoscopic biopsy (muscularis-containing biopsy) used to diagnose motility disturbances. One incision is situated below the umbilicus, and one in the left fossa. The bowel loop is identified laparoscopically, and will then be exteriorized through the incision below the umbilicus. The full thickness biopsy of at least 10X10 mm will then be taken with a surgical knife. The bowel loop is closed with absorbable sutures, and repositioned into the abdomen (56). Drawbacks of biopsies taken at surgery are the manipulation of the patients' diet (fasting), and the bowel preparation or preoperative treatment with antibiotics (29,58). Biopsies taken at surgery have the advantage of larger sample size than endoscopic biopsies, and various analyses may be applied such as molecular typing of bacteria in intestinal tissue of Crohn's patients (59).

Differential Diagnosis

Multiple diseases can present with findings similar to those seen with Adamantiades-Behget's disease and should be considered when a patient presents with recurrent oral or genital ulcers, inflammatory eye disease, or other manifestations of vasculitis. Included in the differential diagnosis are systemic lupus erythematosus (Chapter 1), seronegative spondyloarthropathies, inflammatory bowel disease (Crohn's or ulcerative colitis) (Chapter 20), herpes or other viral infections (Chapter 10), other forms of vasculitis (Chapter 8), and inflammatory skin diseases such as pemphigus vulgaris or pemphigoid lesions (Chapter 37). All patients presenting with oral and genital ulcerations should undergo testing for herpes simplex virus using culture or polymerase chain reaction methods, to ensure that viral infection is not present.

Histopathologic Features of Colorectal Cancers with MSI

MSI-high colorectal cancers have a distinct clinicopathologic phenotype (Kim et al, 1994 Jass et al, 1998 Alexander et al, 2001). MSI-high colorectal cancers are more frequent in younger patients. Most are right-sided (proximal to the splenic flexure), bulky (large) tumors, with an exophytic growth pattern are poorly differentiated, with signet-ring-cell, mucinous, medullary, or variegated (mixed) histologic subtypes have an intense lym-phocytic response with Crohn's-like lymphoid reaction (lymphoid follicles with germinal centers at the tumor edge) and peritumoral and intratumoral lymphocytosis and show an expanding (pushing) invasive pattern at the margins. However, one third of colorectal carcinomas with MSI do not have these histologic characteristics.

Common diseasecommon variant or not

At the time of writing, there are not enough data to be able to evaluate the extent to which the CD-CV hypothesis is true. There are a number of examples of common variants for complex diseases that are known (Lohmueller et al., 2003), and also clear examples of moderate allelic heterogeneity (at NOD2 CARD15, involved in Crohn's disease Hugot et al., 2001) and functional rare variants (associated with plasma levels of HDL cholesterol and LDL, and rates of sterol absorption Cohen

Success and failure of treatment

Low CD4 cells at baseline as well as low viral load before the start of therapy are just two of many factors (Florence 2003, Kaufmann 2005, Moore 2005, Wolbers 2007). Age also plays an important role in older patients, immunological response is often only moderate in comparison to virological response. Several studies demonstrated that the probability of not achieving a rise in the CD4-cell count increases with patient age and with progressive decrease in thymus size as detected by computed tomography (Goetz 2001, Marimoutou 2001, Piketty 2001, Teixera 2001, Viard 2001, Wolbers 2007). Patients who are intravenous drug users also have relatively poor increases in CD4 cells (Dragstedt 2004). In the Swiss cohort, the CD4 cells increased more in women than in men (Wolbers 2007). Other causes for a lack of immunological response may be immuno- or myelosup-pressive concomitant therapies. We have seen patients, who have had a suppressed viral load below 50 CD4 cells l for years, who only...

Modifying the intestinal ecosystem

Linkage of the CARD15 polymorphisms and other PRR polymorphisms with a subset of human Crohn's disease incriminates defective interpretation of the local microenvironment Enteroadherent and intramucosal bacteria are increased in Crohn's disease Crohn's-like lesions that respond to antibiotics or correction of immune defect 5.4.5 Probiotic and prebiotic studies in Crohn's disease The evidence for therapeutic efficacy of probiotics in Crohn's disease is varied and inconclusive (Table 5.4). There have been very few randomised controlled clinical trials. Small patient numbers, differences in disease activity and variations in disease distribution have confounded most trials. One of the earliest studies examined the use of Saccharomyces boulardii (Biocodex Laboratories) in patients with moderately active Crohn's disease. There was a significant decrease in the Crohn's disease activity index (CDAI) compared with the control group (Plein and Hotz, 1993). S. boulardii has been used also in...

Sources of further information and advice

Canada Crohn's and Colitis Foundation of Canada Europe European Federation of Crohn's and Ulcerative Colitis Associations Ireland Irish Society for Colitis and Crohn's Disease Carmichael Centre, North Burnswick St., Dublin 7. Tel + 353 (0)1 872 1416 www.iscc.ie UK National Association for Colitis and Crohn's Disease 4 Beaumont House, Sutton Road, St Albans, Hertfordshire AL1 5HH, UK. Tel + 44 (0) 172 784 4296 (0) 845 130 2233 www.nacc.org.uk USA Crohn's and Colitis Foundation of America Greig ER, Rampton DS. Management of Crohn's disease, London Martin Dunitz, 2003.

Hereditary Nonpolyposis Colorectal Cancer

Pathologically, colorectal cancers from HNPCC patients are characterized by poor differentiation, mucin production, Crohn's-like reaction, and an intense lymphocytic infiltrate (Jass et al, 1994). Even though some of these characteristics (mucin and poor differentiation) indicate a worse prognosis, HNPCC patients with colorectal cancer have been reported to have a better prognosis stage for stage than patients with sporadic colorectal cancer (Watson et al, 1998 Lynch and de la Chapelle, 1999). It is important to note that adenomas do occur in patients with HNPCC. Currently it is believed that adenomas in patients with HNPCC progress to carcinoma more quickly than do adenomas in patients with sporadic colorectal cancer.

Colorectal Cancer Background and aetiology

Chronic inflammatory conditions often predispose to car-cinogenesis and in the colon and rectum this is best demonstrated by chronic UC. The risk of developing malignancy is related to the duration and extent of colitis. An approximate incidence of 10 per annum after a decade of extensive colitis is often cited. However, careful surveillance for dysplasia and precursor lesions followed by colectomy can reduce this risk. Similar risks and surveillance strategies apply to Crohn's colitis.

The Importance Of The Enteric Microbiota In Inflammatory Bowel Disease

Description of first susceptibility gene for Crohn's disease (CARD15 NOD2) Compelling evidence for the interactive role of genes, bacteria, and immunity has been derived from experimental animal models of both Crohn's-like and colitis-like disease (38,39). There are now about 30 different spontaneously occurring or genetically engineered (knockout or transgenic) animal models for inflammatory bowel disease (40-42). Colonization with normal enteric microbiota is required for full expression of disease. Thus, the normal microbiota is a common factor driving the inflammatory process irrespective of the genetic underlying predisposition and immunological effector mechanism (43,44). Several different microorganisms have been demonstrated to induce colitis in animal models. These include Enterococcus faecalis, causing colitis in the antiinflammatory interleukin-10 (IL-10) knockout mice, and Bacteroides vulgatus, which induced inflammation in the HLA-B27 rat model (45,46). This evidence has...

Modulation of Lymphocyte Homing for Therapeutic Purposes

Recent events have prompted intense discussion on the validity of this argument. Clinical trials with Natalizumab (Tysabri), a mAb that blocks the binding of both a401 (VLA-4) to VCAM-1 and a407 to MAdCAM-1 on Th1 cells that infiltrate the brain and gut, respectively (von Andrian and Engelhardt 2003), have shown that the mAb is efficacious in the treatment of both Crohn disease (Ghosh et al. 2003) and, especially, multiple sclerosis (Miller et al. 2003). These exciting clinical results were initially hailed as validation The gut mucosa is arguably the most paradigmatic example of tissue-specific homing. Blockade of a407 in a spontaneous model of colitis in nonhuman primates rapidly reverts the disease (Hesterberg et al. 1996). Similarly, in a chronic colitis model caused by transfer of CD45RBHi CD4 T cells into SCID mice, blocking 07 integrins and or MAdCAM-1 inhibited the development of colitis (Picarella et al. 1997). Consistent with these data, Natalizumab has been efficacious in...

Chemically Induced Responses

A wide range of animal models have been applied to studies on IBD. Naturally occurring animal models have been important tools in studies related to human ulcerative colitis and Crohn's disease. IBD-like symptoms have also been induced chemically. The application of such chemicals may induce ulceration of the intestinal mucosa as well as several immunological responses that are typical to IBD in humans. Simple methods for T-cell induced onset of IBD may be initiated by di-nitro chlorobenzene (DNCP) as described by Glick and Falchuk (127). This method involves both systemic and local application of DNCP. Other chemically induced forms of IBD may be induced by intra

Microbial Degradation of Mucin

Mucin in the GI tract is produced by goblet cells in the mucosa and glandular mucous cells in the submucosa. Mucin consists of a peptide core with oligosaccharide side chains O-glycosidically bound, and it has several important physiological and patho-physiological roles. It acts as lubricant, as a barrier and stabilizer for the intestinal microclimate as well as a source of energy for the microbiota. There is growing evidence that the mucin pattern may be a relevant issue to take into account in the pathophysiology of some intestinal diseases, such as ulcerative colitis, Crohn's disease, gastric and duodenal ulceration, and colon adenocarcinoma.

Steps to Effective Bowel Management

The cause of the dysfunction or problem is diagnosed, the wrong treatment may be prescribed, leading to an unfavorable outcome. The assessment should include the following vital signs hydration status abdominal status perianal or peristomal skin integrity frequency of bowel movements in the previous 2 weeks consistency of stool (liquid, soft formed, or hard and hard to eliminate) number of impactions since cancer diagnosis appetite (ranging from 3 big meals per day to only sips of liquid) daily fluid intake daily fiber intake medications currently being taken, particularly those that affect bowel elimination presence of abdominal pain or cramping concomitant diseases that affect bowel function (e.g., diabetes, Crohn's disease, and irritable bowel syndrome) presence of abdominal distention frequency of bowel movements before cancer diagnosis usual time of day that bowel movements occur effective corrective measures previously used for bowel problems extent of cancer current treatments...

Acquired anorectal disorders

Rarely, Crohn's disease and immunodeficiency can present with laterally located anal fissures. Perianal abscess occurs commonly in infants and is treated by incision and drainage. Approximately one third of abscesses develop into a fistula-in-ano. Fistulas which persist after infancy are treated by fistulectomy. Crohn's disease should be considered in older children with multiple fistulas.

The pathogenesis of IBD

Both Crohn's disease and ulcerative colitis represent the clinical outcome of a complex interaction of immune, genetic, and environmental factors. The normal physiological response to indigenous micro-organisms is one of immunological quiescence. Deviations from this, and in particular, genetically-influenced aberrant immune responses to luminal antigens are now recognised to underlie IBD. The intestinal barrier can be impaired in IBD. Defects in epithelial barrier function may precede the onset of inflammation and lead to persistent immune activation (Irvine and Marshall, 2000). Leukocyte recruitment from the gut vasculature contributes to the initiation and perpetuation of mucosal inflammatory responses. Upregulation of various transcription factors including nuclear factor (NF)-kB, the master coordinator of immune responses to danger signals, drives the subsequent excessive local release of a diverse array of immune mediators. These include cytokines, growth factors, reactive...

Inflammatory Autoimmune

Crohn's disease is an inflammatory disease of the GI tract, of unknown etiology. It is characterized by mucosal ulceration that extends through all layers of the digestive tract wall and is not limited to any one area of the GI system from mouth to anus. Approximately 10 of patients with Crohn's disease have pharyngeal involvement. Most commonly, ulcerative lesions are seen on the pharyngeal walls. The epidemiology, pathogenesis, diagnosis, treatment, and prognosis are discussed in more detail in Chapter 20.

Some success stories

In 2001 three papers reported on the association between the gene NOD2 and Crohn's disease (an inflammatory bowel disease), however, the paths of the research that led to these independent findings were quite different. The first (Hugot et al., 2001) followed the classic research paradigm of genome-wide linkage study (which identified the pericen-tromeric region of chromosome 16), fine mapping study (where more microsatellite markers are genotyped in the linkage region) and association study. This study identified three causal mutations, a single base-pair insertion (3020Cins) and two missense variants. In contrast, the other studies (Hampe etal., 2001 Ogura etal., 2001) selected the NOD2 gene as a candidate gene based on position (within the reported linkage region), structural homology to plant apoptosis regulatory and disease resistance genes and known function of NOD proteins in recognizing bacterial components. Both studies identified the single base-pair insertion and reported...

Future trends

Although naturally occurring probiotics may have insufficient efficacy in Crohn's disease, the genetic modification of commensal bacteria for the site-specific delivery of therapeutic molecules represents a realistic pharmabiotic strategy. Proof of principle has already been demonstrated in animal models of enterocolitis. Genetically engineered Lactococcus lactis has been used to deliver anti-inflammatory IL-10 or the cytoprotective trefoil factor locally to the gut (Steidler et al., 2000 Vandenbroucke et al., 2004). The safety issues related to genetic modification have been addressed by replacing the thymidylate synthase (thy A) gene in L. lactis with a synthetic therapeutic transgene. When the modified bacteria are deprived of thymine or thymidine they are not viable. Neither thymine nor thymidine are readily available in the external environment, thereby limiting the viability of the excreted organism. Moreover, the transgene would be eliminated from the bacterial genome if the...

Epidemiology

One of the major clues to MS etiology comes from analysis of the remarkable worldwide pattern of MS. This shows a crude but inconsistent north-south gradient in North America and Europe a lower prevalence in most of Asia, Africa, and South America (although many of these studies are less than definitive because of uncertainty about the completeness of case ascertainment) and a reverse south-north gradient in Australia and New Zealand (Chapters 1 and 2). This nonrandom pattern is different from that seen with many other acute or chronic autoimmune diseases of the central and peripheral nervous systems (PNS), such as acute disseminated encephalomyelitis (ADEM), the Guillain-Barre syndrome (GBS), and chronic inflammatory demyelinating polyneuropathy (CIDP) however, a similar worldwide pattern can be seen for type 1 diabetes in Europe and other allergic or autoimmune disorders such as Crohn's disease are not randomly distributed (15).

Fistulainano

The so-called 'cryptoglandular hypothesis' ascribes the aetiology of fistula-in-ano to the glands that sit in the inter-sphincteric space around the anal canal. Spread of sepsis from an infected gland leads to perianal abscess which usually presents acutely (see above). Epithelialisation of the track leads to establishment of a fistula-in-ano. A classification of fistulas by the late Sir Alan Parks in 1976, described four main groups intersphincteric, transsphincteric, supras-phincteric and extrasphincteric. A full assessment of a fistula-in-ano requires the identification of the internal and external openings, the primary track, any secondary extension and any diseases complicating the situation. Extensions occur in approximately 10-15 of patients, and are more prevalent in recurrent or Crohn's fistulas.

Genetic factors

The genetic component of IBD was initially suggested by early reports of familial aggregation of these diseases. In 1934, Crohn and colleagues reported the first familial aggregation of CD. In the 1950s and 1960s many other groups confirmed that IBD are more familial than expected by chance. On average, 6-8 of UC patients and 8-10 of CD patients have at least one affected relative (for review see Russell and Satsangi, 2004). Interestingly, values as high as 20 or more have been reported in children, suggesting that either pediatric CD is more genetic or that familial environmental risk factors are important. The non-random distribution of the affected siblings within sibships with multiple cases strongly argues for the second hypothesis of an environmental factor shared by nuclear family members (Hugot et al., 2003b). Crohn's disease Ulcerative colitis Total cases

Stomatitis

Herpangina

Stomatitis refers to an inflammatory process involving the mucous membrane of the mouth that may manifest itself through a variety of signs and symptoms including erythema, vesiculation, bulla formation, desquamation, sloughing, ulceration, pseudomembrane formation, and associated discomfort. Stomatitis may arise due to factors that may be of either local, isolated conditions or of systemic origin. For example, a solitary oral ulcer with a history of a recurrent pattern may be classified as recurrent aphthous stomatitis, a purely local phenomenon. Another clinically-similar-appearing lesion, on the other hand, may represent an oral mucosal manifestation of a more generalized disease process such as Crohn's disease. Stomatitis may involve any site in the oral cavity, including the vermillion of the lips, labial buccal mucosa, dorsal ventral tongue, floor of mouth and hard soft palate, and gingivae. Patients will generally relate a history of recurrence of similar lesions. One of the...